	type	lncrna	mir	gene	tissue/cells	disease	species	experimental	pubmed	title	description	mirid	cite
1	LncRNA	IPS1	miR-399	PHO2	Arabidopsis Thaliana	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	17643101	Target mimicry provides a new mechanism ofr regulation of microRNA activity	IPS1 contains a motif with sequence complementarity to the phosphate (Pi) starvation-induced miRNA miR-399, but the pairing is interrupted by a mismatched loop at the expected miRNA cleavage site. We show that IPS1 RNA is not cleaved but instead sequesters miR-399. Thus, IPS1 overexpression results in increased accumulation of the miR-399 target PHO2 mRNA and, concomitantly, in reduced shoot Pi content. Engineering of IPS1 to be cleavable abolishes its inhibitory activity on miR-399. We coin the term ‘target mimicry’ to de ne this mechanism of inhibition of miRNA activity. Target mimicry can be generalized beyond the control of Pi homeostasis, as demonstrated using arti cial target mimics.	MI0001020	Nat Genet 2007 Aug 39, 1033-7 doi:10.1038/ng2079 PMID:17643101
2	Artifically engineered RNA	MIM156	miR-156	SPL	Heynh (Ecotype Col-0)	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	17643101	Target mimicry provides a new mechanism ofr regulation of microRNA activity	To demonstrate that target mimicry provides insight into general principles of miRNA function, we modified the miR-399–complementary motif of IPS1 to mimic target sites for miR-156 (‘MIM156’) and miR-319 (‘MIM319’). In contrast to the weak effects previously reported for overexpression of cleavable miR-156 or miR-319 target sites, we found that plants overexpressing MIM156 and MIM319 had marked phenotypes.	MI0000178	Nat Genet 2007 Aug 39, 1033-7 doi:10.1038/ng2079 PMID:17643101
3	Artifically engineered RNA	MIM139	miR-139	NA	Heynh (Ecotype Col-0)	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	17643101	Target mimicry provides a new mechanism ofr regulation of microRNA activity.	To demonstrate that target mimicry provides insight into general principles of miRNA function, we modified the miR-399–complementary motif of IPS1 to mimic target sites for miR-156 (‘MIM156’) and miR-319 (‘MIM319’). In contrast to the weak effects previously reported for overexpression of cleavable miR-156 or miR-319 target sites, we found that plants overexpressing MIM156 and MIM319 had marked phenotypes.	MI0000261	Nat Genet 2007 Aug 39, 1033-7 doi:10.1038/ng2079 PMID:17643101
4	Artifically engineered RNA	Drosophila microRNA sponge (miR-7SP)	miR-7	NA	Transgenic Fruitflies	NA	Drosophila (flies)	Western blot;qRT-PCR	19915559	Transgenic microRNA inhibition with spatiotemporal specificity in intact organisms	Here we introduce the Drosophila melanogaster microRNA sponge (miR-SP) as a powerful transgenic technology to dissect the function of everymicroRNA with precise spatiotemporal resolution. miR-SPs can be used to characterize tissue-specific microRNA loss-of-function phenotypes, define the spatial regulation of their effectors and uncover interactions between microRNAs and other genes. Using themiR-SP system, we identified an essential role of the conserved microRNA miR-8, in neuromuscular junction formation. Tissue-specific silencing revealed that postsynaptic activity of miR-8 is important for normal neuromuscular junction morphogenesis.	MI0008947	Nat Methods 2009 Dec 6, 897-903 doi:10.1038/nmeth.1402 PMID:19915559
5	Artifically engineered RNA	Drosophila microRNA sponge (miR-8SP)	miR-8	NA	Transgenic Fruitflies	NA	Drosophila (flies)	Western blot;qRT-PCR	19915559	Transgenic microRNA inhibition with spatiotemporal specificity in intact organisms	Here we introduce the Drosophila melanogaster microRNA sponge (miR-SP) as a powerful transgenic technology to dissect the function of everymicroRNA with precise spatiotemporal resolution. miR-SPs can be used to characterize tissue-specific microRNA loss-of-function phenotypes, define the spatial regulation of their effectors and uncover interactions between microRNAs and other genes. Using themiR-SP system, we identified an essential role of the conserved microRNA miR-8, in neuromuscular junction formation. Tissue-specific silencing revealed that postsynaptic activity of miR-8 is important for normal neuromuscular junction morphogenesis.	MI0008945	Nat Methods 2009 Dec 6, 897-903 doi:10.1038/nmeth.1402 PMID:19915559
6	Artifically engineered RNA	Drosophila microRNA sponge (miR-9aSP)	miR-9a	NA	Transgenic Fruitflies	NA	Drosophila (flies)	Western blot;qRT-PCR	19915559	Transgenic microRNA inhibition with spatiotemporal specificity in intact organisms	Here we introduce the Drosophila melanogaster microRNA sponge (miR-SP) as a powerful transgenic technology to dissect the function of everymicroRNA with precise spatiotemporal resolution. miR-SPs can be used to characterize tissue-specific microRNA loss-of-function phenotypes, define the spatial regulation of their effectors and uncover interactions between microRNAs and other genes. Using themiR-SP system, we identified an essential role of the conserved microRNA miR-8, in neuromuscular junction formation. Tissue-specific silencing revealed that postsynaptic activity of miR-8 is important for normal neuromuscular junction morphogenesis.	MI0008995	Nat Methods 2009 Dec 6, 897-903 doi:10.1038/nmeth.1402 PMID:19915559
7	Artifically engineered RNA	Drosophila microRNA sponge (miR-276aSP)	miR-276a	NA	Transgenic Fruitflies	NA	Drosophila (flies)	Western blot;qRT-PCR	19915559	Transgenic microRNA inhibition with spatiotemporal specificity in intact organisms	Here we introduce the Drosophila melanogaster microRNA sponge (miR-SP) as a powerful transgenic technology to dissect the function of everymicroRNA with precise spatiotemporal resolution. miR-SPs can be used to characterize tissue-specific microRNA loss-of-function phenotypes, define the spatial regulation of their effectors and uncover interactions between microRNAs and other genes. Using themiR-SP system, we identified an essential role of the conserved microRNA miR-8, in neuromuscular junction formation. Tissue-specific silencing revealed that postsynaptic activity of miR-8 is important for normal neuromuscular junction morphogenesis.	MI0008992	Nat Methods 2009 Dec 6, 897-903 doi:10.1038/nmeth.1402 PMID:19915559
8	Viral RNA	HSURs1	miR-27a	FOXO1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
9	Viral RNA	HSURs1	miR-27a	RUNX1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
10	Viral RNA	HSURs1	miR-27a	PAX3	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
11	Viral RNA	HSURs1	miR-27b	FOXO1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
12	Viral RNA	HSURs1	miR-27b	RUNX1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
13	Viral RNA	HSURs1	miR-27b	PAX3	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
14	Viral RNA	HSURs2	miR-27a	FOXO1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
15	Viral RNA	HSURs2	miR-27a	RUNX1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
16	Viral RNA	HSURs2	miR-27a	PAX3	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
17	Viral RNA	HSURs2	miR-27b	FOXO1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
18	Viral RNA	HSURs2	miR-27b	RUNX1	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
19	Viral RNA	HSURs2	miR-27b	PAX3	T Cells	NA	Saimiriine herpesvirus 2 (herpesvirus saimiri)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
20	Artifically engineered RNA	anti-miR-K12-7-sponge	miR-K12-7(KSHV)	MICB	Human B Cell Lines	Herpesviruses	Saimiriine herpesvirus 2 (herpesvirus saimiri)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0002479	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
21	Artifically engineered RNA	anti-miR-BART2-5p-sponge	miR-BART2-5p(EBV)	MICB	Human B Cell Lines	Herpesviruses	Saimiriine herpesvirus 2 (herpesvirus saimiri)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0001068	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
22	Artifically engineered RNA	anti-miR-K12-8	miR-K12-8(KSHV)	NA	Human B Cell Lines	Herpesviruses	Saimiriine herpesvirus 2 (herpesvirus saimiri)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0002478	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
23	Artifically engineered RNA	anti-miR-BART4	miR-BART4(EBV)	NA	Human B Cell Lines	Herpesviruses	Saimiriine herpesvirus 2 (herpesvirus saimiri)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0003726	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
24	Viral RNA	HSURs1	miR-27a	FOXO1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
25	Viral RNA	HSURs1	miR-27a	RUNX1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
26	Viral RNA	HSURs1	miR-27a	PAX3	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
27	Viral RNA	HSURs1	miR-27b	FOXO1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
28	Viral RNA	HSURs1	miR-27b	RUNX1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
29	Viral RNA	HSURs1	miR-27b	PAX3	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
30	Viral RNA	HSURs2	miR-27a	FOXO1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
31	Viral RNA	HSURs2	miR-27a	RUNX1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
32	Viral RNA	HSURs2	miR-27a	PAX3	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000085	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
33	Viral RNA	HSURs2	miR-27b	FOXO1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
34	Viral RNA	HSURs2	miR-27b	RUNX1	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
35	Viral RNA	HSURs2	miR-27b	PAX3	T Cells	NA	Homo sapiens (human)	qRT-PCR;Northern blot	20558719	Down-regulation of a host microRNA by a Herpesvirus saimiri noncoding RNA.	We noted that conserved sequences in HSURs 1 and 2 constitute potential binding sites for three host-cell microRNAs (miRNAs). Coimmunoprecipitation experiments confirmed that HSURs 1 and 2 interact with the predicted miRNAs in virally transformed T cells. The abundance of one of these miRNAs, miR-27, is dramatically lowered in transformed cells, with consequent effects on the expression of miR-27 target genes.	MI0000440	Science 2010 Jun 18 328, 1563-6 doi:10.1126/science.1187197 PMID:20558719
36	Artifically engineered RNA	anti-miR-K12-7-sponge	miR-K12-7(KSHV)	MICB	Human B Cell Lines	Herpesviruses	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0002479	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
37	Artifically engineered RNA	anti-miR-BART2-5p-sponge	miR-BART2-5p(EBV)	MICB	Human B Cell Lines	Herpesviruses	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0001068	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
38	Artifically engineered RNA	anti-miR-K12-8	miR-K12-8(KSHV)	NA	Human B Cell Lines	Herpesviruses	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0002478	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
39	Artifically engineered RNA	anti-miR-BART4	miR-BART4(EBV)	NA	Human B Cell Lines	Herpesviruses	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19380116	Diverse herpesvirus microRNAs target the stress-induced immune ligand MICB to escape recognition by natural killer cells.	Here, we show functional conservation amongdiverse microRNAs derived from different herpesviruses, including HCMV, Kaposis sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV), in their ability to directly target MICB mRNA and reduce its expression. Although the various viral microRNAs share no sequence homology, they are functionally similar and target MICB at different yet adjacent sites during authentic viral infection. The finding that different herpesvirus microRNAs target MICB indicates that MICB plays a pivotal role in the clash between herpesviruses and humans.	MI0003726	Cell Host Microbe 2009 Apr 23 5, 376-85 doi:10.1016/j.chom.2009.03.003 PMID:19380116
40	Coding-mRNA	FN1	miR-491	CD44	Human Breast Carcinoma Cell Line Mda-Mb-231	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22637644	The non-coding 3 UTR of CD44 induces metastasis by regulating extracellular matrix functions	Here, we demonstrate that the overexpression of the CD44 3 UTR results in enhanced cell motility, invasion and cell adhesion in human breast carcinoma cell line MDA-MB-231. Furthermore, we found that expression of the CD44 3 UTR enhances metastasis in vivo.Computational analysis indicated that miRNAs that interact with the CD44 3 UTR also have binding sites in other matrix-encoding mRNA 3 UTRs, including collagen type 1a1 (Col1a1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671. Protein analysis demonstrated that expression of CD44, Col1a1 and FN1 were synergistically upregulated in vitro and in vivo upon transfection of the CD44 3 UTR. The non-coding 3 UTR of CD44 interacts with multiple miRNAs that target extracellular matrix properties and thus can be used to antagonize miRNA activities.	MI0003126	J Cell Sci 2012 Apr 15 125, 2075-85 doi:10.1242/jcs100818 PMID:22637644
41	Coding-mRNA	FN1	miR-512-3p	CD44	Human Breast Carcinoma Cell Line Mda-Mb-231	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22637644	The non-coding 3 UTR of CD44 induces metastasis by regulating extracellular matrix functions	Here, we demonstrate that the overexpression of the CD44 3 UTR results in enhanced cell motility, invasion and cell adhesion in human breast carcinoma cell line MDA-MB-231. Furthermore, we found that expression of the CD44 3 UTR enhances metastasis in vivo.Computational analysis indicated that miRNAs that interact with the CD44 3 UTR also have binding sites in other matrix-encoding mRNA 3 UTRs, including collagen type 1a1 (Col1a1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671. Protein analysis demonstrated that expression of CD44, Col1a1 and FN1 were synergistically upregulated in vitro and in vivo upon transfection of the CD44 3 UTR. The non-coding 3 UTR of CD44 interacts with multiple miRNAs that target extracellular matrix properties and thus can be used to antagonize miRNA activities.	MI0003140	J Cell Sci 2012 Apr 15 125, 2075-85 doi:10.1242/jcs100818 PMID:22637644
42	Coding-mRNA	FN1	miR-671	CD44	Human Breast Carcinoma Cell Line Mda-Mb-231	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22637644	The non-coding 3 UTR of CD44 induces metastasis by regulating extracellular matrix functions	Here, we demonstrate that the overexpression of the CD44 3 UTR results in enhanced cell motility, invasion and cell adhesion in human breast carcinoma cell line MDA-MB-231. Furthermore, we found that expression of the CD44 3 UTR enhances metastasis in vivo.Computational analysis indicated that miRNAs that interact with the CD44 3 UTR also have binding sites in other matrix-encoding mRNA 3 UTRs, including collagen type 1a1 (Col1a1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671. Protein analysis demonstrated that expression of CD44, Col1a1 and FN1 were synergistically upregulated in vitro and in vivo upon transfection of the CD44 3 UTR. The non-coding 3 UTR of CD44 interacts with multiple miRNAs that target extracellular matrix properties and thus can be used to antagonize miRNA activities.	MI0003760	J Cell Sci 2012 Apr 15 125, 2075-85 doi:10.1242/jcs100818 PMID:22637644
43	Coding-mRNA	Col1a1	miR-328	CD44	Human Breast Carcinoma Cell Line Mda-Mb-231	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22637644	The non-coding 3 UTR of CD44 induces metastasis by regulating extracellular matrix functions	Here, we demonstrate that the overexpression of the CD44 3 UTR results in enhanced cell motility, invasion and cell adhesion in human breast carcinoma cell line MDA-MB-231. Furthermore, we found that expression of the CD44 3 UTR enhances metastasis in vivo.Computational analysis indicated that miRNAs that interact with the CD44 3 UTR also have binding sites in other matrix-encoding mRNA 3 UTRs, including collagen type 1a1 (Col1a1) repressed by miR-328 and fibronectin type 1 (FN1) repressed by miR-512-3p, miR-491 and miR-671. Protein analysis demonstrated that expression of CD44, Col1a1 and FN1 were synergistically upregulated in vitro and in vivo upon transfection of the CD44 3 UTR. The non-coding 3 UTR of CD44 interacts with multiple miRNAs that target extracellular matrix properties and thus can be used to antagonize miRNA activities.	MI0000804	J Cell Sci 2012 Apr 15 125, 2075-85 doi:10.1242/jcs100818 PMID:22637644
44	Coding-mRNA	CDC42	miR-216a	CD44	Human Mammary Carcinoma Cells Mt-1	Mammary Carcinoma	Homo sapiens (human)	Immunohistochemistry;Luciferase reporter assay;Western blot	21149267	Expression of CD44 3 -untranslated region regulates endogenous microRNA functions in tumorigenesis and angiogenesis	Computational algorithms have predicted three miRNAs, miR-216a, miR-330 and miR-608, can bind to both the CD44 and CDC42 3-UTRs. This was confirmed with luciferase assays, western blotting and immunohistochemical staining and correlated with a series of siRNA assays. Thus, the non-coding CD44 3-UTR serves as a competitor for miRNA binding and subsequently inactivates miRNA functions, by freeing the target mRNAs from being repressed.	MI0000292	Nucleic Acids Res 2011 Apr 39, 3026-41 doi:10.1093/nar/gkq1003 PMID:21149267
45	Coding-mRNA	CDC42	miR-330	CD44	Human Mammary Carcinoma Cells Mt-1	Mammary Carcinoma	Homo sapiens (human)	Immunohistochemistry;Luciferase reporter assay;Western blot	21149267	Expression of CD44 3 -untranslated region regulates endogenous microRNA functions in tumorigenesis and angiogenesis	Computational algorithms have predicted three miRNAs, miR-216a, miR-330 and miR-608, can bind to both the CD44 and CDC42 3-UTRs. This was confirmed with luciferase assays, western blotting and immunohistochemical staining and correlated with a series of siRNA assays. Thus, the non-coding CD44 3-UTR serves as a competitor for miRNA binding and subsequently inactivates miRNA functions, by freeing the target mRNAs from being repressed.	MI0000803	Nucleic Acids Res 2011 Apr 39, 3026-41 doi:10.1093/nar/gkq1003 PMID:21149267
46	Coding-mRNA	CDC42	miR-608	CD44	Human Mammary Carcinoma Cells Mt-1	Mammary Carcinoma	Homo sapiens (human)	Immunohistochemistry;Luciferase reporter assay;Western blot	21149267	Expression of CD44 3 -untranslated region regulates endogenous microRNA functions in tumorigenesis and angiogenesis	Computational algorithms have predicted three miRNAs, miR-216a, miR-330 and miR-608, can bind to both the CD44 and CDC42 3-UTRs. This was confirmed with luciferase assays, western blotting and immunohistochemical staining and correlated with a series of siRNA assays. Thus, the non-coding CD44 3-UTR serves as a competitor for miRNA binding and subsequently inactivates miRNA functions, by freeing the target mRNAs from being repressed.	MI0003621	Nucleic Acids Res 2011 Apr 39, 3026-41 doi:10.1093/nar/gkq1003 PMID:21149267
47	LncRNA	HULC	miR-372	PRKACB	Hl-7702, Huh-1, Huh-4, Hep3B, Hepg2, Huh-7, Snu-449, Snu-475	Liver Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;Chromatin immunoprecipitation assays	20423907	CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer	We demonstrated HULC may act as an endogenous sponge, which down-regulates a series of microRNAs (miRNAs) activities, including miR-372. Inhibition of miR-372 leads to reducing translational repression of its target gene, PRKACB, which in turn induces phosphorylation of CREB.	MI0000780	Nucleic Acids Res 2010 Sep 38, 5366-83 doi:10.1093/nar/gkq285 PMID:20423907
48	Host gene	linc-MD1	miR-133	HuR	Mucle Tissues	Early Phases Of Myogenesis	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24440503	A Feedforward Regulatory Loop between HuR and the Long Noncoding RNA linc-MD1 Controls Early Phases of Myogenesis	We show that HuR is under the repressive control of miR-133 and that the sponging activity of linc-MD1 consolidates HuR expression in afeedforward positive loop	MI0000450	Mol Cell 2014 Feb 6 53, 506-14 doi:10.1016/j.molcel.2013.12.012 PMID:24440503
49	Host gene	H19	miR-675	RUNX1	Gastric Tissues	Gastric Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24388988	The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1	we found that miR-675 was positively expressed with H19 and was a pivotal mediator in H19-induced gastric cancer cell growth promotion.Subsequently, the tumor suppressor Runt Domain Transcription Factor1 (RUNX1) was confirmed to be a direct target of miR-675 using a luciferase reporter assay and western blotting analyses.	MI0005416	Biochem Biophys Res Commun 2014 Jun 6 448, 315-22 doi:10.1016/j.bbrc.2013.12.126 PMID:24388988
50	LncRNA	BACE1-AS	miR-485-5p	BACE1	Hek293T	Alzheimers Disease	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	20507594	Evidence for natural antisense transcript-mediated inhibition of microRNA function	We report here that BACE1-antisense prevents miRNA-induced repression of BACE1 mRNA by masking the binding site for miR-485-5p. Indeed, miR-485-5p and BACE1-antisense compete for binding within the same region in the open reading frame of the BACE1 mRNA. We observed opposing effects of BACE1-antisense and miR-485-5p on BACE1 protein in vitro and showed that Locked Nucleic Acid-antimiR mediated knockdown of miR-485-5p as well as BACE1-antisense over-expression can prevent the miRNA-induced BACE1 suppression. We found that the expression of BACE1-antisense as well as miR-485-5p are dysregulated in RNA samples from Alzheimer's disease subjects compared to control individuals. Our data demonstrate an interface between two distinct groups of regulatory RNAs in the computation of BACE1 gene expression. Moreover, bioinformatics analyses revealed a theoretical basis for many other potential interactions between natural antisense transcripts and miRNAs at the binding sites of the latter.	MI0002469	Genome Biol 2010  11, R56 doi:10.1186/gb-2010-11-5-r56 PMID:20507594
51	Circular RNA	CDR1-NAT	miR-671	CDR1	Hek293T	Cerebellar Degeneration	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21964070	miRNA-dependent gene silencing involving Ago2-mediated cleavage of a circular antisense RNA	Specifically, we show that miR-671 directs cleavage of a circular antisense transcript of the Cerebellar Degeneration-Related protein 1 (CDR1) locus in an Ago2-slicer-dependent manner. The resulting downregulation of circular antisense has a concomitant decrease in CDR1 mRNA levels, independently of heterochromatin formation.	MI0003760	Embo j 2011 Sep 30 30, 4414-22 doi:10.1038/emboj.2011.359 PMID:21964070
52	LncRNA	HOTAIR	miR-331-3p	HER	Gastric Carcinogenesis	Gastric Cancer	Homo sapiens (human)	Western blot;luciferase reporter assays	24775712	Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer	Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were gained from bioinformatic analysis, luciferase assays and RNA binding protein immunoprecipitation (RIP). The positive HOTAIR/HER2 interaction was identified and verified by immunohistochemistry assay and bivariate correlation analysis.	MI0000812	Mol Cancer 2014 Apr 28 13, 92 doi:10.1186/1476-4598-13-92 PMID:24775712
53	LncRNA	MRAK088388	miR-29b-3p	N4bp2	Pulmonary Fibrosis	Pulmonary Fibrosis	Homo sapiens (human)	qRT-PCR	24702795	Analysing the relationship between lncRNA and protein-coding gene and the role of lncRNA as ceRNA in pulmonary fibrosis.	In this study, we selected two differentially expressed lncRNAs MRAK088388 and MRAK081523 to explore their regulatory mechanisms. MRAK088388 and MRAK081523 were analysed as long-intergenic non-coding RNAs (lincRNAs), and identified as orthologues of mouse lncRNAs AK088388 and AK081523, respectively. qRT-PCR and in situ hybridization (ISH) showed that they were significantly up-regulated, and located in the cytoplasm of interstitial lung cells. We also showed that MRAK088388 and N4bp2 had the same miRNA response elements (MREs) for miR-200, miR-429, miR-29, and miR-30, whereas MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98, and let-7. Moreover, the expression levels of N4bp2 and Plxna4 significantly increased in fibrotic rats, and were highly correlated with those of MRAK088388 and MRAK081523, respectively. Among their shared miRNAs, miR-29b-3p and let-7i-5p decreased in the model group, and were negatively correlated with the expression of MRAK088388 and MRAK081523, respectively. MRAK088388 and MRAK081523 could regulate N4bp2 and Plxna4 expression by sponging miR-29b-3p and let-7i-5p, respectively, and possessed regulatory functions as ceRNAs.	MI0000105	J Cell Mol Med 2014 Jun 18, 991-1003 doi:10.1111/jcmm.12243 PMID:24702795
54	LncRNA	MRAK081523	let-7i	N4bp2	Pulmonary Fibrosis	Pulmonary Fibrosis	Homo sapiens (human)	qRT-PCR	24702795	Analysing the relationship between lncRNA and protein-coding gene and the role of lncRNA as ceRNA in pulmonary fibrosis.	In this study, we selected two differentially expressed lncRNAs MRAK088388 and MRAK081523 to explore their regulatory mechanisms. MRAK088388 and MRAK081523 were analysed as long-intergenic non-coding RNAs (lincRNAs), and identified as orthologues of mouse lncRNAs AK088388 and AK081523, respectively. qRT-PCR and in situ hybridization (ISH) showed that they were significantly up-regulated, and located in the cytoplasm of interstitial lung cells. We also showed that MRAK088388 and N4bp2 had the same miRNA response elements (MREs) for miR-200, miR-429, miR-29, and miR-30, whereas MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98, and let-7. Moreover, the expression levels of N4bp2 and Plxna4 significantly increased in fibrotic rats, and were highly correlated with those of MRAK088388 and MRAK081523, respectively. Among their shared miRNAs, miR-29b-3p and let-7i-5p decreased in the model group, and were negatively correlated with the expression of MRAK088388 and MRAK081523, respectively. MRAK088388 and MRAK081523 could regulate N4bp2 and Plxna4 expression by sponging miR-29b-3p and let-7i-5p, respectively, and possessed regulatory functions as ceRNAs.	MI0000434	J Cell Mol Med 2014 Jun 18, 991-1003 doi:10.1111/jcmm.12243 PMID:24702795
55	Pseudogene	CDK4PS	miR-34	CDK4	Phoenix A, 293T And Pc3	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000268	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
56	Pseudogene	PsiCx43	miR-1	Cx43	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000651	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
57	Pseudogene	KRASP1	miR-143	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000459	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
58	Pseudogene	KRASP1	let-7a	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000060	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
59	Pseudogene	KRASP1	let-7b	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000063	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
60	Pseudogene	KRASP1	let-7c	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000064	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
61	Pseudogene	KRASP1	let-7e	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000066	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
62	Pseudogene	KRASP1	let-7i	KRAS	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000434	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
63	Pseudogene	FOXO3B	miR-182	FOXO3	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000272	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
64	Pseudogene	E2F3P1	miR-17	E2F3	Phoenix A, 293T And Pc3	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	To extend our studies beyond PTEN and its pseudogene, we examined other cancer-related pseudogenes and genes. Alignments of gene and pseudogenes sequences show that microRNA-binding sites are well conserved; for example, the miR-145 binding site on OCT4 and its pseudogenes OCT4-pg1, 3, 4 and 5; miR-1 family binding sites on CONNEXIN 43 (CX43) and its pseudogene. Notably, OCT4-pg1 and -pg5 are exclusively expressed in cancer tissues and not in normal tissues17. Furthermore OCT4-pg5 is truncated at the 5’ end and expresses only a partial open reading frame region followed by the 3’UTR. Further examples of such conservation include: miR-34 family binding site on CDK4PS; miR-182 binding site on FOXO3B; miR-17 family binding site on E2F3P1; miR-143 and let-7 family binding sites on KRAS1P.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
65	LncRNA	lincRNA-ROR	miR-145	OCT4	Embryonic Stem Cell	Stem Cell Self-Renewal	Homo sapiens (human)	Luciferase reporter assay	23541921	Endogenous miRNA sponge lincRNA-ROR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal	We demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We engineered linc-RoR-overexpressing plasmids that have either wild-type (WT) or mutant (Mut) transcripts with mutations in the two miR-145-binding sites. We found that the ectopically expressed linc-RoR WT reduced the concentration of miR-145 during the cotransfection of the linc-RoR expression vector and low concentration of miRNA mimics in HEK293 cells. We also found that linc-RoR expression levels were decreased after transfection of miR-145 mimics, which indicated that both miR-145 and linc-RoR were cleaved and degraded during this process. These data suggest that linc-RoR functions as an miRNA sponge to reduce the efficient concentration of miR-145. In addition, OCT4 and NANOG mRNA was rescued at up to 80% of the levels in wild-type hESCs after miR-145 inhibitor transfection.	MI0000461	Dev Cell 2013 Apr 15 25, 69-80 doi:10.1016/j.devcel.2013.03.002 PMID:23541921
66	LncRNA	lincRNA-ROR	miR-145	Nanog	Embryonic Stem Cell	Stem Cell Self-Renewal	Homo sapiens (human)	Luciferase reporter assay	23541921	Endogenous miRNA sponge lincRNA-ROR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal	We demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We engineered linc-RoR-overexpressing plasmids that have either wild-type (WT) or mutant (Mut) transcripts with mutations in the two miR-145-binding sites. We found that the ectopically expressed linc-RoR WT reduced the concentration of miR-145 during the cotransfection of the linc-RoR expression vector and low concentration of miRNA mimics in HEK293 cells. We also found that linc-RoR expression levels were decreased after transfection of miR-145 mimics, which indicated that both miR-145 and linc-RoR were cleaved and degraded during this process. These data suggest that linc-RoR functions as an miRNA sponge to reduce the efficient concentration of miR-145. In addition, OCT4 and NANOG mRNA was rescued at up to 80% of the levels in wild-type hESCs after miR-145 inhibitor transfection.	MI0000461	Dev Cell 2013 Apr 15 25, 69-80 doi:10.1016/j.devcel.2013.03.002 PMID:23541921
67	LncRNA	lincRNA-ROR	miR-145	Sox2	Embryonic Stem Cell	Stem Cell Self-Renewal	Homo sapiens (human)	Luciferase reporter assay	23541921	Endogenous miRNA sponge lincRNA-ROR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal	We demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We engineered linc-RoR-overexpressing plasmids that have either wild-type (WT) or mutant (Mut) transcripts with mutations in the two miR-145-binding sites. We found that the ectopically expressed linc-RoR WT reduced the concentration of miR-145 during the cotransfection of the linc-RoR expression vector and low concentration of miRNA mimics in HEK293 cells. We also found that linc-RoR expression levels were decreased after transfection of miR-145 mimics, which indicated that both miR-145 and linc-RoR were cleaved and degraded during this process. These data suggest that linc-RoR functions as an miRNA sponge to reduce the efficient concentration of miR-145. In addition, OCT4 and NANOG mRNA was rescued at up to 80% of the levels in wild-type hESCs after miR-145 inhibitor transfection.	MI0000461	Dev Cell 2013 Apr 15 25, 69-80 doi:10.1016/j.devcel.2013.03.002 PMID:23541921
68	LncRNA	lincRNA-ROR	miR-145	NA	Core Stem Cell	Stem Cell Self-Renewal	Homo sapiens (human)	qRT-PCR	24589415	Linc-RNA-RoR acts as a "sponge" against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	After construction of adenovirus vectors carrying green fluorescent protein (GFP), these vectors were transfected into ETs to estimate the effects of overexpression or knocked down expression of miR-145, linc-RoR or Dicer. Flow cytometry was employed to ascertain transfection efficiency, and real-time polymerase chain reaction (RT-PCR) was employed to compare their levels. Colony formation was analyzed using cultured gelatin-coated tissue cultures. miR-145 potential targeting sites in linc-RoR were mutated using a site-directed mutagenesis kit to verify its competing endogenous RNA (ceRNA) effects.Expression of linc-RoR and core stem cell TFs was associated with the pluripotent state of ETs, whereas miR-145 expression increased after ET differentiation. Greater expression of miR-145 could lead to down-regulation of linc-RoR and core TFs, and decreased colony formation. Converse effects could be achieved after knocked-down miR-145 expression. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. Knocked-down Dicer expression could improve the expression of linc-RoR and core TFs.	MI0000461	Gynecol Oncol 2014 May 133, 333-9 doi:10.1016/j.ygyno.2014.02.033 PMID:24589415
69	LncRNA	PTCSC3	miR-574-5p	NA	Bcpap, Ftc133 And 8505C	Thyroid Cancer	Homo sapiens (human)	qRT-PCR	23599737	A long non-coding RNA, PTCSC3, as a tumor suppressor and a target of miRNAs in thyroid cancer cells	Following transfection with PTCSC3, all three thyroid cancer cells originating from various pathological types of thyroid cancers demonstrated significant growth inhibition, cell cycle arrest and increased apoptosis. The top 20 miRNAs to have a potential interaction with PTCSC3 were identified, out of which miR-574-5p was selected to further confirm the inverse correlation with PTCSC3 in thyroid cancer cells in vitro. In the present study, PTCSC3 as atumor suppressor was investigated as a competing endogenous RNA for miR-574-5p.	MI0003581	Exp Ther Med 2013 Apr 5, 1143-1146 doi:10.3892/etm.2013.933 PMID:23599737
70	Coding-mRNA	DNMT1	miR-148a	NA	Hepg2, Smmc-7721 And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24714841	MicroRNA-148a is silenced by hypermethylation and interacts with DNA methyltransferase 1 in hepatocellular carcinogenesis.	DNMT1, the DNA methyltransferase that maintains methylation patterns, is aberrantly upregulated in HCC cell lines, and its overexpression is responsible for hypermethylation of the miR-148a promoter. Intriguingly, the expression of DNMT1, which is a target of miR-148a, is inversely correlated with the expression of miR-148a in HCC cells. These results lead us to propose the existence of a negative feedback regulatory loop between miR-148a and DNMT1 in HCC.	MI0000253	Int J Oncol 2014 Jun 44, 1915-22 doi:10.3892/ijo.2014.2373 PMID:24714841
71	Artifically engineered RNA	miR-18 GFP sponge(pcDNA5-CMV-d2eGFP vector)	miR-18	E2F1	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	This difference likely results from the presence of two miR-20 binding sites and one miR-18 site in the E2F1 3' UTR, plus the added inhibition of the coexpressed miR-20 family member miR-17-5. These effects were recapitulated in a luciferase assay wherein the RLuc reporter was fused to a fragment of the E2F1 UTR spanning the two miR-20 sites	MI0000072	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
72	Artifically engineered RNA	miR-20 GFP sponge(pcDNA5-CMV-d2eGFP vector)	miR-17	E2F1	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	This difference likely results from the presence of two miR-20 binding sites and one miR-18 site in the E2F1 3' UTR, plus the added inhibition of the coexpressed miR-20 family member miR-17-5. These effects were recapitulated in a luciferase assay wherein the RLuc reporter was fused to a fragment of the E2F1 UTR spanning the two miR-20 sites	MI0000071	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
73	Artifically engineered RNA	miR-20 GFP sponge(pcDNA5-CMV-d2eGFP vector)	miR-17	CD69	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	we used a luciferase reporter regulated by a large fragment of the CD69 3' UTR17 or by the E2F5 UTR. As predicted by the TargetScan 4.0 and miRanda algorithms, respectively, these UTRs are each regulated by a single miR-20 site18,19. Correspondingly, each reporter was derepressed upon treatment with a miR-20 sponge in 293T cells 	MI0000071	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
74	Artifically engineered RNA	miR-20 GFP sponge(pcDNA5-CMV-d2eGFP vector)	miR-17	E2F5	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	we used a luciferase reporter regulated by a large fragment of the CD69 3' UTR17 or by the E2F5 UTR. As predicted by the TargetScan 4.0 and miRanda algorithms, respectively, these UTRs are each regulated by a single miR-20 site18,19. Correspondingly, each reporter was derepressed upon treatment with a miR-20 sponge in 293T cells 	MI0000071	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
75	Artifically engineered RNA	mir-30c pTZ-U6+27	miR-30c	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them microRNA sponges, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000254	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
76	Artifically engineered RNA	miR-30e bulged CMV sponge	miR-30e	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000749	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
77	Artifically engineered RNA	miR-21 bulged CMV sponge	miR-21	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000077	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
78	Artifically engineered RNA	miR-16 perfect CMV sponge and U6 sponge	miR-16	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000070	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
79	Artifically engineered RNA	psiCHECK2-let-7 4x	let-7a	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
80	Artifically engineered RNA	psiCHECK2-let-7 4x	let-7b	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
81	Artifically engineered RNA	psiCHECK2-H19 4x	let-7a	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
82	Artifically engineered RNA	psiCHECK2-H19 4x	let-7b	NA	Hek293T	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
83	Artifically engineered RNA	pMXs-GIN-miR140-5pT	miR-140-5p	NA	Helas3	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;Northern blot	19223327	Vectors expressing efficient RNA decoys achieve the long-term suppression of specific microRNA activity in mammalian cells	We tested various RNA decoys which were designed to efficiently expose indigestible complementary RNAs to a specific miRNA molecule. These inhibitory RNAs were at the same time designed to be expressed in lentiviral vectors and to be transported into the cytoplasm after transcription by RNA polymerase III. We report the optimal conditions that we have established for the design of such RNA decoys (we term these molecules TuD RNAs; tough decoy RNAs).	MI0000456	Nucleic Acids Res 2009 Apr 37, e43 doi:10.1093/nar/gkp040 PMID:19223327
84	Artifically engineered RNA	pMXs-GIN-miR140-3pT	miR-140-3p	NA	Helas3	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;Northern blot	19223327	Vectors expressing efficient RNA decoys achieve the long-term suppression of specific microRNA activity in mammalian cells	we tested various RNA decoys which were designed to efficiently expose indigestible complementary RNAs to a specific miRNA molecule. These inhibitory RNAs were at the same time designed to be expressed in lentiviral vectors and to be transported into the cytoplasm after transcription by RNA polymerase III. We report the optimal conditions that we have established for the design of such RNA decoys (we term these molecules TuD RNAs; tough decoy RNAs).	MI0000456	Nucleic Acids Res 2009 Apr 37, e43 doi:10.1093/nar/gkp040 PMID:19223327
85	Artifically engineered RNA	TuD-miR21-4ntin	miR-21	PDCD4	Pa-1 Cells	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;Northern blot	19223327	Vectors expressing efficient RNA decoys achieve the long-term suppression of specific microRNA activity in mammalian cells	we tested various RNA decoys which were designed to efficiently expose indigestible complementary RNAs to a specific miRNA molecule. These inhibitory RNAs were at the same time designed to be expressed in lentiviral vectors and to be transported into the cytoplasm after transcription by RNA polymerase III. We report the optimal conditions that we have established for the design of such RNA decoys (we term these molecules TuD RNAs; tough decoy RNAs).	MI0000077	Nucleic Acids Res 2009 Apr 37, e43 doi:10.1093/nar/gkp040 PMID:19223327
86	Artifically engineered RNA	anti-miR-183	miR-183	b-TrCP1	Hek293T	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot	19647520	CRD-BP protects the coding region of betaTrCP1 mRNA from miR-183-mediated degradation.	Here we show that degradation of mRNA of betaTrCP1 is miRNA dependent and identify miR-183 as a microRNA that interacts with the coding region of betaTrCP1 mRNA. Argonaute2 interacts with the sameregion of betaTrCP1 mRNA in an miR-183-dependent manner. Inhibition of miR-183 function or disruption of the miR-183-binding site stabilizes betaTrCP1 mRNA and elevates betaTrCP1 levels, resulting in activation of the SCF(betaTrCP) E3 ubiquitin ligase.	MI0000273	Mol Cell 2009 Jul 31 35, 240-6 doi:10.1016/j.molcel.2009.06.007 PMID:19647520
87	Artifically engineered RNA	GFP-sponge16	miR-16	FGFR1	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
88	Artifically engineered RNA	GFP-sponge16	miR-16	PI3KCa	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
89	Artifically engineered RNA	GFP-sponge16	miR-16	MDM4	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
90	Artifically engineered RNA	GFP-sponge16	miR-16	VEGFa	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
91	Artifically engineered RNA	GFP-sponge16	miR-16	JUN	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
92	Artifically engineered RNA	GFP-sponge16	miR-16	Jag1	Mononuclear Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	20962322	MicroRNAs 15a/16-1 function as tumor suppressor genes in multiple myeloma.	Here, we functionally validate the role of the microRNAs-15a/16-1 cluster, centered at the deleted region, as TSGs and delineate their downstream target genes in MM. Using "sponge" lentiviral vectors to competitive stably inhibit mature microRNAs in vitro and in vivo, we have documented enhanced proliferative and invasive capacity of cells with stably inhibition of miR-16. Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. Expression profiling analysis of miR-16-deficient cells identified a large number of downstream target genes including FGFR1, PI3KCa, MDM4, VEGFa, as well as secondary affected genes such as JUN and Jag1.	MI0000070	Blood 2010 Oct 20, 10.1182/blood-2009-11-253294 doi:10.1182/blood-2009-11-253294 PMID:20962322
93	Artifically engineered RNA	anti-let-7 sponge	let-7a	NA	Neural Stem Cell	Neural Stem-Cell Commitment	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	18604195	A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment.	We tested the ability of so-called sponge constructs to de-repress the let-7 and mir-125 target gene lin-41. Sponge constructs express an mRNA with cloned arrays of semi-complementary binding sites for a specific miRNA in the 3'UTR, and function as competitive inhibitors26 . Lin-41 is a marker of undif- ferentiated ES and EC cells27 , and is expressed at low levels in NS cells. Transfection of NS cells with sponge constructs targeting either let-7 or mir-125 increased the level of Lin-41 protein, compared with the sponge vector alone or a sponge construct targeting mir-29. This result demonstrates that mRNAs targeted by let-7 and mir-125, such as lin-41, are subject to ongoing post-transcriptional suppression in NS cells.	MI0000060	Nat Cell Biol 2008 Aug 10, 987-93 doi:10.1038/ncb1759 PMID:18604195
94	Artifically engineered RNA	anti-mir-29 sponge	miR-29	NA	Neural Stem Cell	Neural Stem-Cell Commitment	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	18604195	A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment.	We tested the ability of so-called sponge constructs to de-repress the let-7 and mir-125 target gene lin-41. Sponge constructs express an mRNA with cloned arrays of semi-complementary binding sites for a specific miRNA in the 3'UTR, and function as competitive inhibitors26 . Lin-41 is a marker of undif- ferentiated ES and EC cells27 , and is expressed at low levels in NS cells. Transfection of NS cells with sponge constructs targeting either let-7 or mir-125 increased the level of Lin-41 protein, compared with the sponge vector alone or a sponge construct targeting mir-29. This result demonstrates that mRNAs targeted by let-7 and mir-125, such as lin-41, are subject to ongoing post-transcriptional suppression in NS cells.	MI0000087	Nat Cell Biol 2008 Aug 10, 987-93 doi:10.1038/ncb1759 PMID:18604195
95	Artifically engineered RNA	anti-mir-125 sponge	miR-125	NA	Neural Stem Cell	Neural Stem-Cell Commitment	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	18604195	A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment.	We tested the ability of so-called sponge constructs to de-repress the let-7 and mir-125 target gene lin-41. Sponge constructs express an mRNA with cloned arrays of semi-complementary binding sites for a specific miRNA in the 3'UTR, and function as competitive inhibitors26 . Lin-41 is a marker of undif- ferentiated ES and EC cells27 , and is expressed at low levels in NS cells. Transfection of NS cells with sponge constructs targeting either let-7 or mir-125 increased the level of Lin-41 protein, compared with the sponge vector alone or a sponge construct targeting mir-29. This result demonstrates that mRNAs targeted by let-7 and mir-125, such as lin-41, are subject to ongoing post-transcriptional suppression in NS cells.	MI0000469	Nat Cell Biol 2008 Aug 10, 987-93 doi:10.1038/ncb1759 PMID:18604195
96	Artifically engineered RNA	anti-mir128 sponge	miR-128	NA	Neural Stem Cell	Neural Stem-Cell Commitment	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	18604195	A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment.	We tested the ability of so-called sponge constructs to de-repress the let-7 and mir-125 target gene lin-41. Sponge constructs express an mRNA with cloned arrays of semi-complementary binding sites for a specific miRNA in the 3'UTR, and function as competitive inhibitors26 . Lin-41 is a marker of undif- ferentiated ES and EC cells27 , and is expressed at low levels in NS cells. Transfection of NS cells with sponge constructs targeting either let-7 or mir-125 increased the level of Lin-41 protein, compared with the sponge vector alone or a sponge construct targeting mir-29. This result demonstrates that mRNAs targeted by let-7 and mir-125, such as lin-41, are subject to ongoing post-transcriptional suppression in NS cells.	MI0000447	Nat Cell Biol 2008 Aug 10, 987-93 doi:10.1038/ncb1759 PMID:18604195
97	Circular RNA	CDR1as	miR-671	CDR1	Hek293	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21964070	miRNA-dependent gene silencing involving Ago2-mediated cleavage of a circular antisense RNA	we report that miRNAs can also regulate gene expression by targeting non-coding antisense transcripts in human cells. Specifically, we show that miR-671 directs cleavage of a circular antisense transcript of the Cerebellar Degeneration-Related protein 1 (CDR1) locus in an Ago2-slicer-dependent manner. The resulting downregulation of circular antisense has a concomitant decrease in CDR1 mRNA levels, independently of heterochromatin formation.	MI0003760	Embo j 2011 Sep 30 30, 4414-22 doi:10.1038/emboj.2011.359 PMID:21964070
98	Artifically engineered RNA	eGFP-miR-155 sponge	miR-155	JARID2	B-Cell Lymphomas	Cell Survival	Homo sapiens (human)	Reporter assay;Other	19759154	Reticuloendotheliosis virus strain T induces miR-155, which targets JARID2 and promotes cell survival	Eight miR-155 target sites with a bulge from nt 9 to 12 were cloned into the 3'UTR of the MS2 viral coat protein. We first investigated the functionality of the miR-155 sponge by the luciferase assay. In the presence of miR-155, luciferase levels of JARID2 3'UTR were reduced. With increasing amounts of miR-155 sponge, miR-155 function was inhibited and the repression of luciferase JARID2 3'UTR was abrogated	MI0000681	J Virol 2009 Dec 83, 12009-17 doi:10.1128/jvi.01182-09 PMID:19759154
99	Artifically engineered RNA	eGFP-miR-155 sponge	miR-155	JARID2	B-Cell Lymphomas	Cell Survival	Gallus gallus (chicken)	Reporter assay;Other	19759154	Reticuloendotheliosis virus strain T induces miR-155, which targets JARID2 and promotes cell survival	Eight miR-155 target sites with a bulge from nt 9 to 12 were cloned into the 3'UTR of the MS2 viral coat protein. We first investigated the functionality of the miR-155 sponge by the luciferase assay. In the presence of miR-155, luciferase levels of JARID2 3'UTR were reduced. With increasing amounts of miR-155 sponge, miR-155 function was inhibited and the repression of luciferase JARID2 3'UTR was abrogated	MI0001176	J Virol 2009 Dec 83, 12009-17 doi:10.1128/jvi.01182-09 PMID:19759154
100	Artifically engineered RNA	sh-miR-p21	miR-K1	p21	B Cell Lymphoma Cell Line	Cell Cycle Arrest	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20219912	A human herpesvirus microRNA inhibits p21 expression and attenuates p21-mediated cell cycle arrest.	Here, we report that cellular mRNAs encoding the cellular cyclin-dependent kinase inhibitor p21, a key inducer of cell cycle arrest, are direct targets for KSHV miR-K1. Ectopically expressed KSHV miR-K1 specifically inhibited the expression of endogenous p21 in KSHV-negative cells and strongly attenuated the cell cycle arrest that normally occurs upon p53 activation, yet miR-K1 did not prevent the induction of other p53-responsive genes. Stable knockdown of miR-K1 in latently KSHV-infected human primary effusion lymphoma (PEL) B cells revealed a derepression of p21 expression and enhanced cell cycle arrest following activation of p53. Our data demonstrate that miR-K1 represses the expression of p21, a protein with known tumor suppressor functions, and suggest that this KSHV miRNA is likely to contribute to the oncogenic potential of this opportunistic viral pathogen.	NA	J Virol 2010 May 84, 5229-37 doi:10.1128/jvi.00202-10 PMID:20219912
101	Artifically engineered RNA	sh-miR-p21	miR-K1	p21	B Cell Lymphoma Cell Line	Cell Cycle Arrest	Gammaherpesvirus (KSHV)	Western blot;qRT-PCR;luciferase reporter assays	20219912	A human herpesvirus microRNA inhibits p21 expression and attenuates p21-mediated cell cycle arrest.	Here, we report that cellular mRNAs encoding the cellular cyclin-dependent kinase inhibitor p21, a key inducer of cell cycle arrest, are direct targets for KSHV miR-K1. Ectopically expressed KSHV miR-K1 specifically inhibited the expression of endogenous p21 in KSHV-negative cells and strongly attenuated the cell cycle arrest that normally occurs upon p53 activation, yet miR-K1 did not prevent the induction of other p53-responsive genes. Stable knockdown of miR-K1 in latently KSHV-infected human primary effusion lymphoma (PEL) B cells revealed a derepression of p21 expression and enhanced cell cycle arrest following activation of p53. Our data demonstrate that miR-K1 represses the expression of p21, a protein with known tumor suppressor functions, and suggest that this KSHV miRNA is likely to contribute to the oncogenic potential of this opportunistic viral pathogen.	NA	J Virol 2010 May 84, 5229-37 doi:10.1128/jvi.00202-10 PMID:20219912
102	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
103	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
104	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
105	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
106	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
107	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
108	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
109	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
110	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
111	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
112	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
113	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
114	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
115	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
116	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
117	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
118	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
119	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
120	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
121	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
122	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
123	Circular RNA	ciRS-7	miR-7	NA	Brain Tissues	Neocortical and Hippocampal Neurons	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446346	Natural RNA circles function as efficient microRNA sponges	Here we show that this circRNA acts as a miR-7 sponge; we term this circular transcript ciRS-7 (circular RNA sponge for miR-7). ciRS-7 contains more than 70 selectively conserved miRNA target sites, and it is highly and widely associated with Argonaute (AGO) proteins in a miR-7-dependent manner. Although the circRNA is completely resistant to miRNA-mediated target destabilization, it strongly suppresses miR-7 activity, resulting in increased levels of miR-7 targets. In the mouse brain, we observe overlapping co-expression of ciRS-7 and miR-7, particularly in neocortical and hippocampal neurons, suggesting a high degree of endogenous interaction. We further show that the testis-specific circRNA, sex-determining region Y (Sry), serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon. This study serves as the first, to our knowledge, functional analysis of a naturally expressed circRNA.	MI0000263	Nature 2013 Mar 21 495, 384-8 doi:10.1038/nature11993 PMID:23446346
124	Circular RNA	sry	miR-138	NA	Brain Tissues	Neocortical and Hippocampal Neurons	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446346	Natural RNA circles function as efficient microRNA sponges	Here we show that this circRNA acts as a miR-7 sponge; we term this circular transcript ciRS-7 (circular RNA sponge for miR-7). ciRS-7 contains more than 70 selectively conserved miRNA target sites, and it is highly and widely associated with Argonaute (AGO) proteins in a miR-7-dependent manner. Although the circRNA is completely resistant to miRNA-mediated target destabilization, it strongly suppresses miR-7 activity, resulting in increased levels of miR-7 targets. In the mouse brain, we observe overlapping co-expression of ciRS-7 and miR-7, particularly in neocortical and hippocampal neurons, suggesting a high degree of endogenous interaction. We further show that the testis-specific circRNA, sex-determining region Y (Sry), serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon. This study serves as the first, to our knowledge, functional analysis of a naturally expressed circRNA.	MI0000455	Nature 2013 Mar 21 495, 384-8 doi:10.1038/nature11993 PMID:23446346
125	LncRNA	linc-MD1	miR-133	MAML1	Myoblasts	Muscle Differentiation	Homo sapiens (human)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000450	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
126	LncRNA	linc-MD1	miR-135	MAML1	Myoblasts	Muscle Differentiation	Homo sapiens (human)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000452	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
127	LncRNA	linc-MD1	miR-133	MEF2C	Myoblasts	Muscle Differentiation	Homo sapiens (human)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000450	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
128	LncRNA	linc-MD1	miR-135	MEF2C	Myoblasts	Muscle Differentiation	Homo sapiens (human)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000452	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
129	LncRNA	AK020764	miR-142-3p	NA	Cd8 T Cells	Adaptive Immunity	Homo sapiens (human)	qRT-PCR	19494298	Genome-wide identification of long noncoding RNAs in CD8+ T cells.	Two miRNAs, mir-142-5p and mir-142-3p, recently shown to be among the most highly expressed miRNAs in naive, memory, and effector CD8 T cell populations (76), are hosted within the first intron of a long ncRNA (AK020764) that is also strongly expressed in CD8 T cells.	MI0000458	J Immunol 2009 Jun 15 182, 7738-48 doi:10.4049/jimmunol.0900603 PMID:19494298
130	LncRNA	AK020764	miR-142-5p	NA	Cd8 T Cells	Adaptive Immunity	Homo sapiens (human)	qRT-PCR	19494298	Genome-wide identification of long noncoding RNAs in CD8+ T cells.	Two miRNAs, mir-142-5p and mir-142-3p, recently shown to be among the most highly expressed miRNAs in naive, memory, and effector CD8 T cell populations (76), are hosted within the first intron of a long ncRNA (AK020764) that is also strongly expressed in CD8 T cells.	MI0000458	J Immunol 2009 Jun 15 182, 7738-48 doi:10.4049/jimmunol.0900603 PMID:19494298
131	LncRNA	H19	let-7a	Dicer	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
132	LncRNA	H19	let-7a	Hmga2	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
133	LncRNA	H19	let-7a	Igf1	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
134	LncRNA	H19	let-7a	Igf2	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000060	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
135	LncRNA	H19	let-7b	Dicer	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
136	LncRNA	H19	let-7b	Hmga2	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
137	LncRNA	H19	let-7b	Igf1	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
138	LncRNA	H19	let-7b	Igf2	Mucle	Muscle Differentiation	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000063	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
139	Host gene	H19	miR-675-3p	Smad	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0005416	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
140	Host gene	H19	miR-675-5p	Cdc6	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0005416	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
141	Host gene	H19	miR-675-3p	Smad	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0005416	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
142	Host gene	H19	miR-675-5p	Cdc6	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0005416	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
143	LncRNA	H19	let-7a	Hmga2	Panc-1,Sw1990, Aspc-1, Bxpc-3, Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Western blot	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT	We found that the expression level of H19 was significantly upregulated in most PDAC tissues, intriguingly, when tumor tissues were stratified based on clinical progression, we found that H19 levels were remark- ably increased in primary tumors that subsequently metasta- sized compared with those in nonmetastatic PDAC tissues, which suggested that H19 might play a role in PDAC metas- tasis. Secondly, H19 function was investigated in siRNA- mediated knockdown studies and we demonstrated that H19 enhanced PDAC cell migration and invasion. Thirdly, given that H19 exerted pro-oncogenic activities in PDAC, whereas let-7 exhibited a well-known tumor suppressor in PDAC [33–35], and that H19 acted as a molecular sponge to bind with let-7 and inhibited its function in muscle differentiation as previously reported [16], we postulate that H19/let-7 reguation may also contribute to PDAC metastasis. To confirm this speculation, we want to explore whether H19 inhibited let-7 function and affected its target gene. Since oncogenic HMGA2 was reported as the let-7 wellkown target and was dysregulated in many types of tumor, including PDAC [22, 36], additionally, HMGA2 is proved to be a key factor in- volved in the epithelia-mesenchymal transition (EMT), which is vital for tumor invasion and metastasis [24, 37–44]. We detected the expression level of HMGA2 as well as EMT markers after treated PDAC cells with H19-siRNA, and we proved that H19 indeed inhibit endogenous let-7 function, leading to derepression of HMGA2 which mediated EMT. Last but not least, we proved that downregulation of let-7 could significantly restore the impaired migration and inva- sion induced byH19-siRNA, which indicated that let-7 played pivotal roles, at least partially in H19-induced PDAC metastasis.	MI0000060	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
144	LncRNA	H19	let-7b	Hmga2	Panc-1,Sw1990, Aspc-1, Bxpc-3, Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Western blot	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT	We found that the expression level of H19 was significantly upregulated in most PDAC tissues, intriguingly, when tumor tissues were stratified based on clinical progression, we found that H19 levels were remark- ably increased in primary tumors that subsequently metasta- sized compared with those in nonmetastatic PDAC tissues, which suggested that H19 might play a role in PDAC metas- tasis. Secondly, H19 function was investigated in siRNA- mediated knockdown studies and we demonstrated that H19 enhanced PDAC cell migration and invasion. Thirdly, given that H19 exerted pro-oncogenic activities in PDAC, whereas let-7 exhibited a well-known tumor suppressor in PDAC [33–35], and that H19 acted as a molecular sponge to bind with let-7 and inhibited its function in muscle differentiation as previously reported [16], we postulate that H19/let-7 reguation may also contribute to PDAC metastasis. To confirm this speculation, we want to explore whether H19 inhibited let-7 function and affected its target gene. Since oncogenic HMGA2 was reported as the let-7 wellkown target and was dysregulated in many types of tumor, including PDAC [22, 36], additionally, HMGA2 is proved to be a key factor in- volved in the epithelia-mesenchymal transition (EMT), which is vital for tumor invasion and metastasis [24, 37–44]. We detected the expression level of HMGA2 as well as EMT markers after treated PDAC cells with H19-siRNA, and we proved that H19 indeed inhibit endogenous let-7 function, leading to derepression of HMGA2 which mediated EMT. Last but not least, we proved that downregulation of let-7 could significantly restore the impaired migration and inva- sion induced byH19-siRNA, which indicated that let-7 played pivotal roles, at least partially in H19-induced PDAC metastasis.	MI0000063	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
145	LncRNA	H19	let-7c	Hmga2	Panc-1,Sw1990, Aspc-1, Bxpc-3, Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Western blot	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT	We found that the expression level of H19 was significantly upregulated in most PDAC tissues, intriguingly, when tumor tissues were stratified based on clinical progression, we found that H19 levels were remark- ably increased in primary tumors that subsequently metasta- sized compared with those in nonmetastatic PDAC tissues, which suggested that H19 might play a role in PDAC metas- tasis. Secondly, H19 function was investigated in siRNA- mediated knockdown studies and we demonstrated that H19 enhanced PDAC cell migration and invasion. Thirdly, given that H19 exerted pro-oncogenic activities in PDAC, whereas let-7 exhibited a well-known tumor suppressor in PDAC [33–35], and that H19 acted as a molecular sponge to bind with let-7 and inhibited its function in muscle differentiation as previously reported [16], we postulate that H19/let-7 reguation may also contribute to PDAC metastasis. To confirm this speculation, we want to explore whether H19 inhibited let-7 function and affected its target gene. Since oncogenic HMGA2 was reported as the let-7 wellkown target and was dysregulated in many types of tumor, including PDAC [22, 36], additionally, HMGA2 is proved to be a key factor in- volved in the epithelia-mesenchymal transition (EMT), which is vital for tumor invasion and metastasis [24, 37–44]. We detected the expression level of HMGA2 as well as EMT markers after treated PDAC cells with H19-siRNA, and we proved that H19 indeed inhibit endogenous let-7 function, leading to derepression of HMGA2 which mediated EMT. Last but not least, we proved that downregulation of let-7 could significantly restore the impaired migration and inva- sion induced byH19-siRNA, which indicated that let-7 played pivotal roles, at least partially in H19-induced PDAC metastasis.	MI0000064	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
146	LncRNA	H19	let-7e	Hmga2	Panc-1,Sw1990, Aspc-1, Bxpc-3, Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Western blot	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT	We found that the expression level of H19 was significantly upregulated in most PDAC tissues, intriguingly, when tumor tissues were stratified based on clinical progression, we found that H19 levels were remark- ably increased in primary tumors that subsequently metasta- sized compared with those in nonmetastatic PDAC tissues, which suggested that H19 might play a role in PDAC metas- tasis. Secondly, H19 function was investigated in siRNA- mediated knockdown studies and we demonstrated that H19 enhanced PDAC cell migration and invasion. Thirdly, given that H19 exerted pro-oncogenic activities in PDAC, whereas let-7 exhibited a well-known tumor suppressor in PDAC [33–35], and that H19 acted as a molecular sponge to bind with let-7 and inhibited its function in muscle differentiation as previously reported [16], we postulate that H19/let-7 reguation may also contribute to PDAC metastasis. To confirm this speculation, we want to explore whether H19 inhibited let-7 function and affected its target gene. Since oncogenic HMGA2 was reported as the let-7 wellkown target and was dysregulated in many types of tumor, including PDAC [22, 36], additionally, HMGA2 is proved to be a key factor in- volved in the epithelia-mesenchymal transition (EMT), which is vital for tumor invasion and metastasis [24, 37–44]. We detected the expression level of HMGA2 as well as EMT markers after treated PDAC cells with H19-siRNA, and we proved that H19 indeed inhibit endogenous let-7 function, leading to derepression of HMGA2 which mediated EMT. Last but not least, we proved that downregulation of let-7 could significantly restore the impaired migration and inva- sion induced byH19-siRNA, which indicated that let-7 played pivotal roles, at least partially in H19-induced PDAC metastasis.	MI0000066	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
147	LncRNA	H19	let-7i	Hmga2	Panc-1,Sw1990, Aspc-1, Bxpc-3, Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Western blot	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7’s suppression on its target HMGA2-mediated EMT	We found that the expression level of H19 was significantly upregulated in most PDAC tissues, intriguingly, when tumor tissues were stratified based on clinical progression, we found that H19 levels were remark- ably increased in primary tumors that subsequently metasta- sized compared with those in nonmetastatic PDAC tissues, which suggested that H19 might play a role in PDAC metas- tasis. Secondly, H19 function was investigated in siRNA- mediated knockdown studies and we demonstrated that H19 enhanced PDAC cell migration and invasion. Thirdly, given that H19 exerted pro-oncogenic activities in PDAC, whereas let-7 exhibited a well-known tumor suppressor in PDAC [33–35], and that H19 acted as a molecular sponge to bind with let-7 and inhibited its function in muscle differentiation as previously reported [16], we postulate that H19/let-7 reguation may also contribute to PDAC metastasis. To confirm this speculation, we want to explore whether H19 inhibited let-7 function and affected its target gene. Since oncogenic HMGA2 was reported as the let-7 wellkown target and was dysregulated in many types of tumor, including PDAC [22, 36], additionally, HMGA2 is proved to be a key factor in- volved in the epithelia-mesenchymal transition (EMT), which is vital for tumor invasion and metastasis [24, 37–44]. We detected the expression level of HMGA2 as well as EMT markers after treated PDAC cells with H19-siRNA, and we proved that H19 indeed inhibit endogenous let-7 function, leading to derepression of HMGA2 which mediated EMT. Last but not least, we proved that downregulation of let-7 could significantly restore the impaired migration and inva- sion induced byH19-siRNA, which indicated that let-7 played pivotal roles, at least partially in H19-induced PDAC metastasis.	MI0000434	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
148	LncRNA	GAS5	miR-21	NA	Breast Tumor Specimens	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;RNA immunoprecipitation;luciferase reporter assays	23933812	Negative regulation of lncRNA GAS5 by miR-21.	Using the lncRNA RT-PCR (reverse transcription-polymerase chain reaction) array carrying 83 human disease-related lncRNAs, we show that miR-21 is capable of suppressing the lncRNA growth arrest-specific 5 (GAS5). This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor. We further show that the biotin-labeled GAS5-RNA probe is able to pull down the key component (AGO2) of the RNA-induced silencing complex (RISC) and we subsequently identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs.	MI0000077	Cell Death Differ 2013 Nov 20, 1558-68 doi:10.1038/cdd.2013.110 PMID:23933812
149	LncRNA	CARL	miR-539	PHB2	Heart Tissues	Myocardial Infarction	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24710105	CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation.	A lncRNA, named cardiac apoptosis-related lncRNA (CARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2. The results show that PHB2 is able to inhibit mitochondrial fission and apoptosis. miR-539 is responsible for the dysfunction of PHB2 and regulates mitochondrial fission and apoptosis by targeting PHB2. Further, we show that CARL can act as an endogenous miR-539 sponge that regulates PHB2 expression, mitochondrial fission and apoptosis. Our present study reveals a model of mitochondrial fission regulation that is composed of CARL, miR-539 and PHB2. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.	MI0003514	Nat Commun 2014 Apr 7 5, 3596 doi:10.1038/ncomms4596 PMID:24710105
150	LncRNA	CHRF	miR-489	Myd88	Cardiac Fibroblasts	Cardiac Hypertrophy	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24557880	A Long Noncoding RNA, CHRF Regulates Cardiac Hypertrophy by Targeting miR-489	we explored the molecular mechanism by which miR-489 expression is regulated, and found that a long non-codingRNA that we named cardiac hypertrophy related factor (CHRF) acts as an endogenous sponge of miR-489, which downregulates miR-489 expression levels. We identified miR-489 and lncRNAs (cardiac hypertrophy related factor, CHRF) from hypertrophic cardiomyocytes. Here, we tested the hypothesis that miR-489 and CHRF can participate in the regulation of cardiac hypertrophy in vivo and in vitro.	MI0003124	Circ Res 2014 Apr 25 114, 1377-88 doi:10.1161/circresaha.114.302476 PMID:24557880
151	Artifically engineered RNA	mir-15 sponge	miR-15a	NA	Hek293T	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000069	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
152	Artifically engineered RNA	mir-15 sponge	miR-15b	NA	Hek293T	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000438	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
153	Artifically engineered RNA	mir-16 sponge	miR-16	NA	Hek293T	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000070	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
154	Artifically engineered RNA	AdDecoy133	miR-133	RhoA	Heart Tissues	Cardiac Hypertrophy	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000450	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
155	Artifically engineered RNA	AdDecoy133	miR-133	Cdc42	Heart Tissues	Cardiac Hypertrophy	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000450	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
156	Artifically engineered RNA	AdDecoy133	miR-133	Nelf-A	Heart Tissues	Cardiac Hypertrophy	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000450	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
157	Artifically engineered RNA	AdDecoy133	miR-133	WHSC2	Heart Tissues	Cardiac Hypertrophy	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000450	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
158	Artifically engineered RNA	PGK-223T	miR-223	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000300	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
159	Artifically engineered RNA	SFFV-223T	miR-223	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000300	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
160	Artifically engineered RNA	SFFV-16T	miR-16	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000070	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
161	Artifically engineered RNA	SFFV-23T	miR-23a	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000079	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
162	Artifically engineered RNA	SFFV-142	miR-142-3p	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000458	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
163	Artifically engineered RNA	SFFV-221	miR-221	NA	U937 Cells	Histiocytic Lymphoma	Homo sapiens (human)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000298	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
164	Artifically engineered RNA	sponge-182	miR-182	Casp2	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000272	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
165	Artifically engineered RNA	sponge-182	miR-182	Arrdc3	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000272	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
166	Artifically engineered RNA	sponge-182	miR-182	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000272	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
167	Artifically engineered RNA	sponge-183	miR-183	Arrdc3	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000273	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
168	Artifically engineered RNA	sponge-183	miR-183	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000273	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
169	Artifically engineered RNA	sponge-183	miR-183	Casp2	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000273	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
170	Artifically engineered RNA	sponge-96	miR-96	Arrdc3	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000098	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
171	Artifically engineered RNA	sponge-96	miR-96	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000098	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
172	Artifically engineered RNA	sponge-96	miR-96	Casp2	Y79 Cells,Hek293	Retinoblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000098	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
173	Artifically engineered RNA	mir-31 sponge	miR-31	Fzd3	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-31, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-31 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
174	Artifically engineered RNA	mir-31 sponge	miR-31	ITGA5	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-32, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-32 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
175	Artifically engineered RNA	mir-31 sponge	miR-31	M-RIP	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-33, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-33 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
176	Artifically engineered RNA	mir-31 sponge	miR-31	MMP16	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-34, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-34 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
177	Artifically engineered RNA	mir-31 sponge	miR-31	RDX	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-35, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-35 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
178	Artifically engineered RNA	mir-31 sponge	miR-31	RhoA	Breast Cells, Hek293T Cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-36, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-36 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000089	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
179	Artifically engineered RNA	decoy vector mir-15	miR-15a	CCND1	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Homo sapiens (human)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000069	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
180	Artifically engineered RNA	decoy vector mir-16	miR-16	WNT3A	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Homo sapiens (human)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000070	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
181	Artifically engineered RNA	decoy vector mir-15	miR-15a	CCND1	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Homo sapiens (human)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000069	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
182	Artifically engineered RNA	decoy vector mir-16	miR-16	WNT3A	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Homo sapiens (human)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000070	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
183	Artifically engineered RNA	mir-92 sponge	miR-92	KCC2	Cerebellar Granule Neurons Cells	Neuronal Homeostasis	Homo sapiens (human)	Western blot;Northern blot;luciferase reporter assays	20050974	MicroRNA-92 modulates K(+) Cl( ) co-transporter KCC2 expression in cerebellar granule neurons	Here we show that lentiviral-mediated microRNA-92 over-expression reduced KCC2 protein levels and positively shifted reversal potential of GABA induced Cl(-) currents in CGNs. In addition KCC2 re-expression reversed microRNA-92 electrophysiological phenotype. Consistently microRNA-92 inhibition induced both an increase of the level of KCC2and a negative shift in GABA reversal potential.	MI0000093	J Neurochem 2010 May 113, 591-600 doi:10.1111/j.1471-4159.2009.06560.x PMID:20050974
184	Artifically engineered RNA	LV-ets-1-3UTR-MRE	miR-326	Ets1	Hek293T,Th Cells	Multiple Sclerosis	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19838199	MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis	The braodly used microRNA inhibitor LNA-anti-miR-326 (a locked nucleic acid– modified antisense oligonucleotide directed against miR-326) pro- duced an inhibitory effect on TH-17 differentiation similar to that of infection with LV-sponge. We also differentiated TH-17 cells in vitro with a bicistronic retrovirus encoding miR-326, an internal ribosomal entry site and GFP. Relative to infection by control retrovi- rus (encoding mutant miR-326), transduction of miR-326-encoding virus resulted in a substantially higher percentage of IL-17-expressing cells in the GFP+ population, whereas infection with virus encoding a specific inhibitor of miR-326 resulted in a much lower percentage of IL-17-expressing GFP+ cells.	MI0000808	Nat Immunol 2009 Dec 10, 1252-9 doi:10.1038/ni.1798 PMID:19838199
185	Artifically engineered RNA	LNA-anti-miR-326	miR-326	Ets1	Hek293T,Th Cells	Multiple Sclerosis	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19838199	MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis	The braodly used microRNA inhibitor LNA-anti-miR-326 (a locked nucleic acid– modified antisense oligonucleotide directed against miR-326) pro- duced an inhibitory effect on TH-17 differentiation similar to that of infection with LV-sponge. We also differentiated TH-17 cells in vitro with a bicistronic retrovirus encoding miR-326, an internal ribosomal entry site and GFP. Relative to infection by control retrovi- rus (encoding mutant miR-326), transduction of miR-326-encoding virus resulted in a substantially higher percentage of IL-17-expressing cells in the GFP+ population, whereas infection with virus encoding a specific inhibitor of miR-326 resulted in a much lower percentage of IL-17-expressing GFP+ cells.	MI0000808	Nat Immunol 2009 Dec 10, 1252-9 doi:10.1038/ni.1798 PMID:19838199
186	Artifically engineered RNA	let-7 sponge	let-7b	NA	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000063	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
187	Artifically engineered RNA	mir-22 sponge	miR-22	NA	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000078	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
188	Artifically engineered RNA	mir-124 sponge	miR-124	NA	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000443	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
189	Artifically engineered RNA	mir-125 sponge	miR-125	NR2A	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000469	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
190	Artifically engineered RNA	mir-132 sponge	miR-132	NA	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000449	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
191	Artifically engineered RNA	mir-143 sponge	miR-143	NA	Hippocampal Neurons, Hek293T	NA	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000459	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
192	Artifically engineered RNA	lenti-decoy 133	miR-133	KLF15	Cardiac Myocytes	Cardiac Myocytes	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	19720047	MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes	Cardiac myocytes infected with lenti-decoy, in which the 3UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targetingKLF15 and is involved in metabolic control in cardiomyocytes.	MI0000450	Biochem Biophys Res Commun 2009 Nov 13 389, 315-20 doi:10.1016/j.bbrc.2009.08.136 PMID:19720047
193	Artifically engineered RNA	lenti-decoy 133	miR-133	GLUT4	Cardiac Myocytes	Cardiac Myocytes	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	19720047	MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes	Cardiac myocytes infected with lenti-decoy, in which the 3UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targetingKLF15 and is involved in metabolic control in cardiomyocytes.	MI0000450	Biochem Biophys Res Commun 2009 Nov 13 389, 315-20 doi:10.1016/j.bbrc.2009.08.136 PMID:19720047
194	Artifically engineered RNA	anti-miR-204	miR-204	Runx2	Mesenchymal Progenitor Cells And Bone Marrow Stromal Cell (Bmsc)	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20039258	MicroRNA-204 regulates Runx2 protein expression and mesenchymal progenitor cell differentiation	Retroviral overexpression of miR-204 or transfection of miR-204 oligo decreased Runx2 proteinlevels and miR-204 inhibition significantly elevated Runx2 protein levels, suggesting that miR-204 acts as an endogenous attenuator of Runx2in mesenchymal progenitor cells and BMSCs. Mutations of putative miR-204 binding sites upregulated the Runx2 3-UTR reporter activity, suggesting that miR-204/211 bind to Runx2 3-UTR. Perturbation of miR-204 resulted in altered differentiation fate of mesenchymal progenitorcells and BMSCs: osteoblast differentiation was inhibited and adipocyte differentiation was promoted when miR-204 was overexpressed in these cells, where asosteogenesis was upregulated and adipocyte formation was impaired when miR-204 was inhibited.	MI0000284	Stem Cells 2010 Feb 28, 357-64 doi:10.1002/stem.288 PMID:20039258
195	Artifically engineered RNA	anti-miR-211	miR-211	Runx2	Mesenchymal Progenitor Cells And Bone Marrow Stromal Cell (Bmsc)	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20039258	MicroRNA-204 regulates Runx2 protein expression and mesenchymal progenitor cell differentiation	Retroviral overexpression of miR-204 or transfection of miR-204 oligo decreased Runx2 proteinlevels and miR-204 inhibition significantly elevated Runx2 protein levels, suggesting that miR-204 acts as an endogenous attenuator of Runx2in mesenchymal progenitor cells and BMSCs. Mutations of putative miR-204 binding sites upregulated the Runx2 3-UTR reporter activity, suggesting that miR-204/211 bind to Runx2 3-UTR. Perturbation of miR-204 resulted in altered differentiation fate of mesenchymal progenitorcells and BMSCs: osteoblast differentiation was inhibited and adipocyte differentiation was promoted when miR-204 was overexpressed in these cells, where asosteogenesis was upregulated and adipocyte formation was impaired when miR-204 was inhibited.	MI0000287	Stem Cells 2010 Feb 28, 357-64 doi:10.1002/stem.288 PMID:20039258
196	Artifically engineered RNA	mir-183 sponge	miR-183	Slc1a1	Mouse Retina	Retina	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000273	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
197	Artifically engineered RNA	mir-96 sponge	miR-96	Slc1a1	Mouse Retina	Retina	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000098	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
198	Artifically engineered RNA	mir-182 sponge	miR-182	Slc1a1	Mouse Retina	Retina	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000272	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
199	Artifically engineered RNA	LKR13-Tet-On-KRAB-TE-let-7g	let-7c	HMGA2	Hek293, A549, Calu-1, And H1650	Non-Small Cell Lung Cancer	Homo sapiens (human)	Luciferase reporter assay	18308936	Suppression of non-small cell lung tumor development by the let-7 microRNA family	Here, we show that let-7 functionally inhibits non-small cell tumor development. Ectopic expression of let-7g in K-Ras(G12D)-expressing murine lung cancer cells induced both cell cycle arrest and cell death. In tumorxenografts, we observed significant growth reduction of both murine and human non-small cell lung tumors when overexpression of let-7g was induced from lentiviral vectors. In let-7g expressing tumors, reductions in Ras family and HMGA2 protein levels were detected. Importantly, let-7g-mediated tumor suppression was more potent in lung cancer cell lines harboring oncogenic K-Ras mutations than in lines with other mutations. Ectopic expression of K-Ras(G12D) largely rescued let-7g mediated tumor suppression, whereas ectopic expression of HMGA2 was less effective. Finally, in an autochthonous model of NSCLC in the mouse, let-7g expression substantially reduced lung tumor burden.	MI0000064	Proc Natl Acad Sci U S A 2008 Mar 11 105, 3903-8 doi:10.1073/pnas.0712321105 PMID:18308936
200	Artifically engineered RNA	LKR13-Tet-On-KRAB-TE-let-7g	let-7c	Ras	Hek293, A549, Calu-1, And H1650	Non-Small Cell Lung Cancer	Homo sapiens (human)	Luciferase reporter assay	18308936	Suppression of non-small cell lung tumor development by the let-7 microRNA family	Here, we show that let-7 functionally inhibits non-small cell tumor development. Ectopic expression of let-7g in K-Ras(G12D)-expressing murine lung cancer cells induced both cell cycle arrest and cell death. In tumorxenografts, we observed significant growth reduction of both murine and human non-small cell lung tumors when overexpression of let-7g was induced from lentiviral vectors. In let-7g expressing tumors, reductions in Ras family and HMGA2 protein levels were detected. Importantly, let-7g-mediated tumor suppression was more potent in lung cancer cell lines harboring oncogenic K-Ras mutations than in lines with other mutations. Ectopic expression of K-Ras(G12D) largely rescued let-7g mediated tumor suppression, whereas ectopic expression of HMGA2 was less effective. Finally, in an autochthonous model of NSCLC in the mouse, let-7g expression substantially reduced lung tumor burden.	MI0000064	Proc Natl Acad Sci U S A 2008 Mar 11 105, 3903-8 doi:10.1073/pnas.0712321105 PMID:18308936
201	Artifically engineered RNA	mir-9 sponge	miR-9	CDH1	4T1 Breast Cancer Cell Line	Breast Cancer	Homo sapiens (human)	Reporter assay;Western blot	20173740	miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis	Conversely, inhibiting miR-9 by using a miRNA sponge in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin.	MI0000466	Nat Cell Biol 2010 Mar 12, 247-56 doi:10.1038/ncb2024 PMID:20173740
202	Artifically engineered RNA	mir-9 sponge	miR-9	VEGF	4T1 Breast Cancer Cell Line	Breast Cancer	Homo sapiens (human)	Reporter assay;Western blot	20173740	miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis	Conversely, inhibiting miR-9 by using a miRNA sponge in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin.	MI0000466	Nat Cell Biol 2010 Mar 12, 247-56 doi:10.1038/ncb2024 PMID:20173740
203	Artifically engineered RNA	G-U6-144BT	miR-144	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Homo sapiens (human)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0000460	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
204	Artifically engineered RNA	G-U6-144PT	miR-144	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Homo sapiens (human)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0000460	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
205	Artifically engineered RNA	G-U6-451BT	miR-451	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Homo sapiens (human)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0001729	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
206	Artifically engineered RNA	G-U6-451PT	miR-451	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Homo sapiens (human)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0001729	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
207	Artifically engineered RNA	mir-21 sponge	miR-21	SPRY2	Mouse Cardiocyte	Colon Cancer	Homo sapiens (human)	Luciferase reporter assay	18508928	MicroRNA-21 targets Sprouty2 and promotes cellular outgrowths	Although the sponges induce a modest variable decrease of the endogenous miRNA, our eraser wipes it out. The apparent loss of the miRNA signal on the Northern blots cannot be explained by competition of the complementary eraser RNA with the labeled miRNA probe used for the detection, as proposed by Ebert et al. (2007) blue right-pointing triangle because Northern blots are normally run under extreme denaturing conditions. In cardiocytes, miR-specific erasers rendered endogenous miR-21 and miR-199a undetectable on Northern blots.	MI0000077	Mol Biol Cell 2008 Aug 19, 3272-82 doi:10.1091/mbc.e08-02-0159 PMID:18508928
208	Artifically engineered RNA	pH1ant-miR-18a	miR-18a	NA	K562 Cells	Lymphocytic Leukemias	Homo sapiens (human)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000072	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
209	Artifically engineered RNA	pH1ant-miR-19b	miR-19b	NA	K562 Cells	Lymphocytic Leukemias	Homo sapiens (human)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000074	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
210	Artifically engineered RNA	pH1ant-miR-20a	miR-20a	E2F1	K562 Cells	Lymphocytic Leukemias	Homo sapiens (human)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000076	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
211	Artifically engineered RNA	anti-miR-145	miR-145	TIRAP	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Homo sapiens (human)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000461	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
212	Artifically engineered RNA	anti-miR-146a	miR-146a	TIRAP	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Homo sapiens (human)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000477	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
213	Artifically engineered RNA	anti-miR-145	miR-145	TRAF6	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Homo sapiens (human)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000461	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
214	Artifically engineered RNA	anti-miR-146a	miR-146a	TRAF6	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Homo sapiens (human)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000477	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
215	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
216	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
217	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
218	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
219	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
220	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
221	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
222	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
223	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
224	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
225	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
226	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
227	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
228	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
229	Pseudogene	PTENP1	miR-17	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000071	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
230	Pseudogene	PTENP1	miR-21	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000077	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
231	Pseudogene	PTENP1	miR-214	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post- transcriptional regulation.	MI0000290	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
232	Pseudogene	PTENP1	miR-19	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000073	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
233	Pseudogene	PTENP1	miR-26	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000083	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
234	Pseudogene	PTENP1	miR-19b	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000074	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
235	Pseudogene	PTENP1	miR-20a	PTEN	293T , Pc3,Rwpe-1, Pwr-1E And Vcap	Colon Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20577206	A coding-independent function of gene and pseudogene mRNAs regulates tumour biology	We found perfectly conserved seed matches for the PTEN-targeting miR-17, miR-21, miR-214, miR-19 and miR-26 families. To measure the role of these microRNAs on both PTEN and PTENP1 expression, we designed specific PCR primer sets in the non-homologous 3’UTR regions. In DU145 prostate cancer cells, PTEN-targeting microRNAs miR-19b and miR-20a suppress both PTEN and PTENP1 mRNA abundance. In these cells, a pool of inhibitors of endogenously expressed PTEN-targeting microRNAs derepressed both PTEN and PTENP1 transcript levels. The use of chimeric luciferase plasmids indicated the microRNA:PTENP1 interaction was direct. These data indicate that PTENP1 and PTEN are subjected to the same microRNA-mediated, post-transcriptional regulation.	MI0000076	Nature 2010 Jun 24 465, 1033-8 doi:10.1038/nature09144 PMID:20577206
236	Circular RNA	ciRS-7	miR-7	NA	Brain Tissues	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446346	Natural RNA circles function as efficient microRNA sponges	We further show that the testis-specific circRNA, sex-determining region Y (Sry)9, serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon.	MI0000730	Nature 2013 Mar 21 495, 384-8 doi:10.1038/nature11993 PMID:23446346
237	Circular RNA	sry	miR-138	NA	Brain Tissues	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446346	Natural RNA circles function as efficient microRNA sponges	We further show that the testis-specific circRNA, sex-determining region Y (Sry)9, serves as a miR-138 sponge, suggesting that miRNA sponge effects achieved by circRNA formation are a general phenomenon.	MI0000164	Nature 2013 Mar 21 495, 384-8 doi:10.1038/nature11993 PMID:23446346
238	LncRNA	linc-MD1	miR-133	MAML1	Myoblasts	Muscle Differentiation	Mus musculus (mouse)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000159	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
239	LncRNA	linc-MD1	miR-135	MAML1	Myoblasts	Muscle Differentiation	Mus musculus (mouse)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000161	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
240	LncRNA	linc-MD1	miR-133	MEF2C	Myoblasts	Muscle Differentiation	Mus musculus (mouse)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000159	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
241	LncRNA	linc-MD1	miR-135	MEF2C	Myoblasts	Muscle Differentiation	Mus musculus (mouse)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	22000014	A long noncoding RNA controls muscle differentiation by functioning as a competing endogenous RNA	linc-MD1 "sponges" miR-133 and miR-133 [corrected] to regulate the expression of MAML1 and MEF2C, transcription factors that activate muscle-specific gene expression.	MI0000161	Cell 2011 Oct 14 147, 358-69 doi:10.1016/j.cell.2011.09.028 PMID:22000014
242	LncRNA	AK020764	miR-142-3p	NA	Cd8 T Cells	Adaptive Immunity	Mus musculus (mouse)	qRT-PCR	19494298	Genome-wide identification of long noncoding RNAs in CD8+ T cells.	Two miRNAs, mir-142-5p and mir-142-3p, recently shown to be among the most highly expressed miRNAs in naive, memory, and effector CD8 T cell populations (76), are hosted within the first intron of a long ncRNA (AK020764) that is also strongly expressed in CD8 T cells.	MI0000167	J Immunol 2009 Jun 15 182, 7738-48 doi:10.4049/jimmunol.0900603 PMID:19494298
243	LncRNA	AK020764	miR-142-5p	NA	Cd8 T Cells	Adaptive Immunity	Mus musculus (mouse)	qRT-PCR	19494298	Genome-wide identification of long noncoding RNAs in CD8+ T cells.	Two miRNAs, mir-142-5p and mir-142-3p, recently shown to be among the most highly expressed miRNAs in naive, memory, and effector CD8 T cell populations (76), are hosted within the first intron of a long ncRNA (AK020764) that is also strongly expressed in CD8 T cells.	MI0000167	J Immunol 2009 Jun 15 182, 7738-48 doi:10.4049/jimmunol.0900603 PMID:19494298
244	LncRNA	H19	let-7a	Dicer	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000556	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
245	LncRNA	H19	let-7a	Hmga2	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000556	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
246	LncRNA	H19	let-7a	Igf1	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000556	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
247	LncRNA	H19	let-7a	Igf2	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000556	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
248	LncRNA	H19	let-7b	Dicer	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000558	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
249	LncRNA	H19	let-7b	Hmga2	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000558	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
250	LncRNA	H19	let-7b	Igf1	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000558	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
251	LncRNA	H19	let-7b	Igf2	Mucle Tissues	Precocious Muscle Differentiation	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24055342	The imprinted H19 lncRNA antagonizes let-7 microRNAs	We noted that vertebrate H19 harbors both canonical and noncanonical binding sites for the let-7 family of microRNAs, which plays important roles in development, cancer, and metabolism. Using H19 knockdown and overexpression, combined with in vivo crosslinking and genome-wide transcriptome analysis, we demonstrate that H19 modulates let-7 availability by acting as a molecular sponge. The physiological significance of this interaction is highlighted in cultures in which H19 depletion causes precocious muscle differentiation, a phenotype recapitulated by let-7 overexpression. Our results reveal an unexpected mode of action of H19 and identify this lncRNA as an important regulator of the major let-7 family of microRNAs.	MI0000558	Mol Cell 2013 Oct 10 52, 101-12 doi:10.1016/j.molcel.2013.08.027 PMID:24055342
252	Host gene	H19	miR-675-3p	Smad	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0004123	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
253	Host gene	H19	miR-675-5p	Cdc6	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0004123	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
254	Host gene	H19	miR-675-3p	Smad	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0004123	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
255	Host gene	H19	miR-675-5p	Cdc6	Myoblast Cells And Mouse Satellite Cells	Muscle Differentiation And Regeneration	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24532688	The H19 long noncoding RNA gives rise to microRNAs miR-675-3p and miR-675-5p to promote skeletal muscle differentiation and regeneration	H19 exon1 encodes two conserved microRNAs, miR-675-3p andmiR-675-5p, both of which are induced during skeletal muscle differentiation.miR-675-3p and miR-675-5p functionby directly targeting and down-regulating the anti-differentiation Smadtranscription factors critical for the bone morphogenetic protein (BMP) pathwayand the DNA replication initiation factor Cdc6.	MI0004123	Genes Dev 2014 Mar 1 28, 491-501 doi:10.1101/gad.234419.113 PMID:24532688
256	LncRNA	GAS5	miR-21	NA	Breast Tumor Specimens	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;RNA immunoprecipitation;luciferase reporter assays	23933812	Negative regulation of lncRNA GAS5 by miR-21.	Using the lncRNA RT-PCR (reverse transcription-polymerase chain reaction) array carrying 83 human disease-related lncRNAs, we show that miR-21 is capable of suppressing the lncRNA growth arrest-specific 5 (GAS5). This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor. We further show that the biotin-labeled GAS5-RNA probe is able to pull down the key component (AGO2) of the RNA-induced silencing complex (RISC) and we subsequently identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs.	MI0000569	Cell Death Differ 2013 Nov 20, 1558-68 doi:10.1038/cdd.2013.110 PMID:23933812
257	LncRNA	CARL	miR-539	PHB2	Heart Tissues	Myocardial Infarction	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24710105	CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation.	A lncRNA, named cardiac apoptosis-related lncRNA (CARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2. The results show that PHB2 is able to inhibit mitochondrial fission and apoptosis. miR-539 is responsible for the dysfunction of PHB2 and regulates mitochondrial fission and apoptosis by targeting PHB2. Further, we show that CARL can act as an endogenous miR-539 sponge that regulates PHB2 expression, mitochondrial fission and apoptosis. Our present study reveals a model of mitochondrial fission regulation that is composed of CARL, miR-539 and PHB2. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.	MI0003520	Nat Commun 2014 Apr 7 5, 3596 doi:10.1038/ncomms4596 PMID:24710105
258	LncRNA	CHRF	miR-489	Myd88	Cardiac Fibroblasts	Cardiac Hypertrophy	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24557880	A Long Noncoding RNA, CHRF Regulates Cardiac Hypertrophy by Targeting miR-489	we explored the molecular mechanism by which miR-489 expression is regulated, and found that a long non-codingRNA that we named cardiac hypertrophy related factor (CHRF) acts as an endogenous sponge of miR-489, which downregulates miR-489 expression levels. We identified miR-489 and lncRNAs (cardiac hypertrophy related factor, CHRF) from hypertrophic cardiomyocytes. Here, we tested the hypothesis that miR-489 and CHRF can participate in the regulation of cardiac hypertrophy in vivo and in vitro.	MI0003476	Circ Res 2014 Apr 25 114, 1377-88 doi:10.1161/circresaha.114.302476 PMID:24557880
259	Artifically engineered RNA	mir-15 sponge	miR-15a	NA	Hek293T	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000564	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
260	Artifically engineered RNA	mir-15 sponge	miR-15b	NA	Hek293T	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000140	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
261	Artifically engineered RNA	mir-16 sponge	miR-16	NA	Hek293T	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17694064	MicroRNA sponges: competitive inhibitors of small RNAs in mammalian cells	We made decoy targets for several microRNA seed families, named them ‘microRNA sponges’, and tested their ability to derepress microRNA targets in mammalian cells.	MI0000565	Nat Methods 2007 Sep 4, 721-6 doi:10.1038/nmeth1079 PMID:17694064
262	Artifically engineered RNA	AdDecoy133	miR-133	RhoA	Heart Tissues	Cardiac Hypertrophy	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000159	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
263	Artifically engineered RNA	AdDecoy133	miR-133	Cdc42	Heart Tissues	Cardiac Hypertrophy	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000159	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
264	Artifically engineered RNA	AdDecoy133	miR-133	NelfA	Heart Tissues	Cardiac Hypertrophy	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000159	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
265	Artifically engineered RNA	AdDecoy133	miR-133	WHSC2	Heart Tissues	Cardiac Hypertrophy	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	17468766	MicroRNA-133 controls cardiac hypertrophy	Suppression of miR-133 by ‘decoy’ sequences induced hypertrophy,which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused markedand sustained cardiac hypertrophy.	MI0000159	Nat Med 2007 May 13, 613-8 doi:10.1038/nm1582 PMID:17468766
266	Artifically engineered RNA	PGK-223T	miR-223	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000703	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
267	Artifically engineered RNA	SFFV-223T	miR-223	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000703	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
268	Artifically engineered RNA	SFFV-16T	miR-16	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000565	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
269	Artifically engineered RNA	SFFV-23T	miR-23a	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000571	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
270	Artifically engineered RNA	SFFV-142	miR-142-3p	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000167	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
271	Artifically engineered RNA	SFFV-221	miR-221	NA	U937 Cells	Histiocytic Lymphoma	Mus musculus (mouse)	Western blot	19043411	Stable knockdown of microRNA in vivo by lentiviral vectors	In PGK-223T–transduced cells, we observed lower GFP fluorescence for all vector copy numbers tested, indicating thatmiR-223 was regulating its target. Next we replaced the PGK1 promoter with the stronger spleen focus forming virus enhancer/promoter (SFFV) in both vectors, and transduced U937 cells with the constructs, which we named SFFV-GFP and SFFV-223T. Again, uorescence increased proportionally with the number of integrated vectors	MI0000709	Nat Methods 2009 Jan 6, 63-6 doi:10.1038/nmeth.1277 PMID:19043411
272	Artifically engineered RNA	sponge-182	miR-182	Casp2	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000224	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
273	Artifically engineered RNA	sponge-182	miR-182	Arrdc3	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000224	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
274	Artifically engineered RNA	sponge-182	miR-182	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000224	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
275	Artifically engineered RNA	sponge-183	miR-183	Arrdc3-2	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000225	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
276	Artifically engineered RNA	sponge-183	miR-183	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000225	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
277	Artifically engineered RNA	sponge-183	miR-183	Casp2	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000225	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
278	Artifically engineered RNA	sponge-96	miR-96	Arrdc3	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000583	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
279	Artifically engineered RNA	sponge-96	miR-96	Neurod4	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000583	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
280	Artifically engineered RNA	sponge-96	miR-96	Casp2	Y79 Cells,Hek293	Retinoblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	21768104	Sponge transgenic mouse model reveals important roles for the microRNA-183 (miR-183)/96/182 cluster in postmitotic photoreceptors of the retina.	The miR-183/96/182 cluster sponge element was composed of 10 copies each of sequences complementary to miR-183, miR-96, and miR-182 with mismatches at positions 9–12 to enhance stability. This sequence was inserted into the 3'-UTR of EGFP in a pNOVA expression vector regulated by an Opsin promoter and ending with an SV40 polyadenylation signal	MI0000583	J Biol Chem 2011 Sep 9 286, 31749-60 doi:10.1074/jbc.M111.259028 PMID:21768104
281	Artifically engineered RNA	mir-31 sponge	miR-31	Fzd3	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-31, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-31 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
282	Artifically engineered RNA	mir-31 sponge	miR-31	ITGA5	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-32, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-32 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
283	Artifically engineered RNA	mir-31 sponge	miR-31	M-RIP	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-33, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-33 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
284	Artifically engineered RNA	mir-31 sponge	miR-31	MMP16	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-34, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-34 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
285	Artifically engineered RNA	mir-31 sponge	miR-31	RDX	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-35, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-35 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
286	Artifically engineered RNA	mir-31 sponge	miR-31	RhoA	Breast Cells, Hek293T Cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR;Western blot	19524507	A pleiotropically acting microRNA, miR-36, inhibits breast cancer metastasis	We deploy a stable microRNA sponge strategy to inhibit miR-36 in vivo; this allows otherwise-nonaggressive breast cancer cells to metastasize.	MI0000579	Cell 2009 Jun 12 137, 1032-46 doi:10.1016/j.cell.2009.03.047 PMID:19524507
287	Artifically engineered RNA	decoy vector mir-15	miR-15a	CCND1	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Mus musculus (mouse)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000564	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
288	Artifically engineered RNA	decoy vector mir-16	miR-16	WNT3A	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Mus musculus (mouse)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000565	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
289	Artifically engineered RNA	decoy vector mir-15	miR-15a	CCND1	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Mus musculus (mouse)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000564	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
290	Artifically engineered RNA	decoy vector mir-16	miR-16	WNT3A	Human Prostate Cancer Line,Mouse Prostate	Prostate Cancer	Mus musculus (mouse)	Luciferase reporter assay	18931683	The miR-15a-miR-16-1 cluster controls prostate cancer by targeting multiple oncogenic activities	Delivery of antagomirs specific for miR-15a and miR-16 to normal mouse prostate results in marked hyperplasia, and knockdown of miR-15a and miR-16 promotes survival, proliferation and invasiveness of untransformed prostate cells, which become tumorigenic in immunodeficient NOD-SCID mice.	MI0000565	Nat Med 2008 Nov 14, 1271-7 doi:10.1038/nm.1880 PMID:18931683
291	Artifically engineered RNA	mir-92 sponge	miR-92	KCC2	Cerebellar Granule Neurons Cells	Neuronal Homeostasis	Mus musculus (mouse)	Western blot;Northern blot;luciferase reporter assays	20050974	MicroRNA-92 modulates K(+) Cl( ) co-transporter KCC2 expression in cerebellar granule neurons	Here we show that lentiviral-mediated microRNA-92 over-expression reduced KCC2 protein levels and positively shifted reversal potential of GABA induced Cl(-) currents in CGNs. In addition KCC2 re-expression reversed microRNA-92 electrophysiological phenotype. Consistently microRNA-92 inhibition induced both an increase of the level of KCC2and a negative shift in GABA reversal potential.	MI0000719	J Neurochem 2010 May 113, 591-600 doi:10.1111/j.1471-4159.2009.06560.x PMID:20050974
292	Artifically engineered RNA	LV-ets-1-3UTR-MRE	miR-326	Ets1	Hek293T,Th Cells	Multiple Sclerosis	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	19838199	MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis	The braodly used microRNA inhibitor LNA-anti-miR-326 (a locked nucleic acid– modified antisense oligonucleotide directed against miR-326) pro- duced an inhibitory effect on TH-17 differentiation similar to that of infection with LV-sponge. We also differentiated TH-17 cells in vitro with a bicistronic retrovirus encoding miR-326, an internal ribosomal entry site and GFP. Relative to infection by control retrovi- rus (encoding mutant miR-326), transduction of miR-326-encoding virus resulted in a substantially higher percentage of IL-17-expressing cells in the GFP+ population, whereas infection with virus encoding a specific inhibitor of miR-326 resulted in a much lower percentage of IL-17-expressing GFP+ cells.	MI0000598	Nat Immunol 2009 Dec 10, 1252-9 doi:10.1038/ni.1798 PMID:19838199
293	Artifically engineered RNA	LNA-anti-miR-326	miR-326	Ets1	Hek293T,Th Cells	Multiple Sclerosis	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	19838199	MicroRNA miR-326 regulates TH-17 differentiation and is associated with the pathogenesis of multiple sclerosis	The braodly used microRNA inhibitor LNA-anti-miR-326 (a locked nucleic acid– modified antisense oligonucleotide directed against miR-326) pro- duced an inhibitory effect on TH-17 differentiation similar to that of infection with LV-sponge. We also differentiated TH-17 cells in vitro with a bicistronic retrovirus encoding miR-326, an internal ribosomal entry site and GFP. Relative to infection by control retrovi- rus (encoding mutant miR-326), transduction of miR-326-encoding virus resulted in a substantially higher percentage of IL-17-expressing cells in the GFP+ population, whereas infection with virus encoding a specific inhibitor of miR-326 resulted in a much lower percentage of IL-17-expressing GFP+ cells.	MI0000598	Nat Immunol 2009 Dec 10, 1252-9 doi:10.1038/ni.1798 PMID:19838199
294	Artifically engineered RNA	let-7 sponge	let-7a	NA	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000556	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
295	Artifically engineered RNA	mir-22 sponge	miR-22	NA	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000570	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
296	Artifically engineered RNA	mir-124 sponge	miR-124	NA	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000150	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
297	Artifically engineered RNA	mir-125 sponge	miR-125	NR2A	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000151	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
298	Artifically engineered RNA	mir-132 sponge	miR-132	NA	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000158	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
299	Artifically engineered RNA	mir-143 sponge	miR-143	NA	Hippocampal Neurons, Hek293T	NA	Mus musculus (mouse)	Luciferase reporter assay;qRT-PCR	20159450	Regulation of synaptic structure and function by FMRP-associated microRNAs miR-125b and miR-132.	We show that miR-125b and miR-132, as well as several other miRNAs, are associated with FMRP in mouse brain. miR-125b and miR-132 had largely opposing effects on dendritic spine morphology and synaptic physiology in hippocampal neurons. FMRP knockdown ameliorates the effect of miRNA overexpression on spine morphology. We identified NMDA receptor subunit NR2A as a target of miR-125b and show that NR2A mRNA is specifically associated with FMRP in brain. In hippocampal neurons, NR2A expression is negatively regulated through its 3 UTR by FMRP, miR-125b, and Argonaute 1. Regulation of NR2A 3UTR by FMRP depends in part on miR-125b	MI0000257	Neuron 2010 Feb 11 65, 373-84 doi:10.1016/j.neuron.2010.01.005 PMID:20159450
300	Artifically engineered RNA	lenti-decoy 133	miR-133	KLF15	Cardiac Myocytes	Cardiac Myocytes	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	19720047	MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes	Cardiac myocytes infected with lenti-decoy, in which the 3UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targetingKLF15 and is involved in metabolic control in cardiomyocytes.	MI0000159	Biochem Biophys Res Commun 2009 Nov 13 389, 315-20 doi:10.1016/j.bbrc.2009.08.136 PMID:19720047
301	Artifically engineered RNA	lenti-decoy 133	miR-133	GLUT4	Cardiac Myocytes	Cardiac Myocytes	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	19720047	MicroRNA-133 regulates the expression of GLUT4 by targeting KLF15 and is involved in metabolic control in cardiac myocytes	Cardiac myocytes infected with lenti-decoy, in which the 3UTR with tandem sequences complementary to miR-133 was linked to the luciferase reporter gene, had decreased miR-133 levels and increased levels of GLUT4. The expression levels of KLF15 and GLUT4 were decreased at the left ventricular hypertrophy and congestive heart failure stage in a rat model. The present results indicated that miR-133 regulates the expression of GLUT4 by targetingKLF15 and is involved in metabolic control in cardiomyocytes.	MI0000159	Biochem Biophys Res Commun 2009 Nov 13 389, 315-20 doi:10.1016/j.bbrc.2009.08.136 PMID:19720047
302	Artifically engineered RNA	anti-miR-204	miR-204	Runx2	Mesenchymal Progenitor Cells And Bone Marrow Stromal Cell (Bmsc)	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20039258	MicroRNA-204 regulates Runx2 protein expression and mesenchymal progenitor cell differentiation	Retroviral overexpression of miR-204 or transfection of miR-204 oligo decreased Runx2 proteinlevels and miR-204 inhibition significantly elevated Runx2 protein levels, suggesting that miR-204 acts as an endogenous attenuator of Runx2in mesenchymal progenitor cells and BMSCs. Mutations of putative miR-204 binding sites upregulated the Runx2 3-UTR reporter activity, suggesting that miR-204/211 bind to Runx2 3-UTR. Perturbation of miR-204 resulted in altered differentiation fate of mesenchymal progenitorcells and BMSCs: osteoblast differentiation was inhibited and adipocyte differentiation was promoted when miR-204 was overexpressed in these cells, whereasosteogenesis was upregulated and adipocyte formation was impaired when miR-204 was inhibited.	MI0000247	Stem Cells 2010 Feb 28, 357-64 doi:10.1002/stem.288 PMID:20039258
303	Artifically engineered RNA	anti-miR-211	miR-211	Runx2	Mesenchymal Progenitor Cells And Bone Marrow Stromal Cell (Bmsc)	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20039258	MicroRNA-204 regulates Runx2 protein expression and mesenchymal progenitor cell differentiation	Retroviral overexpression of miR-204 or transfection of miR-204 oligo decreased Runx2 proteinlevels and miR-204 inhibition significantly elevated Runx2 protein levels, suggesting that miR-204 acts as an endogenous attenuator of Runx2in mesenchymal progenitor cells and BMSCs. Mutations of putative miR-204 binding sites upregulated the Runx2 3-UTR reporter activity, suggesting that miR-204/211 bind to Runx2 3-UTR. Perturbation of miR-204 resulted in altered differentiation fate of mesenchymal progenitorcells and BMSCs: osteoblast differentiation was inhibited and adipocyte differentiation was promoted when miR-204 was overexpressed in these cells, whereasosteogenesis was upregulated and adipocyte formation was impaired when miR-204 was inhibited.	MI0000708	Stem Cells 2010 Feb 28, 357-64 doi:10.1002/stem.288 PMID:20039258
304	Artifically engineered RNA	mir-183 sponge	miR-183	Slc1a1	Mouse Retina	Retina	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000225	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
305	Artifically engineered RNA	mir-96 sponge	miR-96	Slc1a1	Mouse Retina	Retina	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000583	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
306	Artifically engineered RNA	mir-182 sponge	miR-182	Slc1a1	Mouse Retina	Retina	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	20478254	Characterizing light-regulated retinal microRNAs reveals rapid turnover as a common property of neuronal microRNAs	To get further support for the role of the miR-183/96/182 cluster in regulating Slc1a1 mRNA, we generated EGFP constructs expressing miR-183/96/182-speci c ‘‘sponges’’ in their 30 -UTR (Ebert et al., 2007). Three sponges, each containing eight sites complementary to one of the three miR-183/96/182 cluster miRNAs and a sponge containing four sites speci c to each of the three miRNAs (triple sponge) were constructed. When tested in mouse NIH 3T3 cells, all sponges markedly relieved the repression of FL-Slc1a1_wt reporter induced by the cotransfection of either single miR-183/ 96/182 cluster miRNAs or a mixture of the three	MI0000224	Cell 2010 May 14 141, 618-31 doi:10.1016/j.cell.2010.03.039 PMID:20478254
307	Artifically engineered RNA	LKR13-Tet-On-KRAB-TE-let-7g	let-7c	HMGA2	Hek293, A549, Calu-1, And H1650	Non-Small Cell Lung Cancer	Mus musculus (mouse)	Luciferase reporter assay	18308936	Suppression of non-small cell lung tumor development by the let-7 microRNA family	Here, we show that let-7 functionally inhibits non-small cell tumor development. Ectopic expression of let-7g in K-Ras(G12D)-expressing murine lung cancer cells induced both cell cycle arrest and cell death. In tumorxenografts, we observed significant growth reduction of both murine and human non-small cell lung tumors when overexpression of let-7g was induced from lentiviral vectors. In let-7g expressing tumors, reductions in Ras family and HMGA2 protein levels were detected. Importantly, let-7g-mediated tumor suppression was more potent in lung cancer cell lines harboring oncogenic K-Ras mutations than in lines with other mutations. Ectopic expression of K-Ras(G12D) largely rescued let-7g mediated tumor suppression, whereas ectopic expression of HMGA2 was less effective. Finally, in an autochthonous model of NSCLC in the mouse, let-7g expression substantially reduced lung tumor burden.	MI0000559	Proc Natl Acad Sci U S A 2008 Mar 11 105, 3903-8 doi:10.1073/pnas.0712321105 PMID:18308936
308	Artifically engineered RNA	LKR13-Tet-On-KRAB-TE-let-7g	let-7c	Ras	Hek293, A549, Calu-1, And H1650	Non-Small Cell Lung Cancer	Mus musculus (mouse)	Luciferase reporter assay	18308936	Suppression of non-small cell lung tumor development by the let-7 microRNA family	Here, we show that let-7 functionally inhibits non-small cell tumor development. Ectopic expression of let-7g in K-Ras(G12D)-expressing murine lung cancer cells induced both cell cycle arrest and cell death. In tumorxenografts, we observed significant growth reduction of both murine and human non-small cell lung tumors when overexpression of let-7g was induced from lentiviral vectors. In let-7g expressing tumors, reductions in Ras family and HMGA2 protein levels were detected. Importantly, let-7g-mediated tumor suppression was more potent in lung cancer cell lines harboring oncogenic K-Ras mutations than in lines with other mutations. Ectopic expression of K-Ras(G12D) largely rescued let-7g mediated tumor suppression, whereas ectopic expression of HMGA2 was less effective. Finally, in an autochthonous model of NSCLC in the mouse, let-7g expression substantially reduced lung tumor burden.	MI0000559	Proc Natl Acad Sci U S A 2008 Mar 11 105, 3903-8 doi:10.1073/pnas.0712321105 PMID:18308936
309	Artifically engineered RNA	mir-9 sponge	miR-9	CDH1	4T1 Breast Cancer Cell Line	Breast Cancer	Mus musculus (mouse)	Reporter assay;Western blot	20173740	miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis	Conversely, inhibiting miR-9 by using a miRNA sponge in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin.	MI0000157	Nat Cell Biol 2010 Mar 12, 247-56 doi:10.1038/ncb2024 PMID:20173740
310	Artifically engineered RNA	mir-9 sponge	miR-9	VEGF	4T1 Breast Cancer Cell Line	Breast Cancer	Mus musculus (mouse)	Reporter assay;Western blot	20173740	miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis	Conversely, inhibiting miR-9 by using a miRNA sponge in highly malignant cells inhibits metastasis formation. Expression of miR-9 is activated by MYC and MYCN, both of which directly bind to the mir-9-3 locus. Significantly, in human cancers, miR-9 levels correlate with MYCN amplification, tumour grade and metastatic status. These findings uncover a regulatory and signalling pathway involving a metastasis-promoting miRNA that is predicted to directly target expression of the key metastasis-suppressing protein E-cadherin.	MI0000157	Nat Cell Biol 2010 Mar 12, 247-56 doi:10.1038/ncb2024 PMID:20173740
311	Artifically engineered RNA	G-U6-144BT	miR-144	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Mus musculus (mouse)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0000168	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
312	Artifically engineered RNA	G-U6-144PT	miR-144	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Mus musculus (mouse)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0000168	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
313	Artifically engineered RNA	G-U6-451BT	miR-451	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Mus musculus (mouse)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0001730	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
314	Artifically engineered RNA	G-U6-451PT	miR-451	NA	Murine Hematopoietic	Mammalian Hematopoiesis	Mus musculus (mouse)	qRT-PCR	19911427	A genetic strategy for single and combinatorial analysis of miRNA function in mammalian hematopoietic stem cells	We developed decoy target sequences for each miRNA expressed by lentiviral vectors marked with distinct fluorescent proteins and used them to probe the functions of miR-144 and miR-451 in the murine hematopoietic system in a competitive repopulation setting. Murinehematopoietic chimeras expressing lentiviral-encoded inhibitory sequences specific for miR-144 or miR-451 exhibited markedly reduced Ter119(+) erythroblast counts, with the combined knockdown showing additive effect. These chimeras showed abnormal patterns of erythroid differentiation primarily affecting the proerythroblast to basophilic erythroblast transition, coinciding with the stage where expression of themiRNA cluster is dramatically induced and posttranscriptional gene regulation becomes prominent. These results reveal a role for the miR-144/451 locus in mammalian erythropoiesis and provide the first evidence of functional cooperativity between clustered miRNAs in thehematopoietic system	MI0001730	Stem Cells 2010 Feb 28, 287-96 doi:10.1002/stem.257 PMID:19911427
315	Artifically engineered RNA	mir-21 sponge	miR-21	SPRY2	Mouse Cardiocyte	Mammalian Hematopoiesis	Mus musculus (mouse)	Luciferase reporter assay	18508928	MicroRNA-21 targets Sprouty2 and promotes cellular outgrowths	Although the sponges induce a modest variable decrease of the endogenous miRNA, our eraser wipes it out. The apparent loss of the miRNA signal on the Northern blots cannot be explained by competition of the complementary eraser RNA with the labeled miRNA probe used for the detection, as proposed by Ebert et al. (2007) blue right-pointing triangle because Northern blots are normally run under extreme denaturing conditions. In cardiocytes, miR-specific erasers rendered endogenous miR-21 and miR-199a undetectable on Northern blots.	MI0000569	Mol Biol Cell 2008 Aug 19, 3272-82 doi:10.1091/mbc.e08-02-0159 PMID:18508928
316	Artifically engineered RNA	pH1ant-miR-18a	miR-18a	NA	K562 Cells	Lymphocytic Leukemias	Mus musculus (mouse)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000567	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
317	Artifically engineered RNA	pH1ant-miR-19b	miR-19b	NA	K562 Cells	Lymphocytic Leukemias	Mus musculus (mouse)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000718	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
318	Artifically engineered RNA	pH1ant-miR-20a	miR-20a	E2F1	K562 Cells	Lymphocytic Leukemias	Mus musculus (mouse)	Western blot	18025036	Lentivirus-mediated antagomir expression for specific inhibition of miRNA function	Here, we describe the induction of stable loss-of-function phenotypes for specific miRNAs by lentivirus-mediated antagomirexpression. Lentivirally expressed antagomirs are transcribed from a H1-promoter located within the lentiviral 3LTR and were directed against miRNAs encoded on the polycistronic miR17-92 transcript. Functional silencing of miR-18a, miR-19b and miR-20a by the corresponding antagomirs specifically relieves miRNA-mediated reporter gene repression. Inhibition of miRNA function correlates to reduction of miRNA amplification by miRNA-specific quantitative RT-PCR. Furthermore, protein expression of E2F1, a known miR-20 target, is enhanced by lentivirally expressed anti-miR-20 antagomirs in a dose-dependent manner, whereas over-expression of miR-20a reduces E2F1 levels.	MI0000568	Nucleic Acids Res 2007  35, e149 doi:10.1093/nar/gkm971 PMID:18025036
319	Artifically engineered RNA	anti-miR-145	miR-145	TIRAP	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Mus musculus (mouse)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000169	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
320	Artifically engineered RNA	anti-miR-146a	miR-146a	TIRAP	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Mus musculus (mouse)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000170	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
321	Artifically engineered RNA	anti-miR-145	miR-145	TRAF6	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Mus musculus (mouse)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000169	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
322	Artifically engineered RNA	anti-miR-146a	miR-146a	TRAF6	Hematopoietic Stem/Progenitor Cells (Hspcs)	5Q-Syndrome Phenotype	Mus musculus (mouse)	Immunoprecipitaion;Western blot;Communoprecipitaion	19898489	Identification of miR-145 and miR-146a as mediators of the 5q- syndrome phenotype.	We show that deletion of chromosome 5q correlates with loss of two miRNAs that are abundant in hematopoietic stem/progenitor cells (HSPCs), miR-145 and miR-146a, and we identify Toll–interleukin-1 receptor domain–containing adaptor protein (TIRAP) and tumor necrosis factor receptor–associated factor-6 (TRAF6) as respective targets of these miRNAs. TIRAP is known to lie upstream of TRAF6 in innate immune signaling. Knockdown of miR-145 and miR-146a together or enforced expression of TRAF6 in mouse HSPCs resulted in thrombocytosis, mild neutropenia and megakaryocytic dysplasia. A subset of mice transplanted with TRAF6-expressing marrow progressed either to marrow failure or acute myeloid leukemia.	MI0000170	Nat Med 2010 Jan 16, 49-58 doi:10.1038/nm.2054 PMID:19898489
323	Circular RNA	CDR1as	miR-7	PAK1	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
324	Circular RNA	CDR1as	miR-7	FAK1	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
325	Circular RNA	CDR1as	miR-7	EGFR	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
326	Circular RNA	CDR1as	miR-7	IGF1R	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
327	Circular RNA	CDR1as	miR-7	LSH	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
328	Circular RNA	CDR1as	miR-7	RAF1	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
329	Circular RNA	CDR1as	miR-7	SNCA	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
330	Circular RNA	CDR1as	miR-7	SRSF1	Neocortical,Hippocampal Neurons,Brain	NA	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
331	Circular RNA	CDR1as	miR-7	PAK1	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
332	Circular RNA	CDR1as	miR-7	FAK1	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
333	Circular RNA	CDR1as	miR-7	EGFR	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
334	Circular RNA	CDR1as	miR-7	IGF1R	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
335	Circular RNA	CDR1as	miR-7	LSH	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
336	Circular RNA	CDR1as	miR-7	RAF1	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
337	Circular RNA	CDR1as	miR-7	SNCA	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
338	Circular RNA	CDR1as	miR-7	SRSF1	Neocortical,Hippocampal Neurons,Brain	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000730	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
339	Circular RNA	CDR1as	miR-7	PAK1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
340	Circular RNA	CDR1as	miR-7	FAK1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
341	Circular RNA	CDR1as	miR-7	EGFR	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
342	Circular RNA	CDR1as	miR-7	IGF1R	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
343	Circular RNA	CDR1as	miR-7	LSH	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
344	Circular RNA	CDR1as	miR-7	RAF1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
345	Circular RNA	CDR1as	miR-7	SNCA	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
346	Circular RNA	CDR1as	miR-7	SRSF1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
347	Circular RNA	CDR1as	miR-7	PAK1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
348	Circular RNA	CDR1as	miR-7	FAK1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
349	Circular RNA	CDR1as	miR-7	EGFR	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
350	Circular RNA	CDR1as	miR-7	IGF1R	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
351	Circular RNA	CDR1as	miR-7	LSH	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
352	Circular RNA	CDR1as	miR-7	RAF1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
353	Circular RNA	CDR1as	miR-7	SNCA	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
354	Circular RNA	CDR1as	miR-7	SRSF1	Neocortical,Hippocampal Neurons,Brain	NA	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
355	Viral RNA	viral transcript m169	miR-27a	NA	Murine Embryonic Fibroblasts And Bone Marrow Stroma Cells	Mcmv Infection	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Northern blot	22346748	Degradation of Cellular miR-27 by a Novel, Highly Abundant Viral Transcript Is Important for Efficient Virus Replication In Vivo	In this paper, we show that their regulation is mediated by the highly abundant viral transcript m169. It targets miR-27a/b via a single binding site in its 3'-UTR, which can be efficiently retargeted to other cellular and viral miRNAs, enabling the efficient knock-down of individual miRNAs of interest. Degradation of miR-27a/b is preceded by its 3'-tailing and -trimming.	MI0000085	PLoS Pathog 2012 Feb 8, e1002510 doi:10.1371/journal.ppat.1002510 PMID:22346748
356	Viral RNA	viral transcript m169	miR-27b	NA	Murine Embryonic Fibroblasts And Bone Marrow Stroma Cells	Mcmv Infection	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Northern blot	22346748	Degradation of Cellular miR-27 by a Novel, Highly Abundant Viral Transcript Is Important for Efficient Virus Replication In Vivo	In this paper, we show that their regulation is mediated by the highly abundant viral transcript m169. It targets miR-27a/b via a single binding site in its 3'-UTR, which can be efficiently retargeted to other cellular and viral miRNAs, enabling the efficient knock-down of individual miRNAs of interest. Degradation of miR-27a/b is preceded by its 3'-tailing and -trimming.	MI0000440	PLoS Pathog 2012 Feb 8, e1002510 doi:10.1371/journal.ppat.1002510 PMID:22346748
357	Viral RNA	viral transcript m169	miR-27a	NA	Murine Embryonic Fibroblasts And Bone Marrow Stroma Cells	Mcmv Infection	Murid herpesvirus 1 (murine cytomegalovirus)	qRT-PCR;luciferase reporter assays;Northern blot	22346748	Degradation of Cellular miR-27 by a Novel, Highly Abundant Viral Transcript Is Important for Efficient Virus Replication In Vivo	In this paper, we show that their regulation is mediated by the highly abundant viral transcript m169. It targets miR-27a/b via a single binding site in its 3'-UTR, which can be efficiently retargeted to other cellular and viral miRNAs, enabling the efficient knock-down of individual miRNAs of interest. Degradation of miR-27a/b is preceded by its 3'-tailing and -trimming.	MI0000085	PLoS Pathog 2012 Feb 8, e1002510 doi:10.1371/journal.ppat.1002510 PMID:22346748
358	Viral RNA	viral transcript m169	miR-27b	NA	Murine Embryonic Fibroblasts And Bone Marrow Stroma Cells	Mcmv Infection	Murid herpesvirus 1 (murine cytomegalovirus)	qRT-PCR;luciferase reporter assays;Northern blot	22346748	Degradation of Cellular miR-27 by a Novel, Highly Abundant Viral Transcript Is Important for Efficient Virus Replication In Vivo	In this paper, we show that their regulation is mediated by the highly abundant viral transcript m169. It targets miR-27a/b via a single binding site in its 3'-UTR, which can be efficiently retargeted to other cellular and viral miRNAs, enabling the efficient knock-down of individual miRNAs of interest. Degradation of miR-27a/b is preceded by its 3'-tailing and -trimming.	MI0000440	PLoS Pathog 2012 Feb 8, e1002510 doi:10.1371/journal.ppat.1002510 PMID:22346748
359	Circular RNA	CDR1as	miR-7	NA	Y79 Cells	Impaired Midbrain Development	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	We found that a human circRNA, antisense to the cerebellar degeneration-related protein 1 transcript (CDR1as), is densely bound by microRNA (miRNA) effector complexes and harbours 63 conserved binding sites for the ancient miRNA miR-7. Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0000263	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
360	Circular RNA	CDR1as	miR-7	NA	Y79 Cells	Impaired Midbrain Development	Danio rerio (zebrafish)	Western blot;qRT-PCR;luciferase reporter assays	23446348	Circular RNAs are a large class of animal RNAs with regulatory potency	We found that a human circRNA, antisense to the cerebellar degeneration-related protein 1 transcript (CDR1as), is densely bound by microRNA (miRNA) effector complexes and harbours 63 conserved binding sites for the ancient miRNA miR-7. Further analyses indicated that CDR1as functions to bind miR-7 in neuronal tissues. Human CDR1as expression in zebrafish impaired midbrain development, similar to knocking down miR-7, suggesting that CDR1as is a miRNA antagonist with a miRNA-binding capacity ten times higher than any other known transcript.	MI0001361	Nature 2013 Mar 21 495, 333-8 doi:10.1038/nature11928 PMID:23446348
361	LncRNA	Ncrms	miR-135a	NA	Brain Tissues	Medulloblastoma	Mus musculus (mouse)	qRT-PCR	20380817	Long non-coding RNAs in nervous system function and disease.	Ncrms serves as a host gene for miR-135a (Rodriguez et al., 2004), an oncogenic miRNA that is dysregulated in medulloblastoma.	MI0000161	Brain Res 2010 Jun 18 1338, 20-35 doi:10.1016/j.brainres.2010.03.110 PMID:20380817
362	LncRNA	AK088388	miR-29b-3p	Plxna4	Pulmonary Fibrosis	Pulmonary Fibrosis	Mus musculus (mouse)	qRT-PCR	24702795	Analysing the relationship between lncRNA and protein-coding gene and the role of lncRNA as ceRNA in pulmonary fibrosis.	In this study, we selected two differentially expressed lncRNAs MRAK088388 and MRAK081523 to explore their regulatory mechanisms. MRAK088388 and MRAK081523 were analysed as long-intergenic non-coding RNAs (lincRNAs), and identified as orthologues of mouse lncRNAs AK088388 and AK081523, respectively. qRT-PCR and in situ hybridization (ISH) showed that they were significantly up-regulated, and located in the cytoplasm of interstitial lung cells. We also showed that MRAK088388 and N4bp2 had the same miRNA response elements (MREs) for miR-200, miR-429, miR-29, and miR-30, whereas MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98, and let-7. Moreover, the expression levels of N4bp2 and Plxna4 significantly increased in fibrotic rats, and were highly correlated with those of MRAK088388 and MRAK081523, respectively. Among their shared miRNAs, miR-29b-3p and let-7i-5p decreased in the model group, and were negatively correlated with the expression of MRAK088388 and MRAK081523, respectively. MRAK088388 and MRAK081523 could regulate N4bp2 and Plxna4 expression by sponging miR-29b-3p and let-7i-5p, respectively, and possessed regulatory functions as ceRNAs.	MI0000143	J Cell Mol Med 2014 Jun 18, 991-1003 doi:10.1111/jcmm.12243 PMID:24702795
363	LncRNA	AK081523	let-7i	Plxna4	Pulmonary Fibrosis	Pulmonary Fibrosis	Mus musculus (mouse)	qRT-PCR	24702795	Analysing the relationship between lncRNA and protein-coding gene and the role of lncRNA as ceRNA in pulmonary fibrosis.	In this study, we selected two differentially expressed lncRNAs MRAK088388 and MRAK081523 to explore their regulatory mechanisms. MRAK088388 and MRAK081523 were analysed as long-intergenic non-coding RNAs (lincRNAs), and identified as orthologues of mouse lncRNAs AK088388 and AK081523, respectively. qRT-PCR and in situ hybridization (ISH) showed that they were significantly up-regulated, and located in the cytoplasm of interstitial lung cells. We also showed that MRAK088388 and N4bp2 had the same miRNA response elements (MREs) for miR-200, miR-429, miR-29, and miR-30, whereas MRAK081523 and Plxna4 had the same MREs for miR-218, miR-141, miR-98, and let-7. Moreover, the expression levels of N4bp2 and Plxna4 significantly increased in fibrotic rats, and were highly correlated with those of MRAK088388 and MRAK081523, respectively. Among their shared miRNAs, miR-29b-3p and let-7i-5p decreased in the model group, and were negatively correlated with the expression of MRAK088388 and MRAK081523, respectively. MRAK088388 and MRAK081523 could regulate N4bp2 and Plxna4 expression by sponging miR-29b-3p and let-7i-5p, respectively, and possessed regulatory functions as ceRNAs.	MI0000138	J Cell Mol Med 2014 Jun 18, 991-1003 doi:10.1111/jcmm.12243 PMID:24702795
364	Artifically engineered RNA	anti-miR-122 TuD	miR-122	NA	Liver, Heart	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22388288	Long-term, efficient inhibition of microRNA function in mice using rAAV vectors	To accelerate analysis of miRNA biology in mammals, we combined recombinant adeno-associated virus (rAAV) vectors with miRNA tough decoys (TuDs) to inhibit specific miRNAs. rAAV producing anti-miR-122 TuD but not anti-let-7 TuD reduced serum cholesterol by >30% for 25 weeks in wild-type mice.	MI0000256	Nat Methods 2012 Mar 4 9, 403-9 doi:10.1038/nmeth.1903 PMID:22388288
365	Artifically engineered RNA	antagomir-10b	miR-10b	HOXD10	4T1 Breast Cancer Cell Line	Breast Cancer	Mus musculus (mouse)	qRT-PCR	20351690	Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model	Here we show that systemic treatment oftumor-bearing mice with miR-10b antagomirs-a class of chemically modified anti-miRNA oligonucleotide-suppresses breast cancermetastasis. Both in vitro and in vivo, silencing of miR-10b with antagomirs significantly decreases miR-10b levels and increases the levels of a functionally important miR-10b target, Hoxd10. Administration of miR-10b antagomirs to mice bearing highly metastatic cells does not reduce primary mammary tumor growth but markedly suppresses formation of lung metastases in a sequence-specific manner.	MI0000221	Nat Biotechnol 2010 Apr 28, 341-7 doi:10.1038/nbt.1618 PMID:20351690
366	Artifically engineered RNA	antagomir-10b	miR-10b	RHOC	4T1 Breast Cancer Cell Line	Breast Cancer	Mus musculus (mouse)	qRT-PCR	20351690	Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model	Here we show that systemic treatment oftumor-bearing mice with miR-10b antagomirs-a class of chemically modified anti-miRNA oligonucleotide-suppresses breast cancermetastasis. Both in vitro and in vivo, silencing of miR-10b with antagomirs significantly decreases miR-10b levels and increases the levels of a functionally important miR-10b target, Hoxd10. Administration of miR-10b antagomirs to mice bearing highly metastatic cells does not reduce primary mammary tumor growth but markedly suppresses formation of lung metastases in a sequence-specific manner.	MI0000221	Nat Biotechnol 2010 Apr 28, 341-7 doi:10.1038/nbt.1618 PMID:20351690
367	Coding-mRNA	Zfp874b	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
368	Coding-mRNA	Fuca2	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
369	Coding-mRNA	Tbc1d10a	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
370	Coding-mRNA	1810037l17Rik	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
371	Coding-mRNA	Camk1d	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
372	Coding-mRNA	Abcc3	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
373	Coding-mRNA	GStm1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
374	Coding-mRNA	Mettl16	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
375	Coding-mRNA	Ugdh	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
376	Coding-mRNA	Zfc3h1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
377	Coding-mRNA	Prss53	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
378	Coding-mRNA	Zscan21	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
379	Coding-mRNA	Bbx	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
380	Coding-mRNA	Stx7	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
381	Coding-mRNA	Asb1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
382	Coding-mRNA	Psma1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
383	Coding-mRNA	Hadh	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
384	Coding-mRNA	Ptpn23	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
385	Coding-mRNA	Tdo2	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
386	Coding-mRNA	Grem2	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
387	Coding-mRNA	Mrs2	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
388	Coding-mRNA	Obfc1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
389	Coding-mRNA	Zfp874a	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
390	Coding-mRNA	Arl12b	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
391	Coding-mRNA	Lima1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
392	Coding-mRNA	Ggps1	miR-122-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000256	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
393	Coding-mRNA	Git2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
394	Coding-mRNA	Fzd6	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
395	Coding-mRNA	Raf1	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
396	Coding-mRNA	Ccs	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
397	Coding-mRNA	Camk1	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
398	Coding-mRNA	Syne1	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
399	Coding-mRNA	Fkbp7	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
400	Coding-mRNA	Gmcl1	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
401	Coding-mRNA	Dmgdh	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
402	Coding-mRNA	Psmd2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
403	Coding-mRNA	Sdhb	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
404	Coding-mRNA	Orm2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
405	Coding-mRNA	Slc5a2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
406	Coding-mRNA	Cyp4f17	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
407	Coding-mRNA	Fars2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
408	Coding-mRNA	Ptp4a1	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
409	Coding-mRNA	Mrpl38	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
410	Coding-mRNA	Nfyc	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
411	Coding-mRNA	Gstm6	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
412	Coding-mRNA	Mkrn2	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
413	Coding-mRNA	Cox5a	miR-5102	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0018010	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
414	Coding-mRNA	Ss18l1	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
415	Coding-mRNA	Fxc1	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
416	Coding-mRNA	Med23	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
417	Coding-mRNA	Ftcd	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
418	Coding-mRNA	Dnajb12	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
419	Coding-mRNA	Snx27	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
420	Coding-mRNA	Atp5l	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
421	Coding-mRNA	Kif3b	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
422	Coding-mRNA	Hdac8	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
423	Coding-mRNA	Lztfl1	miR-22-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000570	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
424	Coding-mRNA	Foxq1	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
425	Coding-mRNA	Eny2	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
426	Coding-mRNA	Nags	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
427	Coding-mRNA	Qtrtd1	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
428	Coding-mRNA	Tpd52	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
429	Coding-mRNA	Tbc1d23	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
430	Coding-mRNA	Ak2	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
431	Coding-mRNA	Ugt2b34	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
432	Coding-mRNA	Stk17b	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
433	Coding-mRNA	Strada	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
434	Coding-mRNA	Zc3h15	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
435	Coding-mRNA	Tmem176a	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
436	Coding-mRNA	9030624J02Rik	miR-140-5p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
437	Coding-mRNA	Spred2	miR-140-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
438	Coding-mRNA	Cdk10	miR-140-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
439	Coding-mRNA	D0H4S114	miR-140-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
440	Coding-mRNA	Vamp7	miR-140-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
441	Coding-mRNA	Uba52	miR-140-3p	NA	Liver Tissues	Liver Regenerating	Mus musculus (mouse)	qRT-PCR	23597149	Dynamic recruitment of microRNAs to their mRNA targets in the regenerating liver.	We determined miRNA recruitment at selected time points posthepatectomy previ- ously shown to correspond to the G1 (1h), S (36H) and M (48H) phases of the hepatocyte cell cycle, and in the quies- cent liver, corresponding to G0 [30,31]. Cell cycle stage was confirmed by activation of genes associated with G1 (jun, fos, myc), S (cyclin D1) and M (Foxm1) cell cycle phases determined by RNA-seq analysis of samples from these time points. Following UV-crosslinking of the RISC to microRNA and mRNA, we quantified miRNAs immunoprecipitated with an antibody that recognizes Argonaute 1 through 4 proteins and therefore immunoprecipitates all RISCs [32] by ultra-high throughput sequencing. Next, we turned our attention to the mRNAs that were identified in the RISC using our HITS-CLIP assay. We speculated that miRNA regulation would be more signifi- cant for those mRNAs that were highly enriched in the RISC relative to their overall abundance in the tissue. Therefore, to identify ‘expression-weighted footprints’ ,we used RNA-seq to quantify total mRNA expression in qui- escent liver, and 1 h, 36 h and 48 h posthepatectomy. Next, we calculated RISC enrichment for all mRNAs rela- tive to their overall abundance . To identify potential ceRNA networks, we selected all mRNAs that had one major footprint targeted by a single miRNA. For this analysis, footprints within 20 bp of each other were merged. If (1) the second strongest distinct footprint was less than 25% of the strongest footprint, and (2) the most loaded miRNA in the strongest footprint was 10x higher than the second-most loaded miRNA in the footprint, then the mRNA and miRNA were included in a ceRNA network. This process was performed for each time point. Networks for each miRNA were then merged across all time-points to create summary networks.	MI0000165	BMC Genomics 2013 Apr 18 14, 264 doi:10.1186/1471-2164-14-264 PMID:23597149
442	Pseudogene	Pbcas4	miR-185	BCAS4	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
443	Pseudogene	Pbcas4	miR-185	Bcl2	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
444	Pseudogene	Pbcas4	miR-185	Ill7rd	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
445	Pseudogene	Pbcas4	miR-185	Pnpla3	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
446	Pseudogene	Pbcas4	miR-185	Shisa7	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
447	Pseudogene	Pbcas4	miR-185	Tapbp	Neuroblastoma Cells	Neuroblastoma	Mus musculus (mouse)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000227	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
448	LncRNA	lincRNA-p21	let-7a	JUNB	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000556	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
449	LncRNA	lincRNA-p21	let-7a	CTNNB1	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000556	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
450	LncRNA	lincRNA-p21	let-7b	JUNB	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000558	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
451	LncRNA	lincRNA-p21	let-7b	CTNNB1	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000558	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
452	LncRNA	lincRNA-p21	let-7c	JUNB	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000559	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
453	LncRNA	lincRNA-p21	let-7c	CTNNB1	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000559	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
454	LncRNA	lincRNA-p21	let-7e	JUNB	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000561	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
455	LncRNA	lincRNA-p21	let-7e	CTNNB1	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000561	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
456	LncRNA	lincRNA-p21	let-7i	JUNB	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000138	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
457	LncRNA	lincRNA-p21	let-7i	CTNNB1	Hela Cells	Cervical Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000138	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
458	Coding-mRNA	VAPA	miR-17	PTEN	Du145 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000687	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
459	Coding-mRNA	VAPA	miR-19a	PTEN	Du146 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000688	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
460	Coding-mRNA	VAPA	miR-20a	PTEN	Du147 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000568	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
461	Coding-mRNA	VAPA	miR-20b	PTEN	Du148 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0003536	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
462	Coding-mRNA	VAPA	miR-26b	PTEN	Du149 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000575	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
463	Coding-mRNA	VAPA	miR-106a	PTEN	Du150 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000406	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
464	Coding-mRNA	VAPA	miR-106b	PTEN	Du151 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000407	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
465	Coding-mRNA	CNOT6L	miR-17	PTEN	Du152 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000687	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
466	Coding-mRNA	CNOT6L	miR-19a	PTEN	Du153 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000688	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
467	Coding-mRNA	CNOT6L	miR-20a	PTEN	Du154 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000568	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
468	Coding-mRNA	CNOT6L	miR-20b	PTEN	Du155 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0003536	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
469	Coding-mRNA	CNOT6L	miR-26b	PTEN	Du156 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000575	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
470	Coding-mRNA	CNOT6L	miR-106a	PTEN	Du157 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000406	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
471	Coding-mRNA	CNOT6L	miR-106b	PTEN	Du158 Prostate Cancer Cells	Prostate Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000407	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
472	Coding-mRNA	PTEN	miR-136	VCAN	Breast Carcinoma Cell Line	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Using computational prediction confirmed with in vitro and in vivo experiments, we report that the expression of versican3UTR not only antagonizes miR-199a-3p but can also lower its steady state expression. We found that expression of versican 3UTR in a mouse breast carcinoma cell line, 4T1, decreased miR-199a-3p levels. The decrease in miRNA activity consequently translated into differences in tumor growth	MI0000162	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
473	Coding-mRNA	PTEN	miR-144	VCAN	Breast Carcinoma Cell Line	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Using computational prediction confirmed with in vitro and in vivo experiments, we report that the expression of versican3UTR not only antagonizes miR-199a-3p but can also lower its steady state expression. We found that expression of versican 3UTR in a mouse breast carcinoma cell line, 4T1, decreased miR-199a-3p levels. The decrease in miRNA activity consequently translated into differences in tumor growth	MI0000168	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
474	Coding-mRNA	VCAN	miR-144	RB1	Breast Carcinoma Cell Line	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Computational analysis indicated that both miR-199a-3p and miR-144 targeted a cell cycle regulator, Rb1. In addition, miR-144 and miR-136, which have also been shown to interact with versican 3UTR, was found to target PTEN. Expression of Rb1 and PTEN were up-regulated synergistically in vitro and in vivo, suggesting that the 3UTR binds and modulates miRNA activities, freeing Rb1 and PTEN mRNAs for translation.	MI0000168	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
475	Coding-mRNA	VCAN	miR-199a-3p	RB1	Breast Carcinoma Cell Line	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Computational analysis indicated that both miR-199a-3p and miR-144 targeted a cell cycle regulator, Rb1. In addition, miR-144 and miR-136, which have also been shown to interact with versican 3UTR, was found to target PTEN. Expression of Rb1 and PTEN were up-regulated synergistically in vitro and in vivo, suggesting that the 3UTR binds and modulates miRNA activities, freeing Rb1 and PTEN mRNAs for translation.	MI0000241	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
476	Coding-mRNA	CD34	miR-133a	VCAN	Liver Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0000159	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
477	Coding-mRNA	CD34	miR-144	VCAN	Liver Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0000168	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
478	Coding-mRNA	CD34	miR-431	VCAN	Liver Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0001524	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
479	Coding-mRNA	FN1	miR-133a	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0000159	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
480	Coding-mRNA	FN1	miR-199a-3p	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0000241	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
481	Coding-mRNA	FN1	miR-431	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0001524	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
482	Coding-mRNA	HMGA2	let-7a	TGFBR3	368T1 And 482N1 Cells	Lung Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000556	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
483	Coding-mRNA	HMGA2	let-7b	TGFBR3	368T1 And 482N1 Cells	Lung Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000558	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
484	Coding-mRNA	HMGA2	let-7c	TGFBR3	368T1 And 482N1 Cells	Lung Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000559	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
485	Coding-mRNA	HMGA2	let-7e	TGFBR3	368T1 And 482N1 Cells	Lung Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000561	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
486	Coding-mRNA	HMGA2	let-7i	TGFBR3	368T1 And 482N1 Cells	Lung Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000138	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
487	Pseudogene	Pbcas4	miR-185	BCAS4	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
488	Pseudogene	Pbcas4	miR-185	Bcl2	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
489	Pseudogene	Pbcas4	miR-185	Ill7rd	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
490	Pseudogene	Pbcas4	miR-185	Pnpla3	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
491	Pseudogene	Pbcas4	miR-185	Shisa7	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
492	Pseudogene	Pbcas4	miR-185	Tapbp	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	Pbcas4 knockdown;qRT-PCR	23153069	Evidence for conserved post-transcriptional roles of unitary pseudogenes and for frequent bifunctionality of mRNAs	Mouse genes containing predicted MREs for either miR-185/882 or miR-665 that are predicted also in their human ortholog are nearly twice as likely to be among the genes down-regulated upon Pbcas4 knockdown than among those that are up-regulated. Consistent with the expression of Pbcas4 and the 5 protein-coding gene candidates being post-transcriptionally regulated by miR-185, a 68-fold increase in this miRNA resulted in significantly reduced abundance of mouse Pbcas4and each of the 5 predicted protein-coding transcript targets.	MI0000482	Genome Biol 2012 Nov 15 13, R102 doi:10.1186/gb-2012-13-11-r102 PMID:23153069
493	LncRNA	lincRNA-p21	let-7a	JUNB	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000060	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
494	LncRNA	lincRNA-p21	let-7a	CTNNB1	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000060	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
495	LncRNA	lincRNA-p21	let-7b	JUNB	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000063	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
496	LncRNA	lincRNA-p21	let-7b	CTNNB1	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000063	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
497	LncRNA	lincRNA-p21	let-7c	JUNB	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000064	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
498	LncRNA	lincRNA-p21	let-7c	CTNNB1	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000064	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
499	LncRNA	lincRNA-p21	let-7e	JUNB	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000066	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
500	LncRNA	lincRNA-p21	let-7e	CTNNB1	Human Cervical Carcinoma Hela Cells	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22841487	LincRNA-p21 suppresses target mRNA translation	lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and b-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.	MI0000066	Mol Cell 2012 Aug 24 47, 648-55 doi:10.1016/j.molcel.2012.06.027 PMID:22841487
501	Coding-mRNA	VAPA	miR-17	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000071	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
502	Coding-mRNA	VAPA	miR-19a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000073	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
503	Coding-mRNA	VAPA	miR-20a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000076	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
504	Coding-mRNA	VAPA	miR-20b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0001519	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
505	Coding-mRNA	VAPA	miR-26b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000084	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
506	Coding-mRNA	VAPA	miR-106a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000113	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
507	Coding-mRNA	VAPA	miR-106b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000734	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
508	Coding-mRNA	CNOT6L	miR-17	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000071	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
509	Coding-mRNA	CNOT6L	miR-19a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000073	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
510	Coding-mRNA	CNOT6L	miR-20a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000076	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
511	Coding-mRNA	CNOT6L	miR-20b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0001519	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
512	Coding-mRNA	CNOT6L	miR-26b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000084	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
513	Coding-mRNA	CNOT6L	miR-106a	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000113	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
514	Coding-mRNA	CNOT6L	miR-106b	PTEN	Du145 Prostate Cancer Cells, Glioblastoma	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	A combined computational and experimental approach has been used to identify CNOT6L and VAPA as protein-coding transcripts that regulate PTEN transcript and protein expression in a Dicer-dependent manner, antagonize downstream PI(3)K signalling and possess growth- and tumour-suppressive properties	MI0000734	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
515	Coding-mRNA	PTEN	miR-136	VCAN	Breast Carcinoma Cell Line	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Using computational prediction confirmed with in vitro and in vivo experiments, we report that the expression of versican3UTR not only antagonizes miR-199a-3p but can also lower its steady state expression. We found that expression of versican 3UTR in a mouse breast carcinoma cell line, 4T1, decreased miR-199a-3p levels. The decrease in miRNA activity consequently translated into differences in tumor growth	MI0000475	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
516	Coding-mRNA	PTEN	miR-144	VCAN	Breast Carcinoma Cell Line	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Using computational prediction confirmed with in vitro and in vivo experiments, we report that the expression of versican3UTR not only antagonizes miR-199a-3p but can also lower its steady state expression. We found that expression of versican 3UTR in a mouse breast carcinoma cell line, 4T1, decreased miR-199a-3p levels. The decrease in miRNA activity consequently translated into differences in tumor growth	MI0000460	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
517	Coding-mRNA	VCAN	miR-144	RB1	Breast Carcinoma Cell Line	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Computational analysis indicated that both miR-199a-3p and miR-144 targeted a cell cycle regulator, Rb1. In addition, miR-144 and miR-136, which have also been shown to interact with versican 3UTR, was found to target PTEN. Expression of Rb1 and PTEN were up-regulated synergistically in vitro and in vivo, suggesting that the 3UTR binds and modulates miRNA activities, freeing Rb1 and PTEN mRNAs for translation.	MI0000460	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
518	Coding-mRNA	VCAN	miR-199a-3p	RB1	Breast Carcinoma Cell Line	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	21049042	Expression of versican 3 -untranslated region modulates endogenous microRNA functions	Computational analysis indicated that both miR-199a-3p and miR-144 targeted a cell cycle regulator, Rb1. In addition, miR-144 and miR-136, which have also been shown to interact with versican 3UTR, was found to target PTEN. Expression of Rb1 and PTEN were up-regulated synergistically in vitro and in vivo, suggesting that the 3UTR binds and modulates miRNA activities, freeing Rb1 and PTEN mRNAs for translation.	MI0000242	PLoS One 2010 Oct 25 5, e13599 doi:10.1371/journal.pone.0013599 PMID:21049042
519	Coding-mRNA	CD34	miR-133a	VCAN	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0000450	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
520	Coding-mRNA	CD34	miR-144	VCAN	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0000460	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
521	Coding-mRNA	CD34	miR-431	VCAN	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	23180826	Versican 3 -untranslated region (3 -UTR) functions as a ceRNA in inducing the development of hepatocellular carcinoma by regulating miRNA activity	We found that versican 3-UTR could bind to miRNAs miR-133a, miR-199a*, miR-144, and miR-431 and also interacted with CD34 and fibronectin. As a consequence, expression of versican, CD34, and fibronectin was up-regulated by ectopic transfection of the versican 3-UTR, which was confirmed in HepG2 cells and in transgenic mice as compared with wild-type controls. Transfection with siRNAs targeting the versican 3-UTR abolished the effects of the 3-UTR.	MI0001721	Faseb j 2013 Mar 27, 907-19 doi:10.1096/fj.12-220905 PMID:23180826
522	Coding-mRNA	FN1	miR-133a	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0000450	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
523	Coding-mRNA	FN1	miR-199a-3p	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0000242	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
524	Coding-mRNA	FN1	miR-431	VCAN	Astrocytoma Cell Line U343	Astrocytoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	19223980	A 3 -untranslated region (3 UTR) induces organ adhesion by regulating miR-199a* functions.	Computational analysis indicated that a large number of microRNAs could bind to this fragment potentially including miR-199a*. Expression of versican and fibronectin, two targets of miR-199a*, are up-regulated in transgenic mice, suggesting that the 3UTR binds and modulates miR-199a* activities, freeing mRNAs of versican and fibronectin from being repressed by miR-199a*. Confirmation of the binding was performed by PCR using mature miR-199a* as a primer and the targeting was performed by luciferase assays. Enhanced adhesion by expression of the 3UTR was confirmed by in vitro assays.	MI0001721	PLoS One 2009  4, e4527 doi:10.1371/journal.pone.0004527 PMID:19223980
525	Coding-mRNA	HMGA2	let-7a	TGFBR3	Lung Cancer	Lung Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000060	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
526	Coding-mRNA	HMGA2	let-7b	TGFBR3	Lung Cancer	Lung Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000063	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
527	Coding-mRNA	HMGA2	let-7c	TGFBR3	Lung Cancer	Lung Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000064	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
528	Coding-mRNA	HMGA2	let-7e	TGFBR3	Lung Cancer	Lung Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000066	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
529	Coding-mRNA	HMGA2	let-7i	TGFBR3	Lung Cancer	Lung Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24305048	Hmga2 functions as a competing endogenous RNA to promote lung cancer progression.	Here we show that Hmga2 promotes lung cancer progression in mouse and human cells by operating as a competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family. Hmga2 can promote the transformation of lung cancercells independent of protein-coding function but dependent upon the presence of let-7 sites; this occurs without changes in the levels of let-7 isoforms, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. These effects are also observed in vivo, where Hmga2 ceRNA activity driveslung cancer growth, invasion and dissemination. Finally, analysis of NSCLC-patient gene-expression data reveals that HMGA2 and TGFBR3 are coordinately regulated in NSCLC-patient material, a vital corollary to ceRNA function. Taken together, these results suggest that Hmga2 promotes lung carcinogenesis both as a protein-coding gene and as a non-coding RNA; such dual-function regulation of gene-expression networks reflects a novel means by which oncogenes promote disease progression.	MI0000434	Nature 2014 Jan 9 505, 212-7 doi:10.1038/nature12785 PMID:24305048
530	LncRNA	MALAT1	miR-9	NA	L428 Hodgkin Lymphoma Cell Line,Hek293 And U87Mg Glioblastoma Cells	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	23985560	microRNA-9 targets the long non-coding RNA MALAT1 for degradation in the nucleus	Growing evidence supports an important role for miR-9 in tumorigenesis16,17. In order to gain insights into miR-9 mechanisms of action we performed RNA-seq transcriptome analyses in the L428 Hodgkin Lymphoma cell line transfected with an LNA-modified inhibitor of miR-9 or a scrambled control. Among the upregulated transcripts, MALAT1 was found to be >16 fold upregulated. To further confirm that the miR-9:MALAT1 interaction occurs through the predicted miR-9 binding sites, we cloned two fragments of MALAT1 encompassing the two putative binding sites downstream the luciferase gene and performed luciferase assays in U87MG cells transfected with reporter plasmids containing the two putative miR-9 binding sites. In both cases, miR-9 over-expression resulted in a significant decrease in luciferase activity, while an opposite effect was observed upon miR-9 inhibition. Moreover, directed mutagenesis of the predicted miR-9 binding sites abolished this effect.	MI0000466	Sci Rep 2013  3, 2535 doi:10.1038/srep02535 PMID:23985560
531	LncRNA	MALAT1	miR-9	NA	L428 Hodgkin Lymphoma Cell Line,Hek293 And U87Mg Glioblastoma Cells	Glioblastoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	23985560	microRNA-9 targets the long non-coding RNA MALAT1 for degradation in the nucleus	Growing evidence supports an important role for miR-9 in tumorigenesis16,17. In order to gain insights into miR-9 mechanisms of action we performed RNA-seq transcriptome analyses in the L428 Hodgkin Lymphoma cell line transfected with an LNA-modified inhibitor of miR-9 or a scrambled control. Among the upregulated transcripts, MALAT1 was found to be >16 fold upregulated. To further confirm that the miR-9:MALAT1 interaction occurs through the predicted miR-9 binding sites, we cloned two fragments of MALAT1 encompassing the two putative binding sites downstream the luciferase gene and performed luciferase assays in U87MG cells transfected with reporter plasmids containing the two putative miR-9 binding sites. In both cases, miR-9 over-expression resulted in a significant decrease in luciferase activity, while an opposite effect was observed upon miR-9 inhibition. Moreover, directed mutagenesis of the predicted miR-9 binding sites abolished this effect.	MI0000157	Sci Rep 2013  3, 2535 doi:10.1038/srep02535 PMID:23985560
532	LncRNA	HOTAIR	miR-130a	c-Myc	Gbc Cell Lines (Gbc-Sd, Sgc-996,Noz And Eh-Gb2)	Gallbladder Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24953832	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer	A computational screen of HOTAIR promoter was conducted to search for transcription-factor-binding sites. HOTAIR promoter activities were examined by luciferase reporter assay. The function of the c-Myc binding site in the HOTAIR promoter region was tested by a promoter assay with nucleotide substitutions in the putative E-box. The association of c-Myc with the HOTAIR promoter in vivo was confirmed by chromatin immunoprecipitation assay and Electrophoretic mobility shift assay. A search for miRNAs with complementary base paring with HOTAIR was performed utilizing online software program. Gain and loss of function approaches were employed to investigate the expression changes of HOTAIR or miRNA-130a. The expression levels of HOTAIR, c-Myc and miRNA-130a were examined in 65 matched pairs of gallbladder cancer tissues. The effects of HOTAIR and miRNA-130a on gallbladder cancer cell invasion and proliferation was tested using in vitro cell invasion and flow cytometric assays.	MI0000448	Mol Cancer 2014 Jun 23 13, 156 doi:10.1186/1476-4598-13-156 PMID:24953832
533	Protein	HIV-1 Gag protein	miR-146a	NA	Hek293 Cells Line	Hiv-1 Infection	Human immunodeficiency virus 1(HIV-1)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24938790	MicroRNA binding to the HIV-1 Gag protein inhibits Gag assembly and virus production	Recently, miRNAs have been shown to also interact with proteins outside RISCs, impacting cellular processes through mechanisms not involving gene silencing. Here, we define a previously unappreciated activity of miRNAs in inhibiting RNA-protein interactions that in the context of HIV-1 biology blocks HIV virus budding and reduces virus infectivity. This occurs by miRNA binding to the nucleocapsid domain of the Gag protein, the main structural component of HIV-1 virions. The resulting miRNA-Gag complexes interfere with viral-RNA-mediated Gag assembly and viral budding at the plasma membrane, with imperfectly assembled Gag complexes endocytosed and delivered to lysosomes. The blockade of virus production by miRNA is reversed by adding the miRNA's target mRNA and stimulated by depleting Argonaute-2, suggesting that when miRNAs are not mediating gene silencing, they can block HIV-1 production through disruption of Gag assembly on membranes. This prompted us to examine whether Gag could bind to endogenous miRNAs,not just exogenous miRNAs.Supporting this hypothesis, Gag-miRNA immunoprecipitation experiments revealed that in addition to miRNA-146a,other host miRNA species coimmunoprecipitated wit hGag,including miR-17,miR-19,and miR-16,consistent with previous work showing that Gagcannonspecifically bind to nucleicacids(20). Overall, our findings have significant implications for understanding how cells modulate HIV-1 infection by miRNA expression and raise the possibility that miRNAs can function to disrupt RNA-mediated protein assembly processes in other cellular contexts.	MI0000477	Proc Natl Acad Sci U S A 2014 Jul 1 111, E2676-83 doi:10.1073/pnas.1408037111 PMID:24938790
534	Protein	HIV-1 Gag protein	miR-17	NA	Hek293 Cells Line	Hiv-1 Infection	Human immunodeficiency virus 1(HIV-1)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24938790	MicroRNA binding to the HIV-1 Gag protein inhibits Gag assembly and virus production	Recently, miRNAs have been shown to also interact with proteins outside RISCs, impacting cellular processes through mechanisms not involving gene silencing. Here, we define a previously unappreciated activity of miRNAs in inhibiting RNA-protein interactions that in the context of HIV-1 biology blocks HIV virus budding and reduces virus infectivity. This occurs by miRNA binding to the nucleocapsid domain of the Gag protein, the main structural component of HIV-1 virions. The resulting miRNA-Gag complexes interfere with viral-RNA-mediated Gag assembly and viral budding at the plasma membrane, with imperfectly assembled Gag complexes endocytosed and delivered to lysosomes. The blockade of virus production by miRNA is reversed by adding the miRNA's target mRNA and stimulated by depleting Argonaute-2, suggesting that when miRNAs are not mediating gene silencing, they can block HIV-1 production through disruption of Gag assembly on membranes. This prompted us to examine whether Gag could bind to endogenous miRNAs,not just exogenous miRNAs.Supporting this hypothesis, Gag-miRNA immunoprecipitation experiments revealed that in addition to miRNA-146a,other host miRNA species coimmunoprecipitated wit hGag,including miR-17,miR-19,and miR-16,consistent with previous work showing that Gagcannonspecifically bind to nucleicacids(20). Overall, our findings have significant implications for understanding how cells modulate HIV-1 infection by miRNA expression and raise the possibility that miRNAs can function to disrupt RNA-mediated protein assembly processes in other cellular contexts.	MI0000071	Proc Natl Acad Sci U S A 2014 Jul 1 111, E2676-83 doi:10.1073/pnas.1408037111 PMID:24938790
535	Protein	HIV-1 Gag protein	miR-16	NA	Hek293 Cells Line	Hiv-1 Infection	Human immunodeficiency virus 1(HIV-1)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24938790	MicroRNA binding to the HIV-1 Gag protein inhibits Gag assembly and virus production	Recently, miRNAs have been shown to also interact with proteins outside RISCs, impacting cellular processes through mechanisms not involving gene silencing. Here, we define a previously unappreciated activity of miRNAs in inhibiting RNA-protein interactions that in the context of HIV-1 biology blocks HIV virus budding and reduces virus infectivity. This occurs by miRNA binding to the nucleocapsid domain of the Gag protein, the main structural component of HIV-1 virions. The resulting miRNA-Gag complexes interfere with viral-RNA-mediated Gag assembly and viral budding at the plasma membrane, with imperfectly assembled Gag complexes endocytosed and delivered to lysosomes. The blockade of virus production by miRNA is reversed by adding the miRNA's target mRNA and stimulated by depleting Argonaute-2, suggesting that when miRNAs are not mediating gene silencing, they can block HIV-1 production through disruption of Gag assembly on membranes. This prompted us to examine whether Gag could bind to endogenous miRNAs,not just exogenous miRNAs.Supporting this hypothesis, Gag-miRNA immunoprecipitation experiments revealed that in addition to miRNA-146a,other host miRNA species coimmunoprecipitated wit hGag,including miR-17,miR-19,and miR-16,consistent with previous work showing that Gagcannonspecifically bind to nucleicacids(20). Overall, our findings have significant implications for understanding how cells modulate HIV-1 infection by miRNA expression and raise the possibility that miRNAs can function to disrupt RNA-mediated protein assembly processes in other cellular contexts.	MI0000070	Proc Natl Acad Sci U S A 2014 Jul 1 111, E2676-83 doi:10.1073/pnas.1408037111 PMID:24938790
536	Protein	HIV-1 Gag protein	miR-19	NA	Hek293 Cells Line	Hiv-1 Infection	Human immunodeficiency virus 1(HIV-1)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24938790	MicroRNA binding to the HIV-1 Gag protein inhibits Gag assembly and virus production	Recently, miRNAs have been shown to also interact with proteins outside RISCs, impacting cellular processes through mechanisms not involving gene silencing. Here, we define a previously unappreciated activity of miRNAs in inhibiting RNA-protein interactions that in the context of HIV-1 biology blocks HIV virus budding and reduces virus infectivity. This occurs by miRNA binding to the nucleocapsid domain of the Gag protein, the main structural component of HIV-1 virions. The resulting miRNA-Gag complexes interfere with viral-RNA-mediated Gag assembly and viral budding at the plasma membrane, with imperfectly assembled Gag complexes endocytosed and delivered to lysosomes. The blockade of virus production by miRNA is reversed by adding the miRNA's target mRNA and stimulated by depleting Argonaute-2, suggesting that when miRNAs are not mediating gene silencing, they can block HIV-1 production through disruption of Gag assembly on membranes. This prompted us to examine whether Gag could bind to endogenous miRNAs,not just exogenous miRNAs.Supporting this hypothesis, Gag-miRNA immunoprecipitation experiments revealed that in addition to miRNA-146a,other host miRNA species coimmunoprecipitated wit hGag,including miR-17,miR-19,and miR-16,consistent with previous work showing that Gagcannonspecifically bind to nucleicacids(20). Overall, our findings have significant implications for understanding how cells modulate HIV-1 infection by miRNA expression and raise the possibility that miRNAs can function to disrupt RNA-mediated protein assembly processes in other cellular contexts.	MI0000073	Proc Natl Acad Sci U S A 2014 Jul 1 111, E2676-83 doi:10.1073/pnas.1408037111 PMID:24938790
537	LncRNA	lincRNA-ROR	miR-205	ZEB1	Mcf7, Bt474, Mda-Mb-435, Mda-Mb-231, Bt549 And Mda-Mb-436	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis	we used a psiCHECK2 reporter plasmid to test the relationship between linc-ROR and miRNAs. We cloned the linc-ROR full-length transcript or ZEB2 3'-UTR (untranslated region) into the 3'-UTR of Renilla luciferase (Rluc) gene of psiCHECK2. The psiCHECK2 plasmid also contains a downstream constitutively expressed firefly luciferase gene as an internal control for normalization. We then showed that transient co-transfection of mir-205-5p mimics into HEK293T cells inhibited the Rluc activity in a dose-dependent manner, while the mir-34a-5p and let-7a-5p mimics had little influence on Rluc activity of psiCHECK2-ROR . To determine whether linc-ROR acts as a sponge to mir-205, we transfected psiCHECK2-ZEB2 into HEK293T cells together with the mir-205-5p mimics and increasing amounts of linc-ROR, and we detected that the Rluc activity increased in response to linc-ROR in a dose-dependent manner . Together, these results strongly point to a role of linc-ROR as a molecular sponge for mir-205, and presumably linc-ROR may regulate EMT program through preventing degradation of mir-205 targets (ZEB1 and ZEB2). This was in accordance with the ZEB1 and ZEB2 expression levels after linc-ROR/mir-205 overexpression or silencing. Our data also showed that several ZEB1/2-related miRNAs such as mir-205 and mir-200 family members were downregulated in linc-ROR-overexpressing cells. Thus, we conclude that lin-ROR functions as a molecular sponge for mir-205 to affect mir-205 targets in the process of EMT.	MI0000285	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
538	LncRNA	lincRNA-ROR	miR-205	ZEB2	Mcf7, Bt474, Mda-Mb-435, Mda-Mb-231, Bt549 And Mda-Mb-436	Breast Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis	we used a psiCHECK2 reporter plasmid to test the relationship between linc-ROR and miRNAs. We cloned the linc-ROR full-length transcript or ZEB2 3'-UTR (untranslated region) into the 3'-UTR of Renilla luciferase (Rluc) gene of psiCHECK2. The psiCHECK2 plasmid also contains a downstream constitutively expressed firefly luciferase gene as an internal control for normalization. We then showed that transient co-transfection of mir-205-5p mimics into HEK293T cells inhibited the Rluc activity in a dose-dependent manner , while the mir-34a-5p and let-7a-5p mimics had little influence on Rluc activity of psiCHECK2-ROR . To determine whether linc-ROR acts as a sponge to mir-205, we transfected psiCHECK2-ZEB2 into HEK293T cells together with the mir-205-5p mimics and increasing amounts of linc-ROR, and we detected that the Rluc activity increased in response to linc-ROR in a dose-dependent manner . Together, these results strongly point to a role of linc-ROR as a molecular sponge for mir-205, and presumably linc-ROR may regulate EMT program through preventing degradation of mir-205 targets (ZEB1 and ZEB2). This was in accordance with the ZEB1 and ZEB2 expression levels after linc-ROR/mir-205 overexpression or silencing. Our data also showed that several ZEB1/2-related miRNAs such as mir-205 and mir-200 family members were downregulated in linc-ROR-overexpressing cells. Thus, we conclude that lin-ROR functions as a molecular sponge for mir-205 to affect mir-205 targets in the process of EMT.	MI0000285	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
539	LncRNA	lincRNA-ROR	miR-205	ZEB1	Mcf7, Bt474, Mda-Mb-435, Mda-Mb-231, Bt549 And Mda-Mb-436	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis	we used a psiCHECK2 reporter plasmid to test the relationship between linc-ROR and miRNAs. We cloned the linc-ROR full-length transcript or ZEB2 3'-UTR (untranslated region) into the 3'-UTR of Renilla luciferase (Rluc) gene of psiCHECK2. The psiCHECK2 plasmid also contains a downstream constitutively expressed firefly luciferase gene as an internal control for normalization. We then showed that transient co-transfection of mir-205-5p mimics into HEK293T cells inhibited the Rluc activity in a dose-dependent manner , while the mir-34a-5p and let-7a-5p mimics had little influence on Rluc activity of psiCHECK2-ROR . To determine whether linc-ROR acts as a sponge to mir-205, we transfected psiCHECK2-ZEB2 into HEK293T cells together with the mir-205-5p mimics and increasing amounts of linc-ROR, and we detected that the Rluc activity increased in response to linc-ROR in a dose-dependent manner . Together, these results strongly point to a role of linc-ROR as a molecular sponge for mir-205, and presumably linc-ROR may regulate EMT program through preventing degradation of mir-205 targets (ZEB1 and ZEB2). This was in accordance with the ZEB1 and ZEB2 expression levels after linc-ROR/mir-205 overexpression or silencing. Our data also showed that several ZEB1/2-related miRNAs such as mir-205 and mir-200 family members were downregulated in linc-ROR-overexpressing cells. Thus, we conclude that lin-ROR functions as a molecular sponge for mir-205 to affect mir-205 targets in the process of EMT.	MI0000248	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
540	LncRNA	lincRNA-ROR	miR-205	ZEB2	Mcf7, Bt474, Mda-Mb-435, Mda-Mb-231, Bt549 And Mda-Mb-436	Breast Cancer	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis	we used a psiCHECK2 reporter plasmid to test the relationship between linc-ROR and miRNAs. We cloned the linc-ROR full-length transcript or ZEB2 3'-UTR (untranslated region) into the 3'-UTR of Renilla luciferase (Rluc) gene of psiCHECK2. The psiCHECK2 plasmid also contains a downstream constitutively expressed firefly luciferase gene as an internal control for normalization. We then showed that transient co-transfection of mir-205-5p mimics into HEK293T cells inhibited the Rluc activity in a dose-dependent manner , while the mir-34a-5p and let-7a-5p mimics had little influence on Rluc activity of psiCHECK2-ROR . To determine whether linc-ROR acts as a sponge to mir-205, we transfected psiCHECK2-ZEB2 into HEK293T cells together with the mir-205-5p mimics and increasing amounts of linc-ROR, and we detected that the Rluc activity increased in response to linc-ROR in a dose-dependent manner . Together, these results strongly point to a role of linc-ROR as a molecular sponge for mir-205, and presumably linc-ROR may regulate EMT program through preventing degradation of mir-205 targets (ZEB1 and ZEB2). This was in accordance with the ZEB1 and ZEB2 expression levels after linc-ROR/mir-205 overexpression or silencing. Our data also showed that several ZEB1/2-related miRNAs such as mir-205 and mir-200 family members were downregulated in linc-ROR-overexpressing cells. Thus, we conclude that lin-ROR functions as a molecular sponge for mir-205 to affect mir-205 targets in the process of EMT.	MI0000248	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
541	Coding-mRNA	RB1	NA	STAT3	Snb19 And Sf188	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX1, suggesting that these interactions mediate crosstalk between canonical oncogenic pathways. siRNA silencing of 13 miR-mediated PTEN regulators, whose locus deletions are predictive of PTEN expression variability, was sufficient to downregulate PTEN in a 3UTR-dependent manner and to increase tumor cell growth rates.	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
542	Coding-mRNA	RB1	NA	PDGFRA	Snb19 And Sf189	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX2, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
543	Coding-mRNA	RB1	NA	PTEN	Snb19 And Sf190	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX2, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
544	Coding-mRNA	STAT3	NA	RUNX1	Snb19 And Sf191	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX3, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
545	Coding-mRNA	RUNX1	NA	PTEN	Snb19 And Sf192	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX4, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
546	Coding-mRNA	RUNX1	NA	PDGFRA	Snb19 And Sf193	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX5, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
547	Coding-mRNA	RUNX1	NA	VEGFA	Snb19 And Sf194	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX6, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
548	Coding-mRNA	VEGFA	NA	PTEN	Snb19 And Sf195	Glioma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000015	An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma	Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype implementation, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX7, suggesting that these interactions mediate crosstalk between	NA	Cell 2011 Oct 14 147, 370-81 doi:10.1016/j.cell.2011.09.041 PMID:22000015
549	Artifically engineered RNA	Miravirsen	miR-122	NA	Liver Tissues	Hcv Infection	Homo sapiens (human)	qRT-PCR	23534542	Treatment of HCV infection by targeting microRNA.	Miravirsen is a 15-nucleotide locked nucleic acid–modified antisense oligonucleotide complementary to and with a high affinity and specificity for the 5' region of mature miR-122. Miravirsen can sequester and thus inhibit miR-122 Mechanism of Action of Miravirsen.). The administration of miravirsen to chimpanzees with chronic HCV infection provided long-lasting viral suppression without evidence of resistant mutations at the two miR-122 binding sites of the 5' untranslated region of the HCV genome, and no adverse events were observed in phase 1 studies in healthy volunteers.16,17 Here, we report on the safety and activity of miravirsen in patients with chronic HCV infection.	MI0000442	N Engl J Med 2013 May 2 368, 1685-94 doi:10.1056/NEJMoa1209026 PMID:23534542
550	Coding-mRNA	IGF1R	miR-139-5p	NA	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
551	Coding-mRNA	ROCK2	miR-139-5p	NA	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
552	Coding-mRNA	RAP1B	miR-139-5p	NA	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
553	Coding-mRNA	IGF1R	miR-139-5p	ROCK2	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
554	Coding-mRNA	ROCK2	miR-139-5p	RAP1B	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
555	Coding-mRNA	RAP1B	miR-139-5p	IGF1R	Colorectal Tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;RNA immunoprecipitation	24942287	A Post-Transcriptional Regulation of Tumor Suppressor MiR-139-5p and A Network of MiR-139-5p Mediated mRNAs Interactions in Colorectal Cancer.	We describe post-transcriptional regulation of this intronic microRNA in human colorectal cancer. miR-139-5p is expressed independently of its overexpressed host gene PDE2A in colorectal cancer tissues and cell lines. The miR-139-5p target genes IGF1R, ROCK2 and RAP1B exert regulatory effects on the miR-139-5p expression level, relying on their ability to compete for miR-139-5p binding.With dual-luciferasereporter assay and knockdown experiment, these overexpressed target genes also regulate each others' protein levels through 3'-UTRs, thus regulating tumor cell growth and motility properties. Our study provides a mechanistic, experimentally validated rationale for intronic microRNA dysregulation in colorectal cancer, revealing novel oncogenic roles of IGF1R, ROCK2 and RAP1B 3'-UTRs.	MI0000261	Febs j 2014 Aug 281, 3609-24 doi:10.1111/febs.12880 PMID:24942287
556	Host gene	H19	miR-675	TGFBI	Metastatic Prostate Cancer Cell Line M12	Prostate Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	24988946	lncRNA H19/MiR-675 axis represses prostate cancer metastasis by targeting TGFBI.	Prostate cancer (PCa) is a leading cause of cancer-related mortality in men worldwide and there is a lack of effective treatment options for advanced (metastatic) PCa. Currently, limited knowledge is available concerning the role of long noncoding RNAs (lncRNAs) in prostate cancer metastasis. In this study, we found that lncRNA H19 (H19) and H19-derived miR-675 were significantly down-regulated in the metastatic prostate cancer cell line M12 compared to the non-metastatic prostate epithelial cell line P69. Up-regulation of H19 in P69 & PC3 cells significantly increased the level of miR-675 and repressed cell migration; however, ectopic expression of H19 in M12 cells could not increase the level of miR-675 and therefore had no effect on cell migration. Furthermore, we found that the expression level of either H19 or miR-675 in P69 cells was negatively associated with the expression of transforming growth factor b-induced protein (TGFBI), an ECM protein involved in cancer metastasis. Dual luciferase reporter assays showed that miR-675 directly bound with 3'UTR of TGFBI mRNA to repress its translation. Taken together, we show for the first time that H19/miR-675 axis acts as a suppressor of prostate cancer metastasis, which may have possible diagnostic and therapeutic potentials for advanced prostate cancer.	MI0005416	Febs j 2014 Aug 281, 3766-75 doi:10.1111/febs.12902 PMID:24988946
557	Coding-mRNA	SERINC1	NA	PTEN	Du145, Hct116	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	We investigated the ability of these putative PTEN ceRNAs to modulate PTEN levels by first examining the effect of depletion of these candidates on endogenous PTEN protein levels in DU145 prostate cancer cells. For this analysis, we also included two genes, ACSL4 and UNC5CL, which are not predicted targets of these PTEN-targeting microRNAs as negative controls. These experiments were per- formed using siRNA pools (a combination of four independent siRNAs), which are designed to achieve strong on-target gene knockdown with minimal off-target effects. Real-time PCR analysis confirmed efficient siRNA-mediated knockdown of candidate PTEN ceRNAs. Depletion of SERINC1, ZNF460, VAPA,or CNOT6L transcripts did indeed result in a significant reduction in PTEN protein levels, whereas depletion of ACSL4 or UNC5CL did not have a significant effect.	NA	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
558	Coding-mRNA	ZNF460	NA	PTEN	Du145, Hct116	Glioblastoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	We investigated the ability of these putative PTEN ceRNAs to modulate PTEN levels by first examining the effect of depletion of these candidates on endogenous PTEN protein levels in DU145 prostate cancer cells. For this analysis, we also included two genes, ACSL4 and UNC5CL, which are not predicted targets of these PTEN-targeting microRNAs as negative controls. These experiments were per- formed using siRNA pools (a combination of four independent siRNAs), which are designed to achieve strong on-target gene knockdown with minimal off-target effects. Real-time PCR analysis confirmed efficient siRNA-mediated knockdown of candidate PTEN ceRNAs. Depletion of SERINC1, ZNF460, VAPA,or CNOT6L transcripts did indeed result in a significant reduction in PTEN protein levels, whereas depletion of ACSL4 or UNC5CL did not have a significant effect.	NA	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
559	Coding-mRNA	SERINC1	NA	PTEN	Du145, Hct116	Glioblastoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	We investigated the ability of these putative PTEN ceRNAs to modulate PTEN levels by first examining the effect of depletion of these candidates on endogenous PTEN protein levels in DU145 prostate cancer cells. For this analysis, we also included two genes, ACSL4 and UNC5CL, which are not predicted targets of these PTEN-targeting microRNAs as negative controls. These experiments were per- formed using siRNA pools (a combination of four independent siRNAs), which are designed to achieve strong on-target gene knockdown with minimal off-target effects. Real-time PCR analysis confirmed efficient siRNA-mediated knockdown of candidate PTEN ceRNAs. Depletion of SERINC1, ZNF460, VAPA,or CNOT6L transcripts did indeed result in a significant reduction in PTEN protein levels, whereas depletion of ACSL4 or UNC5CL did not have a significant effect.	NA	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
560	Coding-mRNA	ZNF460	NA	PTEN	Du145, Hct116	Glioblastoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000013	Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs	We investigated the ability of these putative PTEN ceRNAs to modulate PTEN levels by first examining the effect of depletion of these candidates on endogenous PTEN protein levels in DU145 prostate cancer cells. For this analysis, we also included two genes, ACSL4 and UNC5CL, which are not predicted targets of these PTEN-targeting microRNAs as negative controls. These experiments were per- formed using siRNA pools (a combination of four independent siRNAs), which are designed to achieve strong on-target gene knockdown with minimal off-target effects. Real-time PCR analysis confirmed efficient siRNA-mediated knockdown of candidate PTEN ceRNAs. Depletion of SERINC1, ZNF460, VAPA,or CNOT6L transcripts did indeed result in a significant reduction in PTEN protein levels, whereas depletion of ACSL4 or UNC5CL did not have a significant effect.	NA	Cell 2011 Oct 14 147, 344-57 doi:10.1016/j.cell.2011.09.029 PMID:22000013
561	Coding-mRNA	ZEB2	miR-25	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000689	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
562	Coding-mRNA	ZEB2	miR-92a	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000719	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
563	Coding-mRNA	ZEB2	miR-181	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000223	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
564	Coding-mRNA	ZEB2	miR-200b	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000243	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
565	Coding-mRNA	ZEB2	miR-25	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000082	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
566	Coding-mRNA	ZEB2	miR-92a	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000093	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
567	Coding-mRNA	ZEB2	miR-181	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000269	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
568	Coding-mRNA	ZEB2	miR-200b	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	We show that ZEB2 modulates PTEN protein levels in a microRNA-dependent, protein coding-independent manner. Attenuation of ZEB2 expression activates the PI3K/AKT pathway, enhances cell transformation, and commonly occurs in human melanomas and other cancers expressing low PTEN levels.	MI0000342	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
569	Coding-mRNA	AFF1	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
570	Coding-mRNA	JARID2	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
571	Coding-mRNA	MBNL1	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
572	Coding-mRNA	RBM9	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
573	Coding-mRNA	TNRC6a	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
574	Coding-mRNA	TNRC6b	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
575	Coding-mRNA	AFF1	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
576	Coding-mRNA	JARID2	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
577	Coding-mRNA	MBNL1	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
578	Coding-mRNA	RBM9	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
579	Coding-mRNA	TNRC6a	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
580	Coding-mRNA	TNRC6b	NA	PTEN	A375, Wm35, 451Lu And Wm278	Melanoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	22000016	In vivo identification of tumor-suppressive PTEN ceRNAs in an oncogenic BRAF-induced mouse model of melanoma	To examine whether the identified putative PTEN ceRNAs regulate expression of PTEN, we performed RNAi-mediated gene silencing in human melanoma cells using pools of four siRNAs to reduce off-target effects. We selected eight putative PTEN ceRNAs (AFF1, DCBLD2, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2) and depleted them in WM35 cells. Knockdown of seven genes led to reduction of PTEN, six of which significantly attenuated PTEN expression (AFF1, JARID2, MBNL1, RBM9, TNRC6a, TNRC6b, and ZEB2). A reduction of PTEN mRNA levels following PTEN ceRNA silencing was also evident in WM35 cells.	NA	Cell 2011 Oct 14 147, 382-95 doi:10.1016/j.cell.2011.09.032 PMID:22000016
581	Coding-mRNA	SNAI1	miR-153	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000463	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
582	Coding-mRNA	SNAI1	miR-199a	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000242	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
583	Coding-mRNA	SNAI1	miR-203	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000283	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
584	Coding-mRNA	SNAI1	miR-204	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000284	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
585	Coding-mRNA	SNAI1	miR-22	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000078	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
586	Coding-mRNA	SNAI1	miR-34c	NA	Rmug-L Cell Line	Ovarian Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25326810	The SNAI1 3'UTR functions as a sponge for multiple migration-/invasion-related microRNAs.	Since SNAI1 3'UTR primarily influenced migration and invasion of RMUG-L cells, we narrowed our search to miRNAs that have been demonstrated to have contributions to migration and invasion in ovarian cancer or other cancers. Namely, seven candidate miRNAs including miR-153, miR-199a-5p, miR-203, miR-204, miR-22, miR-34a, and miR-34c were subjected to further validation.Luciferase assays indicated that decreased activity of miR-153, miR-199a, miR-203, miR-204, miR-22 and miR-34c resulted from increased levels of Renilla luciferase after SNAI1 3'UTR overexpression in RMUG-L cells.	MI0000743	Tumour Biol 2015 Feb 36, 1067-72 doi:10.1007/s13277-014-2733-z PMID:25326810
587	LncRNA	lnc-SCA7	miR-124	ATXN7	Embryonic Stem Cells	Neuroblastoma	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	25306109	Cross-talking noncoding RNAs contribute to cell-specific neurodegeneration in SCA7.	As observed in N2A cells, lnc-SCA7 knockdown (76% relative to control) in wild-type ES cells significantly reduced the expression of Atxn7 (82% of control). In contrast, in Dcr-deficient ES cells a similar level of lnc-SCA7 knockdown had no significant effect on Atxn7 expression. This is consistent with the regulation of Atxn7 expression by lnc-SCA7 being miRNA-dependent. This conclusion was further supported by the dependence of the reduction in reporter activity after cotransfection of miR-124 mimics and recombinant lnc-SCA7 or Atxn7 luciferase-reporter constructs (23% and 42% of control, respectively) on the presence of the predicted miR-124 MREs in these transcripts. More specifically, transfected constructs bearing inverted seed sequences of all miR-124 MREs predicted within lnc-SCA7 (six MREs) and Atxn7 (two MREs) (hereafter referred to as lnc-SCA7-mut and Atxn7-mut, respec tively) abolished the effect of miR-124 on reporter activity. As expected, neither lnc-SCA7-mut nor Atxn7-mut overexpression (7.7- and 9.7-fold, respectively) had a significant impact on transcript levels of Atxn7 or lnc-SCA7 , consistently with the ability of lnc-SCA7 and Atxn7 transcripts to modulate each other’s abundance in a miR-124 dependent manner.	MI0000150	Nat Struct Mol Biol 2014 Nov 21, 955-961 doi:10.1038/nsmb.2902 PMID:25306109
588	LncRNA	HOST2	let-7b	HMGA2	Ovcar3 Cell Line	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	25292198	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b.	A luciferase reporter vector encoding 1500–2000 nt of the HOST2 sequence (harboring all of complementary positions of seven miRNAs, renamed pGL3-HOST2-wt) and a Renilla luciferase (Rluc) gene in the 3' UTR and a downstream, constitutively expressed firefly luciferase gene, which served as an internal control for normalization, were constructed. These vectors were then sequentially co-transfected with mimics of the above-mentioned, predicted miRNAs and a scramble mimic (as the control, renamed miCon) into OVCAR-3 cells (Aiferase activity of pGL3-HOST2-wt (WT), whereas little to no significant reduction in luciferase activity was observed when the cells were co-transfected with the other five predicted miRNAs. TThe data indicated that mutating the seed regions for let-7b and miR-1266 barely abrogated its luciferase activity. We also found that the inhibition effect of let-7b was more stable than that of miR-1266. Given that let-7 regulates target-gene expression by binding to imperfect complementary sequences in messenger RNAs (mRNAs), leading to translational repression and/or mRNA destabilization {(32)}, and because we knew nothing about miR-1266, we only focused on the regulatory role of let-7b for the HOST2 transcript in the further work. Meanwhile, the expression of let-7b was detected in the 30 OBT and 50 EOC tissue samples and was shown to be lower in EOC than in OBT (P < 0.01). After transfecting the let-7b mimic into OVCAR-3 cells, HOST2 expression was observed to be markedly down-regulated at the mRNA level when compared with that in cells transfected with miCon. These results indicated that let-7b repressed HOST2 expression in EOC, but the reason for let-7b expression being lower in EOC than in OBT was uncertain.When HOST2 was down-regulated, the expression of HMGA2, c-Myc, Dicer and Imp3 were also significantly reduced at the RNA and protein level, which was consistent with an increase in let-7b expression. Concomitantly, cell migration, invasion and proliferation were all inhibited, similar to what we have shown. Thus, the expression of the four targets were analyzed using reciprocal, HOST2 over-expressed experiments, where pcDNA3.0-HOST2 and a control empty vector (pcDNA3.0) were, respectively, transfected into HEK293 cells to increase the endogenous HOST2 level. Cells transfected with pcDNA3.0-HOST2 expressed HOST2 5-fold higher than cells transfection with pcDNA3.0. Significant increases of HMGA2, c-Myc, Dicer and Imp3 at the mRNA and protein levels in response to HOST2 over-expression were all observed. Together, these HOST2 loss- and gain-of-function studies suggest that ectopically expressed HOST2 sequesters endogenous let-7b and inhibits its functions, leading to derepression of the target genes of let-7b. To confirm that these effects were indeed due to down-regulated let-7b, we performed transfection experiments using ilet-7. As expected, increased mRNA as well as protein levels of HMGA2, c-Myc, Dicer and Imp3 were all observed in ilet-7-treated HEK293 cells when compared with iCon-treated cells.	MI0000063	Hum Mol Genet 2015 Feb 1 24, 841-52 doi:10.1093/hmg/ddu502 PMID:25292198
589	LncRNA	HOST2	let-7b	c-Myc	Ovcar3 Cell Line	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	25292198	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b.	A luciferase reporter vector encoding 1500–2000 nt of the HOST2 sequence (harboring all of complementary positions of seven miRNAs, renamed pGL3-HOST2-wt) and a Renilla luciferase (Rluc) gene in the 3' UTR and a downstream, constitutively expressed firefly luciferase gene, which served as an internal control for normalization, were constructed. These vectors were then sequentially co-transfected with mimics of the above-mentioned, predicted miRNAs and a scramble mimic (as the control, renamed miCon) into OVCAR-3 cells (Aiferase activity of pGL3-HOST2-wt (WT), whereas little to no significant reduction in luciferase activity was observed when the cells were co-transfected with the other five predicted miRNAs. TThe data indicated that mutating the seed regions for let-7b and miR-1266 barely abrogated its luciferase activity. We also found that the inhibition effect of let-7b was more stable than that of miR-1266. Given that let-7 regulates target-gene expression by binding to imperfect complementary sequences in messenger RNAs (mRNAs), leading to translational repression and/or mRNA destabilization {(32)}, and because we knew nothing about miR-1266, we only focused on the regulatory role of let-7b for the HOST2 transcript in the further work. Meanwhile, the expression of let-7b was detected in the 30 OBT and 50 EOC tissue samples and was shown to be lower in EOC than in OBT (P < 0.01). After transfecting the let-7b mimic into OVCAR-3 cells, HOST2 expression was observed to be markedly down-regulated at the mRNA level when compared with that in cells transfected with miCon. These results indicated that let-7b repressed HOST2 expression in EOC, but the reason for let-7b expression being lower in EOC than in OBT was uncertain.When HOST2 was down-regulated, the expression of HMGA2, c-Myc, Dicer and Imp3 were also significantly reduced at the RNA and protein level, which was consistent with an increase in let-7b expression. Concomitantly, cell migration, invasion and proliferation were all inhibited, similar to what we have shown. Thus, the expression of the four targets were analyzed using reciprocal, HOST2 over-expressed experiments, where pcDNA3.0-HOST2 and a control empty vector (pcDNA3.0) were, respectively, transfected into HEK293 cells to increase the endogenous HOST2 level. Cells transfected with pcDNA3.0-HOST2 expressed HOST2 5-fold higher than cells transfection with pcDNA3.0. Significant increases of HMGA2, c-Myc, Dicer and Imp3 at the mRNA and protein levels in response to HOST2 over-expression were all observed. Together, these HOST2 loss- and gain-of-function studies suggest that ectopically expressed HOST2 sequesters endogenous let-7b and inhibits its functions, leading to derepression of the target genes of let-7b. To confirm that these effects were indeed due to down-regulated let-7b, we performed transfection experiments using ilet-7. As expected, increased mRNA as well as protein levels of HMGA2, c-Myc, Dicer and Imp3 were all observed in ilet-7-treated HEK293 cells when compared with iCon-treated cells.	MI0000063	Hum Mol Genet 2015 Feb 1 24, 841-52 doi:10.1093/hmg/ddu502 PMID:25292198
590	LncRNA	HOST2	let-7b	DICER	Ovcar3 Cell Line	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	25292198	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b.	A luciferase reporter vector encoding 1500–2000 nt of the HOST2 sequence (harboring all of complementary positions of seven miRNAs, renamed pGL3-HOST2-wt) and a Renilla luciferase (Rluc) gene in the 3' UTR and a downstream, constitutively expressed firefly luciferase gene, which served as an internal control for normalization, were constructed. These vectors were then sequentially co-transfected with mimics of the above-mentioned, predicted miRNAs and a scramble mimic (as the control, renamed miCon) into OVCAR-3 cells (Aiferase activity of pGL3-HOST2-wt (WT), whereas little to no significant reduction in luciferase activity was observed when the cells were co-transfected with the other five predicted miRNAs. TThe data indicated that mutating the seed regions for let-7b and miR-1266 barely abrogated its luciferase activity. We also found that the inhibition effect of let-7b was more stable than that of miR-1266. Given that let-7 regulates target-gene expression by binding to imperfect complementary sequences in messenger RNAs (mRNAs), leading to translational repression and/or mRNA destabilization {(32)}, and because we knew nothing about miR-1266, we only focused on the regulatory role of let-7b for the HOST2 transcript in the further work. Meanwhile, the expression of let-7b was detected in the 30 OBT and 50 EOC tissue samples and was shown to be lower in EOC than in OBT (P < 0.01). After transfecting the let-7b mimic into OVCAR-3 cells, HOST2 expression was observed to be markedly down-regulated at the mRNA level when compared with that in cells transfected with miCon. These results indicated that let-7b repressed HOST2 expression in EOC, but the reason for let-7b expression being lower in EOC than in OBT was uncertain.When HOST2 was down-regulated, the expression of HMGA2, c-Myc, Dicer and Imp3 were also significantly reduced at the RNA and protein level, which was consistent with an increase in let-7b expression. Concomitantly, cell migration, invasion and proliferation were all inhibited, similar to what we have shown. Thus, the expression of the four targets were analyzed using reciprocal, HOST2 over-expressed experiments, where pcDNA3.0-HOST2 and a control empty vector (pcDNA3.0) were, respectively, transfected into HEK293 cells to increase the endogenous HOST2 level. Cells transfected with pcDNA3.0-HOST2 expressed HOST2 5-fold higher than cells transfection with pcDNA3.0. Significant increases of HMGA2, c-Myc, Dicer and Imp3 at the mRNA and protein levels in response to HOST2 over-expression were all observed. Together, these HOST2 loss- and gain-of-function studies suggest that ectopically expressed HOST2 sequesters endogenous let-7b and inhibits its functions, leading to derepression of the target genes of let-7b. To confirm that these effects were indeed due to down-regulated let-7b, we performed transfection experiments using ilet-7. As expected, increased mRNA as well as protein levels of HMGA2, c-Myc, Dicer and Imp3 were all observed in ilet-7-treated HEK293 cells when compared with iCon-treated cells.	MI0000063	Hum Mol Genet 2015 Feb 1 24, 841-52 doi:10.1093/hmg/ddu502 PMID:25292198
591	LncRNA	HOST2	let-7b	IMP3	Ovcar3 Cell Line	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	25292198	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b.	A luciferase reporter vector encoding 1500–2000 nt of the HOST2 sequence (harboring all of complementary positions of seven miRNAs, renamed pGL3-HOST2-wt) and a Renilla luciferase (Rluc) gene in the 3' UTR and a downstream, constitutively expressed firefly luciferase gene, which served as an internal control for normalization, were constructed. These vectors were then sequentially co-transfected with mimics of the above-mentioned, predicted miRNAs and a scramble mimic (as the control, renamed miCon) into OVCAR-3 cells (Aiferase activity of pGL3-HOST2-wt (WT), whereas little to no significant reduction in luciferase activity was observed when the cells were co-transfected with the other five predicted miRNAs. TThe data indicated that mutating the seed regions for let-7b and miR-1266 barely abrogated its luciferase activity. We also found that the inhibition effect of let-7b was more stable than that of miR-1266. Given that let-7 regulates target-gene expression by binding to imperfect complementary sequences in messenger RNAs (mRNAs), leading to translational repression and/or mRNA destabilization {(32)}, and because we knew nothing about miR-1266, we only focused on the regulatory role of let-7b for the HOST2 transcript in the further work. Meanwhile, the expression of let-7b was detected in the 30 OBT and 50 EOC tissue samples and was shown to be lower in EOC than in OBT (P < 0.01). After transfecting the let-7b mimic into OVCAR-3 cells, HOST2 expression was observed to be markedly down-regulated at the mRNA level when compared with that in cells transfected with miCon. These results indicated that let-7b repressed HOST2 expression in EOC, but the reason for let-7b expression being lower in EOC than in OBT was uncertain.When HOST2 was down-regulated, the expression of HMGA2, c-Myc, Dicer and Imp3 were also significantly reduced at the RNA and protein level, which was consistent with an increase in let-7b expression. Concomitantly, cell migration, invasion and proliferation were all inhibited, similar to what we have shown. Thus, the expression of the four targets were analyzed using reciprocal, HOST2 over-expressed experiments, where pcDNA3.0-HOST2 and a control empty vector (pcDNA3.0) were, respectively, transfected into HEK293 cells to increase the endogenous HOST2 level. Cells transfected with pcDNA3.0-HOST2 expressed HOST2 5-fold higher than cells transfection with pcDNA3.0. Significant increases of HMGA2, c-Myc, Dicer and Imp3 at the mRNA and protein levels in response to HOST2 over-expression were all observed. Together, these HOST2 loss- and gain-of-function studies suggest that ectopically expressed HOST2 sequesters endogenous let-7b and inhibits its functions, leading to derepression of the target genes of let-7b. To confirm that these effects were indeed due to down-regulated let-7b, we performed transfection experiments using ilet-7. As expected, increased mRNA as well as protein levels of HMGA2, c-Myc, Dicer and Imp3 were all observed in ilet-7-treated HEK293 cells when compared with iCon-treated cells.	MI0000063	Hum Mol Genet 2015 Feb 1 24, 841-52 doi:10.1093/hmg/ddu502 PMID:25292198
592	Artifically engineered RNA	miR-7-specific decoy transcript	miR-7	CDC7	Cho Cells	Recombinant Protein Production By Cho	Homo sapiens (human)	qRT-PCR	24166820	CHO cell culture longevity and recombinant protein yield are enhanced by depletion of miR-7 activity via sponge decoy vectors.	We generated stable CHO clones that overexpressed a miR-7-specific decoy transcript (sponge) downstream of a green fluorescent protein reporter gene. The miR-7 sponge efficiently diverted miR-7 away from its endogenous targets as exemplified by the increased expression of CDC7. Although the sponge effectively sequestered miR-7, it also appeared to protect the bound miRNA sequence from degradation in the cell, as exemplified by the apparent increase in mature miR-7 levels without any change in primary transcription. Phenotypically, CHO clones with sequestered miR-7 displayed improved maximum cell density (40%), significantly improved viability and an almost two-fold increase in yield of secreted protein in a fed-batch culture. These findings demonstrate that miRNA sponge transcripts could potentially be used in cell line development projects to generate producer clones that grow to higher densities and last longer in the bioreactor - thereby improving product yield.	MI0000263	Biotechnol J 2014 Mar 9, 396-404 doi:10.1002/biot.201300325 PMID:24166820
593	LncRNA	Linc00974	miR-642	NA	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays;Immunohistochemical assay	25476897	A novel biomarker Linc00974 interacting with KRT19 promotes proliferation and metastasis in hepatocellular carcinoma.	MiR-642 was identified, by acting as the competing endogenous RNA in regulating Linc00974 and KRT19. Linc00974 was increased owing to an abnormal hypomethylation promoter, which induced the upregulation of KRT19 via ceRNA interaction, resulting in the activation of the Notch and TGF-b pathways as detected by cDNA microarray.	MI0003657	Cell Death Dis 2014 Dec 4 5, e1549 doi:10.1038/cddis.2014.518 PMID:25476897
594	LncRNA	CASC2	miR-21	NA	U251 And U87	Glioma	Homo sapiens (human)	qRT-PCR	25446261	Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21.	Overexpression of CASC2 inhibited the malignancy of glioma cells, including proliferation, migration, and invasion, and promoted cell apoptosis. MicroRNA-21 (miR-21) has been reported to be overexpressed in human glioma tissues and cell lines, which is responsible for the malignant progression of glioma. We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner.	MI0000077	Cell Signal 2015 Feb 27, 275-82 doi:10.1016/j.cellsig.2014.11.011 PMID:25446261
595	Artifically engineered RNA	Adenoviral vector	miR-221	NA	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR	25436097	Inhibiting the oncogenic mir-221 by microRNA sponge: toward microRNA-based therapeutics for hepatocellular carcinoma.	Novel adeno and adeno-associated viral vectors (AAVs) were developed.Analysis of viral vectors activity in HCC cells revealed their capability to reduce miR-221 endogenous levels, which was accompanied by the increase in CDKN1B/ p27 protein, a known target of miR-221. An increase in apoptosis was also measured in Hep3B cells after infection with any of the two viral vectors in comparison with control vectors, with stronger effects induced by adenovirus compared to AAV vectors.	MI0000298	Gastroenterol Hepatol Bed Bench 2014 Winter 7, 43-54,  PMID:25436097
596	Artifically engineered RNA	Adeno-associated viral vector	miR-222	NA	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR	25436097	Inhibiting the oncogenic mir-222 by microRNA sponge: toward microRNA-based therapeutics for hepatocellular carcinoma.	Novel adeno and adeno-associated viral vectors (AAVs) were developed.Analysis of viral vectors activity in HCC cells revealed their capability to reduce miR-221 endogenous levels, which was accompanied by the increase in CDKN1B/ p28 protein, a known targeof miR-221. An increase in apoptosis was also measured in Hep3B cells after infection with any of the two viral vectors in comparison with control vectors, with stronger effects induced by adenovirus compared to AAV vectors.	MI0000299	Gastroenterol Hepatol Bed Bench 2014 Winter 7, 43-54,  PMID:25436097
597	Artifically engineered RNA	FC sponge	miR-9	REST	Brain Tissues	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	25406064	MicroRNA-9 controls dendritic development by targeting REST.	In order to target miR-9 in vivo, we developed a transgenic miRNA sponge mouse line allowing conditional inactivation of the miR-9 family in a spatio-temporal-controlled manner. Using this novel approach, we found that the sponge variants displayed similar efficacies to inhibit miR-9 activity	MI0000157	Elife 2014 Nov 18 3 doi:10.7554/eLife.02755 PMID:25406064
598	Artifically engineered RNA	Bg sponge	miR-10	NA	Brain Tissues	NA	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	25406064	MicroRNA-10 controls dendritic development by targeting REST.	In order to target miR-9 in vivo, we developed a transgenic miRNA sponge mouse line allowing conditional inactivation of the miR10 family in a spatio-temporal-controlled manner. Using this novel approach, we found that the sponge variants displayed similarowth- and tumour-suppressive properti	MI0000685	Elife 2014 Nov 18 3 doi:10.7554/eLife.02755 PMID:25406064
599	Artifically engineered RNA	miR-223 antagomiR	miR-223	NA	Monocyte	Innate Immune Responses	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	25400635	Small Talk in the Innate Immune System via RNA-Containing Extracellular Vesicles.	EV released by macrophages mediate functional transfer of miR-223, which regulates myeloid cell proliferation/differentiation and tumor development (54–56). Ismail et al. showed that EV release was increased upon differentiation of monocytes into macrophages and that the macrophage-derived EV induced cellular differentiation in targeted monocytes (46). The authors demonstrated that endogenous miR-223 released via EV by macrophages was functional in miR-223-negative target cells transfected with a miRNA-reporter vector. In addition, treatment of monocytes with miR-223 antagomiR was shown to reduce differentiation of these cells. Although evidence for causation was not provided, these data give a strong indication that the EV-induced effects on monocyte differentiation were caused by EV-mediated transfer of miR-223. 	MI0000300	Front Immunol 2014  5, 542 doi:10.3389/fimmu.2014.00542 PMID:25400635
600	Artifically engineered RNA	miR-188-3p sponge	miR-188-3p	BACE1	Brain Tissues	Alzheimers Disease	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	25378159	Synaptic and Cognitive Improvements by Inhibition of 2-AG Metabolism Are through Upregulation of MicroRNA-188-3p in a Mouse Model of Alzheimer's Disease.	To further determine whether the effect of 2-AG on BACE1 expression is mediated through miR-188-3p,weusedthemiRNA“sponge”technique,which renders a continuous miRNA loss of function by complementary binding to a miRNA of interest.Knockdown of miR-188-3p in cells by miR-188-30 sponge eliminated 2-AG-induced suppression of BACE1,where as 2-AG still suppressed BACE1 expression in cells treated with the scramble controls. These results indicate that the suppression of BACE1 by 2-AG is mediated through miR-188-3p.	MI0000230	J Neurosci 2014 Nov 5 34, 14919-33 doi:10.1523/jneurosci.1165-14.2014 PMID:25378159
601	Viral RNA	HCV RNA	miR-122	STAT3	Huh7 Cells	Cellular Antiviral Response	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	25377467	Hepatitis C virus represses the cellular antiviral response by upregulating the expression of signal transducer and activator of transcription 3 through sponging microRNA-122.	miR-122 inhibited the expression of signal transducer and activator of transcription 3 (STAT3), an antivirus response repressor.The HCV RNA acted as an miRNA sponge, which upregulated the expression of STAT3 by sealing miR-122. 	MI0000442	Mol Med Rep 2015 Mar 11, 1733-7 doi:10.3892/mmr.2014.2897 PMID:25377467
602	Protein	HBx	miR-15b	Globo-H	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR	25364579	Hepatitis B virus X protein accelerates the development of hepatoma.	HBx suppresses the expression of miR-15b, which directly targets fucosyltransferase 2 and increases the levels of Globo-H to enhance HCC cell proliferation.	MI0000140	Cancer Biol Med 2014 Sep 11, 182-90 doi:10.7497/j.issn.2095-3941.2014.03.004 PMID:25364579
603	Protein	HBx	miR-205	ACSL1	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR	25364579	Hepatitis B virus X protein accelerates the development of hepatoma.	MiR-205 was downregulated in the liver of HBx-transgenic mice. HBx can abrogate the effect of miR-205 on tumor suppression in carcinogenesis12. The downregulation of miR-205 mediated by HBx remarkably increases the expression levels of acyl-CoA synthetase long-chain family member 1 (ACSL1), and its metabolite triglyceride levels are remarkably increased in HBx-induced liver cancer tissues, as shown in an HBx transgenic mice model.	MI0000248	Cancer Biol Med 2014 Sep 11, 182-90 doi:10.7497/j.issn.2095-3941.2014.03.004 PMID:25364579
604	Protein	HBx	miR-148a	AKT	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR	25364579	Hepatitis B virus X protein accelerates the development of hepatoma.	HBx suppresses the p53-mediated activation of miR-148a, resulting in the upregulation of AKT and ERK and subsequent activation of mTOR to promote cancer growth and metastasis in a mouse model of HCC.	MI0000550	Cancer Biol Med 2014 Sep 11, 182-90 doi:10.7497/j.issn.2095-3941.2014.03.004 PMID:25364579
605	Coding-mRNA	Ang-2	miR-351	VEGF	Vascular Cells	Microvascular Dysfunction	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays; Intraocular injection of miRNA mimic	25172656	miRNA-dependent cross-talk between VEGF and Ang-2 in hypoxia-induced microvascular dysfunction.	We assessed whether the expression of Ang-2 and VEGF is interdependent through the sequestration of common miRNAs. Bioinformatics prediction and 3'-UTR luciferase assay revealed that Ang-2 and VEGF is commonly targeted by miR-351. Silencing either Ang-2 or VEGF increases the availabilities of shared miR-351, therefore reduces the activity of Luc-Ang-2 3'-UTR. The interdependence of VEGF and Ang-2 is miRNA- and 3'-UTR dependent, as silencing Dicer abolishes the interdependence. We also found that miR-351 dependency of VEGF-Ang-2 crosstalk occurs in retinal endothelial cells and rat retinas. miR-351 over-expression significantly reduces the level of VEGF and Ang-2 expression in vivo and in vitro. Overall, miRNA-dependent crosstalk between Ang-2 and VEGF plays a role in hypoxia-induced microvascular response. miRNA-based therapy can affect the expression of Ang-2 and VEGF, which represents a therapeutic potential for the treatment of vascular disease.	MI0000643	Biochem Biophys Res Commun 2014 Sep 26 452, 428-35 doi:10.1016/j.bbrc.2014.08.096 PMID:25172656
606	Coding-mRNA	VCAN	miR-185	NA	Fibroblasts	Wound Repair And Fibroblast	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24594381	Versican 3'-untranslated region (3'UTR) promotes dermal wound repair and fibroblast migration by regulating miRNA activity	We demonstrated that both the versican 3'UTR and b-catenin 3'UTR shared common binding sites for miR-185, miR-203*, miR-434-3p, miR-680, and miR-690. It appeared that over-expression of the versican 3'UTR bound and inhibited the activity of these miRNAs, resulting in promotion of versican expression and b-catenin expression.	MI0000227	Biochim Biophys Acta 2014 Jul 1843, 1373-85 doi:10.1016/j.bbamcr.2014.02.015 PMID:24594381
607	Coding-mRNA	VCAN	miR-203*	NA	Fibroblasts	Wound Repair And Fibroblast	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24594381	Versican 3'-untranslated region (3'UTR) promotes dermal wound repair and fibroblast migration by regulating miRNA activity	We demonstrated that both the versican 3'UTR and b-catenin 3'UTR shared common binding sites for miR-185, miR-203*, miR-434-3p, miR-680, and miR-690. It appeared that over-expression of the versican 3'UTR bound and inhibited the activity of these miRNAs, resulting in promotion of versican expression and b-catenin expression.	MI0000246	Biochim Biophys Acta 2014 Jul 1843, 1373-85 doi:10.1016/j.bbamcr.2014.02.015 PMID:24594381
608	Coding-mRNA	VCAN	miR-434-3p	NA	Fibroblasts	Wound Repair And Fibroblast	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24594381	Versican 3'-untranslated region (3'UTR) promotes dermal wound repair and fibroblast migration by regulating miRNA activity	We demonstrated that both the versican 3'UTR and b-catenin 3'UTR shared common binding sites for miR-185, miR-203*, miR-434-3p, miR-680, and miR-690. It appeared that over-expression of the versican 3'UTR bound and inhibited the activity of these miRNAs, resulting in promotion of versican expression and b-catenin expression.	MI0001526	Biochim Biophys Acta 2014 Jul 1843, 1373-85 doi:10.1016/j.bbamcr.2014.02.015 PMID:24594381
609	Coding-mRNA	VCAN	miR-680	NA	Fibroblasts	Wound Repair And Fibroblast	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24594381	Versican 3'-untranslated region (3'UTR) promotes dermal wound repair and fibroblast migration by regulating miRNA activity	We demonstrated that both the versican 3'UTR and b-catenin 3'UTR shared common binding sites for miR-185, miR-203*, miR-434-3p, miR-680, and miR-690. It appeared that over-expression of the versican 3'UTR bound and inhibited the activity of these miRNAs, resulting in promotion of versican expression and b-catenin expression.	MI0004640	Biochim Biophys Acta 2014 Jul 1843, 1373-85 doi:10.1016/j.bbamcr.2014.02.015 PMID:24594381
610	Coding-mRNA	VCAN	miR-690	NA	Fibroblasts	Wound Repair And Fibroblast	Mus musculus (mouse)	Western blot;qRT-PCR;luciferase reporter assays	24594381	Versican 3'-untranslated region (3'UTR) promotes dermal wound repair and fibroblast migration by regulating miRNA activity	We demonstrated that both the versican 3'UTR and b-catenin 3'UTR shared common binding sites for miR-185, miR-203*, miR-434-3p, miR-680, and miR-690. It appeared that over-expression of the versican 3'UTR bound and inhibited the activity of these miRNAs, resulting in promotion of versican expression and b-catenin expression.	MI0004658	Biochim Biophys Acta 2014 Jul 1843, 1373-85 doi:10.1016/j.bbamcr.2014.02.015 PMID:24594381
611	Artifically engineered RNA	V-139	miR-139	TCP2	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	We expressed the miR319 target mimic in Arabidopsis by the modified TRV vector. A sequence containing four copies of the target mimic flanked by restriction enzyme sites was prepared and ligated into the TRV RNA2 vector with BamHI and SalI, producing TRV:MIM319 (V-319). A partial sequence of GUS was used to prepare a control vector (V-GUS). Agrobacterium containing either V-319 or V-GUS was mixed with Agrobacterium containing the TRV RNA1 vector and infiltrated into young leaves of Arabidopsis when plants were at the 4-leaf stage. At 7 days post infil- tration (dpi), one leaf of each treated plant was collected for detecting viral infection by RT-PCR. Plants without viral infection were excluded in the next phenotype monitoring. At least 12 infected plants were used in each of three replicate experiments. Phenotype monitoring showed that V-319-treated plants had downwardly curled leaves at 15 dpi. And at the flowering time, the majority of flowers in V-319-treated plants had short and small sepals and petals, while a few flowers lacked petals and did not have fully developed anthers. Flowers with short sepals and petals were fertile but the seed pods produced were smaller, while flowers lacking petals and anthers were infertile. The phenotype of V-319-treated plants was thus totally consistent with the earlier report, indicating that miR319 had been sequestered efficiently by V-319. The miR319 host targets TCP2, TCP4, MYB33 and MYB65, but not TCP3, were expressed at higher levels in leaves and all targets were expressed at higher levels in flowers in V-319-treated plants than in the controls. 	MI0000261	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
612	Artifically engineered RNA	V-139	miR-139	TCP4	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	We expressed the miR319 target mimic in Arabidopsis by the modified TRV vector. A sequence containing four copies of the target mimic flanked by restriction enzyme sites was prepared and ligated into the TRV RNA2 vector with BamHI and SalI, producing TRV:MIM319 (V-319). A partial sequence of GUS was used to prepare a control vector (V-GUS). Agrobacterium containing either V-319 or V-GUS was mixed with Agrobacterium containing the TRV RNA1 vector and infiltrated into young leaves of Arabidopsis when plants were at the 4-leaf stage. At 7 days post infil- tration (dpi), one leaf of each treated plant was collected for detecting viral infection by RT-PCR. Plants without viral infection were excluded in the next phenotype monitoring. At least 12 infected plants were used in each of three replicate experiments. Phenotype monitoring showed that V-319-treated plants had downwardly curled leaves at 15 dpi. And at the flowering time, the majority of flowers in V-319-treated plants had short and small sepals and petals, while a few flowers lacked petals and did not have fully developed anthers. Flowers with short sepals and petals were fertile but the seed pods produced were smaller, while flowers lacking petals and anthers were infertile. The phenotype of V-319-treated plants was thus totally consistent with the earlier report, indicating that miR319 had been sequestered efficiently by V-319. The miR319 host targets TCP2, TCP4, MYB33 and MYB65, but not TCP3, were expressed at higher levels in leaves and all targets were expressed at higher levels in flowers in V-319-treated plants than in the controls. 	MI0000261	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
613	Artifically engineered RNA	V-139	miR-139	MYB33	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	We expressed the miR319 target mimic in Arabidopsis by the modified TRV vector. A sequence containing four copies of the target mimic flanked by restriction enzyme sites was prepared and ligated into the TRV RNA2 vector with BamHI and SalI, producing TRV:MIM319 (V-319). A partial sequence of GUS was used to prepare a control vector (V-GUS). Agrobacterium containing either V-319 or V-GUS was mixed with Agrobacterium containing the TRV RNA1 vector and infiltrated into young leaves of Arabidopsis when plants were at the 4-leaf stage. At 7 days post infil- tration (dpi), one leaf of each treated plant was collected for detecting viral infection by RT-PCR. Plants without viral infection were excluded in the next phenotype monitoring. At least 12 infected plants were used in each of three replicate experiments. Phenotype monitoring showed that V-319-treated plants had downwardly curled leaves at 15 dpi. And at the flowering time, the majority of flowers in V-319-treated plants had short and small sepals and petals, while a few flowers lacked petals and did not have fully developed anthers. Flowers with short sepals and petals were fertile but the seed pods produced were smaller, while flowers lacking petals and anthers were infertile. The phenotype of V-319-treated plants was thus totally consistent with the earlier report, indicating that miR319 had been sequestered efficiently by V-319. The miR319 host targets TCP2, TCP4, MYB33 and MYB65, but not TCP3, were expressed at higher levels in leaves and all targets were expressed at higher levels in flowers in V-319-treated plants than in the controls. 	MI0000261	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
614	Artifically engineered RNA	V-139	miR-139	MYB65	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	We expressed the miR319 target mimic in Arabidopsis by the modified TRV vector. A sequence containing four copies of the target mimic flanked by restriction enzyme sites was prepared and ligated into the TRV RNA2 vector with BamHI and SalI, producing TRV:MIM319 (V-319). A partial sequence of GUS was used to prepare a control vector (V-GUS). Agrobacterium containing either V-319 or V-GUS was mixed with Agrobacterium containing the TRV RNA1 vector and infiltrated into young leaves of Arabidopsis when plants were at the 4-leaf stage. At 7 days post infil- tration (dpi), one leaf of each treated plant was collected for detecting viral infection by RT-PCR. Plants without viral infection were excluded in the next phenotype monitoring. At least 12 infected plants were used in each of three replicate experiments. Phenotype monitoring showed that V-319-treated plants had downwardly curled leaves at 15 dpi. And at the flowering time, the majority of flowers in V-319-treated plants had short and small sepals and petals, while a few flowers lacked petals and did not have fully developed anthers. Flowers with short sepals and petals were fertile but the seed pods produced were smaller, while flowers lacking petals and anthers were infertile. The phenotype of V-319-treated plants was thus totally consistent with the earlier report, indicating that miR319 had been sequestered efficiently by V-319. The miR319 host targets TCP2, TCP4, MYB33 and MYB65, but not TCP3, were expressed at higher levels in leaves and all targets were expressed at higher levels in flowers in V-319-treated plants than in the controls. 	MI0000261	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
615	Artifically engineered RNA	V-156	miR-156	SPL2	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	To test the suitability of VbMS, TRV:MIM156 (V-156) was constructed and used to analyze loss-of-function of miR156 in Arabidopsis. miR156 of Arabidopsis targets a series of SQUAMOSA promoter-binding protein-like (SPL) genes and regulates vegetative phase change. Thus inhibition of the new rosette leaves in V-156-treated plants is expressed by their smaller size. The results were also consistent with the findings that plants overexpressing miR156 initiated rosette leaves faster than wild-type. At 25 and 35 dpi, the thinner plant shape and the smaller number of leaves on V-156-treated plants was obvious, which is consistent with the phenotype reported in plants overexpressing the target mimic MIM156, and is nearly opposite to the report that plants overexpressing miR156 had a substantial increase in total leaf number on the main and side shoots The miR156 host targets, SPL2, SPL3, and SPL10 were expressed at higher levels in V-156-treated plants than in the controls. Molecular evidence together with the change in phenotype therefore demonstrated that the VbMS system had efficiently inhibited the activity of miR156 in A. thaliana.	MI0000178	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
616	Artifically engineered RNA	V-156	miR-156	SPL3	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	To test the suitability of VbMS, TRV:MIM156 (V-156) was constructed and used to analyze loss-of-function of miR156 in Arabidopsis. miR156 of Arabidopsis targets a series of SQUAMOSA promoter-binding protein-like (SPL) genes and regulates vegetative phase change. Thus inhibition of the new rosette leaves in V-156-treated plants is expressed by their smaller size. The results were also consistent with the findings that plants overexpressing miR156 initiated rosette leaves faster than wild-type. At 25 and 35 dpi, the thinner plant shape and the smaller number of leaves on V-156-treated plants was obvious, which is consistent with the phenotype reported in plants overexpressing the target mimic MIM156, and is nearly opposite to the report that plants overexpressing miR156 had a substantial increase in total leaf number on the main and side shoots The miR156 host targets, SPL2, SPL3, and SPL10 were expressed at higher levels in V-156-treated plants than in the controls. Molecular evidence together with the change in phenotype therefore demonstrated that the VbMS system had efficiently inhibited the activity of miR156 in A. thaliana.	MI0000178	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
617	Artifically engineered RNA	V-156	miR-156	SPL10	Arabidopsis	NA	Arabidopsis thaliana (thale cress)	qRT-PCR	24664983	A virus-based miRNA suppression (VbMS) system for miRNA loss-of-function analysis in plants	To test the suitability of VbMS, TRV:MIM156 (V-156) was constructed and used to analyze loss-of-function of miR156 in Arabidopsis. miR156 of Arabidopsis targets a series of SQUAMOSA promoter-binding protein-like (SPL) genes and regulates vegetative phase change. Thus inhibition of the new rosette leaves in V-156-treated plants is expressed by their smaller size. The results were also consistent with the findings that plants overexpressing miR156 initiated rosette leaves faster than wild-type. At 25 and 35 dpi, the thinner plant shape and the smaller number of leaves on V-156-treated plants was obvious, which is consistent with the phenotype reported in plants overexpressing the target mimic MIM156, and is nearly opposite to the report that plants overexpressing miR156 had a substantial increase in total leaf number on the main and side shoots The miR156 host targets, SPL2, SPL3, and SPL10 were expressed at higher levels in V-156-treated plants than in the controls. Molecular evidence together with the change in phenotype therefore demonstrated that the VbMS system had efficiently inhibited the activity of miR156 in A. thaliana.	MI0000178	Biotechnol J 2014 May 9, 702-8 doi:10.1002/biot.201300523 PMID:24664983
618	Artifically engineered RNA	miR221 sponge	miR-221	RELA	Hct116 And Rko Cell Lines	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24931456	A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFkB and STAT3 in colorectal cancer cells.	Colorectal cancer cell lines were transfected with MIR221 or MIR222 sponges. The activity levels of NFKB and STAT3 were measured in dual luciferase reporter assays. Immunoblot and real-time PCR analyses to measure protein and mRNA levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. In agreement with the causal roles of NFKB and STAT3 in CAC development, our data vevealed dramatically decreased levels of RELA and STAT3 protein expression in tumors from mice treated with the MIR221/222 sponge. Intriguingly, treatment with the MIR221/222 sponge significantly inhibited colitis, as indicated by body weight loss, colon shortening and inflammatory factor production.	MI0000298	Gastroenterology 2014 Oct 147, 847-859.e11 doi:10.1053/j.gastro.2014.06.006 PMID:24931456
619	Artifically engineered RNA	miR221 sponge	miR-221	PDLIM2	Hct116 And Rko Cell Lines	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24931456	A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFkB and STAT3 in colorectal cancer cells.	Colorectal cancer cell lines were transfected with MIR221 or MIR222 sponges. The activity levels of NFKB and STAT3 were measured in dual luciferase reporter assays. Immunoblot and real-time PCR analyses to measure protein and mRNA levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. In agreement with the causal roles of NFKB and STAT3 in CAC development, our data vevealed dramatically decreased levels of RELA and STAT3 protein expression in tumors from mice treated with the MIR221/222 sponge. Intriguingly, treatment with the MIR221/222 sponge significantly inhibited colitis, as indicated by body weight loss, colon shortening and inflammatory factor production.	MI0000298	Gastroenterology 2014 Oct 147, 847-859.e11 doi:10.1053/j.gastro.2014.06.006 PMID:24931456
620	Artifically engineered RNA	miR222 sponge	miR-222	RELA	Hct116 And Rko Cell Lines	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24931456	A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFkB and STAT3 in colorectal cancer cells.	Colorectal cancer cell lines were transfected with MIR221 or MIR222 sponges. The activity levels of NFKB and STAT3 were measured in dual luciferase reporter assays. Immunoblot and real-time PCR analyses to measure protein and mRNA levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. In agreement with the causal roles of NFKB and STAT3 in CAC development, our data vevealed dramatically decreased levels of RELA and STAT3 protein expression in tumors from mice treated with the MIR221/222 sponge. Intriguingly, treatment with the MIR221/222 sponge significantly inhibited colitis, as indicated by body weight loss, colon shortening and inflammatory factor production.	MI0000299	Gastroenterology 2014 Oct 147, 847-859.e11 doi:10.1053/j.gastro.2014.06.006 PMID:24931456
621	Artifically engineered RNA	miR222 sponge	miR-222	PDLIM2	Hct116 And Rko Cell Lines	Colorectal Cancer	Homo sapiens (human)	Western blot;qRT-PCR;luciferase reporter assays	24931456	A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFkB and STAT3 in colorectal cancer cells.	Colorectal cancer cell lines were transfected with MIR221 or MIR222 sponges. The activity levels of NFKB and STAT3 were measured in dual luciferase reporter assays. Immunoblot and real-time PCR analyses to measure protein and mRNA levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. In agreement with the causal roles of NFKB and STAT3 in CAC development, our data vevealed dramatically decreased levels of RELA and STAT3 protein expression in tumors from mice treated with the MIR221/222 sponge. Intriguingly, treatment with the MIR221/222 sponge significantly inhibited colitis, as indicated by body weight loss, colon shortening and inflammatory factor production.	MI0000299	Gastroenterology 2014 Oct 147, 847-859.e11 doi:10.1053/j.gastro.2014.06.006 PMID:24931456
622	Viral RNA	HBV	miR-15a	SMAD7	Liver Tissues	Hepatocellular Carcinoma	Hepatitis B virus (HBV)	Western blot;qRT-PCR;luciferase reporter assays	25540364	HBV regulates apoptosis and tumorigenesis through miR15a-Smad7-TGF-B pathway	We examined the protein level of Smad7 in miR-15a transfected cells. The immunoblotting data showed that the protein level of Smad7 was significantly reduced in miR-15a transfected cells data showed that miR-15a can reduce the relative luciferase activity of pGLO-Smad7 3’UTR but not pGLO-Smad7 3’UTR-mut we examined the amount of Smad7 mRNA in HBV-transgenic BALB/c mice by real-time PCR. The data showed that the relative amount of Smad7 mRNA in liver tissue of HBV-transgenic BALB/c mice was 2-fold higher than that in control mice (p<0.01). We next examined the correlation between miR-15a and Smad7 mRNA in liver tissue from HCC patients which were all chronic HBV carriers. There was negative correlation between miR-15a and Smad7 mRNA levels. We then analyzed the levels of Smad7 mRNA and HBV transcripts in liver tissue from the  HCC patients by real-time PCR. miR-15a mimic enhances the activation of TGF-B luciferase reporter while miR-15a inhibitor inhibits the activation of TGF-B signaling. In conclusion, we demonstrate that HBV mRNAs act as ceRNAs of miR-15a and regulate TGF-B signaling in the development of HBV-related HCC.	MI0000069	J Virol 2015 Mar 89, 2739-49 doi:10.1128/jvi.02784-14 PMID:25540364
623	Coding-mRNA	AEG-1	miR-30a	SNAIL	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	25484183	AEG-1 3'-untranslated region functions as a ceRNA in inducing epithelial-mesenchymal transition of human non-small cell lung cancer by regulating miR-30a activity.	Astrocyte Elevated Gene-1 (AEG-1), also known as metadherin (MTDH) and LYRIC/3D3. RT-PCR analyses were performed to examine the expres- sion of AEG-1 and hallmark EMT genes by using human-specific primers. Cell analysis of miR-30a mimics, inhibitor and negative control transfected cells were subjected to PCR analysis, Western blot and immunoblot analysis. AEG-1 protein expression in the same cells was inhibited by miR-30a. For ceRNA verification, HEK 293T cells were co-transfected with pMiR-Report/Snail, pMiR-Report/Mut-Snail, pMiR-Report/Vimentin, or pMiR-Report/Mut-Vimentin and AEG-1 mRNA 3' UTR vector (PAU)or control vector (PSI). The cells were lysed and luciferase activity was measured by luminometer 48 h afterwards. Overexpression of AEG-1 3' UTR increased the 3' UTR activity of luc-Snail and luc-Vimentin as assumed, due to less available common miRNAs. The protein level increased by western blot analysis in the AEG-1 3'UTR overexpression lung cancer A549 cells. Therefore, AEG-1 3'UTR as a ceRNA regulated the expression of Snail and Vimentin post-transcriptly based on the activity of miR-30a. we also used AEG-1 CDS overexpression plasmid (PA) to increase the protein expression of AEG-1, and determine the expression of Vimentin and Snail by western blot analysis. It was suggested the regulation effect of AEG-1 on the expression of Snail was not only at RNA level but also protein level.	MI0000088	Eur J Cell Biol 2015 Jan 94, 22-31 doi:10.1016/j.ejcb.2014.10.006 PMID:25484183
624	Coding-mRNA	AEG-1	miR-30a	VIMENTIN	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	25484183	AEG-1 3'-untranslated region functions as a ceRNA in inducing epithelial-mesenchymal transition of human non-small cell lung cancer by regulating miR-30a activity.	Astrocyte Elevated Gene-1 (AEG-1), also known as metadherin (MTDH) and LYRIC/3D3. RT-PCR analyses were performed to examine the expres- sion of AEG-1 and hallmark EMT genes by using human-specific primers. Cell analysis of miR-30a mimics, inhibitor and negative control transfected cells were subjected to PCR analysis, Western blot and immunoblot analysis. AEG-1 protein expression in the same cells was inhibited by miR-30a. For ceRNA verification, HEK 293T cells were co-transfected with pMiR-Report/Snail, pMiR-Report/Mut-Snail, pMiR-Report/Vimentin, or pMiR-Report/Mut-Vimentin and AEG-1 mRNA 3' UTR vector (PAU)or control vector (PSI). The cells were lysed and luciferase activity was measured by luminometer 48 h afterwards. Overexpression of AEG-1 3' UTR increased the 3' UTR activity of luc-Snail and luc-Vimentin as assumed, due to less available common miRNAs. The protein level increased by western blot analysis in the AEG-1 3'UTR overexpression lung cancer A549 cells. Therefore, AEG-1 3'UTR as a ceRNA regulated the expression of Snail and Vimentin post-transcriptly based on the activity of miR-30a. we also used AEG-1 CDS overexpression plasmid (PA) to increase the protein expression of AEG-1, and determine the expression of Vimentin and Snail by western blot analysis. It was suggested the regulation effect of AEG-1 on the expression of Snail was not only at RNA level but also protein level.	MI0000088	Eur J Cell Biol 2015 Jan 94, 22-31 doi:10.1016/j.ejcb.2014.10.006 PMID:25484183
625	LncRNA	H19	miR-141	ZEB1	Mkn45 And 7901 Cells	Gastric Cancer	Homo sapiens (human)	Luciferase reporter assay;qRT-PCR	26160158	The Interaction Between MiR-141 and lncRNA-H19 in Regulating Cell Proliferation and Migration in Gastric Cancer.	H19 expression was found to be inversely correlated to miR-141 expression in gastric cancer cells and tissues. H19 promotes malignancy including proliferation and invasion whereas miR-141 suppresses malignancy in human cancer cells. MiR-141 binds to H19 in a sequence specific manner, and suppresses H19 expression and functions including proliferation and invasion. MiR-141 could also regulate H19 target genes and miR-141 inhibitor restores H19 siRNA function, while H19 regulates miR-141 target gene ZEB1.	MI0000457	Cell Physiol Biochem 2015  36, 1440-52 doi:10.1159/000430309 PMID:26160158
626	LncRNA	H19	miR-138	ZEB1	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000455	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
627	LncRNA	H19	miR-138	ZEB2	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000455	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
628	LncRNA	H19	miR-138	Vimentin	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000455	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
629	LncRNA	H19	miR-200a	ZEB1	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000737	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
630	LncRNA	H19	miR-200a	ZEB2	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000737	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
631	LncRNA	H19	miR-200a	Vimentin	Sw620 Cells And Hct-116 Cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer	We found that H19 was highly expressed in mesenchymal-like cancer cells and primary CRC tissues. Stable expression of H19 significantly promotes EMT progression and accelerates in vivo and in vitro tumor growth. Furthermore, by using bioinformatics study and RNA immunoprecipitation combined with luciferase reporter assays, we demonstrated that H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. Taken together, these observations imply that the lncRNA H19 modulated the expression of multiple genes involved in EMT by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and EMT progression.	MI0000737	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
632	LncRNA	HOTAIR	miR-218	BMI1	Liver Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation; luciferase reporter assays	26024833	Hotair Mediates Hepatocarcinogenesis through Suppressing MiRNA-218 Expression and Activating P14 and P16 Signaling.	In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis. Further investigation revealed that Hotair knockdown dramatically inhibited cell viability and induced G1-phase arrest in vitro and suppressed tumorigenicity in vivo by promoting miR-218 expression. Oncogene Bmi-1 was demonstrated to be a functional target of miR-218 and the main downstream targets P16Ink4a and P14ARF signaling were activated in Hotair-suppressed tumorigenesis. In primary human HCC specimens, Hotair and Bmi-1 were concordantly upregulated whereas miR-218 was downregulated in these tissues. Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.	MI0000294	J Hepatol 2015 Oct 63, 886-95 doi:10.1016/j.jhep.2015.05.016 PMID:26024833
633	LncRNA	HOTAIR	miR-218	BMI1	Liver Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	RNA immunoprecipitation; luciferase reporter assays	26024833	Hotair Mediates Hepatocarcinogenesis through Suppressing MiRNA-218 Expression and Activating P14 and P16 Signaling.	In this study, we reported that Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis. Further investigation revealed that Hotair knockdown dramatically inhibited cell viability and induced G1-phase arrest in vitro and suppressed tumorigenicity in vivo by promoting miR-218 expression. Oncogene Bmi-1 was demonstrated to be a functional target of miR-218 and the main downstream targets P16Ink4a and P14ARF signaling were activated in Hotair-suppressed tumorigenesis. In primary human HCC specimens, Hotair and Bmi-1 were concordantly upregulated whereas miR-218 was downregulated in these tissues. Furthermore, Hotair was inversely associated with miR-218 expression and positively correlated with Bmi-1 expression in these clinical tissues.	MI0000700	J Hepatol 2015 Oct 63, 886-95 doi:10.1016/j.jhep.2015.05.016 PMID:26024833
634	Protein	HBx	miR-148a	ERK	Liver Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR	25364579	Hepatitis B virus X protein accelerates the development of hepatoma.	HBx suppresses the p53-mediated activation of miR-148a, resulting in the upregulation of AKT and ERK and subsequent activation of mTOR to promote cancer growth and metastasis in a mouse model of HCC.	MI0000550	Cancer Biol Med 2014 Sep 11, 182-90 doi:10.7497/j.issn.2095-3941.2014.03.004 PMID:25364579
635	LncRNA	MIAT	miR-150-5p	VEGF	Hmvecs	Diabetes Mellitus-Induced Microvascular Dysfunction	Homo sapiens (human)	luciferase reporter assays, RNA immunoprecipitation	25587098	lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA	Using quantitative polymerase chain reaction, we demonstrated increased expression of lncRNA-MIAT in diabetic retinas and endothelial cells cultured in high glucose medium. Visual electrophysiology examination, TUNEL staining, retinal trypsin digestion, vascular permeability assay, and in vitro studies revealed that MIAT knockdown obviously ameliorated diabetes mellitus-induced retinal microvascular dysfunction in vivo, and inhibited endothelial cell proliferation, migration, and tube formation in vitro. Bioinformatics analysis, luciferase assay, RNA immunoprecipitation, and in vitro studies revealed that MIAT functioned as a competing endogenous RNA, and formed a feedback loop with vascular endothelial growth factor and miR-150-5p to regulate endothelial cell function.	MI0000479	Circ Res 2015 Mar 27 116, 1143-56 doi:10.1161/circresaha.116.305510 PMID:25587098
636	LncRNA	MIAT	miR-150-5p	VEGF	Hmvecs	Diabetes Mellitus-Induced Microvascular Dysfunction	Mus musculus (mouse)	luciferase reporter assays, RNA immunoprecipitation	25587098	lncRNA-MIAT regulates microvascular dysfunction by functioning as a competing endogenous RNA	Using quantitative polymerase chain reaction, we demonstrated increased expression of lncRNA-MIAT in diabetic retinas and endothelial cells cultured in high glucose medium. Visual electrophysiology examination, TUNEL staining, retinal trypsin digestion, vascular permeability assay, and in vitro studies revealed that MIAT knockdown obviously ameliorated diabetes mellitus-induced retinal microvascular dysfunction in vivo, and inhibited endothelial cell proliferation, migration, and tube formation in vitro. Bioinformatics analysis, luciferase assay, RNA immunoprecipitation, and in vitro studies revealed that MIAT functioned as a competing endogenous RNA, and formed a feedback loop with vascular endothelial growth factor and miR-150-5p to regulate endothelial cell function.	MI0000479	Circ Res 2015 Mar 27 116, 1143-56 doi:10.1161/circresaha.116.305510 PMID:25587098
637	LncRNA	CCAT2	miR-424	NA	Skov3, Omc685, A2780 And Ho8910	Ovarian Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28550684	Long Noncoding RNA CCAT2 Knockdown Suppresses Tumorous Progression By Sponging miR-424 in epithelial Ovarian Vancer.	CCAT2 knockdown induced by interfering oligonucleotides could inhibit proliferation and promote apoptosis and induce cell cycle arrest at G0/G1 phase. Bioinformatics prediction analysis predicted that miR-424 targeted CCAT2, which was confirmed by luciferase reporter assay. Moreover, miR-424 inhibitor rescued the tumorigenesis inhibition induced by CCAT2 knockdown.	MI0001446	Oncol Res 2018 Mar 5 26, 241-247 doi:10.3727/096504017x14953948675412 PMID:28550684
638	LncRNA	MEG3	miR-9	FOXO1	Te1, Te13, Eca109, Yes2	Esophageal Squamous Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay;Western blot assay	28539329	Aberrant Methylation-mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer.	We found that transfection with miR-9 mimic significantly reduced the luciferase activities of the pGL3-MEG3 reporter vector but not empty vector or mutant vector pGL3-MEG3-M1-2 in Eca109 cell line, suggesting the binding of miR-9 to these sitesmiR-9 mimic was transfected into Eca109 cells, luciferase activity was significantly repressed in each site, whereas the repressions were completely abolished when mutation was introduced in each site. Ectopically expressed MEG3, but not the mutant, reduced the level of miR-9, suggesting the sponge role of MEG3 for miR-9.	MI0000466	Mol Cancer Res 2017 Jul 15, 800-810 doi:10.1158/1541-7786.Mcr-16-0385 PMID:28539329
639	LncRNA	MEG3	miR-9	E-cadherin	Te1, Te13, Eca109, Yes2	Esophageal Squamous Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay;Western blot assay	28539329	Aberrant Methylation-mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer.	We found that transfection with miR-9 mimic significantly reduced the luciferase activities of the pGL3-MEG3 reporter vector but not empty vector or mutant vector pGL3-MEG3-M1-2 in Eca109 cell line, suggesting the binding of miR-9 to these sitesmiR-9 mimic was transfected into Eca109 cells, luciferase activity was significantly repressed in each site, whereas the repressions were completely abolished when mutation was introduced in each site. Ectopically expressed MEG3, but not the mutant, reduced the level of miR-9, suggesting the sponge role of MEG3 for miR-9.	MI0000466	Mol Cancer Res 2017 Jul 15, 800-810 doi:10.1158/1541-7786.Mcr-16-0385 PMID:28539329
640	LncRNA	PVT1	miR-203a	E2F3	Hek-293	Asthma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28510638	a-Asarone suppresses the proliferation and migration of ASMCs through targeting the lncRNA-PVT1/miR-203a/E2F3 signal pathway in RSV-infected rats.	we established an RSV-infected Sprague–Dawley rat model and demonstrated that lncRNA-PVT1 is involved in the mechanism of a-asarone in treating RSV-induced asthma, and lncRNA-PVT1 regulates the expression of E2F3 by functioning as a ceRNA which competitively sponges miR-203a.	MI0000283	Acta Biochim Biophys Sin (Shanghai) 2017 Jul 1 49, 598-608 doi:10.1093/abbs/gmx048 PMID:28510638
641	LncRNA	PVT1	miR-203a	E2F3	Hek-293	Asthma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28510638	a-Asarone suppresses the proliferation and migration of ASMCs through targeting the lncRNA-PVT1/miR-203a/E2F3 signal pathway in RSV-infected rats.	we established an RSV-infected Sprague–Dawley rat model and demonstrated that lncRNA-PVT1 is involved in the mechanism of a-asarone in treating RSV-induced asthma, and lncRNA-PVT1 regulates the expression of E2F3 by functioning as a ceRNA which competitively sponges miR-203a.	MI0000283	Acta Biochim Biophys Sin (Shanghai) 2017 Jul 1 49, 598-608 doi:10.1093/abbs/gmx048 PMID:28510638
642	LncRNA	XLOC_008466	miR-874	MMP2	A549, H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;	28501870	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.	Up-regulation of XLOC_008466 in NSCLC patients was related to lymph node metastasis and the TNM stage. In vitro, down-regulation of XLOC_008466 inhibited cell proliferation and invasion of A549 and H460 cells in vitro, but promoted cell apoptosis. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression.	MI0005532	Cell Physiol Biochem 2017  42, 126-136 doi:10.1159/000477121 PMID:28501870
643	LncRNA	XLOC_008466	miR-874	XIAP	A549, H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;	28501870	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874.	Up-regulation of XLOC_008466 in NSCLC patients was related to lymph node metastasis and the TNM stage. In vitro, down-regulation of XLOC_008466 inhibited cell proliferation and invasion of A549 and H460 cells in vitro, but promoted cell apoptosis. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression.	MI0005532	Cell Physiol Biochem 2017  42, 126-136 doi:10.1159/000477121 PMID:28501870
644	LncRNA	MALAT1	miR-146b-5p	TRAF6	Mhcc97-H, Smmc-7721, Hep3B And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay;Northern blot assay	28404923	Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis.	TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6. Furthermore, we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b-5p to down-regulate its expression in HCC. In general, our results indicate that miR-146b-5p inhibits tumor growth and metastasis of HCC by targeting TRAF6 mediated Akt phosphorylation.	MIMAT0002809	Oncotarget 2017 Apr 25 8, 28683-28695 doi:10.18632/oncotarget.15640 PMID:28404923
645	LncRNA	LINC00668	miR-297	VEGFA	Scc4, Scc9, Scc1, Scc25, Tu183, Hsu3,Fadu, Oec-M1, Snu1041, And Scc15	Oral Squamous Cell Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28564590	Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma.	Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Furthermore, LINC00668 knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67 in vivo. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling.	MI0005775	Biochem Biophys Res Commun 2017 Aug 5 489, 404-412 doi:10.1016/j.bbrc.2017.05.155 PMID:28564590
646	LncRNA	CASC2	miR-21	PTEN	Ddp-Resistant Cancer Cells	Cervical Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28495512	Modulation of CASC2/miR-21/PTEN pathway sensitizes cervical cancer to cisplatin.	A lower expression of CACS2 was observed in the DDP-resistant cervical cancer tissues, compared to DDP-sensitive cancer tissues; CACS2 overexpression could sensitize DDP-resistant cervical cancer cell (HeLa/DDP and CaSki/DDP) to DDP. Further functional experiments indicate that CASC2 upregulated PTEN expression by direct inhibiting miR-21 in the DDP-resistant cancer cells, leading to the down-regulation of p-AKT protein. In DDP-resistant cervical cancer tissues, miR-21 was up-regulated while PTEN was down-regulated. 	MI0000077	Arch Biochem Biophys 2017 Jun 1 623-624, 20-30 doi:10.1016/j.abb.2017.05.001 PMID:28495512
647	LncRNA	HOTAIR	miR-217	HIF1A	769-P And Achn	Renal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28492542	LncRNA HOTAIR regulates HIF-1a/AXL signaling through inhibition of miR-217 in renal cell carcinoma.	HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1a expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. Furthermore, HOTAIR knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67, HIF-1a, and AXL, but upregulated the expression of miR-217 in vivo.	MI0000293	Cell Death Dis 2017 May 11 8, e2772 doi:10.1038/cddis.2017.181 PMID:28492542
648	LncRNA	HOTAIR	miR-217	AXL	769-P And Achn	Renal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28492542	LncRNA HOTAIR regulates HIF-1a/AXL signaling through inhibition of miR-217 in renal cell carcinoma.	HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1a expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. Furthermore, HOTAIR knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67, HIF-1a, and AXL, but upregulated the expression of miR-217 in vivo.	MI0000293	Cell Death Dis 2017 May 11 8, e2772 doi:10.1038/cddis.2017.181 PMID:28492542
649	LncRNA	HOTAIR	miR-217	HIF1A	769-P And Achn	Renal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28492542	LncRNA HOTAIR regulates HIF-1a/AXL signaling through inhibition of miR-217 in renal cell carcinoma.	HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1a expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. Furthermore, HOTAIR knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67, HIF-1a, and AXL, but upregulated the expression of miR-217 in vivo.	MI0000293	Cell Death Dis 2017 May 11 8, e2772 doi:10.1038/cddis.2017.181 PMID:28492542
650	LncRNA	HOTAIR	miR-217	AXL	769-P And Achn	Renal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28492542	LncRNA HOTAIR regulates HIF-1a/AXL signaling through inhibition of miR-217 in renal cell carcinoma.	HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues. Gain- and loss-of-function of HOTAIR revealed that HOTAIR functioned as a ceRNA for miR-217 to facilitate HIF-1a expression and then upregulated AXL level promoting Rcc proliferation, migration, and EMT process, and inhibiting apoptosis. Furthermore, HOTAIR knockdown suppressed tumor growth and reduced the expression of proliferation antigen ki-67, HIF-1a, and AXL, but upregulated the expression of miR-217 in vivo.	MI0000293	Cell Death Dis 2017 May 11 8, e2772 doi:10.1038/cddis.2017.181 PMID:28492542
651	LncRNA	CCR492	let-7	c-Myc	Embryonic Broblasts	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27344374	The long intergenic non-coding RNA CCR492 functions as a let-7 competitive endogenous RNA to regulate c-Myc expression.	By loss-of-function experiments we found that lincRNA CCR492 is required for G1/S progression, localizes in the cell cytoplasm and contains 4 let-7 microRNA recognition elements (MREs). Mechanistically, CCR492 functions as a competing endogenous RNA (ceRNA) to antagonize the function of let-7 microRNAs, leading to the de-repression of c-Myc. Moreover, we show that ectopic expression of CCR492 along with a constitutively active H-Ras promotes cell transformation.	MI0000060	Biochim Biophys Acta 2016 Oct 1859, 1322-32 doi:10.1016/j.bbagrm.2016.06.010 PMID:27344374
652	LncRNA	CCR492	let-7	c-Myc	Embryonic Broblasts	NA	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27344374	The long intergenic non-coding RNA CCR492 functions as a let-7 competitive endogenous RNA to regulate c-Myc expression.	By loss-of-function experiments we found that lincRNA CCR492 is required for G1/S progression, localizes in the cell cytoplasm and contains 4 let-7 microRNA recognition elements (MREs). Mechanistically, CCR492 functions as a competing endogenous RNA (ceRNA) to antagonize the function of let-7 microRNAs, leading to the de-repression of c-Myc. Moreover, we show that ectopic expression of CCR492 along with a constitutively active H-Ras promotes cell transformation.	MI0000060	Biochim Biophys Acta 2016 Oct 1859, 1322-32 doi:10.1016/j.bbagrm.2016.06.010 PMID:27344374
653	LncRNA	n340790	miR-1254	NA	Human Thyroid Follicular Epithelial Cell Line	Thyroid Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28559970	The lncRNA n340790 accelerates carcinogenesis of thyroid cancer by regulating miR-1254.	we found that n340790 was highly expressed, miR-1254 exhibited low levels of expression in human thyroid cancer tissues, and both of these molecules were good prognostic factors for thyroid cancer. n340790 and miR-1254 were simultaneously and strongly correlated with invasion, metastasis, and TNM stage of thyroid cancer. n340790 plays vital roles in the development of thyroid cancer both in vitro and in vivo. Furthermore, n340790 could act as an endogenous sponge by directly binding to miR-1254 and decreasing miR-1254 expression.	MIMAT0005905	Am J Transl Res 2017  9, 2181-2194,  PMID:28559970
654	LncRNA	HOXA11-AS	miR-124-3p	ROCK1	U2Os, Mg-63 And Khos	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28558357	Long non-coding RNA HOXA11-AS functions as a competing endogenous RNA to regulate ROCK1 expression by sponging miR-124-3p in osteosarcoma.	HOXA11-AS silencing suppressed OS cells proliferation, invasion and induced cell arrest in G0/G1 phase. Furthermore, our data showed that HOXA11-AS acts as an endogenous sponge by directly binding miR-124-3p, and decreasing the expression of miR-124-3p. HOXA11-AS may regulate tumor progression by affecting miR-124-3p targets, and ROCK1 expression. 	MIMAT0000422	Biomed Pharmacother 2017 Aug 92, 437-444 doi:10.1016/j.biopha.2017.05.081 PMID:28558357
655	LncRNA	ANRIL	miR-186	NA	Hela, Caski, Siha, Ht-3 And C33A	Cervical Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28550682	Long Noncoding RNA ANRIL Promotes Cervical Cancer Development By Acting as a Sponge of miR-186.	RT-PCR showed that ANRIL expression was significantly up-regulated in cervical cancer tumors and cell lines. Nevertheless, ANRIL knockdown transfected with interference oligonucleotide inhibited the proliferation activity and invasive ability, and promoted apoptosis of cervical cancer cell lines. Bioinformatics prediction program and luciferase assay predicted and validated that miR-186 directly targeted ANRIL. Expression level of miR-186 was down-regulated in cervical cancer tumors and cell lines and negatively correlated to that of ANRIL. Moreover, rescue experiments showed that miR-186 inhibitor could reverse the suppression of ANRIL knockdown. 	MI0000483	Oncol Res 2018 Apr 10 26, 345-352 doi:10.3727/096504017x14953948675449 PMID:28550682
656	LncRNA	UCA1	miR-122	NA	U87 And U251	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28548636	Long Non-coding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells.	UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative and invasive activity of glioma cell lines (U87 and U251). Bioinformatics analysis and luciferase reporter assay verified the complementary binding within UCA1 and miR-122 at 3'-UTR. Functional experiments revealed that UCA1 acted as miR-122 'sponge' to modulate glioma cell proliferation, migration and invasion via downregulating miR-122.	MI0000442	Oncol Res 2018 Jan 19 26, 103-110 doi:10.3727/096504017x14934860122864 PMID:28548636
657	LncRNA	TCONS_00075467	miR-328	CACNA1C	Rabbit Atria	Atrial Fibrillation	Oryctolagus cuniculus (rabbit)	luciferase reporter assays;qRT-PCR	28546098	Altered long non-coding RNA expression profile in rabbit atria with atrial fibrillation: TCONS_00075467 modulates atrial electrical remodeling by sponging miR-328 to regulate CACNA1C.	the expression of miRNA-328 was negatively correlated with TCONS_00075467. We further demonstrated that TCONS_00075467 could sponge miRNA-328 in vitro and in vivo to regulate the downstream protein coding gene CACNA1C. In addition, miRNA-328 could partly reverse the effects of TCONS_00075467 on electrical remodeling. In summary, dysregulated lncRNAs may play important roles in modulating electrical remodeling during AF.	MI0000804	J Mol Cell Cardiol 2017 Jul 108, 73-85 doi:10.1016/j.yjmcc.2017.05.009 PMID:28546098
658	LncRNA	NEAT1	miR-34a	c-Met	Achn, 786-O, A498, And Caki-1	Renal Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28968960	The long non-coding RNA NEAT1 enhances epithelial-to-mesenchymal transition and chemoresistance via the miR-34a/c-Met axis in renal cell carcinoma.	NEAT1 is up-regulated in RCC tissue compared to corresponding non-tumor tissue. High NEAT1 expression was associated with tumor progression and poor survival in RCC patients. NEAT1 knockdown suppressed RCC cell proliferation by inhibiting cell cycle progression, and inhibited RCC cell migration and invasion by reversing the epithelial-to- mesenchymal transition phenotype. Down-regulation of NEAT1 increased the sensitivity of RCC cells to sorafenib in vitro. Mechanistic analysis revealed that NEAT1 acts as a competitive sponge for miR-34a, which prevents inhibition of c-Met. 	MI0000268	Oncotarget 2017 Sep 8 8, 62927-62938 doi:10.18632/oncotarget.17757 PMID:28968960
659	LncRNA	UCA1	miR-16	MDR1	Leukemia Cell Lines	Chronic Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;Western blot assay	27854515	lncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in chronic myeloid leukemia Cells.	UCA1 was identified as an important modulator of MDR1 by a model system of leukemia cell lines with a gradual increase of MDR1 expression and IM resistance. Overexpression of UCA1 increased MDR1 expression to promote IM resistance of CML cells	MI0000070	DNA Cell Biol 2017 Jan 36, 18-25 doi:10.1089/dna.2016.3533 PMID:27854515
660	LncRNA	UCA1	miR-16	GLS2	Bladder Tissues And Cell Lines	Bladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26373319	Long non-coding RNA UCA1 promotes glutamine metabolism by targeting miR-16 in human bladder cancer.	luciferase reporter assays indicated that there was a miR-16 binding site in urothelial carcinoma-associated 1, and it showed appreciable levels of sponge effects on miR-16 as readouts in a dose-dependent manner. Moreover, the 'seed region' of miR-16 directly bound to the 3'UTR of GLS2 mRNA and regulated GLS2 expression level.	MI0000070	Jpn J Clin Oncol 2015 Nov 45, 1055-63 doi:10.1093/jjco/hyv132 PMID:26373319
661	LncRNA	HOXA-AS2	miR-520c-3p	TGFBR2	Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	Silencing of HOXA-AS2 inhibited the progression of breast cancer cells in vitro and in vivo. Furthermore, microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
662	LncRNA	HOXA-AS2	miR-520c-3p	TGFBR2	Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	Silencing of HOXA-AS2 inhibited the progression of breast cancer cells in vitro and in vivo. Furthermore, microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
663	LncRNA	HOXA-AS2	miR-520c-3p	RELA	Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	Silencing of HOXA-AS2 inhibited the progression of breast cancer cells in vitro and in vivo. Furthermore, microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
664	LncRNA	HOXA-AS2	miR-520c-3p	RELA	Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	Silencing of HOXA-AS2 inhibited the progression of breast cancer cells in vitro and in vivo. Furthermore, microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
665	LncRNA	H19	miR-152	DNMT1	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28544374	Long non-coding RNA H19 promotes the proliferation and invasion of breast cancer through upregulating DNMT1 expression by sponging miR-152.	 Downregulation of H19 and DNMT1 significantly retarded breast cancer cell proliferation and invasion. H19 act as an endogenous sponge by directly binding to miR-152. miR-152 directly targeted DNMT1 and was regulated by H19. Besides, H19 overexpression dramatically relieved the inhibition of miR-152 on DNMT1 expression. miR-152 inhibition and DNMT1 overexpression obviously reversed the inhibitory effects of H19 downregulation on cell proliferation and invasion. 	MI0000462	J Biochem Mol Toxicol 2017 Sep 31 doi:10.1002/jbt.21933 PMID:28544374
666	LncRNA	MALAT1	miR-143-3p	ZEB1	Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28543721	Long non-coding RNA MALAT1 regulates ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression.	MALAT1 was upregulated in HCC tissues. ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1. The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p. Transfection with siR-MALAT1 significantly inhibited cell proliferation and invasion, while knockdown of miR-181a partially reversed these effects.	MIMAT0000435	J Cell Biochem 2017 Dec 118, 4836-4843 doi:10.1002/jcb.26158 PMID:28543721
667	LncRNA	AF113014	miR-20a	EGR2	Smmc7721, Hepg2, Sk-Hep1 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28542387	LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells.	AF113014 inhibited proliferation of HCC cells both in vitro and in vivo, whereas the opposite effect was observed when AF113014 knockdown. Moreover, we identified that Egr2, a tumor suppressor gene, was a downstream target gene of AF113014. Furthermore, we discovered that AF113014 up-regulated Egr2 expression through interacting with miR-20a by using dual-luciferase reporter assay, qRT-PCR and Western blotting analysis.	MI0000076	PLoS One 2017  12, e0177843 doi:10.1371/journal.pone.0177843 PMID:28542387
668	LncRNA	N-BLR	miR-141-3p	ZEB1	Colon Samples	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28535802	N-BLR, a primate-specific non-coding transcript leads to colorectal cancer invasion and migration	hrough in vitro and in vivo experiments we found that N-BLR facilitates migration primarily via crosstalk with E-cadherin and ZEB1. We showed that this crosstalk is mediated by a pyknon, a short ~20 nucleotide-long DNA motif contained in the N-BLR transcript and is targeted by members of the miR-200 family. 	MIMAT0000432	Genome Biol 2017 May 24 18, 98 doi:10.1186/s13059-017-1224-0 PMID:28535802
669	LncRNA	N-BLR	miR-200c-3p	ZEB1	Colon Samples	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28535802	N-BLR, a primate-specific non-coding transcript leads to colorectal cancer invasion and migration	hrough in vitro and in vivo experiments we found that N-BLR facilitates migration primarily via crosstalk with E-cadherin and ZEB1. We showed that this crosstalk is mediated by a pyknon, a short ~20 nucleotide-long DNA motif contained in the N-BLR transcript and is targeted by members of the miR-200 family. 	MIMAT0000617	Genome Biol 2017 May 24 18, 98 doi:10.1186/s13059-017-1224-0 PMID:28535802
670	LncRNA	N-BLR	miR-141-3p	ZEB1	Colon Samples	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	28535802	N-BLR, a primate-specific non-coding transcript leads to colorectal cancer invasion and migration	hrough in vitro and in vivo experiments we found that N-BLR facilitates migration primarily via crosstalk with E-cadherin and ZEB1. We showed that this crosstalk is mediated by a pyknon, a short ~20 nucleotide-long DNA motif contained in the N-BLR transcript and is targeted by members of the miR-200 family. 	MIMAT0000432	Genome Biol 2017 May 24 18, 98 doi:10.1186/s13059-017-1224-0 PMID:28535802
671	LncRNA	N-BLR	miR-200c-3p	ZEB1	Colon Samples	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	28535802	N-BLR, a primate-specific non-coding transcript leads to colorectal cancer invasion and migration	hrough in vitro and in vivo experiments we found that N-BLR facilitates migration primarily via crosstalk with E-cadherin and ZEB1. We showed that this crosstalk is mediated by a pyknon, a short ~20 nucleotide-long DNA motif contained in the N-BLR transcript and is targeted by members of the miR-200 family. 	MIMAT0000617	Genome Biol 2017 May 24 18, 98 doi:10.1186/s13059-017-1224-0 PMID:28535802
672	LncRNA	MALAT1	miR-145	TGFB1	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
673	LncRNA	MALAT1	miR-145	TGFBR2	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
674	LncRNA	MALAT1	miR-145	SMAD3	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
675	LncRNA	MALAT1	miR-145	TGFB1	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
676	LncRNA	MALAT1	miR-145	TGFBR2	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
677	LncRNA	MALAT1	miR-145	SMAD3	Endothelial Progenitor Cells 	Endothelial-To-Mesenchymal Transition	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28535533	MALAT1 Modulates TGF-b1-Induced endothelial-to-mesenchymal transition through Downregulation of miR-145.	Expression levels of EndMT markers were assessed by qRT-PCR and western blotting. Alpha-smooth muscle actin (a-SMA) expression was measured by cell immunofluorescence staining. The regulatory relationship between MALAT1 and miR-145 and its target genes, TGFBR2 (TGFb receptortype II) and SMAD3 (mothers against decapentaplegic homolog 3) was analyzed using the luciferase reporter assay.	MI0000461	Cell Physiol Biochem 2017  42, 357-372 doi:10.1159/000477479 PMID:28535533
678	LncRNA	HOTTIP	miR-30b	HOXA13	Escc Cells	Esophageal Squamous Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28534516	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells.	harboring a miR-30b-binding site, HOTTIP as a molecular sponge mainly regulated miR-30b level in the nucleus and modulated the repression of HOXA13 mediated by miR-30b in the cytoplasm, resulting in the positive HOTTIP/HOXA13 correlation. In addition, HOTTIP upregulated snail1 by competitively binding miR-30b, subsequently promoting epithelial-mesenchymal transition (EMT) and invasion. HOTTIP directly bound the adaptor protein WDR5 and drove histone H3 lysine 4 trimethylation and HOXA13 gene transcription in ESCC cells.	MI0000441	Oncogene 2017 Sep 21 36, 5392-5406 doi:10.1038/onc.2017.133 PMID:28534516
679	LncRNA	n336694	miR-106b	NA	Sh-Sy5Y	Alzheimers Disease	Homo sapiens (human)	qRT-PCR;Western blot assay	28528185	Simvastatin ameliorate memory deficits and inflammation in clinical and mouse model of Alzheimer's disease via modulating the expression of miR-106b.	long non-coding RNA (lnc RNA) n336694 and miR-106b was overexpressed in APP/PS1 mice brain tissues, the relationship between lnc RNA n336694 and miR-106b was explored using the method of Target Scan bioinformatics predictions, the results revealed that miR-106b might be a potential target of lnc RNA n336694. Furthermore, miR-106b mediated apoptosis in SH-SY5Y cell and simvastatin could suppressed this process.	MI0000734	Biomed Pharmacother 2017 Aug 92, 46-57 doi:10.1016/j.biopha.2017.05.060 PMID:28528185
680	LncRNA	n336694	miR-106b	NA	Sh-Sy5Y	Alzheimers Disease	Mus musculus (mouse)	qRT-PCR;Western blot assay	28528185	Simvastatin ameliorate memory deficits and inflammation in clinical and mouse model of Alzheimer's disease via modulating the expression of miR-106b.	long non-coding RNA (lnc RNA) n336694 and miR-106b was overexpressed in APP/PS1 mice brain tissues, the relationship between lnc RNA n336694 and miR-106b was explored using the method of Target Scan bioinformatics predictions, the results revealed that miR-106b might be a potential target of lnc RNA n336694. Furthermore, miR-106b mediated apoptosis in SH-SY5Y cell and simvastatin could suppressed this process.	MI0000734	Biomed Pharmacother 2017 Aug 92, 46-57 doi:10.1016/j.biopha.2017.05.060 PMID:28528185
681	LncRNA	LAMC1	miR-124	CD151	Qgy-7703 And Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	28524360	LAMC1 mRNA promotes malignancy of hepatocellular carcinoma cells by competing for MicroRNA-124 binding with CD151.	miR-124 negatively regulates LAMC1 expression through two miRNA binding sites within its 3' untranslated region (3'UTR) and suppresses migration and invasion of HCC cells through regulating LAMC1. The wild type LAMC1 miRNA response elements (MREs) facilitate expression of CD151, and this regulation is miR-124 dependent. In clinical hepatic tissues, LAMC1 and CD151 mRNAs exhibit positive correlation. Importantly, LAMC1 MREs promote HCC malignancy by absorbing miR-124 and by assisting CD151 expression. We conclude that LAMC1 mRNA acts as a trans regulator to stimulate CD151 expression by competing for miR-124 binding in HCC cells.	MI0000443	IUBMB Life 2017 Aug 69, 595-605 doi:10.1002/iub.1642 PMID:28524360
682	LncRNA	MALAT1	miR-204	SMAD4	Aortic Valve Interstitial Cell	Calcific Aortic Valve Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR; RNA pull-down assay	28522163	LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.	In vitro experiments revealed that MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers, including alkaline phosphatase, mineralized bone matrix formation and osteocalcin. Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1. 	MI0000284	Int J Cardiol 2017 Sep 15 243, 404-412 doi:10.1016/j.ijcard.2017.05.037 PMID:28522163
683	LncRNA	PVT1	miR-488-3p	NA	Mg63	Osteoarthritis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;MS2 RNA immunoprecipitation	28520497	LncRNA PVT1 Regulates Chondrocyte Apoptosis in Osteoarthritis by Acting as a Sponge for miR-488-3p.	miR-488-3p was predicted to be a targeted microRNA of PVT1. Different methods, including MS2 RNA immunoprecipitation (RIP), luciferase activity, and anti-AGO2 RIP, were performed to detect the interaction between PVT1 and miR-488-3p, which suggested that PVT1 negatively regulated miR-488-3p in OA chondrocytes. Moreover, PVT1 promoted the apoptosis of OA and normal chondrocytes through miR-488-3p. 	MIMAT0004763	DNA Cell Biol 2017 Jul 36, 571-580 doi:10.1089/dna.2017.3678 PMID:28520497
684	LncRNA	GAS5	miR-221	ARHI	Osteosarcoma Tissues	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot	28519068	Long noncoding RNA GAS5 suppresses cell growth and epithelial-mesenchymal transition in osteosarcoma by regulating the miR-221/ARHI pathway.	GAS5 and ARHI levels were significantly reduced, while miR-221 increased, both in osteosarcoma tissues and cells. Overexpression of GAS5 suppressed the proliferation, migration and epithelial-mesenchymal transition (EMT) of osteosarcoma cells. GAS5 could directly bind to miR-221 to decrease miR-221 expression and enhance ARHI expression. The effect of GAS5 overexpression on the proliferation, migration and EMT was reversed by miR-221 mimics or ARHI siRNA in osteosarcoma cells.	MI0000298	J Cell Biochem 2017 Dec 118, 4772-4781 doi:10.1002/jcb.26145 PMID:28519068
685	LncRNA	lincRNA-ROR	miR-145	OCT4	Lung Cancer Stem Cell	Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot	28516515	Interaction of lincRNA ROR and p53/miR-145 correlates with lung cancer stem cell signatures.	high p53 level, low miR-145 level, and high ROR level were associated with poor prognosis in NSCLC.silencing ROR failed to change p53 mRNA level but promoted p53 protein level, suggesting a posttranscriptional regulation mechanism involved in si-ROR-mediated promotion of p53. While silencing p53 moderately downregulated ROR. Additionally, silencing ROR or p53 upregulated miR-145. However, silencing both ROR and p53 failed to make obvious change to miR-145 mRNA level and p53 protein level. 	MI0000461	J Cell Biochem 2017 May 18, 10.1002/jcb.25960 doi:10.1002/jcb.25960 PMID:28516515
686	LncRNA	lincRNA-ROR	miR-145	Sox2	Lung Cancer Stem Cell	Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot	28516515	Interaction of lincRNA ROR and p53/miR-145 correlates with lung cancer stem cell signatures.	high p53 level, low miR-145 level, and high ROR level were associated with poor prognosis in NSCLC.silencing ROR failed to change p53 mRNA level but promoted p53 protein level, suggesting a posttranscriptional regulation mechanism involved in si-ROR-mediated promotion of p53. While silencing p53 moderately downregulated ROR. Additionally, silencing ROR or p53 upregulated miR-145. However, silencing both ROR and p53 failed to make obvious change to miR-145 mRNA level and p53 protein level. 	MI0000461	J Cell Biochem 2017 May 18, 10.1002/jcb.25960 doi:10.1002/jcb.25960 PMID:28516515
687	Circular RNA	hsa_circ_0058106	miR-185-3p	SMAD7	Npc Cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004611	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
688	Circular RNA	hsa_circ_0058106	miR-185-3p	WNT2B	Npc Cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004611	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
689	Circular RNA	hsa_circ_0058107	miR-185-3p	SMAD7	Npc Cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	26390174	MiR-185-3p and miR-324-3p Predict Radiosensitivity of nasopharyngeal carcinoma and Modulate Cancer Cell Growth and Apoptosis by Targeting SMAD7.	MiR-185-3p and miR-324-3p expression in the tumor tissues before and after RT or chemoradiotherapy (CRT) were determined. Overall survival and recurrence-free survival curves were estimated to assess the prognostic values of these 2 miRNAs. Their target was predicted using an online database and verified using dual luciferase assay, qRT-PCR, and Western blot analysis. In addition, the function of miR-185-3p/miR-324-3p-SMAD7 axis in NPC cells was investigated.	MIMAT0004611	Med Sci Monit 2015 Sep 21 21, 2828-36 doi:10.12659/msm.895660 PMID:26390174
690	Circular RNA	hsa_circ_0024108	miR-185-3p	WNT2B	Npc Cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004611	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
691	Circular RNA	hsa_circ_0024108	miR-296-3p	EAG1	Glioblastoma	Glioblastoma	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004679	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
692	Circular RNA	hsa_circ_0024108	miR-296-3p	NF2	Glioblastoma	Glioblastoma	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004679	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
693	Circular RNA	hsa_circ_0024108	miR-296-3p	ICAM-1	Prostate Cancer	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004679	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
694	Circular RNA	hsa_circ_0024108	miR-296-3p	CX3CR1	Non-Small Cell Lung Cancer	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004679	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
695	Circular RNA	hsa_circ_0024108	miR-623	MMP-2	Lung Adenocarcinoma	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MI0003637	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
696	Circular RNA	hsa_circ_0024108	miR-623	MMP-9	Lung Adenocarcinoma	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MI0003637	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
697	Circular RNA	hsa_circ_0024108	miR-670-5p	PROX1	Hepatocellular Carcinoma	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0010357	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
698	Circular RNA	hsa_circ_0036722	miR-1254	NA	Non Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0005905	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
699	Circular RNA	hsa_circ_0036722	miR-145-5p	NA	Nasopharyngeal Carcinoma	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0000437	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
700	Circular RNA	hsa_circ_0036722	miR-145-5p	NA	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0000437	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
701	Circular RNA	hsa_circ_0036722	miR-145-5p	SOX2	Prostate Cancer	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0000437	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
702	Circular RNA	hsa_circ_0036722	miR-185-3p	WNT2B	Nasopharyngeal Carcinoma	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0004611	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
703	Circular RNA	hsa_circ_0036722	miR-671-5p	FOXM1	Breast Cancer	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0003880	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
704	Circular RNA	hsa_circ_0036722	miR-671-5p	VSNL1	Glioblastoma	Glioblastoma	Homo sapiens (human)	qRT-PCR;Western blot	28514762	Novel circular RNA expression profiles reflect progression of patients with hypopharyngeal squamous cell carcinoma.	Among the predicted miRNA targets of validated circRNAs, several are closely associated with cancer according to published data, and these miRNAs are considered promising candidates for future study. We further analyzed their interactions with corresponding circRNAs. The analysis included MRE sequences, miRNA seed types, AU-richness near seed sequences, and relative positions of MREs in the linearized sequences of circRNAs. A/U (marked with red bars in Table 4) near MRE facilitates accessibility, whereas G/C (marked with black bars) means low accessibility.	MIMAT0003880	Oncotarget 2017 Jul 11 8, 45367-45379 doi:10.18632/oncotarget.17488 PMID:28514762
705	LncRNA	PTCSC3	miR-574-5p	SCAI	Ptc-1 Cells	Papillary Thyroid Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot	28513866	LncRNA PTCSC3/miR-574-5p governs cell proliferation and migration of papillary thyroid carcinoma via Wnt/b-catenin signaling.	Overexpressed PTCSC3 suppressed cell proliferation and migration, promoted the expression of SCAI, but inhibited b-catenin. PTCSC3 absorbed miR-574-5p, and miR-574-5p targeted to SCAI; SCAI could regulate the activity of Wnt/b-catenin. PTCSC3/miR-574-5p regulated the activity of Wnt/b-catenin via SCAI and mediated cell proliferation and migration of PTC-1. 	MIMAT0004795	J Cell Biochem 2017 Dec 118, 4745-4752 doi:10.1002/jcb.26142 PMID:28513866
706	LncRNA	TUG1	miR-142	ZEB2	T24 And Biu-87	Bladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot	28503069	Downregulation of long noncoding RNA TUG1 inhibits proliferation and induces apoptosis through the TUG1/miR-142/ZEB2 axis in bladder cancer cells.	Knockdown of either TUG1 or ZEB2 inhibited proliferation and induced apoptosis in bladder cancer cells. Interestingly, ZEB2 overexpression reversed the effects of TUG1 knockdown on cell proliferation and apoptosis. Moreover, ZEB2 was verified as a direct target of miR-142 and miR-142 could specially bind to TUG1. In addition, downregulation of TUG1 inhibited the Wnt/b-catenin pathway by regulating ZEB2 expression in bladder cancer cells.	MI0000458	Onco Targets Ther 2017  10, 2461-2471 doi:10.2147/ott.S124595 PMID:28503069
707	LncRNA	AC023115.3	miR-26a	GSK3B	U87Mg And U251Mg	Glioblastoma	Homo sapiens (human)	qRT-PCR;Western blot	28499919	Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy.	 long non-coding RNA AC023115.3 is induced by cisplatin in human glioblastoma cells and that elevated AC023115.3 promotes cisplatin-induced apoptosis by inhibiting autophagy. Further mechanistic studies revealed that AC023115.3 acts as a competing endogenous RNA for miR-26a and attenuates the inhibitory effect of miR-26a on GSK3b, a proline-directed serine-threonine kinase that promotes the degradation of Mcl1, leading to an increase in GSK3b and a decrease in autophagy. Additionally, we discovered that AC023115.3 improves chemosensitivity of glioma cells to cisplatin by regulating the miR-26a-GSK3b-Mcl1 pathway.	MI0000083	Biochim Biophys Acta Mol Cell Res 2017 Aug 1864, 1393-1404 doi:10.1016/j.bbamcr.2017.05.008 PMID:28499919
708	LncRNA	UCC	miR-143	KRAS	Sw480 And Sw620 Cells	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.	Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. 	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
709	LncRNA	UCC	miR-143	IGF1R	Sw480 And Sw620 Cells	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.	Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. 	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
710	LncRNA	UCC	miR-143	BCL2	Sw480 And Sw620 Cells	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.	Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. 	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
711	LncRNA	UCC	miR-143	HK2	Sw480 And Sw620 Cells	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.	Bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation assays showed that miR-143 can interact with UCC, and we found that UCC expression inversely correlates with miR-143 expression in CRC specimens. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA. 	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
712	LncRNA	CRNDE	miR-136	E2F1	Sw480, Hct116 And Ht-29	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;Western blot assay	28115855	Long noncoding RNA CRNDE functions as a competing endogenous RNA to promote metastasis and oxaliplatin resistance by sponging miR-136 in colorectal cancer	Knockdown of CRNDE with OXA treatment decreased cell viability and promoted DNA damage and cell apoptosis, while the overexpression of CRNDE with OXA treatment reduced DNA damage and cell apoptosis. Further in-depth mechanistic studies revealed that CRNDE functioned as a competing endogenous RNA for miR-136, led to the de-repression of its endogenous target, E2F transcription factor 1 (E2F1). 	MI0000475	Onco Targets Ther 2017  10, 205-216 doi:10.2147/ott.S116178 PMID:28115855
713	LncRNA	TUSC7	miR-211-3p	NA	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28214867	The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer.	We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p.	MIMAT0022694	Cell Physiol Biochem 2017  41, 635-644 doi:10.1159/000457938 PMID:28214867
714	LncRNA	XIST	miR-181a	PTEN	Hcclm3, Hepg2, Hep3B, Smmc-7721, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28388883	Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression	PTEN was found to be a target gene of miR-181a. MiR-181a had multiple binding sites with the long non-coding RNA (lncRNA) XIST. The regulation of miR-181a on PTEN was mediated by lncRNA XIST. The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects.	MI0000269	BMC Cancer 2017 Apr 7 17, 248 doi:10.1186/s12885-017-3216-6 PMID:28388883
715	LncRNA	PVT1	miR-186	HIF1A	Gastric Cancer Tissue	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28122299	The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer	Quantitative real-time PCR (QRT-PCR) was used to determine the expression of PVT1 and miR-186 in GC tissues. The MTT cell proliferation and transwell invasion assays were used to detect the cell proliferation and invasion abilities. Western-blotting analysis was used to detect the protein expression of PCNA and HIF-1a. To understand the tumorigenic mechanism of PVT1, luciferase reporter assays were performed to evaluate whether the miR-186 was a target of PVT1 in GC cells	MI0000483	Biomed Pharmacother 2017 Apr 88, 302-308 doi:10.1016/j.biopha.2017.01.049 PMID:28122299
716	LncRNA	PVT1	miR-186	PCNA	Gastric Cancer Tissue	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28122299	The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer	Quantitative real-time PCR (QRT-PCR) was used to determine the expression of PVT1 and miR-186 in GC tissues. The MTT cell proliferation and transwell invasion assays were used to detect the cell proliferation and invasion abilities. Western-blotting analysis was used to detect the protein expression of PCNA and HIF-1a. To understand the tumorigenic mechanism of PVT1, luciferase reporter assays were performed to evaluate whether the miR-186 was a target of PVT1 in GC cells	MI0000483	Biomed Pharmacother 2017 Apr 88, 302-308 doi:10.1016/j.biopha.2017.01.049 PMID:28122299
717	LncRNA	FBXL19-AS1	miR-203	NA	Lovo,Ht29,Hct116, And Sw620	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28479250	Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203.	knockdown of FBXL19-AS1 played tumor-suppressive effects by inhibiting cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo. Overexpression of FBXL19-AS1 was markedly correlated with TNM stage and LNM in CRC. Bioinformatics analysis predicted that miR-203 was potentially targeted by FBXL19-AS1, which was confirmed by dual-luciferase reporter assay. Pearson's correlation analysis showed that miR-203 expression was negatively related to FBXL19-AS1 in tumor tissues. Finally, miR-203 inhibition abrogated the effect of FBXL19-AS1 knockdown on the proliferation and invasion of LoVo cells.	MI0000283	Biochem Biophys Res Commun 2017 Jun 17 488, 67-73 doi:10.1016/j.bbrc.2017.05.008 PMID:28479250
718	LncRNA	H19	miR-29b	COL1A1	Nih3T3	Pulmonary Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27613097	The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis.	H19 expression was positively correlated with COL1A1 and Acta2 expression; H19 knockdown inhibited COL1A1 and Acta2 expression. Moreover, H19 interacted with miR-29b through directly binding to the 3'UTR; miR-29b inhibited COL1A1 expression by directly binding to the 3'UTR. In conclusion, we revealed the promotive effect of H19 on BLM-induced IPF, and demonstrated the mechanism by which H19/miR-29b interaction exerts its effect on regulating pulmonary fibrosis. 	MI0000105	Biochem Biophys Res Commun 2016 Oct 21 479, 417-423 doi:10.1016/j.bbrc.2016.09.028 PMID:27613097
719	LncRNA	H19	miR-29b	Acta2	Nih3T3	Pulmonary Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27613097	The effect of H19-miR-29b interaction on bleomycin-induced mouse model of idiopathic pulmonary fibrosis.	H19 expression was positively correlated with COL1A1 and Acta2 expression; H19 knockdown inhibited COL1A1 and Acta2 expression. Moreover, H19 interacted with miR-29b through directly binding to the 3'UTR; miR-29b inhibited COL1A1 expression by directly binding to the 3'UTR. In conclusion, we revealed the promotive effect of H19 on BLM-induced IPF, and demonstrated the mechanism by which H19/miR-29b interaction exerts its effect on regulating pulmonary fibrosis. 	MI0000105	Biochem Biophys Res Commun 2016 Oct 21 479, 417-423 doi:10.1016/j.bbrc.2016.09.028 PMID:27613097
720	LncRNA	CCAT1	miR-181b	FGFR3	U87 And Ln229 Glioma Cells	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28475287	lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b.	An RNA interference approach was used to downregulate CCAT1 expression and we analyzed the underlying mechanism of CCAT1 by using bioinformatics analysis, CCK-8 assay, Transwell assay, flow cytometry, luciferase assay, RNA immunoprecipitation, real-time PCR, Western blot, and xenograft models. CCAT1 expression was significantly increased, while miR-181b decreased, in glioma tissues. Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b. Additionally, we found that CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRa.	MI0000270	J Cell Biochem 2017 Dec 118, 4548-4557 doi:10.1002/jcb.26116 PMID:28475287
721	LncRNA	CCAT1	miR-181b	PDGFRA	U87 And Ln229 Glioma Cells	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28475287	lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b.	An RNA interference approach was used to downregulate CCAT1 expression and we analyzed the underlying mechanism of CCAT1 by using bioinformatics analysis, CCK-8 assay, Transwell assay, flow cytometry, luciferase assay, RNA immunoprecipitation, real-time PCR, Western blot, and xenograft models. CCAT1 expression was significantly increased, while miR-181b decreased, in glioma tissues. Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b. Additionally, we found that CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRa.	MI0000270	J Cell Biochem 2017 Dec 118, 4548-4557 doi:10.1002/jcb.26116 PMID:28475287
722	LncRNA	SNHG1	miR-338-3p	CST3	Esophageal Carcinoma Tissues	Esophageal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28423738	LncRNA Snhg1, a non-degradable sponge for miR-338, promotes expression of proto-oncogene CST3 in primary esophageal cancer cells.	 luciferase reporter gene and RNA pull-down assays indicated that Snhg1 could be directly bound by miR-338. Snhg1 acted as a non-degradable sponge to relieve the suppression on CST3 caused by miR-338.proto-oncogene CST3 was predicted and validated as a target gene of miR-338. Gain-and-loss-function experiments indicated that miR-338 suppressed expression of CST3 protein (also Cystatin C, CysC)	MIMAT0000763	Oncotarget 2017 May 30 8, 35750-35760 doi:10.18632/oncotarget.16189 PMID:28423738
723	LncRNA	linc-NeD125	miR-19a-3p	CDK6	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000073	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
724	LncRNA	linc-NeD125	miR-19a-3p	MYCN	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000073	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
725	LncRNA	linc-NeD125	miR-19a-3p	SNCAIP	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000073	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
726	LncRNA	linc-NeD125	miR-19a-3p	KDM6A	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000073	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
727	LncRNA	linc-NeD125	miR-19b-3p	CDK6	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000074	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
728	LncRNA	linc-NeD125	miR-19b-3p	MYCN	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000074	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
729	LncRNA	linc-NeD125	miR-19b-3p	SNCAIP	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000074	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
730	LncRNA	linc-NeD125	miR-19b-3p	KDM6A	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000074	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
731	LncRNA	linc-NeD125	miR-106a-5p	CDK6	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000103	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
732	LncRNA	linc-NeD125	miR-106a-5p	MYCN	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000103	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
733	LncRNA	linc-NeD125	miR-106a-5p	SNCAIP	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000103	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
734	LncRNA	linc-NeD125	miR-106a-5p	KDM6A	D283 Med Cells	Medulloblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28415684	The long noncoding RNA linc-NeD125 controls the expression of medulloblastoma driver genes by microRNA sponge activity.	When expressed at the high levels found in G4 MBs, linc-NeD125 functions as a competing endogenous RNA (ceRNA) that, sequestering miR-19a-3p, miR-19b-3p, and mir-106a-5p, de-represses the expression of their targets CDK6, MYCN, SNCAIP and KDM6A, major driver genes of G4 MB. 	MIMAT0000103	Oncotarget 2017 May 9 8, 31003-31015 doi:10.18632/oncotarget.16049 PMID:28415684
735	LncRNA	CCAT1	miR-33a	NA	Melanoma Cells	Melanoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28409554	LncRNA CCAT1 Upregulates Proliferation and Invasion in Melanoma Cells Via Suppressing miR-33a.	Expression of CCAT1 was significantly up-regulated in melanoma tissue and cell lines. CCAT1 knockdown observably suppressed the proliferation, migration and invasion ability. Bioinformatics analysis predicted that miR-33a acted as target of CCAT1, confirmed by Dual-luciferase reporter assay.CCAT1 knockdown reversed the tumor-promoting of miR-33a inhibitor.	MI0000091	Oncol Res 2018 Mar 5 26, 201-208 doi:10.3727/096504017x14920318811749 PMID:28409554
736	LncRNA	SNHG1	miR-199a-3p	CDK7	Pc3, Du145, Lncap, Rwpe-1 And Hek293T	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28400279	SNHG1 lncRNA negatively regulates miR-199a-3p to enhance CDK7 expression and promote cell proliferation in prostate cancer.	SNHG1 could interact with miR-199a-3p and inhibit the activity of miR-199a-3p in prostate cancer cells. In addition, miR-199a-3p could target the 3' UTR of CDK7 and suppress CDK7 expression. More importantly, SNHG1 increased CDK7 expression by competitively binding miR-199a-3p, and then promoted cell proliferation and cell cycle progression in prostate cancer.	MIMAT0000232	Biochem Biophys Res Commun 2017 May 20 487, 146-152 doi:10.1016/j.bbrc.2017.03.169 PMID:28400279
737	LncRNA	MEG3	miR-15a-5p	Inha	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
738	LncRNA	MEG3	miR-15a-5p	Acsl3	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
739	LncRNA	MEG3	miR-15a-5p	Kif21b	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
740	LncRNA	MEG3	miR-15a-5p	Igfbp2	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
741	Circular RNA	Igf1r	miR-15a-5p	Inha	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
742	Circular RNA	Igf1r	miR-15a-5p	Acsl3	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
743	Circular RNA	Igf1r	miR-15a-5p	Kif21b	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
744	Circular RNA	Igf1r	miR-15a-5p	Igfbp2	Mouse Germline Stem Cells	NA	Mus musculus (mouse)	qRT-PCR	28404936	Systematic identification and comparison of expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in mouse germline stem cells	We explored the expression profiles of mRNAs, lncRNAs, and circRNAs in male and female mouse germline stem cells by high-throughput sequencing.Six putative novel lncRNA transcripts identified in SSCs and FGSCs libraries were randomly selected to validate using RT-PCR. CeRNA network inferred that lncRNA Meg3 and cirRNA Igf1r could bind competitively with miRNA-15a-5p increasing target gene Inha, Acsl3, Kif21b, and Igfbp2 expressions.	MIMAT0000068	Oncotarget 2017 Apr 18 8, 26573-26590 doi:10.18632/oncotarget.15719 PMID:28404936
745	LncRNA	TP73-AS1	miR-142	HMGB1	U118, U251, Snb119, Ln229 And Shg-44	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28379612	The long non-coding RNA TP73-AS1 interacted with miR-142 to modulate brain glioma growth through HMGB1/RAGE pathway.	MiR-142 has been reported to play a pivotal role in cancers; here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding. Further, HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142.	MI0000458	J Cell Biochem 2018 Apr 119, 3007-3016 doi:10.1002/jcb.26021 PMID:28379612
746	LncRNA	TP73-AS1	miR-142	RAGE	U118, U251, Snb119, Ln229 And Shg-44	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28379612	The long non-coding RNA TP73-AS1 interacted with miR-142 to modulate brain glioma growth through HMGB1/RAGE pathway.	MiR-142 has been reported to play a pivotal role in cancers; here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding. Further, HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142.	MI0000458	J Cell Biochem 2018 Apr 119, 3007-3016 doi:10.1002/jcb.26021 PMID:28379612
747	LncRNA	TP73-AS1	miR-142	HMGB1	U118, U251, Snb119, Ln229 And Shg-44	Glioma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28379612	The long non-coding RNA TP73-AS1 interacted with miR-142 to modulate brain glioma growth through HMGB1/RAGE pathway.	MiR-142 has been reported to play a pivotal role in cancers; here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding. Further, HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142.	MI0000458	J Cell Biochem 2018 Apr 119, 3007-3016 doi:10.1002/jcb.26021 PMID:28379612
748	LncRNA	TP73-AS1	miR-142	RAGE	U118, U251, Snb119, Ln229 And Shg-44	Glioma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28379612	The long non-coding RNA TP73-AS1 interacted with miR-142 to modulate brain glioma growth through HMGB1/RAGE pathway.	MiR-142 has been reported to play a pivotal role in cancers; here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding. Further, HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142.	MI0000458	J Cell Biochem 2018 Apr 119, 3007-3016 doi:10.1002/jcb.26021 PMID:28379612
749	LncRNA	XIST	miR-494	PTEN	Rat Spinal Cord Tissue	Spinal Cord Injury	Rattus (rat)	luciferase reporter assays;qRT-PCR;Western blot assay	28368292	Long Coding RNA XIST Contributes to Neuronal Apoptosis through the Downregulation of AKT Phosphorylation and Is Negatively Regulated by miR-494 in Rat Spinal Cord Injury.	knockdown of lncRNA-XIST by Lv-shRNA had a prominent protective effect on SCI recovery by suppressing apoptosis through reactivation of the PI3K/AKT signaling pathway in rat spinal cord tissue. In particular, our results suggested that lncRNA-XIST may act as a competitive endogenous RNA, effectively becoming a sink for miR-494, leading to derepression of its target gene, phosphatase and tensin homolog deleted on chromosome ten (PTEN). antagomiR-494 could reverse the protective effects of lncRNA-XIST knockdown on SCI rats through blocking the PTEN/PI3K/AKT signaling pathway.	MI0003134	Int J Mol Sci 2017 Apr 1 18 doi:10.3390/ijms18040732 PMID:28368292
750	LncRNA	XIST	miR-494	Akt	Rat Spinal Cord Tissue	Spinal Cord Injury	Rattus (rat)	luciferase reporter assays;qRT-PCR;Western blot assay	28368292	Long Coding RNA XIST Contributes to Neuronal Apoptosis through the Downregulation of AKT Phosphorylation and Is Negatively Regulated by miR-494 in Rat Spinal Cord Injury.	knockdown of lncRNA-XIST by Lv-shRNA had a prominent protective effect on SCI recovery by suppressing apoptosis through reactivation of the PI3K/AKT signaling pathway in rat spinal cord tissue. In particular, our results suggested that lncRNA-XIST may act as a competitive endogenous RNA, effectively becoming a sink for miR-494, leading to derepression of its target gene, phosphatase and tensin homolog deleted on chromosome ten (PTEN). antagomiR-494 could reverse the protective effects of lncRNA-XIST knockdown on SCI rats through blocking the PTEN/PI3K/AKT signaling pathway.	MI0003134	Int J Mol Sci 2017 Apr 1 18 doi:10.3390/ijms18040732 PMID:28368292
751	LncRNA	MALAT1	miR-142-3p	HMGB1	Saos2, Mg63, Sw1353, U2Os, Hos	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28346809	MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.	knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis	MIMAT0000434	Cell Cycle 2017 Mar 19 16, 578-587 doi:10.1080/15384101.2017.1288324 PMID:28346809
752	LncRNA	MALAT1	miR-129-5p	HMGB1	Saos2, Mg63, Sw1353, U2Os, Hos	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28346809	MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.	knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis	MIMAT0000242	Cell Cycle 2017 Mar 19 16, 578-587 doi:10.1080/15384101.2017.1288324 PMID:28346809
753	LncRNA	UCA1	miR-204	ATF2	Lncap, Pc-3, Du145	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28337266	Long non-coding RNA UCA1 promotes cell progression by acting as a competing endogenous RNA of ATF2 in prostate cancer.	UCA1 regulated ATF2 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to ATF2 3'UTR, which suppressed the degradation of ATF2 mRNA by miR-204.	MI0000284	Am J Transl Res 2017  9, 366-375,  PMID:28337266
754	LncRNA	UCA1	miR-204	ATF2	Lncap, Pc-3, Du145	Prostate Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28337266	Long non-coding RNA UCA1 promotes cell progression by acting as a competing endogenous RNA of ATF2 in prostate cancer.	UCA1 regulated ATF2 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to ATF2 3'UTR, which suppressed the degradation of ATF2 mRNA by miR-204.	MI0000284	Am J Transl Res 2017  9, 366-375,  PMID:28337266
755	LncRNA	LOC100129148	miR-539-5p	KLF12	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28328537	Long non-coding RNA LOC100129148 functions as an oncogene in human nasopharyngeal carcinoma by targeting miR-539-5p.	Over-expressed LOC100129148 favored, but silenced LOC100129148 hampered cell proliferation in NPC cells. Additionally, LOC100129148 enhanced the KLF12 expression through functioning as a competitive 'sponge' for miR-539-5p.	MIMAT0003163	Aging (Albany NY) 2017 Mar 21 9, 999-1011 doi:10.18632/aging.101205 PMID:28328537
756	LncRNA	H19	miR-181d	b-catenin	U87, U251, Ln229, U373 And U118	Glioblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28327666	Hypoxia induces H19 expression through direct and indirect Hif-1a activity, promoting oncogenic effects in glioblastoma.	After transfecting a luciferase reporter plasmid harboring the putative miR-181d binding site from H19, the relative luciferase activity decreased in cells transfected with miR-181d mimics but not miR-16-1 mimics,miR-181d overexpression decreased the b-catenin levels, and H19 upregulation facilitated b-catenin accumulation by aborting the inhibition of miR-181d in both U87 and U251 cells.	MI0003139	Sci Rep 2017 Mar 22 7, 45029 doi:10.1038/srep45029 PMID:28327666
757	LncRNA	H19	miR-181d	b-catenin	U87, U251, Ln229, U373 And U118	Glioblastoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	28327666	Hypoxia induces H19 expression through direct and indirect Hif-1a activity, promoting oncogenic effects in glioblastoma.	After transfecting a luciferase reporter plasmid harboring the putative miR-181d binding site from H19, the relative luciferase activity decreased in cells transfected with miR-181d mimics but not miR-16-1 mimics,miR-181d overexpression decreased the b-catenin levels, and H19 upregulation facilitated b-catenin accumulation by aborting the inhibition of miR-181d in both U87 and U251 cells.	MI0003139	Sci Rep 2017 Mar 22 7, 45029 doi:10.1038/srep45029 PMID:28327666
758	LncRNA	BX649188.1	kshv-miR-K12-7-3p	NA	Kshv-Positive B Cell Lymphoma (Bc-3) Cells	NA	Kaposis sarcoma-associated herpesvirus	luciferase reporter assays;qRT-PCR	28323040	Machine learning-based identification of endogenous cellular microRNA sponges against viral microRNAs.	Viral miRNA binding sites were predicted using a newly-developed machine learning-based method, and candidate interactions between miRNAs and sponge RNAs were experimentally validated using luciferase reporter assay, western blot analysis, and flow cytometry. We found that BX649188.1 functions as a potential natural miRNA sponge against kshv-miR-K12-7-3p.	MIMAT0002187	Methods 2017 Oct 1 129, 33-40 doi:10.1016/j.ymeth.2017.03.017 PMID:28323040
759	LncRNA	BX649188.1	kshv-miR-K12-7-3p	NA	293T	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28323040	Machine learning-based identification of endogenous cellular microRNA sponges against viral microRNAs.	Viral miRNA binding sites were predicted using a newly-developed machine learning-based method, and candidate interactions between miRNAs and sponge RNAs were experimentally validated using luciferase reporter assay, western blot analysis, and flow cytometry. We found that BX649188.1 functions as a potential natural miRNA sponge against kshv-miR-K12-7-3p.	MIMAT0002187	Methods 2017 Oct 1 129, 33-40 doi:10.1016/j.ymeth.2017.03.017 PMID:28323040
760	LncRNA	MEG3	miR-133a-3p	SLC39A1	Bone Marrow Mesenchymal Stem Cells	Postmenopausal Osteoporosis	Homo sapiens (human)	qRT-PCR	28320084	LncRNA MEG3 inhibited osteogenic differentiation of bone marrow mesenchymal stem cells from postmenopausal osteoporosis by targeting miR-133a-3p.	In the differentiation process from BMSCs to osteoblasts, the expressions of MEG3 and miR-133a-3p were markedly decreased, and MEG3 overexpression reversed the osteogenic induction-mediated downregulation of miR-133a-3p, which was accompanied by significant decline in SLC39A1 expression. Furthermore, miR-133a-3p silencing or upregulation eliminated the effects of MEG3 on the osteogenic differentiation of BMSCs through direct binding.	MIMAT0000427	Biomed Pharmacother 2017 May 89, 1178-1186 doi:10.1016/j.biopha.2017.02.090 PMID:28320084
761	LncRNA	HOTAIR	miR-19	PTEN	Heart Tissues,Cultural Cardiomyocytes	Cardiac Hypertrophy	Homo sapiens (human)	qRT-PCR	28316060	HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy.	 HOTAIR expression was negatively correlated with miR-19 in TAC-operated mice. HOTAIR overexpression reduced cell surface area and the expression of hypertrophic markers ANP, BNP, and b-MHC in response to Ang-II stimulation as well as knockdown of miR-19. The further molecular mechanisms of HOTAIR action in CH demonstrated that HOTAIR may act as a competing endogenous RNA (ceRNA) for miR-19, thereby modulating the dis-inhibition of its endogenous target PTEN and playing an important role in inhibiting CH progress. 	MI0000075	Mol Cell Biochem 2017 Aug 432, 179-187 doi:10.1007/s11010-017-3008-y PMID:28316060
762	LncRNA	HOTAIR	miR-19	PTEN	Heart Tissues,Cultural Cardiomyocytes	Cardiac Hypertrophy	Mus musculus (mouse)	qRT-PCR	28316060	HOTAIR functions as a competing endogenous RNA to regulate PTEN expression by inhibiting miR-19 in cardiac hypertrophy.	 HOTAIR expression was negatively correlated with miR-19 in TAC-operated mice. HOTAIR overexpression reduced cell surface area and the expression of hypertrophic markers ANP, BNP, and b-MHC in response to Ang-II stimulation as well as knockdown of miR-19. The further molecular mechanisms of HOTAIR action in CH demonstrated that HOTAIR may act as a competing endogenous RNA (ceRNA) for miR-19, thereby modulating the dis-inhibition of its endogenous target PTEN and playing an important role in inhibiting CH progress. 	MI0000075	Mol Cell Biochem 2017 Aug 432, 179-187 doi:10.1007/s11010-017-3008-y PMID:28316060
763	LncRNA	TUG1	miR-186	CPEB2	Colorectal Cancer Tissues	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28302487	TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis.	TUG1 knockdown re-sensitized the MTX resistance in colorectal cancer cells, which were MTX-resistant colorectal cell line. Furthermore, bioinformatics analysis showed that miR-186 could directly bind to TUG1, suggesting TUG1 might worked as a ceRNA to sponge miR-186. Extensively, our study also showed that CPEB2 was the direct target of miR-186 in colorectal cancer cells.	MI0000483	Biochem Biophys Res Commun 2017 Sep 16 491, 552-557 doi:10.1016/j.bbrc.2017.03.042 PMID:28302487
764	LncRNA	LncRNA-ATB	miR-200a	b-catenin	Liver Tissues,Hepatic Stellate Cells	Hcv-Related Hepatic Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28302418	LncRNA-ATB/microRNA-200a/b-catenin regulatory axis involved in the progression of HCV-related hepatic fibrosis.	LncRNA-ATB was up-regulated in fibrotic liver tissues and activated LX-2 cells treated with CM from HepG2-CORE cells. Dual luciferase reporter assays confirmed that lncRNA-ATB contained common binding sites for miR-200a and b-catenin. Decreased expression of miR-200a and increased expression of b-catenin were observed in liver tissues of patients with HCV-related hepatic fibrosis and activated HSCs. Knockdown of lncRNA-ATB could down-regulate b-catenin expression by up-regulating the endogenous miR-200a and suppress the activation of LX-2 cells.	MI0000737	Gene 2017 Jun 30 618, 1-7 doi:10.1016/j.gene.2017.03.008 PMID:28302418
765	LncRNA	lncRNA-MODR	miR-454	RUNX2	Maxillary Sinus Membrane Stem Cells	Osteogenic Differentiation	Homo sapiens (human)	qRT-PCR;Western blot	28301382	Long Noncoding RNA Sponges miR-454 to Promote Osteogenic Differentiation in Maxillary Sinus Membrane Stem Cells.	lncRNA-MODR overexpression upregulated, whereas lncRNA-MODR silencing decreased the expression of the osteogenic key marker, runt-related transcription factor 2 (RUNX2). In-depth analyses showed that lncRNA-MODR acts as a molecular sponge for microRNA-454 (miR-454) and that prevents RUNX2 from mi-454-mediated suppression.	MI0003820	Implant Dent 2017 Apr 26, 178-186 doi:10.1097/id.0000000000000569 PMID:28301382
766	LncRNA	XIST	miR-133a	EGFR	Pancreatic Cancer Tissues	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28295543	LncRNA XIST Promotes Pancreatic Cancer Proliferation Through miR-133a/EGFR.	Exogenous miR-133a expression significantly inhibited PC cell proliferation. Moreover, as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting. In PC tissues, miR-133a expression was down-regulated and EGFR expression was up-regulated; miR-133a was inversely correlated with EGFR and XIST.	MI0000450	J Cell Biochem 2017 Oct 118, 3349-3358 doi:10.1002/jcb.25988 PMID:28295543
767	Circular RNA	CircCOL3A1-859267	miR-29a-3p	NA	Human Dermal Fibroblasts Cells	Dermal Fibroblasts	Homo sapiens (human)	qRT-PCR	28286269	Circular RNA profiling reveals that circCOL3A1-859267 regulate type I collagen expression in photoaged human dermal fibroblasts.	Overexpression of circCOL3A1-859267 inhibited UVA-induced decrease of type I collagen expression and silencing of it reduced type I collagen intensity. Via a bioinformatic method, 44 miRNAs were predicted to binding with circCOL3A1-859267, 5 of them have been confirmed or predicted to interact with type I collagen. 	MIMAT0000086	Biochem Biophys Res Commun 2017 Apr 29 486, 277-284 doi:10.1016/j.bbrc.2017.03.028 PMID:28286269
768	Circular RNA	CircCOL3A1-859267	miR-29b-3p	NA	Human Dermal Fibroblasts Cells	Dermal Fibroblasts	Homo sapiens (human)	qRT-PCR	28286269	Circular RNA profiling reveals that circCOL3A1-859267 regulate type I collagen expression in photoaged human dermal fibroblasts.	Overexpression of circCOL3A1-859267 inhibited UVA-induced decrease of type I collagen expression and silencing of it reduced type I collagen intensity. Via a bioinformatic method, 44 miRNAs were predicted to binding with circCOL3A1-859267, 5 of them have been confirmed or predicted to interact with type I collagen. 	MIMAT0000100	Biochem Biophys Res Commun 2017 Apr 29 486, 277-284 doi:10.1016/j.bbrc.2017.03.028 PMID:28286269
769	Circular RNA	CircCOL3A1-859267	miR-29c-3p	NA	Human Dermal Fibroblasts Cells	Dermal Fibroblasts	Homo sapiens (human)	qRT-PCR	28286269	Circular RNA profiling reveals that circCOL3A1-859267 regulate type I collagen expression in photoaged human dermal fibroblasts.	Overexpression of circCOL3A1-859267 inhibited UVA-induced decrease of type I collagen expression and silencing of it reduced type I collagen intensity. Via a bioinformatic method, 44 miRNAs were predicted to binding with circCOL3A1-859267, 5 of them have been confirmed or predicted to interact with type I collagen. 	MIMAT0000681	Biochem Biophys Res Commun 2017 Apr 29 486, 277-284 doi:10.1016/j.bbrc.2017.03.028 PMID:28286269
770	Circular RNA	CircCOL3A1-859267	miR-767-5p	NA	Human Dermal Fibroblasts Cells	Dermal Fibroblasts	Homo sapiens (human)	qRT-PCR	28286269	Circular RNA profiling reveals that circCOL3A1-859267 regulate type I collagen expression in photoaged human dermal fibroblasts.	Overexpression of circCOL3A1-859267 inhibited UVA-induced decrease of type I collagen expression and silencing of it reduced type I collagen intensity. Via a bioinformatic method, 44 miRNAs were predicted to binding with circCOL3A1-859267, 5 of them have been confirmed or predicted to interact with type I collagen. 	MIMAT0003882	Biochem Biophys Res Commun 2017 Apr 29 486, 277-284 doi:10.1016/j.bbrc.2017.03.028 PMID:28286269
771	LncRNA	Lnc-mg	miR-125b	IGF2	Skeletal Muscle Cells	Promote Myogenesis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28281528	Lnc-mg is a long non-coding RNA that promotes myogenesis.	conditional knockout of lnc-mg in skeletal muscle results in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promotes muscle hypertrophy. In vitro analysis of primary skeletal muscle cells shows that lnc-mg increases gradually during myogenic differentiation and its overexpression improves cell differentiation. Mechanistically, lnc-mg promotes myogenesis, by functioning as a competing endogenous RNA (ceRNA) for microRNA-125b to control protein abundance of insulin-like growth factor 2. 	MI0000446	Nat Commun 2017 Mar 10 8, 14718 doi:10.1038/ncomms14718 PMID:28281528
772	LncRNA	Lnc-mg	miR-125b	IGF2	Skeletal Muscle Cells	Promote Myogenesis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28281528	Lnc-mg is a long non-coding RNA that promotes myogenesis.	conditional knockout of lnc-mg in skeletal muscle results in muscle atrophy and the loss of muscular endurance during exercise. Alternatively, skeletal muscle-specific overexpression of lnc-mg promotes muscle hypertrophy. In vitro analysis of primary skeletal muscle cells shows that lnc-mg increases gradually during myogenic differentiation and its overexpression improves cell differentiation. Mechanistically, lnc-mg promotes myogenesis, by functioning as a competing endogenous RNA (ceRNA) for microRNA-125b to control protein abundance of insulin-like growth factor 2. 	MI0000446	Nat Commun 2017 Mar 10 8, 14718 doi:10.1038/ncomms14718 PMID:28281528
773	LncRNA	HOTAIRM1	miR-3960	HOXA1	Monocyte/Dendritic Cell 	Monocyte	Homo sapiens (human)	qRT-PCR	28280365	Downregulation of long noncoding RNA HOTAIRM1 promotes monocyte/dendritic cell differentiation through competitively binding to endogenous miR-3960.	 based on the "competing endogenous RNA" hypothesis, we discovered miR-3960 targeting both HOTAIRM1 and the DC differentiation repression gene, HOXA1, by most possibly constructing a potential competing endogenous RNA network. Increased miR-3960 expression could downregulate both of these two long RNAs and finally lead peripheral blood cells to differentiate into DCs.	MI0016964	Onco Targets Ther 2017  10, 1307-1315 doi:10.2147/ott.S124201 PMID:28280365
774	LncRNA	HOTAIRM1	miR-3960	HOXA1	Monocyte/Dendritic Cell 	Dendritic Cell Differentiation	Homo sapiens (human)	qRT-PCR	28280365	Downregulation of long noncoding RNA HOTAIRM1 promotes monocyte/dendritic cell differentiation through competitively binding to endogenous miR-3960.	 based on the "competing endogenous RNA" hypothesis, we discovered miR-3960 targeting both HOTAIRM1 and the DC differentiation repression gene, HOXA1, by most possibly constructing a potential competing endogenous RNA network. Increased miR-3960 expression could downregulate both of these two long RNAs and finally lead peripheral blood cells to differentiate into DCs.	MI0016964	Onco Targets Ther 2017  10, 1307-1315 doi:10.2147/ott.S124201 PMID:28280365
775	LncRNA	CRNDE	miR-451	NA	U266 And Rpmi8226	Myeloma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28276319	Long Non-coding RNA CRNDE Promotes Multiple Myeloma Cell Growth By Suppressing MiR-451.	After being transfected with siRNA, miR-451 expression observably increases. Bioinformatics analysis and luciferase assay reveal the interaction complementary bonding between CRNDE and miR-451. Pearson's correlation shows that CRNDE is negatively correlated to miR-451 expression in human MM samples. Subsequently, miR-451 inhibitor rescues the tumorigenesis inhibition induced by CRNDE knockdown. 	MI0001729	Oncol Res 2017 Aug 7 25, 1207-1214 doi:10.3727/096504017x14886679715637 PMID:28276319
776	LncRNA	MEG3	miR-19a	PTEN	U87 And U251	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28276316	Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion By Acting As Competing Endogenous RNA of MiR-19a.	 luciferase results verify the putative target site and also reveal the complementary binding between miR-19a and MEG3. MiR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis.	MI0000073	Oncol Res 2017 Nov 2 25, 1471-1478 doi:10.3727/096504017x14886689179993 PMID:28276316
777	LncRNA	PVT1	miR-424	NA	Cervical Cancer Tissue And Cell Lines	Cervical Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28276314	Long Non-Coding RNA PVT1 Facilitates Cervical Cancer Progression Via Negative Regulating of miR-424.	After transfecting PVT1 siRNA, the proliferation, migration and invasion of cervical cancer cells were markedly decreased. MiRNA expression profiles demonstrate that miR-424 was markedly down-regulated in cervical cancer tissue. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay.miR-424 lower-expression could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines.	MI0001446	Oncol Res 2017 Sep 21 25, 1391-1398 doi:10.3727/096504017x14881559833562 PMID:28276314
778	LncRNA	PVT1	miR-152	CD151	Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28258379	Long Noncoding RNA PVT1 Acts as a "Sponge" to Inhibit microRNA-152 in Gastric Cancer Cells.	we found that PVT1 have three binding sequences for miR-152. Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues.	MI0000462	Dig Dis Sci 2017 Nov 62, 3021-3028 doi:10.1007/s10620-017-4508-z PMID:28258379
779	LncRNA	PVT1	miR-152	FGF2	Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28258379	Long Noncoding RNA PVT1 Acts as a "Sponge" to Inhibit microRNA-152 in Gastric Cancer Cells.	we found that PVT1 have three binding sequences for miR-152. Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues.	MI0000462	Dig Dis Sci 2017 Nov 62, 3021-3028 doi:10.1007/s10620-017-4508-z PMID:28258379
780	Circular RNA	cir-ITCH	miR-7	ITCH	A549 And Nic-H460	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27642589	Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/b-Catenin Pathway.	cir-ITCH was enhanced in different lung cancer cell lines, A549 and NIC-H460. Ectopic expression of cir-ITCH markedly elevated its parental cancer-suppressive gene, ITCH, expression and inhibited proliferation of lung cancer cells. Molecular analysis further revealed that cir-ITCH acted as sponge of oncogenic miR-7 and miR-214 to enhance ITCH expression and thus suppressed the activation of Wnt/b-catenin signaling.	MI0000263	Biomed Res Int 2016  2016, 1579490 doi:10.1155/2016/1579490 PMID:27642589
781	Circular RNA	cir-ITCH	miR-214	ITCH	A549 And Nic-H460	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27642589	Circular RNA-ITCH Suppresses Lung Cancer Proliferation via Inhibiting the Wnt/b-Catenin Pathway.	cir-ITCH was enhanced in different lung cancer cell lines, A549 and NIC-H460. Ectopic expression of cir-ITCH markedly elevated its parental cancer-suppressive gene, ITCH, expression and inhibited proliferation of lung cancer cells. Molecular analysis further revealed that cir-ITCH acted as sponge of oncogenic miR-7 and miR-214 to enhance ITCH expression and thus suppressed the activation of Wnt/b-catenin signaling.	MI0000290	Biomed Res Int 2016  2016, 1579490 doi:10.1155/2016/1579490 PMID:27642589
782	Coding-mRNA	STARD13	miR-340	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000802	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
783	Coding-mRNA	STARD13	miR-448	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0001637	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
784	Coding-mRNA	STARD13	miR-374	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000782	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
785	Coding-mRNA	STARD13	miR-203	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000283	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
786	Coding-mRNA	STARD13	let-7a	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000556	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
787	Coding-mRNA	STARD13	miR-216	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000292	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
788	Coding-mRNA	STARD13	miR-23	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000079	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
789	Coding-mRNA	STARD13	miR-153	FAS	Hepg2 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	To understand the molecular mechanisms of STARD13 3'-UTR- mediated cellular apoptosis, miRNA binding sites were predicted in the 3'-UTRs of STARD13 and Fas and nine common miRNAs were identified to bind to the 3'-UTRs of STARD13 and Fas. Thus we assumed that STARD13 3'-UTR could act as a ceRNA for Fas. The hypothesis was further tested by confirming that STARD13 3'-UTR modulates Fas expression in a miRNA- and 3'-UTR-dependent way.	MI0000463	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
790	LncRNA	lincRNA-ROR	miR-145	ARF6	Hek293T, Mcf-7, Hs578T, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25253741	lincRNA-ROR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6.	Investigation of miR-145-regulated pathways involved in tumor invasion revealed a novel target, the small GTPase ADP-ribosylation factor 6 (Arf6). Subsequent analysis demonstrated that ARF6, a known regulator of breast tumor cell invasion, is dramatically upregulated in TNBC and in breast tumor metastasis. Mechanistically, ARF6 regulates E-cadherin localization and affects cell-cell adhesion. These results reveal a lincRNA-ROR/miR-145/ARF6 pathway that regulates invasion in TNBCs.	MI0000461	Mol Cancer Res 2015 Feb 13, 330-8 doi:10.1158/1541-7786.Mcr-14-0251 PMID:25253741
791	LncRNA	CASC2	miR-101	CPEB1	U251 And U87	Astrocytoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28252647	CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis.	Overexpression of CASC2c promotes the malignant characteristic of astrocytoma cells.CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1.	MI0000103	Cell Death Dis 2017 Mar 2 8, e2639 doi:10.1038/cddis.2017.11 PMID:28252647
792	Coding-mRNA	SRF	miR-101-3p	NA	Bgc-823, Mnk-45, Mgc-803, Sgc-7901, Ags And Hgc-27	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28251884	MiR-101-3p Suppresses HOX Transcript Antisense RNA (HOTAIR)-induced Proliferation and Invasion Through Directly Targeting SRF in Gastric Carcinoma Cells.	Overexpression miR-101-3p suppressed both the proliferation and invasion of AGS gastric adenocarcinoma cells and knockdown of miR-101-3p displayed an opposite effect. In addition, miR-101-3p could directly target and suppress the expression SRF gene, which is a transcription factor of HOTAIR, a well-characterized tumor promoter lncRNA. MiR-101-3p negatively regulated SRF-mediated transcription of HOTAIR.	MIMAT0000099	Oncol Res 2017 Sep 21 25, 1383-1390 doi:10.3727/096504017x14879366402279 PMID:28251884
793	Artifically engineered RNA	miR-181-sponge	miR-181a	PTEN	H9C2 Cells	Heart Disease	Mus musculus (mouse)	qRT-PCR;Western blot assay	28242633	Divergent Effects of miR-181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets.	miR-181a/b targets phosphatase and tensin homolog (PTEN), and the sponge-expressing stable cells had increased PTEN activity and decreased PI3K signaling.Our results suggest divergent effects of different miR-181 family members: miR-181a/b targets PTEN in the cytosol, resulting in an increase in infarct size in miR-181a/b-/- mice due to increased PTEN signaling, whereas miR-181c targets mt-COX1 in the mitochondria, resulting in decreased infarct size in miR-181c/d-/- mice.	MI0000269	J Am Heart Assoc 2017 Feb 27 6 doi:10.1161/jaha.116.004694 PMID:28242633
794	Artifically engineered RNA	miR-181-sponge	miR-181b	PTEN	H9C2 Cells	Heart Disease	Mus musculus (mouse)	qRT-PCR;Western blot assay	28242633	Divergent Effects of miR-181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets.	miR-181a/b targets phosphatase and tensin homolog (PTEN), and the sponge-expressing stable cells had increased PTEN activity and decreased PI3K signaling.Our results suggest divergent effects of different miR-181 family members: miR-181a/b targets PTEN in the cytosol, resulting in an increase in infarct size in miR-181a/b-/- mice due to increased PTEN signaling, whereas miR-181c targets mt-COX1 in the mitochondria, resulting in decreased infarct size in miR-181c/d-/- mice.	MI0000270	J Am Heart Assoc 2017 Feb 27 6 doi:10.1161/jaha.116.004694 PMID:28242633
795	Artifically engineered RNA	miR-181-sponge	miR-181c	MT-CO1	H9C2 Cells	Heart Disease	Mus musculus (mouse)	qRT-PCR;Western blot assay	28242633	Divergent Effects of miR-181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets.	miR-181a/b targets phosphatase and tensin homolog (PTEN), and the sponge-expressing stable cells had increased PTEN activity and decreased PI3K signaling.Our results suggest divergent effects of different miR-181 family members: miR-181a/b targets PTEN in the cytosol, resulting in an increase in infarct size in miR-181a/b-/- mice due to increased PTEN signaling, whereas miR-181c targets mt-COX1 in the mitochondria, resulting in decreased infarct size in miR-181c/d-/- mice.	MI0000271	J Am Heart Assoc 2017 Feb 27 6 doi:10.1161/jaha.116.004694 PMID:28242633
796	Coding-mRNA	SP1	miR-7a	Klf4	Mdpc6T	Odontoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28238937	Sp1 is a competitive endogenous RNA of Klf4 during odontoblast differentiation.	In situ hybridization verified that Sp1 was co-expressed with Klf4 in the differentiating and the mature odontoblasts in vivo. Knockdown of Sp1 using siRNA resulted in a significant reduction of Klf4 and vice visa. This interaction was further confirmed to be miRNA dependent. Common miRNAs of Klf4 and Sp1 were predicted, among which miR-7a, miR-29b and miR-135a were able to downregulate both Klf4 and Sp1 expression after their separate overexpression in the mDPC6T cells. Dual luciferase assays showed that these miRNAs separately regulated the 3'UTRs of both Klf4 and Sp1, and the down-regulation of Klf4 3 'UTR by Sp1 siRNA was abolished when these three miRNAs' binding sites were mutated in the Klf4 3 'UTR. 	MI0000728	Int J Biochem Cell Biol 2017 Apr 85, 159-165 doi:10.1016/j.biocel.2017.02.008 PMID:28238937
797	Coding-mRNA	SP1	miR-135a	Klf4	Mdpc6T	Odontoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28238937	Sp1 is a competitive endogenous RNA of Klf4 during odontoblast differentiation.	In situ hybridization verified that Sp1 was co-expressed with Klf4 in the differentiating and the mature odontoblasts in vivo. Knockdown of Sp1 using siRNA resulted in a significant reduction of Klf4 and vice visa. This interaction was further confirmed to be miRNA dependent. Common miRNAs of Klf4 and Sp1 were predicted, among which miR-7a, miR-29b and miR-135a were able to downregulate both Klf4 and Sp1 expression after their separate overexpression in the mDPC6T cells. Dual luciferase assays showed that these miRNAs separately regulated the 3'UTRs of both Klf4 and Sp1, and the down-regulation of Klf4 3 'UTR by Sp1 siRNA was abolished when these three miRNAs' binding sites were mutated in the Klf4 3 'UTR. 	MI0000161	Int J Biochem Cell Biol 2017 Apr 85, 159-165 doi:10.1016/j.biocel.2017.02.008 PMID:28238937
798	Coding-mRNA	SP1	miR-29b	Klf4	Mdpc6T	Odontoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28238937	Sp1 is a competitive endogenous RNA of Klf4 during odontoblast differentiation.	In situ hybridization verified that Sp1 was co-expressed with Klf4 in the differentiating and the mature odontoblasts in vivo. Knockdown of Sp1 using siRNA resulted in a significant reduction of Klf4 and vice visa. This interaction was further confirmed to be miRNA dependent. Common miRNAs of Klf4 and Sp1 were predicted, among which miR-7a, miR-29b and miR-135a were able to downregulate both Klf4 and Sp1 expression after their separate overexpression in the mDPC6T cells. Dual luciferase assays showed that these miRNAs separately regulated the 3'UTRs of both Klf4 and Sp1, and the down-regulation of Klf4 3 'UTR by Sp1 siRNA was abolished when these three miRNAs' binding sites were mutated in the Klf4 3 'UTR. 	MI0000105	Int J Biochem Cell Biol 2017 Apr 85, 159-165 doi:10.1016/j.biocel.2017.02.008 PMID:28238937
799	LncRNA	SNHG16	miR-98	E2F5	Mda-Mb-231, Mcf-7, Mda-Mb-468 And Hek293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;RNA immunoprecipitation	28232182	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.	SNHG16 as a competitive endogenous RNA (ceRNA) of E2F transcription factor 5 protein (E2F5) via competition for the shared miR-98 through bioinformatics analysis, and proved this regulation using relative quantitative real-time PCR (qRT-PCR), western blot, RNA immunoprecipitation (RIP) assay and luciferase reporter assay. our findings indicated that SNHG16 induces breast cancer cell migration by competitively binding miR-98 with E2F5, and SNHG16 can serve as a potential therapeutic target for breast cancer treatment.	MI0000100	Biochem Biophys Res Commun 2017 Apr 1 485, 272-278 doi:10.1016/j.bbrc.2017.02.094 PMID:28232182
800	Coding-mRNA	HNRNPK	miR-1207-5p	PTOV1-AS1	Hela	Cervical Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28228215	hnRNPK-regulated PTOV1-AS1 modulates heme oxygenase-1 expression via miR-1207-5p.	The knockdown of hnRNPK or PTOV1-AS1 suppressed HO-1 expression by increasing the enrichment of HO-1 mRNA in miR-1207-5p-mediated miRISC. Downregulation of HO-1 by a miR-1207-5p mimic or knockdown of hnRNPK and PTOV1-AS1 inhibited the proliferation and clonogenic ability of HeLa cells.	MIMAT0005871	BMB Rep 2017 Apr 50, 220-225 doi:10.5483/bmbrep.2017.50.4.024 PMID:28228215
801	LncRNA	RPPH1	miR-330-5p	CDC42	Mouse Brains	Alzheimers Disease	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28223918	Rpph1 Upregulates CDC42 Expression and Promotes Hippocampal Neuron Dendritic Spine Formation by Competing with miR-330-5p.	The underlying mechanisms for the involvement of ceRNA in AD were validated using the Dual Luciferase Reporter Assay, detection of transcription levels by quantitative RT-PCR and translation levels by Western blotting, and morphological examination in primary cultured neurons. In the ceRNA network, four lncRNAs (C030034L19Rik, Rpph1, A830012C17Rik, and Gm15477) and five miRNAs (miR-182-5p, miR-330-5p, miR-326-3p, miR-132-3p, and miR-484) are enriched in nine pathways and an AD-related gene pool. Rpph1 binds to miR326-3p/miR-330-5p and causes the release of their downstream target Cdc42, which leads to CDC42 upregulation.	MIMAT0004693	Front Mol Neurosci 2017  10, 27 doi:10.3389/fnmol.2017.00027 PMID:28223918
802	LncRNA	RPPH1	miR-326-3p	CDC42	Mouse Brains	Alzheimers Disease	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28223918	Rpph1 Upregulates CDC42 Expression and Promotes Hippocampal Neuron Dendritic Spine Formation by Competing with miR-330-5p.	The underlying mechanisms for the involvement of ceRNA in AD were validated using the Dual Luciferase Reporter Assay, detection of transcription levels by quantitative RT-PCR and translation levels by Western blotting, and morphological examination in primary cultured neurons. In the ceRNA network, four lncRNAs (C030034L19Rik, Rpph1, A830012C17Rik, and Gm15477) and five miRNAs (miR-182-5p, miR-330-5p, miR-326-3p, miR-132-3p, and miR-484) are enriched in nine pathways and an AD-related gene pool. Rpph1 binds to miR326-3p/miR-330-5p and causes the release of their downstream target Cdc42, which leads to CDC42 upregulation.	MIMAT0000559	Front Mol Neurosci 2017  10, 27 doi:10.3389/fnmol.2017.00027 PMID:28223918
803	LncRNA	RPPH1	miR-330-5p	CDC42	Hek 293T Cells	Alzheimers Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28223918	Rpph1 Upregulates CDC42 Expression and Promotes Hippocampal Neuron Dendritic Spine Formation by Competing with miR-330-5p.	The underlying mechanisms for the involvement of ceRNA in AD were validated using the Dual Luciferase Reporter Assay, detection of transcription levels by quantitative RT-PCR and translation levels by Western blotting, and morphological examination in primary cultured neurons. In the ceRNA network, four lncRNAs (C030034L19Rik, Rpph1, A830012C17Rik, and Gm15477) and five miRNAs (miR-182-5p, miR-330-5p, miR-326-3p, miR-132-3p, and miR-484) are enriched in nine pathways and an AD-related gene pool. Rpph1 binds to miR326-3p/miR-330-5p and causes the release of their downstream target Cdc42, which leads to CDC42 upregulation.	MIMAT0004693	Front Mol Neurosci 2017  10, 27 doi:10.3389/fnmol.2017.00027 PMID:28223918
804	LncRNA	RPPH1	miR-326-3p	CDC42	Hek 293T Cells	Alzheimers Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28223918	Rpph1 Upregulates CDC42 Expression and Promotes Hippocampal Neuron Dendritic Spine Formation by Competing with miR-330-5p.	The underlying mechanisms for the involvement of ceRNA in AD were validated using the Dual Luciferase Reporter Assay, detection of transcription levels by quantitative RT-PCR and translation levels by Western blotting, and morphological examination in primary cultured neurons. In the ceRNA network, four lncRNAs (C030034L19Rik, Rpph1, A830012C17Rik, and Gm15477) and five miRNAs (miR-182-5p, miR-330-5p, miR-326-3p, miR-132-3p, and miR-484) are enriched in nine pathways and an AD-related gene pool. Rpph1 binds to miR326-3p/miR-330-5p and causes the release of their downstream target Cdc42, which leads to CDC42 upregulation.	MIMAT0000559	Front Mol Neurosci 2017  10, 27 doi:10.3389/fnmol.2017.00027 PMID:28223918
805	Circular RNA	Circ-TTBK2	miR-217	HNF1B	U87 And U251	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;RNA immunoprecipitation	28219405	TTBK2 circular RNA promotes glioma malignancy by regulating miR-217/HNF1b/Derlin-1 pathway	Enhanced expression of circ-TTBK2 promoted cell proliferation, migration, and invasion, while inhibited apoptosis. MiR-217 was downregulated in glioma tissues and cell lines. We also found that circ-TTBK2, but not linear TTBK2, acted asmiR-217 sponge in a sequence-specific manner. In addition, upregulated circ-TTBK2 decreased miR-217 expression and there was a reciprocal negative feedback between them in an Argonaute2-dependent manner. Moreover, reintroduction of miR-217 significantly reversed circ-TTBK2-mediated promotion of glioma progression. HNF1b was a direct target of miR-217, and played oncogenic role in glioma cells.	MI0000293	J Hematol Oncol 2017 Feb 20 10, 52 doi:10.1186/s13045-017-0422-2 PMID:28219405
806	Pseudogene	PTENP1	miR-106b	PTEN	Ges-1	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28212532	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.	In order to identify and characterize the PTENP1~miRNA~PTEN ceRNA network in GC, we first determined PTENP1 levels in clinical GC samples and found that PTENP1 and PTEN were concurrently downregulated in these samples. We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay.	MI0000734	Oncotarget 2017 Apr 18 8, 26079-26089 doi:10.18632/oncotarget.15317 PMID:28212532
807	Pseudogene	PTENP1	miR-93	PTEN	Ges-1	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28212532	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.	In order to identify and characterize the PTENP1~miRNA~PTEN ceRNA network in GC, we first determined PTENP1 levels in clinical GC samples and found that PTENP1 and PTEN were concurrently downregulated in these samples. We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay.	MI0000095	Oncotarget 2017 Apr 18 8, 26079-26089 doi:10.18632/oncotarget.15317 PMID:28212532
808	LncRNA	TUG1	miR-335-5p	ROCK1	Mg-63, U2Os And Mnng/Hos	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28205334	Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells.	TUG1 and Rho-associated coiled-coil-containing protein kinase 1 (ROCK1), a metastasis-related gene targeted by microRNA-335-5p (miR-335-5p), had the same miR-335-5p combining site. The subsequent luciferase assay verified TUG1 was a target of miR-335-5p. Furthermore, the results of a real-time quantitative PCR showed that TUG1 and miR-335-5p could affect each other's expression. respectively. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p.	MIMAT0000765	Cancer Sci 2017 May 108, 859-867 doi:10.1111/cas.13201 PMID:28205334
809	LncRNA	STX12	miR-148a	SMAD5	Pancreaticstellate Cells	Pancreatitis	Homo sapiens (human)	qRT-PCR;Western blot assay	28202235	STX12 lncRNA/miR-148a/SMAD5 participate in the regulation of pancreatic stellate cell activation through a mechanism involving competing endogenous RNA.	The expression of STX12 was downregulated (relative expression level: 0.23±0.01, P<0.01), while the expression of miR-148a was significantly elevated (relative expression level: 1.54±0.02, p<0.01), and the expression of miR-130b was markedly reduced (relative expression level: 0.69±0.02, p<0.01). The expression of SMAD5 was decreased (relative expression level: 0.70±0.04, p<0.05), whereas the expression of IL6ST displayed no significant change (p=0.24).	MI0000253	Pancreatology 2017 Mar-Apr 17, 237-246 doi:10.1016/j.pan.2017.01.010 PMID:28202235
810	LncRNA	STX12	miR-148a	SMAD5	Pancreaticstellate Cells	Pancreatitis	Mus musculus (mouse)	qRT-PCR;Western blot assay	28202235	STX12 lncRNA/miR-148a/SMAD5 participate in the regulation of pancreatic stellate cell activation through a mechanism involving competing endogenous RNA.	The expression of STX12 was downregulated (relative expression level: 0.23±0.01, P<0.01), while the expression of miR-148a was significantly elevated (relative expression level: 1.54±0.02, p<0.01), and the expression of miR-130b was markedly reduced (relative expression level: 0.69±0.02, p<0.01). The expression of SMAD5 was decreased (relative expression level: 0.70±0.04, p<0.05), whereas the expression of IL6ST displayed no significant change (p=0.24).	MI0000253	Pancreatology 2017 Mar-Apr 17, 237-246 doi:10.1016/j.pan.2017.01.010 PMID:28202235
811	LncRNA	Lnc-MKI67IP-3	let-7e	IKBB	Vascular Endothelial Cells	Inflammatory Responses Of Vecs	Homo sapiens (human)	qRT-PCR;Western blot assay	28195197	Let-7e modulates the inflammatory response in vascular endothelial cells through ceRNA crosstalk	lnc-MKI67IP-3 acted as a sponge or competing endogenous RNA (ceRNA) for let-7e, suppressing its pro-inflammatory effects, and let-7e decreased lnc-MKI67IP-3 expression, thereby forming a positive feedback loop to aggravate inflammation. Moreover, let-7e, lnc-MKI67IP-3 and IkBb were also abnormal in oxLDL-treated VECs and atherosclerotic plaques.	MI0000066	Sci Rep 2017 Feb 14 7, 42498 doi:10.1038/srep42498 PMID:28195197
812	LncRNA	PVT1	miR-200b	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0000342	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
813	LncRNA	PVT1	miR-200c	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0000650	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
814	LncRNA	PVT1	miR-429	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0001641	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
815	LncRNA	TCONS_147426	miR-200b	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0000342	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
816	LncRNA	TCONS_147426	miR-200c	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0000650	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
817	LncRNA	TCONS_147426	miR-429	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)	short and long RNA-seq	28187158	Role of the long non-coding RNA PVT1 in the dysregulation of the ceRNA-ceRNA network in human breast cancer.	We found a drastic rewiring in the cross-talks between ceRNAs from the physiological to the pathological condition. The main actor of this dysregulated lncRNA-associated ceRNA network was the lncRNA PVT1, which revealed a net biding preference towards the miR-200 family members in normal breast tissues. Despite its up-regulation in breast cancer tissues, mimicked by the miR-200 family members, PVT1 stops working as ceRNA in the cancerous state. The specific conditions required for a ceRNA landscape to occur are still far from being determined. Here, we emphasized the importance of the relative concentration of the ceRNAs, and their related miRNAs. In particular, we focused on the withdrawal in breast cancer tissues of the PVT1 ceRNA activity and performed a gene expression and sequence analysis of its multiple isoforms. We found that the PVT1 isoform harbouring the binding site for a representative miRNA of the miR-200 family shows a drastic decrease in its relative concentration with respect to the miRNA abundance in breast cancer tissues, providing a plausibility argument to the breakdown of the sponge program orchestrated by the oncogene PVT1.	MI0001641	PLoS One 2017  12, e0171661 doi:10.1371/journal.pone.0171661 PMID:28187158
818	LncRNA	MALAT1	miR-203	TYMS	U87 And U251	Glioblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28187000	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.	The gain and loss-function experiments revealed thatmiR-203 was down-regulated by MALAT1 and this interaction has reciprocal effects. Besides, thymidylate synthase (TS) mRNA was identified as a direct target of miR-203.LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression.	MI0000283	Oncotarget 2017 Apr 4 8, 22783-22799 doi:10.18632/oncotarget.15199 PMID:28187000
819	Coding-mRNA	XIAP	miR-29a-5p	FSCN1	Mcf-7, Mda-Mb-231, Bt549, Skbr3, T47D	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	28186968	XIAP 3'-untranslated region as a ceRNA promotes FSCN1 function in inducing the progression of breast cancer by binding endogenous miR-29a-5p.	Expression of XIAP and FSCN1 were up-regulated synergistically after transfecting XIAP 3'UTR in vitro and in vivo. Interactions between XIAP and FSCN1 appear to be a key determinant of these processes. Co-transfection with Dicer siRNA reversed the XIAP 3'UTR-mediated oncogenicity, suggesting the miRNAs might be involved in that process. we demonstrated that one miRNA, miR-29a-5p, can bind to both the XIAP and FSCN1 3'UTRs and play an important role in that interactions. We showed that the 3'UTR of XIAP was able to antagonize miR-29a-5p, and resulted in the increased translation of XIAP and FSCN1.	MIMAT0004503	Oncotarget 2017 Mar 7 8, 16784-16800 doi:10.18632/oncotarget.15159 PMID:28186968
820	LncRNA	NEAT1	miR-181d-5p	SOX5	Glioma Endothelial Cells	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28185956	Long non-coding RNA NEAT1 regulates permeability of the blood-tumor barrier via miR-181d-5p-mediated expression changes in ZO-1, occludin, and claudin-5.	Knockdown of NEAT1 impaired the integrity and increased the permeability of the BTB, accompanied by downregulation of expression of the tight junction proteins ZO-1, occludin and claudin-5 in GECs. Both bioinformatics data and results of luciferase reporter assays demonstrated that NEAT1 influenced BTB permeability by binding to miR-181d-5p. Knockdown of NEAT1 also down-regulated the expression of sex determining region Y-box protein 5 (SOX5), which was defined as a direct and functional downstream target of miR-181d-5p. SOX5 interacts with the promoter region of ZO-1, occludin and claudin-5 in GECs.	MIMAT0002821	Biochim Biophys Acta Mol Basis Dis 2017 Sep 1863, 2240-2254 doi:10.1016/j.bbadis.2017.02.005 PMID:28185956
821	LncRNA	ENST00000535511	miR-133b	UBD	Crc Tumor/Non-Tumor Tissues	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	28177879	Comprehensive analysis of differentially expressed profiles of lncRNAs and construction of miR-133b mediated ceRNA network in colorectal cancer.	A miR-133b-meditated lncRNA-mRNA ceRNA network was revealed, a subset of which was validated in 14 paired CRC patient tumor/non-tumor samples. An innovate method was employed that combined analyses of two microarray data sets to construct a miR-133b-mediated lncRNA-mRNA competing endogenous RNAs (ceRNA) network. Quantitative RT-PCR analysis was used to validate part of this network. GSEA was used to predict the potential functions of these lncRNAs.	MI0000822	Oncotarget 2017 Mar 28 8, 21095-21105 doi:10.18632/oncotarget.15045 PMID:28177879
822	LncRNA	LINC00858	miR-422a	KLK4	A549, Sk-Mes-1, H1299, 95D, H460, H520, H1975, H157, Sk-Lu-1, And Spc-A-1	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28177876	Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer.	Ectopic expression of LINC00858 in NSCLC cells promoted cell proliferation and induced cell migration and invasion. Moreover, LINC00858 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-422a and thereby modulating the expression of kallikrein-related peptidase 4 (KLK4).	MI0001444	Aging (Albany NY) 2017 Feb 6 9, 475-486 doi:10.18632/aging.101171 PMID:28177876
823	LncRNA	MEG3	miR-214	NA	A2780Cp Cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	28175963	Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer.	There were at least two binding sites between MEG3 and miR-214. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance.	MI0000290	Cancer Chemother Pharmacol 2017 Mar 79, 479-487 doi:10.1007/s00280-017-3238-4 PMID:28175963
824	LncRNA	HULC	miR-6825-5p	USP22	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027550	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
825	LncRNA	HULC	miR-6845-5p	USP22	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027590	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
826	LncRNA	HULC	miR-6886-3p	USP22	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027673	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
827	LncRNA	HULC	miR-6825-5p	Sirt1	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027550	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
828	LncRNA	HULC	miR-6845-5p	Sirt1	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027590	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
829	LncRNA	HULC	miR-6886-3p	Sirt1	Hepg2, Hep3B, Plc, Huh7, Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells.	Ectopic expression of HULC elicited the autophagy of HCC cells through stabilizing silent information regulator 1 (Sirt1) protein. The investigation for the corresponding mechanism by which HULC stabilized Sirt1 revealed that HULC upregulated ubiquitin-specific peptidase 22 (USP22), leading to the decrease of ubiquitin-mediated degradation of Sirt1 protein by removing the conjugated polyubiquitin chains from Sirt1. Moreover, we found that miR-6825-5p, miR-6845-5p and miR-6886-3p could decrease the level of USP22 protein by binding to the 3'-untranlated region of USP22 mRNA. All the three microRNAs (miRNAs) were downregulated by HULC, which resulted in the elevation of USP22. In addition, we showed that the level of HULC was positively correlated with that of Sirt1 protein in human HCC tissues. 	MIMAT0027673	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
830	LncRNA	PlncRNA1	miR-34c	MAZ	Intestinal Epithelial Cell Line	Inflammatory Bowel Disease	Homo sapiens (human)	qRT-PCR;Western blot assay	28153728	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease.	Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin. The protect effects of PlncRNA1 overexpression on intestinal epithelial barrier function was reversed by overexpression of miR-34c.	MI0000743	Biochem Biophys Res Commun 2017 Apr 22 486, 6-13 doi:10.1016/j.bbrc.2017.01.115 PMID:28153728
831	LncRNA	PlncRNA1	miR-34c	ZO-1	Intestinal Epithelial Cell Line	Inflammatory Bowel Disease	Homo sapiens (human)	qRT-PCR;Western blot assay	28153728	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease.	Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin. The protect effects of PlncRNA1 overexpression on intestinal epithelial barrier function was reversed by overexpression of miR-34c.	MI0000743	Biochem Biophys Res Commun 2017 Apr 22 486, 6-13 doi:10.1016/j.bbrc.2017.01.115 PMID:28153728
832	LncRNA	PlncRNA1	miR-34c	OCEL1	Intestinal Epithelial Cell Line	Inflammatory Bowel Disease	Homo sapiens (human)	qRT-PCR;Western blot assay	28153728	MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease.	Tight junction (TJ) proteins ZO-1 and occludin were regulated by MAZ, while, miR-34c targeted MAZ to regulate its expression, in addition, PlncRNA1 and miR-34c bound together to regulate the expressions of MAZ, ZO-1 and occludin. The protect effects of PlncRNA1 overexpression on intestinal epithelial barrier function was reversed by overexpression of miR-34c.	MI0000743	Biochem Biophys Res Commun 2017 Apr 22 486, 6-13 doi:10.1016/j.bbrc.2017.01.115 PMID:28153728
833	LncRNA	MALAT1	miR-101	NA	Kyse30, Kyse450, And Kyse150	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	28150831	MicroRNA-mediated silence of onco-lncRNA MALAT1 in different ESCC cells via ligand-functionalized hydroxyl-rich nanovectors.	Poly(glycidyl methacrylate)-based star-like polycations with flanking folic acid (FA) ligands and rich hydrophilic hydroxyl groups (denoted as s-PGEA-FA) were proposed as efficient nanovectors to deliver miR-101 and miR-217 for silencing onco-lncRNA MALAT1 in different ESCC cells. The inhibition of ESCC by s-PGEA-FA/miRNA nanocomplexes would be achieved via subsequently targeting onco-lncRNA MALAT1 in ESCC cells. 	MI0000103	Nanoscale 2017 Feb 16 9, 2521-2530 doi:10.1039/c6nr09668a PMID:28150831
834	LncRNA	MALAT1	miR-217	NA	Kyse30, Kyse450, And Kyse150	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	28150831	MicroRNA-mediated silence of onco-lncRNA MALAT1 in different ESCC cells via ligand-functionalized hydroxyl-rich nanovectors.	Poly(glycidyl methacrylate)-based star-like polycations with flanking folic acid (FA) ligands and rich hydrophilic hydroxyl groups (denoted as s-PGEA-FA) were proposed as efficient nanovectors to deliver miR-101 and miR-217 for silencing onco-lncRNA MALAT1 in different ESCC cells. The inhibition of ESCC by s-PGEA-FA/miRNA nanocomplexes would be achieved via subsequently targeting onco-lncRNA MALAT1 in ESCC cells. 	MI0000293	Nanoscale 2017 Feb 16 9, 2521-2530 doi:10.1039/c6nr09668a PMID:28150831
835	Coding-mRNA	TFF3	miR-491-5p	PRINS	Ht-29/B6	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28149533	TFF3-dependent resistance of human colorectal adenocarcinoma cells HT-29/B6 to apoptosis is mediated by miR-491-5p regulation of lncRNA PRINS.	 In silico-based expression analysis revealed TFF3-mediated regulation of selected microRNAs as well as long non-coding RNAs (lncRNAs), whereas miR-491-5p was identified to target the lncRNA 'psoriasis susceptibility-related RNA gene induced by stress' (PRINS). RNA interference-based gain- and loss-of-function experiments examined miR-491-PRINS axis to exert the TFF3-mediated phenotype. Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS.	MIMAT0002807	Cell Death Discov 2017  3, 16106 doi:10.1038/cddiscovery.2016.106 PMID:28149533
836	Circular RNA	ciRS-7	miR-7	PIK3CD	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
837	Circular RNA	ciRS-7	miR-7	p70S6K	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
838	Circular RNA	ciRS-7	miR-7	mTOR	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
839	Circular RNA	Cdr1as	miR-7	PIK3CD	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
840	Circular RNA	Cdr1as	miR-7	p70S6K	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
841	Circular RNA	Cdr1as	miR-7	mTOR	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27614453	The circular RNA ciRS-7 (Cdr1as) acts as a risk factor of hepatic microvascular invasion in hepatocellular carcinoma.	The expression of ciRS-7 in HCC tissues with concurrent MVI was inversely correlated with that of miR-7 (r = -0.39, p = 0.007) and positively related with that of two miR-7-targeted genes [PIK3CD (r = 0.55, p < 0.001) and p70S6K (r = 0.34, p = 0.021)]. In addition, the median recurrent time of patients from higher ciRS-7 level group was shorter than that of lower ciRS-7 group (18 vs. 25 months), but no significant difference was observed (p = 0.38)	MI0008947	J Cancer Res Clin Oncol 2017 Jan 143, 17-27 doi:10.1007/s00432-016-2256-7 PMID:27614453
842	LncRNA	MALAT1	miR-202	Gli2	Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;RNA immunoprecipitation	27887846	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression.	MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202. In addition, knockdown of Malat1 inhibited GC cells proliferation, S-phase cell number, and induced cell apoptosis via negatively regulating miR-202 in vitro.	MI0003130	Biomed Pharmacother 2017 Jan 85, 264-271 doi:10.1016/j.biopha.2016.11.014 PMID:27887846
843	LncRNA	H19	miR-200a	ZEB1	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000737	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
844	LncRNA	H19	miR-200a	ZEB2	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000737	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
845	LncRNA	H19	miR-200b	ZEB1	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000342	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
846	LncRNA	H19	miR-200b	ZEB2	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000342	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
847	LncRNA	H19	miR-200c	ZEB1	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000650	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
848	LncRNA	H19	miR-200c	ZEB2	Mg63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27008415	H19 Functions as a ceRNA in Promoting Metastasis Through Decreasing miR-200s Activity in Osteosarcoma.	We performed gain- and loss-of-function assays and found that H19 promotes migration and invasion in osteosarcoma cells. Furthermore, we showed that H19 promotes metastasis through upregulation of ZEB1 and ZEB2 by competitively binding the miR-200 family. 	MI0000650	DNA Cell Biol 2016 May 35, 235-40 doi:10.1089/dna.2015.3171 PMID:27008415
849	LncRNA	UCA1	miR-182	iASPP	U373Mg, T98Mg, Swo38, U251 And Shg44	Glioma	Homo sapiens (human)	luciferase reporter assays	28137422	The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP.	Upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation.	MI0000272	Arch Biochem Biophys 2017 Jun 1 623-624, 1-8 doi:10.1016/j.abb.2017.01.013 PMID:28137422
850	LncRNA	MHENCR	miR-425	IGF1	A375 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qRT-PCR;Western blot assay	28123636	Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway.	Functional experiments revealed that MHENCR knockdown significantly inhibited melanoma cells proliferation, induced cell cycle arrest and apoptosis, and also attenuated melanoma cells migration in vitro. Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.	MI0001448	Am J Transl Res 2017  9, 90-102,  PMID:28123636
851	LncRNA	MHENCR	miR-425	SPIN1	A375 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qRT-PCR;Western blot assay	28123636	Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway.	Functional experiments revealed that MHENCR knockdown significantly inhibited melanoma cells proliferation, induced cell cycle arrest and apoptosis, and also attenuated melanoma cells migration in vitro. Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.	MI0001448	Am J Transl Res 2017  9, 90-102,  PMID:28123636
852	LncRNA	MHENCR	miR-489	IGF1	A375 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qRT-PCR;Western blot assay	28123636	Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway.	Functional experiments revealed that MHENCR knockdown significantly inhibited melanoma cells proliferation, induced cell cycle arrest and apoptosis, and also attenuated melanoma cells migration in vitro. Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.	MI0003124	Am J Transl Res 2017  9, 90-102,  PMID:28123636
853	LncRNA	MHENCR	miR-489	SPIN1	A375 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qRT-PCR;Western blot assay	28123636	Long noncoding RNA MHENCR promotes melanoma progression via regulating miR-425/489-mediated PI3K-Akt pathway.	Functional experiments revealed that MHENCR knockdown significantly inhibited melanoma cells proliferation, induced cell cycle arrest and apoptosis, and also attenuated melanoma cells migration in vitro. Furthermore, we identified MHENCR as a competitively endogenous RNA, which specifically bound to miR-425 and miR-489, upregulated their target genes IGF1 and SPIN1 expression, and further activated PI3K-Akt pathway.	MI0003124	Am J Transl Res 2017  9, 90-102,  PMID:28123636
854	LncRNA	HOTAIR	miR-34a	Sox2	Mcf7,Mb231	Breast Cancer	Homo sapiens (human)	qRT-PCR	28122024	Long Non-Coding RNA HOTAIR Regulates the Proliferation, Self-Renewal Capacity, Tumor Formation and Migration of the Cancer Stem-Like Cell (CSC) Subpopulation Enriched from Breast Cancer Cells.	Full-length HOTAIR transcriptionally inhibits miR-34a specifically, leading to upregulation of Sox2, which is targeted by miR-34a. Ectopic introduction of miR-34a mimics reverses the effects of HOTAIR on the physiological processes of CSCs, indicating that HOTAIR affects these processes, including self-renewal capacity; these effects are dependent on the regulation of Sox2 via miR-34a	MI0000268	PLoS One 2017  12, e0170860 doi:10.1371/journal.pone.0170860 PMID:28122024
855	LncRNA	GAS5	miR-135b	NA	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	28117028	LncRNA GAS5 Inhibits Tumorigenesis and Enhances Radiosensitivity By Suppressing miR-135b Expression in Non-Small Cell Lung Cancer.	Luciferase reporter assay confirmed that GAS5 could directly target miR-135b and negatively regulate its expression. Moreover, rescue experiments demonstrated that miR-135b upregulation markedly abolished GAS5 overexpression-induced tumorigenesis inhibition and radiosensitivity improvement. 	MI0000810	Oncol Res 2017 Sep 21 25, 1305-1316 doi:10.3727/096504017x14850182723737 PMID:28117028
856	LncRNA	MTDH	miR-130b	PTEN	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Homo sapiens (human)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
857	LncRNA	MTDH	miR-130b	PPP2CA	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Homo sapiens (human)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
858	LncRNA	MTDH	miR-130b	SMAD7	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Homo sapiens (human)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
859	LncRNA	MTDH	miR-130b	PTEN	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Mus musculus (mouse)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
860	LncRNA	MTDH	miR-130b	PPP2CA	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Mus musculus (mouse)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
861	LncRNA	MTDH	miR-130b	SMAD7	U87, U251, T98G, Shg44, Ln229 And Hek293T	Glioma	Mus musculus (mouse)	qRT-PCR;Western blot assay	28107197	MTDH promotes glioma invasion through regulating miR-130b-ceRNAs.	MTDH upregulated miR-130b transcription via acting as a coactivator of NF-kB. MiR-130b promoted EMT-like change and invasion of glioma cells through targeting multiple EMT-related genes, including PTEN, PPP2CA and SMAD7. In addition, PTEN acted as the competing endogenous RNA (ceRNA) to affect PPP2CA and SMAD7 expression, and inhibited EMT-like change in glioma cells. Furthermore, miR-130b mediated EMT-like change induced by MTDH, and MTDH inhibited the expression levels of PTEN, PPP2CA and SMAD7.	MI0000748	Oncotarget 2017 Mar 14 8, 17738-17749 doi:10.18632/oncotarget.14717 PMID:28107197
862	LncRNA	H19	let-7	LIN28	Mda-Mb-231, Sk-Br-3 And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	28102845	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.	We found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples. Intriguingly, this gain of LIN28 expression can also feedback to reverse the H19 loss-mediated suppression of BCSC properties.	MI0000060	Cell Death Dis 2017 Jan 19 8, e2569 doi:10.1038/cddis.2016.438 PMID:28102845
863	LncRNA	H19	let-7	LIN28	Mda-Mb-231, Sk-Br-3 And Mcf-7	Breast Cancer	Mus musculus (mouse)	luciferase reporter assays	28102845	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.	We found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples. Intriguingly, this gain of LIN28 expression can also feedback to reverse the H19 loss-mediated suppression of BCSC properties.	MI0000060	Cell Death Dis 2017 Jan 19 8, e2569 doi:10.1038/cddis.2016.438 PMID:28102845
864	LncRNA	CRNDE	miR-181a-5p	TCF4	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
865	LncRNA	CRNDE	miR-181a-5p	Wnt	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
866	LncRNA	CRNDE	miR-181a-5p	b-catenin	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
867	LncRNA	CRNDE	miR-181a-5p	TCF4	Hct116 And Sw480	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
868	LncRNA	CRNDE	miR-181a-5p	Wnt	Hct116 And Sw480	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
869	LncRNA	CRNDE	miR-181a-5p	b-catenin	Hct116 And Sw480	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/b-catenin signaling.	CRNDE knockdown and miR-181a-5p overexpression in CRC cell lines led to inhibited cell proliferation and reduced chemoresistance. We also determined that b-catenin and TCF4 were inhibitory targets of miR-181a-5p, and that Wnt/b-catenin signaling was inhibited by both CRNDE knockdown and miR-181a-5p overexpression. 	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
870	LncRNA	LINC00152	miR-138	HIF1A	Gbc-Sd, Noz	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28077595	Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1a via miR-138.	In vivo, LINC00152 overexpression significantly promoted tumour peritoneal spreading and metastasis. Mechanistic analyses indicated that LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of hypoxia inducible factor-1a (HIF-1a). We revealed that miR-138 is a suppressor of GBC cell metastasis and EMT progression, and a similar phenomenon was observed in HIF-1a knockdown NOZ cells.	MI0000455	Open Biol 2017 Jan 7 doi:10.1098/rsob.160247 PMID:28077595
871	LncRNA	LINC00152	miR-138	HIF1A	Gbc-Sd, Noz	Gallbladder Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28077595	Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1a via miR-138.	In vivo, LINC00152 overexpression significantly promoted tumour peritoneal spreading and metastasis. Mechanistic analyses indicated that LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of hypoxia inducible factor-1a (HIF-1a). We revealed that miR-138 is a suppressor of GBC cell metastasis and EMT progression, and a similar phenomenon was observed in HIF-1a knockdown NOZ cells.	MI0000455	Open Biol 2017 Jan 7 doi:10.1098/rsob.160247 PMID:28077595
872	LncRNA	ZEB1-AS1	miR-200a	ZEB1	Hos And Saos-2	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000737	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
873	LncRNA	ZEB1-AS1	miR-200b	ZEB1	Hos And Saos-2	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000342	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
874	LncRNA	ZEB1-AS1	miR-200c	ZEB1	Hos And Saos-2	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000650	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
875	LncRNA	ZEB1-AS1	miR-141	ZEB1	Hos And Saos-2	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000457	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
876	LncRNA	ZEB1-AS1	miR-429	ZEB1	Hos And Saos-2	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0001641	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
877	LncRNA	ZEB1-AS1	miR-200a	ZEB1	Hos And Saos-2	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000737	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
878	LncRNA	ZEB1-AS1	miR-200b	ZEB1	Hos And Saos-2	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000342	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
879	LncRNA	ZEB1-AS1	miR-200c	ZEB1	Hos And Saos-2	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000650	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
880	LncRNA	ZEB1-AS1	miR-141	ZEB1	Hos And Saos-2	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0000457	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
881	LncRNA	ZEB1-AS1	miR-429	ZEB1	Hos And Saos-2	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	28075045	Interplay Between Long Noncoding RNA ZEB1-AS1 and miR-200s Regulates Osteosarcoma Cell Proliferation and Migration.	Functional experiments showed that consistent with ZEB1-AS1 depletion, miR-200s overexpression and ZEB1 depletion both inhibit osteosarcoma cell proliferation and migration. Overexpression of miR-200s partially abolished the effects of ZEB1-AS1 on osteosarcoma cell proliferation and migration. Moreover, the combination of ZEB1-AS1 depletion and miR-200s overexpression significantly inhibits osteosarcoma cell proliferation and migration. In conclusion, this study revealed a novel regulatory mechanism between ZEB1-AS1, miR-200s, and ZEB1.	MI0001641	J Cell Biochem 2017 Aug 118, 2250-2260 doi:10.1002/jcb.25879 PMID:28075045
882	LncRNA	SNHG12	miR-199a-5p	MLK3	Hcc Cell Lines	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay,ChIRP assay	28073380	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma.	SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues. There were direct interactions between miR-199a/b-5p and the binding site of SNHG12. SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-kB pathway.	MIMAT0000231	J Exp Clin Cancer Res 2017 Jan 10 36, 11 doi:10.1186/s13046-016-0486-9 PMID:28073380
883	LncRNA	SNHG12	miR-199b-5p	MLK3	Hcc Cell Lines	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay,ChIRP assay	28073380	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma.	SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues. There were direct interactions between miR-199a/b-5p and the binding site of SNHG12. SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-kB pathway.	MIMAT0000263	J Exp Clin Cancer Res 2017 Jan 10 36, 11 doi:10.1186/s13046-016-0486-9 PMID:28073380
884	LncRNA	MALAT1	miR-218	EZH2	Ht29, Sw480, Sw620	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28069878	MALAT1 Is Associated with Poor Response to Oxaliplatin-Based Chemotherapy in Colorectal Cancer Patients and Promotes Chemoresistance through EZH2.	LncRNA MALAT1 knockdown enhances E-cadherin expression and inhibits oxaliplatin-induced EMT in colorectal cancer cells. EZH2 is highly expressed and associated with the 3' end region of lncRNA MALAT1 in colorectal cancer, and this association suppressed the expression of E-cadherin. Furthermore, targeted inhibition of MALAT1 or EZH2 reversed EMT and chemoresistance induced by oxaliplatin.	MI0000294	Mol Cancer Ther 2017 Apr 16, 739-751 doi:10.1158/1535-7163.Mct-16-0591 PMID:28069878
885	Circular RNA	Circ100284	miR-217	EZH2	Keratinocyte Cells	Carcinogenesis	Homo sapiens (human)	qRT-PCR;Western blot assay	28062277	Circ100284, via miR-217 regulation of EZH2, is involved in the arsenite-accelerated cell cycle of human keratinocytes in carcinogenesis.	Knockdown of circ100284 with siRNA inhibited the cell cycle acceleration induced by arsenite, but this inhibition was reversed by co-transfection with circ100284 siRNA and by a miR-217 inhibitor. Knockdown of circ100284 with siRNA or transfected with miR-217 mimic inhibited the capacity of T-HaCaT cells for colony formation, invasion, and migration, effects that were reversed by co-transfection with a miR-217 inhibitor or by epigenetic expression of EZH2. These results suggest that, in HaCaT cells, arsenite increases circ100284 levels, which act as a sponge for miR-217 and up-regulate the miR-217 target, EZH2, which, in turn, up-regulates cyclin D1and CDK4, and thus accelerates the cell cycle and leads to malignant transformation. 	MI0000293	Biochim Biophys Acta Mol Basis Dis 2017 Mar 1863, 753-763 doi:10.1016/j.bbadis.2016.12.018 PMID:28062277
886	Artifically engineered RNA	miR-199-sponge	miR-199a-5p	PGC1A	Mouse Heart	Physiological Cardiac Hypertrophy	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26976621	miR-199-sponge transgenic mice develop physiological cardiac hypertrophy.	We generated a sponge transgenic mouse model with a specific disruption of miR-199 in the heart. To our surprise, we found that knockdown of endogenous miR-199 caused physiological cardiac hypertrophy characterized by an increased heart weight and cardiomyocyte size, but with normal cardiac morphology and function. Furthermore, we also identified PGC1a as the target gene of the miR-199 family, and PGC1a was also increased in sponge transgenic mice.	MIMAT0000231	Cardiovasc Res 2016 May 15 110, 258-67 doi:10.1093/cvr/cvw052 PMID:26976621
887	Artifically engineered RNA	miR-199-sponge	miR-199a-5p	PGC1A	Mouse Heart	Physiological Cardiac Hypertrophy	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26976621	miR-199-sponge transgenic mice develop physiological cardiac hypertrophy.	We generated a sponge transgenic mouse model with a specific disruption of miR-199 in the heart. To our surprise, we found that knockdown of endogenous miR-199 caused physiological cardiac hypertrophy characterized by an increased heart weight and cardiomyocyte size, but with normal cardiac morphology and function. Furthermore, we also identified PGC1a as the target gene of the miR-199 family, and PGC1a was also increased in sponge transgenic mice.	MIMAT0000231	Cardiovasc Res 2016 May 15 110, 258-67 doi:10.1093/cvr/cvw052 PMID:26976621
888	LncRNA	XIST	miR-144	Titin	Trophoblast Cells	Proliferation And Invasion Of Ht Cells 	Homo sapiens (human)	luciferase reporter assays	28059474	CsA Promotes XIST Expression to Regulate Human Trophoblast Cells Proliferation and Invasion Through miR-144/Titin Axis.	XIST and miR-144 reciprocally inhibited each other in HT cells; as exhibited by luciferase reporter gene assays, miR-144 bind to XIST by direct targeting. XIST suppressed miR-144 expression to promote titin expression. As exhibited by the Spearman's correlation analysis, in CsA treated HT cells, miR-144 was inversely correlated with titin and XIST, respectively; XIST was positively correlated with titin.	MI0000460	J Cell Biochem 2017 Aug 118, 2208-2218 doi:10.1002/jcb.25867 PMID:28059474
889	LncRNA	TUG1	miR-9	MTHFD2	Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	28053623	LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells.	TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of MCF-7 cells. The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells.	MI0000466	J Breast Cancer 2016 Dec 19, 349-357 doi:10.4048/jbc.2016.19.4.349 PMID:28053623
890	LncRNA	SPRY4-IT1	miR-101-3p	EZH2	Ej, Umuc3 And T24T	Bladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27998761	LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2.	knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression.	MIMAT0000099	Cancer Lett 2017 Mar 1 388, 281-291 doi:10.1016/j.canlet.2016.12.005 PMID:27998761
891	LncRNA	SPRY4-IT1	miR-101-3p	EZH2	Ej, Umuc3 And T24T	Bladder Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27998761	LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2.	knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression.	MIMAT0000099	Cancer Lett 2017 Mar 1 388, 281-291 doi:10.1016/j.canlet.2016.12.005 PMID:27998761
892	Circular RNA	CircPVT1	miR-125a	E2F2	Mgc-803 And Ags	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays	27986464	Circular RNA profile identifies circPVT1 as a proliferative factor and prognostic marker in gastric cancer.	The expression of circPVT1 is often upregulated in GC tissues due to the amplification of its genomic locus. circPVT1 may promote cell proliferation by acting as a sponge for members of the miR-125 family. The level of circPVT1 was observed as an independent prognostic marker for overall survival and disease-free survival of patients with GC.	MI0000469	Cancer Lett 2017 Mar 1 388, 208-219 doi:10.1016/j.canlet.2016.12.006 PMID:27986464
893	Circular RNA	CircPVT1	miR-125b	E2F2	Mgc-803 And Ags	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays	27986464	Circular RNA profile identifies circPVT1 as a proliferative factor and prognostic marker in gastric cancer.	The expression of circPVT1 is often upregulated in GC tissues due to the amplification of its genomic locus. circPVT1 may promote cell proliferation by acting as a sponge for members of the miR-125 family. The level of circPVT1 was observed as an independent prognostic marker for overall survival and disease-free survival of patients with GC.	MI0000446	Cancer Lett 2017 Mar 1 388, 208-219 doi:10.1016/j.canlet.2016.12.006 PMID:27986464
894	LncRNA	TUG1	miR-145-5p	NA	Bgc-823 And Sgc-7901	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays	27983921	Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p.	 The biological function of TUG1 and miR-145-5p in GC cell proliferation and invasion in vitro and tumor growth in vivo was investigated by MTT assay, Transwell invasion assay, and tumor xenograft experiments. The regulating relationship between TUG1 and miR-145-5 was confirmed by luciferase reporter assay. 	MIMAT0000437	Oncol Res 2017 May 24 25, 789-798 doi:10.3727/096504016x14783677992682 PMID:27983921
895	LncRNA	H19	miR-675	NA	U251 And U87	Glioma	Homo sapiens (human)	qRT-PCR	27981546	LncRNA H19 is overexpressed in glioma tissue, is negatively associated with patient survival, and promotes tumor growth through its derivative miR-675.	In cell culture experiments, silencing of lncRNA H19 diminished proliferation of glioma cell lines. These effects of lncRNA H19 appeared to be intermediated by miR-675. The latter was overexpressed in glioma tissue and was negatively associated with patient survival. Supporting the involvement of miR-675, its antagomir decreased proliferation of glioma cell lines, whereas its mimic increased proliferation of NHA cells.	MI0005416	Eur Rev Med Pharmacol Sci 2016 Dec 20, 4891-4897,  PMID:27981546
896	LncRNA	MALAT1	miR-183	ITGB1	A375, C32, Edmel3, G361, Hbl, Wm1115, Sk-Mel-1, M14, Mv3, A875, M2	Melanoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27966454	Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation.	Decreased level of miR-183 was relevant to poor overall survival, while miR-183 up-regulation resulted in a marked suppression of cell growth in vitro and in vivo. We further found that the expression and function of miR-183 were suppressed by MALAT1. Integrin b1 (ITGB1) was then speculated and confirmed as a direct target of miR-183. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1. 	MI0000273	Oncotarget 2017 Jan 10 8, 3509-3518 doi:10.18632/oncotarget.13862 PMID:27966454
897	Coding-mRNA	KDM4A	miR-137	NA	Pancreatic Cancer Tissues	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26904954	miR-137 Modulates a Tumor Suppressor Network-Inducing Senescence in Pancreatic Cancer Cells.	Restoring the KDM4A expression contributed to bypass of miR-137-induced senescence and inhibition of endogenous miR-137 with an miRNA sponge-compromised Ras-induced senescence. miR-137 levels are significantly reduced in human pancreatic tumors, consistent with previous studies revealing a defective senescence response in this cancer type. Restoration of miR-137 expression inhibited proliferation and promoted senescence of pancreatic cancer cells.	MI0000454	Cell Rep 2016 Mar 1 14, 1966-78 doi:10.1016/j.celrep.2016.01.068 PMID:26904954
898	Artifically engineered RNA	Ad-miR-221-SP	miR-221	NA	Vascular Smooth Muscle Cell	Vein Graft Neointimal Hyperplasia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26828387	MicroRNA-221 sponge therapy attenuates neointimal hyperplasia and improves blood flows in vein grafts.	miR-221 sponges can significantly decrease the expression of miR-221 and proliferation in cultured VSMC. Cellular proliferation rates were significantly reduced in miR-221 sponge treated grafts as compared with controls at 6 weeks after bypass surgery (19.8% versus 43.6%, P=0.0028). miR-221 sponge gene transfer reduced the neointimal area (210.75 ± 24.13 versus 67.01 ± 12.02, P<0.0001), neointimal thickness (171.86 ± 27.87 versus 64.13 ± 16.23, P<0.0001) and neointima/media ratio (0.74 ± 0.21 versus 1.95 ± 0.25, P<0.0001) in vein grafts versus controls.	MI0000298	Int J Cardiol 2016 Apr 1 208, 79-86 doi:10.1016/j.ijcard.2016.01.006 PMID:26828387
899	Viral RNA	HBx-LINE1	miR-122	NA	Mouse Liver Cell	Liver Injury	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Northern blot assay	26409216	Hepatitis B virus-human chimeric transcript HBx-LINE1 promotes hepatic injury via sequestering cellular microRNA-122.	HBx-LINE1 in HBV-positive HCC tissues was inversely correlated with miR-122. Each HBx-LINE1 consists of six miR-122-binding sites, and forced expression of HBx-LINE1 effectively depleted cellular miR-122, promoting hepatic cell epithelial-mesenchymal transition (EMT)-like changes, including b-catenin signaling activation, E-cadherin reduction and cell migration enhancement. Mice administered with HBx-LINE1 display a significant mouse liver cell abnormal mitosis and hepatic injury.	MI0000442	J Hepatol 2016 Feb 64, 278-291 doi:10.1016/j.jhep.2015.09.013 PMID:26409216
900	Viral RNA	HBx-LINE1	miR-122	NA	Mouse Liver Cell	Liver Injury	Hepatitis B virus (HBV)	luciferase reporter assays;qRT-PCR;Northern blot assay	26409216	Hepatitis B virus-human chimeric transcript HBx-LINE1 promotes hepatic injury via sequestering cellular microRNA-122.	HBx-LINE1 in HBV-positive HCC tissues was inversely correlated with miR-122. Each HBx-LINE1 consists of six miR-122-binding sites, and forced expression of HBx-LINE1 effectively depleted cellular miR-122, promoting hepatic cell epithelial-mesenchymal transition (EMT)-like changes, including b-catenin signaling activation, E-cadherin reduction and cell migration enhancement. Mice administered with HBx-LINE1 display a significant mouse liver cell abnormal mitosis and hepatic injury.	MI0000442	J Hepatol 2016 Feb 64, 278-291 doi:10.1016/j.jhep.2015.09.013 PMID:26409216
901	Artifically engineered RNA	miR-130a sponge	miR-130a	NA	Ht126	Colon Cancer	Homo sapiens (human)	vector transfection	27974852	Four microRNAs Signature for Survival Prognosis in Colon Cancer using TCGA Data.	We used HT126 colon cancer cells in the study to explore the anti-cancer effects of miR-130a sponge. In the study, cell growth assay showed miR-130a sponge inhibited colon cancer cells growth in a dose dependent manner in 96h. When it combined with anti-cancer drug 5-FU, the miR-130a sponge sensitized the anti-cancer drug effect of 5-FU to block cancer cell growth in 96h.	MI0000448	Sci Rep 2016 Dec 15 6, 38306 doi:10.1038/srep38306 PMID:27974852
902	Circular RNA	HRCR	miR-223	ARC	Adult Male C57Bl/6 Mice	Heart Failure	Mus musculus (mouse)	qRT-PCR;Western blot assay	26802132	A circular RNA protects the heart from pathological hypertrophy and heart failure by targeting miR-223.	miR-223 transgenic mice developed cardiac hypertrophy and heart failure, whereas miR-223-deficient mice were protected from hypertrophic stimuli, indicating that miR-223 acts as a positive regulator of cardiac hypertrophy. We identified ARC as a miR-223 downstream target to mediate the function of miR-223 in cardiac hypertrophy. Apoptosis repressor with CARD domain transgenic mice showed reduced hypertrophic responses. Further, we found that a circRNA HRCR functions as an endogenous miR-223 sponge to sequester and inhibit miR-223 activity, which resulted in the increase of ARC expression.	MI0000300	Eur Heart J 2016 Sep 1 37, 2602-11 doi:10.1093/eurheartj/ehv713 PMID:26802132
903	LncRNA	XIST	miR-497	MACC1	Sgc-7901, Bgc-823, Hgc-27 And Mkn-28	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27911852	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.	We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis.	MI0003138	Oncotarget 2017 Jan 17 8, 4125-4135 doi:10.18632/oncotarget.13670 PMID:27911852
904	LncRNA	XIST	miR-497	MACC1	Sgc-7901, Bgc-823, Hgc-27 And Mkn-28	Gastric Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27911852	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.	We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis.	MI0003138	Oncotarget 2017 Jan 17 8, 4125-4135 doi:10.18632/oncotarget.13670 PMID:27911852
905	LncRNA	RMRP	miR-206	KRAS	A549, Spc-A1, H1299 And H23	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27906963	LncRNA-RMRP Acts as an Oncogene in Lung Cancer.	Overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	MI0000490	PLoS One 2016  11, e0164845 doi:10.1371/journal.pone.0164845 PMID:27906963
906	LncRNA	RMRP	miR-206	FMNL2	A549, Spc-A1, H1299 And H23	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27906963	LncRNA-RMRP Acts as an Oncogene in Lung Cancer.	Overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	MI0000490	PLoS One 2016  11, e0164845 doi:10.1371/journal.pone.0164845 PMID:27906963
907	LncRNA	RMRP	miR-206	SOX9	A549, Spc-A1, H1299 And H23	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27906963	LncRNA-RMRP Acts as an Oncogene in Lung Cancer.	Overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration. Our data proved that RMRP acted as an oncogene LncRNA to promote the expression of KRAS, FMNL2 and SOX9 by inhibiting miR-206 expression in lung cancer.	MI0000490	PLoS One 2016  11, e0164845 doi:10.1371/journal.pone.0164845 PMID:27906963
908	LncRNA	MALAT1	miR-155	FBXW7	U87 And Shg139	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27904771	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function.	MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. The miR-155-induced tumorigenesis is mediated through FBXW7 function. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway. 	MI0000681	Am J Cancer Res 2016  6, 2561-2574,  PMID:27904771
909	Circular RNA	ZNF609	miR-150-5p	AKT3	293, Sh-Sy5Y	Hirschsprungs Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27903978	Circular RNA ZNF609 functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-150-5p in Hirschsprung's disease.	Suppression of cir-ZNF609 inhibited the proliferation and migration of cells. We screened out several putative cir-ZNF609 ceRNAs of which the AKT3 transcript was selected. RNA immunoprecipitation and luciferase reporter assays demonstrated that cir-ZNF609 may act as a sponge for miR-150-5p to modulate the expression of AKT3.	MIMAT0000451	Oncotarget 2017 Jan 3 8, 808-818 doi:10.18632/oncotarget.13656 PMID:27903978
910	Circular RNA	ZNF609	miR-150-5p	AKT3	293, Sh-Sy5Y	Hirschsprungs Disease	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27903978	Circular RNA ZNF609 functions as a competitive endogenous RNA to regulate AKT3 expression by sponging miR-150-5p in Hirschsprung's disease.	Suppression of cir-ZNF609 inhibited the proliferation and migration of cells. We screened out several putative cir-ZNF609 ceRNAs of which the AKT3 transcript was selected. RNA immunoprecipitation and luciferase reporter assays demonstrated that cir-ZNF609 may act as a sponge for miR-150-5p to modulate the expression of AKT3.	MIMAT0000451	Oncotarget 2017 Jan 3 8, 808-818 doi:10.18632/oncotarget.13656 PMID:27903978
911	LncRNA	HOTAIR	miR-1	NA	Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27895772	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.	The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1. 	MI0000651	Oncol Lett 2016 Nov 12, 4061-4067 doi:10.3892/ol.2016.5127 PMID:27895772
912	LncRNA	HOTAIR	miR-1	NA	Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27895772	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.	The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells, which suggests that HOTAIR harbors a miRNA-1 binding site. The present data revealed that this binding site is vital for the regulation of miRNA-1 by HOTAIR. Furthermore, HOTAIR negatively regulated the expression of miRNA-1 in HepG2 cells. Additionally, the present study demonstrated that the oncogenic activity of HOTAIR is in part based on the negative regulation of miR-1. 	MI0000651	Oncol Lett 2016 Nov 12, 4061-4067 doi:10.3892/ol.2016.5127 PMID:27895772
913	LncRNA	H19	miR-29b-3p	TGFB1	Mouse Tendon Defect Model	Tendon Injures	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27895107	Long noncoding RNA H19 accelerates tenogenic differentiation and promotes tendon healing through targeting miR-29b-3p and activating TGF-b1 signaling.	Stable overexpression of H19 significantly accelerated TGF-b1-induced tenogenic differentiation in vitro and accelerated tendon healing in a mouse tendon defect model. H19 directly targeted miR-29b-3p, which is considered to be a negative regulator of tenogenesis. Furthermore, miR-29b-3p directly suppressed the expression of TGF-b1 and type I collagen, thereby forming a novel regulatory feedback loop between H19 and TGF-b1 to mediate tenogenic differentiation. 	MIMAT0000100	Faseb j 2017 Mar 31, 954-964 doi:10.1096/fj.201600722R PMID:27895107
914	LncRNA	H19	miR-29b-3p	TGFB1	Mouse Tendon Defect Model	Tendon Injures	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27895107	Long noncoding RNA H19 accelerates tenogenic differentiation and promotes tendon healing through targeting miR-29b-3p and activating TGF-b1 signaling.	Stable overexpression of H19 significantly accelerated TGF-b1-induced tenogenic differentiation in vitro and accelerated tendon healing in a mouse tendon defect model. H19 directly targeted miR-29b-3p, which is considered to be a negative regulator of tenogenesis. Furthermore, miR-29b-3p directly suppressed the expression of TGF-b1 and type I collagen, thereby forming a novel regulatory feedback loop between H19 and TGF-b1 to mediate tenogenic differentiation. 	MIMAT0000100	Faseb j 2017 Mar 31, 954-964 doi:10.1096/fj.201600722R PMID:27895107
915	LncRNA	5-Mar	miR-30a	SMAD2	Skov3, A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27875077	MARCH5 RNA promotes autophagy, migration, and invasion of ovarian cancer cells.	Mechanistic investigations revealed that MARCH5 RNA may function as a competing endogenous RNA (ceRNA) to regulate the expression of SMAD2 and ATG5 by competing for MIR30A. Knocking down SMAD2 or ATG5 can block the effect of MARCH5 in A2780 cells. Also, silencing the expression of MARCH5 in SKOV3 cells can inhibit the TGFB1-SMAD2/3 pathway. In contrast, the ectopic expression of MARCH5 in A2780 cells can activate the TGFB1-SMAD2/3 pathway. In turn, the TGFB1-SMAD2/3 pathway can regulate MARCH5 and ATG5 through MIR30A.	MI0000088	Autophagy 2017 Feb 13, 333-344 doi:10.1080/15548627.2016.1256520 PMID:27875077
916	LncRNA	5-Mar	miR-30a	ATG5	Skov3, A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27875077	MARCH5 RNA promotes autophagy, migration, and invasion of ovarian cancer cells.	Mechanistic investigations revealed that MARCH5 RNA may function as a competing endogenous RNA (ceRNA) to regulate the expression of SMAD2 and ATG5 by competing for MIR30A. Knocking down SMAD2 or ATG5 can block the effect of MARCH5 in A2780 cells. Also, silencing the expression of MARCH5 in SKOV3 cells can inhibit the TGFB1-SMAD2/3 pathway. In contrast, the ectopic expression of MARCH5 in A2780 cells can activate the TGFB1-SMAD2/3 pathway. In turn, the TGFB1-SMAD2/3 pathway can regulate MARCH5 and ATG5 through MIR30A.	MI0000088	Autophagy 2017 Feb 13, 333-344 doi:10.1080/15548627.2016.1256520 PMID:27875077
917	LncRNA	5-Mar	miR-30a	SMAD2	Skov3, A2780	Ovarian Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	27875077	MARCH5 RNA promotes autophagy, migration, and invasion of ovarian cancer cells.	Mechanistic investigations revealed that MARCH5 RNA may function as a competing endogenous RNA (ceRNA) to regulate the expression of SMAD2 and ATG5 by competing for MIR30A. Knocking down SMAD2 or ATG5 can block the effect of MARCH5 in A2780 cells. Also, silencing the expression of MARCH5 in SKOV3 cells can inhibit the TGFB1-SMAD2/3 pathway. In contrast, the ectopic expression of MARCH5 in A2780 cells can activate the TGFB1-SMAD2/3 pathway. In turn, the TGFB1-SMAD2/3 pathway can regulate MARCH5 and ATG5 through MIR30A.	MI0000088	Autophagy 2017 Feb 13, 333-344 doi:10.1080/15548627.2016.1256520 PMID:27875077
918	LncRNA	5-Mar	miR-30a	ATG5	Skov3, A2780	Ovarian Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	27875077	MARCH5 RNA promotes autophagy, migration, and invasion of ovarian cancer cells.	Mechanistic investigations revealed that MARCH5 RNA may function as a competing endogenous RNA (ceRNA) to regulate the expression of SMAD2 and ATG5 by competing for MIR30A. Knocking down SMAD2 or ATG5 can block the effect of MARCH5 in A2780 cells. Also, silencing the expression of MARCH5 in SKOV3 cells can inhibit the TGFB1-SMAD2/3 pathway. In contrast, the ectopic expression of MARCH5 in A2780 cells can activate the TGFB1-SMAD2/3 pathway. In turn, the TGFB1-SMAD2/3 pathway can regulate MARCH5 and ATG5 through MIR30A.	MI0000088	Autophagy 2017 Feb 13, 333-344 doi:10.1080/15548627.2016.1256520 PMID:27875077
919	LncRNA	SNHG5	miR-32	KLF4	Sgc-7901 And Mgc-803	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27871067	The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.	KLF4 suppression by miR-32 could be partially rescued by SNHG5 overexpression, whereas miR-32 mimic rescued SNHG5 overexpression-mediated suppression of GC cell migration. In addition, we identified a negative correlation between the expression of SNHG5 and miR-32 in GC tissues. Furthermore, KLF4 expression was significantly downregulated in GC specimens, and a negative correlation between miR-32 and KLF4 expression and a positive correlation between KLF4 and SNHG5 expression levels were detected.	MI0000090	Faseb j 2017 Mar 31, 893-903 doi:10.1096/fj.201600994R PMID:27871067
920	LncRNA	AF147447	miR-34c	MUC2	7901 And Mkn45	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27835575	Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c.	LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression. We also found that transcription factor E2F1 could be recruited to lncRNA AF147447 promoter by RNA immunoprecipatation and RNA pull down assays. These findings support a role of lncRNA AF147447 in tumor suppression.	MI0000743	Oncotarget 2016 Dec 13 7, 82770-82782 doi:10.18632/oncotarget.13165 PMID:27835575
921	LncRNA	GAS5	miR-23a	MT2A	Bgc-823 And Mgc-803	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27827524	Long non-coding RNA GAS5 acts as a molecular sponge to regulate miR-23a in gastric cancer.	GAS5 negatively regulated miR-23a expression in GC cells. The bio-informatics prediction showed putative miR-23a binding sites within GAS5 transcripts. Furthermore, our data indicated the positive regulation of GAS5 on the miR-23a target, MT2A, wherein GAS5 suppressed the negative regulation of miR-23a on MT2A by binding its 3'UTR. Additionally, the expression of MT2A was also decreased in GC tissues, showing a positive or negative correlation with GAS5 or miR-23a, respectively.	MI0000079	Minerva Med 2016 Nov 9,   PMID:27827524
922	LncRNA	HOTAIR	miR-1	CCND1	Kyse30, Kyse140, Kyse150, Kyse180, Kyse410, And Kyse510	Esophageal Squamous Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27816685	Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma.	HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. 	MI0000651	Transl Oncol 2016 Dec 9, 489-497 doi:10.1016/j.tranon.2016.09.005 PMID:27816685
923	LncRNA	HOTAIR	miR-1	CCND1	Kyse30, Kyse140, Kyse150, Kyse180, Kyse410, And Kyse510	Esophageal Squamous Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27816685	Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma.	HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. 	MI0000651	Transl Oncol 2016 Dec 9, 489-497 doi:10.1016/j.tranon.2016.09.005 PMID:27816685
924	LncRNA	EWSAT1	miR-326	CCND1	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27816050	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters. 	MI0000808	Aging (Albany NY) 2016 Nov 3 8, 2948-2960 doi:10.18632/aging.101103 PMID:27816050
925	LncRNA	EWSAT1	miR-330-5p	CCND1	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27816050	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters. 	MIMAT0004693	Aging (Albany NY) 2016 Nov 3 8, 2948-2960 doi:10.18632/aging.101103 PMID:27816050
926	LncRNA	H19	let-7	StAR	Hek293	Ovarian Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27813675	The Steroidogenic Acute Regulatory Protein (StAR) Is Regulated by the H19/let-7 Axis.	Using human and murine cell lines, we show that overexpression of H19 stimulates StAR expression by antagonizing let-7, which inhibits StAR at the post-transcriptional level. Our results uncover a novel mechanism underlying the regulation of StAR expression and represent the first example of lncRNA-mediated control of the rate-limiting step of steroidogenesis.	MI0000060	Endocrinology 2017 Feb 1 158, 402-409 doi:10.1210/en.2016-1340 PMID:27813675
927	LncRNA	H19	let-7	StAR	Hek293	Ovarian Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27813675	The Steroidogenic Acute Regulatory Protein (StAR) Is Regulated by the H19/let-7 Axis.	Using human and murine cell lines, we show that overexpression of H19 stimulates StAR expression by antagonizing let-7, which inhibits StAR at the post-transcriptional level. Our results uncover a novel mechanism underlying the regulation of StAR expression and represent the first example of lncRNA-mediated control of the rate-limiting step of steroidogenesis.	MI0000060	Endocrinology 2017 Feb 1 158, 402-409 doi:10.1210/en.2016-1340 PMID:27813675
928	LncRNA	PVT1	miR-195	BCL2	Khos, 143B, Lm7, U2Os, And Mg-63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27813492	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.	The interaction between PVT1 and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PVT1 negatively regulated miR-195 in osteosarcoma cells. Simultaneously, we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells. Moreover, silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT11-induced apoptosis of U2OS cells.	MI0000489	Oncotarget 2016 Dec 13 7, 82620-82633 doi:10.18632/oncotarget.13012 PMID:27813492
929	LncRNA	PVT1	miR-195	CCND1	Khos, 143B, Lm7, U2Os, And Mg-63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27813492	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.	The interaction between PVT1 and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PVT1 negatively regulated miR-195 in osteosarcoma cells. Simultaneously, we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells. Moreover, silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT11-induced apoptosis of U2OS cells.	MI0000489	Oncotarget 2016 Dec 13 7, 82620-82633 doi:10.18632/oncotarget.13012 PMID:27813492
930	LncRNA	PVT1	miR-195	FASN	Khos, 143B, Lm7, U2Os, And Mg-63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27813492	Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195.	The interaction between PVT1 and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PVT1 negatively regulated miR-195 in osteosarcoma cells. Simultaneously, we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells. Moreover, silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT11-induced apoptosis of U2OS cells.	MI0000489	Oncotarget 2016 Dec 13 7, 82620-82633 doi:10.18632/oncotarget.13012 PMID:27813492
931	LncRNA	GAS5	miR-2467-5p	NODAL	EMbryonic Stem Cells	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0019952	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
932	LncRNA	GAS5	miR-3200-3p	NODAL	EMbryonic Stem Cells	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0015085	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
933	LncRNA	GAS5	let-7a	NODAL	EMbryonic Stem Cells	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MI0000060	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
934	LncRNA	GAS5	let-7e-5p	NODAL	EMbryonic Stem Cells	NA	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0000066	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
935	LncRNA	GAS5	miR-2467-5p	NODAL	EMbryonic Stem Cells	NA	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0019952	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
936	LncRNA	GAS5	miR-3200-3p	NODAL	EMbryonic Stem Cells	NA	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0015085	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
937	LncRNA	GAS5	let-7a	NODAL	EMbryonic Stem Cells	NA	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MI0000060	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
938	LncRNA	GAS5	let-7e-5p	NODAL	EMbryonic Stem Cells	NA	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27811843	Long non-coding RNA GAS5 controls human embryonic stem cell self-renewal by maintaining NODAL signalling.	Phenotypic analysis shows that GAS5 knockdown significantly impairs hESC self-renewal, but its overexpression significantly promotes hESC self-renewal. Using RNA sequencing and functional analysis, we demonstrate that GAS5 maintains NODAL signalling by protecting NODAL expression from miRNA-mediated degradation. Therefore, we propose that the above pluripotency factors, GAS5 and NODAL form a feed-forward signalling loop that maintains hESC self-renewal. 	MIMAT0000066	Nat Commun 2016 Nov 4 7, 13287 doi:10.1038/ncomms13287 PMID:27811843
939	LncRNA	H19	let-7a	IL6	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000060	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
940	LncRNA	H19	let-7b	IL6	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000063	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
941	LncRNA	HULC	miR-372	IL6	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000780	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
942	LncRNA	HULC	miR-373	IL6	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000781	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
943	LncRNA	H19	let-7a	CXCR4	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000060	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
944	LncRNA	H19	let-7b	CXCR4	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000063	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
945	LncRNA	HULC	miR-372	CXCR4	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000780	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
946	LncRNA	HULC	miR-373	CXCR4	Rbe Human Cholangiocarcinoma Cells And Hek293T 	Cholangiocarcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner.	H19 and HULC promoted cholangiocyte migration and invasion via the inflammation pathway. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000781	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
947	LncRNA	HOXA11-AS	miR-1297	E2F1	Gastric Cell Lines	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27651312	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1.	HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells.	MI0006358	Cancer Res 2016 Nov 1 76, 6299-6310 doi:10.1158/0008-5472.Can-16-0356 PMID:27651312
948	LncRNA	HOXA11-AS	miR-1297	E2F1	Gastric Cell Lines	Gastric Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	27651312	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1.	HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells.	MI0006358	Cancer Res 2016 Nov 1 76, 6299-6310 doi:10.1158/0008-5472.Can-16-0356 PMID:27651312
949	LncRNA	SOX2OT	miR-375	NA	Nt-2 Cells	Gastric Cancer	Helicobacter pylori	qRT-PCR	27800139	The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT.	Expression of miR-375 and SOX2OT and SOX2 were quantified using real-time polymerase chain reaction and compared with control cells transfected with pEGFP-C1-Mock clone.Following ectopic expression of miR-375, SOX2OT and SOX2 expression analysis revealed a significant decrease in their expression level (P < 0.05) in NT-2 cells compared to the control.	MI0000783	Jundishapur J Microbiol 2016 Sep 9, e23464 doi:10.5812/jjm.23464 PMID:27800139
950	Coding-mRNA	SOX2	miR-375	NA	Nt-2 Cells	Gastric Cancer	Helicobacter pylori	qRT-PCR	27800139	The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT.	Expression of miR-375 and SOX2OT and SOX2 were quantified using real-time polymerase chain reaction and compared with control cells transfected with pEGFP-C1-Mock clone.Following ectopic expression of miR-375, SOX2OT and SOX2 expression analysis revealed a significant decrease in their expression level (P < 0.05) in NT-2 cells compared to the control.	MI0000783	Jundishapur J Microbiol 2016 Sep 9, e23464 doi:10.5812/jjm.23464 PMID:27800139
951	LncRNA	SOX2OT	miR-375	NA	Nt-2 Cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	27800139	The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT.	Expression of miR-375 and SOX2OT and SOX2 were quantified using real-time polymerase chain reaction and compared with control cells transfected with pEGFP-C1-Mock clone.Following ectopic expression of miR-375, SOX2OT and SOX2 expression analysis revealed a significant decrease in their expression level (P < 0.05) in NT-2 cells compared to the control.	MI0000783	Jundishapur J Microbiol 2016 Sep 9, e23464 doi:10.5812/jjm.23464 PMID:27800139
952	Coding-mRNA	SOX2	miR-375	NA	Nt-2 Cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	27800139	The Effect of MicroRNA-375 Overexpression, an Inhibitor of Helicobacter pylori-Induced Carcinogenesis, on lncRNA SOX2OT.	Expression of miR-375 and SOX2OT and SOX2 were quantified using real-time polymerase chain reaction and compared with control cells transfected with pEGFP-C1-Mock clone.Following ectopic expression of miR-375, SOX2OT and SOX2 expression analysis revealed a significant decrease in their expression level (P < 0.05) in NT-2 cells compared to the control.	MI0000783	Jundishapur J Microbiol 2016 Sep 9, e23464 doi:10.5812/jjm.23464 PMID:27800139
953	LncRNA	PVT1	miR-146a	NA	Lncap, Pc-3 And Du145	Prostate Cancer	Homo sapiens (human)	qRT-PCR	27794184	LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a.	The expression level of miR-146a was assessed by quantitative RT-PCR. The correlation analysis and methylation status analysis was made to confirm the interaction between PVT1 and miR-146a. Biological function analysis was performed through gain-of-function and loss-of-function strategies. Our results showed that miR-146a was downregulated and negatively correlated with PVT1 level in prostate cancer. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter.	MI0000477	Cancer Med 2016 Dec 5, 3512-3519 doi:10.1002/cam4.900 PMID:27794184
954	LncRNA	MALAT1	miR-200c	TGFB	Rl-952, Hec-1-B And Jec	Endometrial Cancer	Homo sapiens (human)	MG-63 and U2OS	27693631	Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma.	we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-b increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro. A xenograft tumor model was used to show that targeting the miR-200c/MALAT1 axis inhibited EEC growth and EMT-associated protein expression in vivo. I	MI0000650	Cancer Lett 2016 Dec 1 383, 28-40 doi:10.1016/j.canlet.2016.09.019 PMID:27693631
955	LncRNA	MALAT1	miR-200c	TGFB	Rl-952, Hec-1-B And Jec	Endometrial Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27693631	Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma.	we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-b increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro. A xenograft tumor model was used to show that targeting the miR-200c/MALAT1 axis inhibited EEC growth and EMT-associated protein expression in vivo. I	MI0000650	Cancer Lett 2016 Dec 1 383, 28-40 doi:10.1016/j.canlet.2016.09.019 PMID:27693631
956	LncRNA	LINC00161	miR-645	IFIT2	Mg-63 And U2Os	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27609068	Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.	Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. 	MI0003660	Cancer Lett 2016 Nov 28 382, 137-146 doi:10.1016/j.canlet.2016.08.024 PMID:27609068
957	LncRNA	Unigene56159	miR-140-5p	Slug	Hbv(-) And Hbv(+) Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay;Fluorescent reporter assays	27597739	Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells.	Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug.	MIMAT0000431	Cancer Lett 2016 Nov 28 382, 166-175 doi:10.1016/j.canlet.2016.08.029 PMID:27597739
958	LncRNA	Unigene56159	miR-140-5p	Slug	Hbv(-) And Hbv(+) Hcc Tissues	Hepatocellular Carcinoma	Hepatitis B virus (HBV)	qRT-PCR;Western blot assay;Fluorescent reporter assays	27597739	Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells.	Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug.	MIMAT0000431	Cancer Lett 2016 Nov 28 382, 166-175 doi:10.1016/j.canlet.2016.08.029 PMID:27597739
959	LncRNA	RMRP	miR-206	CCND2	Ags, Bgc-823, Hgc-27, Mgc-803 And Sgc-7901	Gastric Cancer	Homo sapiens (human)	qRT-PCR	27192121	LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.	Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression. 	MI0000490	Oncotarget 2016 Jun 21 7, 37812-37824 doi:10.18632/oncotarget.9336 PMID:27192121
960	LncRNA	RMRP	miR-206	CCND2	Ags, Bgc-823, Hgc-27, Mgc-803 And Sgc-7901	Gastric Cancer	Mus musculus (mouse)	qRT-PCR	27192121	LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.	Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression. 	MI0000490	Oncotarget 2016 Jun 21 7, 37812-37824 doi:10.18632/oncotarget.9336 PMID:27192121
961	LncRNA	MALAT1	miR-206	ANXA2	Gbc-Sd And Sgc-996	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
962	LncRNA	MALAT1	miR-206	KRAS	Gbc-Sd And Sgc-996	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
963	LncRNA	MALAT1	miR-206	ANXA2	Gbc-Sd And Sgc-996	Gallbladder Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
964	LncRNA	MALAT1	miR-206	KRAS	Gbc-Sd And Sgc-996	Gallbladder Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206. Because miR-206 directly suppresses expression of ANXA2 and KRAS, which are thought to promote GBC progression, Malat1 binding of miR-206 in GBC tissue and cells has an oncogenic effect. Conversely, Malat1 knockdown inhibits proliferation and invasion by GBC cells while increasing apoptosis.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
965	Coding-mRNA	CTU1	miR-138	KNG1	U87	Glioblastoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
966	Coding-mRNA	KIAA1274	miR-138	KNG1	U87	Glioblastoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
967	Coding-mRNA	RAX	miR-138	KNG1	U87	Glioblastoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
968	Coding-mRNA	CTU1	miR-138	KNG1	U87	Glioblastoma	Danio rerio (zebrafish)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
969	Coding-mRNA	KIAA1274	miR-138	KNG1	U87	Glioblastoma	Danio rerio (zebrafish)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
970	Coding-mRNA	RAX	miR-138	KNG1	U87	Glioblastoma	Danio rerio (zebrafish)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
971	Coding-mRNA	CTU1	miR-138	KNG1	U87	Glioblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
972	Coding-mRNA	KIAA1274	miR-138	KNG1	U87	Glioblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
973	Coding-mRNA	RAX	miR-138	KNG1	U87	Glioblastoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27764797	Aberrant ceRNA-mediated regulation of KNG1 contributes to glioblastoma-induced angiogenesis.	Validation experiments in U87 glioblastoma cells showed that the regulation of KNG1 by CTU1, KIAA1274, and RAX was mediated by miR-138. The siRNA-mediated knockdown of CTU1, KIAA1274, or RAX in U87 cells and immortalized human endothelial cells (iHECs) significantly reduced KNG1 expression (P < 0.05 for all), which resulted in the upregulation of oncogenic EGFR signaling in both cell lines, and stimulated angiogenic processes in cultured iHECs and zebrafish and mouse xenograft models of glioblastoma-induced angiogenesis. Angiogenic transduction of iHECs occurred via the uptake of U87-derived exosomes enriched in miR-138, with the siRNA-mediated knockdown of KNG1, CTU1, KIAA1274, or RAX increasing the level of miR-138 enrichment to varying extents and enhancing the angiogenic effects of the U87-derived exosomes on iHECs.	MI0000455	Oncotarget 2016 10/14, 10.18632/oncotarget.12659 doi:10.18632/oncotarget.12659
974	LncRNA	PCA3	miR-1261	PRKD3	Rwpe-1,Lncap	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27743381	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells.	we demonstrated that binding of Snail to the promoter region of PCA3 could activate the expression of PCA3. Down-regulation of PCA3 by silencing could increase the expression of the miRNA-1261, which then targeted at the PRKD3 gene (protein kinase D3) through competitive sponging.	MI0006396	Tumour Biol 2016 Oct 14, 10.1007/s13277-016-5450-y doi:10.1007/s13277-016-5450-y PMID:27743381
975	LncRNA	HOTAIRM1	miR-20a	ULK1	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000076	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
976	LncRNA	HOTAIRM1	miR-106b	E2F1	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000734	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
977	LncRNA	HOTAIRM1	miR-125b	DRAM2	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000446	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
978	LncRNA	HOTAIRM1	miR-20a	ULK1	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000076	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
979	LncRNA	HOTAIRM1	miR-106b	E2F1	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000734	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
980	LncRNA	HOTAIRM1	miR-125b	DRAM2	Nb4 And U937-Pr9	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27740626	The lncRNA HOTAIRM1 regulates the degradation of PML-RARA oncoprotein and myeloid cell differentiation by enhancing the autophagy pathway.	Through the use of a dual luciferase activity assay, AGO2 RNA immunoprecipitation and RNA pull-down, HOTAIRM1 was revealed to act as a microRNA sponge in a pathway that included miR-20a/106b, miR-125b and their targets ULK1, E2F1 and DRAM2. 	MI0000446	Cell Death Differ 2017 Feb 24, 212-224 doi:10.1038/cdd.2016.111 PMID:27740626
981	LncRNA	H19	miR-342-3p	FOXM1	Gbc-Sd, Ehgb-1 And Noz	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27716361	Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer.	 By dual-luciferase reporter assays, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays, we verified that H19 was identified as a direct target of miR-342-3p. QRT-PCR and Western-blotting assays demonstrated that H19 silencing down-regulated, whereas over-expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively 'sponging' miR-342-3p.	MIMAT0000753	J Exp Clin Cancer Res 2016 Oct 3 35, 160 doi:10.1186/s13046-016-0436-6 PMID:27716361
982	LncRNA	H19	miR-342-3p	FOXM1	Gbc-Sd, Ehgb-1 And Noz	Gallbladder Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27716361	Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer.	 By dual-luciferase reporter assays, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays, we verified that H19 was identified as a direct target of miR-342-3p. QRT-PCR and Western-blotting assays demonstrated that H19 silencing down-regulated, whereas over-expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively 'sponging' miR-342-3p.	MIMAT0000753	J Exp Clin Cancer Res 2016 Oct 3 35, 160 doi:10.1186/s13046-016-0436-6 PMID:27716361
983	Artifically engineered RNA	miR-15a-16-1 sponge	miR-15a	FASN	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	27713175	Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer.	Sponge construct consisting of eight repeats of the FASN 3'-UTR region targeted by these microRNAs could markedly increase endogenous FASN levels in mammary cells. When FASN expression was restored by ectopic expression in breast cancer cells, retarded cell proliferation caused by miR-15a-16-1 was partially rescued.	MI0000069	Oncotarget 2016 Nov 29 7, 78566-78576 doi:10.18632/oncotarget.12479 PMID:27713175
984	Artifically engineered RNA	miR-15a-16-1 sponge	miR-16-1	FASN	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	27713175	Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer.	Sponge construct consisting of eight repeats of the FASN 3'-UTR region targeted by these microRNAs could markedly increase endogenous FASN levels in mammary cells. When FASN expression was restored by ectopic expression in breast cancer cells, retarded cell proliferation caused by miR-15a-16-1 was partially rescued.	MI0000070	Oncotarget 2016 Nov 29 7, 78566-78576 doi:10.18632/oncotarget.12479 PMID:27713175
985	Artifically engineered RNA	miR-497-195 sponge	miR-497	FASN	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	27713175	Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer.	Sponge construct consisting of eight repeats of the FASN 3'-UTR region targeted by these microRNAs could markedly increase endogenous FASN levels in mammary cells. When FASN expression was restored by ectopic expression in breast cancer cells, retarded cell proliferation caused by miR-15a-16-1 was partially rescued.	MI0003138	Oncotarget 2016 Nov 29 7, 78566-78576 doi:10.18632/oncotarget.12479 PMID:27713175
986	Artifically engineered RNA	miR-497-195 sponge	miR-195	FASN	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	luciferase reporter assays	27713175	Fatty acid synthase is a primary target of MiR-15a and MiR-16-1 in breast cancer.	Sponge construct consisting of eight repeats of the FASN 3'-UTR region targeted by these microRNAs could markedly increase endogenous FASN levels in mammary cells. When FASN expression was restored by ectopic expression in breast cancer cells, retarded cell proliferation caused by miR-15a-16-1 was partially rescued.	MI0000489	Oncotarget 2016 Nov 29 7, 78566-78576 doi:10.18632/oncotarget.12479 PMID:27713175
987	Artifically engineered RNA	AAV9	miR-433	AZIN1	Heart Tissues	Cardiac Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27698941	Crucial Role of miR-433 in Regulating Cardiac Fibrosis.	Decreased level of AZIN1 activated TGF-b1 while down-regulation of JNK1 resulted in activation of ERK and p38 kinase leading to Smad3 activation and ultimately cardiac fibrosis. Importantly, systemic neutralization of miR-433 or adeno-associated virus 9 (AAV9)-mediated cardiac transfer of a miR-433 sponge attenuated cardiac fibrosis and ventricular dysfunction following myocardial infarction. 	MI0001723	Theranostics 2016  6, 2068-2083 doi:10.7150/thno.15007 PMID:27698941
988	Artifically engineered RNA	AAV9	miR-433	JNK1	Heart Tissues	Cardiac Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27698941	Crucial Role of miR-433 in Regulating Cardiac Fibrosis.	Decreased level of AZIN1 activated TGF-b1 while down-regulation of JNK1 resulted in activation of ERK and p38 kinase leading to Smad3 activation and ultimately cardiac fibrosis. Importantly, systemic neutralization of miR-433 or adeno-associated virus 9 (AAV9)-mediated cardiac transfer of a miR-433 sponge attenuated cardiac fibrosis and ventricular dysfunction following myocardial infarction.	I0001723	Theranostics 2016  6, 2068-2083 doi:10.7150/thno.15007 PMID:27698941
989	Artifically engineered RNA	AAV9	miR-433	AZIN1	Heart Tissues	Cardiac Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27698941	Crucial Role of miR-433 in Regulating Cardiac Fibrosis.	Decreased level of AZIN1 activated TGF-b1 while down-regulation of JNK1 resulted in activation of ERK and p38 kinase leading to Smad3 activation and ultimately cardiac fibrosis. Importantly, systemic neutralization of miR-433 or adeno-associated virus 9 (AAV9)-mediated cardiac transfer of a miR-433 sponge attenuated cardiac fibrosis and ventricular dysfunction following myocardial infarction.	MI0001723	Theranostics 2016  6, 2068-2083 doi:10.7150/thno.15007 PMID:27698941
990	Artifically engineered RNA	AAV9	miR-433	JNK1	Heart Tissues	Cardiac Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27698941	Crucial Role of miR-433 in Regulating Cardiac Fibrosis.	Decreased level of AZIN1 activated TGF-b1 while down-regulation of JNK1 resulted in activation of ERK and p38 kinase leading to Smad3 activation and ultimately cardiac fibrosis. Importantly, systemic neutralization of miR-433 or adeno-associated virus 9 (AAV9)-mediated cardiac transfer of a miR-433 sponge attenuated cardiac fibrosis and ventricular dysfunction following myocardial infarction.	MI0001723	Theranostics 2016  6, 2068-2083 doi:10.7150/thno.15007 PMID:27698941
991	Circular RNA	CircRNA_002581	miR-122	Slc1a5	Liver Tissues	Nonalcoholic Steatohepatitis	Mus musculus (mouse)	qRT-PCR	27677588	CircRNA expression pattern and circRNA-miRNA-mRNA network in the pathogenesis of nonalcoholic steatohepatitis.	Liver circRNA and mRNA profile was initially screened by microarray and ensuing qRT-PCR verification was carried out.Randomly selected 13 of 14 mRNAs and 2 of 8 circRNAs were successfully verified by qRT-PCR. Through predicted overlapped miRNA verification, four circRNA-miRNA-mRNA pathways were constructed, including circRNA_002581-miR-122-Slc1a5, circRNA_002581- miR-122-Plp2, circRNA_002581-miR-122-Cpeb1 and circRNA_007585-miR-326- UCP2.	MI0000442	Oncotarget 2016 Oct 11 7, 66455-66467 doi:10.18632/oncotarget.12186 PMID:27677588
992	Circular RNA	CircRNA_002581	miR-122	Plp2	Liver Tissues	Nonalcoholic Steatohepatitis	Mus musculus (mouse)	qRT-PCR	27677588	CircRNA expression pattern and circRNA-miRNA-mRNA network in the pathogenesis of nonalcoholic steatohepatitis.	Liver circRNA and mRNA profile was initially screened by microarray and ensuing qRT-PCR verification was carried out.Randomly selected 13 of 14 mRNAs and 2 of 8 circRNAs were successfully verified by qRT-PCR. Through predicted overlapped miRNA verification, four circRNA-miRNA-mRNA pathways were constructed, including circRNA_002581-miR-122-Slc1a5, circRNA_002581- miR-122-Plp2, circRNA_002581-miR-122-Cpeb1 and circRNA_007585-miR-326- UCP2.	MI0000442	Oncotarget 2016 Oct 11 7, 66455-66467 doi:10.18632/oncotarget.12186 PMID:27677588
993	Circular RNA	CircRNA_002581	miR-122	Cpeb1	Liver Tissues	Nonalcoholic Steatohepatitis	Mus musculus (mouse)	qRT-PCR	27677588	CircRNA expression pattern and circRNA-miRNA-mRNA network in the pathogenesis of nonalcoholic steatohepatitis.	Liver circRNA and mRNA profile was initially screened by microarray and ensuing qRT-PCR verification was carried out.Randomly selected 13 of 14 mRNAs and 2 of 8 circRNAs were successfully verified by qRT-PCR. Through predicted overlapped miRNA verification, four circRNA-miRNA-mRNA pathways were constructed, including circRNA_002581-miR-122-Slc1a5, circRNA_002581- miR-122-Plp2, circRNA_002581-miR-122-Cpeb1 and circRNA_007585-miR-326- UCP2.	MI0000442	Oncotarget 2016 Oct 11 7, 66455-66467 doi:10.18632/oncotarget.12186 PMID:27677588
994	Circular RNA	CircRNA_007585	miR-326	UCP2	Liver Tissues	Nonalcoholic Steatohepatitis	Mus musculus (mouse)	qRT-PCR	27677588	CircRNA expression pattern and circRNA-miRNA-mRNA network in the pathogenesis of nonalcoholic steatohepatitis.	Liver circRNA and mRNA profile was initially screened by microarray and ensuing qRT-PCR verification was carried out.Randomly selected 13 of 14 mRNAs and 2 of 8 circRNAs were successfully verified by qRT-PCR. Through predicted overlapped miRNA verification, four circRNA-miRNA-mRNA pathways were constructed, including circRNA_002581-miR-122-Slc1a5, circRNA_002581- miR-122-Plp2, circRNA_002581-miR-122-Cpeb1 and circRNA_007585-miR-326- UCP2.	MI0000808	Oncotarget 2016 Oct 11 7, 66455-66467 doi:10.18632/oncotarget.12186 PMID:27677588
995	Artifically engineered RNA	miR-483 sponge	miR-483	IGF1	Granulosa-Like Tumor Cell Line	Polycystic Ovary Syndrome	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27662007	miR-483 is Down-Regulated in Polycystic Ovarian Syndrome and Inhibits KGN Cell Proliferation via Targeting Insulin-Like Growth Factor 1 (IGF1).	Overexpression of miR-483 inhibited cell viability and proliferation, and induced cell cycle arrest. miR-483 also inhibited CCNB1, CCND1, and CDK2. miR-483 sponge induced the opposite effects. miR-483 directly targeted IGF1 3'UTR, and IGF1 promoted KGN cell proliferation and reversed miR-483-inhibited cell viability.	MI0002467	Med Sci Monit 2016 Sep 23 22, 3383-3393 doi:10.12659/msm.897301 PMID:27662007
996	LncRNA	MALAT1	miR-375	NA	Siha And Caski	Cervical Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27658300	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.	QRT-PCR analysis showed that miR-375 overexpression significantly reduced MALAT1 expression, while MALAT1 overexpression reversely suppressed miR-375 levels. Therefore, we infer that there is a reciprocal regulation between miR-375 and MALAT1 in the cells.	MI0000783	PLoS One 2016  11, e0163460 doi:10.1371/journal.pone.0163460 PMID:27658300
997	LncRNA	MIAT	miR-150	ANP	H9C2	Cardiac Hypertrophy	Homo sapiens (human)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
998	LncRNA	MIAT	miR-150	BNP	H9C2	Cardiac Hypertrophy	Homo sapiens (human)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
999	LncRNA	MIAT	miR-150	b-MHC	H9C2	Cardiac Hypertrophy	Homo sapiens (human)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
1000	LncRNA	MIAT	miR-150	b-MHC	H9C2	Cardiac Hypertrophy	Mus musculus (mouse)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
1001	LncRNA	MIAT	miR-150	b-MHC	H9C2	Cardiac Hypertrophy	Mus musculus (mouse)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
1002	LncRNA	MIAT	miR-150	b-MHC	H9C2	Cardiac Hypertrophy	Mus musculus (mouse)	qRT-PCR	27649667	LncRNA MIAT enhances cardiac hypertrophy partly through sponging miR-150.	MIAT siRNA substantially alleviated the Ang II induced upregulation of ANP, BNP and b-MHC in H9c2 cells and markedly attenuated the Ang II induced increase of the cell surface area and the protein synthesis. MIAT overexpression in H9c2 cells significantly reduced the miR-150 expression.	MI0000479	Eur Rev Med Pharmacol Sci 2016 Sep 20, 3653-60,  PMID:27649667
1003	LncRNA	MEG3	miR-181b	ALOX15	Ht22 Cell	Ischemic Infarct	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27642276	The Mechanism of Long Non-coding RNA MEG3 for Neurons Apoptosis Caused by Hypoxia: Mediated by miR-181b-12/15-LOX Signaling Pathway.	Knockdown of MEG3 contributes to attenuation of hypoxia-induced apoptosis of HT22 cell. Also, expression level of MEG3 negatively correlated with miR-181b expression and positively correlated with 12/15-LOX expression. In contrary to MEG3, miR-181b overexpression attenuated hypoxia-induced HT22 cell apoptosis, as well as suppressed hypoxia-induced increase in 12/15-LOX expression. By luciferase reporter assay, we concluded that miR-181b directly binds to 12/15-LOX 3'-UTR, thereby negatively regulates 12/15-LOX expression.	MI0000270	Front Cell Neurosci 2016  10, 201 doi:10.3389/fncel.2016.00201 PMID:27642276
1004	LncRNA	MEG3	miR-181b	ALOX12	Ht22 Cell	Ischemic Infarct	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27642276	The Mechanism of Long Non-coding RNA MEG3 for Neurons Apoptosis Caused by Hypoxia: Mediated by miR-181b-12/15-LOX Signaling Pathway.	Knockdown of MEG3 contributes to attenuation of hypoxia-induced apoptosis of HT22 cell. Also, expression level of MEG3 negatively correlated with miR-181b expression and positively correlated with 12/15-LOX expression. In contrary to MEG3, miR-181b overexpression attenuated hypoxia-induced HT22 cell apoptosis, as well as suppressed hypoxia-induced increase in 12/15-LOX expression. By luciferase reporter assay, we concluded that miR-181b directly binds to 12/15-LOX 3'-UTR, thereby negatively regulates 12/15-LOX expression.	MI0000270	Front Cell Neurosci 2016  10, 201 doi:10.3389/fncel.2016.00201 PMID:27642276
1005	LncRNA	XIST	miR-101	EZH2	Gc7901, Hgc27, Bgc823, Mkn45, Mkn28, And Ags	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27620004	Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression.	An inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted.	MI0000103	J Exp Clin Cancer Res 2016 Sep 13 35, 142 doi:10.1186/s13046-016-0420-1 PMID:27620004
1006	LncRNA	XIST	miR-101	EZH2	Gc7901, Hgc27, Bgc823, Mkn45, Mkn28, And Ags	Gastric Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27620004	Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression.	An inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted.	MI0000103	J Exp Clin Cancer Res 2016 Sep 13 35, 142 doi:10.1186/s13046-016-0420-1 PMID:27620004
1007	LncRNA	lncRpa	miR-671	caspase8	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1008	Circular RNA	CircRar1	miR-671	caspase8	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1009	LncRNA	lncRpa	miR-671	p38	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1010	Circular RNA	CircRar1	miR-671	p38	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1011	LncRNA	lncRpa	miR-671	caspase8	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1012	Circular RNA	CircRar1	miR-671	caspase8	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1013	LncRNA	lncRpa	miR-671	p38	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1014	Circular RNA	CircRar1	miR-671	p38	Mouse Model Of Lead-Induced Neurotoxicity	Lead-Induced Neurotoxicity	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27604105	A novel regulatory network among LncRpa, CircRar1, MiR-671 and apoptotic genes promotes lead-induced neuronal cell apoptosis.	High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR-671.	MI0003760	Arch Toxicol 2017 Apr 91, 1671-1684 doi:10.1007/s00204-016-1837-1 PMID:27604105
1015	LncRNA	lncMD	miR-125b	IGF2	Bovine Skeletal Muscle Tissues	Muscle Differentiation	Homo sapiens (human)	RACE,luciferase reporter assays	27589905	The developmental transcriptome sequencing of bovine skeletal muscle reveals a long noncoding RNA, lncMD, promotes muscle differentiation by sponging miR-125b.	lncMD acts as a molecular sponge for miR-125b and that insulin-like growth factor 2 (IGF2) is a direct target of miR-125b in cattle. Moreover, lncMD level was positively correlated with IGF2 mRNA level in bovine muscle tissues, a vital corollary to ceRNA function. Altogether, our research showed that lncMD acts as a ceRNA to sequester miR-125b, leading to heightened IGF2 expression and thus promotes muscle differentiation.	MI0000446	Biochim Biophys Acta 2016 Nov 1863, 2835-2845 doi:10.1016/j.bbamcr.2016.08.014 PMID:27589905
1016	LncRNA	lncMD	miR-125b	IGF2	Bovine Skeletal Muscle Tissues	Muscle Differentiation	Mus musculus (mouse)	RACE,luciferase reporter assays	27589905	The developmental transcriptome sequencing of bovine skeletal muscle reveals a long noncoding RNA, lncMD, promotes muscle differentiation by sponging miR-125b.	lncMD acts as a molecular sponge for miR-125b and that insulin-like growth factor 2 (IGF2) is a direct target of miR-125b in cattle. Moreover, lncMD level was positively correlated with IGF2 mRNA level in bovine muscle tissues, a vital corollary to ceRNA function. Altogether, our research showed that lncMD acts as a ceRNA to sequester miR-125b, leading to heightened IGF2 expression and thus promotes muscle differentiation.	MI0000446	Biochim Biophys Acta 2016 Nov 1863, 2835-2845 doi:10.1016/j.bbamcr.2016.08.014 PMID:27589905
1017	LncRNA	lncMD	miR-125b	IGF2	Bovine Skeletal Muscle Tissues	Muscle Differentiation	Canis lupus familiaris (dog)	RACE,luciferase reporter assays	27589905	The developmental transcriptome sequencing of bovine skeletal muscle reveals a long noncoding RNA, lncMD, promotes muscle differentiation by sponging miR-125b.	lncMD acts as a molecular sponge for miR-125b and that insulin-like growth factor 2 (IGF2) is a direct target of miR-125b in cattle. Moreover, lncMD level was positively correlated with IGF2 mRNA level in bovine muscle tissues, a vital corollary to ceRNA function. Altogether, our research showed that lncMD acts as a ceRNA to sequester miR-125b, leading to heightened IGF2 expression and thus promotes muscle differentiation.	MI0000446	Biochim Biophys Acta 2016 Nov 1863, 2835-2845 doi:10.1016/j.bbamcr.2016.08.014 PMID:27589905
1018	LncRNA	lncMD	miR-125b	IGF2	Bovine Skeletal Muscle Tissues	Muscle Differentiation	Ornithorhynchus anatinus (platypus)	RACE,luciferase reporter assays	27589905	The developmental transcriptome sequencing of bovine skeletal muscle reveals a long noncoding RNA, lncMD, promotes muscle differentiation by sponging miR-125b.	lncMD acts as a molecular sponge for miR-125b and that insulin-like growth factor 2 (IGF2) is a direct target of miR-125b in cattle. Moreover, lncMD level was positively correlated with IGF2 mRNA level in bovine muscle tissues, a vital corollary to ceRNA function. Altogether, our research showed that lncMD acts as a ceRNA to sequester miR-125b, leading to heightened IGF2 expression and thus promotes muscle differentiation.	MI0000446	Biochim Biophys Acta 2016 Nov 1863, 2835-2845 doi:10.1016/j.bbamcr.2016.08.014 PMID:27589905
1019	LncRNA	HOTAIR	miR-214	PIK3R3	Skov3, Ovcar3, And A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	26826873	HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3.	The mRNA level of HOTAIR and PIK3R3 in ovarian cancer SKOV3 cells was decreased when transected with miR-214 or miR-217 compared to negative control (p<0.05). The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced (p<0.05). The proliferation, migration and invasion was decreased in ovarian SKOV3 when HOTAIR or PIK3R3 was silenced (p<0.05).	MI0000290	Med Sci Monit 2016 Jan 31 22, 325-31 doi:10.12659/msm.894913 PMID:26826873
1020	LncRNA	MALAT1	miR-101b	Rac1	C57Bl/6J Mice Liver	Liver Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26697839	MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis.	There was a negative feedback loop between the levels of MALAT1 and miR-101b. Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs. 	MI0000649	Cell Cycle 2015  14, 3885-96 doi:10.1080/15384101.2015.1120917 PMID:26697839
1021	LncRNA	MALAT1	miR-101b	Rac1	C57Bl/6J Mice Liver	Liver Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	26697839	MALAT1 functions as a competing endogenous RNA to mediate Rac1 expression by sequestering miR-101b in liver fibrosis.	There was a negative feedback loop between the levels of MALAT1 and miR-101b. Luciferase reporter assay indicated that MALAT1 and RAS-related C3 botulinum substrate 1 (Rac1) are targets of miR-101b. We uncovered that MALAT1 regulates Rac1 expression through miR-101b as a competing endogenous RNA (ceRNA), thereby influencing the proliferation, cell cycle and activation of primary HSCs. 	MI0000649	Cell Cycle 2015  14, 3885-96 doi:10.1080/15384101.2015.1120917 PMID:26697839
1022	LncRNA	PVT1	miR-152	PTCH1	Liver Fibrotic Tissues	Liver Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27588491	Long non-coding RNA PVT1 activates hepatic stellate cells through competitively binding microRNA-152.	Patched1 (PTCH1), a negative regulator factor of Hh pathway, was enhanced by PVT1 knockdown. PTCH1 demethylation caused by miR-152 was responsible for the effects of PVT1 knockdown on PTCH1 expression. Notably, miR-152 inhibitor reversed the effects of PVT1 knockdown on HSC activation. Luciferase reporter assays and pull-down assays showed a direct interaction between miR-152 and PVT1. Collectively, we demonstrate that PVT1 epigenetically down-regulates PTCH1 expression via competitively binding miR-152, contributing to EMT process in liver fibrosis.	MI0000462	Oncotarget 2016 Sep 27 7, 62886-62897 doi:10.18632/oncotarget.11709 PMID:27588491
1023	LncRNA	PVT1	miR-152	PTCH1	Liver Fibrotic Tissues	Liver Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27588491	Long non-coding RNA PVT1 activates hepatic stellate cells through competitively binding microRNA-152.	Patched1 (PTCH1), a negative regulator factor of Hh pathway, was enhanced by PVT1 knockdown. PTCH1 demethylation caused by miR-152 was responsible for the effects of PVT1 knockdown on PTCH1 expression. Notably, miR-152 inhibitor reversed the effects of PVT1 knockdown on HSC activation. Luciferase reporter assays and pull-down assays showed a direct interaction between miR-152 and PVT1. Collectively, we demonstrate that PVT1 epigenetically down-regulates PTCH1 expression via competitively binding miR-152, contributing to EMT process in liver fibrosis.	MI0000462	Oncotarget 2016 Sep 27 7, 62886-62897 doi:10.18632/oncotarget.11709 PMID:27588491
1024	LncRNA	MALAT1	miR-25	RBM24	Npc Fresh Tumor Tissues	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27584791	RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma.	Ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.	MI0000082	Cell Death Dis 2016 Sep 1 7, e2352 doi:10.1038/cddis.2016.252 PMID:27584791
1025	LncRNA	MALAT1	miR-25	RBM24	Npc Fresh Tumor Tissues	Nasopharyngeal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27584791	RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma.	Ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.	MI0000082	Cell Death Dis 2016 Sep 1 7, e2352 doi:10.1038/cddis.2016.252 PMID:27584791
1026	LncRNA	RBM24	miR-143	MIR143HG	293T And Sk-N-Be	Hirschsprungs Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27565737	Negative feedback circuitry between MIR143HG and RBM24 in Hirschsprung disease.	As RBM24 mRNA is a target of miR-143, upregulation of RBM24 upon an increase in the level of MIR143HG could be attributed to sequestration of miR-143 by MIR143HG (sponge effect). The RBM24 protein was shown to bind to MIR143HG, and subsequently, accelerated its degradation by destabilizing its transcript and facilitating its interaction with Ago2, thus forming a negative feedback between MIR143HG and RBM24. In addition, experiments using siRNA against DROSHA indicated that RBM24 could promote the biogenesis of miR-143. 	MI0000459	Biochim Biophys Acta 2016 Nov 1862, 2127-2136 doi:10.1016/j.bbadis.2016.08.017 PMID:27565737
1027	LncRNA	MIR143HG	miR-143	RBM24	293T And Sk-N-Be	Hirschsprungs Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27565737	Negative feedback circuitry between MIR143HG and RBM24 in Hirschsprung disease.	As RBM24 mRNA is a target of miR-143, upregulation of RBM24 upon an increase in the level of MIR143HG could be attributed to sequestration of miR-143 by MIR143HG (sponge effect). The RBM24 protein was shown to bind to MIR143HG, and subsequently, accelerated its degradation by destabilizing its transcript and facilitating its interaction with Ago2, thus forming a negative feedback between MIR143HG and RBM24. In addition, experiments using siRNA against DROSHA indicated that RBM24 could promote the biogenesis of miR-143. 	MI0000459	Biochim Biophys Acta 2016 Nov 1862, 2127-2136 doi:10.1016/j.bbadis.2016.08.017 PMID:27565737
1028	LncRNA	MALAT1	miR-22	MMP14	A375	Melanoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27564100	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.	MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22. The effects of MALAT1 in malignant melanoma is verified using a xenograft model.	MI0000078	Oncotarget 2016 Sep 27 7, 63901-63912 doi:10.18632/oncotarget.11564 PMID:27564100
1029	LncRNA	MALAT1	miR-22	Snail	A375	Melanoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27564100	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.	MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22. The effects of MALAT1 in malignant melanoma is verified using a xenograft model.	MI0000078	Oncotarget 2016 Sep 27 7, 63901-63912 doi:10.18632/oncotarget.11564 PMID:27564100
1030	LncRNA	H19	miR-29a	VASH2	Rain Microvascular Endothelial Cell Line	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27543358	Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a.	Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a. In addition, miR-29a targeted 3'-UTR region of vasohibin 2 (VASH2) and decreased its expression. VASH2 has been identified as an angiogenic factor. Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a. 	MI0000087	Cancer Lett 2016 Oct 28 381, 359-69 doi:10.1016/j.canlet.2016.08.009 PMID:27543358
1031	LncRNA	H19	miR-29a	VASH2	Rain Microvascular Endothelial Cell Line	Glioma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27543358	Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a.	Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a. In addition, miR-29a targeted 3'-UTR region of vasohibin 2 (VASH2) and decreased its expression. VASH2 has been identified as an angiogenic factor. Knockdown of H19 also decreased the VASH2 expression by up-regulating miR-29a. 	MI0000087	Cancer Lett 2016 Oct 28 381, 359-69 doi:10.1016/j.canlet.2016.08.009 PMID:27543358
1032	LncRNA	SNHG6-003	miR-26a	TAK1	Hcc Cell Lines Bel-7402, Smmc-7721, Mhcc-97H, Sk-Hep-1, Huh7 Andhcc-Lm3	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;tissue micorarray	27530352	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.	SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-b-activated kinase 1 (TAK1). Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern. 	MI0000083	Oncogene 2017 Feb 23 36, 1112-1122 doi:10.1038/onc.2016.278 PMID:27530352
1033	LncRNA	SNHG6-003	miR-26a	TAK1	Hcc Cell Lines Bel-7402, Smmc-7721, Mhcc-97H, Sk-Hep-1, Huh7 Andhcc-Lm3	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;tissue micorarray	27530352	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.	SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-b-activated kinase 1 (TAK1). Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern. 	MI0000083	Oncogene 2017 Feb 23 36, 1112-1122 doi:10.1038/onc.2016.278 PMID:27530352
1034	LncRNA	AK048794	miR-592	FAM91A1	Embryonic Stem Cells	Embryonic Stem Cell Pluripotency	Mus musculus (mouse)	RACE,luciferase reporter assays;Western blot assay	27520307	AK048794 maintains the mouse embryonic stem cell pluripotency by functioning as an miRNA sponge for miR-592.	We demonstrated that lncRNA - AK048794, regulated by transcription factor GATA1, functioned as a competing endogenous RNA (ceRNA) for miR-592 and led to the de-repression of its endogenous target FAM91A1, which is involved in mESC pluripotency maintenance.	MI0003604	Biochem J 2016 Oct 15 473, 3639-3654 doi:10.1042/bcj20160540 PMID:27520307
1035	LncRNA	linc-223	miR-125-5p	IRF4	Hl-60 And K562	Acute Myeloid Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27517498	The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA.	linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo. Furthermore, data from primary AML samples show significant downregulation of linc-223 in different AML subtypes.	MIMAT0000443	Oncotarget 2016 Sep 13 7, 60155-60168 doi:10.18632/oncotarget.11165 PMID:27517498
1036	LncRNA	linc-223	miR-125-5p	IRF4	Hl-60 And K562	Acute Myeloid Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27517498	The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA.	linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo. Furthermore, data from primary AML samples show significant downregulation of linc-223 in different AML subtypes.	MIMAT0000443	Oncotarget 2016 Sep 13 7, 60155-60168 doi:10.18632/oncotarget.11165 PMID:27517498
1037	LncRNA	lncRNA-POIR	miR-182	FoxO1	Ppdlscs, Hpdlscs	Periodontitis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27512949	Long noncoding RNA related to periodontitis interacts with miR-182 to upregulate osteogenic differentiation in periodontal mesenchymal stem cells of periodontitis patients.	Using quantitative real-time PCRs (qPCRs) and luciferase reporter assays, we demonstrated that lncRNA-POIR may act as a competing endogenous RNA (ceRNA) for miR-182, leading to derepression of its target gene, FoxO1. In this process, lncRNA-POIR and miR-182 suppress each other and form a network to regulate FoxO1. FoxO1 increased bone formation of pPDLSCs by competing with TCF-4 for b-catenin and inhibiting the canonical Wnt pathway.	MI0000272	Cell Death Dis 2016 Aug 11 7, e2327 doi:10.1038/cddis.2016.125 PMID:27512949
1038	LncRNA	lncRNA-POIR	miR-182	FoxO1	Ppdlscs, Hpdlscs	Periodontitis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27512949	Long noncoding RNA related to periodontitis interacts with miR-182 to upregulate osteogenic differentiation in periodontal mesenchymal stem cells of periodontitis patients.	Using quantitative real-time PCRs (qPCRs) and luciferase reporter assays, we demonstrated that lncRNA-POIR may act as a competing endogenous RNA (ceRNA) for miR-182, leading to derepression of its target gene, FoxO1. In this process, lncRNA-POIR and miR-182 suppress each other and form a network to regulate FoxO1. FoxO1 increased bone formation of pPDLSCs by competing with TCF-4 for b-catenin and inhibiting the canonical Wnt pathway.	MI0000272	Cell Death Dis 2016 Aug 11 7, e2327 doi:10.1038/cddis.2016.125 PMID:27512949
1039	LncRNA	Cdr1as	miR-7a	PARP	Mcm	Myocardial Infarction	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26998750	The Circular RNA Cdr1as Promotes Myocardial Infarction by Mediating the Regulation of miR-7a on Its Target Genes Expression.	Cdr1as and miR-7a were both upregulated in MI mice with increased cardiac infarct size, or cardiomyocytes under hypoxia treatment. Cdr1as overexpression in MCM cells promoted cell apoptosis, but was then reversed by miR-7a overexpression. The SP1 was identified as a new miR-7a target, in line with previously identified PARP, while miR-7a-induced decrease of cell apoptosis under hypoxia treatment was proven to be inhibited by PARP-SP1 overexpression. Moreover, Cdr1as overexpression in vivo increased cardiac infarct size with upregulated expression of PARP and SP1, while miR-7a overexpression reversed these changes.	MI0000728	PLoS One 2016  11, e0151753 doi:10.1371/journal.pone.0151753 PMID:26998750
1040	LncRNA	Cdr1as	miR-7a	SP1	Mcm	Myocardial Infarction	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26998750	The Circular RNA Cdr1as Promotes Myocardial Infarction by Mediating the Regulation of miR-7a on Its Target Genes Expression.	Cdr1as and miR-7a were both upregulated in MI mice with increased cardiac infarct size, or cardiomyocytes under hypoxia treatment. Cdr1as overexpression in MCM cells promoted cell apoptosis, but was then reversed by miR-7a overexpression. The SP1 was identified as a new miR-7a target, in line with previously identified PARP, while miR-7a-induced decrease of cell apoptosis under hypoxia treatment was proven to be inhibited by PARP-SP1 overexpression. Moreover, Cdr1as overexpression in vivo increased cardiac infarct size with upregulated expression of PARP and SP1, while miR-7a overexpression reversed these changes.	MI0000728	PLoS One 2016  11, e0151753 doi:10.1371/journal.pone.0151753 PMID:26998750
1041	LncRNA	Cdr1as	miR-7a	PARP	Mcm	Myocardial Infarction	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26998750	The Circular RNA Cdr1as Promotes Myocardial Infarction by Mediating the Regulation of miR-7a on Its Target Genes Expression.	Cdr1as and miR-7a were both upregulated in MI mice with increased cardiac infarct size, or cardiomyocytes under hypoxia treatment. Cdr1as overexpression in MCM cells promoted cell apoptosis, but was then reversed by miR-7a overexpression. The SP1 was identified as a new miR-7a target, in line with previously identified PARP, while miR-7a-induced decrease of cell apoptosis under hypoxia treatment was proven to be inhibited by PARP-SP1 overexpression. Moreover, Cdr1as overexpression in vivo increased cardiac infarct size with upregulated expression of PARP and SP1, while miR-7a overexpression reversed these changes.	MI0000728	PLoS One 2016  11, e0151753 doi:10.1371/journal.pone.0151753 PMID:26998750
1042	LncRNA	Cdr1as	miR-7a	SP1	Mcm	Myocardial Infarction	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26998750	The Circular RNA Cdr1as Promotes Myocardial Infarction by Mediating the Regulation of miR-7a on Its Target Genes Expression.	Cdr1as and miR-7a were both upregulated in MI mice with increased cardiac infarct size, or cardiomyocytes under hypoxia treatment. Cdr1as overexpression in MCM cells promoted cell apoptosis, but was then reversed by miR-7a overexpression. The SP1 was identified as a new miR-7a target, in line with previously identified PARP, while miR-7a-induced decrease of cell apoptosis under hypoxia treatment was proven to be inhibited by PARP-SP1 overexpression. Moreover, Cdr1as overexpression in vivo increased cardiac infarct size with upregulated expression of PARP and SP1, while miR-7a overexpression reversed these changes.	MI0000728	PLoS One 2016  11, e0151753 doi:10.1371/journal.pone.0151753 PMID:26998750
1043	Protein	HuR	miR-21	PDCD4	Mcf7,Huh7	Breast Cancer	Homo sapiens (human)	qRT-PCR,RNA immunoprecipitation	26189797	RNA-binding protein HuR sequesters microRNA-21 to prevent translation repression of proinflammatory tumor suppressor gene programmed cell death 4.	Cells stably expressing miR-21 showed higher proliferation and reduced apoptosis, which was reversed by HuR expression. Inflammatory stimulus caused nuclear-cytoplasmic relocalization of HuR, reversing the translation repression of PDCD4. Unprecedentedly, HuR was also found to bind to miR-21 directly, preventing its interaction with the PDCD4 3'-UTR, thereby preventing the translation repression of PDCD4.	MI0000077	Oncogene 2016 Mar 31 35, 1703-15 doi:10.1038/onc.2015.235 PMID:26189797
1044	Protein	HuR	miR-21	PDCD4	Mcf7,Huh7	Breast Cancer	Mus musculus (mouse)	qRT-PCR,RNA immunoprecipitation	26189797	RNA-binding protein HuR sequesters microRNA-21 to prevent translation repression of proinflammatory tumor suppressor gene programmed cell death 4.	Cells stably expressing miR-21 showed higher proliferation and reduced apoptosis, which was reversed by HuR expression. Inflammatory stimulus caused nuclear-cytoplasmic relocalization of HuR, reversing the translation repression of PDCD4. Unprecedentedly, HuR was also found to bind to miR-21 directly, preventing its interaction with the PDCD4 3'-UTR, thereby preventing the translation repression of PDCD4.	MI0000077	Oncogene 2016 Mar 31 35, 1703-15 doi:10.1038/onc.2015.235 PMID:26189797
1045	LncRNA	RSU1P2	let-7a	IGF1R	Hela And C33A,	Cervical Cancer	Homo sapiens (human)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1046	LncRNA	RSU1P2	let-7a	N-myc	Hela And C33A,	Cervical Cancer	Homo sapiens (human)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1047	LncRNA	RSU1P2	let-7a	EphA4	Hela And C33A,	Cervical Cancer	Homo sapiens (human)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1048	LncRNA	RSU1P2	let-7a	IGF1R	Hela And C33A,	Cervical Cancer	Mus musculus (mouse)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1049	LncRNA	RSU1P2	let-7a	N-myc	Hela And C33A,	Cervical Cancer	Mus musculus (mouse)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1050	LncRNA	RSU1P2	let-7a	EphA4	Hela And C33A,	Cervical Cancer	Mus musculus (mouse)	EGFP reporter assay;qRT-PCR;Western blot assay	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. 	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
1051	Pseudogene	CTNNAP1	miR-141	CTNNA1	Sw480 And Sw620	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27487124	Downregulated pseudogene CTNNAP1 promote tumor growth in human cancer by downregulating its cognate gene CTNNA1 expression.	The mechanistic experiments revealed that pseudogene CTNNAP1 played a pivotal role in the regulation of its cognate gene CTNNA1 by competition for microRNA-141. Moreover, gain-of-function approaches showed that overexpression of CTNNAP1 or CTNNA1 significantly inhibited cell proliferation and tumor growth in vitro and in vivo by inducing G0/G1 cell cycle arrest. 	MI0000457	Oncotarget 2016 Aug 23 7, 55518-55528 doi:10.18632/oncotarget.10833 PMID:27487124
1052	Pseudogene	CTNNAP1	miR-141	CTNNA1	Sw480 And Sw620	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27487124	Downregulated pseudogene CTNNAP1 promote tumor growth in human cancer by downregulating its cognate gene CTNNA1 expression.	The mechanistic experiments revealed that pseudogene CTNNAP1 played a pivotal role in the regulation of its cognate gene CTNNA1 by competition for microRNA-141. Moreover, gain-of-function approaches showed that overexpression of CTNNAP1 or CTNNA1 significantly inhibited cell proliferation and tumor growth in vitro and in vivo by inducing G0/G1 cell cycle arrest. 	MI0000457	Oncotarget 2016 Aug 23 7, 55518-55528 doi:10.18632/oncotarget.10833 PMID:27487124
1053	LncRNA	MALAT1	miR-122	IGF1R	Sgc7901, Mkn45 And Bgc823	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27486823	The lncRNA MALAT1 is a novel biomarker for gastric cancer metastasis.	knockdown of MALAT1 could inhibit cell proliferation, cell cycle progression, migration and invasion, and promote apoptosis in gastric cancer cells. Furthermore, the miR-122-IGF-1R signaling correlated with the dysregulated MALAT1 expression in gastric cancer.	MI0000442	Oncotarget 2016 Aug 30 7, 56209-56218 doi:10.18632/oncotarget.10941 PMID:27486823
1054	Coding-mRNA	c-Myc	let-7a	PML	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000060	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1055	Coding-mRNA	c-Myc	let-7c	PML	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000064	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1056	Coding-mRNA	c-Myc	let-7g	PML	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000433	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1057	Coding-mRNA	c-Myc	let-7a	RARA	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000060	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1058	Coding-mRNA	c-Myc	let-7c	RARA	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000064	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1059	Coding-mRNA	c-Myc	let-7g	RARA	Nb4	Acute Promyelocytic Leukemia	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000433	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1060	Coding-mRNA	c-Myc	let-7a	PML	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000556	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1061	Coding-mRNA	c-Myc	let-7c	PML	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000064	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1062	Coding-mRNA	c-Myc	let-7g	PML	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000433	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1063	Coding-mRNA	c-Myc	let-7a	RARA	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000060	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1064	Coding-mRNA	c-Myc	let-7c	RARA	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000064	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1065	Coding-mRNA	c-Myc	let-7g	RARA	Nb4	Acute Promyelocytic Leukemia	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27486764	C-Myc functions as a competing endogenous RNA in acute promyelocytic leukemia.	ttenuation of c-Myc transcript results in PML/RARa-degraded cellular phenotypes in APL cells, but these Myc reduction-associated cell phenotypes are sufficient to abrogate in a microRNA dependent manner. We also show that let-7microRNA family members promote differentiation of All-Trans-Retinoic Acid (ATRA)-induced NB4 cells and their activities are affected by expression levels of both c-Myc and PML/RARa through altering miRNA targets.	MI0000433	Oncotarget 2016 Aug 30 7, 56422-56430 doi:10.18632/oncotarget.10896 PMID:27486764
1066	LncRNA	lncRNA-MSR	miR-152	TMSB4	Osteoarthritis Tissues	Osteoarthritis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay;Western blot assay	27469625	The TMSB4 Pseudogene LncRNA Functions as a Competing Endogenous RNA to Promote Cartilage Degradation in Human Osteoarthritis.	The TMSB4 pseudogene,lncRNA-MSR, was upregulated in the damaged cartilage and was activated in chondrocytes in response to mechanical stress. Furthermore,lncRNA-MSR regulated the expression of TMSB4 by competing with miRNA-152 in chondrocytes.	MI0000462	Mol Ther 2016 Oct 24, 1726-1733 doi:10.1038/mt.2016.151 PMID:27469625
1067	LncRNA	Lnc-Ang362	miR-221	NA	Vascular Smooth Muscle Cells	Cardiovascular Disease	Homo sapiens (human)	siRNA knockdown,RNA sequencing	23697773	Novel Long Non-Coding RNAs Are Regulated by Angiotensin II in Vascular Smooth Muscle Cells.	Analysis of transcript abundance identified all protein-coding and lncRNAs regulated by Ang II. We further discovered that one Ang II-regulated lncRNA functions as the host transcript for miR-221 and miR-222, two miRNAs implicated in cell proliferation. Additionally, siRNA-mediated knockdown of Lnc-Ang362 reduced proliferation of VSMCs.	MI0000298	Circ Res 2013 Jul 19 113, 266-78 doi:10.1161/circresaha.112.300849 PMID:23697773
1068	LncRNA	Lnc-Ang362	miR-222	NA	Vascular Smooth Muscle Cells	Cardiovascular Disease	Homo sapiens (human)	siRNA knockdown,RNA sequencing	23697773	Novel Long Non-Coding RNAs Are Regulated by Angiotensin II in Vascular Smooth Muscle Cells.	Analysis of transcript abundance identified all protein-coding and lncRNAs regulated by Ang II. We further discovered that one Ang II-regulated lncRNA functions as the host transcript for miR-221 and miR-222, two miRNAs implicated in cell proliferation. Additionally, siRNA-mediated knockdown of Lnc-Ang362 reduced proliferation of VSMCs.	MI0000299	Circ Res 2013 Jul 19 113, 266-78 doi:10.1161/circresaha.112.300849 PMID:23697773
1069	LncRNA	HOTAIR	miR-148b-3p	PRC2	A172	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27446363	miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.	siRNA was used to suppress the expression of HOTAIR and reverse transcription-quantitative polymerase chain reaction was used to detect the expression of miR-148b-3p. The results confirmed that HOTAIR mRNA expression was inversely correlated with miR-148b-3p expression in A172 glioma cells.	MIMAT0000759	Oncol Lett 2016 Aug 12, 879-886 doi:10.3892/ol.2016.4743 PMID:27446363
1070	LncRNA	MALAT1	miR-363-3p	MCL1	Cbc Cells	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27420766	The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer.	Luciferase reporter assays and RNA pull down assays showed that MALAT1 is a target of miR-363-3p. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenousRNA (ceRNA) for miR-363-3p in GBC cells.	MIMAT0000707	J Cell Mol Med 2016 Dec 20, 2299-2308 doi:10.1111/jcmm.12920 PMID:27420766
1071	LncRNA	SNHG16	NA	SCD	Colorectal Cancer Cell Lines	Colorectal Cancer	Homo sapiens (human)	AGO-CLIP;qRT-PCR	27396952	SNHG16 is regulated by the Wnt pathway in colorectal cancer and affects genes involved in lipid metabolism.	Argonaute CrossLinking and ImmunoPrecipitation (AGO-CLIP) demonstrated that SNHG16 heavily binds AGO and has 27 AGO/miRNA target sites along its length, indicating that SNHG16 may act as a competing endogenous RNA (ceRNA) “sponging” miRNAs off their cognate targets. Most interestingly, half of the miRNA families with high confidence targets on SNHG16 also target the 3'UTR of Stearoyl-CoA Desaturase (SCD). 	NA	Mol Oncol 2016 Oct 10, 1266-82 doi:10.1016/j.molonc.2016.06.003 PMID:27396952
1072	LncRNA	LINC00324	miR-615-5p	BTG2	Huvec,Hek-293 And Hs68 	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27373735	Screening and validation of lncRNAs and circRNAs as miRNA sponges.	To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. 	MIMAT0004804	Brief Bioinform 2017 Sep 1 18, 780-788 doi:10.1093/bib/bbw053 PMID:27373735
1073	LncRNA	LINC00324	miR-615-5p	ADCYAP1R1	Huvec,Hek-293 And Hs68 	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27373735	Screening and validation of lncRNAs and circRNAs as miRNA sponges.	To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. 	MIMAT0004804	Brief Bioinform 2017 Sep 1 18, 780-788 doi:10.1093/bib/bbw053 PMID:27373735
1074	LncRNA	LINC00324	miR-4281	NA	Huvec,Hek-293 And Hs68 	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27373735	Screening and validation of lncRNAs and circRNAs as miRNA sponges.	To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. 	MI0015885	Brief Bioinform 2017 Sep 1 18, 780-788 doi:10.1093/bib/bbw053 PMID:27373735
1075	LncRNA	LOC400043	miR-28-3p	NA	Huvec,Hek-293 And Hs68 	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27373735	Screening and validation of lncRNAs and circRNAs as miRNA sponges.	To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. 	MIMAT0004502	Brief Bioinform 2017 Sep 1 18, 780-788 doi:10.1093/bib/bbw053 PMID:27373735
1076	LncRNA	LOC400043	miR-96-5p	NA	Huvec,Hek-293 And Hs68 	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27373735	Screening and validation of lncRNAs and circRNAs as miRNA sponges.	To uncover the roles of miRNA sponges, loss-of-function experiments were conducted, which revealed the biological roles as miRNA sponges. LINC00324 is important for the cell survival by binding to miR-615-5p leading to the de-repression of its target BTG2 LOC400043 controls several biological functions via sequestering miR-28-3p and miR-96-5p, thereby changing the expressions of transcriptional regulators. 	MIMAT0000095	Brief Bioinform 2017 Sep 1 18, 780-788 doi:10.1093/bib/bbw053 PMID:27373735
1077	LncRNA	CA9	miR-34a	JAGGED1	Mcf7	Hypoxic Human Mammospheres	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26553365	Carbonic Anhydrase 9 mRNA/microRNA34a Interplay in hypoxic human mammospheres.	The over-expression of cloned CA9-mRNA-3'UTR increases the mRNA half-life and protein levels of two miR34a targets JAGGED1 and NOTCH3. The data here reported shows that the SNAI2-dependent down-regulation of miR34a substantially contributes to the post-transcriptional up-regulation of CA9, and that CA9-mRNA-3'UTR acts as an endogenous microRNA sponge. 	MI0000268	J Cell Physiol 2016 Jul 231, 1534-41 doi:10.1002/jcp.25245 PMID:26553365
1078	LncRNA	CA9	miR-34a	NOTCH3	Mcf7	Hypoxic Human Mammospheres	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26553365	Carbonic Anhydrase 9 mRNA/microRNA34a Interplay in hypoxic human mammospheres.	The over-expression of cloned CA9-mRNA-3'UTR increases the mRNA half-life and protein levels of two miR34a targets JAGGED1 and NOTCH3. The data here reported shows that the SNAI2-dependent down-regulation of miR34a substantially contributes to the post-transcriptional up-regulation of CA9, and that CA9-mRNA-3'UTR acts as an endogenous microRNA sponge. 	MI0000268	J Cell Physiol 2016 Jul 231, 1534-41 doi:10.1002/jcp.25245 PMID:26553365
1079	LncRNA	H19	miR-29a-3p	DNMT3B	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1080	Circular RNA	MYLK	miR-29a-3p	DNMT3B	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1081	Circular RNA	CTDP1	miR-29a-3p	DNMT3B	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1082	LncRNA	H19	miR-29a-3p	VEGFA	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1083	Circular RNA	MYLK	miR-29a-3p	VEGFA	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1084	Circular RNA	CTDP1	miR-29a-3p	VEGFA	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1085	LncRNA	H19	miR-29a-3p	ITGB1	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1086	Circular RNA	MYLK	miR-29a-3p	ITGB1	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1087	Circular RNA	CTDP1	miR-29a-3p	ITGB1	Bladder Carcinoma Tissues	Bladder Cancer	Homo sapiens (human)	microarray;qRT-PCR	27363013	Comprehensive analysis of differentially expressed profiles of lncRNAs and circRNAs with associated co-expression and ceRNA networks in bladder carcinoma.	We selected differentially expressed 8 lncRNAs and 9 circRNAs, sharing a common binding site of MRE. For instance, lncRNA H19, circular MYLK and circular CTDP1 are ceRNA of miR-29a-3p targeting DNMT3B, ITGB1, VEGFA and HAS3. Whereas, lncRNA RP11-89K21.2 and circular PC are ceRNA of miR-185-3p targeting ADD1and BAP1. These RNA interactions would supply novel perspective for the tumorigenesis mechanisms of BC.	MIMAT0000086	Oncotarget 2016 Jul 26 7, 47186-47200 doi:10.18632/oncotarget.9706 PMID:27363013
1088	LncRNA	NEAT1	miR-377-3p	E2F3	A549, Spc-A1, H1299, 95D, Sk-Mes-1, And Nci-H520	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27351135	Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.	By using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. 	MIMAT0000730	Oncotarget 2016 Aug 9 7, 51784-51814 doi:10.18632/oncotarget.10108 PMID:27351135
1089	LncRNA	NEAT1	miR-377-3p	E2F3	A549, Spc-A1, H1299, 95D, Sk-Mes-1, And Nci-H520	Non-Small Cell Lung Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27351135	Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.	By using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. 	MIMAT0000730	Oncotarget 2016 Aug 9 7, 51784-51814 doi:10.18632/oncotarget.10108 PMID:27351135
1090	LncRNA	LncRNA-ATB	miR-200a	TGFB2	U251 And A172	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;RNA immunoprecipitation	27267902	Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.	ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-b2.	MI0000737	J Exp Clin Cancer Res 2016 Jun 6 35, 90 doi:10.1186/s13046-016-0367-2 PMID:27267902
1091	LncRNA	LncRNA-ATB	miR-200a	TGFB2	U251 And A172	Glioma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;RNA immunoprecipitation	27267902	Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.	ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-b2.	MI0000737	J Exp Clin Cancer Res 2016 Jun 6 35, 90 doi:10.1186/s13046-016-0367-2 PMID:27267902
1092	LncRNA	HULC	miR-200a-3p	ZEB1	Huh-6, Huh-7, Hepg2, Bel-7402, Mhcc-97H, Sk-Hep1 And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot assay	27285757	LncRNA HULC enhances epithelial-mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1 signaling pathway.	HULC functioned as a competing endogenous RNA (ceRNA) to mediate EMT via up-regulating ZEB1. In this way, it sequesters the miR-200a-3p signaling pathway to facilitate HCC metastasis. HULC comes into play as an oncogene in HCC, acting mechanistically by inducing HCC cells to activate EMT. Such an effect promotes tumor progression and metastasis through the miR-200a-3p/ZEB1 signaling pathway. 	MIMAT0000682	Oncotarget 2016 Jul 5 7, 42431-42446 doi:10.18632/oncotarget.9883 PMID:27285757
1093	LncRNA	HULC	miR-200a-3p	ZEB1	Huh-6, Huh-7, Hepg2, Bel-7402, Mhcc-97H, Sk-Hep1 And Smmc-7721	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot assay	27285757	LncRNA HULC enhances epithelial-mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1 signaling pathway.	HULC functioned as a competing endogenous RNA (ceRNA) to mediate EMT via up-regulating ZEB1. In this way, it sequesters the miR-200a-3p signaling pathway to facilitate HCC metastasis. HULC comes into play as an oncogene in HCC, acting mechanistically by inducing HCC cells to activate EMT. Such an effect promotes tumor progression and metastasis through the miR-200a-3p/ZEB1 signaling pathway. 	MIMAT0000682	Oncotarget 2016 Jul 5 7, 42431-42446 doi:10.18632/oncotarget.9883 PMID:27285757
1094	LncRNA	LncRNA-NRF	miR-873	RIPK1	Cardiomyocytes	Ischemia And Reperfusion	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27258785	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.	In exploring the molecular mechanism by which miR-873 expression is regulated, we identify NRF as an endogenous sponge RNA and repress miR-873 expression. NRF directly binds to miR-873 and regulates RIPK1/RIPK3 expression and necrosis. Knockdown of NRF antagonizes necrosis in cardiomyocytes and reduces necrosis and myocardial infarction upon I/R injury.	MI0005564	Cell Death Differ 2016 Aug 23, 1394-405 doi:10.1038/cdd.2016.28 PMID:27258785
1095	LncRNA	LncRNA-NRF	miR-873	RIPK3	Cardiomyocytes	Ischemia And Reperfusion	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27258785	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.	In exploring the molecular mechanism by which miR-873 expression is regulated, we identify NRF as an endogenous sponge RNA and repress miR-873 expression. NRF directly binds to miR-873 and regulates RIPK1/RIPK3 expression and necrosis. Knockdown of NRF antagonizes necrosis in cardiomyocytes and reduces necrosis and myocardial infarction upon I/R injury.	MI0005564	Cell Death Differ 2016 Aug 23, 1394-405 doi:10.1038/cdd.2016.28 PMID:27258785
1096	LncRNA	LncRNA-NRF	miR-873	RIPK1	Cardiomyocytes	Ischemia And Reperfusion	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27258785	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.	In exploring the molecular mechanism by which miR-873 expression is regulated, we identify NRF as an endogenous sponge RNA and repress miR-873 expression. NRF directly binds to miR-873 and regulates RIPK1/RIPK3 expression and necrosis. Knockdown of NRF antagonizes necrosis in cardiomyocytes and reduces necrosis and myocardial infarction upon I/R injury.	MI0005564	Cell Death Differ 2016 Aug 23, 1394-405 doi:10.1038/cdd.2016.28 PMID:27258785
1097	LncRNA	LncRNA-NRF	miR-873	RIPK3	Cardiomyocytes	Ischemia And Reperfusion	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	27258785	The long noncoding RNA NRF regulates programmed necrosis and myocardial injury during ischemia and reperfusion by targeting miR-873.	In exploring the molecular mechanism by which miR-873 expression is regulated, we identify NRF as an endogenous sponge RNA and repress miR-873 expression. NRF directly binds to miR-873 and regulates RIPK1/RIPK3 expression and necrosis. Knockdown of NRF antagonizes necrosis in cardiomyocytes and reduces necrosis and myocardial infarction upon I/R injury.	MI0005564	Cell Death Differ 2016 Aug 23, 1394-405 doi:10.1038/cdd.2016.28 PMID:27258785
1098	LncRNA	lncRNA-RNCR3	miR-185-5p	KLF2	Huvecs,Vsmcs	Vascular Dysfunction	Homo sapiens (human)	qRT-PCR	27253412	Role of long non-coding RNA-RNCR3 in atherosclerosis-related vascular dysfunction.	RNCR3 knockdown accelerates the development of atherosclerosis, aggravates hypercholesterolemia and inflammatory factor releases, and decreases EC and VSMC proliferation in vivo. RNCR3 knockdown also reduces the proliferation and migration, and accelerates apoptosis development of EC and VSMC in vitro. RNCR3 acts as a ceRNA, and forms a feedback loop with Kruppel-like factor 2 and miR-185-5p to regulate cell function.	MIMAT0000455	Cell Death Dis 2016 Jun 2 7, e2248 doi:10.1038/cddis.2016.145 PMID:27253412
1099	LncRNA	lncRNA-RNCR3	miR-185-5p	KLF2	Huvecs,Vsmcs	Vascular Dysfunction	Mus musculus (mouse)	qRT-PCR	27253412	Role of long non-coding RNA-RNCR3 in atherosclerosis-related vascular dysfunction.	RNCR3 knockdown accelerates the development of atherosclerosis, aggravates hypercholesterolemia and inflammatory factor releases, and decreases EC and VSMC proliferation in vivo. RNCR3 knockdown also reduces the proliferation and migration, and accelerates apoptosis development of EC and VSMC in vitro. RNCR3 acts as a ceRNA, and forms a feedback loop with Kruppel-like factor 2 and miR-185-5p to regulate cell function.	MIMAT0000455	Cell Death Dis 2016 Jun 2 7, e2248 doi:10.1038/cddis.2016.145 PMID:27253412
1100	LncRNA	LINC00673	miR-1231	PTPN11	Bxpc-3, Cfpac-1 And 293T	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27213290	Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation.	 LINC00673 is able to reinforce the interaction of PTPN11 with PRPF19, an E3 ubiquitin ligase, and promote PTPN11 degradation through ubiquitination, which causes diminished SRC-ERK oncogenic signaling and enhanced activation of the STAT1-dependent antitumor response. A G>A change at rs11655237 in exon 4 of LINC00673 creates a target site for miR-1231 binding, which diminishes the effect of LINC00673 in an allele-specific manner and thus confers susceptibility to tumorigenesis. 	MI0006321	Nat Genet 2016 Jul 48, 747-57 doi:10.1038/ng.3568 PMID:27213290
1101	Viral RNA	HBV	miR-146a	RIG-I	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1102	Viral RNA	HBV	miR-146a	RIG-G	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1103	Viral RNA	HBV	miR-146a	RIG-I	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1104	Viral RNA	HBV	miR-146a	RIG-G	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1105	Viral RNA	HBV	miR-146a	RIG-I	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Hepatitis B virus (HBV)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1106	Viral RNA	HBV	miR-146a	RIG-G	Hek293,Hepg2 And Hepg2.2.15	Liver Cancer	Hepatitis B virus (HBV)	luciferase reporter assays;qRT-PCR;Western blot assay	27210312	Hepatitis B virus inhibits intrinsic RIG-I and RIG-G immune signaling via inducing miR146a.	miR-146a was demonstrated to negatively regulate the expression of RIG-I-like receptors by directly targeting both RIG-I and RIG-G. Further investigation showed that antagonizing miR146a by anti-sense inhibitors or sponge approach accelerated HBV clearance and reduced HBV load both in vitro and in a HBV-carrying mouse model. Therefore, our findings indicated that HBV-induced miR146a attenuates cell-intrinsic anti-viral innate immunity through targeting RIG-I and RIG-G, and silencing miR146a might be an effective target to reverse HBV-induced immune suppression.	MI0000477	Sci Rep 2016 May 23 6, 26150 doi:10.1038/srep26150 PMID:27210312
1107	LncRNA	H19	miR-141	NA	Hfob1.19	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27186302	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.	The overexpressed miR-141 suppressed H19 and miR-675 expression in hFOB1.19 cells. Besides, miR-141 suppression significantly increased cell viability but this effect was blocked by silencing H19 or miR-675 inhibitor, which is similar to the effects on VEGF and IGF2 expression.	MI0000457	Am J Transl Res 2016  8, 1780-8,  PMID:27186302
1108	Artifically engineered RNA	i-lncRNA	miR-21	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1109	Artifically engineered RNA	i-lncRNA	miR-125b	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000446	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1110	Artifically engineered RNA	i-lncRNA	miR-155	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1111	Artifically engineered RNA	i-lncRNA	miR-21	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1112	Artifically engineered RNA	i-lncRNA	miR-155	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1113	Artifically engineered RNA	i-lncRNA	miR-221	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1114	Artifically engineered RNA	i-lncRNA	miR-21	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1115	Artifically engineered RNA	i-lncRNA	miR-155	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1116	Artifically engineered RNA	i-lncRNA	miR-221	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1117	Artifically engineered RNA	i-lncRNA	miR-17	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000071	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1118	Artifically engineered RNA	i-lncRNA	miR-21	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1119	Artifically engineered RNA	i-lncRNA	miR-125b	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000446	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1120	Artifically engineered RNA	i-lncRNA	miR-155	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1121	Artifically engineered RNA	i-lncRNA	miR-221	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1122	Artifically engineered RNA	i-lncRNA	miR-17	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000071	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1123	Artifically engineered RNA	i-lncRNA	miR-21	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1124	Artifically engineered RNA	i-lncRNA	miR-125b	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000446	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1125	Artifically engineered RNA	i-lncRNA	miR-155	PTEN	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1126	Artifically engineered RNA	i-lncRNA	miR-21	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1127	Artifically engineered RNA	i-lncRNA	miR-155	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1128	Artifically engineered RNA	i-lncRNA	miR-221	p27kip1	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1129	Artifically engineered RNA	i-lncRNA	miR-21	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1130	Artifically engineered RNA	i-lncRNA	miR-155	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1131	Artifically engineered RNA	i-lncRNA	miR-221	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1132	Artifically engineered RNA	i-lncRNA	miR-17	TIMP3	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000071	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1133	Artifically engineered RNA	i-lncRNA	miR-21	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000077	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1134	Artifically engineered RNA	i-lncRNA	miR-125b	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000446	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1135	Artifically engineered RNA	i-lncRNA	miR-155	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000681	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1136	Artifically engineered RNA	i-lncRNA	miR-221	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000298	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1137	Artifically engineered RNA	i-lncRNA	miR-17	RECK	Oci-Ly10, Sudhl-4, Db	Diffuse Large B-Cell Lymphoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27172795	Therapeutic strategy with artificially-designed i-lncRNA targeting multiple oncogenic microRNAs exhibits effective antitumor activity in diffuse large B-cell lymphoma.	The in vitro experiments confirmed that the i-lncRNA expression significantly inhibited cell proliferation, induced cell cycle arrest and apoptosis in DLBCL cell lines, mainly through upregulating the expression of PTEN, p27kip1, TIMP3, RECK and downregulating the expression of p38/MAPK, survivin, CDK4, c-myc.	MI0000071	Oncotarget 2016 Aug 2 7, 49143-49155 doi:10.18632/oncotarget.9237 PMID:27172795
1138	LncRNA	MEG3	miR-1297	PTEN	Nccit	Testicular Germ Cell Tumor	Homo sapiens (human)	qRT-PCR;Western blot assay	27158395	Crosstalk between Meg3 and miR-1297 regulates growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway.	Luciferase report assay showed that Meg3 overexpression abolished the effects of miR-1297 on 3'-UTR of PTEN mRNA, possibly through competitive binding, which was supported by double fluorescent in situ hybridization showing co-localization of intracellular Meg3 and miR-1297 signals in TGCT cells. Moreover, Meg3 overexpression abolished the inhibitory effects of miR-1297 on PTEN, resulting in deactivation of Akt and decreases in cell growth. 	MI0006358	Am J Transl Res 2016  8, 1091-9,  PMID:27158395
1139	LncRNA	NEAT1	miR-548ar-3p	FUS	Mcf-7 And Mda-Mb-231)	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation	27147820	NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548.	Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis. These results indicate a novel interaction between NEAT1, miR-548ar-3p, and FUS and their role in the regulation of breast cancer cell apoptosis.	MIMAT0022266	Gene Regul Syst Bio 2016  10, 11-7 doi:10.4137/grsb.S29414 PMID:27147820
1140	LncRNA	HOTAIR	miR-141	SKA2	U87, U251 And A172	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27121316	Epigenetic modification of miR-141 regulates SKA2 by an endogenous 'sponge' HOTAIR in glioma.	Mechanistic investigations revealed that HOTAIR might act as an endogenous 'sponge' of miR-141, thereby regulating the derepression of SKA2. Further, we explored the molecular mechanism by which miR-141 expression was regulated, and found that the miR-141 promoter was hypermethylated and that promoter methylation of miR-141 was mediated by DNMT1 in glioma cells. 	MI0000457	Oncotarget 2016 May 24 7, 30610-25 doi:10.18632/oncotarget.8895 PMID:27121316
1141	LncRNA	HOTAIR	miR-141	SKA2	U87, U251 And A172	Glioma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27121316	Epigenetic modification of miR-141 regulates SKA2 by an endogenous 'sponge' HOTAIR in glioma.	Mechanistic investigations revealed that HOTAIR might act as an endogenous 'sponge' of miR-141, thereby regulating the derepression of SKA2. Further, we explored the molecular mechanism by which miR-141 expression was regulated, and found that the miR-141 promoter was hypermethylated and that promoter methylation of miR-141 was mediated by DNMT1 in glioma cells. 	MI0000457	Oncotarget 2016 May 24 7, 30610-25 doi:10.18632/oncotarget.8895 PMID:27121316
1142	LncRNA	H19	miR-17-5p	YES1	Tpc-1, Nim, And Bcpap	Thyroid Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27093644	Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer.	H19 was identified as a target of miR-17-5p, by Dual-Luciferase Reporter assays and RNA-binding protein immunoprecipitation assays. H19 antagonized the function of miR-17-5p on upregulation of its target YES1 and inhibited miR-17-5p-induced cell cycle progression.	MIMAT0000070	Febs j 2016 Jun 283, 2326-39 doi:10.1111/febs.13741 PMID:27093644
1143	LncRNA	H19	miR-17-5p	YES1	Tpc-1, Nim, And Bcpap	Thyroid Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	27093644	Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer.	H19 was identified as a target of miR-17-5p, by Dual-Luciferase Reporter assays and RNA-binding protein immunoprecipitation assays. H19 antagonized the function of miR-17-5p on upregulation of its target YES1 and inhibited miR-17-5p-induced cell cycle progression.	MIMAT0000070	Febs j 2016 Jun 283, 2326-39 doi:10.1111/febs.13741 PMID:27093644
1144	Circular RNA	Circ_001569	miR-145	E2F5	Crc Cell Lines	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27058418	Emerging roles of circRNA_001569 targeting miR-145 in the proliferation and invasion of colorectal cancer.	hsa_circ_001569 was identified as a sponge of miR-145 and up-regulated miR-145 functional targets E2F5, BAG4 and FMNL2. In CRC tissues, circ_001569 negatively correlated with miR-145, and miR-145 correlated negatively with E2F5, BAG4 and FMNL2 expressions. 	MI0000461	Oncotarget 2016 May 3 7, 26680-91 doi:10.18632/oncotarget.8589 PMID:27058418
1145	Circular RNA	Circ_001569	miR-145	BAG4	Crc Cell Lines	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27058418	Emerging roles of circRNA_001569 targeting miR-145 in the proliferation and invasion of colorectal cancer.	hsa_circ_001569 was identified as a sponge of miR-145 and up-regulated miR-145 functional targets E2F5, BAG4 and FMNL2. In CRC tissues, circ_001569 negatively correlated with miR-145, and miR-145 correlated negatively with E2F5, BAG4 and FMNL2 expressions. 	MI0000461	Oncotarget 2016 May 3 7, 26680-91 doi:10.18632/oncotarget.8589 PMID:27058418
1146	Circular RNA	Circ_001569	miR-145	FMNL2	Crc Cell Lines	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27058418	Emerging roles of circRNA_001569 targeting miR-145 in the proliferation and invasion of colorectal cancer.	hsa_circ_001569 was identified as a sponge of miR-145 and up-regulated miR-145 functional targets E2F5, BAG4 and FMNL2. In CRC tissues, circ_001569 negatively correlated with miR-145, and miR-145 correlated negatively with E2F5, BAG4 and FMNL2 expressions. 	MI0000461	Oncotarget 2016 May 3 7, 26680-91 doi:10.18632/oncotarget.8589 PMID:27058418
1147	LncRNA	H19	miR-630	EZH2	Np69, Cne2	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27040767	Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma.	H19 affected the expression of enhancer of zeste homolog 2 (EZH2), which has also been observed to be up-regulated in NPC and to promote cell invasion. Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner.	MI0003644	Biochem Biophys Res Commun 2016 May 13 473, 913-919 doi:10.1016/j.bbrc.2016.03.150 PMID:27040767
1148	LncRNA	HOTAIR	miR-1	MAPK1	Skov3, Es-2, Ovcar3, A2780, And Coc1	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion.	The mRNA level of HOTAIR and MAPK1 in ovarian SKOV3 decreased when transected with miR-1, miR-214-3p, or miR-330-5p compared to negative control (p<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05).	MI0000651	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
1149	LncRNA	HOTAIR	miR-214-3p	MAPK1	Skov3, Es-2, Ovcar3, A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion.	The mRNA level of HOTAIR and MAPK1 in ovarian SKOV3 decreased when transected with miR-1, miR-214-3p, or miR-330-5p compared to negative control (p<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05).	MIMAT0000271	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
1150	LncRNA	HOTAIR	miR-330-5p	MAPK1	Skov3, Es-2, Ovcar3, A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion.	The mRNA level of HOTAIR and MAPK1 in ovarian SKOV3 decreased when transected with miR-1, miR-214-3p, or miR-330-5p compared to negative control (p<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05).	MIMAT0004693	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
1151	Artifically engineered RNA	miR-23 sponge	miR-23	LE1	Cho Cells	Re-Programming Of Cho Cells	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26097147	Re-programming CHO cell metabolism using miR-23 tips the balance towards a highly productive phenotype.	CHO clones depleted of miR-23 using a miR-sponge decoy demonstrated an average ~three-fold enhanced specific productivity with no impact on cell growth. Using a cell respirometer, mitochondrial activity was found to be enhanced by ~30% at Complex I and II of the electron transport system. Additionally, label-free proteomic analysis uncovered various potential novel targets of miR-23 including LE1 and IDH1, both implicated in oxidative metabolism and mitochondrial activity.	MI0000079	Biotechnol J 2015 Jul 10, 1029-40 doi:10.1002/biot.201500101 PMID:26097147
1152	Artifically engineered RNA	miR-23 sponge	miR-23	IDH1	Cho Cells	Re-Programming Of Cho Cells	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26097147	Re-programming CHO cell metabolism using miR-23 tips the balance towards a highly productive phenotype.	CHO clones depleted of miR-23 using a miR-sponge decoy demonstrated an average ~three-fold enhanced specific productivity with no impact on cell growth. Using a cell respirometer, mitochondrial activity was found to be enhanced by ~30% at Complex I and II of the electron transport system. Additionally, label-free proteomic analysis uncovered various potential novel targets of miR-23 including LE1 and IDH1, both implicated in oxidative metabolism and mitochondrial activity.	MI0000079	Biotechnol J 2015 Jul 10, 1029-40 doi:10.1002/biot.201500101 PMID:26097147
1153	Coding-mRNA	GPER	miR-148a	HOTAIR	Mda-Mb-231And Bt549	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	25928008	Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer.	E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients. After the mutation of the predicted miR-148a binding sites in HOTAIR, miR-148a had no effect on HOTAIR.	MI0000253	J Transl Med 2015 Apr 25 13, 131 doi:10.1186/s12967-015-0489-x PMID:25928008
1154	LncRNA	H19	miR-874	AQP3	Caco-2 Cells	Intestinal Barrier Dysfunction	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27059301	LncRNA H19 functions as a competing endogenous RNA to regulate AQP3 expression by sponging miR-874 in the intestinal barrier.	H19 function as a competing endogenous RNA (ceRNA) to regulate the expression of AQP3 through competition for miR-874, thus playing a significant role in maintaining intestinal barrier function.	MI0005532	FEBS Lett 2016 May 590, 1354-64 doi:10.1002/1873-3468.12171 PMID:27059301
1155	LncRNA	H19	miR-874	AQP3	Caco-2 Cells	Intestinal Barrier Dysfunction	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	27059301	LncRNA H19 functions as a competing endogenous RNA to regulate AQP3 expression by sponging miR-874 in the intestinal barrier.	H19 function as a competing endogenous RNA (ceRNA) to regulate the expression of AQP3 through competition for miR-874, thus playing a significant role in maintaining intestinal barrier function.	MI0005532	FEBS Lett 2016 May 590, 1354-64 doi:10.1002/1873-3468.12171 PMID:27059301
1156	LncRNA	HNF1A-AS1	miR-30b-5p	BCL2	Hepg2, Smmc-7721, Plc/Prf/5, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27084450	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p.	HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. 	MIMAT0000420	Biochem Biophys Res Commun 2016 May 13 473, 1268-1275 doi:10.1016/j.bbrc.2016.04.054 PMID:27084450
1157	LncRNA	HNF1A-AS1	miR-30b-5p	ATG5	Hepg2, Smmc-7721, Plc/Prf/5, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27084450	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p.	HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b. 	MIMAT0000420	Biochem Biophys Res Commun 2016 May 13 473, 1268-1275 doi:10.1016/j.bbrc.2016.04.054 PMID:27084450
1158	LncRNA	GAS5	miR-21	PTEN	Skbr-3	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27034004	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer.	 GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. 	MI0000077	Oncotarget 2016 May 10 7, 27778-86 doi:10.18632/oncotarget.8413 PMID:27034004
1159	LncRNA	GAS5	miR-21	PTEN	Skbr-3	Breast Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	27034004	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer.	 GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN. 	MI0000077	Oncotarget 2016 May 10 7, 27778-86 doi:10.18632/oncotarget.8413 PMID:27034004
1160	LncRNA	Ftx	miR-545	RIG-I	Hepg2, Hep3B, Huh7, Smmc-7721 And Bel-7402	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26992218	Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.	RIG-I as a direct target of miR-545. The expression of RIG-I was downregulated in HCC tissues and was inversely correlated with miR-545 expression. Our data revealed that ectopic expression of RIG-I abrogated the effects of lncRNA Ftx or miR-545 on HCC cells. LncRNA Ftx/miR-545-mediated downregulation of RIG-I led to increased Akt phosphorylation in vitro and in vivo.	MI0003516	Oncotarget 2016 May 3 7, 25350-65 doi:10.18632/oncotarget.8129 PMID:26992218
1161	LncRNA	Ftx	miR-545	RIG-I	Hepg2, Hep3B, Huh7, Smmc-7721 And Bel-7402	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26992218	Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.	RIG-I as a direct target of miR-545. The expression of RIG-I was downregulated in HCC tissues and was inversely correlated with miR-545 expression. Our data revealed that ectopic expression of RIG-I abrogated the effects of lncRNA Ftx or miR-545 on HCC cells. LncRNA Ftx/miR-545-mediated downregulation of RIG-I led to increased Akt phosphorylation in vitro and in vivo.	MI0003516	Oncotarget 2016 May 3 7, 25350-65 doi:10.18632/oncotarget.8129 PMID:26992218
1162	Coding-mRNA	CDH5	miR-10b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000267	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1163	Coding-mRNA	HOXD1	miR-10b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000267	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1164	Coding-mRNA	HOXD10	miR-10b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000267	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1165	Coding-mRNA	CDH5	miR-9	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000466	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1166	Coding-mRNA	HOXD1	miR-9	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000466	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1167	Coding-mRNA	HOXD10	miR-9	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000466	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1168	Coding-mRNA	CDH5	miR-125b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000446	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1169	Coding-mRNA	HOXD1	miR-125b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000446	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1170	Coding-mRNA	HOXD10	miR-125b	STARD13	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000446	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1171	Coding-mRNA	STARD13	miR-10b	NA	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000267	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1172	Coding-mRNA	STARD13	miR-9	NA	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000466	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1173	Coding-mRNA	STARD13	miR-125b	NA	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26985770	STARD13-correlated ceRNA network inhibits EMT and metastasis of breast cancer.	CDH5, HOXD1, and HOXD10 as putative STARD13 ceRNAs and they display concordant patterns with STARD13 in different metastatic potential breast cancer cell lines and tissues. Notably, 3'UTRs of these genes suppress breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT) in vitro and in vivo, which are activated through the crosstalk between STARD13 and its ceRNAs in 3'UTR- and miRNA-dependent manners.	MI0000446	Oncotarget 2016 Apr 26 7, 23197-211 doi:10.18632/oncotarget.8099 PMID:26985770
1174	Artifically engineered RNA	miR-135b sponge	miR-135b	LATS2	Mhcc97	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26429530	miR-135b promotes the invasion and metastasis of hepatocellular carcinoma cells	The invasive and migratory abilities in vitro and in vivo were significantly suppressed in miR-135b down-regulated MHCC97 hepatocellular carcinoma cells silenced by the pcDNA-miR-135b-Sponge plasmid. Western blotting and dual-luciferase report system analysis showed that multiple key components in the Hippo pathway, including large tumor suppressor homolog 2 (LATS2), beta-transducin repeats-containing proteins (b-TrCP), N-myc downstream-regulated gene 2 (NDR2) as well as leucine zipper tumor suppressor gene 1 (LZTS1) were targeted by miR-135b.	MI0000810	Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2015 Oct 31, 1316-21,  PMID:26429530
1175	Artifically engineered RNA	miR-135b sponge	miR-135b	b-TrCP	Mhcc97	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26429530	miR-135b promotes the invasion and metastasis of hepatocellular carcinoma cells	The invasive and migratory abilities in vitro and in vivo were significantly suppressed in miR-135b down-regulated MHCC97 hepatocellular carcinoma cells silenced by the pcDNA-miR-135b-Sponge plasmid. Western blotting and dual-luciferase report system analysis showed that multiple key components in the Hippo pathway, including large tumor suppressor homolog 2 (LATS2), beta-transducin repeats-containing proteins (b-TrCP), N-myc downstream-regulated gene 2 (NDR2) as well as leucine zipper tumor suppressor gene 1 (LZTS1) were targeted by miR-135b.	MI0000810	Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2015 Oct 31, 1316-21,  PMID:26429530
1176	Artifically engineered RNA	miR-135b sponge	miR-135b	NDR2	Mhcc97	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26429530	miR-135b promotes the invasion and metastasis of hepatocellular carcinoma cells	The invasive and migratory abilities in vitro and in vivo were significantly suppressed in miR-135b down-regulated MHCC97 hepatocellular carcinoma cells silenced by the pcDNA-miR-135b-Sponge plasmid. Western blotting and dual-luciferase report system analysis showed that multiple key components in the Hippo pathway, including large tumor suppressor homolog 2 (LATS2), beta-transducin repeats-containing proteins (b-TrCP), N-myc downstream-regulated gene 2 (NDR2) as well as leucine zipper tumor suppressor gene 1 (LZTS1) were targeted by miR-135b.	MI0000810	Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2015 Oct 31, 1316-21,  PMID:26429530
1177	Artifically engineered RNA	miR-135b sponge	miR-135b	LZTS1	Mhcc97	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26429530	miR-135b promotes the invasion and metastasis of hepatocellular carcinoma cells	The invasive and migratory abilities in vitro and in vivo were significantly suppressed in miR-135b down-regulated MHCC97 hepatocellular carcinoma cells silenced by the pcDNA-miR-135b-Sponge plasmid. Western blotting and dual-luciferase report system analysis showed that multiple key components in the Hippo pathway, including large tumor suppressor homolog 2 (LATS2), beta-transducin repeats-containing proteins (b-TrCP), N-myc downstream-regulated gene 2 (NDR2) as well as leucine zipper tumor suppressor gene 1 (LZTS1) were targeted by miR-135b.	MI0000810	Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2015 Oct 31, 1316-21,  PMID:26429530
1178	LncRNA	FER1L4	miR-106a-5p	NA	Rko, Lovo, Hct116, Sw480 And Sw620	Colon Cancer	Homo sapiens (human)	qRT-PCR	26224446	Long non-coding RNA Fer-1-like protein 4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer.	Among the colon cancer cell lines, FER1L4 levels were relatively lower, with concurrent high levels of miR-106a-5p. Restoration of FER1L4 decreased the expression of miR-106a-5p, and had a significant influence on colon cancer cell proliferation, migration and invasion.	MIMAT0000103	Cancer Sci 2015 Oct 106, 1323-32 doi:10.1111/cas.12759 PMID:26224446
1179	LncRNA	MIAT	miR-150-5p	HLEC	Sra01/04 Cell	NA	Homo sapiens (human)	microarray,Immunofluoresence assay	26818536	Role of long non-coding RNA MIAT in proliferation, apoptosis and migration of lens epithelial cells: a clinical and in vitro study.	MIAT knockdown could repress tumour necrosis factor-a-induced abnormal proliferation and migration of HLECs, suggesting a potential role of MIAT in PCO-related pathological process. Moreover, we found that MIAT acted as a ceRNA, and formed a feedback loop with Akt and miR-150-5p to regulate HLEC function.	MIMAT0000451	J Cell Mol Med 2016 Mar 20, 537-48 doi:10.1111/jcmm.12755 PMID:26818536
1180	Pseudogene	Foxo3P	miR-221	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0000298	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1181	Pseudogene	Foxo3P	miR-136-3p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0004606	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1182	Pseudogene	Foxo3P	miR-138	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0000455	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1183	Pseudogene	Foxo3P	miR-149-3p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0004609	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1184	Pseudogene	Foxo3P	miR-433	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0001723	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1185	Pseudogene	Foxo3P	miR-762	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0003892	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1186	Pseudogene	Foxo3P	miR-3614-5p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0017992	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1187	Pseudogene	Foxo3P	miR-3622b-5p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0018005	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1188	Circular RNA	Circ-Foxo3	miR-221	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0000298	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1189	Circular RNA	Circ-Foxo3	miR-136-3p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0004606	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1190	Circular RNA	Circ-Foxo3	miR-138	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0000455	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1191	Circular RNA	Circ-Foxo3	miR-149-3p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0004609	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1192	Circular RNA	Circ-Foxo3	miR-433	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0001723	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1193	Circular RNA	Circ-Foxo3	miR-762	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MI0003892	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1194	Circular RNA	Circ-Foxo3	miR-3614-5p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0017992	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1195	Circular RNA	Circ-Foxo3	miR-3622b-5p	Foxo3	Mda-Mb-468 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26657152	Foxo3 activity promoted by non-coding effects of circular RNA and Foxo3 pseudogene in the inhibition of tumor growth and angiogenesis.	We found that the transcripts of Foxo3 mRNA, Foxo3P and Foxo3 circular RNA were all targets of miR-22, miR-136*, miR-138, miR-149*, miR-433, miR-762, miR-3614–5p and miR-3622b–5p. Together, these mechanisms effectively promoted the translation of the Foxo3 mRNA.	MIMAT0018005	Oncogene 2016 Jul 28 35, 3919-31 doi:10.1038/onc.2015.460 PMID:26657152
1196	Viral RNA	HBx	miR-7	EGFR	Hep3B, Hepg2	Hepatocellular Carcinoma	Hepatitis B virus (HBV)	luciferase reporter assays;qRT-PCR	23840262	Hepatitis B Virus-Encoded X Protein Downregulates EGFR Expression via Inducing MicroRNA-7 in Hepatocellular Carcinoma Cells.	we found that HBx upregulates miR-7 expression to target 3'UTR of EGFR mRNA, which in turn results in the reduction of EGFR protein expression in HCC cells. HBx-mediated EGFR suppression renders HCC cells a slow-growth behavior. Deprivation of HBx or miR-7 expression or restoration of EGFR expression can increase the growth rate of HCC cells.	MI0008947	Evid Based Complement Alternat Med 2013  2013, 682380 doi:10.1155/2013/682380 PMID:23840262
1197	Viral RNA	HBx	miR-7	EGFR	Hep3B, Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	23840262	Hepatitis B Virus-Encoded X Protein Downregulates EGFR Expression via Inducing MicroRNA-7 in Hepatocellular Carcinoma Cells.	we found that HBx upregulates miR-7 expression to target 3'UTR of EGFR mRNA, which in turn results in the reduction of EGFR protein expression in HCC cells. HBx-mediated EGFR suppression renders HCC cells a slow-growth behavior. Deprivation of HBx or miR-7 expression or restoration of EGFR expression can increase the growth rate of HCC cells.	MI0008947	Evid Based Complement Alternat Med 2013  2013, 682380 doi:10.1155/2013/682380 PMID:23840262
1198	LncRNA	ESAT-6	miR-155	SOCS1	Raw264.7	Tuberculosis	Homo sapiens (human)	qRT-PCR;Western blot assay	25721573	Early secreted antigen ESAT-6 of Mycobacterium Tuberculosis promotes apoptosis of macrophages via targeting the microRNA155-SOCS1 interaction.	ESAT-6 significantly increased miR-155 expression, which was dependent on TLR2/NF-κB activation in macrophages. Induced expression of miRNA-155 was required for the ESAT-6-mediated protective immune response and macrophage apoptosis. ESAT-6 promoted macrophage apoptosis by targeting the miR-155-SOCS1 pathway. The differential expression levels of TLR2, BIC, and SOCS1 were involved in regulating the immune response in human peripheral blood mononuclear cells of patients with active tuberculosis (TB) and latent TB (LTB).	MI0000681	Cell Physiol Biochem 2015  35, 1276-88 doi:10.1159/000373950 PMID:25721573
1199	LncRNA	ESAT-6	miR-155	SOCS1	Raw264.7	Tuberculosis	Mus musculus (mouse)	qRT-PCR;Western blot assay	25721573	Early secreted antigen ESAT-6 of Mycobacterium Tuberculosis promotes apoptosis of macrophages via targeting the microRNA155-SOCS1 interaction.	ESAT-6 significantly increased miR-155 expression, which was dependent on TLR2/NF-κB activation in macrophages. Induced expression of miRNA-155 was required for the ESAT-6-mediated protective immune response and macrophage apoptosis. ESAT-6 promoted macrophage apoptosis by targeting the miR-155-SOCS1 pathway. The differential expression levels of TLR2, BIC, and SOCS1 were involved in regulating the immune response in human peripheral blood mononuclear cells of patients with active tuberculosis (TB) and latent TB (LTB).	MI0000681	Cell Physiol Biochem 2015  35, 1276-88 doi:10.1159/000373950 PMID:25721573
1200	LncRNA	MIR31HG	miR-193b	CCND1	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1201	LncRNA	MIR31HG	miR-193b	MCL1	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1202	LncRNA	MIR31HG	miR-193b	NT5E	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1203	LncRNA	MIR31HG	miR-193b	KRAS	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1204	LncRNA	MIR31HG	miR-193b	uPA	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1205	LncRNA	MIR31HG	miR-193b	ETS1	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1206	LncRNA	MIR31HG	miR-193b	ACTB	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	Using luciferase reporter and RIP assays, we provide evidence that miR-193b directly targeted MIR31HG by binding to two microRNA binding sites in the MIR31HG sequence. On the other hand, MIR31HG may act as an endogenous 'sponge' by competing for miR-193b binding to regulate the miRNA targets.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
1207	LncRNA	BC032469	miR-1207-5p	hTERT	Sgc-7901, Mkn28, Ags And Mkn45	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26549025	Long noncoding RNA BC032469, a novel competing endogenous RNA, upregulates hTERT expression by sponging miR-1207-5p and promotes proliferation in gastric cancer.	Downregulation of BC032469 resulted in a significant inhibition of proliferation in vitro and in vivo. Mechanistically, BC032469 could directly bind to miR-1207-5p and effectively functioned as a sponge for miR-1207-5p to modulate the derepression of hTERT.	MIMAT0005871	Oncogene 2016 Jul 7 35, 3524-34 doi:10.1038/onc.2015.413 PMID:26549025
1208	LncRNA	miR-183 sponge	miR-183	RAB21	Mcf-7,Mda-Mb-231,Sk-Br-3,T47D, Zr-75-1, Mcf-10A	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25394902	MiR-183/-96/-182 cluster is up-regulated in most breast cancers and increases cell proliferation and migration.	To investigate the biological effects of the miR-183/-96 /-182 cluster in breast cancer, we generated miR-96, miR-182 and miR-183 overexpression stable cell lines to check the overdose effects; we also used miR-Down antagomir for each miRNA as well as miR-183/-96 /-182 cluster sponge lentivirus to check the knockdown effects.The data showed that RAB21 protein was significantly decreased in the miR-183 overexpression cell lines, but not in miR-96 and miR-182 overexpression cell lines compared with the empty vector control cell lines and wild-type cells	MI0000273	Breast Cancer Res 2014 Nov 14 16, 473 doi:10.1186/s13058-014-0473-z PMID:25394902
1209	LncRNA	lincRNA-ROR	miR-145	Nanog	Pancreatic Cancer Tissues	Pancreatic Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	26636540	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer.	The effects of ROR on PCSCs were studied by RNA interference approaches in vitro and in vivo. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were gained from bioinformatic analysis, luciferase assays and RNA binding protein immunoprecipitation. The positive ROR/Nanog interaction was identified and verified by immunohistochemistry assay. Compared with adjacent non-tumor tissues, ROR was up-regulated in most tumor tissues. Knockdown of ROR by RNA interference in PCSCs inhibited proliferation, induced apoptosis and decreased migration. Moreover, ROR silencing resulted in significantly decreased tumourigenicity of PCSCs in nude mice than controls. In particular, ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Nanog.	MI0000461	Oncotarget 2016 Jan 12 7, 1608-18 doi:10.18632/oncotarget.6450 PMID:26636540
1210	LncRNA	lincRNA-ROR	miR-145	Nanog	Pancreatic Cancer Tissues	Pancreatic Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	26636540	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer.	The effects of ROR on PCSCs were studied by RNA interference approaches in vitro and in vivo. Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were gained from bioinformatic analysis, luciferase assays and RNA binding protein immunoprecipitation. The positive ROR/Nanog interaction was identified and verified by immunohistochemistry assay. Compared with adjacent non-tumor tissues, ROR was up-regulated in most tumor tissues. Knockdown of ROR by RNA interference in PCSCs inhibited proliferation, induced apoptosis and decreased migration. Moreover, ROR silencing resulted in significantly decreased tumourigenicity of PCSCs in nude mice than controls. In particular, ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Nanog.	MI0000461	Oncotarget 2016 Jan 12 7, 1608-18 doi:10.18632/oncotarget.6450 PMID:26636540
1211	LncRNA	TGFB2-OT1	miR-3960	CERS1	Huvec	Inflammation Of Vascular	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26565952	A new microRNA signal pathway regulated by long noncoding RNA TGFB2-OT1 in autophagy and inflammation of vascular endothelial cells.	TGFB2-OT1 acted as a competing endogenous RNA, bound to MIR3960, MIR4488 and MIR4459, then regulated the expression of the miRNA targets CERS1 (ceramide synthase 1), NAT8L (N-acetyltransferase 8-like [GCN5-related, putative]), and LARP1 (La ribonucleoprotein domain family, member 1). CERS1 and NAT8L participate in autophagy by affecting mitochondrial function. TGFB2-OT1 increased the LARP1 level, which promoted SQSTM1 (sequestosome 1) expression, NFKB RELA and CASP1 activation, and then production of IL6, IL8 and IL1B in VECs.	MI0016964	Autophagy 2015  11, 2172-83 doi:10.1080/15548627.2015.1106663 PMID:26565952
1212	LncRNA	TGFB2-OT1	miR-4488	NAT8L	Huvec	Inflammation Of Vascular	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26565952	A new microRNA signal pathway regulated by long noncoding RNA TGFB2-OT1 in autophagy and inflammation of vascular endothelial cells.	TGFB2-OT1 acted as a competing endogenous RNA, bound to MIR3960, MIR4488 and MIR4459, then regulated the expression of the miRNA targets CERS1 (ceramide synthase 1), NAT8L (N-acetyltransferase 8-like [GCN5-related, putative]), and LARP1 (La ribonucleoprotein domain family, member 1). CERS1 and NAT8L participate in autophagy by affecting mitochondrial function. TGFB2-OT1 increased the LARP1 level, which promoted SQSTM1 (sequestosome 1) expression, NFKB RELA and CASP1 activation, and then production of IL6, IL8 and IL1B in VECs.	MI0016849	Autophagy 2015  11, 2172-83 doi:10.1080/15548627.2015.1106663 PMID:26565952
1213	LncRNA	TGFB2-OT1	miR-4459	LARP1	Huvec	Inflammation Of Vascular	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26565952	A new microRNA signal pathway regulated by long noncoding RNA TGFB2-OT1 in autophagy and inflammation of vascular endothelial cells.	TGFB2-OT1 acted as a competing endogenous RNA, bound to MIR3960, MIR4488 and MIR4459, then regulated the expression of the miRNA targets CERS1 (ceramide synthase 1), NAT8L (N-acetyltransferase 8-like [GCN5-related, putative]), and LARP1 (La ribonucleoprotein domain family, member 1). CERS1 and NAT8L participate in autophagy by affecting mitochondrial function. TGFB2-OT1 increased the LARP1 level, which promoted SQSTM1 (sequestosome 1) expression, NFKB RELA and CASP1 activation, and then production of IL6, IL8 and IL1B in VECs.	MI0016805	Autophagy 2015  11, 2172-83 doi:10.1080/15548627.2015.1106663 PMID:26565952
1214	LncRNA	GAS5	miR-222	p27	(Ccl4) Liver Injury Model	Liver Fibrosis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26446789	Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA.	Quantitative RT-PCR demonstrated that the copy numbers of GAS5 per cell are higher than those of miR-222. GAS5 increased the level of p27 protein by functioning as a competing endogenous RNA for miR-222, thereby inhibiting the activation and proliferation of HSCs.	MI0000299	J Biol Chem 2015 Nov 20 290, 28286-28298 doi:10.1074/jbc.M115.683813 PMID:26446789
1215	LncRNA	GAS5	miR-222	p27	(Ccl4) Liver Injury Model	Liver Fibrosis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	26446789	Long Non-coding RNA Growth Arrest-specific Transcript 5 (GAS5) Inhibits Liver Fibrogenesis through a Mechanism of Competing Endogenous RNA.	Quantitative RT-PCR demonstrated that the copy numbers of GAS5 per cell are higher than those of miR-222. GAS5 increased the level of p27 protein by functioning as a competing endogenous RNA for miR-222, thereby inhibiting the activation and proliferation of HSCs.	MI0000299	J Biol Chem 2015 Nov 20 290, 28286-28298 doi:10.1074/jbc.M115.683813 PMID:26446789
1216	Artifically engineered RNA	miR-21 sponge	miR-21	PDCD4	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25477028	Downregulation of microRNA-21 expression restrains non-small cell lung cancer cell proliferation and migration through upregulation of programmed cell death 4.	Inhibition of miR-21 expression following transfection of miR-21-sponge reduced cell proliferation, migration, and invasion of A549 cells. Depletion of PDCD4 by siRNA transfection reversed the reduction of cell proliferation, migration, and invasion induced by inhibition of miR-21 in A549 cells. It indicates that miR-21 is highly expressed in patients with NSCLC and inhibition of miR-21 expression reduces proliferation, migration, and invasion of A549 cells by upregulating PDCD4 expression.	MI0000077	Cancer Gene Ther 2015 Jan 22, 23-9 doi:10.1038/cgt.2014.66 PMID:25477028
1217	LncRNA	MALAT1	miR-145	NA	Hela And Caski	Cervical Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay;Northern blot assay	26311052	Long non-coding RNA MALAT1 modulates radiosensitivity of HR-HPV+ cervical cancer via sponging miR-145.	 By performing RNA-binding protein immunoprecipitation (RIP) assay and RNA pull-down assay, we confirmed that miR-145 and MALAT1 were in the same Ago2 complex and there was a reciprocal repression between them. Then, we explored the function of MALAT1-miR-145 in radiosensitivity of cervical cancers cells and demonstrated that si-MALAT1 and miR-145 had some level of synergic effect in reducing cancer cell colony formation, cell cycle regulation, and inducing apoptosis. 	MI0000461	Tumour Biol 2016 Feb 37, 1683-91 doi:10.1007/s13277-015-3946-5 PMID:26311052
1218	LncRNA	FER1L4	miR-106a-5p	PTEN	Ags, Mgc-803 And Sgc-7901	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	26306906	Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression.	Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein.	MIMAT0000103	Sci Rep 2015 Aug 26 5, 13445 doi:10.1038/srep13445 PMID:26306906
1219	LncRNA	MEG3	miR-181a	BCL2	Hgc-27 And Mgc-803	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26253106	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate gastric cancer progression.	ectopic expression of MEG3 in HGC-27 and MGC-803 cells inhibited cell proliferation, migration, invasion, and promoted cell apoptosis, which might be due to MEG3 sequestering oncogenic miR-181 s in GC cells. Furthermore, MEG3 could up-regulated Bcl-2 via its competing endogenous RNA (ceRNA) activity on miR-181a	MI0000269	J Exp Clin Cancer Res 2015 Aug 8 34, 79 doi:10.1186/s13046-015-0197-7 PMID:26253106
1220	LncRNA	lincRNA-ROR	let-7i-5p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0000415	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1221	LncRNA	lincRNA-ROR	let-7b-5p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0000063	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1222	LncRNA	lincRNA-ROR	let-7e-5p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0000066	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1223	LncRNA	lincRNA-ROR	let-7e-3p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0004485	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1224	LncRNA	lincRNA-ROR	let-7b-3p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0004482	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1225	LncRNA	lincRNA-ROR	let-7c-3p	NA	Panc-1 And Sw1990	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells.	linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. 	MIMAT0026472	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
1226	Circular RNA	CircRNA_0007874	miR-9	p21	Hepg2, Smmc-7721, Qgy-7701 And Sk-Hep1	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	28520103	Circular RNA MTO1 acts as the sponge of miR-9 to suppress hepatocellular carcinoma progression.	We analyzed the expression profile of human circRNAs in HCC tissues and identified circMTO1 (mitochondrial translation optimization 1 homologue; hsa_circRNA_0007874/hsa_circRNA_104135) as one circRNA significantly down-regulated in HCC tissues. HCC patients with low circMTO1 expression had shortened survival. By using a biotin-labeled circMTO1 probe to perform RNA in vivo precipitation in HCC cells, we identified miR-9 as the circMTO1-associated miRNA. Furthermore, silencing of circMTO1 in HCC could down-regulate p21, the target of oncogenic miR-9, resulting in the promotion of HCC cell proliferation and invasion. In addition, the tumor-promoting effect of circMTO1 silencing was blocked by miR9 inhibitor. Intratumoral administration of cholesterol-conjugated circMTO1 small interfering RNA promoted tumor growth in HCC-bearing mice in vivo.	MI0000466	Hepatology 2017 Oct 66, 1151-1164 doi:10.1002/hep.29270 PMID:28520103
1227	Circular RNA	CircRNA_104135	miR-9	p21	Hepg2, Smmc-7721, Qgy-7701 And Sk-Hep1	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	28520103	Circular RNA MTO1 acts as the sponge of miR-9 to suppress hepatocellular carcinoma progression.	We analyzed the expression profile of human circRNAs in HCC tissues and identified circMTO1 (mitochondrial translation optimization 1 homologue; hsa_circRNA_0007874/hsa_circRNA_104135) as one circRNA significantly down-regulated in HCC tissues. HCC patients with low circMTO1 expression had shortened survival. By using a biotin-labeled circMTO1 probe to perform RNA in vivo precipitation in HCC cells, we identified miR-9 as the circMTO1-associated miRNA. Furthermore, silencing of circMTO1 in HCC could down-regulate p21, the target of oncogenic miR-9, resulting in the promotion of HCC cell proliferation and invasion. In addition, the tumor-promoting effect of circMTO1 silencing was blocked by miR9 inhibitor. Intratumoral administration of cholesterol-conjugated circMTO1 small interfering RNA promoted tumor growth in HCC-bearing mice in vivo.	MI0000466	Hepatology 2017 Oct 66, 1151-1164 doi:10.1002/hep.29270 PMID:28520103
1228	LncRNA	HOTAIR	miR-148a	Snail2	Kyse30, Kyse150, Te-1, Eca-1, Eca-109	Esophageal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28441714	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.	In vitro analysis showedlncRNA-HOTAIR enhanced EC cell proliferation, invasion and migration, and promoted the EMT. Mechanistic investigations revealedlncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.	MI0000253	Biomed Pharmacother 2017 Jun 90, 888-896 doi:10.1016/j.biopha.2017.03.103 PMID:28441714
1229	LncRNA	HOTAIR	miR-148a	E-cadherin	Kyse30, Kyse150, Te-1, Eca-1, Eca-109	Esophageal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28441714	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.	In vitro analysis showedlncRNA-HOTAIR enhanced EC cell proliferation, invasion and migration, and promoted the EMT. Mechanistic investigations revealedlncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.	MI0000253	Biomed Pharmacother 2017 Jun 90, 888-896 doi:10.1016/j.biopha.2017.03.103 PMID:28441714
1230	LncRNA	HOTAIR	miR-148a	N-cadherin	Kyse30, Kyse150, Te-1, Eca-1, Eca-109	Esophageal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28441714	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.	In vitro analysis showedlncRNA-HOTAIR enhanced EC cell proliferation, invasion and migration, and promoted the EMT. Mechanistic investigations revealedlncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.	MI0000253	Biomed Pharmacother 2017 Jun 90, 888-896 doi:10.1016/j.biopha.2017.03.103 PMID:28441714
1231	LncRNA	HOTAIR	miR-148a	Vimentin	Kyse30, Kyse150, Te-1, Eca-1, Eca-109	Esophageal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28441714	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer.	In vitro analysis showedlncRNA-HOTAIR enhanced EC cell proliferation, invasion and migration, and promoted the EMT. Mechanistic investigations revealedlncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression.	MI0000253	Biomed Pharmacother 2017 Jun 90, 888-896 doi:10.1016/j.biopha.2017.03.103 PMID:28441714
1232	Circular RNA	Circ_0016347	miR-214	caspase1	Saos-2 And Mg-63	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28424426	Circular RNA hsa-circ-0016347 promotes proliferation, invasion and metastasis of osteosarcoma cells.	circ-0016347 acted as a positive regulator in osteosarcoma cells proliferation and invasion. Moreover, circ-0016347 was identified as a sponge of miR-214 that upregulated the expression of caspase-1, which is the functional target of miR-214.	MI0000290	Oncotarget 2017 Apr 11 8, 25571-25581 doi:10.18632/oncotarget.16104 PMID:28424426
1233	Circular RNA	Circ_0016347	miR-214	caspase1	Saos-2 And Mg-63	Osteosarcoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28424426	Circular RNA hsa-circ-0016347 promotes proliferation, invasion and metastasis of osteosarcoma cells.	circ-0016347 acted as a positive regulator in osteosarcoma cells proliferation and invasion. Moreover, circ-0016347 was identified as a sponge of miR-214 that upregulated the expression of caspase-1, which is the functional target of miR-214.	MI0000290	Oncotarget 2017 Apr 11 8, 25571-25581 doi:10.18632/oncotarget.16104 PMID:28424426
1234	Circular RNA	ciRS-7	miR-7	PTEN	Mgc-803 And Hgc-27	Gastric Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	28608528	Overexpression of circular RNA ciRS-7 abrogates the tumor suppressive effect of miR-7 on Gastric cancer via PTEN/PI3K/AKT signaling pathway.	overexpression of ciRS-7 blocked the miR-7-induced tumor suppression in MGC-803 and HGC-27 cells and led to a more aggressive oncogenic phenotype, via antagonizing miR-7-mediated PTEN/PI3K/AKT pathway.	MI0008947	J Cell Biochem 2018 Jan 119, 440-446 doi:10.1002/jcb.26201 PMID:28608528
1235	Circular RNA	ciRS-7	miR-7	PI3K	Mgc-803 And Hgc-27	Gastric Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	28608528	Overexpression of circular RNA ciRS-7 abrogates the tumor suppressive effect of miR-7 on Gastric cancer via PTEN/PI3K/AKT signaling pathway.	overexpression of ciRS-7 blocked the miR-7-induced tumor suppression in MGC-803 and HGC-27 cells and led to a more aggressive oncogenic phenotype, via antagonizing miR-7-mediated PTEN/PI3K/AKT pathway.	MI0008947	J Cell Biochem 2018 Jan 119, 440-446 doi:10.1002/jcb.26201 PMID:28608528
1236	Circular RNA	ciRS-7	miR-7	PTEN	Mgc-803 And Hgc-27	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28608528	Overexpression of circular RNA ciRS-7 abrogates the tumor suppressive effect of miR-7 on Gastric cancer via PTEN/PI3K/AKT signaling pathway.	overexpression of ciRS-7 blocked the miR-7-induced tumor suppression in MGC-803 and HGC-27 cells and led to a more aggressive oncogenic phenotype, via antagonizing miR-7-mediated PTEN/PI3K/AKT pathway.	MI0008947	J Cell Biochem 2018 Jan 119, 440-446 doi:10.1002/jcb.26201 PMID:28608528
1237	Circular RNA	ciRS-7	miR-7	PI3K	Mgc-803 And Hgc-27	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28608528	Overexpression of circular RNA ciRS-7 abrogates the tumor suppressive effect of miR-7 on Gastric cancer via PTEN/PI3K/AKT signaling pathway.	overexpression of ciRS-7 blocked the miR-7-induced tumor suppression in MGC-803 and HGC-27 cells and led to a more aggressive oncogenic phenotype, via antagonizing miR-7-mediated PTEN/PI3K/AKT pathway.	MI0008947	J Cell Biochem 2018 Jan 119, 440-446 doi:10.1002/jcb.26201 PMID:28608528
1238	LncRNA	XIST	miR-449a	BCL2	Nl9980, Nci-H1299, Nci-H460, Spc-A-1 And A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	28248928	The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer	knockdown of XIST significantly suppressed the tumor growth in NSCLC A549 xenograft mouse model. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2.	MI0001648	Acta Pharmacol Sin 2017 Mar 38, 371-381 doi:10.1038/aps.2016.133 PMID:28248928
1239	LncRNA	XIST	miR-449a	BCL2	Nl9980, Nci-H1299, Nci-H460, Spc-A-1 And A549	Non-Small Cell Lung Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	28248928	The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer	knockdown of XIST significantly suppressed the tumor growth in NSCLC A549 xenograft mouse model. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2.	MI0001648	Acta Pharmacol Sin 2017 Mar 38, 371-381 doi:10.1038/aps.2016.133 PMID:28248928
1240	LncRNA	TUG1	miR-9	Bcl2l11	Male Sprague-Dawley (Sd) Rats	Ischemia	Homo sapiens (human)	qRT-PCR;Western blot assay	28202414	LncRNA TUG1 sponges microRNA-9 to promote neurons apoptosis by up-regulated Bcl2l11 under ischemia.	Knockdown of TUG1 decreased the ratio of apoptotic cells and promoted cells survival in vitro, which may be regulated by the elevated miRNA-9 expression and decreased Bcl2l11 protein. Furthermore, TUG1 could directly interact with miR-9 and down-regulating miR-9 could efficiently reverse the function of TUG1 on the Bcl2l11 expression. 	MI0000466	Biochem Biophys Res Commun 2017 Mar 25 485, 167-173 doi:10.1016/j.bbrc.2017.02.043 PMID:28202414
1241	LncRNA	TUG1	miR-9	Bcl2l11	Male Sprague-Dawley (Sd) Rats	Ischemia	Mus musculus (mouse)	qRT-PCR;Western blot assay	28202414	LncRNA TUG1 sponges microRNA-9 to promote neurons apoptosis by up-regulated Bcl2l11 under ischemia.	Knockdown of TUG1 decreased the ratio of apoptotic cells and promoted cells survival in vitro, which may be regulated by the elevated miRNA-9 expression and decreased Bcl2l11 protein. Furthermore, TUG1 could directly interact with miR-9 and down-regulating miR-9 could efficiently reverse the function of TUG1 on the Bcl2l11 expression. 	MI0000466	Biochem Biophys Res Commun 2017 Mar 25 485, 167-173 doi:10.1016/j.bbrc.2017.02.043 PMID:28202414
1242	LncRNA	TUG1	miR-300	NA	Eh-Gb1, Gbc-Sd, Noz, Sgc-996	Gallbladder Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28178615	Long non-coding RNA TUG1 promotes cell proliferation and metastasis by negatively regulating miR-300 in gallbladder carcinoma.	Mechanically, we found that TUG1 is upregulated by TGF-b1, and knockdown of TUG1 inhibited GBC cell EMT. Furthermore, we identified that miR-300, which has been reported as a suppressor in other types of cancer, is negatively regulated by TUG1	MI0005525	Biomed Pharmacother 2017 Apr 88, 863-869 doi:10.1016/j.biopha.2017.01.150 PMID:28178615
1243	Artifically engineered RNA	MIM169a	miR-169a	NF-YA10	Oryza Sativa	Magnaporthe	Oryza sativa (rice)	qRT-PCR	28144248	Osa-miR169 Negatively Regulates Rice Immunity against the Blast Fungus Magnaporthe oryzae.	Overexpression of a target mimicry that acts as a sponge to trap miR169a led to enhanced resistance to M. oryzae. In addition, three of miR169's target genes were also differentially up-regulated in the resistant accession upon M. oryzae infection. 	NA	Front Plant Sci 2017  8, 2 doi:10.3389/fpls.2017.00002 PMID:28144248
1244	Artifically engineered RNA	MIM169a	miR-169a	NF-YA1	Oryza Sativa	Magnaporthe	Oryza sativa (rice)	qRT-PCR	28144248	Osa-miR169 Negatively Regulates Rice Immunity against the Blast Fungus Magnaporthe oryzae.	Overexpression of a target mimicry that acts as a sponge to trap miR169a led to enhanced resistance to M. oryzae. In addition, three of miR169's target genes were also differentially up-regulated in the resistant accession upon M. oryzae infection. 	NA	Front Plant Sci 2017  8, 2 doi:10.3389/fpls.2017.00002 PMID:28144248
1245	Artifically engineered RNA	MIM169a	miR-169a	NF-YA2	Oryza Sativa	Magnaporthe	Oryza sativa (rice)	qRT-PCR	28144248	Osa-miR169 Negatively Regulates Rice Immunity against the Blast Fungus Magnaporthe oryzae.	Overexpression of a target mimicry that acts as a sponge to trap miR169a led to enhanced resistance to M. oryzae. In addition, three of miR169's target genes were also differentially up-regulated in the resistant accession upon M. oryzae infection. 	NA	Front Plant Sci 2017  8, 2 doi:10.3389/fpls.2017.00002 PMID:28144248
1246	Artifically engineered RNA	MIM169a	miR-169a	NF-YA6	Oryza Sativa	Magnaporthe	Oryza sativa (rice)	qRT-PCR	28144248	Osa-miR169 Negatively Regulates Rice Immunity against the Blast Fungus Magnaporthe oryzae.	Overexpression of a target mimicry that acts as a sponge to trap miR169a led to enhanced resistance to M. oryzae. In addition, three of miR169's target genes were also differentially up-regulated in the resistant accession upon M. oryzae infection. 	NA	Front Plant Sci 2017  8, 2 doi:10.3389/fpls.2017.00002 PMID:28144248
1247	LncRNA	TUG1	miR-377	PPAR	Sv40 Mes13	Diabetic Nephropathy	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	28137588	Long noncoding RNA TUG1 alleviates extracellular matrix accumulation via mediating microRNA-377 targeting of PPARr in diabetic nephropathy.	PPARr was predicted to be the target of miR-377 and the prediction was verified by luciferase assays. Expression of miR-377 was up-regulated in mesangial cell treated with high glucose (25 mM), and overexpression of miR-377 inhibited PPARr expression and promoted PAI-1 and TGF-b1 expression. The expression of TUG1 antagonized the effect of miR-377 on the downregulation of its target PPARr and inhibited extracellular matrix accumulation, including PAI-1, TGF-b1, fibronectin (FN) and collagen IV (Col IV), induced by high glucose. 	MI0000785	Biochem Biophys Res Commun 2017 Mar 11 484, 598-604 doi:10.1016/j.bbrc.2017.01.145 PMID:28137588
1248	LncRNA	FTH1P3	miR-224-5p	fizzled5	Scc4, Scc9, Scc1, Scc25, Tu183, Hsu3, Fadu,Oec-M1, Snu1041, And Scc15	Oral Squamous Cell Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	28093311	Long non-coding RNA FTH1P3 facilitates oral squamous cell carcinoma progression by acting as a molecular sponge of miR-224-5p to modulate fizzled 5 expression.	FTH1P3 acted as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-224-5p and thereby modulating the expression of fizzled 5. Importantly, expression analysis revealed that both FTH1P3 and fizzled 5 were up-regulated in OSCC cell lines and tissues, and over-expression of fizzled 5 also functioned as an oncogene in OSCC cells.	MIMAT0000281	Gene 2017 Apr 5 607, 47-55 doi:10.1016/j.gene.2017.01.009 PMID:28093311
1249	LncRNA	HULC	miR-200a	cMyc	K562, Kg-1 And Thp-1	Chronic Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;Western blot assay	28069548	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.	Experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity. Furthermore, HULC could modulate c-Myc and Bcl-2 by miR-200a as an endogenous sponge. 	MI0000737	Gene 2017 Apr 5 607, 41-46 doi:10.1016/j.gene.2017.01.004 PMID:28069548
1250	LncRNA	HULC	miR-200a	BCL2	K562, Kg-1 And Thp-1	Chronic Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;Western blot assay	28069548	Long noncoding RNA HULC promotes cell proliferation by regulating PI3K/AKT signaling pathway in chronic myeloid leukemia.	Experiments demonstrated that HULC silencing markedly suppressed the phosphorylation of PI3K and AKT, indicating that enhancement of imatinib-induced apoptosis by HULC inhibition is related with the reduction of c-Myc expression and inhibition of PI3K/Akt pathway activity. Furthermore, HULC could modulate c-Myc and Bcl-2 by miR-200a as an endogenous sponge. 	MI0000737	Gene 2017 Apr 5 607, 41-46 doi:10.1016/j.gene.2017.01.004 PMID:28069548
1251	LncRNA	HOTAIR	miR-7	HuR	 Scc25, Hn4, Cal27, Scc4, Hn30, Hn12, Hn13 And Fadu	Neck Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot assay	27941336	A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and neck squamous cell carcinoma Progression and Metastasis	HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. qRT-PCR and western blot results showed that upregulating miR-7 dramatically decreased HuR expression levels, while transfection with miR-7 inhibitor increased HuR expression in SCC25 and FaDu cells, indicating that miR-7 can bind to HuR.	MI0008947	Cell Physiol Biochem 2016  40, 1039-1051 doi:10.1159/000453160 PMID:27941336
1252	Circular RNA	ciRS-7	miR-7	UBE2A	Brain Tissues	Alzheimers Disease	Homo sapiens (human)	qRT-PCR;Western blot assay	27929395	Deficiency in the Ubiquitin Conjugating Enzyme UBE2A in Alzheimer's Disease (AD) is Linked to Deficits in a Natural Circular miRNA-7 Sponge (circRNA; ciRS-7).	Deficits in ciRS-7-mediated "sponging events", resulting in excess ambient miRNA-7 appear to drive the selective down-regulation in the expression of miRNA-7-sensitive mRNA targets, such as that encoding the ubiquitin conjugating enzyme E2A (UBE2A; chr Xq24). UBE2A, which normally serves as a central effector in the ubiquitin-26S proteasome system, coordinates the clearance of amyloid peptides via proteolysis, is known to be depleted in sporadic AD brain and, hence, contributes to amyloid accumulation and the formation of senile plaque deposits.	MI0008947	Genes (Basel) 2016 Dec 5 7 doi:10.3390/genes7120116 PMID:27929395
1253	LncRNA	DDAH1-V3	miR-21	DDAH1	Huvec	Cardiovascular Disease	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27663503	DDAH1-V3 transcript might act as miR-21 sponge to maintain balance of DDAH1-V1 in cultured HUVECs.	Overexpression of miR-21 decreased mRNA expression and mRNA half-life time of all DDAH1 transcripts significantly (P < 0.05), and DDAH1-V2 displayed significantly decreased half-life time than DDAH1-V1 and -V3 with or without miR-21 transfection (P < 0.05, respectively). MiR-21 (100 nM) decreased DDAH1 protein expression and eNOS activity significantly (P < 0.05), which was reversed by PmirGLO-miR-21 transfection (P < 0.05). Transfection of PmirGLO-miR-21 alone increased intracellular miR-21 expression by approximately 5.6-fold, but only showed a trend of increase in DDAH1 protein expression.	MI0000077	Nitric Oxide 2016 Nov 30 60, 59-68 doi:10.1016/j.niox.2016.09.008 PMID:27663503
1254	LncRNA	TUG1	miR-9-5p	POU2F1	Osteosarcoma Cell Lines 	Osteosarcoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27658774	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression.	TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells, which involved the derepression of POU class 2 homeobox 1 (POU2F1) expression.	MIMAT0000441	Tumour Biol 2016 Nov 37, 15031-15041 doi:10.1007/s13277-016-5391-5 PMID:27658774
1255	LncRNA	UFC1	miR-34a	NA	Articular Cartilage Tissues	Osteoarthritis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	27529373	Long Noncoding RNA UFC1 Promotes Proliferation of Chondrocyte in Osteoarthritis by Acting as a Sponge for miR-34a.	UFC1 was significantly reduced in OA patients. Functional assays demonstrated that UFC1 promotes chondrocytes proliferation and inhibits cell apoptosis. Furthermore, we found that UFC1 regulates survival of OA chondrocytes through physically association with miR-34a.	MI0000268	DNA Cell Biol 2016 Nov 35, 691-695 doi:10.1089/dna.2016.3397 PMID:27529373
1256	Circular RNA	CircTCF25	miR-103a-3p	CDK6	Bladder Carcinoma Cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27484176	Screening differential circular RNA expression profiles reveals the regulatory role of circTCF25-miR-103a-3p/miR-107-CDK6 pathway in bladder carcinoma.	We predicted that circTCF25 could sequester miR-103a-3p/miR-107, which potentially lead to the up-regulation of thirteen targets related to cell proliferation, migration and invasion. Subsequently, we demonstrated that over-expression of circTCF25 could down-regulate miR-103a-3p and miR-107, increase CDK6 expression, and promote proliferation and migration in vitro and vivo.	MIMAT0000101	Sci Rep 2016 Aug 3 6, 30919 doi:10.1038/srep30919 PMID:27484176
1257	Circular RNA	CircTCF25	miR-107	CDK6	Bladder Carcinoma Cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	27484176	Screening differential circular RNA expression profiles reveals the regulatory role of circTCF25-miR-103a-3p/miR-107-CDK6 pathway in bladder carcinoma.	We predicted that circTCF25 could sequester miR-103a-3p/miR-107, which potentially lead to the up-regulation of thirteen targets related to cell proliferation, migration and invasion. Subsequently, we demonstrated that over-expression of circTCF25 could down-regulate miR-103a-3p and miR-107, increase CDK6 expression, and promote proliferation and migration in vitro and vivo.	MI0000114	Sci Rep 2016 Aug 3 6, 30919 doi:10.1038/srep30919 PMID:27484176
1258	LncRNA	XIST	miR-34a-5p	E2F3	Sune-1, Cne-1, Hne-1, Cne-2,C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27461945	Long non-coding RNA XIST exerts oncogenic functions in human nasopharyngeal carcinoma by targeting miR-34a-5p.	multivariate analysis demonstrated XIST was an independent risk factor for prognosis. XIST over-expression enhanced, while XIST silencing hampered the cell growth in NPC. Additionally, mechanistic analysis revealed that XIST up-regulated the expression of miR-34a-5p targeted gene E2F3 through acting as a competitive 'sponge' of miR-34a-5p. 	MIMAT0000255	Gene 2016 Oct 30 592, 8-14 doi:10.1016/j.gene.2016.07.055 PMID:27461945
1259	LncRNA	TUG1	miR-26a	PTEN	U251 And Shg-44 Cells	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27298156	Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells.	Experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3'UTR. Additionally, the expression of PTEN was also upregulated in glioma tissues, showing a positive or negative correlation with TUG1 or miR-26a, respectively.	MI0000083	J Dermatol Sci 2016 Sep 83, 210-8 doi:10.1016/j.jdermsci.2016.05.012 PMID:27298156
1260	Coding-mRNA	PIK3C2A	miR-124	CD151	Qgy- 7703 And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27270320	PIK3C2A mRNA functions as a miR-124 sponge to facilitate CD151 expression and enhance malignancy of hepatocellular carcinoma cells.	Direct and negative regulation of PIK3C2A and CD151 by miR-124 was confirmed in HCC cells. miR-124 and the two potential ceRNAs are all recruited to the RNA-induced silencing complex (RISC). In HCC cell lines QGY- 7703 and SMMC-7721, and normal hepatic cell line HL-7702, miR-124 plays a tumor suppressor role by targeting PIK3C2A and CD151. The MREs within PIK3C2A 3'UTR can independently stimulate CD151 expression level by acting as miR-124 decoys.	MI0000443	Oncotarget 2016 Jul 12 7, 43376-43389 doi:10.18632/oncotarget.9716 PMID:27270320
1261	Circular RNA	CircHIPK3	miR-124	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000443	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1262	Circular RNA	CircHIPK3	miR-152	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000462	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1263	Circular RNA	CircHIPK3	miR-193a	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000487	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1264	Circular RNA	CircHIPK3	miR-29a	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000087	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1265	Circular RNA	CircHIPK3	miR-29b	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000105	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1266	Circular RNA	CircHIPK3	miR-338	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000814	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1267	Circular RNA	CircHIPK3	miR-379	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0000787	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1268	Circular RNA	CircHIPK3	miR-584	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0003591	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1269	Circular RNA	CircHIPK3	miR-654	NA	Hek-293T	Breast Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay,RNA FISH	27050392	Circular RNA profiling reveals an abundant circHIPK3 that regulates cell growth by sponging multiple miRNAs	We further performed a luciferase screening and observed that circHIPK3 could bind to multiple miRNAs, including a well-known tumor suppressor miRNA miR-124.Compared with the control RNA, 9 miRNAs (miR-124, miR-152, miR-193a, miR-29a, miR-29b, miR-338, miR-379, miR-584 and miR-654) out of the 424 miRNAs were able to reduce the luciferase reporter activities by at least 30%.	MI0003676	Nat Commun 2016 Apr 6 7, 11215 doi:10.1038/ncomms11215 PMID:27050392
1270	LncRNA	UCA1	miR-204-5p	CREB1	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1271	LncRNA	UCA1	miR-204-5p	RAB22A	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1272	LncRNA	UCA1	miR-204-5p	BCL2	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1273	LncRNA	UCA1	miR-204-5p	CREB1	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1274	LncRNA	UCA1	miR-204-5p	RAB22A	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1275	LncRNA	UCA1	miR-204-5p	BCL2	Hek-293T, Hct8, Hct116, Ht29, Lovo, And Sw480,	Colorectal Cancer	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Northern blot assay	27046651	LncRNA-UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p.	Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
1276	LncRNA	TUSC7	miR-10a	EphA4	Hepg2, Mhcc97L, Hep3B, Smmc-7721, Mhcc97H, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	27002617	Long non-coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma.	 TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis.	MI0000266	Tumour Biol 2016 Aug 37, 11429-41 doi:10.1007/s13277-016-4892-6 PMID:27002617
1277	LncRNA	TUG1	miR-106a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000113	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1278	LncRNA	TUG1	miR-106b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000734	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1279	LncRNA	TUG1	miR-17-5p	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MIMAT0000070	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1280	LncRNA	TUG1	miR-20a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000076	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1281	LncRNA	TUG1	miR-20b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0001519	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1282	LncRNA	TUG1	miR-26a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000083	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1283	LncRNA	TUG1	miR-26b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000084	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1284	LncRNA	TUG1	miR-93	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000095	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1285	LncRNA	CTB-89H12.4	miR-106a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000113	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1286	LncRNA	CTB-89H12.4	miR-106b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000734	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1287	LncRNA	CTB-89H12.4	miR-17-5p	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MIMAT0000070	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1288	LncRNA	CTB-89H12.4	miR-19a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000073	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1289	LncRNA	CTB-89H12.4	miR-19b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000074	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1290	LncRNA	CTB-89H12.4	miR-20a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000076	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1291	LncRNA	CTB-89H12.4	miR-20b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0001519	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1292	LncRNA	CTB-89H12.4	miR-26a	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000083	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1293	LncRNA	CTB-89H12.4	miR-26b	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000084	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1294	LncRNA	CTB-89H12.4	miR-93	PTEN	Du145 And 22Rv1	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26975529	Integrative analyses reveal a long noncoding RNA-mediated sponge regulatory network in prostate cancer.	We confirm the tumour-suppressive function of two lncRNAs (TUG1 and CTB-89H12.4) and their regulation of PTEN expression in prostate cancer. Surprisingly, one of the two lncRNAs, TUG1, was previously known for its function in polycomb repressive complex 2 (PRC2)-mediated transcriptional regulation, suggesting its sub-cellular localization-dependent function.	MI0000095	Nat Commun 2016 Mar 15 7, 10982 doi:10.1038/ncomms10982 PMID:26975529
1295	Artifically engineered RNA	miR-449 sponge	miR-449	SIRT1	Nrk-52E Cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;Western blot assay	26968221	Inhibiting microRNA-449 Attenuates Cisplatin-Induced Injury in NRK-52E Cells Possibly via Regulating the SIRT1/P53/BAX Pathway.	Results showed that cisplatin treatment in NRK-52E cells significantly up-regulated miR-449 levels (P<0.05), inhibited cell viability (P<0.05), accelerated cell apoptosis (P<0.05), and changed SIRT1, acetylated p53, and BAX protein levels (P<0.01). However, inhibiting miR-449 by its sponge transfection in cisplatin-treated cells significantly promoted cell viability (P<0.05), suppressed cell apoptosis (P<0.05), elevated SIRT1 expression (P<0.01), and inhibited acetylated p53 and BAX protein levels (P<0.001).	MI0001648	Med Sci Monit 2016 Mar 12 22, 818-23 doi:10.12659/msm.897187 PMID:26968221
1296	Artifically engineered RNA	miR-449 sponge	miR-449	p53	Nrk-52E Cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;Western blot assay	26968221	Inhibiting microRNA-449 Attenuates Cisplatin-Induced Injury in NRK-52E Cells Possibly via Regulating the SIRT1/P53/BAX Pathway.	Results showed that cisplatin treatment in NRK-52E cells significantly up-regulated miR-449 levels (P<0.05), inhibited cell viability (P<0.05), accelerated cell apoptosis (P<0.05), and changed SIRT1, acetylated p53, and BAX protein levels (P<0.01). However, inhibiting miR-449 by its sponge transfection in cisplatin-treated cells significantly promoted cell viability (P<0.05), suppressed cell apoptosis (P<0.05), elevated SIRT1 expression (P<0.01), and inhibited acetylated p53 and BAX protein levels (P<0.001).	MI0001648	Med Sci Monit 2016 Mar 12 22, 818-23 doi:10.12659/msm.897187 PMID:26968221
1297	Artifically engineered RNA	miR-449 sponge	miR-449	BAX	Nrk-52E Cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;Western blot assay	26968221	Inhibiting microRNA-449 Attenuates Cisplatin-Induced Injury in NRK-52E Cells Possibly via Regulating the SIRT1/P53/BAX Pathway.	Results showed that cisplatin treatment in NRK-52E cells significantly up-regulated miR-449 levels (P<0.05), inhibited cell viability (P<0.05), accelerated cell apoptosis (P<0.05), and changed SIRT1, acetylated p53, and BAX protein levels (P<0.01). However, inhibiting miR-449 by its sponge transfection in cisplatin-treated cells significantly promoted cell viability (P<0.05), suppressed cell apoptosis (P<0.05), elevated SIRT1 expression (P<0.01), and inhibited acetylated p53 and BAX protein levels (P<0.001).	MI0001648	Med Sci Monit 2016 Mar 12 22, 818-23 doi:10.12659/msm.897187 PMID:26968221
1298	Circular RNA	CircRNA-CER	miR-136	MMP13	Knee Tissues	Cartilage Degradation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26931159	Circular RNA Related to the Chondrocyte ECM Regulates MMP13 Expression by Functioning as a MiR-136 'Sponge' in Human Cartilage Degradation.	CircRNA-CER expression increased with interleukin-1 and tumor necrosis factor levels in chondrocytes. Silencing of circRNA-CER using small interfering RNA suppressed MMP13 expression and increased ECM formation. CircRNA-CER could compete for miR-136 with MMP13.	MI0000475	Sci Rep 2016 Mar 2 6, 22572 doi:10.1038/srep22572 PMID:26931159
1299	Artifically engineered RNA	miR-134 sponge	miR-134	MBD3	Neural Progenitor Cells	Cell Pluripotency	Homo sapiens (human)	qRT-PCR;Western blot assay	26929159	MiR-134-Mbd3 axis regulates the induction of pluripotency.	Inhibition of miR-134 by miR-134 sponge promoted the efficiency of reprogramming which also was highly similar to mESCs. On the contrary, up-regulation of miR-134 repressed iPSCs induction. We also found that inhibition of miR-134 promoted the maturation of pre-iPSCs and increased its pluripotency. We also showed that miR-134 can directly target to the pluripotency related factor Methyl-CpG-binding domain protein 3 (Mdb3) 3' untranslated regions (3' UTR) to down-regulate its expression. And Mbd3 was found to promote the induction of iPSCs and could block the repression of reprogramming caused by overexpression of miR-134.	MI0000474	J Cell Mol Med 2016 Jun 20, 1150-8 doi:10.1111/jcmm.12805 PMID:26929159
1300	Viral RNA	BVDV	miR-7	NA	Huh-7,Hek293, Hela And A549	NA	Bovine viral diarrhea virus 1(BVDV)	luciferase reporter assays	26962949	A broad RNA virus survey reveals both miRNA dependence and functional sequestration	For BVDV, around 40% of miR-17 interactions mapped to the virus, suggesting an analogous sponge effect.Along these lines, we reasoned that the BVDV miR-17 sponge effect should result in specific de-repression of cellular miR-17 targets, measurable by mRNA-seq. 	MI0008947	Cell Host Microbe 2016 Mar 9 19, 409-23 doi:10.1016/j.chom.2016.02.007 PMID:26962949
1301	LncRNA	HCV	miR-7	NA	Huh-7,Hek293, Hela And A549	NA	Hepatitis C virus (HCV)	luciferase reporter assays	26962949	A broad RNA virus survey reveals both miRNA dependence and functional sequestration	For HCV, around 50% of miR-122 interactions mapped to the virus, consistent with our modeling estimates of the available miR-122 pool during infection.	MI0008947	Cell Host Microbe 2016 Mar 9 19, 409-23 doi:10.1016/j.chom.2016.02.007 PMID:26962949
1302	LncRNA	UVA1	miR-485-5p	MMP14	Omc685, A2780,And Skov3	Ovarian Cancer	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26867765	UCA1 functions as a competing endogenous RNA to suppress epithelial ovarian cancer metastasis.	Knockdown of UCA1 reduced the invasion and migration ability of EOC cells. The results showed that UCA1 could function as an endogenous sponge by directly binding to miR-485-5p. Depletion of UCA1 was involved in the downregulation of matrix metallopeptidase 14 (MMP14) expression, a target gene of miR-485-5p. 	MIMAT0002175	Tumour Biol 2016 Aug 37, 10633-41 doi:10.1007/s13277-016-4917-1 PMID:26867765
1303	LncRNA	H19	miR-141	CTNNB1	Hek293,Hmscs	Osteoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26853553	H19 activates Wnt signaling and promotes osteoblast differentiation by functioning as a competing endogenous RNA.	Meanwhile, by using bioinformatic investigations and RIP assays combined with luciferase reporter assays, we demonstrated that H19 functioned as an miRNA sponge for miR-141 and miR-22, both of which were negative regulators of osteogenesis and Wnt/b-catenin pathway. Further investigations revealed that H19 antagonized the functions of these two miRNAs and led to de-repression of their shared target gene b-catenin, which eventually activated Wnt/b-catenin pathway and hence potentiated osteogenesis. 	MI0000457	Sci Rep 2016 Feb 8 6, 20121 doi:10.1038/srep20121 PMID:26853553
1304	LncRNA	H19	miR-22	CTNNB1	Hek293,Hmscs	Osteoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	26853553	H19 activates Wnt signaling and promotes osteoblast differentiation by functioning as a competing endogenous RNA.	Meanwhile, by using bioinformatic investigations and RIP assays combined with luciferase reporter assays, we demonstrated that H19 functioned as an miRNA sponge for miR-141 and miR-22, both of which were negative regulators of osteogenesis and Wnt/b-catenin pathway. Further investigations revealed that H19 antagonized the functions of these two miRNAs and led to de-repression of their shared target gene b-catenin, which eventually activated Wnt/b-catenin pathway and hence potentiated osteogenesis. 	MI0000078	Sci Rep 2016 Feb 8 6, 20121 doi:10.1038/srep20121 PMID:26853553
1305	Artifically engineered RNA	miR-10 sponge	miR-10	HOXD-10	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	qRT-PCR;immunoblotting	26820121	MiRNA-10b sponge: An anti-breast cancer study in vitro.	qRT-PCR results found that the sponge plasmid effectively inhibited the expression of miRNA-10b, and upregulated the expression of the miRNA 10b target protein HOXD-10. The results from the CCK-8 assay found that the miRNA-10b sponge inhibited the growth of breast cancer cell lines MDA-MB-231 and MCF-7. Results of the plate cloning experiments indicated that the miRNA-10b sponge suppressed the colony formation of the MDA-MB-231 and MCF-7 cells.	MI0000685	Oncol Rep 2016 Apr 35, 1950-8 doi:10.3892/or.2016.4596 PMID:26820121
1306	Artifically engineered RNA	miR-27a sponge	miR-27a	Siglec1	Hek293T, Thp1 And Raw264.7 	Antiviral Innate Response	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26700765	Type I IFN-Inducible Downregulation of MicroRNA-27a Feedback Inhibits Antiviral Innate Response by Upregulating Siglec1/TRIM27.	We constructed "Sponge" transgenic mice against miR-27a expression and found that Siglec1 and TRIM27 expression were elevated whereas type I IFN production was inhibited and viral replication was aggregated in vivo. Therefore, type I IFN-induced downregulation of miR-27a can upregulate Siglec1 and TRIM27 expression, feedback inhibiting type I IFN production in antiviral innate response.	MI0000085	J Immunol 2016 Feb 1 196, 1317-26 doi:10.4049/jimmunol.1502134 PMID:26700765
1307	Artifically engineered RNA	miR-27a sponge	miR-27a	TRIM27	Hek293T, Thp1 And Raw264.7 	Antiviral Innate Response	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26700765	Type I IFN-Inducible Downregulation of MicroRNA-27a Feedback Inhibits Antiviral Innate Response by Upregulating Siglec1/TRIM27.	We constructed "Sponge" transgenic mice against miR-27a expression and found that Siglec1 and TRIM27 expression were elevated whereas type I IFN production was inhibited and viral replication was aggregated in vivo. Therefore, type I IFN-induced downregulation of miR-27a can upregulate Siglec1 and TRIM27 expression, feedback inhibiting type I IFN production in antiviral innate response.	MI0000085	J Immunol 2016 Feb 1 196, 1317-26 doi:10.4049/jimmunol.1502134 PMID:26700765
1308	Artifically engineered RNA	miR-27a sponge	miR-27a	Siglec1	Hek293T, Thp1 And Raw264.7 	Antiviral Innate Response	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	26700765	Type I IFN-Inducible Downregulation of MicroRNA-27a Feedback Inhibits Antiviral Innate Response by Upregulating Siglec1/TRIM27.	We constructed "Sponge" transgenic mice against miR-27a expression and found that Siglec1 and TRIM27 expression were elevated whereas type I IFN production was inhibited and viral replication was aggregated in vivo. Therefore, type I IFN-induced downregulation of miR-27a can upregulate Siglec1 and TRIM27 expression, feedback inhibiting type I IFN production in antiviral innate response.	MI0000085	J Immunol 2016 Feb 1 196, 1317-26 doi:10.4049/jimmunol.1502134 PMID:26700765
1309	Artifically engineered RNA	miR-27a sponge	miR-27a	TRIM27	Hek293T, Thp1 And Raw264.7 	Antiviral Innate Response	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR	26700765	Type I IFN-Inducible Downregulation of MicroRNA-27a Feedback Inhibits Antiviral Innate Response by Upregulating Siglec1/TRIM27.	We constructed "Sponge" transgenic mice against miR-27a expression and found that Siglec1 and TRIM27 expression were elevated whereas type I IFN production was inhibited and viral replication was aggregated in vivo. Therefore, type I IFN-induced downregulation of miR-27a can upregulate Siglec1 and TRIM27 expression, feedback inhibiting type I IFN production in antiviral innate response.	MI0000085	J Immunol 2016 Feb 1 196, 1317-26 doi:10.4049/jimmunol.1502134 PMID:26700765
1310	Artifically engineered RNA	miR-155 sponge	miR-155	Mecp2	Hela And Hek293T	Down Syndrome	Homo sapiens (human)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0000681	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1311	Artifically engineered RNA	miR-155 sponge	miR-155	Ship1	Hela And Hek293T	Down Syndrome	Homo sapiens (human)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0000681	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1312	Artifically engineered RNA	miR-802 sponge	miR-802	FoxM1	Hela And Hek293T	Down Syndrome	Homo sapiens (human)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0003906	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1313	Artifically engineered RNA	miR-802 sponge	miR-802	Mecp2	Hela And Hek293T	Down Syndrome	Homo sapiens (human)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0003906	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1314	Artifically engineered RNA	miR-155 sponge	miR-155	Mecp2	Hela And Hek293T	Down Syndrome	Mus musculus (mouse)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0000681	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1315	Artifically engineered RNA	miR-155 sponge	miR-155	Ship1	Hela And Hek293T	Down Syndrome	Mus musculus (mouse)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0000681	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1316	Artifically engineered RNA	miR-802 sponge	miR-802	FoxM1	Hela And Hek293T	Down Syndrome	Mus musculus (mouse)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0003906	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1317	Artifically engineered RNA	miR-802 sponge	miR-802	Mecp2	Hela And Hek293T	Down Syndrome	Mus musculus (mouse)	qRT-PCR	26546125	Genome-wide miR-155 and miR-802 target gene identification in the hippocampus of Ts65Dn Down syndrome mouse model by miRNA sponges.	We developed a lentiviral miRNA-sponge strategy (Lv-miR155-802T) to identify in vivo relevant miR-155 and miR-802 target mRNAs. Hippocampal injections of lentiviral sponges in Ts65Dn mice normalized the expression of miR-155 and miR-802 and rescued the levels of their targets methyl-CpG-binding protein 2 gene (Mecp2), SH2 (Src homology 2)-containing inositol phosphatase-1 (Ship1) and Forkhead box protein M1 (FoxM1). Transcriptomic data of Lv-miR155-802T miRNA-sponge treated hippocampi correlated with candidate targets highlighting miRNA dosage-sensitive genes.	MI0003906	BMC Genomics 2015 Nov 6 16, 907 doi:10.1186/s12864-015-2160-6 PMID:26546125
1318	LncRNA	LINC00162	miR-320a	Nucleolin	Ntera-2 (Nt2) And Nccit	Testicular Embryonal Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MI0000542	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
1319	LncRNA	LINC00162	miR-383	Nucleolin	Ntera-2 (Nt2) And Nccit	Testicular Embryonal Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Northern blot assay	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MI0000791	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
1320	LncRNA	PCGEM1	miR-770	GFP	Osteoarthritic Synoviocytes	Osteoarthritis	Homo sapiens (human)	qRT-PCR;Western blot assay	26340084	PCGEM1 stimulates proliferation of osteoarthritic synoviocytes by acting as a sponge for miR-770.	Transfection of the miR-770 precursor resulted in reduced proliferation, and induced apoptosis of human synoviocytes. This effect of miR-770 expression was reversed by co-introduction of PCGEM1. Target validation showed a direct binding between PCGEM1 and miR-770. 	MI0005118	J Orthop Res 2016 Mar 34, 412-8 doi:10.1002/jor.23046 PMID:26340084
1321	Artifically engineered RNA	miR-497 sponge	miR-497	BCL2	Neonatal Rat Cardiomyocytes	Anoxia	Homo sapiens (human)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1322	Artifically engineered RNA	miR-497 sponge	miR-497	LC3B-II	Neonatal Rat Cardiomyocytes	Anoxia	Homo sapiens (human)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1323	Artifically engineered RNA	miR-497 sponge	miR-497	BCL2	Neonatal Rat Cardiomyocytes	Anoxia	Mus musculus (mouse)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1324	Artifically engineered RNA	miR-497 sponge	miR-497	LC3B-II	Neonatal Rat Cardiomyocytes	Anoxia	Mus musculus (mouse)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1325	Artifically engineered RNA	miR-497 sponge	miR-497	BCL2	Neonatal Rat Cardiomyocytes	Reoxygenation Injury	Homo sapiens (human)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1326	Artifically engineered RNA	miR-497 sponge	miR-497	LC3B-II	Neonatal Rat Cardiomyocytes	Reoxygenation Injury	Homo sapiens (human)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1327	Artifically engineered RNA	miR-497 sponge	miR-497	BCL2	Neonatal Rat Cardiomyocytes	Reoxygenation Injury	Mus musculus (mouse)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1328	Artifically engineered RNA	miR-497 sponge	miR-497	LC3B-II	Neonatal Rat Cardiomyocytes	Reoxygenation Injury	Mus musculus (mouse)	qRT-PCR;Western blot assay	26299920	Inhibition of microRNA-497 ameliorates anoxia/reoxygenation injury in cardiomyocytes by suppressing cell apoptosis and enhancing autophagy.	In response to AR, silencing of miR-497 using a miR-497 sponge significantly reduced cell apoptosis and enhanced autophagic flux. Furthermore, the infarct size induced by IR in adenovirus (Ad)-miR-497 sponge infected mice was significantly smaller than in mice receiving Ad-vector or vehicle treatment, while Ad-miR-497 increased infarct size. The expression of Bcl-2 and LC3B-II in NRCs or in murine heart was significantly decreased by miR-497 mimic and enhanced by miR-497 sponge	MI0003138	Oncotarget 2015 Aug 7 6, 18829-44 doi:10.18632/oncotarget.4774 PMID:26299920
1329	Artifically engineered RNA	miR-17 sponge	miR-17	NA	Sw954	Vulvar Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR	26297962	Design of a miRNA sponge for the miR-17 miRNA family as a therapeutic strategy against vulvar carcinoma.	A luciferase reporter assay with a psiCheck2 vector was used to test the specificity of the sponge sequences for miR-17 family miRNA binding. Taqman qRT-PCR was used to test how the sponges affected miRNA expression. In FFPE samples, higher expression of miR-20a and miR-106a correlated with deeper tumor invasion (P = 0.0187 and P = 0.0404, respectively). The luciferase reporter assay validated the specificity of the sponge for miR-17 family members. Using qRT-PCR, we confirmed this specificity with decreased expression in 5 (out of six) miRNAs of the miR-17 family in SW954 cells.	MI0000071	Mol Cell Probes 2015 Dec 29, 420-426 doi:10.1016/j.mcp.2015.08.002 PMID:26297962
1330	LncRNA	lincRNA-p21	miR-130b	NA	SVEC4	NA	Homo sapiens (human)	qRT-PCR	26273737	The Role of Long Intergenic Noncoding RNA p21 in Vascular Endothelial Cells.	lincRNA-p21 acted as an endogenous sponge by directly binding to miR-130b and decreased miR-130b expression. In addition, miR-130b reversed the inhibitory effect of lincRNA-p21 on the growth of vascular endothelial cells. 	MI0000748	DNA Cell Biol 2015 Nov 34, 677-83 doi:10.1089/dna.2015.2966 PMID:26273737
1331	LncRNA	NEAT1	miR-449b-5p	c-Met	Glioma Tissues	Glioma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;RNA immunoprecipitation	26242266	Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis.	Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. RNA immunoprecipitation assay combined with luciferase reporter assay confirmed miR-449b-5p-specific binding to NEAT1. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met.	MIMAT0003327	Tumour Biol 2016 Jan 37, 673-83 doi:10.1007/s13277-015-3843-y PMID:26242266
1332	Circular RNA	Cdr1as	miR-7	Myrip	Min6	Diabetes Mellitus	Homo sapiens (human)	qRT-PCR	26211738	The circular RNA Cdr1as, via miR-7 and its targets, regulates insulin transcription and secretion in islet cells.	we show the first characterization of Cdr1as expression in islet cells, which was upregulated by long-term forskolin and PMA stimulation, but not high glucose, indicating the involvement of cAMP and PKC pathways. Remarkably, both insulin content and secretion were significantly increased by overexpression of Cdr1as in islet cells. We further identified a new target Myrip in the Cdr1as/miR-7 pathway that regulates insulin granule secretion, and also another target Pax6 that enhances insulin transcription. 	MI0008947	Sci Rep 2015 Jul 27 5, 12453 doi:10.1038/srep12453 PMID:26211738
1333	Circular RNA	Cdr1as	miR-7	Pax6	Min6	Diabetes Mellitus	Homo sapiens (human)	qRT-PCR	26211738	The circular RNA Cdr1as, via miR-7 and its targets, regulates insulin transcription and secretion in islet cells.	we show the first characterization of Cdr1as expression in islet cells, which was upregulated by long-term forskolin and PMA stimulation, but not high glucose, indicating the involvement of cAMP and PKC pathways. Remarkably, both insulin content and secretion were significantly increased by overexpression of Cdr1as in islet cells. We further identified a new target Myrip in the Cdr1as/miR-7 pathway that regulates insulin granule secretion, and also another target Pax6 that enhances insulin transcription. 	MI0008947	Sci Rep 2015 Jul 27 5, 12453 doi:10.1038/srep12453 PMID:26211738
1334	Circular RNA	Cdr1as	miR-7	Myrip	Min6	Diabetes Mellitus	Mus musculus (mouse)	qRT-PCR	26211738	The circular RNA Cdr1as, via miR-7 and its targets, regulates insulin transcription and secretion in islet cells.	we show the first characterization of Cdr1as expression in islet cells, which was upregulated by long-term forskolin and PMA stimulation, but not high glucose, indicating the involvement of cAMP and PKC pathways. Remarkably, both insulin content and secretion were significantly increased by overexpression of Cdr1as in islet cells. We further identified a new target Myrip in the Cdr1as/miR-7 pathway that regulates insulin granule secretion, and also another target Pax6 that enhances insulin transcription. 	MI0008947	Sci Rep 2015 Jul 27 5, 12453 doi:10.1038/srep12453 PMID:26211738
1335	Circular RNA	Cdr1as	miR-7	Pax6	Min6	Diabetes Mellitus	Mus musculus (mouse)	qRT-PCR	26211738	The circular RNA Cdr1as, via miR-7 and its targets, regulates insulin transcription and secretion in islet cells.	we show the first characterization of Cdr1as expression in islet cells, which was upregulated by long-term forskolin and PMA stimulation, but not high glucose, indicating the involvement of cAMP and PKC pathways. Remarkably, both insulin content and secretion were significantly increased by overexpression of Cdr1as in islet cells. We further identified a new target Myrip in the Cdr1as/miR-7 pathway that regulates insulin granule secretion, and also another target Pax6 that enhances insulin transcription. 	MI0008947	Sci Rep 2015 Jul 27 5, 12453 doi:10.1038/srep12453 PMID:26211738
1336	Artifically engineered RNA	miR-21 sponge	miR-21	PDCD4	Mcf-7 And Hela	Breast Cancer	Homo sapiens (human)	Western blot assay	26169933	miRNA oligonucleotide and sponge for miRNA-21 inhibition mediated by PEI-PLL in breast cancer therapy.	miR-21 inhibition could induce the cell cycle arrest in G1 phase, upregulate the expression of Programmed Cell Death Protein 4 (PDCD4) and thus active the caspase-3 apoptosis pathway. Interestingly, the PEI-PLL/Sponge and PEI-PLL/AMO also sensitized the MCF-7 cells to anti-tumor drugs, doxorubicin (DOX) and cisplatin (CDDP). 	MI0000077	Acta Biomater 2015 Oct 25, 184-93 doi:10.1016/j.actbio.2015.07.020 PMID:26169933
1337	LncRNA	H19	let-7	IGF1R	Eutopic Endometrium Tissues	Endometriosis	Homo sapiens (human)	qRT-PCR;Western blot assay	26089099	H19 lncRNA alters stromal cell growth via IGF signaling in the endometrium of women with endometriosis.	 We show that decreased H19 increases let-7 activity, which in turn inhibits Igf1r expression at the post-transcriptional level, thereby contributing to reduced proliferation of endometrial stromal cells. We propose that perturbation of this newly identified H19/Let-7/IGF1R regulatory pathway may contribute to impaired endometrial preparation and receptivity for pregnancy in women with endometriosis. 	MI0000060	EMBO Mol Med 2015 Aug 7, 996-1003 doi:10.15252/emmm.201505245 PMID:26089099
1338	LncRNA	H19	let-7	IGF1R	Eutopic Endometrium Tissues	Endometriosis	Mus musculus (mouse)	qRT-PCR;Western blot assay	26089099	H19 lncRNA alters stromal cell growth via IGF signaling in the endometrium of women with endometriosis.	 We show that decreased H19 increases let-7 activity, which in turn inhibits Igf1r expression at the post-transcriptional level, thereby contributing to reduced proliferation of endometrial stromal cells. We propose that perturbation of this newly identified H19/Let-7/IGF1R regulatory pathway may contribute to impaired endometrial preparation and receptivity for pregnancy in women with endometriosis. 	MI0000060	EMBO Mol Med 2015 Aug 7, 996-1003 doi:10.15252/emmm.201505245 PMID:26089099
1339	LncRNA	CCAT1	let-7a	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000060	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1340	LncRNA	CCAT1	let-7b	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000063	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1341	LncRNA	CCAT1	let-7c	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000064	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1342	LncRNA	CCAT1	let-7e	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000066	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1343	LncRNA	CCAT1	let-7a	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000060	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1344	LncRNA	CCAT1	let-7b	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000063	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1345	LncRNA	CCAT1	let-7c	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000064	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1346	LncRNA	CCAT1	let-7e	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000066	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1347	LncRNA	MALAT1	miR-133a	Srf	C2C12 Myoblast Cells,Hek293	Myogenesis	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25868726	Malat1 regulates serum response factor through miR-133 as a competing endogenous RNA in myogenesis.	Malat1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased Malat1 expression as well. Further study revealed that Malat1 contained an miR-133 functional target site, and the interplay between Malat1 and Srf was miR-133 dependent. 	MI0000159	Faseb j 2015 Jul 29, 3054-64 doi:10.1096/fj.14-259952 PMID:25868726
1348	LncRNA	MALAT1	miR-133a	Srf	C2C12 Myoblast Cells,Hek293	Myogenesis	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25868726	Malat1 regulates serum response factor through miR-133 as a competing endogenous RNA in myogenesis.	Malat1 in the mouse myoblast C2C12 cell line inhibited myocyte differentiation and decreased Srf at both the RNA and protein levels. Srf silencing decreased Malat1 expression as well. Further study revealed that Malat1 contained an miR-133 functional target site, and the interplay between Malat1 and Srf was miR-133 dependent. 	MI0000159	Faseb j 2015 Jul 29, 3054-64 doi:10.1096/fj.14-259952 PMID:25868726
1349	LncRNA	UCA1	miR-216b	FGFR1	Mhcc97L, Smmc7721, Mhcc97H, Hepg2 And Sk-Hep1	Hepatocellular Carcinoma	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25760077	Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway.	 UCA1 could reverse the inhibitory effect of miR-216b on the growth and metastasis of HCC cells, which might be involved in the derepression of fibroblast growth factor receptor 1 (FGFR1) expression, a target gene of miR-216b, and the activation of ERK signaling pathway.	MI0005569	Oncotarget 2015 Apr 10 6, 7899-917 doi:10.18632/oncotarget.3219 PMID:25760077
1350	Viral RNA	HCV	miR-122	NA	Hepatoma Cell Line	Hcv Infection	Hepatitis C virus (HCV)	luciferase reporter assays;Single-cell reporter measurements	25768906	Hepatitis C virus RNA functionally sequesters miR-122.	Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and site number. We describe a quantitative mathematical model of HCV-induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.	MI0000442	Cell 2015 Mar 12 160, 1099-110 doi:10.1016/j.cell.2015.02.025 PMID:25768906
1351	Viral RNA	HCV	miR-122	NA	Hepatoma Cell Line	Hcv Infection	Homo sapiens (human)	luciferase reporter assays;Single-cell reporter measurements	25768906	Hepatitis C virus RNA functionally sequesters miR-122.	Single-cell expression data from reporters containing miR-122 sites showed significant de-repression during HCV infection depending on expression level and site number. We describe a quantitative mathematical model of HCV-induced miR-122 sequestration and propose that such miR-122 inhibition by HCV RNA may result in global de-repression of host miR-122 targets, providing an environment fertile for the long-term oncogenic potential of HCV.	MI0000442	Cell 2015 Mar 12 160, 1099-110 doi:10.1016/j.cell.2015.02.025 PMID:25768906
1352	Pseudogene	OCT4-pg5	miR-145	OCT4	An3Ca, Spec-2, Hec-1B, Kle And Rl95–2 	Endometrial Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	25634023	OCT4 pseudogene 5 upregulates OCT4 expression to promote proliferation by competing with miR-145 in endometrial carcinoma.	We observed that OCT4-pg5 was abnormally activated in the endometrial carcinomas, and that overexpression of OCT4-pg5 contributed to enhanced cell proliferation and OCT4-PI3K/AKT-cyclin D1 signaling. Moreover, the miR-145 mimic depleted OCT4 expression, whereas elevated OCT4-pg5 restored OCT4 expression and OCT4-PI3K/AKT-cyclin D1 signaling. 	MI0000461	Oncol Rep 2015 Apr 33, 1745-52 doi:10.3892/or.2015.3763 PMID:25634023
1353	LncRNA	H19	miR-17-5p	NA	Hela Cells And Myoblasts	Myoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25531890	miR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction.	miR-106a overexpression experiments confirmed that miR-CLIP captured functional targets, including H19, a long noncoding RNA that is expressed during skeletal muscle cell differentiation. We showed that miR-17-5p family members bind H19 in HeLa cells and myoblasts. During myoblast differentiation, levels of H19, miR-17-5p family members and mRNA targets changed in a manner suggesting that H19 acts as a 'sponge' for these miRNAs.	MIMAT0000070	Nat Chem Biol 2015 Feb 11, 107-14 doi:10.1038/nchembio.1713 PMID:25531890
1354	LncRNA	H19	miR-106a	NA	Hela Cells And Myoblasts	Myoblast Differentiation	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25531890	miR-CLIP capture of a miRNA targetome uncovers a lincRNA H19-miR-106a interaction.	miR-106a overexpression experiments confirmed that miR-CLIP captured functional targets, including H19, a long noncoding RNA that is expressed during skeletal muscle cell differentiation. We showed that miR-17-5p family members bind H19 in HeLa cells and myoblasts. During myoblast differentiation, levels of H19, miR-17-5p family members and mRNA targets changed in a manner suggesting that H19 acts as a 'sponge' for these miRNAs.	MI0000113	Nat Chem Biol 2015 Feb 11, 107-14 doi:10.1038/nchembio.1713 PMID:25531890
1355	LncRNA	H19	let-7a	INSR	Human Muscle Tissues	Glucose Metabolism	Homo sapiens (human)	luciferase reporter assays;qRT-PCR;Western blot assay	25399420	The H19/let-7 double-negative feedback loop contributes to glucose metabolism in muscle cells.	Here we report that H19 is significantly decreased in muscle of human subjects with type-2 diabetes and insulin resistant rodents. This decrease leads to increased bioavailability of let-7, causing diminished expression of let-7 targets, which is recapitulated in vitro where H19 depletion results in impaired insulin signaling and decreased glucose uptake. Furthermore, acute hyperinsulinemia downregulates H19, a phenomenon that occurs through PI3K/AKT-dependent phosphorylation of the miRNA processing factor KSRP, which promotes biogenesis of let-7 and its mediated H19 destabilization. 	MI0000060	Nucleic Acids Res 2014 Dec 16 42, 13799-811 doi:10.1093/nar/gku1160 PMID:25399420
1356	LncRNA	H19	let-7a	INSR	Mouse Muscle Tissues	Glucose Metabolism	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25399420	The H19/let-7 double-negative feedback loop contributes to glucose metabolism in muscle cells.	Here we report that H19 is significantly decreased in muscle of human subjects with type-2 diabetes and insulin resistant rodents. This decrease leads to increased bioavailability of let-7, causing diminished expression of let-7 targets, which is recapitulated in vitro where H19 depletion results in impaired insulin signaling and decreased glucose uptake. Furthermore, acute hyperinsulinemia downregulates H19, a phenomenon that occurs through PI3K/AKT-dependent phosphorylation of the miRNA processing factor KSRP, which promotes biogenesis of let-7 and its mediated H19 destabilization. 	MI0000060	Nucleic Acids Res 2014 Dec 16 42, 13799-811 doi:10.1093/nar/gku1160 PMID:25399420
1357	LncRNA	miR168-sponge	miR-168	SlAGO1A	Tomato	NA	Solanum lycopersicum (tomato)	qRT-PCR	25378580	miR168 influences phase transition, leaf epinasty, and fruit development via SlAGO1s in tomato.	SlAGO1A and SlAGO1B accumulate in miR168-sponge transgenic plants, and that expression of miR168-resistant SlAGO1A (4m-SlAGO1A) and SlAGO1B (4m-SlAGO1B) in tomato results in a series of defects affecting growth rate, floral timing, leaves, and fruit. Accumulation of miR156 was found when 4m-SlAGO1A was at an early developmental stage compared to the wild type and original SlAGO1A transgenic plants, and miR172 was highly expressed in adult 4m-SlAGO1A compared to the controls.	NA	J Exp Bot 2014 Dec 65, 6655-66 doi:10.1093/jxb/eru387 PMID:25378580
1358	LncRNA	miR168-sponge	miR-168	SlAGO1B	Tomato	NA	Solanum lycopersicum (tomato)	qRT-PCR	25378580	miR168 influences phase transition, leaf epinasty, and fruit development via SlAGO1s in tomato.	SlAGO1A and SlAGO1B accumulate in miR168-sponge transgenic plants, and that expression of miR168-resistant SlAGO1A (4m-SlAGO1A) and SlAGO1B (4m-SlAGO1B) in tomato results in a series of defects affecting growth rate, floral timing, leaves, and fruit. Accumulation of miR156 was found when 4m-SlAGO1A was at an early developmental stage compared to the wild type and original SlAGO1A transgenic plants, and miR172 was highly expressed in adult 4m-SlAGO1A compared to the controls.	NA	J Exp Bot 2014 Dec 65, 6655-66 doi:10.1093/jxb/eru387 PMID:25378580
1359	LncRNA	miR-21 sponge	miR-21	PTEN	T24 Cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	25266796	A lentiviral sponge for miRNA-21 diminishes aerobic glycolysis in bladder cancer T24 cells via the PTEN/PI3K/AKT/mTOR axis.	A microRNA sponge forcibly expressed using a lentiviral vector was utilised to knock down miR-21 expression in vitro. qPCR and Western blot assays were performed to evaluate the expression of a regulatory factor related to aerobic glycolysis and the signalling pathway it regulates.Decrease in glucose uptake and lactate production was observed upon expression of the miR-21 sponge, which promoted phosphatase and tensin homologue (PTEN) expression, decreased phosphorylated AKT and deactivated mTOR.	MI0000077	Tumour Biol 2015 Jan 36, 383-91 doi:10.1007/s13277-014-2617-2 PMID:25266796
1360	LncRNA	lincRNA-ROR	miR-145	ARF6	Hek293T, Mcf-7, Hs578T, And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot assay	25253741	lincRNA-ROR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6.	Investigation of miR-145-regulated pathways involved in tumor invasion revealed a novel target, the small GTPase ADP-ribosylation factor 6 (Arf6). Subsequent analysis demonstrated that ARF6, a known regulator of breast tumor cell invasion, is dramatically upregulated in TNBC and in breast tumor metastasis. Mechanistically, ARF6 regulates E-cadherin localization and affects cell-cell adhesion. 	MI0000461	Mol Cancer Res 2015 Feb 13, 330-8 doi:10.1158/1541-7786.Mcr-14-0251 PMID:25253741
1361	LncRNA	lincRNA-ROR	miR-145	ARF6	Hek293T, Mcf-7, Hs578T, And Mda-Mb-231	Breast Cancer	Mus musculus (mouse)	qRT-PCR;Western blot assay	25253741	lincRNA-ROR and miR-145 regulate invasion in triple-negative breast cancer via targeting ARF6.	Investigation of miR-145-regulated pathways involved in tumor invasion revealed a novel target, the small GTPase ADP-ribosylation factor 6 (Arf6). Subsequent analysis demonstrated that ARF6, a known regulator of breast tumor cell invasion, is dramatically upregulated in TNBC and in breast tumor metastasis. Mechanistically, ARF6 regulates E-cadherin localization and affects cell-cell adhesion. 	MI0000461	Mol Cancer Res 2015 Feb 13, 330-8 doi:10.1158/1541-7786.Mcr-14-0251 PMID:25253741
1362	LncRNA	PDGF	miR-138	FAK	Mesenchymal Stem Cells	Bone Homeostasis Disorder	Homo sapiens (human)	qRT-PCR;Western blot assay	24792185	PDGF-regulated miRNA-138 inhibits the osteogenic differentiation of mesenchymal stem cells.	We found that PDGF treatment significantly inhibits the osteogenic differentiation of MSCs and that miR-138 gene transcription is controlled by PDGF signaling. Our results confirm that miR-138 inhibits the osteogenic differentiation of MSCs and suppresses the phosphorylation of FAK, ERK1/2, and Runx2. Furthermore, our study clearly demonstrates that downregulation of Runx2 by miR-138 is critical for the PDGF-mediated inhibition of osteogenic differentiation of MSCs.	MI0000455	Biochem Biophys Res Commun 2014 Jun 6 448, 241-7 doi:10.1016/j.bbrc.2014.04.091 PMID:24792185
1363	LncRNA	PDGF	miR-138	ERK1	Mesenchymal Stem Cells	Bone Homeostasis Disorder	Homo sapiens (human)	qRT-PCR;Western blot assay	24792185	PDGF-regulated miRNA-138 inhibits the osteogenic differentiation of mesenchymal stem cells.	We found that PDGF treatment significantly inhibits the osteogenic differentiation of MSCs and that miR-138 gene transcription is controlled by PDGF signaling. Our results confirm that miR-138 inhibits the osteogenic differentiation of MSCs and suppresses the phosphorylation of FAK, ERK1/2, and Runx2. Furthermore, our study clearly demonstrates that downregulation of Runx2 by miR-138 is critical for the PDGF-mediated inhibition of osteogenic differentiation of MSCs.	MI0000455	Biochem Biophys Res Commun 2014 Jun 6 448, 241-7 doi:10.1016/j.bbrc.2014.04.091 PMID:24792185
1364	LncRNA	PDGF	miR-138	Runx2	Mesenchymal Stem Cells	Bone Homeostasis Disorder	Homo sapiens (human)	qRT-PCR;Western blot assay	24792185	PDGF-regulated miRNA-138 inhibits the osteogenic differentiation of mesenchymal stem cells.	We found that PDGF treatment significantly inhibits the osteogenic differentiation of MSCs and that miR-138 gene transcription is controlled by PDGF signaling. Our results confirm that miR-138 inhibits the osteogenic differentiation of MSCs and suppresses the phosphorylation of FAK, ERK1/2, and Runx2. Furthermore, our study clearly demonstrates that downregulation of Runx2 by miR-138 is critical for the PDGF-mediated inhibition of osteogenic differentiation of MSCs.	MI0000455	Biochem Biophys Res Commun 2014 Jun 6 448, 241-7 doi:10.1016/j.bbrc.2014.04.091 PMID:24792185
1365	LncRNA	PDGF	miR-138	ERK2	Mesenchymal Stem Cells	Bone Homeostasis Disorder	Homo sapiens (human)	qRT-PCR;Western blot assay	24792185	PDGF-regulated miRNA-138 inhibits the osteogenic differentiation of mesenchymal stem cells.	We found that PDGF treatment significantly inhibits the osteogenic differentiation of MSCs and that miR-138 gene transcription is controlled by PDGF signaling. Our results confirm that miR-138 inhibits the osteogenic differentiation of MSCs and suppresses the phosphorylation of FAK, ERK1/2, and Runx2. Furthermore, our study clearly demonstrates that downregulation of Runx2 by miR-138 is critical for the PDGF-mediated inhibition of osteogenic differentiation of MSCs.	MI0000455	Biochem Biophys Res Commun 2014 Jun 6 448, 241-7 doi:10.1016/j.bbrc.2014.04.091 PMID:24792185
1366	LncRNA	CCAT1	let-7a	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000060	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1367	LncRNA	CCAT1	let-7b	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000063	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1368	LncRNA	CCAT1	let-7c	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000064	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1369	LncRNA	CCAT1	let-7e	HMGA2	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000066	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1370	LncRNA	CCAT1	let-7a	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000060	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1371	LncRNA	CCAT1	let-7b	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000063	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1372	LncRNA	CCAT1	let-7c	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000064	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1373	LncRNA	CCAT1	let-7e	c-Myc	Smmc-7721, Hep3B, Huh7, And Hepg2	Hepatocellular Carcinoma	Mus musculus (mouse)	luciferase reporter assays;qRT-PCR;Western blot assay	25884472	Long noncoding RNA CCAT1 promotes hepatocellular carcinoma progression by functioning as let-7 sponge.	CCAT1 functions as a molecular sponge for let-7, antagonizes its functions, and leads to the de-repression of its endogenous targets HMGA2 and c-Myc. The effect of CCAT1 on HCC cell proliferation and migration is dependent upon its competitively binding to let-7. We found that the let-7a, let-7b, let-7c, and let-7e mimics reduced the luciferase activities of the WT reporter vector.	MI0000066	J Exp Clin Cancer Res 2015 Feb 19 34, 18 doi:10.1186/s13046-015-0136-7 PMID:25884472
1374	LncRNA	AC026166.2-001	miR-24-3p	p27	Amc-Hn-8, Tu-212, Xenograft Tumor Tissues	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	Microarray,PCR,Western blot,Luciferase reporter assay,knockdown	29463827	Long non-coding RNA AC026166.2-001 inhibits cell proliferation and migration in laryngeal squamous cell carcinoma by regulating the miR-24-3p/p27 axis.	AC026166.2-001 inhibited LSCC cell proliferation and the clone-forming capacity.Cell cycle distribution and related protein changes were measured by flow cytometry.AC026166.2-001 arrested the cell cycle at the G1 phase and induced apoptosis.In addition, AC026166.2-001 decreased cell migration as measured by wound healing assays and transwell migration assays.Moreover,luciferase reporter assay and Western blotting results suggested that AC026166.2-001 acts as a sponge of miR-24-3p and regulates the expression of p27 and cyclin D1.The in vivo results showed that AC026166.2-001 significantly suppressed the growth of LSCC xenografts and promoted apoptosis.overexpression of miR-24-3p significantly reduced the luciferase activity of AC026166.2-001 WT GP-miRGLO vectors but not of AC026166.2-001 MUT.Next,AC026166.2-001 may act as a sponge for miR-24-3p.Quantitative RT-PCR was used to test our assumption and we found that miR-24-3p was down-regulated by AC026166.2-001.	MIMAT0000080	Sci Rep 2018 Feb 20 8, 3375 doi:10.1038/s41598-018-21659-5 PMID:29463827
1375	LncRNA	ADAMTS9-AS2	miR-182	NR3C1	Rectal Adenocarcinoma tissues	Rectal Adenocarcinoma	Homo sapiens (human)	qPCR etc	29512732	Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma.	HULC,CRNDE and PVT1 expression levels were increased, and the expression level of ADAMTS9 AS5 was decreased in READ tumor tissues compared to adjacent non tumor tissues.	MI0000272	Oncol Rep 2018 May 39, 2101-2113 doi:10.3892/or.2018.6296 PMID:29512732
1376	LncRNA	ADAMTS9-AS2	miR-223-3p	TGFBR3	A549, Spc-A1, H23 And Nci-H520	Lung Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot etc	29707897	Upregulated lncRNA ADAMTS9-AS2 suppresses progression of lung cancer through inhibition of miR-223-3p and promotion of TGFBR3.	lncADAMTS9-AS2 was lowly expressed in lung cancer tissues. High expression of ADAMTS9-AS2 in lung cancer cells significantly reduced proliferation ability and inhibited migration, as well as elevating their apoptosis rate. In vivo assay found that ADAMTS9-AS2 suppressed the lung tumor growth. Bioinformatics predicted that miR-223-3p bound directly to the ADAMTS9-AS2 and TGFBR3, which was later confirmed by luciferase reporter system. ADAMTS9-AS2 transfection increased TGFBR3 mRNA and protein expressions in lung cancer cells, but miR-223-3p transfection significantly decreased them. Besides,miR-223-3p induced cellular apoptosis while TGFBR3 group  showed the complete opposite effect. It was proved that ADAMTS9-AS2 and TGFBR3 were the direct genes of miR-223-3p. MiR-223-3p promotes proliferation, migration and invasion of lung cancer cells by targeting TGFBR3. 	MIMAT0000280	IUBMB Life 2018 Jun 70, 536-546 doi:10.1002/iub.1752 PMID:29707897
1377	LncRNA	ADPGK-AS1	miR-205-5p	ZEB1	Hek-293T, Panc-1 And Sw-1990	Pancreatic Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot etc	29667486	LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB1-mediated epithelial-mesenchymal transition.	MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal. Dual-luciferase  reporter gene assay proved that ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR. The expression of MiR-205-5p was negatively correlated with proliferation, migration and invasion, and positively  correlated with apoptosis rate of PC cells, while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1. ADPGK-AS1 strongly promoted the tumorigenesis via downregulating  miR-205-5p expression and induced the EMT process in vivo. ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression  through activating ZEB1-induced EMT. 	MIMAT0000266	Cancer Biol Ther 2018 Jul 3 19, 573-583 doi:10.1080/15384047.2018.1423912 PMID:29667486
1378	LncRNA	ANRIL	miR-125a	NA	Hb56, Hb96,Tscc, Tca8113, Scc-9 And Cal27,Hioec，Hek-293T,Oral Cancer Tissues	Oral Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29635126	The role of long non-coding RNA ANRIL in the carcinogenesis of oral cancer by targeting miR-125a.	ANRIL showed significantly higher, while miR-125a showed lower, expression in OC tissues and sera than in normal controls. MTT, colony formation, flow cytometry analysis, wound-healing, transwell and mice xenograft model assays were used to detect the proliferation, migration, and invasion of ARNIL-overexpressing HB56 cells and ARNIL-knockdown CAL27 cells. The results showed that cell proliferation, migration, and invasion were significantly increased by ARNIL overexpression and decreased by ARNIL silencing in oral cancer cells. Furthermore, we found a negative correlation between ARNIL and miR-125a, and ARNIL acts as a miRNA-sponge by directly interacting with miR-125a. 	MI0000469	Biomed Pharmacother 2018 Jul 103, 38-45 doi:10.1016/j.biopha.2018.01.105 PMID:29635126
1379	LncRNA	ATB	miR-200c	ZEB1	Hepg2，Mcf7，Uvecs,Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29657927	Gene Expression Analysis of Two Epithelial-mesenchymal Transition-related Genes:  Long Noncoding RNA-ATB and SETD8 in Gastric Cancer Tissues. 	In gastric tissue samples,cancerous tissues had relatively lower lncRNAATB expression levels than noncancerous ones,although the difference was not statistically significant.lncRNA-ATB levels were inversely associated with depth of invasion (T).Trastuzumab resistance and invasion-metastasis cascade in breast cancer is mediated by sponging role of lncRNA-ATB for miR-200c and thus increasing ZEB1 and ZNF217 and then inducing EMT. 	MI0000650	Adv Biomed Res 2018  7, 42 doi:10.4103/abr.abr_252_16 PMID:29657927
1380	LncRNA	ATB	miR-200c	ZNF-217	Hepg2，Mcf7，Uvecs,Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29657927	Gene Expression Analysis of Two Epithelial-mesenchymal Transition-related Genes:  Long Noncoding RNA-ATB and SETD8 in Gastric Cancer Tissues. 	In gastric tissue samples,cancerous tissues had relatively lower lncRNAATB expression levels than noncancerous ones,although the difference was not statistically significant.lncRNA-ATB levels were inversely associated with depth of invasion (T).Trastuzumab resistance and invasion-metastasis cascade in breast cancer is mediated by sponging role of lncRNA-ATB for miR-200c and thus increasing ZEB1 and ZNF217 and then inducing EMT. 	MI0000650	Adv Biomed Res 2018  7, 42 doi:10.4103/abr.abr_252_16 PMID:29657927
1381	LncRNA	ATB	miR-494	STAT3	A549	Lung Cancer	Homo sapiens (human)	qPCR,Western blot etc	29693289	LncRNA ATB promotes proliferation and metastasis in A549 cells by down-regulation of microRNA-494.	ATB overexpression promoted proliferation, migration, and invasion of A549 cells. Meanwhile, EMT of  A549 cells was also enhanced. ATB silence showed the opposite influence. Expression of miR-494 was negatively regulated by ATB. Following experiments showed ATB-induced alterations of proliferation, migration, invasion, and EMT were all reversed by miR-494 overexpression. Finally, we proved that ATB increased phosphorylated levels of AKT, JAK1, and STAT3, and those increases were all reversed by miR-494 overexpression. We interestingly figured out that ATB promoted proliferation, migration, invasion, and EMT through down-regulating miR-494 in A549 cells. Moreover, ATB might activate AKT and the JAK/STAT3 pathway via down-regulating miR-494. 	MI0003134	J Cell Biochem 2018 Aug 119, 6935-6942 doi:10.1002/jcb.26894 PMID:29693289
1382	LncRNA	ATB	miR-126	KRAS	Bladder Carcinoma Cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29321082	Long noncoding RNA ATB promotes proliferation, migration and invasion in bladder cancer by suppressing microRNA-126.	lncRNA-ATB was a molecular sponge of miR-126, and exerted tumor promoting effects by down-regulation of miR-126. Moreover, KRAS  was a direct target of miR-126, and negatively regulated by miR-126. Finally,  overexpression of KRAS increased cell viability, migration and invasion, as well   as activated PI3K/AKT and mTOR signal pathways in T24 cells. 	MI0000471	Oncol Res 2018 Aug 23 26, 1063-1072 doi:10.3727/096504018x15152072098476 PMID:29321082
1383	LncRNA	BANCR	miR-532-5p	NCF2	MNK-45, SGC-7901, HGC-27, BGC-23, and AGS	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray,RT-qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29483646	LINC01410-miR-532-NCF2-NF-kB feedback loop promotes gastric cancer angiogenesis and metastasis.	Using the cancer genome atlas (TCGA) data set and bioinformatics analyses, we identified miR-532-5p as a potential tumor suppressor in GC, and found that lncRNA LINC01410 might be a negative regulator of miR-532-5p. We then conducted a series of in vivo and in vitro assays to explore the effect of LINC01410 on miR-532-5p-mediated GC malignancy and the underlying mechanism involved.MiR-532-5p overexpression inhibited GC metastasis and angiogenesis in vitro and in vivo,whereas miR-532-5p silencing had the opposite effect. Further study showed that miR-532-5p attenuated NF-κB signaling by directly inhibiting NCF2 expression, while miR-532-5p silencing in GC enhanced NF-κB activity.Furthermore,we demonstrated miR-532-5p down-regulation was caused by aberrantly high expression of LINC01410 in GC.Mechanistically, overexpression of LINC01410 promoted GC angiogenesis and metastasis by binding to and suppressing miR-532-5p, which resulted in up-regulation of NCF2 and sustained NF-κB pathway activation.Interestingly, NCF2 could in turn increase the promoter activity and expression of LINC01410 via NF-κB, thus forming a positive feedback loop that drives the malignant behavior of GC.one of the most interesting findings from this study is that NF-κB can also regulate expression of LINC01410. Other studies have also reported the similar regulating mechanisms. For instance, lncRNA HCP5 up-regulates expression of Runt-related transcription factor 1 (RUNX1) in glioma cells, while overexpression of RUNX1 can also up-regulate HCP expression.	MIMAT0002888	Oncogene 2018 May 37, 2660-2675 doi:10.1038/s41388-018-0162-y PMID:29483646
1384	LncRNA	BCYRN1	miR-138	VEGF	Siha,Hela ,Caski,Ect1/E6E7 ,Cervical Cancer Tissues	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29552212	Long non-coding RNA BCYRN1 promotes the proliferation and metastasis of cervical  cancer via targeting microRNA-138 in vitro and in vivo.  	MicroRNA (miR)-138 was predicted as a direct target of BCYRN1 and the expression of miR-138 was elevated in HeLa cells transfected with  BCYRN1 siRNA. Subsequently, elevated levels of miR-138 were suppressed by transfection with miR-138 inhibitor in HeLa cells pretreated with BCYRN1 siRNA.BCYRN1 siRNA partially counteracted the effect of  miR-138 inhibitor on promoting cell viability and mobility in HeLa cells. BCYRN1 siRNA was able to prevent tumor growth, and reduced the expression of migration marker proteins metalloproteinase 2 and vascular endothelial cell growth factor, with enhanced expression levels of miR-138. These results suggest that lncRNA BCYRN1 promotes the proliferation and invasion of cervical cancer via targeting miR-138. 	MI0000455	Oncol Lett 2018 Apr 15, 5809-5818 doi:10.3892/ol.2018.8015 PMID:29552212
1385	LncRNA	BCYRN1	miR-138	MMP2	Siha,Hela ,Caski,Ect1/E6E7 ,Cervical Cancer Tissues	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29552212	Long non-coding RNA BCYRN1 promotes the proliferation and metastasis of cervical  cancer via targeting microRNA-138 in vitro and in vivo.  	MicroRNA (miR)-138 was predicted as a direct target of BCYRN1 and the expression of miR-138 was elevated in HeLa cells transfected with  BCYRN1 siRNA. Subsequently, elevated levels of miR-138 were suppressed by transfection with miR-138 inhibitor in HeLa cells pretreated with BCYRN1 siRNA.BCYRN1 siRNA partially counteracted the effect of  miR-138 inhibitor on promoting cell viability and mobility in HeLa cells. BCYRN1 siRNA was able to prevent tumor growth, and reduced the expression of migration marker proteins metalloproteinase 2 and vascular endothelial cell growth factor, with enhanced expression levels of miR-138. These results suggest that lncRNA BCYRN1 promotes the proliferation and invasion of cervical cancer via targeting miR-138. 	MI0000455	Oncol Lett 2018 Apr 15, 5809-5818 doi:10.3892/ol.2018.8015 PMID:29552212
1386	LncRNA	BLACAT1	miR-361	ABCB1	Bgc-823, Sgc-7901, Mgc-803,Ges-1,Gastric Cancer Tissue A	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29710482	Long noncoding RNA BLACAT1 modulates ABCB1 to promote oxaliplatin resistance of gastric cancer via sponging miR-361.	In vitro, BLACAT1 knockdown decreased the expression levels of drug resistance related genes and ABCB1 protein. BLACAT1 knockdown significantly promoted apoptosis and down-regulated the invasion and the IC50 value of oxaliplatin.In vivo, BLACAT1 knockdown suppressed the tumor growth of gastric cancer cells. Bioinformatics tools and luciferase assay indicated that miR-361 both targeted 3-UTR of BLACAT1 and ABCB1mRNA, suggesting the BLACAT1/miR-361/ABCB1 regulatory pathway.	MI0000760	Biomed Pharmacother 2018 Mar 99, 832-838 doi:10.1016/j.biopha.2018.01.130 PMID:29710482
1387	LncRNA	CASC2	miR-181a	TGFB	Hcc1937, Lcc9,Mda-Mb-231, Mcf-7,Breast Cancer Tissues 	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown etc	29523222	Up-regulation of lncRNA CASC2 suppresses cell proliferation and metastasis of breast cancer via inactivating of the TGF-b signaling pathway. 	Overexpression of lncRNA CASC2 significantly repressed proliferation and metastasis while caused cell cycle arrest and much more early apoptosis of breast cancer.The inactivation of TGF- signal pathway was  involved in the function of lncRNA CASC2. lncRNA CASC2 was a key factor in the tumorigenesis and malignancy of breast cancer, thereby possibly was a potential therapy target for the treatment of breast cancer. 	MI0000269	Oncol Res 2019 Feb 21 27, 379-387 doi:10.3727/096504018x15199531937158 PMID:29523222
1388	LncRNA	CASC2	miR-181a	PLXNC	A375, C8161, HMCB, G361, WM115, MM96L, and M14	Melanoma	Homo sapiens (human)	Microarray,qPCR,Western blot,Luciferase reporter assay	29514220	Long non-coding RNA CASC2 inhibits tumorigenesis via the miR-181a/PLXNC1 axis in  melanoma. 	CASC2 could efficiently sponge miR-181a, thereby facilitating the expression of PLXNC1. Up-regulation of CASC2 suppressed the cell proliferation and invasion, but induced the apoptosis of melanoma cells.  LncRNA CASC2 can promote PLXNC1 expression by sponging miR-181a, thereby inhibiting the  proliferation and invasion of melanoma cells, indicating that lncRNA CASC2 functions via the miR-181a/PLXNC1 axis in melanoma.  	MI0000269	Acta Biochim Biophys Sin (Shanghai) 2018 Mar 1 50, 263-272 doi:10.1093/abbs/gmx148 PMID:29514220
1389	LncRNA	CASC2	miR-24	TRAIL	HepG2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29476051	CASC2/miR-24/miR-221 modulates the TRAIL resistance of hepatocellular carcinoma cell through caspase-8/caspase-3.	CASC2, a well-established tumor suppressive long non-coding RNA, could serve as a "Sponge" of miR-24 and miR-221, thus modulating TRAIL-induced tumor cell apoptosis TRAIL resistance of hepatocellular carcinoma. Taken together, we demonstrated a CASC2/miR-24/miR-221 axis, which can affect the TRAIL resistance of hepatocellular carcinoma through regulating caspase 3/8; through acting as a "Sponge" of miR-24 and miR-221, CASC2 may contribute to improving hepatocellular carcinoma TRAIL resistance, and finally promoting the treatment efficiency of TRAIL-based therapies.	MIMAT0000080	Cell Death Dis 2018 Feb 23 9, 318 doi:10.1038/s41419-018-0350-2 PMID:29476051
1390	LncRNA	CASC2	miR-221	TRAIL	HepG2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29476051	CASC2/miR-24/miR-221 modulates the TRAIL resistance of hepatocellular carcinoma cell through caspase-8/caspase-3.	CASC2, a well-established tumor suppressive long non-coding RNA, could serve as a "Sponge" of miR-24 and miR-221, thus modulating TRAIL-induced tumor cell apoptosis TRAIL resistance of hepatocellular carcinoma. Taken together, we demonstrated a CASC2/miR-24/miR-221 axis, which can affect the TRAIL resistance of hepatocellular carcinoma through regulating caspase 3/8; through acting as a "Sponge" of miR-24 and miR-221, CASC2 may contribute to improving hepatocellular carcinoma TRAIL resistance, and finally promoting the treatment efficiency of TRAIL-based therapies.	MI0000298	Cell Death Dis 2018 Feb 23 9, 318 doi:10.1038/s41419-018-0350-2 PMID:29476051
1391	LncRNA	CASC2	miR-18a-5p	RUNX1	A375, A2058 and HTB63	Melanoma	Homo sapiens (human)	RT-qPCR,Western blot,Luciferase reporter assay	29422114	Upregulated lncRNA CASC2 may inhibit malignant melanoma development through regulating miR-18a-5p/RUNX1.	CASC2 acted as a molecular sponge for miR-18a-5p and RUNX1 was a target gene of miR-18a-5p. Moreover, CASC2 overexpression promoted the expression of RUNX1, while upregulated miR-18a-5p significantly reversed the effect of CASC2 on RUNX1 level.Upregulated CASC2 may inhibit cell proliferation, migration and invasion through regulating miR-18a-5p and its target gene RUNX1 in MM.	MIMAT0000072	Oncol Res 2019 Feb 21 27, 371-377 doi:10.3727/096504018x15178740729367 PMID:29422114
1392	LncRNA	CASC2	miR-183	SPRY2	Atcc, Crl-1740, Pc3 	Prostate Cancer	Homo sapiens (human)	RT-PCR,Luciferase reporter assay,in vitro knockdown	29373811	Long non-coding RNA CASC2 regulates Sprouty2 via functioning as a competing endogenous RNA for miR-183 to modulate the sensitivity of prostate cancer cells to docetaxel.	CASC2 and SPRY2 expression was down-regulated in PC tissues and cell lines,the overexpression of CASC2 and SPRY2 could suppress PC cell proliferation, promote PC cell apoptosis, and enhance the sensitivity of PC cells to docetaxel. CASC2 positively regulated SPRY2 expression and inhibited downstream extracellular regulated protein kinases (ERK) signaling activation through SPRY2.miR-183 inhibition enhanced the cytotoxicity of docetaxel on PC cells, which could be partially attenuated by SPRY2 knockdown.	MI0000273	Arch Biochem Biophys 2019 Apr 15 665, 69-78 doi:10.1016/j.abb.2018.01.013 PMID:29373811
1393	LncRNA	CAT104	miR-381	ZEB1	NCI-N87, SGC7901, BGC823, BGC803, and AGS	Gastric Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	29295724	Long non-coding RNA CAT104 promotes cell viability, migration and invasion in gastric carcinoma cells through activation of microRNA-381 inhibiting zinc finger E-box binding homeobox 1 (ZEB1) expression.	CAT104 was highly expressed in human GC NCI-N87, SGC7901, BGC823, BGC803 and AGS cells. Suppression of CAT104 decreased NCI-N87 cell viability, migration and invasion, but promoted apoptosis. CAT104 knockdown enhanced the expression of microRNA-381 (miR-381) expression in NCI-N87 cells. miR-381 participated in the regulation effects of CAT104 on NCI-N87 cell viability, migration, invasion and apoptosis. Zinc finger E-box binding homeobox 1 (ZEB1) was identified as a direct target of miR-381. Overexpression of ZEB1 revealed the miR-381 mimicinduced cell viability, migration and invasion inhibition.Suppression of ZEB1 revealed the miR-381 inhibitor-induced activation of c-Jun N-terminal kinase pathway (JNK) and Wnt/ signaling pathways in NCI-N87 cells.	MI0000789	Oncol Res 2018 Aug 23 26, 1037-1046 doi:10.3727/096504017x15144748428127 PMID:29295724
1394	LncRNA	CAT104	miR-381	ZEB1	Mg63 And Os-732,Hfob1.19, Hek293	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29523223	Knockdown of long non-coding RNA CAT104 inhibits the proliferation, migration and invasion of human osteosarcoma cells by regulating microRNA-381. 	CAT104 was highly expressed in osteosarcoma MG-63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381 and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E box binding homeobox 1 (ZEB1) was a direct target gene of miR-381, which was involved in the regulatory roles of miR381 in OS-732 cell proliferation, migration, invasion and apoptosis, as well as c-Jun Nterminal kinase (JNK) and Wnt/-catenin pathways. Suppression of CAT104 exerted significant inhibitory effects on osteosarcoma cell proliferation, migration and invasion by regulating the expression of miR-381 and downstream ZEB1, as well as JNK and Wnt/-catenin pathways. 	MI0000789	Oncol Res 2018 Dec 27 27, 89-98 doi:10.3727/096504018x15199511344806 PMID:29523223
1395	LncRNA	CCAT1	miR-1290	TCF21	Ovcar-8 And Skov-3,Omc685,Iose386	Ovarian Cancer	Homo sapiens (human)	qPCR	29424889	LncRNA colon cancer-associated transcript 1 (CCAT1) promotes proliferation and metastasis of ovarian cancer via miR-1290.	the expression of lncRNA CCAT1 was closely related to prognosis, tumor size, and lymph node metastasis. lncRNA CCAT1 could sponge miR-1290 in ovarian cancer. high expression of lncRNA CCAT1 could be used as an indicator of the survival time of OC patients.	MIMAT0005880	Eur Rev Med Pharmacol Sci 2018 Jan 22, 322-328 doi:10.26355/eurrev_201801_14175 PMID:29424889
1396	LncRNA	CNALPTC1	miR-30a	BCL9	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000088	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1397	LncRNA	CNALPTC1	miR-30b	BCL9	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000441	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1398	LncRNA	CNALPTC1	miR-30c	BCL9	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000254	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1399	LncRNA	CNALPTC1	miR-30d	BCL9	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000255	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1400	LncRNA	CNALPTC1	miR-30e	BCL9	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000749	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1401	LncRNA	CNALPTC1	miR-30a	SNAI1	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000088	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1402	LncRNA	CNALPTC1	miR-30b	SNAI1	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000441	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1403	LncRNA	CNALPTC1	miR-30c	SNAI1	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000254	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1404	LncRNA	CNALPTC1	miR-30d	SNAI1	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000255	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1405	LncRNA	CNALPTC1	miR-30e	SNAI1	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000749	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1406	LncRNA	CNALPTC1	miR-30a	VIM	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000088	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1407	LncRNA	CNALPTC1	miR-30b	VIM	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000441	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1408	LncRNA	CNALPTC1	miR-30c	VIM	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000254	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1409	LncRNA	CNALPTC1	miR-30d	VIM	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000255	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1410	LncRNA	CNALPTC1	miR-30e	VIM	Tpc-1 And Ihh-4	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,RIP	29416932	Long noncoding RNA CNALPTC1 promotes cell proliferation and migration of papillary thyroid cancer via sponging miR-30 family.	The genomic copy number of CNALPTC1 is amplified and CNALPTC1 expression level is up-regulated in PTC. CNALPTC1 physically associates to miR-30 family and down-regulates miR-30 expression. Furthermore, CNALPTC1 up-regulates the expression of miR-30 targets, such as BCL9, SNAI1, and VIM. The mutation of miR-30 binding site on CNALPTC1 or overexpression of miR-30 abrogates the oncogenic roles of CNALPTC1 in PTC.	MI0000749	Am J Cancer Res 2018  8, 192-206,  PMID:29416932
1411	LncRNA	CRNDE	miR-145	E2F3	5637,T24,Bc Tissues	Bladder Cancer	Homo sapiens (human)	qPCR,in vitro knockdown etc	29710461	Overexpression of CRNDE promotes the progression of bladder cancer.   	CRNDE was significantly increased in bladder cancer, and overexpressed expression of CRNDE was positively related with advanced TNM stage of bladder cancer patients. In addition, in vitro experiments showed that CRNDE strengthened cell migration/proliferation and inhibited cell apoptosis in bladder cancer.CRNDE can suppress E2F3 expression to increase miR-145 expression.	MI0000461	Biomed Pharmacother 2018 Mar 99, 638-644 doi:10.1016/j.biopha.2017.12.055 PMID:29710461
1412	LncRNA	CRNDE	miR-144	FGF2	Rectal Adenocarcinoma tissues	Rectal Adenocarcinoma	Homo sapiens (human)	qPCR etc	29512732	Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma.	HULC, CRNDE and PVT1 expression levels were increased, and the expression level of ADAMTS9 AS3 was decreased in READ tumor tissues compared to adjacent non tumor tissues.	MI0000460	Oncol Rep 2018 May 39, 2101-2113 doi:10.3892/or.2018.6296 PMID:29512732
1413	LncRNA	DANCR	miR-758-3p	BCL-2	Spc-A,Ncl-H1650, Ncl-H1975, Sk-Mes-1,A549,Ncl-H358 And Nci-H1299,16Hbe	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29635134	The long non-coding RNA-DANCR exerts oncogenic functions in non-small cell lung cancer via miR-758-3p.	DANCR was markedly upregulated in NSCLC tumor tissues and cell lines compared with related normal controls.The ectopic expression of DANCR significantly increased the proliferation, migration and invasion of SPC-A1 and NCL-H1299 cells. Furthermore, we investigated whether DANCR regulates NSCLC tumor formation in vivo. Subsequently, we concluded that DANCR promotes NSCLC cell proliferation, migration and invasion by regulating the tumor suppressor miR-758-3p.the DANCR/miR-758-3p axis could be a potential target in the treatment of NSCLC. 	MIMAT0003879	Biomed Pharmacother 2018 Jul 103, 94-100 doi:10.1016/j.biopha.2018.03.053 PMID:29635134
1414	LncRNA	DANCR	miR-33a-5p	AXL	U87Mg, U251Mg, Ln18,U138Mg	Malignant Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays,in vitro knockdown etc	29572052	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated  AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 	MIMAT0000091	Neurochem Int 2018 Sep 118, 233-241 doi:10.1016/j.neuint.2018.03.011 PMID:29572052
1415	LncRNA	DANCR	miR-33b-5p	AXL	U87Mg, U251Mg, Ln18,U138Mg	Malignant Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays,in vitro knockdown etc	29572052	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated  AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 	MIMAT0003301	Neurochem Int 2018 Sep 118, 233-241 doi:10.1016/j.neuint.2018.03.011 PMID:29572052
1416	LncRNA	DANCR	miR-1-3p	AXL	U87Mg, U251Mg, Ln18,U138Mg	Malignant Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays,in vitro knockdown etc	29572052	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated  AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 	MIMAT0000416	Neurochem Int 2018 Sep 118, 233-241 doi:10.1016/j.neuint.2018.03.011 PMID:29572052
1417	LncRNA	DANCR	miR-206	AXL	U87Mg, U251Mg, Ln18,U138Mg	Malignant Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays,in vitro knockdown etc	29572052	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated  AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 	MI0000490	Neurochem Int 2018 Sep 118, 233-241 doi:10.1016/j.neuint.2018.03.011 PMID:29572052
1418	LncRNA	DANCR	miR-613	AXL	U87Mg, U251Mg, Ln18,U138Mg	Malignant Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays,in vitro knockdown etc	29572052	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. 	Long noncoding RNA DANCR mediates cisplatin resistance in glioma cells via activating AXL/PI3K/Akt/NF-κB signaling pathway. DNACR also attenuated cisplatin-induced cell apoptosis in vitro and in vivo. DANCR upregulated  AXL via competitively binding miR-33a-5p, miR-33b-5p, miR-1-3p, miR-206, and miR-613. Through upregulating AXL, DANCR activated PI3K/Akt/NF-κB signaling pathway in glioma cells. Inhibiting AXL/PI3K/Akt/NF-κB signaling pathway reversed the effects of DANCR on cisplatin resistance.DANCR promotes cisplatin resistance via activating AXL/PI3K/Akt/NF-κB signaling pathway in glioma.DANCR would be a potential biomarker for predicting cisplatin sensitivity and a therapeutic target for enhancing cisplatin efficacy in glioma. 	MI0003626	Neurochem Int 2018 Sep 118, 233-241 doi:10.1016/j.neuint.2018.03.011 PMID:29572052
1419	LncRNA	DANCR	miR-335-5p	ROCK1	Mg-63, U2Os, Mnng/Hos, 143B And Hfob	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc	29753317	Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma.	an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma. LncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma. 	MIMAT0000765	Mol Cancer 2018 May 12 17, 89 doi:10.1186/s12943-018-0837-6 PMID:29753317
1420	LncRNA	DANCR	miR-1972	ROCK1	Mg-63, U2Os, Mnng/Hos, 143B And Hfob	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc	29753317	Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma.	an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma. LncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma. 	MIMAT0009447	Mol Cancer 2018 May 12 17, 89 doi:10.1186/s12943-018-0837-6 PMID:29753317
1421	LncRNA	DANCR	miR-613	MMP-9	Weri-Rb1, Y79, So-Rb50, Hxo-Rb44, Arpe-19 And Htert-Rpe1	Retinoblastoma	Homo sapiens (human)	qPCR,Western blot etc	29744877	Long noncoding RNA DANCR aggravates retinoblastoma through miR-34c and miR-613 by targeting MMP-9.	DANCR was up-regulated in RB tissue and cell lines.Moreover, the ectopic overexpression of DANCR indicated poor overall survivals and disease free survival (DFS) for RB patients.In vitro and in vivo experiments, DANCR knockdown suppress the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) correlated protein (N-cadherin, Vimentin) of RB cells. Bioinformatics analysis predicted that miR-34c and miR-613 targeted  with 3'-UTR of DANCR, besides, miR-34c and miR-613 also targeted with 3'-UTR of MMP-9, which was validated by luciferase reporter assay. Functional experiments demonstrated that miR-34c and miR-613 could reverse the oncogenic function of DANCR in RB tumorigenesis. In conclusion, our results reveal that DANCR function as competing endogenous RNA (ceRNA) for miR-34c and miR-613 to modulate progression and metastasis in RB oncogenesis via targeting MMP-9, presenting the in-depth regulation of DANCR in RB and providing a novel insight for ceRNA mechanism for RB. 	MI0003626	J Cell Physiol 2018 Oct 233, 6986-6995 doi:10.1002/jcp.26621 PMID:29744877
1422	LncRNA	DANCR	miR-34c	MMP-9	Weri-Rb1, Y79, So-Rb50, Hxo-Rb44, Arpe-19 And Htert-Rpe1	Retinoblastoma	Homo sapiens (human)	qPCR,Western blot etc	29744877	Long noncoding RNA DANCR aggravates retinoblastoma through miR-34c and miR-613 by targeting MMP-9.	DANCR was up-regulated in RB tissue and cell lines.Moreover, the ectopic overexpression of DANCR indicated poor overall survivals and disease free survival (DFS) for RB patients.In vitro and in vivo experiments, DANCR knockdown suppress the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) correlated protein (N-cadherin, Vimentin) of RB cells. Bioinformatics analysis predicted that miR-34c and miR-613 targeted  with 3'-UTR of DANCR, besides, miR-34c and miR-613 also targeted with 3'-UTR of MMP-9, which was validated by luciferase reporter assay. Functional experiments demonstrated that miR-34c and miR-613 could reverse the oncogenic function of DANCR in RB tumorigenesis. In conclusion, our results reveal that DANCR function as competing endogenous RNA (ceRNA) for miR-34c and miR-613 to modulate progression and metastasis in RB oncogenesis via targeting MMP-9, presenting the in-depth regulation of DANCR in RB and providing a novel insight for ceRNA mechanism for RB. 	MI0000743	J Cell Physiol 2018 Oct 233, 6986-6995 doi:10.1002/jcp.26621 PMID:29744877
1423	LncRNA	DANCR	miR-577	HSP27	Ht29, Hct116, Sw480, Lovo And E Ncm460	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	29717105	Long noncoding RNA DANCR promotes colorectal cancer proliferation and metastasis  via miR-577 sponging.	DANCR was highly expressed and correlated with proliferation and metastasis in CRC.In addition, we demonstrated that DANCR and HSP27 were both targets of microRNA-577 (miR-577) and shared the same binding site.Furthermore,DANCR promoted HSP27 expression and its mediation of proliferation/metastasis via miR-577 sponging. Finally, using an in vivo study, we confirmed that overexpression of DANCR promoted CRC tumor growth and liver metastasis. 	MI0003584	Exp Mol Med 2018 May 1 50, 1-17 doi:10.1038/s12276-018-0082-5 PMID:29717105
1424	LncRNA	DANCR	miR-634	RAB1A	Nb Tissues, Glioma Tissues, Glioma Cell Lines 	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29301870	LncRNA DANCR functions as a competing endogenous RNA to regulate RAB1A expression by sponging miR-634 in glioma.	DANCR was significantly up-regulated in glioma tissues and cell lines (U251, U118, LN229, and U87MG). High DANCR expression was correlated with advanced tumor grade.Inhibition of DANCR suppressed the glioma cells proliferation and induced cells arrested in the G0/G1 phase.In addition,we verified that DANCR could directly interact with miR-634 in glioma cells and this interaction resulted in the inhibition of downstream of RAB1A expression.	MI0003649	Biosci Rep 2018 Feb 28 38 doi:10.1042/bsr20171664 PMID:29301870
1425	LncRNA	DGCR5	miR-22-3p	BCL-2	A549, H460, H1299,  Bes-2B And Hek-293T	Lung Cancer	Homo sapiens (human)	qPCR,Western blot etc	29030962	LncRNA DGCR5 promotes lung adenocarcinoma (LUAD) progression via inhibiting hsa-mir-22-3p.	DGCR5 was upregulated in LUAD tissues and LUAD cell lines. Inhibition of DGCR5 can prevent LUAD progression via playing anti-apoptosis roles. Both mRNA expression and protein levels of BCL-2 were increased by DGCR5 downregulation while reversely BAX was increased. Additionally,a novel microRNA target of DGCR5, hsa-mir-22-3p was identified through bioinformatics search and confirmed by dual-luciferase reporter system. Gain and loss-of-function studies were performed to verify whether DGCR5 exerts its biological functions through regulating hsa-mir-22-3p in vitro. Overexpression of DGCR5 was able to reverse the tumor inhibitory effect of hsa-mir-22-3p mimics. Furthermore, in vivo tests tumor xenografts were established to detect the function of DGCR5 in LUAD tumorigenesis. Downregulated DGCR5 expression was greatly associated with smaller tumor size, implying a favorable prognosis of LUAD patients. Taken these together, DGCR5 could be considered as a prognostic biomarker and therapeutic target in LUAD diagnosis and treatment. 	MIMAT0000077	J Cell Physiol 2018 May 233, 4126-4136 doi:10.1002/jcp.26215 PMID:29030962
1426	LncRNA	DGCR5	miR-330-5p	CD44	A549, H460, H1299 And Hek-293T	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29663359	LncRNA DGCR5 contributes to CSC-like properties via modulating miR-330-5p/CD44 in NSCLC.	DGCR5 was up-regulated in the enriched CSCs of NSCLC. DGCR5 can inhibit the stemness of NSLCL while overexpression of DGCR5 promoted CSC-like traits.In addition, miR-330-5p was predicted as target of DGCR.Meanwhile,miR-330-5p was decreased in CSCs of NSCLC.miR-330-5p mimics repressed the stemness while miR-330-5p inhibition enhanced CSC-like properties by targeting CD44.Taken these together,DGCR5 can act as a crucial regulator of  CSCs in NSCLC by modulating miR-330-5p/CD44 axis. 	MIMAT0004693	J Cell Physiol 2018 Sep 233, 7447-7456 doi:10.1002/jcp.26590 PMID:29663359
1427	LncRNA	Dleu2	miR-16-1	NA	Tu212,A549,Laryngeal Cancer Tissues	Laryngeal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29687850	Long non-coding RNA Dleu2 affects proliferation, migration and invasion ability of laryngeal carcinoma cells through triggering miR-16-1 pathway.   	LncRNA Dleu2 and miR-16-1 levels were significantly declined in the laryngeal carcinoma tissue compared to para-carcinoma tissue. LncRNA Dleu2 and miR-16-1 up-regulation significantly reduced cell proliferation,migration,and invasion compared to the control group. Ago-miR16-1 transfection significantly enhanced the luciferase activity of wild-type Dleu2 compared to control group,suggesting their interaction with each other. LncRNA Dleu2 influences the proliferation, migration, and invasion of laryngeal cancer cells through miR-16-1. Therefore, lncRNA Dleu2 and miR-16-1 may serve as potential biomarkers and targets for laryngeal cancer diagnosis and treatment. 	MI0000070	Eur Rev Med Pharmacol Sci 2018 Apr 22, 1963-1970 doi:10.26355/eurrev_201804_14723 PMID:29687850
1428	LncRNA	ENST01108	miR-489	SIK1	U251 And U87,Glioma Tissues	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29421578	Long non-coding RNA ENST01108 promotes carcinogenesis of glioma by acting as a molecular sponge to modulate miR-489.  	lncRNA ENST01108 (ENST01108) has oncogenic role in glioma. Clinical data suggest that ENST01108 is closely associated with the malignant status in glioma. In vitro experiment demonstrated that overexpression  of ENST01108 promoted glioma cell proliferation, migration, invasion, EMT process and survival, while knockdown of ENST01108 has an opposite effect,indicating that ENST01108 serves as an oncogenic property in glioma carcinogenesis.Further, we identified miR-489 as a direct target of ENST01108 and ENST01108 negatively regulate miR-489 by act as a sponge. SIK1 is verified as the direct target of miR-489 and it is negatively regulated by miR-489. ENST01108 also positively regulate SIKI and it promotes SIKI expression by suppressing miR-489. Taken together, the reciprocal repression of ENST011081 and miR-489 may be served as potential targets for cancer therapeutics in glioma. 	MI0003124	Biomed Pharmacother 2018 Apr 100, 20-28 doi:10.1016/j.biopha.2018.01.126 PMID:29421578
1429	LncRNA	FABP5P3	miR-589-5p	ZMYND19	Lo2,Hep3B,Hepg2,Huh7, Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29522715	LncRNA FABP5P3/miR-589-5p/ZMYND19 axis contributes to hepatocellular carcinoma cell proliferation, migration and invasion.  	FABP5P3 that was up-regulated in HCC tissues.Patients with higher FABP5P3 expression displayed poorer survival rate.FABP5P3 depletion in HCC cell lines and sample cells remarkably inhibited the abilities of proliferation, migration and invasion. FABP5P3 bond to miR-589-5p which served as a tumor suppressor. MiR-589-5p targeted directly the mRNA of ZMYND19 whose function has not been defined in HCC.FABP5P3  promoted HCC development and progression by sponging miR-589-5p and up-regulating ZMYND19 expression.FABP5P3/miR-589-5p/ZMYND19 axis regulates cell proliferation and migration in HCC,which may serve as a new target for HCC treatment.  	MIMAT0004799	Biochem Biophys Res Commun 2018 Apr 6 498, 551-558 doi:10.1016/j.bbrc.2018.03.017 PMID:29522715
1430	LncRNA	FAL1	miR-1236	AFP	Lo2, Smmc-7721, Huh7, Hepg2,Hepg2.2.15,Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29421439	LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells.   	lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC. LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover,lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migratio.	MI0006326	Life Sci 2018 Mar 15 197, 122-129 doi:10.1016/j.lfs.2018.02.006 PMID:29421439
1431	LncRNA	FAL1	miR-1236	ZEB1	Lo2, Smmc-7721, Huh7, Hepg2,Hepg2.2.15,Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29421439	LncRNA FAL1 promotes cell proliferation and migration by acting as a CeRNA of miR-1236 in hepatocellular carcinoma cells.   	lncRNA FAL1 was up-regulated in HCC tissues and functioned as an oncogene in HCC. LncRNA FAL1 could accelerate cell proliferation and metastasis as a ceRNA mechanism by competitively binding to miR-1236. Moreover,lncRNA FAL1 was also up-regulated in serum exosome of HCC patients and could transfer lncRNA FAL1 to HCC cells to increase their abilities of cell proliferation and migratio.	MI0006326	Life Sci 2018 Mar 15 197, 122-129 doi:10.1016/j.lfs.2018.02.006 PMID:29421439
1432	LncRNA	FENDRR	miR-18a-5p	RUNX1	Rwpe-1,P69,Vcap, Lncap, 22Rv1, Pc3,Du145 ,Pca Tissues 	Prostate Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown	29465000	Long non-coding RNA FENDRR reduces prostate cancer malignancy by competitively binding miR-18a-5p with RUNX1.	FENDRR acts as a molecular sponge for miR-18a-5p. Upregulation of FENDRR inhibited cell proliferation, increased apoptosis and decreased invasion and migration ability,which was inhibited by miR-18a-5p mimic. Knockdown of FENDRR resulted in a significant increase of PCa cell proliferation and decrease of apoptosis and this effect was inhibited miR-18a-5p inhibitor.FENDRR and RUNX1 contain potential target sites for miR-18a-5p. miR-18a-5p mimic inhibited RUNX1 expression and luciferase activity.FENDRR could increase RUNX1 expression,which was inhibited by miR-18a-5p.The effect of FENDRR on cell proliferation, apoptosis and invasion and migration ability was suppressed by silence of RUNX1. 	MIMAT0000072	Biomarkers 2018 Jul 23, 435-445 doi:10.1080/1354750x.2018.1443509 PMID:29465000
1433	LncRNA	FEZF1-AS1	miR-4443	NUPR1	U2Os, Saos2, Sw1353, And Mg63, Fetal Osteoblastic Cell Line Hfob	Osteosarcoma	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29510778	Long non-coding RNA FEZF1-AS1 promotes osteosarcoma progression by regulating miR-4443/NUPR1 axis.	FEZF1-AS1 sponged miR-4443 to promote NUPR1 expression in U2OS and MG63 cells.Furthermore,knockdown of miR-4443 abrogated FEZF1-AS1 silence-induced inhibition of cell proliferation,migration and invasion in osteosarcoma.Finally,we found that restoration of NUPR1 rescued the proliferation,migration and invasion abilities of FEZF1-AS1-depleted U2OS and MG63 cells. In collection,FEZF1-AS1 could promote osteosarcoma progression by sponging miR-4443 to promote NUPR1 expression.The FEZF1-AS1/miR-4443/NUPR1 axis may act as a novel therapeutic strategy for osteosarcoma treatment.	MI0016786	Oncol Res 2018 Oct 17 26, 1335-1343 doi:10.3727/096504018x15188367859402 PMID:29510778
1434	LncRNA	FEZF1-AS1	miR-107	ZNF312B	Panc-1, Capan-2, Miapaca-2, Sw1990, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29348628	FEZF1-AS1/miR-107/ZNF312B axis facilitates progression and Warburg effect in pancreatic ductal adenocarcinoma.	A novel lncRNA FEZF1-AS1 and its sense-cognate gene ZNF312B were found to be highly expressed in human PDAC tissues and cell lines, which is associated with disease progression and predicts clinical outcome in PDAC patients.FEZF1-AS1 may act as an endogenous sponge by competing for miR-107, thereby modulating the derepression of ZNF312B. Downregulation of FEZF1-AS1 or ZNF312B significantly inhibited proliferation, colony formation, migration, and invasion of PDAC cells in vitro, whereas the miR-107 inhibitor abrogated the effect of dow-regulation of FEZF1-AS1 or ZNF312B in reducing oncogenic capacities of PDAC cells.In addition, FEZF1-AS1/miR-107/ZNF312B axis-induced promotion of PDAC cells proliferation appeared to be mediated by modulation of the apoptosis and the G1-S checkpoint.	MI0000114	Cell Death Dis 2018 Jan 18 9, 34 doi:10.1038/s41419-017-0052-1 PMID:29348628
1435	LncRNA	FLVCR1-AS1	miR-513c	MET	Lo2,Hep3B, Hepg2, Huh7, And Plc/Prf-5, Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,in vitro knockdown,Luciferase reporter assay etc	29574975	LncRNA FLVCR1-AS1 acts as miR-513c sponge to modulate cancer cell proliferation,  migration, and invasion in hepatocellular carcinoma.  	lncRNA FLVCR1-AS1 was extremely up-regulated in HCC tissues and cell lines. FLVCR1-AS1 expression level was positively correlated with tumor severity.FLVCR1-AS1 knockdown remarkably inhibited HCC cell proliferation,migration,and invasion in vitro and in vivo while induced cell apoptosis. In mechanism, FLVCR1-AS1 acted as a competitive endogenous RNAs to sponge miR-513c which targeted the mRNA of MET for degradation. By directly sponging miR-513c, FLVCR1-AS1 increased MET expression in HCC, and then promoted HCC progression. FLVCR1-AS1 played a positive role in HCC development and progression according to the study in its mechanism,function and clinical manifestation, so that it could be expected to become a new target in HCC prevention and treatment.  	MI0006649	J Cell Biochem 2018 Jul 119, 6045-6056 doi:10.1002/jcb.26802 PMID:29574975
1436	LncRNA	FOXD2-AS1	miR-143	ABCC3	T24 	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29674277	Long noncoding RNA FOXD2-AS1 accelerates the gemcitabine-resistance of bladder cancer by sponging miR-143.	LncRNA FOXD2-AS1 was high-expressed in gemcitabine-resistant bladder cancer cells. In vitro experiments, FOXD2-AS1 knockdown suppressed the 50% inhibitive concentration (IC50) of gemcitabine, drug-resistance related genes (MDR1, MRP2, LRP1) expression,invasion and ABCC3 protein expression in gemcitabine-resistant bladder cancer cells (T24/GEM, 5637/GEM). In vivo of xenograft assay, FOXD2-AS1 knockdown inhibited the tumor growth of bladder cancer cells.Bioinformatics program and validation experiments confirmed that FOXD2-AS1 positively regulated ABCC3 protein through targeting miR-143,acting as a competing endogenous RNA (ceRNA).In summary,the vital roles of FOXD2-AS1/miR-143/ABCC3 axis in gemcitabine resistance of bladder cancer cells, providing a novel therapeutic strategy for bladder cancer. We found that lncRNA FOXD2-AS1 sponged miR-143 to indirectly target ABCC3 protein ex- pression, consisting the FOXD2-AS1/miR-143/ABCC3 axis.	MI0000459	Biomed Pharmacother 2018 Jul 103, 415-420 doi:10.1016/j.biopha.2018.03.138 PMID:29674277
1437	LncRNA	GACAT3	miR-149	SP1	Fhc, Ht29, Hct116,Sw480, Lovo, And 293T,Crc Tissues	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29593420	Novel long noncoding RNA GACAT3 promotes colorectal cancer cell proliferation, invasion, and migration through miR-149.  	GACAT3 was highly expressed in CRC tissues and cell lines. Si-GACAT3 significantly decreased cell proliferation, motility, and invasiveness both in vitro and in vivo. We confirmed that downregulated GACAT3 significantly increased the expression of miR-149, and miR-149 binds to GACAT3 in a sequence-specific manner using luciferase reporter assays and pull-down assay. Further functional experiments indicated that GACAT3 could directly upregulate SP1 and STAT3 expressions by functioning as a competing endogenous RNA for miR-149, and consequentially, promoting CRC cell proliferation and invasion in vitro. 	MI0000478	Onco Targets Ther 2018  11, 1543-1552 doi:10.2147/ott.S144103 PMID:29593420
1438	LncRNA	GACAT3	miR-149	STAT3	Fhc, Ht29, Hct116,Sw480, Lovo, And 293T,Crc Tissues	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29593420	Novel long noncoding RNA GACAT3 promotes colorectal cancer cell proliferation, invasion, and migration through miR-149.  	GACAT3 was highly expressed in CRC tissues and cell lines. Si-GACAT3 significantly decreased cell proliferation, motility, and invasiveness both in vitro and in vivo. We confirmed that downregulated GACAT3 significantly increased the expression of miR-149, and miR-149 binds to GACAT3 in a sequence-specific manner using luciferase reporter assays and pull-down assay. Further functional experiments indicated that GACAT3 could directly upregulate SP1 and STAT3 expressions by functioning as a competing endogenous RNA for miR-149, and consequentially, promoting CRC cell proliferation and invasion in vitro. 	MI0000478	Onco Targets Ther 2018  11, 1543-1552 doi:10.2147/ott.S144103 PMID:29593420
1439	LncRNA	GAS5	miR-221	NA	Sw480,Crc Tissues	Colorectal Cancer	Homo sapiens (human)	qPCR etc	29630521	Prognostic and predictive value of long non-coding RNA GAS5 and mircoRNA-221 in colorectal cancer and their effects on colorectal cancer cell proliferation, migration and invasion.	LncRNA GAS5 is upregulated while the miR-221 is downregulated in the tissues,plasma and exosomes of patients with CRC.The results of ROC showed that the expressions of both lncRNA GAS5 and miR-221 in the tissues, plasma and exosomes had diagnostic value in CRC. While the LncRNA GAS5 expression in tissues,plasma and exosomes were associated with the tumor node metastasis (TNM) stage,Dukes stage, lymph node metastasis (LNM),local recurrence rate and distant metastasis rate,the MiR-221 expression in tissues, plasma and exosomes were associated with tumor size, TNM stage, Dukes stage, LNM, local recurrence rate and distant metastasis rate.LncRNA GAS5 and miR-221 expression in tissues,plasma and exosomes were found to be independent prognostic factors for CRC.Following the overexpression of GAS5, the GAS5 expressions was up-regulated and miR-221 expression was down-regulated;the rate of cell proliferation, migration and invasion were decreased.	MI0000298	Cancer Biomark 2018  22, 283-299 doi:10.3233/cbm-171011 PMID:29630521
1440	LncRNA	GAS5	miR-203a	TIMP2	Mg-63 And Os-732,Hfob1.19	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot	29414815	LncRNA GAS5 Represses Osteosarcoma Cells Growth and Metastasis via Sponging MiR-203a.	LncRNA GAS5 was down-regulated in MG-63 and OS-732 cells compared to hFOB1.19 cells.Silence of lncRNA GAS5 significantly promoted MG-63 cells viability,migration and invasion,and up-regulated Cyclin D1,Cyclin B1,CDK1 and CDK4 expressions.miR-203a was negatively regulated by lncRNA GAS5.The promoting activities of lncRNA GAS5 silence on MG-63 cells growth and metastasis were reversed by miR-203a suppression.lncRNA GAS5 silence,miR-203a overexpression,and TIMP2 silence could activate PI3K/AKT/GSK3β signaling while block NF-κB signaling.LncRNA GAS5 might be a tumor suppressor in osteosarcoma via sponging miR-203a,sequestering miR-203a away from TIMP2.	MI0000283	Cell Physiol Biochem 2018  45, 844-855 doi:10.1159/000487178 PMID:29414815
1441	LncRNA	GAS5	miR-21	AGO4	Ags1, Mgc803, Sgc7901, And Mkn54,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	Overexpression of tumor suppressor lncRNAs PTENP1-AS and GAS5 might,in turn,reduce the oncogenic role of miR-21.We observed upregulation of PTENP1-AS that could increase the EGFR and AGO4 expression in tumors and also noticed that GAS5 could compete with AGO4 and regulate the miR-21.Compared to PTENP1-AS,the GAS5 expression was predominantly upregulated in the gastric tumor samples and the expression level was comparatively higher than competing mRNA AGO4. Collectively,these observations suggest that overexpression of PTENP1-AS and GAS5 in gastric cancer could be abrogating oncogenic activity of miR-21 and confirms that lncRNAs could act as tumor suppressive ceRNAs.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1442	LncRNA	GAS5	miR-301a	CXCR4	Eca109, Te-1, Te-3 And Ec9706, Esophageal Epithelia Cell Line 	Esophageal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29386089	Long non-coding RNA GAS5 promotes proliferation,migration and invasion by regulation of miR-301a in esophageal cancer.	GAS5 expression was increased in EC cells (ECA109, TE-1, TE3 and EC9706) compared to SHEE cells. Knockdown of GAS5 decreased cell viability,migration,invasion,and induced apoptosis in EC9706 cells. Moreover, miR-301a was directly sponged to GAS5,and miR-301a suppression obviously alleviated the pro-tumor effects of GAS5.Furthermore,miR-301a positively regulated CXCR4 expression,and overexpression of CXCR4 induced apoptosis and abolished the promoting effect of miR-301a inhibition on cell viability,migration and invasion.Besides,miR-301a blocked Wnt/β-catenin and NF-κB signal pathways by regulation of CXCR4.	MI0000745	Oncol Res 2018 Sep 14 26, 1285-1294 doi:10.3727/096504018x15166193231711 PMID:29386089
1443	LncRNA	GUARDIN	miR-23a	TRF2	HCT116, U2OS, A549, H1299, 293T and HAFF	Colon Cancer	Homo sapiens (human)	Microarray,Luciferase reporter assay,in vitro knockdown,RNAi etc	29593331	GUARDIN is a p53-responsive long non-coding RNA that is essential for genomic stability.  	GUARDIN is necessary for preventing chromosome end-to-end fusion through maintaining the expression of telomeric repeat-binding factor 2 (TRF2) by sequestering microRNA-23a.Moreover, GUARDIN also sustains breast cancer 1 (BRCA1) stability by acting as an RNA scaffold to facilitate the heterodimerization of BRCA1 and BRCA1-associated RING domain protein 1 (BARD1).As such, GUARDIN silencing triggered apoptosis and senescence,enhanced cytotoxicity of additional genotoxic stress and inhibited cancer xenograft growth. Thus, GUARDIN may constitute a target for cancer treatment. GUARDIN functions to regulate TRF2 and IRF1 through sequestering miR-23a. 	MI0000079	Nat Cell Biol 2018 Apr 20, 492-502 doi:10.1038/s41556-018-0066-7 PMID:29593331
1444	LncRNA	H19	miR-106a-5p	E2F3	A375,Sk-Mel-1,Sk-Mel-5, Melanoma Tissues	Melanoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29350287	Long non-coding RNA H19 promotes glucose metabolism and cell growth in malignant  melanoma via miR-106a-5p/E2F3 axis.  	LncRNA H19 was increased in melanoma tissue,and lncRNA H19 was correlated with poor prognosis of melanoma patients.miR-106a-5p acts as a tumour suppressor in melanoma by targeting E2F3.E2F3 affects the melanoma cell glucose metabolism and growth.lncRNA H19 may function as the sponge of miR-106a-5p to up-regulate E2F3 expression,and consequently promote the glucose metabolism and growth of melanoma.	MIMAT0000103	J Cancer Res Clin Oncol 2018 Mar 144, 531-542 doi:10.1007/s00432-018-2582-z PMID:29350287
1445	LncRNA	H19	miR-675	E2F1	COLO357, CAPAN-1, MIA PaCa-2, BxPC-3, AsPC-1, PANC-1, and T3M4	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29344285	Long noncoding RNA H19 derived miR-675 regulates cell proliferation by down-regulating E2F1 in human pancreatic ductal adenocarcinoma.	the suppressed cell proliferation caused by H19 knockdown could be rescued by inhibiting miR-675 expression.As a transcript of the first exon of H19,the level of miR-675 was negatively correlated with H19 expression in microdissected PDAC tissues.And the decrease of E2F1 protein expression caused by siH19 could be partially reversed by miR-675 knockdown.there might be a H19/miR-675/E2F1 regulatory loop in cell cycle modulation.	MI0005416	J Cancer 2018  9, 389-399 doi:10.7150/jca.21347 PMID:29344285
1446	LncRNA	H19	miR-138	EZH2	Scc-4, Scc-15 , Cal-27, Hsc-3,Hsc-2,Oscc Tissues	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29344674	Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR-138 and releasing EZH2 in oral squamous cell carcinoma.	The correlation between H19 and microRNA (miR)138 was detected.H19 was found to be upregulated in OSCC tissues and its high expression level was associated with the TNM stage and nodal invasion,and also correlated with a shorter overall survival of patients with OSCC.The knockdown of H19 significantly inhibited OSCC cell proliferation,migration,invasion and epithelial-mesenchymal transition (EMT),and induced apoptosis in vitro.it also suppressed subcutaneous tumor growth in vivo.H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR138,the inhibition of miR138 attenuated the inhibitory effects of H19 knockdown on OSCC cells. 	MI0000455	Int J Oncol 2018 Mar 52, 901-912 doi:10.3892/ijo.2018.4247 PMID:29344674
1447	LncRNA	H19	miR-148a	DNMT1	Ags1, Mgc803, Sgc7901, And Mkn46,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	lncRNAs H19,MEG3 and MALAT1 showed significant association with tumor stage and HOTAIR had a significant association with patient survival.H19 is a well-known oncogenic lncRNA that is involved in the reduction of p53 activity inducing proliferation in gastric cancer.In the present study,we observed a higher level of H19 which sponged out the low level expressed miR-148a leading to the overexpression of its target mRNA DNMT1.Similarly,we also observed the KLF4 overexpression due to the H19 mediated sponging of miR-148a. 	MI0000253	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1448	LncRNA	H19	miR-484	ROCK2	A549, H1975, Hcc827, Calu-3, 2Bs And Mrc-5	Lung Cancer	Homo sapiens (human)	qPCR,Western blot etc	29219208	LncRNA H19 promotes epithelial-mesenchymal transition (EMT) by targeting miR-484 in human lung cancer cells.	H19 was highly expressed in both lung cancer tissues and cells. Suppression of H19 significantly decreased A549 cell viability, migration, and invasion, but promoted apoptosis. Overexpression of H19 promoted cell migration, invasion, and EMT process.miR-484 was a target of H19 and overexpression of it reversed the effects of H19 on EMT. miR-484 regulated the expression of ROCK2.Mechanistic study revealed that suppressing H19 decreased the expression of proteins in JNK pathway, and ROCK2 was the main downstream molecule of H19.H19 promoted EMT in lung cancer A549 cells by negatively regulating miR-484.	MIMAT0002174	J Cell Biochem 2018 Jun 119, 4447-4457 doi:10.1002/jcb.26537 PMID:29219208
1449	LncRNA	H19	miR-29b-3p	PGRN	Hct116, Ht-29, Sw620 And Sw480	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29754471	LncRNA H19/miR-29b-3p/PGRN Axis Promoted Epithelial-Mesenchymal Transition of Colorectal Cancer Cells by Acting on Wnt Signaling.	The proliferative and invasive capacities of CRC cells were appraised through transwell, MTT and scratch assays. As a result, overexpressed H19 and down-expressed miR-29b-3p displayed close associations with the CRC patients' poor prognosis.	MIMAT0000100	Mol Cells 2018 May 31 41, 423-435 doi:10.14348/molcells.2018.2258 PMID:29754471
1450	LncRNA	H19	miR-17	STAT3	A549, H1299 And Bes-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29693721	H19 promotes non-small-cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR-17.	H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS-2B cells.Meanwhile,miR-17 was downregulated in NSCLC cell lines.Inhibited H19 can suppress the growth,migration,and invasion of NSCLC cells and bioinformatics search was performed to predict the correlation between H19 and miR-17.Overexpression of miR-17 was able to inhibit the progression of NSCLC cells while reversely miR-17 inhibitors reversed this process.In addition, signal transducers and activators of transcription (STAT3),as an mRNA target of miR-17,was presented in our research.Moreover, we discovered that H19 demonstrated its biological functions via regulating miR-17 and STAT3 in vitro.Silencing H19 greatly increased STAT3 expression by sponging miR-19 in vitro.It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer. 	MI0000071	J Cell Physiol 2018 Oct 233, 6768-6776 doi:10.1002/jcp.26530 PMID:29693721
1451	LncRNA	H19	miR-103	Trx	Hcc1937 And Hcc38	Breast Cancer	Homo sapiens (human)	qPCR etc	29693231	LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness.	Network analysis revealed the existence of five genes related with H19, including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS). The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 	MI0000109	Breast Cancer Res Treat 2018 Aug 170, 507-516 doi:10.1007/s10549-018-4793-z PMID:29693231
1452	LncRNA	H19	miR-107	Trx	Hcc1937 And Hcc38	Breast Cancer	Homo sapiens (human)	qPCR etc	29693231	LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness.	Network analysis revealed the existence of five genes related with H19,including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS).The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 	MI0000114	Breast Cancer Res Treat 2018 Aug 170, 507-516 doi:10.1007/s10549-018-4793-z PMID:29693231
1453	LncRNA	H19	let-7	Trx	Hcc1937 And Hcc38	Breast Cancer	Homo sapiens (human)	qPCR etc	29693231	LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness.	Network analysis revealed the existence of five genes related with H19,including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS).The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 	MI0000060	Breast Cancer Res Treat 2018 Aug 170, 507-516 doi:10.1007/s10549-018-4793-z PMID:29693231
1454	LncRNA	H19	miR-29b-1	Trx	Hcc1937 And Hcc38	Breast Cancer	Homo sapiens (human)	qPCR etc	29693231	LncRNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness.	Network analysis revealed the existence of five genes related with H19,including miR-103, miR-107, let-7, miR-29b-1, and Trx. In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines.In clinical studies, H19 expression was associated with hormone negativity, tumor size, and nodal status.Patients with H19 expression had significantly poor disease-free survival (DFS) and overall survival(OS).The effect of H19 expression on prognosis was the most significant in triple-negative breast cancer compared to that in other subtypes. 	MI0000105	Breast Cancer Res Treat 2018 Aug 170, 507-516 doi:10.1007/s10549-018-4793-z PMID:29693231
1455	LncRNA	H19	miR-675	KIF1B	Sh-Sy5Y, 293T Cells	Neuroblastoma	Homo sapiens (human)	qRT-PCR,Western blot	29465760	Angelica sinensis polysaccharide inhibits proliferation, migration, and invasion by downregulating microRNA-675 in human neuroblastoma cell line SH-SY5Y.	Expressions of lncRNA-H19 and miR-675 were upregulated in neuroblastoma cells,and were downregulated by AP.AP was also identified to upregulate CD44.We next found AP affected SH-SY5Y cells through downregulating miR-675.Key kinases in the PI3K/AKT and JAK/STAT pathways were downregulated by AP stimulation,while these downregulations were abrogated by miR-675 overexpression. KIF1B isoform β (KIF1Bβ) is proved to be a target of miR-675.	MI0005416	Cell Biol Int 2018 Jul 42, 867-876 doi:10.1002/cbin.10954 PMID:29465760
1456	LncRNA	H19	miR-675	EZH2	A172, Ln229, U87Mg, Ln18 And T98G	Glioblastoma	Homo sapiens (human)	RT-qPCR,Western blot,in vitro knockdown,RIP	29643989	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter.	hypothesyze that in glioblastoma H19 exerts its function through the interaction with the catalytic subunit of the PRC2 complex,EZH2.H19 expression in glioblastoma tissues correlates with that of several genes involved in glioblastoma growth and progression.H19 knock-down reduces viability, migration and invasiveness of two distinct human glioblastoma cell lines. Most importantly,we provide a mechanistic perspective about the role of H19 in glioblastoma cells,by showing that its expression is inversely linked to that of NKD1,a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter.Indeed, we showed that H19 binds EZH2 in glioblastoma cells,and that EZH2 binding to NKD1 and other promoters is impaired by H19 silencing.The molecular mechanisms described so far for an oncogenic role of H19 in GBM range from H19 processing to produce miR-675 to a function as sponge for miR-29a, in turn boosting tumor angiogenesis.	MI0005416	Oncotarget 2018 Mar 20 9, 15512-15525 doi:10.18632/oncotarget.24496 PMID:29643989
1457	LncRNA	H19	miR-29a	EZH2	A172, Ln229, U87Mg, Ln18 And T98G	Glioblastoma	Homo sapiens (human)	RT-qPCR,Western blot,in vitro knockdown,RIP	29643989	The lncRNA H19 positively affects the tumorigenic properties of glioblastoma cells and contributes to NKD1 repression through the recruitment of EZH2 on its promoter.	hypothesyze that in glioblastoma H19 exerts its function through the interaction with the catalytic subunit of the PRC2 complex,EZH2.H19 expression in glioblastoma tissues correlates with that of several genes involved in glioblastoma growth and progression.H19 knock-down reduces viability, migration and invasiveness of two distinct human glioblastoma cell lines. Most importantly,we provide a mechanistic perspective about the role of H19 in glioblastoma cells,by showing that its expression is inversely linked to that of NKD1,a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter.Indeed, we showed that H19 binds EZH2 in glioblastoma cells,and that EZH2 binding to NKD1 and other promoters is impaired by H19 silencing.The molecular mechanisms described so far for an oncogenic role of H19 in GBM range from H19 processing to produce miR-675 to a function as sponge for miR-29a, in turn boosting tumor angiogenesis.	MI0000087	Oncotarget 2018 Mar 20 9, 15512-15525 doi:10.18632/oncotarget.24496 PMID:29643989
1458	LncRNA	H19	miR-152	NA	A172, U251, U87, U373 And U563	Glioma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	29422115	Long non-coding RNA H19 promotes proliferation and invasion in human glioma cells by downregulating miR-152.	H19 expression was upregulated and miR-152 expression was downregulated in human glioma cell lines. H19 downregulation or miR-152 upregulation suppressed glioma cell proliferation and invasion in vitro.Moreover, H19 and miR-152 directly regulated each other. Furthermore,decreased miR-152 expression alleviated si-H19-induced inhibitory effects on proliferation and invasion in glioma cells. As expected, H19 silencing hindered glioma growth in vivo.	MI0000462	Oncol Res 2018 Oct 17 26, 1419-1428 doi:10.3727/096504018x15178768577951 PMID:29422115
1459	LncRNA	H19	let-7a	HMGA2	Cal27, Scc9, Scc15, Scc25,Fadu,Tscc Tissues	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29523225	H19 facilitates tongue squamous cell carcinoma migration and invasion via sponging miR-let-7.    	Depletion of H19 impaired the migration and invasion ability of TSCC cells.Mechanisticlly,H19 functions as a competing endogenous RNA  (ceRNA) to sponge miRNA let-7a,leading to an increase in a let-7a target, the key regulator of tumor metastasis HMGA2,which is enriched in TSCC tissues and cell lines.Intriguingly,inhibition of let-7a significantly rescued short hairpin H19 (shH19) induced decrease of TSCC migration and invasion.H19/let-7a/HMGA2/EMT axis plays a critical role in the regulation of TSCC migration and invasion,which may provide a new therapeutic target for TSCC cancers.	MI0000060	Oncol Res 2019 Feb 5 27, 173-182 doi:10.3727/096504018x15202945197589 PMID:29523225
1460	LncRNA	HAGLROS	miR-100-5p	ATG9A	Ges1	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29329543	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy.	HAGLROS,whose expression was significantly increased and correlated with outcomes of GC patients Exogenous down-regulation of HAGLROS expression significantly suppressed the cell proliferation,invasion and migration.HAGLROS was a direct target of transcriptional factor STAT3.Moreover,HAGLROS knockdown decreased mTOR expression and increased autophagy-related genes ATG9A and ATG9B expression.Further,HAGLROS regulated mTOR signals in two manners.HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition.HAGLROS interacted with mTORC1 components to activate mTORC1 signaling pathway which was known to bean important negative signal of autophagy.	MIMAT0000098	Mol Cancer 2018 Jan 12 17, 6 doi:10.1186/s12943-017-0756-y PMID:29329543
1461	LncRNA	HAGLROS	miR-100-5p	ATG9B	Ges1	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29329543	STAT3-induced lncRNA HAGLROS overexpression contributes to the malignant progression of gastric cancer cells via mTOR signal-mediated inhibition of autophagy.	HAGLROS,whose expression was significantly increased and correlated with outcomes of GC patients Exogenous down-regulation of HAGLROS expression significantly suppressed the cell proliferation,invasion and migration.HAGLROS was a direct target of transcriptional factor STAT3.Moreover,HAGLROS knockdown decreased mTOR expression and increased autophagy-related genes ATG9A and ATG9B expression.Further,HAGLROS regulated mTOR signals in two manners.HAGLROS competitively sponged miR-100-5p to increase mTOR expression by antagonizing miR-100-5p-mediated mTOR mRNA inhibition.HAGLROS interacted with mTORC1 components to activate mTORC1 signaling pathway which was known to bean important negative signal of autophagy.	MIMAT0000098	Mol Cancer 2018 Jan 12 17, 6 doi:10.1186/s12943-017-0756-y PMID:29329543
1462	LncRNA	HCP5	miR-22-3p	ST6GAL2	Ftc-133,Ftc-238,Nthy-Ori 3-1,Hek293T,Huvecs ,Ftc Tissues	Follicular Thyroid Cancer	Homo sapiens (human)	RNA-seq,qPCR,RNAi etc	29515098	LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge. 	Overexpression of HCP5 can promote the proliferation,migration,invasiveness and angiogenic ability of FTC cells.HCP5 and alpha-2,6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC.We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells.HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. 	MIMAT0000077	Cell Death Dis 2018 Mar 7 9, 372 doi:10.1038/s41419-018-0382-7 PMID:29515098
1463	LncRNA	HCP5	miR-186-5p	ST6GAL2	Ftc-133,Ftc-238,Nthy-Ori 3-1,Hek293T,Huvecs ,Ftc Tissues	Follicular Thyroid Cancer	Homo sapiens (human)	RNA-seq,qPCR,RNAi etc	29515098	LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge. 	Overexpression of HCP5 can promote the proliferation,migration,invasiveness and angiogenic ability of FTC cells.HCP5 and alpha-2,6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC.We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells.HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. 	MIMAT0000456	Cell Death Dis 2018 Mar 7 9, 372 doi:10.1038/s41419-018-0382-7 PMID:29515098
1464	LncRNA	HCP5	miR-216a-5p	ST6GAL2	Ftc-133,Ftc-238,Nthy-Ori 3-1,Hek293T,Huvecs ,Ftc Tissues	Follicular Thyroid Cancer	Homo sapiens (human)	RNA-seq,qPCR,RNAi etc	29515098	LncRNA HCP5 promotes follicular thyroid carcinoma progression via miRNAs sponge. 	Overexpression of HCP5 can promote the proliferation,migration,invasiveness and angiogenic ability of FTC cells.HCP5 and alpha-2,6-sialyltransferase 2 (ST6GAL2) were co-expressed in FTC.We hypothesised that ST6GAL2 may be regulated by HCP5, which would in turn mediate the activity of FTC cells.HCP5 functions as a competing endogenous RNA (ceRNA) and acts as a sponge for miR-22-3p, miR-186-5p and miR-216a-5p, which activates ST6GAL2. 	MIMAT0000273	Cell Death Dis 2018 Mar 7 9, 372 doi:10.1038/s41419-018-0382-7 PMID:29515098
1465	LncRNA	HOST2	let-7b	c-Myc	Mda-Mb-231, Mda-Mb-468, Sk-Br-3, Mcf-7, And Mcf-10A	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29236319	Effects of long non-coding RNA HOST2 on cell migration and invasion by regulating MicroRNA let-7b in breast cancer.	Compared with adjacent normal tissues,HOST2 expression was higher but let-7b expression lower in breast cancer tissues. HOST2 expression in breast cancer cells was remarkably increased compared with that in the normal breast epithelial MCF-10A cells.In MCF-7 cells,in comparison with the blank and NC groups,expressions of HOST2 and c-Myc were reduced, but let-7b expression was remarkably elevated in the siHOST2 and let-7b mimic groups,the let-7b inhibitor group exhibited higher expressions of HOST2 and c-Myc but lower let-7b expression.Overexpression of HOST2 could promote cell motility,migration and invasion,thus enhancing the growth of breast cancer tumor. By inhibiting HOST2,opposite trends were found.LncRNA HOST2 promotes cell migration and invasion by inhibiting let-7b in breast cancer  patients. 	MI0000063	J Cell Biochem 2018 Jun 119, 4570-4580 doi:10.1002/jcb.26606 PMID:29236319
1466	LncRNA	HOTAIR	miR-331-3p	HER2	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR etc	29683069	Plasma long non-coding RNA HOTAIR as a potential biomarker for gastric cancer.	Plasma long non-coding HOTAIR as anon-invasive biomarker in GC.Plasma HOTAIR was significantly up-regulated in GC patients compared with controls.HOTAIR may also serve as a competitive endogenous RNA (ceRNA). In GC, it prevents transcriptional suppression of HER2 mRNA through competition for miR-331-3p.	MIMAT0000760	Int J Biol Markers 2018 Apr 1, 10.1177/1724600818760244, 1724600818760244 doi:10.1177/1724600818760244 PMID:29683069
1467	LncRNA	HOTAIR	miR-454-3p	EZH2	Du145,Pc3	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown etc	29221985	HOTAIR-mediated reciprocal regulation of EZH2 and DNMT1 contribute to polyphyllin I-inhibited growth of castration-resistant prostate cancer cells in vitro and in  vivo.   	Silenced HOTAIR reduced EZH2 and DNMT1 protein expressions.On the contrary, exogenously expressed HOTAIR resisted PPI-inhibited EZH2 and DNMT1 protein expressions, EZH2 promoter activity and cell growth. Moreover, excessive EZH2 antagonized PPI-suppressed DNMT1 protein expression or vice versa.The interactions among HOTAIR, DNMT1 and EZH2, and reciprocal regulation of DNMT1 and EZH2 contribute to the overall responses of PPI. HOTAIR induced DNA methylation of miR-454-3p via recruiting EZH2 and DNMT1 to the promoter regions of miR-454-3p, this largely reduced miR-454-3p expression,thereby reducing apoptosis and inducing autophagy in human chondrosarcoma cells	MIMAT0003885	Biochim Biophys Acta Gen Subj 2018 Mar 1862, 589-599 doi:10.1016/j.bbagen.2017.12.001 PMID:29221985
1468	LncRNA	HOTAIR	miR-148a	AGO4	Ags1, Mgc803, Sgc7901, And Mkn47,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	HOTAIR had a significant association with patient survival.	MI0000253	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1469	LncRNA	HOTAIR	miR-15b	p53	U-87 Mg	Glioma	Homo sapiens (human)	qPCR,Western blot etc	29323737	MiR-15b/HOTAIR/p53 form a regulatory loop that affects the growth of glioma cells.	The present study further demonstrated that miR-15b, HOTAIR, and p53 formed a mutually regulated loop.MiR-15b upregulated the expression of p53 but inhibited the expression of HOTAIR.In addition,miR-15b was able to regulate the expression of HOTAIR through p53.P53 promoted miR-15b expression but inhibited HOTAIR expression.Furthermore,the examination of cell proliferation,apoptosis,and invasion revealed that both miR-15b and p53 inhibited the proliferation and invasion,but promoted the apoptosis,of glioma cells.In contrast,HOTAIR exerted effects that were the opposite of those exerted by miR-15b and p53 on glioma cells.The upregulation of HOTAIR suppressed the inhibitory effects of miR-15b and p53 on cell proliferation and invasion as well as the promoting effect of miR-15b and p53 on apoptosis.Therefore,it can be concluded that miR-15b,HOTAIR,and p53 constitute a regulatory loop that is capable of regulating the growth of glioma cells. 	MI0000438	J Cell Biochem 2018 Jun 119, 4540-4547 doi:10.1002/jcb.26591 PMID:29323737
1470	LncRNA	HOTAIR	miR-331-3p	NRP2	Mri-H196 And Mri-H186 	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi etc	29130509	ARFHPV E7 oncogene, lncRNA HOTAIR, miR-331-3p and its target, NRP2, form a negative feedback loop to regulate the apoptosis in the tumorigenesis in HPV positive cervical cancer.	NRP2 was identified as a virtual target gene of miR-331-3p with a binding site of miR-331-3p,and HOTAIR was directly sponged to miR-331-3p,miR-331-3p reduced luciferase activity of wild-type of NRP2 3'UTR and HOTAIR, but not those of mutant NRP2 3'UTR and HOTAIR.MiR-331-3p down-regulated NRP2 and E7 expression levels,and further promoted cell apoptosis,while inhibited cell proliferation.Cell transfected with HPV16 E7 displayed lower levels of HOTAIR,NRP2 and P53,a higher level of miR-331-3p,over-expression of E7 further repressed cell apoptosis,while improved cell proliferation compared with control. Normal HPV (+) group exhibited a higher miR-331-3p, and lower mRNA levels of HOTAIR and NRP2 than HPV (-) group.NRP2 protein was highly expressed in HPV (-) group compared to that in HPV (+) group. E7-HOTAIR-miR-331-3p-NRP2-E7 formed a regulatory loop, and could be involved in the pathogenesis of cervical cancer. 	MIMAT0000760	J Cell Biochem 2018 Jun 119, 4397-4407 doi:10.1002/jcb.26503 PMID:29130509
1471	LncRNA	HOTAIR	miR-133a-3p	XIRP1	Cervical Cancer tissues	Cervical Cancer	Homo sapiens (human)	qPCR etc	29620291	Integrated analysis of long non-coding RNA competing interactions revealed potential biomarkers in cervical cancer: Based on a public database.	HOTAIR and UCA1 both were significantly higher expressed in GC tumor tissues than adjacent non-tumor tissues.The results from the qRT-PCR validation in 82 newly diagnosed GC patients and the above bioinformatics results were 100% in agreement. To further analyze the association between the 2 key lncRNAs and clinicopathological characteristics of 82 GC patients, we found that HOTAIR was significantly associated with tumor size and lymphatic metastasis, and UCA1 was significantly associated with tumor size,TNM stage and  lymphatic metastasis. HOTAIR and UCA1 were found to be significantly associated with overall survival.The miR-1 was downexpressed when lncRNA UCA1 was overexpressed in glioma cells.mRNA XIRP1 was found to interact with miRNA miR-133a-3p. Key miRNA miR-133a-3p was predicted to target key lncRNA HOTAIR.	MIMAT0000427	Mol Med Rep 2018 Jun 17, 7845-7858 doi:10.3892/mmr.2018.8846 PMID:29620291
1472	LncRNA	HOTAIR	miR-143-3p	BCL2	Siha, Hela, Caski, C4-1 And Hacat 	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29336659	Long non-coding RNA HOTAIR promotes cervical cancer progression through regulating BCL2 via targeting miR-143-3p.	HOTAIR expression was elevated while miR-143-3p expression was reduced in cervical cancer tissues and cell lines.HOTAIR knockdown suppressed proliferation and enhanced apoptosis in cervical cancer cells.Moreover, HOTAIR could function as a sponge for miR-143-3p.The inhibitory effect of HOTAIR knockdown on cervical cancer cells growth was abolished following decrease of miR-143-3p expression.Furthermore, HOTAIR promoted BCL2 expression by modulating miR-143-3p.BCL2 overexpression attenuated the tumor-suppressive effect of miR-143-3p in cervical cancer.Finally, the carcinogenicity of HOTAIR was validated in mice.HOTAIR acted as a ceRNA to modulate BCL2 expression via competitively binding to miR-143-3p.	MIMAT0000435	Cancer Biol Ther 2018 May 4 19, 391-399 doi:10.1080/15384047.2018.1423921 PMID:29336659
1473	LncRNA	HOTAIR	miR-646	NPM1	Hec-1-A And Ishikawa	Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29466670	Long non-coding RNA HOTAIR mediates the estrogen-induced metastasis of endometrial cancer cells via miR-646/NPM1 axis.	MiR-646 expression was significantly decreased both in human EC tissues and cell lines compared with the control.Moreover, miR-646 expression was negatively related to HOTAIR in human EC tissues.miR-646 overexpression considerably attenuated the E2-promoted viability, migration and invasion of Ishikawa and HEC-1-A cells in vitro.In addition, HOTAIR was confirmed to regulate the viability, migration and invasion of EC cells through negative regulating miR-646.More importantly, we also demonstrated that NPM1 was the target of miR-646,and HOTAIR promoted NPM1 expression through interacting with miR-646 in EC cells.HOTAIR was well documented in recruiting PRC2 components and subsequent chromosomal gene silencing via coordinated histone H3K27 methylation and H3K4 demethylation.We therefore performed RNA pull-down assays in Ishikawa cells by means of transfection of the biotin-labelled miR-646 and its mutation and observed that HOTAIR was pulled down by miR-646 but not by miR-646 mutation, suggesting a direct interaction between HOTAIR and miR-646. 	MI0003661	Am J Physiol Cell Physiol 2018 Jun 1 314, C690-c701 doi:10.1152/ajpcell.00222.2017 PMID:29466670
1474	LncRNA	HOTAIR	miR-23b	MAPK1	Siha, Hela, Caski, And C4-1	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29335299	HOTAIR contributes to cell proliferation and metastasis of cervical cancer via targetting miR-23b/MAPK1 axis.	the expressions of HOTAIR and miR-23b were detected by real-time PCR in 33 paired cervical cancer tissue samples and cervical cell lines. The effects of HOTAIR on the expressions of miR-23b and mitogen-activated protein kinase 1 (MAPK1) were studied by overexpression and RNAi approaches.HOTAIR expression was significantly increased in cervical cancer cells and tissues.In contrast,the expression of miR-23b was obviously decreased.HOTAIR knockdown promoted apoptosis and inhibited cell proliferation and invasion in vitro and in vivo Moreover, our data indicated that HOTAIR may competitively bind miR-23b and modulate the expression of MAPK1 indirectly in cervical cancer cells.	MI0000439	Biosci Rep 2018 Feb 28 38 doi:10.1042/bsr20171563 PMID:29335299
1475	LncRNA	HOTAIR	miR-126-5p	GLS	Nbt, Glioma Cell Lines 	Glioma	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay	29319172	Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote glioma progression by sponging miR-126-5p.	HOTAIR was aberrantly up-regulated in glioma tissues and was negatively correlated with miR-126-5p expression.Next, we determined that HOTAIR promote glioma progression by sponging miR-126-5p.Subsequently,glutaminase (GLS) was confirmed to be a direct target of miR-126-5p.Moreover,HOTAIR could modulate GLS expression by functioning as a competing endogenous RNA (ceRNA) for miR-126-5p. 	MIMAT0000444	J Cell Physiol 2018 Sep 233, 6822-6831 doi:10.1002/jcp.26432 PMID:29319172
1476	LncRNA	HOTAIR	miR-20a-5p	HMGA2	Mcf7, Skbr3, Mda-Mb- 231 ,Mcf- 10A,Bc Tissues	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown	29473328	LncRNA HOTAIR influences cell growth, migration, invasion, and apoptosis via the  miR-20a-5p/HMGA2 axis in breast cancer.   	The expression levels of the lncRNA HOTAIR were upregulated in BC tissues and cells.Knockdown lncRNA HOTAIR inhibited cell propagation and metastasis and facilitated cell apoptosis.MiR-20a-5p was a target of lncRNA HOTAIR and had a negative correlation with lncRNA HOTAIR.MiR-20a-5p overexpression in BC suppressed cell growth,mobility,and invasiveness and facilitated apoptosis.HMGA2 was a target of miR-20a-5p,which significantly induced carcinogenesis of BC.BC cells progression was mediated by lncRNA HOTAIR via affecting miR-20a-5p/HMGA2 in vivo.LncRNA HOTAIR affected cell growth, metastasis,and apoptosis via the miR-20a-5p/HMGA2 axis in breast cancer.  	MIMAT0000075	Cancer Med 2018 Mar 7, 842-855 doi:10.1002/cam4.1353 PMID:29473328
1477	LncRNA	HOTTIP	miR-637	AKT1	Tpc-1 And Hth83	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	29474928	LncRNA HOTTIP promotes papillary thyroid carcinoma cell proliferation, invasion and migration by regulating miR-637.	HOTTIP was upregulated in human PTC tissues and PTC cell lines.In addition, HOTTIP knockdown inhibited the proliferation, invasion and migration in vitro together with in vivo tumorigenesis of PTC cells.Additionally, HOTTIP knockdown downregulated Akt1 expression and suppressed cell proliferation, invasion and migration in PTC cells by regulating miR-637. In contrast, miR-637 inhibitor reversed above-mentioned tendencies caused by HOTTIP knockdown.	MI0003652	Int J Biochem Cell Biol 2018 May 98, 1-9 doi:10.1016/j.biocel.2018.02.013 PMID:29474928
1478	LncRNA	HOTTIP	miR-216a	BCL-2	H69, H69Ar, H446, H446Ar And Alveolar Epithelial Cell Line 	Small Cell Lung Cancer	Homo sapiens (human)	Microarray,RT-qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RNAi,RIP	29367594	Long non-coding RNA HOTTIP promotes BCL-2 expression and induces chemoresistance in small cell lung cancer by sponging miR-216a.	HOTTIP functioned as an oncogene in SCLC progression by binding miR-216a and abrogating its tumor-suppressive function in this setting.On the other hand,HOTTIP increased the expression of anti-apoptotic factor BCL-2,another important target gene of miR-216a,and jointly enhanced chemoresistance of SCLC by regulating BCL-2.	MI0000292	Cell Death Dis 2018 Jan 24 9, 85 doi:10.1038/s41419-017-0113-5 PMID:29367594
1479	LncRNA	HOXA11-AS	miR-214-3p	NA	Hep3B, Smmc-7721, Mhcc97-H, Bel-7402 And Hl-7702	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29761918	LncRNA HOXA11-AS promotes hepatocellular carcinoma progression by repressing miR-214-3p.	HOXA11-AS expression was up-regulated in the HCC tissues,and the higher expression of HOXA11-AS was associated with the advanced stage in the HCC samples.In addition,the expression of HOXA11-AS was up-regulated in HCC cell lines compared with normal liver cell lines. Overexpression of HOXA11-AS promoted HCC proliferation and invasion and induced the epithelial-mesenchymal transition (EMT) and knockdown of HOXA11-AS suppressed the HCC cell proliferation and invasion .However, we showed that miR-214-3p expression was down-regulated in the HCC tissues and cell lines.Ectopic expression of miR-214-3p suppressed HCC cell proliferation and invasion.Furthermore,we indicated that overexpression of HOXA11-AS decreased the miR-214-3p expression and the expression of miR-214-3p was negatively related with the HOXA11-AS expression in HCC samples. Ectopic expression of HOXA11-AS increased HCC proliferation and invasion and induced EMT through inhibiting miR-214-3p expression.These data suggested that HOXA11-AS/miR-214-3p axis was responsible for development of HCC. We ndemonstrated that miR-214-3p expression was down-regulated in the HCC tissues and the expression of miR-214-3p was negatively correlated with the expression of HOXA11-AS.	MIMAT0000271	J Cell Mol Med 2018 May 15 22, 3758-67 doi:10.1111/jcmm.13633 PMID:29761918
1480	LncRNA	HOXA11-AS	miR-642b-3p	PDE4D	A549	Lung Cancer	Homo sapiens (human)	qPCR etc	29616096	A comprehensive analysis of the predicted targets of miR-642b-3p associated with  the long non-coding RNA HOXA11-AS in NSCLC cells.	The transfection efficiency was ~100%,and the  knockdown efficiency of HOXA11 AS in NSCLC cell lines was >75%, as determined by a reverse transcription quantitative polymerase chain reaction.Following the knockdown of HOXA11-AS,miR-642b-3p was significantly downregulated in A549 NSCLC cells.The ROC curve revealed that the area under curve (AUC) of HOXA11-AS was 0.700 for patients with lung adenocarcinoma and 0.964 for patients with squamous cell carcinoma,which may gain a moderate or high diagnostic value of HOXA11-AS level in lung cancer. 	MIMAT0018444	Oncol Lett 2018 May 15, 6147-6160 doi:10.3892/ol.2018.8105 PMID:29616096
1481	LncRNA	HOXD-AS1	miR-130a	E2F8	Hek-293T	Glioblastoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29341117	HOXD-AS1/miR-130a sponge regulates glioma development by targeting E2F8.	HOXD-AS1 expression was upregulated in glioma tissues and in glioma cell lines.HOXD-AS1 overexpression promoted cell migration and invasion in vitro, whereas knockdown of HOXD-AS1 expression repressed these cellular processes. Mechanistic studies further revealed that HOXD-AS1 could compete with the transcription factor E2F8 to bind with miR-130a,thus affecting E2F8 expression. Additionally, reciprocal repression was observed between HOXD-AS1 and miR-130a,and miR-130a mediated the tumor-suppressive effects of HOXD-AS1 knockdown. 	MI0000448	Int J Cancer 2018 Jun 1 142, 2313-2322 doi:10.1002/ijc.31262 PMID:29341117
1482	LncRNA	HOXD-AS1	miR-217	AEG-1	Hct116, Ccd-112Con	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29749477	Long non-coding RNA HOXD-AS1 promotes tumor progression and predicts poor prognosis in colorectal cancer.	HOXD-AS1 was upregulated in CRC tissues and cell lines, and that overexpression of HOXD-AS1 was associated with poor prognosis in patients with CRC. Furthermore, knockdown of HOXDAS1 inhibited cell proliferation, cell invasion, epithelialmesenchymal transition and stem cell formation in vitro,as well as tumor growth and metastasis in vivo.Mechanistically,HOXD-AS1 functioned as a competing endogenous RNA for miR-217. In conclusion, the present study demonstrated that HOXD-AS1 may promote CRC progression and metastasis by competing for miR-217.In addition, HOXD-AS1 may be considered an indicator of prognosis in patients with CRC. The present study confirmed that HOXDAS1 could act as a ceRNA for miR-217.	MI0000293	Int J Oncol 2018 Jul 53, 21-32 doi:10.3892/ijo.2018.4400 PMID:29749477
1483	LncRNA	HOXD-AS1	miR-608	FZD4	Caov-3, Sk-Ov-3 And Ovcar-3 And A Normal Human Ovary Cell Line 	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29416930	HOXD-AS1 promotes cell proliferation, migration and invasion through miR-608/FZD4 axis in ovarian cancer.	HOXD-AS1 was observed to be upregulated in both OC tissues and cell lines.HOXD-AS1 was detected to positively regulate the expression of frizzled family receptor 4 (FZD4) by competitively binding to miR-608.	MI0003621	Am J Cancer Res 2018  8, 170-182,  PMID:29416930
1484	LncRNA	HULC	miR-150	ZEB1	Rectal Adenocarcinoma tissues	Rectal Adenocarcinoma	Homo sapiens (human)	qPCR etc	29512732	Construction of a ceRNA network reveals potential lncRNA biomarkers in rectal adenocarcinoma.	HULC,CRNDE and PVT1 expression levels were increased,and the expression level of ADAMTS9 AS2 was decreased in READ tumor  tissues compared to adjacent non tumor tissues. 	MI0000479	Oncol Rep 2018 May 39, 2101-2113 doi:10.3892/or.2018.6296 PMID:29512732
1485	LncRNA	HULC	miR-200a-3p	ZEB1	Lncap, Pc3,Du145,Rwpe-1,Pca Tissues	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29765457	High lncRNA HULC expression is associated with poor prognosis and promotes tumor  progression by regulating epithelial-mesenchymal transition in prostate cancer.  	HULC expression was upregulated in PCa tissues and cell lines compared to adjacent non-tumor tissues and the normal prostate cell line RWPE-1. High HULC expression was positively associated with advanced clinicopathologic features and poor overall survival (OS) for PCa patients.HULC inhibition suppressed PCa cell growth and metastasis both in vitro and in vivo.Furthermore, HULC knockdown reduced N-cadherin and vimentin expression and increased E-cadherin expression in PCa cells.LncRNA HULC might play oncogenic roles in PCa progression, which provided a novel therapeutic strategy for PCa patients.lncRNA HULC enhanced epithelial mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1.	MIMAT0000682	Arch Med Sci 2018 Apr 14, 679-686 doi:10.5114/aoms.2017.69147 PMID:29765457
1486	LncRNA	KCNQ1OT1	miR-504	CDK16	Huh-7, Smmc-7721,Hep3B, Mhcc97-H And Mhcc97-L,Lo2,293T,Hcc Tissues 	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29532864	Long non-coding RNA KCNQ1OT1 mediates the growth of hepatocellular carcinoma by functioning as a competing endogenous RNA of miR-504.  	The ectopic high expression of KCNQ1OT1 was associated with liver cirrhosis,a larger tumor size, an advanced TNM stage,and a worse overall survival and tumorfree survival.KCNQ1OT1 exerted its effects partly by relying on the microRNA504 (miR504)mediated regulation of cyclindependent kinase 16 (CDK16),in addition to the regulation of the glycogen synthase kinase 3β (GSK3β)/βcatenin/Bcl2 signaling pathway. The present study revealed the functions and mechanisms of action of lncRNA KCNQ1OT1 regarding its role in promoting the growth of HCC.KCNQ1OT1 may prove to be a potential therapeutic target for human HCC. 	MI0003189	Int J Oncol 2018 May 52, 1603-1612 doi:10.3892/ijo.2018.4313 PMID:29532864
1487	LncRNA	KCNQ1OT1	miR-153	MET	Hacat, A375, A875 And Mum-2C	Melanoma	Homo sapiens (human)	Microarray,qPCR,Western blot etc	29667930	KCNQ1OT1 promotes melanoma growth and metastasis.	KCNQ1OT1 expression is up-regulated in melanoma tissues and cells.KCNQ1OT1 promoted cell proliferation and metastasis in melanoma.By directly bindin to miR-153,KCNQ1OT1 acted as a competing endogenous RNA (ceRNA) to de-repress MET expression.	MI0000463	Aging (Albany NY) 2018 Apr 17 10, 632-644 doi:10.18632/aging.101418 PMID:29667930
1488	LncRNA	LINC00152	miR-16	BMI1	U87, Ln229, U251, And T98G,Nhas 	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown	29669323	Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16.	LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples.Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro.LINC00152 knockdown inhibits tumor growth.LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown-mediated suppressive effects on proliferation, migration, and invasion.LINC00152 induced BMI1 expression by sponging miR-16,this effect further promoted glioma cell proliferation and invasion.LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment. 	MI0000070	Cell Physiol Biochem 2018  46, 1055-1064 doi:10.1159/000488836 PMID:29669323
1489	LncRNA	LINC00152	miR-193a-3p	MCL1	Mgc-803, Ags, Sgc-7901, Bgc-823 And  Ges-1 	Gastric Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RNAi etc	29339419	LINC00152 down-regulated miR-193a-3p to enhance MCL1 expression and promote gastric cancer cells proliferation.	LINC00152 was proven to have a higher expression level in GC tissues than in the adjacent normal tissues.GC cells proliferation was inhibited after LINC00152 was down-regulated.LINC00152 inhibited the expression of miR-193a-3p,which negatively regulated MCL1 In addition,GC cells proliferation was inhibited by cell transfection with shRNA-MCL1,and enhanced by transfection with miR-193a-3p mimics. Our study suggested that LINC00152 was overexpressed in GC tissues,and it down-regulated miR-193a-3p to enhance miR-193a-3p expression thereby promoting GC cells proliferation.Furthermore,an interesting discovery is that LINC00152 works as a competing endogenous RNA (ceRNA) through sponging miR-193a-3p and shares the identical responsive elements of miR-193a-3p with some signaling pathway factor like erb-b2 receptor tyrosine kinase 4 (ERBB4).	MIMAT0000459	Biosci Rep 2018 Jun 29 38 doi:10.1042/bsr20171607 PMID:29339419
1490	LncRNA	LINC00152	miR-107	HMGA2	Nhas, U87,U251, Ln229, A172, And U118	Glioblastoma	Homo sapiens (human)	qPCR,Western blot etc	29671226	LncRNA LINC00152 promoted glioblastoma progression through targeting the miR-107  expression.	LINC00152 expression level was upregulated in glioblastoma tissues and cell lines. Overexpression of LINC00152 promoted the U87 and LN229 cell proliferation and invasion. Moreover, overexpression of LINC00152 suppressed the E-cadherin expression, where ectopic expression of LINC00152 promoted the N-cadherin, Vimentin, and Snail expression.These results suggested that LINC00152 enhanced epithelial-to-mesenchymal transition (EMT) program in the glioblastoma cell. Overexpression of LINC00152 suppressed the miR-107 expression in the U87 cell and enhanced the HMGA2 expression,which is a direct target gene of miR-107. In addition, we showed that the miR-107 expression was downregulated in the glioblastoma tissues and cell lines. Interesting, the expression of LINC00152 was negatively related with miR-107 expression in the glioblastoma tissues. Furthermore, LINC00152 promoted the glioblastoma cell proliferation and invasion through inhibiting miR-107 expression.These data suggested that LINC00152 acted as oncogene roles in the glioblastoma cell partly through targeting the miR-107 expression. The LINC00152 expression was correlated with advanced TNM stage and was served as positive prognostic factor of overall survival.	MI0000114	Environ Sci Pollut Res Int 2018 Jun 25, 17674-17681 doi:10.1007/s11356-018-1784-x PMID:29671226
1491	LncRNA	LINC00174	miR-1910-3p	TAZ	Dld1, Hct116, Lovo, Rko, Ls174T, Hct8, Hr28348, Ht29, Sw620, Sw480 And Ncm460	Colorectal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	29729381	STAT1-mediated upregulation of lncRNA LINC00174 functions a ceRNA for miR-1910-3p to facilitate colorectal carcinoma progression through regulation of TAZ.	increased expression of LINC00174 in CRC tissues and cells in comparison to their corresponding controls.Moreover,the aberrant overexpression of LINC00174 indicated the poor prognosis of CRC patients.Silence of LINC00174 was able to repress CRC cell growth in vitro and in vivo.We first reported that transcription factor STAT1 mediated LINC00174 expression in CRC. In addition, rescue assay was performed to further confirm that LINC00174 contributed to CRC progression by regulating miR-1910-3p/TAZ signal pathway. Taken together, our study discovered the oncogenic role of LINC00174 in clinical specimens and cellular experiments,showing the potential LINC00174/miR-1910-3p/TAZ pathway.This results and findings provide a novel insight for CRC tumorigenesis. 	MIMAT0026917	Gene 2018 Aug 5 666, 64-71 doi:10.1016/j.gene.2018.05.001 PMID:29729381
1492	LncRNA	LINC00319	miR-450b-5p	EZH2	H157, 95D, Spc-A-1, A549, Sk-Lu-1, Calu-3, Hcc-78, H1299 And H1975	Lung Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	29408583	Long intergenic non-protein coding RNA 319 aggravates lung adenocarcinoma carcinogenesis by modulating miR-450b-5p/EZH2.	We observed that increased expression of LINC00319 in lung adenocarcinoma tissues and cells in comparison to their corresponding controls.Moreover,the aberrant overexpression of LINC00319 indicated the poor prognosis of lung adenocarcinoma patients.Silence of LINC00319 was able to repress lung adenocarcinoma cell growth in vitro.Rescue assay was performed to further confirm that LINC00319 contributed to lung adenocarcinoma progression by regulating miR-450b-5p/EZH2 signal pathway.Taken together, our study discovered the oncogenic role of LINC00319 in clinical specimens and cellular experiments,showing the potential LINC00319/miR-450b-5p/EZH2 pathway.This results and findings provide a novel insight for lung adenocarcinoma tumorigenesis.	MIMAT0004909	Gene 2018 Apr 15 650, 60-67 doi:10.1016/j.gene.2018.01.096 PMID:29408583
1493	LncRNA	LINC00483	miR-30a-3p	SPAG9	Sgc7901, Bgc823, Mgc803, Mnk28 And Ges-1	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot etc	29761936	Linc00483 as ceRNA regulates proliferation and apoptosis through activating MAPKs in gastric cancer.	linc00483 promoted gastric cancer cell proliferation,invasiveness and metastasis in vitro and in vivo.Mechanistically, upregulated expression of linc00483 in gastric cancer acts as a sponge to absorb endogenous tumour suppressor miR-30a-3p. Furthermore,it restores SPAG9 expression, which is negatively regulated by miR-30a-3p,and actives MAPK signaling pathway in gastric cancer cells.Thus,linc00483 is an oncogenic lncRNA in gastric cancer and targeting linc00483 or its pathway can potentially be useful in development of targeted therapies for patients with gastric cancer.linc00483 is an important regulator in carcinogenesis and may be a useful biomarker to predict prognosis of gastric cancer patients.Linc00483 regulates SPAG9 by acting as a ceRNA and interacting with miR-30a-3p.	MIMAT0000088	J Cell Mol Med 2018 May 15 22, 3875-86 doi:10.1111/jcmm.13661 PMID:29761936
1494	LncRNA	LINC00511	miR-765	LAMC2	Hoec, Tca-8113, Scc-9, Scc-4 And Cal-2	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	Microarray,qPCR,Western blot,Luciferase reporter assay etc	29315846	LINC00511 interacts with miR-765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2.	LINC00511 was obviously upregulated in TSCC tissues and cell lines.Moreover,it was found that LINC00511 served as a competing endogenous RNA (ceRNA) through sponging miR-765 and ultimately modulated the derepression of laminin subunit gamma 2 (LAMC2).The inhibitory effects of miR-765 on TSCC cells proliferation,invasion as well as cell cycle distribution can be restored by the ectopic overexpression of LINC00511. Additionally, the restored capacity of LINC00511 promoted the expression of LAMC2, which was a downstream target of miR-765 and can be negatively regulated by miR-765. A novel molecular axis of LINC00511/miR-765/LAMC2 was investigated to regulate the tumor development of TSCC. LINC00511 promoted the expression of LAMC2 via the ceRNA mechanism of sponging miR-765. 	MI0005116	J Oral Pathol Med 2018 May 47, 468-476 doi:10.1111/jop.12677 PMID:29315846
1495	LncRNA	LINC00675	miR-942	GSK3B	Ht29, Sw620 And Hct116	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29524886	Long non-coding RNA Linc00675 suppresses cell proliferation and metastasis in colorectal cancer via acting on miR-942 and Wnt/β-catenin signaling.	the down-regulation of Linc00675 in both CRC cells and clinical CRC tissues. Expression of Linc00675 was also relatively low in metastatic tumors and advanced tumors.Further studies also showed that overexpression of Linc00675 inhibited the proliferation,invasion and migration of CRC cells. In addition, our data also revealed the negative regulation of miR-942 by Linc00675 and the relatively higher expression of miR-942 in clinical CRC tissues. More importantly, the inhibitory effect of Linc00675 on proliferation, invasion and migration of HCT116 cells was also significantly attenuated in the presence of miR-942 mimic, suggesting that down-regulation of miR-942 represented one of the mechanisms by which Linc00675 inhibited the proliferation and metastasis of CRC. Furthermore, we also demonstrated the inhibition of Wnt/β-catenin signaling in the Linc00675/miR-942 regulated pathway in CRC cells.The role of Linc00675 in the development and progression of cancer may depend on the specific cancer types.	MI0005767	Biomed Pharmacother 2018 May 101, 769-776 doi:10.1016/j.biopha.2018.02.123 PMID:29524886
1496	LncRNA	LINC00894-002	miR-200a-3p	TamR	Mcf-7/Wt And Mcf-7/Tamr	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29738694	Downregulation of LINC00894-002 Contributes to Tamoxifen Resistance by Enhancing the TGF-β Signaling Pathway.	LINC00894-002 exhibits the most sophisticated network pattern and is the most downregulated lncRNA in MCF-7/TamR cells. Moreover,LINC00894-002 is directly upregulated by ERα.Knocking down LINC00894-002 downregulates expression of miR-200a-3p and miR-200b-3p, upregulates the expression of TGF-β2 and ZEB1,and finally contributes to TamR.Herein, we report the first case of an inhibitory lncRNA against TamR through the miR-200-TGF-β2-ZEB1 signaling pathway. 	MIMAT0000682	Biochemistry (Mosc) 2018 May 83, 603-611 doi:10.1134/s0006297918050139 PMID:29738694
1497	LncRNA	LINC00894-002	miR-200b-3p	TamR	Mcf-7/Wt And Mcf-7/Tamr	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29738694	Downregulation of LINC00894-002 Contributes to Tamoxifen Resistance by Enhancing the TGF-β Signaling Pathway.	LINC00894-002 exhibits the most sophisticated network pattern and is the most downregulated lncRNA in MCF-7/TamR cells. Moreover,LINC00894-002 is directly upregulated by ERα.Knocking down LINC00894-002 downregulates expression of miR-200a-3p and miR-200b-3p, upregulates the expression of TGF-β2 and ZEB1,and finally contributes to TamR.Herein, we report the first case of an inhibitory lncRNA against TamR through the miR-200-TGF-β2-ZEB1 signaling pathway. 	MIMAT0000318	Biochemistry (Mosc) 2018 May 83, 603-611 doi:10.1134/s0006297918050139 PMID:29738694
1498	LncRNA	LINC01016	miR-302a-3p	SATB1	Ishikawa And Rl-95-, Embryonic Kidney Cell Line 	Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29467441	LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis.	LINC01016 was substantially upregulated in endometrial cancer tissues,and LINC01016 silencing abolished the malignant behavior of endometrial cancer cells.LINC01016 positively rescued the downstream gene nuclear factor YA (NFYA) by competitively "sponging" miR-302a-3p and miR-3130-3p.In turn, these two miRNAs could inhibit LINC01016 transcription,thus forming two reciprocal repression cycles,which influenced the biological behavior of endometrial cancer cells.MiR-302a-3p and miR-3130-3p could specifically bind with the 3'-UTR regions of NFYA, and NFYA could upregulate the expression of special AT-rich sequence-binding protein 1 (SATB1) as a transcriptional factor.This study was the first to show that the LINC01016-miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis played a crucial role in the occurrence of endometrial cancer.	MIMAT0000684	Cell Death Dis 2018 Feb 21 9, 303 doi:10.1038/s41419-018-0291-9 PMID:29467441
1499	LncRNA	LINC01016	miR-3130-3p	SATB1	Ishikawa And Rl-95-, Embryonic Kidney Cell Line 	Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29467441	LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis.	LINC01016 was substantially upregulated in endometrial cancer tissues,and LINC01016 silencing abolished the malignant behavior of endometrial cancer cells.LINC01016 positively rescued the downstream gene nuclear factor YA (NFYA) by competitively "sponging" miR-302a-3p and miR-3130-3p.In turn, these two miRNAs could inhibit LINC01016 transcription,thus forming two reciprocal repression cycles,which influenced the biological behavior of endometrial cancer cells.MiR-302a-3p and miR-3130-3p could specifically bind with the 3'-UTR regions of NFYA, and NFYA could upregulate the expression of special AT-rich sequence-binding protein 1 (SATB1) as a transcriptional factor.This study was the first to show that the LINC01016-miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis played a crucial role in the occurrence of endometrial cancer.	MIMAT0014994	Cell Death Dis 2018 Feb 21 9, 303 doi:10.1038/s41419-018-0291-9 PMID:29467441
1500	LncRNA	LINC01088	miR-24-1-5p	PAK4	A2780	Ovarian Cancer	Homo sapiens (human)	Microarray,RT-qPCR,Western blot,Luciferase reporter assay	29440672	LINC01088 inhibits tumorigenesis of ovarian epithelial cells by targeting miR-24-1-5p.	the expression of long intergenic non-coding RNA 1088 (LINC01088) was clearly reduced in benign epithelial ovarian tumor tissues compared to matched normal ovarian tissues. This was shown by global cDNA gene chip scanning and real-time qPCR, and validated in 42 clinical specimens.Furthermore, we found that LINC01088 inhibited the growth of ovarian cancer xenografts in nude mice.Correlation analysis between LINC01088 and mircoRNAs (miRNAs) conducted using primary clinical samples and RNA co-precipitation experiments revealed that miR-24-1-5p was one of the targets of LINC01088. Overexpression of miR-24-1-5p facilitated cell proliferation both in vitro and in vivo, however, LINC01088 could partially reverse the cell proliferation induced by miR-24-1-5p.Finally, we demonstrated that p21 activated kinase 4 (PAK4) was one of the downstream key targets of miR-24-1-5p;a remarkable decrease in cell proliferation after overexpression of PAK4.We conclude that LINC01088 might function as a tumor suppressor,inhibiting the tumorigenesis of ovarian epithelial cells through LINC01088/ miR-24-1-5p/ PAK4 axis.	MIMAT0000079	Sci Rep 2018 Feb 13 8, 2876 doi:10.1038/s41598-018-21164-9 PMID:29440672
1501	LncRNA	LINC01234	miR-204-5p	CBFB	Ges-1, Bgc823, Sgc7901, Ags, Hgc27, Mgc803	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29386218	Long Noncoding RNA LINC01234 Functions as a Competing Endogenous RNA to Regulate  CBFB Expression by Sponging miR-204-5p in Gastric Cancer.	LINC01234 expression was significantly upregulated in gastric cancer tissues and was associated with larger tumor size, advanced TNM stage,lymph node metastasis,and shorter survival time.Furthermore,knockdown of LINC01234-induced apoptosis and growth arrest in vitro and inhibited tumorigenesis in mouse xenografts.Mechanistic investigations indicated that LINC01234 functioned as a ceRNA for miR-204-5p,thereby leading to the derepression of its endogenous target core-binding factor β (CBFB).LINC01234 is significantly overexpressed in gastric cancer, and LINC01234-miR-204-5p-CBFB axis plays a critical role in gastric cancer tumorigenesis. 	MIMAT0000265	Clin Cancer Res 2018 Apr 15 24, 2002-2014 doi:10.1158/1078-0432.Ccr-17-2376 PMID:29386218
1502	LncRNA	LINC01296	miR-21a	PDCD4	Ccd841A, Sw480, Dld-1, Hct116, Sw620, Caco-2 And Ht29 	Colon Cancer	Homo sapiens (human)	qPCR,RIP etc	29673421	Long noncoding RNA LINC01296 harbors miR-21a to regulate colon carcinoma proliferation and invasion.	LINC01296 was upregulated in CC cancerous tissues and cell lines compared to adjacent normal tissue and normal liver cell lines. Besides, LINC01296 overexpression was associated with poor prognostic and lower survival rate.Moreover, LINC01296 silencing inhibited the proliferation, invasion of CC cells in vitro detected by epithelialmesenchymal transition (EMT). Bioinformatics analysis revealed that miR-21a targeted 3'-UTR of LINC01296. Rescue experiments confirmed that miR-21a could reverse the function of LINC01296 on CC cells.The expression of LINC01296 and mir-21a is negatively correlated in CC.	MI0000569	Oncol Res 2019 May 7 27, 541-549 doi:10.3727/096504018x15234931503876 PMID:29673421
1503	LncRNA	LINC01296	miR-21a	PTEN	Ccd841A, Sw480, Dld-1, Hct116, Sw620, Caco-2 And Ht29 	Colon Cancer	Homo sapiens (human)	qPCR,RIP etc	29673421	Long noncoding RNA LINC01296 harbors miR-21a to regulate colon carcinoma proliferation and invasion.	LINC01296 was upregulated in CC cancerous tissues and cell lines compared to adjacent normal tissue and normal liver cell lines. Besides, LINC01296 overexpression was associated with poor prognostic and lower survival rate.Moreover, LINC01296 silencing inhibited the proliferation, invasion of CC cells in vitro detected by epithelialmesenchymal transition (EMT). Bioinformatics analysis revealed that miR-21a targeted 3'-UTR of LINC01296. Rescue experiments confirmed that miR-21a could reverse the function of LINC01296 on CC cells.The expression of LINC01296 and mir-21a is negatively correlated in CC.	MI0000569	Oncol Res 2019 May 7 27, 541-549 doi:10.3727/096504018x15234931503876 PMID:29673421
1504	LncRNA	LINC01296	miR-21a	TPM1	Ccd841A, Sw480, Dld-1, Hct116, Sw620, Caco-2 And Ht29 	Colon Cancer	Homo sapiens (human)	qPCR,RIP etc	29673421	Long noncoding RNA LINC01296 harbors miR-21a to regulate colon carcinoma proliferation and invasion.	LINC01296 was upregulated in CC cancerous tissues and cell lines compared to adjacent normal tissue and normal liver cell lines. Besides, LINC01296 overexpression was associated with poor prognostic and lower survival rate.Moreover, LINC01296 silencing inhibited the proliferation, invasion of CC cells in vitro detected by epithelialmesenchymal transition (EMT). Bioinformatics analysis revealed that miR-21a targeted 3'-UTR of LINC01296. Rescue experiments confirmed that miR-21a could reverse the function of LINC01296 on CC cells.The expression of LINC01296 and mir-21a is negatively correlated in CC.	MI0000569	Oncol Res 2019 May 7 27, 541-549 doi:10.3727/096504018x15234931503876 PMID:29673421
1505	LncRNA	ATB	miR-200a	STAT3	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000737	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1506	LncRNA	ATB	miR-200b	STAT3	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000342	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1507	LncRNA	ATB	miR-200c	STAT3	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000650	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1508	LncRNA	ATB	miR-200a	IL-1	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000737	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1509	LncRNA	ATB	miR-200b	IL-1	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000342	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1510	LncRNA	ATB	miR-200c	IL-1	Smmc-7721,Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29331759	Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB. 	Expression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling.	MI0000650	Biomed Pharmacother 2018 Mar 99, 134-141 doi:10.1016/j.biopha.2017.12.108 PMID:29331759
1511	LncRNA	LUCAT1	miR-375	DNMT1	Kyse-30,Te-2, Hce-4,Hce-7, Escc Tissues	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,in vitro knockdown etc	29247823	The long noncoding RNA LUCAT1 promotes tumorigenesis by controlling ubiquitination and stability of DNA methyltransferase 1 in esophageal squamous cell carcinoma. 	LUCAT1 knockdown reduced cell proliferation,induced apoptosis, and upregulated tumor-suppressor genes by reducing DNA methylation in KYSE-30cells. Moreover, LUCAT1 siRNA reduced DNA methyltransferase 1 (DNMT1) protein levels without affecting transcription. LUCAT1 regulates the stability of DNMT1 and inhibits the expression of tumor suppressors through DNA methylation,leading to the formation and metastasis of ESCC.	MIMAT0000728	Cancer Lett 2018 Mar 28 417, 47-57 doi:10.1016/j.canlet.2017.12.016 PMID:29247823
1512	LncRNA	MALAT1	miR-125b	STAT3	Tca8113, Scc-25, Cal-27 And Hn5 Cells,Hs680,Oral Squamous Cell Carcinoma  Tissue	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown, RIP etc	28926115	Long non-coding RNA MALAT1 promotes oral squamous cell carcinoma development via  microRNA-125b/STAT3 axis.	MALAT1 was upregulated in OSCC cell lines.Inhibition of MALAT1 can prevent OSCC proliferation while overexpressing MALAT1 promoted OSCC progression.In addition, miR-125b was a direct target of MALAT1,which indicated a negative correlation between MALAT1 and miR-125b.Downregulated MALAT1 greatly inhibited OSCC tumor growth and reversely upregualated MALAT1 promoted OSCC development via miR-125b/STAT3 axis, respectively.MALAT1 can function as a competing endogenous RNA (ceRNA) to modulate STAT3 expression by absorbing miR-125b in OSCC and could be used as a novel therapeutic target in OSCC diagnosis and treatment. 	MI0000446	J Cell Physiol 2018 Apr 233, 3384-3396 doi:10.1002/jcp.26185 PMID:28926115
1513	LncRNA	MALAT1	miR-101	NA	U251 	Glioblastoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc 	29479863	Long noncoding RNA MALAT1 knockdown reverses chemoresistance to temozolomide via promoting microRNA-101 in glioblastoma.	MALAT1 was significantly upregulated in TMZ-resistant GBM cells.On the other hand,MALAT1 knockdown reduces TMZ resistance of GBM cells both in vitro and in vivo by inhibiting cell proliferation and promoting apoptosis. We also show that miR-101 overexpression reduced TMZ resistance of GBM cells and played an antagonistic role compared with MALAT1. Importantly,we demonstrate that MALAT1 promoted the chemoresistance through suppressing miR-101 signaling pathway via directly binding it in GBM cells. In conclusion,our study indicates that knockdown of MALAT1 reverses chemoresistance to TMZ via promoting miR-101 regulatory network in GBM and thus offers a novel prognostic marker and potential target.	MI0000103	Cancer Med 2018 Apr 7, 1404-1415 doi:10.1002/cam4.1384 PMID:29479863
1514	LncRNA	MALAT1	miR-145-5p	AKAP12	Du145 And Pc3,Hek-293T ,Pca Tissues	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29633510	Long noncoding RNA MALAT1 enhances the docetaxel resistance of prostate cancer cells via miR-145-5p-mediated regulation of AKAP12.  	MALAT1 expression levels were up-regulated in clinical DTX-resistant PCa samples.Overexpressed MALAT1 promoted cell proliferation,migration and invasion but decreased cell apoptosis rate of PCa cells in spite of DTX treatment.We identified miR-145-5p as a target of MALAT1.MiR-145-5p overexpression in PC3-DTX led to inhibited cell proliferation, migration and invasion as well as reduced chemoresistance to DTX,which was attenuated by MALAT1.Moreover,we determined that AKAP12 was a target of miR-145-5p,which significantly induced chemoresistance of PCa cells to DTX. Besides,it was proved that MALAT1 promoted tumour cell proliferation and enhanced DTX-chemoresistance in vivo.There was an lncRNA MALAT1/miR-145-5p/AKAP12 axis involved in DTX resistance of PCa cells and  provided a new thought for PCa therapy.	MIMAT0000437	J Cell Mol Med 2018 Jun 22, 3223-3237 doi:10.1111/jcmm.13604 PMID:29633510
1515	LncRNA	MALAT1	miR-124	foxq1	T24, Biu-87,Hek 293T，Bladder Tissue	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot etc	29736319	LncRNA MALAT1 promotes tumor growth and metastasis by targeting miR-124/foxq1 in  bladder transitional cell carcinoma (BTCC).  	The effects of MALAT1 on BTCC cells were investigated by over-expression approaches in vitro and in vivo.Insights of the mechanism of competitive endogenous RNAs (ceRNAs) were validated through bioinformatic analysis and luciferase assay. MALAT1 up-regulation positively correlated with advanced clinical pathological stage and shorter survival of BTCC patients. Furthermore, MALAT1 over-expression promoted proliferation,migration and invasion of BTCC cells in vitro and in vivo. Particularly, MALAT1 may function as a ceRNA to sponge miR-124,thus modulating the derepression of foxq1, miR-124 target gene,in post-transcriptional levels.The positive MALAT1/foxq1 interaction was confirmed by bivariate correlation analysis, and this positive correlation was of great significance in BTCC tumor growth and metastasis, also accompanied by EMT changes.Overall,this ceRNA regulatory network concerning MALAT1 and the positive MALAT1/foxq1 correlation benefit a better understanding of BTCC pathogenesis and promote the feasibility of lncRNA-directed therapy against this disease.	MI0000443	Am J Cancer Res 2018  8, 748-760,  PMID:29736319
1516	LncRNA	MALAT1	miR-145	KLF4	Ags1, Mgc803, Sgc7901, And Mkn56,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	MALAT1, H19, and TUG1 were among the top twenty overexpressed lncRNAs in gastric tumors.	MI0000461	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1517	LncRNA	MALAT1	miR-17	PTEN	Hct116 And Rko,Crc Tissue	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β 4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary, we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000071	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1518	LncRNA	MALAT1	miR-20a	PTEN	Hct116 And Rko,Crc Tissue	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β 4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary, we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000076	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1519	LncRNA	MALAT1	miR-106b	PTEN	Hct116 And Rko,Crc Tissue	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β 4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary, we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000734	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1520	LncRNA	MALAT1	miR-17	PTEN	Skbr3	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary,we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000071	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1521	LncRNA	MALAT1	miR-20a	PTEN	Skbr3	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary,we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000076	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1522	LncRNA	MALAT1	miR-107b	PTEN	Skbr3	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29574704	A non-canonical tumor suppressive role for the long non-coding RNA MALAT1 in colon and breast cancers.  	MALAT1 exerts a modulatory effect on pro-migratory markers such as epithelial cell adhesion molecule (EpCAM) and integrin β4 (ITGB4),suggesting a potential mechanism for MALAT1-mediated regulation of tumorigenesis.In summary,we establish and characterize a PTEN-miRNA-MALAT1 axis that regulates migration and invasion. MALAT1 lncRNA possesses novel tumor suppressive properties in colon and breast cancers.MALAT1 is regulated by the PTEN-targeting microRNAs miR-17,20a and 106b.	MI0000114	Int J Cancer 2018 Aug 1 143, 668-678 doi:10.1002/ijc.31386 PMID:29574704
1523	LncRNA	MALAT1	miR-143-3p	ZEB1	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc	29604585	Oncogenic long noncoding RNA MALAT1 and HCV-related hepatocellular carcinoma.	Circulatory MALAT1 might represent a putative non-invasive prognostic biomarker indicating worse liver failure score in HCV-related HCC patients with traditional markers.Supporting our bioinformatics prediction, MALAT1 served as a competitive endogenous RNA (ceRNA)to miR-143-3p,which in turn,caused up-regulation of ZEB1 and promoted cancer growth and metastasis in Bel-7402 and HepG2 cell lines.	MIMAT0000435	Biomed Pharmacother 2018 Jun 102, 653-669 doi:10.1016/j.biopha.2018.03.105 PMID:29604585
1524	LncRNA	MALAT1	miR-124	SNARE	Y79, Weri-Rb1, So-Rb50 And Hxo-Rb44  	Retinoblastoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29073720	MALAT1 modulates the autophagy of retinoblastoma cell through miR-124-mediated stx17 regulation.	Through direct targeting miR-124,MALAT1 promotes retinoblastoma cell autophagy. Further,we investigated whether Syntaxin 17 (STX17),a Soluble NSF Attachment Protein receptor (SNARE) of the autophagosome, is involved in MALAT1/miR-124 regulation of retinoblastoma cell autophagy, and the underlying mechanism. 	MI0000443	J Cell Biochem 2018 May 119, 3853-3863 doi:10.1002/jcb.26464 PMID:29073720
1525	LncRNA	MALAT1	miR-509	Rac1	Mg63 And U2Os	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28560950	MALAT1 Promotes the Proliferation and Metastasis of Osteosarcoma Cells By Activating the Rac1/JNK Pathway Via Targeting MiR-509.	MALAT1 was increased in human OS tissues and cell lines.MALAT1 knockdown suppressed OS cell growth and metastasis,induced OS cell apoptosis and delayed tumor growth in an OS xenograft model.We also detected downregulation of microRNA-509 (miR-509), a suppressor of OS growth,in OS tissues and cell lines.Then,we identified that miR-509 is a direct target of MALAT1 and Ras-related C3 botulinum toxin substrate 1 (Rac1) is a direct target of miR-509.MALAT1 may promote OS cell growth through inhibition of miR-509, leading to the activation of Rac1/JNK pathway.Our results suggest a MALAT1/miR-509/Rac1 axis that mediates OS cell proliferation and tumor  progression.	MIMAT0004779	Oncol Res 2018 Apr 27, 10.3727/096504017x14957939026111 doi:10.3727/096504017x14957939026111 PMID:28560950
1526	LncRNA	MALAT1	miR-204	SIRT1	Lo2, Bel7404, Huh7, And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	28720061	The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1.	microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis.microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells.Notably,sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion.This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma. 	MI0000284	Tumour Biol 2017 Jul 39, 1010428317718135 doi:10.1177/1010428317718135 PMID:28720061
1527	LncRNA	MAP3K20	miR-375	JAK2	Hgc27, Sgc7901, Mgc803, Ags And Mkn-45,Ges-1,Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown, RIP etc	29428732	Knockdown of long non-coding RNA MAP3K20 antisense RNA 1 inhibits gastric cancer  growth through epigenetically regulating miR-375.	MLK7-AS1 interacted with Dnmt1 and recruited it to miR-375 promotor, hyper-methylating miR-375 promotor and repressing miR-375 expression. Our findings demonstrate that knockdown of MLK7-AS1 by siRNA inhibits gastric cancer growth by epigenetically regulating miR-375. Knockdown of MLK7-AS1 by siRNA increased the expression of miR-375. MiR-375 wasfound to be an important tumor suppressor in gastric cancer bytargeting Janus kinase 2 (JAK2).	MIMAT0000728	Biochem Biophys Res Commun 2018 Mar 4 497, 527-534 doi:10.1016/j.bbrc.2018.02.072 PMID:29428732
1528	LncRNA	MCM3AP-AS1	miR-211	KLF5	Hek293T Cells	Glioblastoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29375300	The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis.	lncRNA antisense 1 to Micro-chromosome maintenance protein 3-associated protein (MCM3AP-AS1) was upregulated whereas miR-211 was downregulated in glioma-associated endothelial cells (GECs). Furthermore, knockdown of MCM3AP-AS1 increased the expression of miR-211.miR-211 targeted KLF5 3'-UTR and consequently inhibited KLF5 expression. Besides,in this study we found that MCM3AP-AS1 knockdown decreased KLF5 and AGGF1 expression by upregulating miR-211.In addition, KLF5 was associated with the promoter region of AGGF1.Knockdown of KLF5 decreased AGGF1 expression by transcriptional repression, and also inhibited the activation of PI3K/AKT and ERK1/2 signaling pathways. 	MI0000287	Front Mol Neurosci 2017  10, 437 doi:10.3389/fnmol.2017.00437 PMID:29375300
1529	LncRNA	MEG3	miR-21	VEGF	Mkn74, Mkn45,Sgc7901, Ags,Gc Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29710493	LncRNA-MEG3 inhibits proliferation and metastasis by regulating miRNA-21 in gastric cancer.  	MEG3 suppressed proliferation and metastasis of GC cells through inhibiting miR-21 expression.MiR-21 was a target of MEG3.	MI0000077	Biomed Pharmacother 2018 Mar 99, 931-938 doi:10.1016/j.biopha.2018.01.164 PMID:29710493
1530	LncRNA	MEG3	miR-21	PKM2	Ags, Nci-N87, Sgc-7901, Mkn-45, Tmk-1 And Ges-1	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi etc	29749532	MEG3/miR-21 axis affects cell mobility by suppressing epithelialmesenchymal transition in gastric cancer.	MEG3 was downregulated while miR21 was upregulated in gastric cancer tissues and cell lines by qRT-PCR.Overexpression of MEG3 suppressed cell mobility of gastric cancer cells (AGS) by downregulating the expression of MMP3, MMP9 and VEGF.overexpression of MEG3 also suppressed epithelialmesenchymal transition (EMT) by increasing the expression of an epithelial marker (Ecadherin) and downregulating the expression of mesenchymal markers,indicating that MEG3 suppressed cell mobility through the inhibition of EMT in gastric cancer.The expression of miR21 was negatively regulated by MEG3 and overexpression of miR21 promoted cell mobility of AGS through activation of EMT.Cotransfection of lncRNAMEG3 and miR21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3,suggesting that the MEG3/miR21 axis affects cell mobility by suppressing EMT in gastric cancer. Using a mouse xenograft tumor model,we found that the overexpression of MEG3 suppressed tumor growth and metastasis while overexpression of miR21 had the opposite effects.The MEG3/miR21 axis affected gastric cancer growth and metastasis through inhibition of EMT in vivo.In conclusion,we demonstrated that the MEG3/miR21 axis participates in the tumor progression and metastasis of gastric cancer through the regulation of EMT.	MI0000077	Oncol Rep 2018 Jul 40, 39-48 doi:10.3892/or.2018.6424 PMID:29749532
1531	LncRNA	MEG3	miR-1297	PTEN	Hep3B	Liver Cancer	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29449541	Long noncoding RNA MEG3 suppresses liver cancer cells growth through inhibiting β-catenin by activating PKM2 and inactivating PTEN.	Mechanistically, MEG3 promotes the expression and maturition of miR122 which targets PKM2. Therefore,MEG3 decreases the expression and nuclear location of PKM2 dependent on miR122. Furthermore,MEG3 also inhibits CyclinD1 and C-Myc via PKM2 in liver cancer cells. On the other hand,MEG3 promotes β-catenin degradation through ubiquitin-proteasome system dependent on PTEN. Strikingly, MEG3 inhibits β-catenin activity through PKM2 reduction and PTEN increase.Significantly,we also found that excessive β-catenin abrogated the effect of MEG3 in liver cancer.MEG3 overexpression increased the PTEN 3-UTR mRNA methylation compared to control.Crosstalk between MEG3 and miR-1297 regulates the growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway 44.MEG3 may be an underlying therapeutic target for LUAD functioning as ceRNAs for the regulation of miRNA-mRNA in lung adenocarcinoma. 	MIMAT0005886	Cell Death Dis 2018 Feb 15 9, 253 doi:10.1038/s41419-018-0305-7 PMID:29449541
1532	LncRNA	MIAT	miR-141	DDX5	Bgc-823,Mgc-803,Gastric Cancer Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RIP,Western blot,Luciferase reporter assay,in vitro knockdown etc	29540201	Long non-coding RNA MIAT promotes gastric cancer growth and metastasis through regulation of miR-141/DDX5 pathway.	MIAT was highly expressed in GC tissues and cell lines and correlated with differentiation degree, TNM stage, distant metastasis, and lymph node metastasis.MIAT knockdown inhibited GC growth and metastasis both in vitro and in vivo. MIAT acted as miR-141 sponge and regulated its target gene DDX5 expression.In BGC-823 and MGC-803 cells with si-MIAT,DDX5 overexpression resulted in an increase of cell proliferation, migration and invasion. Our data indicated that MIAT played an oncogenic role in GC growth and metastasis,and could serve as a novel molecular target for treating GC.	MI0000457	J Exp Clin Cancer Res 2018 Mar 14 37, 58 doi:10.1186/s13046-018-0725-3 PMID:29540201
1533	LncRNA	MIAT	miR-214	NA	Hepg2, Huh7, Sk-Hep-1, Hle And L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RNAi etc	29097358	lncRNA MIAT promotes proliferation and invasion of HCC cells via sponging miR-214.	Upregulation of MIAT is related to the proliferation and invasion of HCC, and downregulating MIAT expression inhibited HCC cell proliferation and invasion. The H3/H4 histone acetylation level of MIAT promoter in HCC tissues was higher than that in normal tissues. MIAT negatively regulated miR-214 in HCC cells. Inhibition of miR-214 reversed the influence of MIAT downregulation on HCC cell proliferation and invasion. In nude mouse xenograft models, downregulation of MIAT markedly suppressed the tumor growth of HCC via releasing miR-214. In conclusion, lncRNA MIAT promotes the proliferation and invasion of HCC cells through sponging miR-214, which brings a novel target for the therapy and prognosis of hepatocellular carcinoma. NEW & NOTEWORTHY This is the first research showing long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) to have a regulatory effect on hepatocellular carcinoma. Micro-RNA (miR)-214 could be sponged by MIAT to promote the proliferation and invasion of hepatocellular carcinoma cells. The lncRNA MIAT/miR-214 axis brings a novel insight for the therapy and prognosis of hepatocellular carcinoma. 	MI0000290	Am J Physiol Gastrointest Liver Physiol 2018 May 1 314, G559-g565 doi:10.1152/ajpgi.00242.2017 PMID:29097358
1534	LncRNA	MIAT	miR-132	Derlin-1	Hcoepic, Ht-29, Sw480, And Lovo	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29686537	Long non-coding RNA MIAT promotes growth and metastasis of colorectal cancer cells through regulation of miR-132/Derlin-1 pathway.	MIAT was highly expressed in CRC tissues and cells.MIAT knockdown inhibited proliferation,migration and invasion and enhanced apoptosis of CRC cells.Further,we demonstrated that MIAT acted as a competing endogenous RNA for miR-132, antagonized its functions,and resulted in the de-repression of its target gene Derlin-1,which acted as an oncogene in promoting growth and metastasis of CRC cells.In LOVO and SW480 cells with si-MIAT, miR-132 inhibitor resulted in an increase of cell proliferation, migration and invasion and a decrease of cell apoptosis, which was partially abolished by transfection of Derlin-1 shRNA.Our data indicated that highly expressed MIAT was an oncogenic lncRNA that promoted the growth and metastasis of CRC through miR-132/Derlin-1 axis. 	MI0000449	Cancer Cell Int 2018  18, 59 doi:10.1186/s12935-017-0477-8 PMID:29686537
1535	LncRNA	MIAT	miR-34a	NA	Beas-2B,  Human Lung Cancer Cell Lines 	Lung Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29487526	Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a.	LncRNA MIAT expression was associated with tumor size, lymph node metastasis,distant metastasis and TNM stage. Univariate analysis and multivariate analysis revealed that the lncRNA MIAT to be an independent factor for predicating the prognosis of lung cancer patients.Low lncRNA MIAT have longer overall survival time and progression-free survival time than patients with high lncRNA MIAT expression. Moreover,the knockdown of MIAT significantly sensitized PC9 and gefitinib-resistant PC9 cells to gefitinib in vitro and in vivo,and increased the expression of miR-34a and inactivated PI3K/Akt signaling. MIAT interacted with miR-34a and epigenetically controlled the miR-34a expression by hyper-methylating its promotor.MiR-34a promoter methylation status was measured by MSP in tissues and BSP in cells.	MI0000268	Front Pharmacol 2018  9, 82 doi:10.3389/fphar.2018.00082 PMID:29487526
1536	LncRNA	MIR100HG	miR-100	p53	Bxpc-3, Panc-1 And Colo357	Pancreatic Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot etc	29748571	TGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression.	although the pro-tumourigenic miR-100 and miR-125b accordingly increase,the amount of anti-tumourigenic let-7a is unchanged, as TGF-β also induces LIN28B inhibiting its maturation.Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β effectors.We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells.Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell-cell junctions'pathways.Together, we uncover that TGF-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis.	MI0000102	Nat Commun 2018 May 10 9, 1845 doi:10.1038/s41467-018-03962-x PMID:29748571
1537	LncRNA	MIR100HG	miR-125b	p53	Bxpc-3, Panc-1 And Colo357	Pancreatic Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot etc	29748571	TGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression.	although the pro-tumourigenic miR-100 and miR-125b accordingly increase,the amount of anti-tumourigenic let-7a is unchanged, as TGF-β also induces LIN28B inhibiting its maturation.Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β effectors.We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells.Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell-cell junctions'pathways.Together, we uncover that TGF-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis.	MI0000446	Nat Commun 2018 May 10 9, 1845 doi:10.1038/s41467-018-03962-x PMID:29748571
1538	LncRNA	MIR100HG	let-7a	p53	Bxpc-3, Panc-1 And Colo357	Pancreatic Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot etc	29748571	TGF-β induces miR-100 and miR-125b but blocks let-7a through LIN28B controlling PDAC progression.	although the pro-tumourigenic miR-100 and miR-125b accordingly increase,the amount of anti-tumourigenic let-7a is unchanged, as TGF-β also induces LIN28B inhibiting its maturation.Notably, we demonstrate that inactivation of miR-125b or miR-100 affects the TGF-β-mediated response indicating that these miRNAs are important TGF-β effectors.We integrate AGO2-RIP-seq with RNA-seq to identify the global regulation exerted by these miRNAs in PDAC cells.Transcripts targeted by miR-125b and miR-100 significantly overlap and mainly inhibit p53 and cell-cell junctions'pathways.Together, we uncover that TGF-β induces an lncRNA, whose encoded miRNAs, miR-100, let-7a and miR-125b play opposing roles in controlling PDAC tumourigenesis.	MI0000060	Nat Commun 2018 May 10 9, 1845 doi:10.1038/s41467-018-03962-x PMID:29748571
1539	LncRNA	MIR222HG	miR-221	NA	Lncap,Lncap-Abl ,Pca Tumor Tissues	Prostate Cancer	Homo sapiens (human)	qPCR,luciferase reporter assayRIP,in vitro knockdown etc	29540675	Expression of lncRNA MIR222HG co-transcribed from the miR-221/222 gene promoter facilitates the development of castration-resistant prostate cancer.	Upon promoter activation, a set of polyadenylated long non-coding RNA (lncRNA) MIR222HGs was transcribed from this promoter region.Over-expression of these MIR222HGs increased androgen-independent cell growth and repressed the expression of androgen receptor-regulated dihydrotestosterone (DHT)-induced KLK3,TMPRSS2,and FKBP5 in HSPC LNCaP cells, hallmarks of the CRPC phenotype. Clinically, increased expression of MIR222HG is associated with PCa progression to CRPC.MIR222HG may potentially affect miR-mediated expression silencing, subsequently leading to AR  reprogramming. Our study highlights an essential role of a non-coding RNA in CRPC development and that differential activation of a single promoter can up-regulate two different types of non-coding RNAs, miR-221/222 and lncRNA MIR222HG,in CRPC.  	MI0000298	Oncogenesis 2018 Mar 13 7, 30 doi:10.1038/s41389-018-0039-5 PMID:29540675
1540	LncRNA	MIR222HG	miR-222	NA	Lncap,Lncap-Abl ,Pca Tumor Tissues	Prostate Cancer	Homo sapiens (human)	qPCR,luciferase reporter assayRIP,in vitro knockdown etc	29540675	Expression of lncRNA MIR222HG co-transcribed from the miR-221/222 gene promoter facilitates the development of castration-resistant prostate cancer.	Upon promoter activation, a set of polyadenylated long non-coding RNA (lncRNA) MIR222HGs was transcribed from this promoter region.Over-expression of these MIR222HGs increased androgen-independent cell growth and repressed the expression of androgen receptor-regulated dihydrotestosterone (DHT)-induced KLK3,TMPRSS2,and FKBP5 in HSPC LNCaP cells, hallmarks of the CRPC phenotype. Clinically, increased expression of MIR222HG is associated with PCa progression to CRPC.MIR222HG may potentially affect miR-mediated expression silencing, subsequently leading to AR  reprogramming. Our study highlights an essential role of a non-coding RNA in CRPC development and that differential activation of a single promoter can up-regulate two different types of non-coding RNAs, miR-221/222 and lncRNA MIR222HG,in CRPC.  	MI0000299	Oncogenesis 2018 Mar 13 7, 30 doi:10.1038/s41389-018-0039-5 PMID:29540675
1541	LncRNA	MIR503HG	miR-503	Smurf2	Sr-786, Karpas, Mac-1 And Fepd 	Anaplastic Large-Cell Lymphoma	Homo sapiens (human)	qPCR etc	29758012	The Long Non-Coding RNA MIR503HG Enhances Proliferation of Human ALK-Negative Anaplastic Large-Cell Lymphoma.	MIR503HG (miR-503 host gene) was highly expressed in ALK-negative cell lines and was significantly upregulated in tumors in mice formed from ALK-negative ALCL cell lines.Depletion of MIR503HG suppressed tumor cell proliferation in vivo and in vitro;conversely, its overexpression enhanced tumor cell growth.MIR503HG-induced proliferation was mediated by the induction of microRNA-503 (miR-503) and suppression of Smurf2, resulting in stabilization of the tumor growth factor-β receptor (TGFBR) and enhanced tumor cell growth.Collectively, these findings support a potential role for MIR503HG in cancer cell proliferation through the miR-503/Smurf2/TGFBR axis and indicate that MIR503HG is a potential marker in ALK-negative ALCL.	MI0003188	Int J Mol Sci 2018 May 14 19 doi:10.3390/ijms19051463 PMID:29758012
1542	LncRNA	MNX1-AS1	miR-4443	NA	U138, Ln229, T98 And U251	Glioblastoma	Homo sapiens (human)	qPCR etc	29678219	LncRNA MNX1-AS1 promotes glioblastoma progression through inhibition of miR-4443.	the expression of MNX1-AS1 was significantly upregulated in GBM tissues and cell lines. Knockdown of MNX1-AS1 significantly inhibited the proliferation,migration and invasion of GBM cells. In terms of mechanism,we found that MNX1-AS1 could bind to miR-4443 in GBM cells. Overexpression of miR-4443 significantly inhibited the expression of MNX1-AS1, and vice versa. Moreover,there was an inverse correlation between the expression levels of MNX1-AS1 and miR-4443 in GBM tissues. Moreover,we found that overexpression of miR-4443 inhibited the proliferation, migration and invasion of GBM cells. Besides,we showed that inhibition of miR-4443 reversed the effects of MNX1-AS1 knockdown on GBM cell proliferation, migration and invasion. Taken together, we found that MNX1-AS1 promoted the proliferation,migration and invasion of GBM cells through inhibiting miR-4443. 	MI0016786	Oncol Res 2019 Feb 21 27, 341-347 doi:10.3727/096504018x15228909735079 PMID:29678219
1543	LncRNA	MT1JP	miR-214-3p	RUNX3	Sgc-7901, Mgc-803, Hgc-27 And Ags	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi etc	29742512	LncRNA MT1JP Suppresses Gastric Cancer Cell Proliferation and Migration Through MT1JP/MiR-214-3p/RUNX3 Axis.	MT1JP was found downregulated in GC tissues and cells. Low expression of MT1JP was significantly correlated with advanced TNM stage and lymphatic metastasis. The expression of plasma MT1JP was also found decreased in GC patients compared to healthy controls, with an area under the ROC curve (AUC) of 0.649 for diagnosis of GC. Gain- and loss-of-function of MT1JP revealed that MT1JP functioned as a ceRNA for miR-214-3p to facilitate RUNX3 expression and then upregulated p21 and Bim levels suppressing GC cell proliferation, invasion and migration, and promoting apoptosis. Furthermore, MT1JP overexpression suppressed tumor growth and inhibited the expression of miR-214-3p and proliferation antigen Ki-67, but increased the expression of RUNX3, p21 and Bim in vivo. Our results suggest a potential ceRNA regulatory network involving MT1JP regulates RUNX3 expression by competitively binding endogenous miR-214-3p in tumorigenesis and progression of GC. 	MIMAT0000271	Cell Physiol Biochem 2018  46, 2445-2459 doi:10.1159/000489651 PMID:29742512
1544	LncRNA	MT1JP	miR-92a-3p	FBXW7	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29720189	LncRNA MT1JP functions as a ceRNA in regulating FBXW7 through competitively binding to miR-92a-3p in gastric cancer.	LncRNA MT1JP was significantly lower in GC tissues than adjacent normal tissues,and higher MT1JP was remarkably related to lymph node metastasis and advance stage. Besides, GC patients with higher MT1JP expression had a well survival. Functionally,overexpression of lncRNA MT1JP inhibited cell proliferation, migration, invasion and promoted cell apoptosis in vitro, and inhibited tumor growth and metastasis in vivo. Functional analysis showed that lncRNA MT1JP regulated FBXW7 expression by competitively binding to miR-92a-3p. MiR-92a-3p and down-regulated FBXW7 reversed cell phenotypes caused by lncRNA MT1JP by rescue analysis.MT1JP, a down-regulated lncRNA in GC,was associated with malignant tumor phenotypes and survival of GC.MT1JP regulated the progression of GC by functioning as a competing endogenous RNA (ceRNA) to competitively bind to miR-92a-3p and regulate FBXW7 expression.Our study provided new insight into the post-transcriptional regulation mechanism of lncRNA MT1JP,and suggested that MT1JP may act as a potential therapeutic target and prognosis biomarker for GC.	MIMAT0000092	Mol Cancer 2018 May 2 17, 87 doi:10.1186/s12943-018-0829-6 PMID:29720189
1545	LncRNA	MYCNOS-01	miR-485-5p	MYCN	Rms-01, Cell Line	Rhabdomyosarcoma	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,in vitro knockdown	29466962	The long non-coding RNA MYCNOS-01 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells.	MYCNOS-01 transcript levels were generally higher in NB and RMS tumor samples and cell lines with MYCN genomic amplification.RNA interference of MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels.Conversely, MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein levels.Reduction of MYCNOS-01 or MYCN expression decreased cell growth in MYCN-amplified alveolar rhabdomyosarcoma and neuroblastoma cell lines.This is consistent with MYCNOS-01-mediated regulation of MYCN contributing to the phenotype observed.Another possibility therefore is that MYCNOS-01 interacts with an miRNA that targets MYCN for degradation, therefore increasing MYCN protein expression by sequestering away a negative regulating factor.	MIMAT0002175	BMC Cancer 2018 Feb 21 18, 217 doi:10.1186/s12885-018-4129-8 PMID:29466962
1546	LncRNA	MYCNOS-01	miR-485-5p	MYCN	Rms-01, Cell Line	Neuroblastoma	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,in vitro knockdown	29466962	The long non-coding RNA MYCNOS-01 regulates MYCN protein levels and affects growth of MYCN-amplified rhabdomyosarcoma and neuroblastoma cells.	MYCNOS-01 transcript levels were generally higher in NB and RMS tumor samples and cell lines with MYCN genomic amplification.RNA interference of MYCNOS-01 expression did not alter MYCN transcript levels but decreased MYCN protein levels.Conversely, MYCN reduction increased MYCNOS-01 transcript levels,creating a negative feedback loop on MYCN protein levels.Reduction of MYCNOS-01 or MYCN expression decreased cell growth in MYCN-amplified alveolar rhabdomyosarcoma and neuroblastoma cell lines.This is consistent with MYCNOS-01-mediated regulation of MYCN contributing to the phenotype observed.Another possibility therefore is that MYCNOS-01 interacts with an miRNA that targets MYCN for degradation, therefore increasing MYCN protein expression by sequestering away a negative regulating factor.	MIMAT0002175	BMC Cancer 2018 Feb 21 18, 217 doi:10.1186/s12885-018-4129-8 PMID:29466962
1547	LncRNA	n335586	miR-924	CKMT1A	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29753758	LncRNA n335586/miR-924/CKMT1A axis contributes to cell migration and invasion in  hepatocellular carcinoma cells.	the expression of n335586 was significantly increased in HBV positive HCC tissues and cells and was induced by HBV in vitro.Function study indicated that lncRNA n335586 remarkably promoted HCC cells migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and metastasis in vivo.Further mechanistic studies showed lncRNA n335586 promoted HCC cells migration and invasion through facilitating the expression of its host gene CKMT1A by competitively binding miR-924. In conclusion,we demonstrated that the n335586/miR-924/CKMT1A axis contributes to HCC cell migration and invasion, which may be helpful for understanding of pathogenesis of HBV-related HCC.Because lncRNA n335586 overlapped with part of CDS and 3′-UTR of CKMT1A,we speculated that it may operate in ceRNA manner.	MI0005716	Cancer Lett 2018 Aug 10 429, 89-99 doi:10.1016/j.canlet.2018.05.010 PMID:29753758
1548	LncRNA	NCK1-AS1	miR-6857	CDK1	CerEpiC	Cervical Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29416014	LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway.	Functionally,we screened the CC-associated lncRNA NCK1-AS1 as a new candidate lncRNA and regulator which promotes development and progression in CC. qRT-PCR and RNA in situ hybridization (RISH) results showed that NCK1-AS1 was significantly up-regulated in 77.4% of the CC tissue group compared with the normal group.Interestingly,we demonstrated that transcription factor SP1 directly binds to the promoter to activate NCK1-AS1 expression in SiHa cells.In vitro and in vivo assays of silencing NCK1-AS1 significantly inhibited cell proliferation and invasion, with induction of cell arrest in S phase of the cell cycle.Furthermore,Human Transcriptome Array 2.0 analysis after NCK1-AS1 silencing highlighted alterations in cell proliferation and cell cycle pathways.NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation.	MI0022703	Cell Death Dis 2018 Feb 7 9, 198 doi:10.1038/s41419-017-0249-3 PMID:29416014
1549	LncRNA	NCK1-AS1	miR-6857	CDK6	CerEpiC	Cervical Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29416014	LncRNA NCK1-AS1 promotes proliferation and induces cell cycle progression by crosstalk NCK1-AS1/miR-6857/CDK1 pathway.	Functionally,we screened the CC-associated lncRNA NCK1-AS1 as a new candidate lncRNA and regulator which promotes development and progression in CC. qRT-PCR and RNA in situ hybridization (RISH) results showed that NCK1-AS1 was significantly up-regulated in 77.4% of the CC tissue group compared with the normal group.Interestingly,we demonstrated that transcription factor SP1 directly binds to the promoter to activate NCK1-AS1 expression in SiHa cells.In vitro and in vivo assays of silencing NCK1-AS1 significantly inhibited cell proliferation and invasion, with induction of cell arrest in S phase of the cell cycle.Furthermore,Human Transcriptome Array 2.0 analysis after NCK1-AS1 silencing highlighted alterations in cell proliferation and cell cycle pathways.NCK1-AS1 functioned as a molecular sponge for miR-6857, antagonizing its ability to repress CDK1/6 protein translation.	MI0022703	Cell Death Dis 2018 Feb 7 9, 198 doi:10.1038/s41419-017-0249-3 PMID:29416014
1550	LncRNA	NEAT1	miR-365	RGS20	Scc-9,Scc-25, Hn4, Tca-8113,Cal-27,Oscc Tissues	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29484420	lncRNA NEAT1 promotes cell proliferation and invasion by regulating miR-365/RGS20 in oral squamous cell carcinoma.  	Functionally,knockdown of NEAT1 significantly inhibited cell proliferation and invasion and induced cell cycle arrest at the G0/G1 phase and apoptosis, whereas inhibition of miR365 abolished the suppressive effect of NEAT1 knockdown on cellular processes.RGS20,a direct target of miR365,could reverse the tumor suppressive role of miR365 mimic by enhancing cell viability and motility.Moreover, the protein levels of RGS20, cyclin D1, Ecadherin, Ncadherin and vimentin could be regulated by the NEAT1/miR365 axis.NEAT1 silencing also inhibited tumor growth in vivo.NEAT1/miR365/RGS20 axis may be a novel mechanism or therapeutic strategy for OSCC treatment.  	MI0000767	Oncol Rep 2018 Apr 39, 1948-1956 doi:10.3892/or.2018.6283 PMID:29484420
1551	LncRNA	NEAT1	let-7a-5p	Rsf-1	Hk-1, Cne-1, Cne-2 Subclone S18 And Sune1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot etc	29565706	LncRNA NEAT1/let-7a-5p axis regulates the cisplatin resistance in nasopharyngeal carcinoma by targeting Rsf-1 and modulating the Ras-MAPK pathway.	NEAT1 was upregulated and let-7a-5p was downregulated in NPC tissues,as well as NPC cell lines.Inhibition of NEAT1 markedly repressed the cisplatin resistance of NPC cells. NEAT1 was demonstrated to interact with let-7a-5p. Besides, a negative correlation between NEAT1 and let-7a-5p expression was observed in NPC tissues.Rsf-1 was confirmed as a target of let-7a-5p.NEAT1 remarkably reversed the inhibitory effect of let-7q-5p on the cisplatin resistance of NPC cells in vitro. Additionally, NEAT1 knockdown inhibited the Ras-MAPK pathway in NPC cells.NEAT1 knockdown suppressed tumor growth in the presence of cisplatin in vivo.Overall,these findings suggest that NEAT1/let-7a-5p axis regulates the cisplatin resistance in NPC by targeting Rsf-1 and modulating the Ras-MAPK signaling pathway. 	MIMAT0000062	Cancer Biol Ther 2018 Jun 3 19, 534-542 doi:10.1080/15384047.2018.1450119 PMID:29565706
1552	LncRNA	NEAT1	miR-124-3p	ATGL	L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29764424	Long non-coding RNA NEAT1-modulated abnormal lipolysis via ATGL drives hepatocellular carcinoma proliferation.	the lipolytic enzyme,ATGL is highly expressed in human HCC tissues and predicts poor prognosis.high levels of DAG and FFA are present in HCC tissues.Furthermore,the lncRNA-NEAT1 was found to modulate ATGL expression and disrupt lipolysis in HCC cells via ATGL. Notably, ATGL and its products, DAG and FFA, were shown to be responsible for NEAT1-mediated HCC cell growth. NEAT1 regulated ATGL expression by binding miR-124-3p.Additionally, NEAT1 knockdown attenuated HCC cell growth through miR-124-3p/ATGL/DAG+FFA/PPARα signaling. NEAT1-modulates abnormal lipolysis via ATGL to drive HCC proliferation. NEAT1 was demonstrated to function as a competing endogenous RNA (ceRNA) by competitively binding common micro-RNAs.	MIMAT0000422	Mol Cancer 2018 May 15 17, 90 doi:10.1186/s12943-018-0838-5 PMID:29764424
1553	LncRNA	NEAT1	miR-34c	BCL-2	Hfob1.19, Mg63, 143B, Hos And Saos2	Osteosarcoma	Homo sapiens (human)	qPCR,RNAi etc	29654165	Knockdown of the oncogene LncRNA NEAT1 restores the availability of miR-34c and improves the sensitivity to cisplatin in osteosarcoma.	NEAT1 was overexpressed in OS tissues, which positively correlated with tumor size, Enneking stage and distant metastasis of OS patients. The elevated level of NEAT1 was confirmed in OS cell lines including MG63 and HOS in vitro Knockdown of NEAT1 by two siRNAs induced impaired cell vitalities,promotes the apoptosis and G0/G1 arrest in two cell lines,which was associated with inhibited anti-apoptosis signals BCL-2 pathway and cell cycle-related cyclin D1 (CCND1) signals.Moreover, the tumor suppressor microRNA-34c (miR-34c) was negatively regulated and inhibited by NEAT1 in OS. Suppression of miR-34c could up-regulate the expressions of its target genes BCL-2 and CCND1 to antagonize the effects of NEAT1 knockdown. Furthermore, overexpressed NEAT1 reduced the sensitivity of cisplatin (DDP) and inhibited DDP-induced apoptosis and cell cycle arrest via miR-34c. The results in vivo also confirmed that knockdown of NEAT1 sensitized the OS cells to DPP-induced tumor regression, delayed the tumor growth with reduced levels of Ki-67, BCL-2 and cyclin D1 signals, suggesting that NEAT1 is an oncogene and chemotherapy resistant factor in osteosarcoma.	MI0000743	Biosci Rep 2018 Jun 29 38 doi:10.1042/bsr20180375 PMID:29654165
1554	LncRNA	NEAT1	miR-506	STAT3	Bgc823, Sgc-7901, Ags, Mgc803, Mkn28, Cell Lines	Gastric Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29363783	Long noncoding RNA NEAT1-modualted miR-506 regulates gastric cancer development through targeting STAT3.	NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901,AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated.the negative binding correlation between NEAT1 and miR-506. In addition, miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression.downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors.	MI0003193	J Cell Biochem 2019 Apr 120, 4827-4836 doi:10.1002/jcb.26691 PMID:29363783
1555	LncRNA	NEAT1	miR-448	ZEB1	Mcf-7, Mda-Mb-453, Mda-Mb-231, Skbr3 And Mcf-10A	Breast Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29323713	NEAT1 contributes to breast cancer progression through modulating miR-448 and ZEB1.	NEAT1 levels were significantly increased in human breast cancer cells including MCF-7, MDA-MB-453, MDA-MB-231, and SKBR3 cells compared to normal mammary epithelial cells MCF-10A while miR-448 was decreased. We found that downregulation of NEAT1 was able to inhibit the growth of breast cancer cells and miR-448 mimic exerted the similar function. Bioinformatics analysis and dual luciferase reporter assays confirmed the negative correlation between NEAT1 and miR-448 in vitro. In addition, ZEB1 was predicted as a novel mRNA target of miR-448.Overexpression of NEAT1 can induce breast cancer cell growth, migration, and invasion by inhibiting miR-448 and upregulating ZEB1. It was demonstrated that NEAT1 can increase ZEB1 levels while miR-448 mimic can repress ZEB1. It was speculated in our study that NEAT1 can serve as a competing endogenous lncRNA (ceRNA) to modulate ZEB1 by sponging miR-448 in breast cancer.	MIMAT0001532	J Cell Physiol 2018 Nov 233, 8558-8566 doi:10.1002/jcp.26470 PMID:29323713
1556	LncRNA	NEAT1	miR-129-5p	KLK7	Bncc338081, Tpc-1	Papillary Thyroid Cancer	Homo sapiens (human)	Microarray,QRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29319165	Long noncoding RNA NEAT1 regulate papillary thyroid cancer progression by modulating miR-129-5p/KLK7 expression.	LncRNA NEAT1 was highly expressed in PTC tissues and cell lines and could deteriorate PTC by promoting proliferation, invasion, and migration accompanied by less apoptosis. Besides, miR-129-5p/lncRNA NEAT1 were found to negatively correlate with each other by direct target relationship and their combination suppressed the progression of PTC. KLK7,a highly expressed downstream protein in PTC tissues,could be directly regulated by miR-129-5p in a negative way. KLK7 accelerated the deterioration of PTC in vitro experiments which could be reversed by sh-lnc RNA NEAT1 and miR-129-5p mimics.In vivo experiments, silence of lncRNA NEAT1 restrain tumor growth in weight and volume.	MIMAT0000242	J Cell Physiol 2018 Oct 233, 6638-6648 doi:10.1002/jcp.26425 PMID:29319165
1557	LncRNA	NEAT1	miR-106b-5p	ATAD2	Nthy-Ori 3-1, K1,Ihh4,Tpc1,Bcpap,Ptc Tissues	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot	29515109	NEAT1_2 functions as a competing endogenous RNA to regulate ATAD2 expression by sponging microRNA-106b-5p in papillary thyroid cancer. 	The relative expression level of NEAT1_2 was positively associated with TNM stage and tumor size. NEAT1_2 knockdown led to a significant inhibition of growth and metastasis, and induced apoptosis in PTC cells. Knockdown of NEAT1_2 significantly inhibited malignant biological behavior by downregulating the oncogene ATAD2. NEAT1_2 could act as a competing endogenous RNA to regulate the expression of ATAD2 through downregulating miR-106b-5p.	MIMAT0000680	Cell Death Dis 2018 Mar 7 9, 380 doi:10.1038/s41419-018-0418-z PMID:29515109
1558	LncRNA	NNT-AS1	miR-142-3p	ZEB1	Md-Mb-231, Md-Mb-468, Mcf-7 And Mcf-10A 	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29710510	Long non-coding RNA NNT-AS1 affects progression of breast cancer through miR-142-3p/ZEB1 axis.	Loss of function assay was carried out to detect the effects of silenced NNT-AS1 on proliferation, metastasis and EMT process of BC cells. Subcellular fractionation assay demonstrated that NNT-AS1 was located in the cytoplasm of BC cells. we found the combination between NNT-AS1 and miR-142-3p through conducting bioinformatics analysis, RIP and luciferase reporter assays. Similarly, the combination between miR-142-3p and ZEB1 was verified. Finally, the recue assays were carried out to demonstrate the effects of NNT-AS1/miR-142-3p/ZEB1 axis on the biological behaviors of BC cells.All the above findings revealed a fact that NNT-AS1 affects breast cancer progression through modulating miR-142-3p/ZEB1 axis. 	MIMAT0000434	Biomed Pharmacother 2018 Jul 103, 939-946 doi:10.1016/j.biopha.2018.04.087 PMID:29710510
1559	LncRNA	NORAD	miR-202-5p	NA	Sw480 And Hct116, Normal Colorectal Mucosa Cells Cell Line 	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,in vitro knockdown,Luciferase reporter assay	29471886	LncRNA NORAD contributes to colorectal cancer progression by inhibition of miR-202-5p.	NORAD served as a competing endogenous RNA for miR-202-5p.We found that there was an inversely relationship between the expression of NORAD and miR-202-5p in CRC tissues.Moreover, overexpression of miR-202-5p in SW480 and HCT116 cells significantly inhibited cellular proliferation,migration and invasion.Taken together,our study demonstrated NORAD/miR-202-5p axis plays a pivot function on CRC progression.	MIMAT0002810	Oncol Res 2018 Oct 17 26, 1411-1418 doi:10.3727/096504018x15190844870055 PMID:29471886
1560	LncRNA	NR2F1-AS1	miR-363	ABCC1	Huh7, Hepg2,Lo-2, Hcc Tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Microarray,Western blot etc	29602203	LncRNA NR2F1-AS1 regulates hepatocellular carcinoma oxaliplatin resistance by targeting ABCC1 via miR-363. 	miR-363 targeted the 3'-UTR of NR2F1-AS1 and  ABCC1 mRNA,presenting that NR2F1-AS1 promoted ABCC1 expression through endogenous sponging miR-363.NR2F1-AS1 regulates HCC OXA resistance through targeting miR-363-ABCC1 pathway,providing a vital theoretic mechanism and therapeutic target for HCC chemoresistance.	MI0000764	J Cell Mol Med 2018 Jun 22, 3238-3245 doi:10.1111/jcmm.13605 PMID:29602203
1561	LncRNA	OIP5-AS1	miR-186a-5p	ZEB1	Hepg2, Huh-6, Smmc-7721, Qsg-7701 And L-02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP etc	29475118	Kockdown of OIP5-AS1 expression inhibits proliferation, metastasis and EMT progress in hepatoblastoma cells through up-regulating miR-186a-5p and down-regulating ZEB1.	OIP5-AS1 was oncogenic in hepatoblastoma for the high expression of it in hepatoblastoma tissues and cells. OIP5-AS1 knockdown was carried out in cancer cells.Unsurprisingly,this action was verified to be able to inhibit cell proliferation, metastasis and EMT  progress in hepatoblastoma.We discovered OIP5-AS1 is located in nucleus of cancerous cells.It could target to miR-186a-5p and up-regulate the target gene of miR-186a-5p (ZEB1).Based on all above findings,we came into a conclusion that OIP5-AS1 is a ceRNA in Hepatoblastoma cells through modulating miR-186a-5p/ZEB1. 	MI0000483	Biomed Pharmacother 2018 May 101, 14-23 doi:10.1016/j.biopha.2018.02.026 PMID:29475118
1562	LncRNA	PAX8-AS1-N	miR-17-5p	PTEN	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29693272	Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N.	we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p,and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4.In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients.In conclusion,PAX8-AS1-N activation mediated the anti-cancer effects of baicalein via regulating miR-17-5p,and suggested that baicalein and enhancing PAX8-AS1-N would be potential therapeutic strategies against breast cancer. 	MIMAT0000070	J Cell Biochem 2018 Aug 119, 6842-6856 doi:10.1002/jcb.26881 PMID:29693272
1563	LncRNA	PAX8-AS1-N	miR-17-5p	CDKN1A	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29693272	Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N.	we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p,and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4.In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients.In conclusion,PAX8-AS1-N activation mediated the anti-cancer effects of baicalein via regulating miR-17-5p,and suggested that baicalein and enhancing PAX8-AS1-N would be potential therapeutic strategies against breast cancer. 	MIMAT0000070	J Cell Biochem 2018 Aug 119, 6842-6856 doi:10.1002/jcb.26881 PMID:29693272
1564	LncRNA	PAX8-AS1-N	miR-17-5p	ZBTB4	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29693272	Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8-AS1-N.	we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner.PAX8-AS1-N reduced cell viability,inhibited cell-cycle progression,and induced apoptosis of breast cancer cells in vitro.Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability,the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p,and up-regulated miR-17-5p targets,such as PTEN, CDKN1A, and ZBTB4.In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients.In conclusion,PAX8-AS1-N activation mediated the anti-cancer effects of baicalein via regulating miR-17-5p,and suggested that baicalein and enhancing PAX8-AS1-N would be potential therapeutic strategies against breast cancer. 	MIMAT0000070	J Cell Biochem 2018 Aug 119, 6842-6856 doi:10.1002/jcb.26881 PMID:29693272
1565	LncRNA	UCA1	miR-182	PFKFB2	U251 And U87Mg	Glioblastoma	Homo sapiens (human)	qPCR etc	29655792	Long non-coding RNA UCA1/miR-182/PFKFB2 axis modulates glioblastoma-associated stromal cells-mediated glycolysis and invasion of glioma cells.	lncRNA UCA1/miR-182 axis has been regarded as a nodal driver of glioma invasion mediated by GB-associated stromal cells (GASCs) and GASC-secreted chemokine CXCL14.In clinical specimens, CXCL14 upregulation in GASCs also correlated with poor prognosis. Notably, CXCL14-high GASCs mediated lncRNA UCA1 upregulation and miR-182 downregulation in glioma cells. Moreover, miR-182 directly bound to the fructose-2,6-biphosphatase PFKFB2.UCA1/miR-182 axis thereby modulated GASC-induced glycolysis in glioma cells. Overall, UCA1/miR-182/PFKFB2 axis modulates chemokine CXCL14 secretion, glycolysis and invasion of glioma cells in GASCs. 	MI0000272	Biochem Biophys Res Commun 2018 Jun 7 500, 569-576 doi:10.1016/j.bbrc.2018.04.091 PMID:29655792
1566	LncRNA	PlncRNA-1	miR-204	MMP9	Sw480,  Sw620, Hct116, And Ht29	Colorectal Cancer	Homo sapiens (human)	Western blot etc	29738066	Long non-coding RNA PlncRNA-1 promotes cell proliferation and hepatic metastasis  in colorectal cancer.	up-regulated PlncRNA-1 in CRC tissues and cells promoted cell proliferation by accelerating cell cycle process and inhibiting cell apoptosis in vitro, enhanced tumor growth and matastasis in vivo and was associated with cell migration and invasion, EMT process of CRC cells. In addition, PlncRNA-1 was a target of miR-204 and enhanced the expression of an endogenous miR-204 target, MMP9 in CRC cells.Furthermore, we found that PlncRNA-1 activates Wnt/β-catenin pathway through the miR-204 in CRC cells.the PlncRNA-1/miR-204/ Wnt/β-catenin regulatory network may shed light on tumorigenesis in CRC. PlncRNA-1 may act as a ceRNA to regulate the expression level of MMP9 in a miR-204 dependent manner.	MI0000284	J Cell Biochem 2018 Aug 119, 7091-7104 doi:10.1002/jcb.27031 PMID:29738066
1567	LncRNA	PRLB	miR-4766-5p	SIRT1	Breast Cancer tissues	Breast Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RIP etc	29752439	A novel long non-coding RNA-PRLB acts as a tumor promoter through regulating miR-4766-5p/SIRT1 axis in breast cancer.	lncRNA-PRLB was upregulated in human breast cancer tissues and breast cancer cell lines.Further evaluation verified that lncRNA-PRLB was positively correlated with the extent of metastasis, and its expression was correlated with shorter survival time of breast cancer patients.We identified microRNA miR-4766-5p as an inhibitory target of lncRNA-PRLB.Both lncRNA-PRLB overexpression and miR-4766-5p knockdown could remarkably enhance cell growth, metastasis, and chemoresistance.We also determined that sirtuin 1 (SIRT1) was an inhibitory target of miR-4766-5p, and that SIRT1 was inhibited by both lncRNA-PRLB knockdown and miR-4766-5p overexpression. Significantly,we found that the promotion of cell proliferation and metastasis,the acquisition of chemoresistance, and the increased expression of SIRT1 induced by lncRNA-PRLB overexpression could be partly abrogated by ectopic expression of miR-4766-5p.Taken together,our findings indicated that lncRNA could regulate the progression and chemoresistance of breast cancer via modulating the expression levels of miR-4766-5p and SIRT1, which may have a pivotal role in breast cancer treatment and prognosis prediction. The subcellular distribution assay revealed that lncRNA-PRLB is predominately located in the plasma.	MIMAT0019917	Cell Death Dis 2018 May 1 9, 563 doi:10.1038/s41419-018-0582-1 PMID:29752439
1568	LncRNA	PTENP1-AS	miR-21	AGO4	Ags1, Mgc803, Sgc7901, And Mkn45,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	we observed a higher level of H19 which sponged out the low level expressed miR-148a leading to the overexpression of its target mRNA DNMT1.In this study, we observed upregulation of PTENP1-AS increased the EGFR and AGO4 level in tumors.In addition,we also observed that lncRNA GAS5 competes with AGO4 for miR-21.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1569	LncRNA	PVT1	miR-455	RUNX2PVT1	Fhc,Sw480, Sw620, Ht29, Hct116,Colorectal Cancer Tissues	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot etc	29637007	A feedback loop consisting of RUNX2/LncRNA-PVT1/miR-455 is involved in the progression of colorectal cancer.    	PVT1 regulated the growth of CRC tumors by acting as a competing endogenous RNAs (ceRNA) and negatively regulated miR-455. Furthermore, we discovered that RUNX2,a functional transcription factor in CRC,up-regulated PVT1 expression. 	MI0003513	Am J Cancer Res 2018  8, 538-550,  PMID:29637007
1570	LncRNA	PVT1	miR-26b	CTGF	Huvec	Glioma	Homo sapiens (human)	Western blot, Luciferase reporter assay etc	29620147	lncRNA PVT1 promotes the angiogenesis of vascular endothelial cell by targeting miR-26b to activate CTGF/ANGPT2.	PVT1 affected cell proliferation, migration and in vitro vascular tube formation of HUVECs. In addition,it was determined that PVT1 was able to bind and degrade miR26b to promote connective tissue growth factor (CTGF) and angiopoietin 2 (ANGPT2) expression.miR26b was also identified to have a suppressive role in cell proliferation,migration and in vitro vascular tube formation of HUVECs via binding 3'UTR regions and downregulating CTGF and ANGPT2 expression levels.PVT1 was important in angiogenesis of vascular endothelial cell as ceRNA to bind and degrade miR26b,which expanded the current understanding of PVT1 as ceRNA to regulate biological processes.	MI0000084	Int J Mol Med 2018 Jul 42, 489-496 doi:10.3892/ijmm.2018.3595 PMID:29620147
1571	LncRNA	PVT1	miR-26b	ANGPT2	Huvec	Glioma	Homo sapiens (human)	Western blot, Luciferase reporter assay etc	29620147	lncRNA PVT1 promotes the angiogenesis of vascular endothelial cell by targeting miR-26b to activate CTGF/ANGPT2.	PVT1 affected cell proliferation, migration and in vitro vascular tube formation of HUVECs. In addition,it was determined that PVT1 was able to bind and degrade miR26b to promote connective tissue growth factor (CTGF) and angiopoietin 2 (ANGPT2) expression.miR26b was also identified to have a suppressive role in cell proliferation,migration and in vitro vascular tube formation of HUVECs via binding 3'UTR regions and downregulating CTGF and ANGPT2 expression levels.PVT1 was important in angiogenesis of vascular endothelial cell as ceRNA to bind and degrade miR26b,which expanded the current understanding of PVT1 as ceRNA to regulate biological processes.	MI0000084	Int J Mol Med 2018 Jul 42, 489-496 doi:10.3892/ijmm.2018.3595 PMID:29620147
1572	LncRNA	PVT1	miR-186	Twist1	Pc-3, Du145, 22Rv1 And Wpmy	Prostate Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot etc	29452232	Long noncoding RNA PVT1 promotes EMT via mediating microRNA-186 targeting of Twist1 in prostate cancer.	PVT1 promotes prostate cancer invasion and metastasis by modulating EMT.Furthermore,PVT1 can promote EMT by up-regulation of Twist1,a transcription factor associated with EMT.We then confirmed that PVT1 acts as a sponge for miRNA-186-5p and positively regulates Twist1 by a sponge effect.Therefore, this study has revealed a novel MECHANISM for the promotion of EMT in prostate cancer by PVT1.Our findings suggest that the PVT1/miR-186/Twist1 regulatory axis may be a new therapeutic target for prostate cancer. PVT1 can reduce the expression of miR-186 as ceRNA in PCa cell lines and promotes Twist1 expression by suppressing miR-186.	MI0000483	Gene 2018 May 15 654, 36-42 doi:10.1016/j.gene.2018.02.036 PMID:29452232
1573	LncRNA	PVT1	miR-190a-5p	CTGF	U87, U251 And Hek-293T	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	29501773	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p.	PVT1 was up-regulated in glioma specimens and cell lines.Knockdown of PVT1 impaired the malignant behaviors of glioma cells via the suppression of proliferation,migration and invasion,as well as through promotion of apoptosis.Furthermore,PVT1 was identified to affect the glioma cells via binding to miR-190a-5p and miR-488-3p,which were down-regulated and played tumor suppressor roles in glioma cells.Up-regulated miR-190a-5p or miR-488-3p partially rescued the suppressive effect induced by PVT1 knockdown.Myocyte enhancer factor 2C (MEF2C) was a direct downstream target of miR-190a-5p and miR-488-3p,which was proved to be an oncogene and involved in the PVT1 knockdown induced regulation of biological behaviors of glioma cells.Over-expression of MEF2C up-regulated JAGGED1 by increasing the promoter activity of JAGGED1.Over-expression of PVT1 promotes multiple drug-resistance in gastric cancer.	MIMAT0000458	Biochim Biophys Acta Mol Basis Dis 2018 May 1864, 1783-1794 doi:10.1016/j.bbadis.2018.02.022 PMID:29501773
1574	LncRNA	PVT1	miR-488-3p	MEF2C	U87, U251 And Hek-293T	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	29501773	PVT1 regulates the malignant behaviors of human glioma cells by targeting miR-190a-5p and miR-488-3p.	PVT1 was up-regulated in glioma specimens and cell lines. Knockdown of PVT1 impaired the malignant behaviors of glioma cells via the suppression of proliferation,migration and invasion,as well as through promotion of apoptosis.Furthermore,PVT1 was identified to affect the glioma cells via binding to miR-190a-5p and miR-488-3p,which were down-regulated and played tumor suppressor roles in glioma cells.Up-regulated miR-190a-5p or miR-488-3p partially rescued the suppressive effect induced by PVT1 knockdown. Myocyte enhancer factor 2C (MEF2C) was a direct downstream target of miR-190a-5p and miR-488-3p,which was proved to be an oncogene and involved in the PVT1 knockdown induced regulation of biological behaviors of glioma cells.Over-expression of MEF2C up-regulated JAGGED1 by increasing the promoter activity of JAGGED1.Over-expression of PVT1 promotes multiple drug-resistance in gastric cancer.	MIMAT0004763	Biochim Biophys Acta Mol Basis Dis 2018 May 1864, 1783-1794 doi:10.1016/j.bbadis.2018.02.022 PMID:29501773
1575	LncRNA	PVT1	miR-152	BMP3	Panc-1, Aspc-1 And Hek 293T	Pancreatic Cancer	Homo sapiens (human)	qPCR etc	28657147	LncRNA-PVT1 promotes pancreatic cancer cells proliferation and migration through  acting as a molecular sponge to regulate miR-448.	PVT1 functions as an endogenous "sponge" by competing for miR-448 binding to regulate the miRNA target SERBP1,therefore,promotes the proliferation and migration of PC cells. 	MI0000462	J Cell Physiol 2018 May 233, 4044-4055 doi:10.1002/jcp.26072 PMID:28657147
1576	LncRNA	PWRN1	miR-425-5p	PTEN	Hek-293,Ges-1,Mgc-803, Hgc-27, Sgc-7901, Mkn-45, Gc Tissues	Gastric Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RIP,Luciferase reporter assay	29535266	Prader-Willi region non-protein coding RNA 1 suppressed gastric cancer growth as  a competing endogenous RNA of microRNA-425-5p.    	PWRN1 affected PTEN/Akt/MDM2/p53 axis via suppressing miR-425-5p.PWRN1 up-regulated could reduce proliferation and metastasis and increased apoptosis in GC cells, while miR-425-5p had reverse effects. PWRN1 may target an oncogene miR-425-5p.	MIMAT0003393	Clin Sci (Lond) 2018 May 23 132, 1003-1019 doi:10.1042/cs20171588 PMID:29535266
1577	LncRNA	PWRN1	miR-425-5p	Akt	Hek-293,Ges-1,Mgc-803, Hgc-27, Sgc-7901, Mkn-45, Gc Tissues	Gastric Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RIP,Luciferase reporter assay	29535266	Prader-Willi region non-protein coding RNA 1 suppressed gastric cancer growth as  a competing endogenous RNA of microRNA-425-5p.    	PWRN1 affected PTEN/Akt/MDM2/p53 axis via suppressing miR-425-5p.PWRN1 up-regulated could reduce proliferation and metastasis and increased apoptosis in GC cells, while miR-425-5p had reverse effects. PWRN1 may target an oncogene miR-425-5p.	MIMAT0003393	Clin Sci (Lond) 2018 May 23 132, 1003-1019 doi:10.1042/cs20171588 PMID:29535266
1578	LncRNA	PWRN1	miR-425-5p	MDM2	Hek-293,Ges-1,Mgc-803, Hgc-27, Sgc-7901, Mkn-45, Gc Tissues	Gastric Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RIP,Luciferase reporter assay	29535266	Prader-Willi region non-protein coding RNA 1 suppressed gastric cancer growth as  a competing endogenous RNA of microRNA-425-5p.    	PWRN1 affected PTEN/Akt/MDM2/p53 axis via suppressing miR-425-5p.PWRN1 up-regulated could reduce proliferation and metastasis and increased apoptosis in GC cells, while miR-425-5p had reverse effects. PWRN1 may target an oncogene miR-425-5p.	MIMAT0003393	Clin Sci (Lond) 2018 May 23 132, 1003-1019 doi:10.1042/cs20171588 PMID:29535266
1579	LncRNA	PWRN1	miR-425-5p	p53	Hek-293,Ges-1,Mgc-803, Hgc-27, Sgc-7901, Mkn-45, Gc Tissues	Gastric Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,RIP,Luciferase reporter assay	29535266	Prader-Willi region non-protein coding RNA 1 suppressed gastric cancer growth as  a competing endogenous RNA of microRNA-425-5p.    	PWRN1 affected PTEN/Akt/MDM2/p53 axis via suppressing miR-425-5p.PWRN1 up-regulated could reduce proliferation and metastasis and increased apoptosis in GC cells, while miR-425-5p had reverse effects. PWRN1 may target an oncogene miR-425-5p.	MIMAT0003393	Clin Sci (Lond) 2018 May 23 132, 1003-1019 doi:10.1042/cs20171588 PMID:29535266
1580	LncRNA	lincRNA-ROR	miR-145	Sox2	Hb56, Hb96,Tscc, Tca8113, Scc-9 And Cal27, Hek-293T,Oral Cancer Tissues	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay etc	29690669	LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells 	LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens.LincRNA-ROR was related to tumor size, lymph node involvement and distant metastasis,and miR-145 was found related to tumor size and tumor location.CD44(+) CD133(+) cells were successfully isolated from SW1116 by flow cytometry. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05).The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence,while miR-145 was significantly increased.Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog.MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy.Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity.The data may provide insights into the pathophysiological interactions of the components of genetic networks in the development of colon cancer and may lead to new therapies in the future. 	MI0000461	Zhonghua Bing Li Xue Za Zhi 2018 Apr 8 47, 284-290 doi:10.3760/cma.j.issn.0529-5807.2018.04.011 PMID:29690669
1581	LncRNA	lincRNA-ROR	miR-145	Nanog	Hb56, Hb96,Tscc, Tca8113, Scc-9 And Cal27, Hek-293T,Oral Cancer Tissues	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay etc	29690669	LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells 	LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens.LincRNA-ROR was related to tumor size, lymph node involvement and distant metastasis,and miR-145 was found related to tumor size and tumor location.CD44(+) CD133(+) cells were successfully isolated from SW1116 by flow cytometry. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05).The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence,while miR-145 was significantly increased.Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog.MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy.Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity.The data may provide insights into the pathophysiological interactions of the components of genetic networks in the development of colon cancer and may lead to new therapies in the future. 	MI0000461	Zhonghua Bing Li Xue Za Zhi 2018 Apr 8 47, 284-290 doi:10.3760/cma.j.issn.0529-5807.2018.04.011 PMID:29690669
1582	LncRNA	lincRNA-ROR	miR-145	OCT4	Hb56, Hb96,Tscc, Tca8113, Scc-9 And Cal27, Hek-293T,Oral Cancer Tissues	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay etc	29690669	LincRNA-ROR functions as a ceRNA to regulate Oct4, Sox2, and Nanog expression by sponging miR-145 and its effect on biologic characteristics of colonic cancer stem cells 	LincRNA-ROR was frequently up-regulated and inversely correlated with miR-145 down-regulation in the colon cancer specimens.LincRNA-ROR was related to tumor size, lymph node involvement and distant metastasis,and miR-145 was found related to tumor size and tumor location.CD44(+) CD133(+) cells were successfully isolated from SW1116 by flow cytometry. The levels of CD44, CD133, Oct4, Sox2, Nanog, lincRNA-ROR in CD44(+) CD133(+) cells were significantly increased,while miR-145 was decreased compared with CD44(-)CD133(-)cells(P<0.05).The levels of CD44,CD133,lnc-ROR in CD44(+) CD133(+) cells were significantly reduced upon cell adherence,while miR-145 was significantly increased.Bioinformatics analysis revealed that lincRNA-ROR shared miRNA response elements with core transcription factors Oct4,Sox2 and Nanog.MiR-145 significantly inhibited the expression of lincRNA-ROR, Oct4, Sox2 and Nanog. Silencing lincRNA-ROR significantly inhibited colon cancer stem cells proliferation and increased the sensitivity to chemotherapy.Linc-ROR functions as a key ceRNA to prevent core TFs,e.g.Oct4, Sox2, Nanog, from miR-145-mediated suppression in colon cancer stem cells and regulates cell proliferation and chemosensitivity.The data may provide insights into the pathophysiological interactions of the components of genetic networks in the development of colon cancer and may lead to new therapies in the future. 	MI0000461	Zhonghua Bing Li Xue Za Zhi 2018 Apr 8 47, 284-290 doi:10.3760/cma.j.issn.0529-5807.2018.04.011 PMID:29690669
1583	LncRNA	lincRNA-ROR	miR-145	KLF4	Ags1, Mgc803, Sgc7901, And Mkn48,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	LINCROR could sponge the miR-148a, miR-145 and miR-21 and can act as ceRNA modulating the miRNA-mediated post-transcriptional regulation of EGFR, KLF4, DNMT1 and AGO4.The downregulation of LINCROR when its target miR-145 abundantly expressed.In addition,we observed the expression level LINCROR directly correlated with the overexpression of the miR-145.This relationship has been already reported in colon cancer and shown to be involved in overall survival.Our results suggest that reduced LINCROR/high miR-145 might be associated with better prognosis.LINCROR is an active member associated with reprogramming and stemness-related transcription factors.Downregulation of LINCROR by miR-145 might impair the cancer stemness by deregulation of another transcription factor KLF4.	MI0000461	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1584	LncRNA	lincRNA-ROR	miR-145	MUC1	Hek293T, Mcf-10A, Mcf-7, Bt474, Mda-Mb-453 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR etc	29673594	LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1.	lincRNA-ROR was upregulated in TNBC cell lines and tissue samples.The aberrant expression of lincRNA-ROR was shown to increase invasion and metastasis in MDA-MB-231 and loss of function by siRNA reverse these process.Furthermore, lincRNA-ROR functions as a competing endogenous RNAs (ceRNA) which sponges miR-145 and therefore upregulate the expression of Mucin1 (MUC1).Studies showed that downregulated SPRY4-IT1 could facilitate bladder cancer cell apoptosis via acting as a ceRNA for miR-101-3p.	MI0000461	Biochem Biophys Res Commun 2018 Jun 7 500, 614-620 doi:10.1016/j.bbrc.2018.04.119 PMID:29673594
1585	LncRNA	lincRNA-ROR	miR-145	RAD18	Hepg2 And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc	29559320	Long non-coding RNA ROR promotes radioresistance in hepatocelluar carcinoma cells by acting as a ceRNA for microRNA-145 to regulate RAD18 expression.	linc-ROR promotes HCC metastasis via induction of epithelial-mesenchymal transition (EMT).linc-ROR was significantly upregulated in radioresistant HCC cells.Knockdown of linc-ROR reduces in vitro and in vivo radiosensitivity of parental HCC cells by reducing DNA repair capacity, while ectopic expression of linc-ROR enhances radiosensitivity of radioresistant HCC cells.Further mechanistic investigations revealed that lincRNA-ROR exerted its biological effects by acting as a competing endogenous RNA (ceRNA) for miR-145 to regulate RAD18 expression, thereby promoting DNA repair. 	MI0000461	Arch Biochem Biophys 2018 May 1 645, 117-125 doi:10.1016/j.abb.2018.03.018 PMID:29559320
1586	LncRNA	lincRNA-ROR	miR-145	FSCN1	Ec109 And Ec9706, Immortalized Esophageal Epithelial Cell Line, 	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR,Western blot,RIP	29430188	LincRNA-ROR promotes metastasis and invasion of esophageal squamous cell carcinoma by regulating miR-145/FSCN1.	ROR expression in ESCC tumor tissues was significantly higher than in the adjacent tissues. The survival rate of ESCC patients with high ROR expression levels was lower than that of patients with low ROR expression levels. ROR overexpression could downregulate miR-145 by up to 50% was proven by RIP,DLR assay,and qRT-PCR. FSCN1 was a downstream target of ROR/miR-145.Transwell assays were used to show that overexpression of ROR enhanced migration and invasion behavior of ESCC and miR-145 hindered these effects.	MI0000461	Onco Targets Ther 2018  11, 639-649 doi:10.2147/ott.S157638 PMID:29430188
1587	LncRNA	RP11-169D4.1	miR-205-5p	CDH1	Snu899 And Snu46 	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR,Western blot etc	28534968	Functional significance of the long non-coding RNA RP11-169D4.1 as a metastasis suppressor in laryngeal squamous cell carcinoma by regulating CDH1.	RP11-169D4.1 expression was markedly decreased in LSCC tissues and cell lines.The overexpression of RP11-169D4.1 inhibited the proliferation,migration and invasion of LSCC cell lines as well as promoted apoptosis.We further verified that miR-205-5p had binding sites with RP11169D4.1 and that RP11-169D4.1 could regulate the expression of CDH1.Ectopic transfection of RP11-169D4.1 led to a significant reduction in the downstream signaling molecule AKT in LSCC cells. The long non-coding RNA RP11-169D4.1 may serve as a tumor suppressor and a promising therapeutic target in laryngeal cancer,which could inhibit the process of EMT by regulating CDH1. 	MIMAT0000266	Oncol Rep 2017 Jul 38, 211-220 doi:10.3892/or.2017.5645 PMID:28534968
1588	LncRNA	RP11-396F22.1	miR-32	Cpne8	Siha,Hela, C33A And Ms751 	Cervical Cancer	Homo sapiens (human)	Microarray,qPCR,in vitro knockdown etc	29636859	Overexpression of long non-coding RNA RP11-396F22.1 correlates poor prognosis of patients with early-stage cervical cancer.	RP11-396F22.1 might regulate Cpne8 expression via miRNA-32.Indeed,we found that knock down of RP11-396F22.1 significantly down regulated miRNA-32 expression 	MI0000090	Am J Transl Res 2018  10, 684-695,  PMID:29636859
1589	LncRNA	RP11-909B2.1	miR-595	L3MBTL1	Rko	Colorectal Cancer	Homo sapiens (human)	qPCR etc	29737552	Competing endogenous RNA network crosstalk reveals novel molecular markers in colorectal cancer.	the three RNAs-based biomarker network (long non-coding intergenic RNA-[lncRNA RP11-909B2.1], Homo sapiens microRNA-595  [hsa-miRNA-595], and L3MBTL1 mRNA), had high sensitivity and specificity for discriminating CRC from healthy controls and also from benign colorectal neoplasm. The data suggest that among these three RNAs, serum lncRNA RP11-909B2.1 could be a promising independent prognostic factors in CRC.The circulatory RNA based biomarker panel can act as potential biomarker for CRC diagnosis and prognosis. 	MIMAT0003263	J Cell Biochem 2018 Aug 119, 6869-6881 doi:10.1002/jcb.26884 PMID:29737552
1590	LncRNA	RP4	miR-7-5p	SH3GLB1	Sw480	Colorectal Cancer	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,etc	29531464	Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer.	Cell proliferation,tumor growth,and early apoptosis in SW480 cells were negatively regulated by lncRNA RP4.Functional experiments indicated that lncRNA RP4 directly upregulated SH3GLB1 expression by acting as a competing endogenous RNA (ceRNA) for miR-7-5p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3K and Akt phosphorylation in colorectal cancer cells in vivo. 	MIMAT0000252	World J Gastroenterol 2018 Mar 7 24, 1004-1012 doi:10.3748/wjg.v24.i9.1004 PMID:29531464
1591	LncRNA	SMARCC2	miR-551b-3p	TMPRSS4	Ags, Sgc-7901, Mkn-45,Bgc-823, Hgc-27,Gastric Cancer Tissues 	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown, etc	29337109	Molecular mechanisms of lncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis in gastric cancer. 	LncRNA SMARCC2 inhibits the expression of miR-551b-3p through binding to its mRNA response elements in gastric cancer cells. Overexpression of LncRNA SMARCC2 enhances the proliferation and migration of gastric cancer cells, while inhibition of LncRNA SMARCC2 does the opposite. TMPRSS4 is a direct target gene of miR-551b-3p. We conclude that miR-551b-3p functions as a tumour suppressor gene in gastric cancer, and its function is regulated by LncRNA SMARCC2/miR-551b-3p/TMPRSS4 axis.  	MIMAT0003233	Cancer Lett 2018 Apr 1 418, 84-96 doi:10.1016/j.canlet.2018.01.032 PMID:29337109
1592	LncRNA	SNHG1	miR-145-5p	NAUK1	Hek293T , N69, Cne,Hne-1, Npc Tissues，	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29575772	LncRNA SNHG1 functions as a ceRNA to antagonize the effect of miR-145a-5p on the  down-regulation of NUAK1 in nasopharyngeal carcinoma cell	Down-regulation of SNHG1 facilitated the expression of miR-145-5p and further suppressed the level of NAUK1 in CNE and HNE-1 cells. Silencing of SNHG1, up-regulation of miR-145-5p and inhibition of NAUK1 by relative transfection all attenuated the aggressiveness of CNE and HNE-1 cells both in vivo and in vitro. Moreover, the impaired cell migration and invasion by SNHG1 siRNA could be rescued by cotransfection of miR-145-5p in CNE and HNE-1 cells. LncRNA SNHG1 promoted the expression of NUAK1 by down-regulating miR-145-5p and thus promoted the aggressiveness of nasopharyngeal carcinoma cells through AKT signalling pathway and induced epithelial-mesenchymal transition (EMT).  	MIMAT0000437	J Cell Mol Med 2019 Apr 23, 2351-2361 doi:10.1111/jcmm.13497 PMID:29575772
1593	LncRNA	SNHG1	miR-145-5p	MTDH	H358, H1299, A549, And Sk-Mes-1,  Bronchial Epithelial Cell Line	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29466052	Long noncoding RNA SNHG1 promotes non-small cell lung cancer progression by up-regulating MTDH via sponging miR-145-5p.	SNHG1 directly bound to microRNA (miRNA)-145-5p,isolating miR-145-5p from its target gene MTDH.Inhibition of SNHG1 suppressed NSCLC cell viability, proliferation,migration, and invasion in vitro, but its effect was rescued by miR-145-5p inhibition. These results demonstrate that SNHG1 contributes to NSCLC progression by modulating the miR-145-5p/ MTDH axis, and it could potentially be a therapeutic target as well as a diagnostic marker.	MIMAT0000437	Faseb j 2018 Jul 32, 3957-3967 doi:10.1096/fj.201701237RR PMID:29466052
1594	LncRNA	SNHG12	miR-424-5p	NA	C33A, Me-180, Caski, Hela And Siha,Nc104 	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay	29533945	Upregulation of Long Non-Coding RNA Small Nucleolar RNA Host Gene 12 Contributes to Cell Growth and Invasion in Cervical Cancer by Acting as a Sponge for MiR-424-5p.	NHG12 was found to be abnormally elevated in human cervical cancer tissues compared with paired adjacent normal tissues.high SNHG12 expression in tumor tissues was significantly correlated with vascular involvement,lymph node metastasis,advanced FIGO stage and poor prognosis.the knockdown of SNHG12 was found to inhibit proliferation,migration and invasion of cervical cancer cells in vitro, and silencing SNHG12 was shown to suppress tumor growth in a nude mouse model. SNHG12 functioned as an endogenous sponge for miR-424-5p, thereby downregulating the expression of miR-424-5p in cervical cancer.the inhibition of miR-424-5p in SNHG12-depleted cells partially reversed the effects on cervical cancer cell apoptosis, adhesion and invasion.the tumor-promoting role of SNHG12 is to function as a molecular sponge, which negatively regulates miR-424-5p.	MIMAT0001341	Cell Physiol Biochem 2018  45, 2086-2094 doi:10.1159/000488045 PMID:29533945
1595	LncRNA	SNHG12	miR-199a	Argo2	Sgc-7901, Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,RIP,Luciferase reporter assay	29565487	LncRNA SNHG12 regulated the proliferation of gastric carcinoma cell BGC-823 by targeting microRNA-199a/b-5p.  	The expression of lncRNA SNHG12 was positively linked with the proliferative ability of BGC-823. RIP experiment confirmed the binding abilities of lncRNA SNHG12,microRNA-199a/b-5p and Argo2. 	MIMAT0000231	Eur Rev Med Pharmacol Sci 2018 Mar 22, 1297-1306 doi:10.26355/eurrev_201803_14471 PMID:29565487
1596	LncRNA	SNHG12	miR-199b-5p	Argo2	Sgc-7901, Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,RIP,Luciferase reporter assay	29565487	LncRNA SNHG12 regulated the proliferation of gastric carcinoma cell BGC-823 by targeting microRNA-199a/b-5p.  	The expression of lncRNA SNHG12 was positively linked with the proliferative ability of BGC-823. RIP experiment confirmed the binding abilities of lncRNA SNHG12,microRNA-199a/b-5p and Argo2. 	MIMAT0000263	Eur Rev Med Pharmacol Sci 2018 Mar 22, 1297-1306 doi:10.26355/eurrev_201803_14471 PMID:29565487
1597	LncRNA	SNHG14	miR-145	PI3K	Bgc-823, Sgc-7901, And Hgc-27	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29667771	Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis.	LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells.Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability,migration,invasion,and promoted cell apoptosis.In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. Our findings indicate that up-regulation of lncRNA SNHG14 may contribute to gastric cancer development via targeting miR-145/SOX9 axis and involving in PI3K/AKT/mTOR pathway. 	MI0000461	J Cell Biochem 2018 Aug 119, 6905-6913 doi:10.1002/jcb.26889 PMID:29667771
1598	LncRNA	SNHG14	miR-145	AKT	Bgc-823, Sgc-7901, And Hgc-27	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29667771	Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis.	LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells.Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability,migration,invasion,and promoted cell apoptosis.In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. Our findings indicate that up-regulation of lncRNA SNHG14 may contribute to gastric cancer development via targeting miR-145/SOX9 axis and involving in PI3K/AKT/mTOR pathway. 	MI0000461	J Cell Biochem 2018 Aug 119, 6905-6913 doi:10.1002/jcb.26889 PMID:29667771
1599	LncRNA	SNHG14	miR-145	mTOR	Bgc-823, Sgc-7901, And Hgc-27	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29667771	Long non-coding RNA SNHG14 contributes to gastric cancer development through targeting miR-145/SOX9 axis.	LncRNA SNHG14 was markedly up-regulated in gastric cancer tissues and cells.Knockdown of SNHG14 significantly inhibited SGC-7901 cell viability,migration,invasion,and promoted cell apoptosis.In addition, miR-145 was negatively regulated by SNHG14 and the effects of SNHG14 knockdown on cell viability, apoptosis, migration, invasion, and the expression of apoptosis-related proteins and EMT-markers were reversed by inhibition of miR-145 at the same time. Furthermore, SOX9 was verified as a functional target of miR-145, and miR-145 regulated tumor malignant behaviors through regulating SOX9. Besides, knockdown of SNHG14 inhibited the expression of p-PI3K, p-AKT, and p-mTOR and promoted PTEN expression, where miR-145 inhibition had opposite effects. Moreover, the activated PI3K/AKT/mTOR pathway caused by miR-145 inhibition was counteracted after knockdown of SOX9. Our findings indicate that up-regulation of lncRNA SNHG14 may contribute to gastric cancer development via targeting miR-145/SOX9 axis and involving in PI3K/AKT/mTOR pathway. 	MI0000461	J Cell Biochem 2018 Aug 119, 6905-6913 doi:10.1002/jcb.26889 PMID:29667771
1600	LncRNA	SNHG14	miR-92a-3p	NA	U251 And U87 Normal Brain Glial Cell Line 	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	29552296	The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma.	SNHG14 was found to be downregulated in human glioma tissues and cell lines. there was a negative correlation between SNHG14 expression and miR-92a-3p expression.miR-92a-3p could directly bind to SNHG14. miR-92a-3p was significantly upregulated in glioma and acted as an oncogene in glioma cells by inhibiting Bim. Moreover, mechanistic investigations showed that miR-92a-3p could reverse the tumour suppressive effects induced by SNHG14 in glioma, indicating that SNHG14 may act as an endogenous sponge that competes for binding to miR-92a-3p.	MIMAT0000092	Oncotarget 2018 Feb 23 9, 12112-12124 doi:10.18632/oncotarget.23960 PMID:29552296
1601	LncRNA	SNHG15	miR-486	CDK14	A549,H460,Sk-Mes-1,Calu-3,Nhbe, Hek-293T, Nsclc Tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29630731	Long non-coding RNA SNHG15 promotes CDK14 expression via miR-486 to accelerate non-small cell lung cancer cells progression and metastasis. 	LncRNA SNHG15 was significantly upregulated in NSCLC tissue samples and cells, and its overexpression was associated with poor prognosis of NSCLC patients. In vitro, loss-of-functional cellular experiments showed that SNHG15 silencing significantly inhibited the proliferation, promoted the apoptosis, and induced the cycle arrest at G0//G1 phase. In vivo, xenograft assay showed that SNHG15 silencing suppressed tumor growth of NSCLC cells. Besides, SNHG15 silencing decreased CDK14 protein expression both in vivo and vitro. Bioinformatics tools and luciferase reporter assay confirmed that miR-486 both targeted the 3'-UTR of SNHG15 and CDK14 and was negatively correlated with their expression levels. In summary, our study conclude that the ectopic overexpression of SNHG15 contribute to the NSCLC tumorigenesis by regulating CDK14 protein via sponging miR-486, providing a novel insight for NSCLC pathogenesis and potential therapeutic strategy for NSCLC patients.  	MI0002470	J Cell Physiol 2018 Sep 233, 7164-7172 doi:10.1002/jcp.26543 PMID:29630731
1602	LncRNA	SNHG15	miR-98	E2F5	Achn, Osrc-2, 786-O, 769-P, Caki-1 And Hk-2	Renal Cancer	Homo sapiens (human)	qPCR,Western blot etc	29750422	Knockdown of SNHG15 suppresses renal cell carcinoma proliferation and EMT by regulating the NF-κB signaling pathway.	In the present study, the expression levels of small nucleolar RNA host gene 15 (SNHG15) were significantly upregulated in renal cell carcinoma (RCC) tissues and cell lines compared with in adjacent tissues and a proximal tubule epithelial cell line, as determined by reverse transcriptionquantitative polymerase chain reaction. Subsequently, knockdown of SNHG15 expression with small interfering RNA inhibited RCC proliferation, invasion and migration, was determined by western blotting and Transwell assays. Furthermore, the present study suggested that SNHG15 may be involved in the nuclear factorκB signaling pathway, induce the epithelialmesenchymal transition process, and promote RCC invasion and migration. SNHG8 has been suggested as a potential biomarker and drug target candidate for gastric cancer, and is associated with EpsteinBarr virus. SNHG16 exerts its effects by acting as a ceRNA, competitively binding miR98 with E2F transcription factor 5 protein.	MI0000100	Int J Oncol 2018 Jul 53, 384-394 doi:10.3892/ijo.2018.4395 PMID:29750422
1603	LncRNA	SNHG16	miR-4518	PRMT5	Nhas, U251, H4, Sw1783 And Ln229	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29529599	LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma.	SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518.SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway. the overall survival rate was lower in the high SNHG12 expression group than in the low SNHG12 expression group	MI0016884	Cell Physiol Biochem 2018  45, 1975-1985 doi:10.1159/000487974 PMID:29529599
1604	LncRNA	SNHG16	miR-4518	PI3K	Nhas, U251, H4, Sw1783 And Ln229	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29529599	LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma.	SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518.SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway. the overall survival rate was lower in the high SNHG12 expression group than in the low SNHG12 expression group	MI0016884	Cell Physiol Biochem 2018  45, 1975-1985 doi:10.1159/000487974 PMID:29529599
1605	LncRNA	SNHG16	miR-4518	Akt	Nhas, U251, H4, Sw1783 And Ln229	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29529599	LncRNA SNHG16 Functions as an Oncogene by Sponging MiR-4518 and Up-Regulating PRMT5 Expression in Glioma.	SNHG16 was highly expressed in glioma tissues and cell lines, which was related to poorer clinicopathologic features and shorter survival time. Knockdown of SNHG16 inhibits the viability and induces apoptosis of glioma cells. Further investigation revealed that SNHG16 could up-regulate the expression of miR-4518 targeted gene PRMT5 via acting as an endogenous sponge of miR-4518.SNHG16 also affects the expression of Bcl-2 family proteins and the activation of PI3K/Akt signaling pathway. the overall survival rate was lower in the high SNHG12 expression group than in the low SNHG12 expression group	MI0016884	Cell Physiol Biochem 2018  45, 1975-1985 doi:10.1159/000487974 PMID:29529599
1606	LncRNA	SNHG20	miR-140-5p	ADAM10	Hela, Siha, C33A, Sw756, And Me-180	Cervical Cancer	Homo sapiens (human)	qPCR etc	29604594	LncRNA SNHG20 promotes cell proliferation and invasion via miR-140-5p-ADAM10 axis in cervical cancer.	SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could  act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion. 	MIMAT0000431	Biomed Pharmacother 2018 Jun 102, 749-757 doi:10.1016/j.biopha.2018.03.024 PMID:29604594
1607	LncRNA	SNHG5	miR-377	CASP1	Pc9 ,A549,Hek-293T,Lung Adenocarcinoma Tissues	Lung Cancer	Homo sapiens (human)	Western blot,in vitro knockdown,Luciferase reporter assay,RNAi etc	29592872	The long non-coding RNA SNHG5 regulates gefitinib resistance in lung adenocarcinoma cells by targeting miR-377/CASP1 axis.  	Overexpression of SNHG5 suppressed the expression of miR-377, while the knockdown of SNHG5 increased the miR-377 expression. MiR-377 expression was significantly upregulated in LAD specimens with acquired gefitinib resistance and was negatively correlated with SNHG5 expression. In addition, CASP1 was predicted as a downstream target of miR-377.Knockdown of CASP1 in SNHG5-overexpression PC9GR cells abolished their gefitinib resistance. 	MI0000785	Biosci Rep 2018 Aug 31 38 doi:10.1042/bsr20180400 PMID:29592872
1608	LncRNA	SNHG7	miR-503	Cyclin-D1	Lncap, Vcap, 22Rv1, Du145, Pc-3	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot etc	29571017	Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503.	SNHG7 expression was significantly up-regulated in prostate cancer tissue and cell lines.Besides, the overexpression of SNHG7 was closely correlated with the poor prognosis. In vitro and in vivo, SNHG7 knockdown markedly inhibited prostate cancer proliferation and cycle-related protein (CDK4, CDK6, Cyclin D1), induced cell cycle arrest at G0/G1 phase and suppressed tumor growth. Moreover, miR-503 was predicted by bioinformatics tools and validated using luciferase reporter assay to both directly inhibited SNHG7 and Cyclin D1 expression by targeting their RNA 3'-UTR. We found that lncRNA SNHG7 acts a ceRNA for miR-503 and harbors miR-503 to positively regulates Cyclin D1 expression.	MI0003188	Biomed Pharmacother 2018 Jun 102, 326-332 doi:10.1016/j.biopha.2018.03.011 PMID:29571017
1609	LncRNA	SNHG7	miR-5095	CTNNB1	Heb, And Human Gbm Cell Lines 	Glioblastoma	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29360452	Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095.	the expression of SNHG7 was significantly upregulated in GBM tissues and cell lines compared with non-cancerous brain tissues. Furthermore,SNHG7 knockdown remarkably suppressed the proliferation, migration and invasion of A172 and U87cells while inducing their apoptosis. Subsequently,SNHG7 knockdown significantly inhibited tumor growth and metastasis invivo by using xenograft experiments in nude mice.SNHG7 directly inhibited miR-5095,which targeted the 3'UTR of CTNNB1 mRNA and subsequently downregulated the Wnt/β-catenin signaling pathway in GBM.Using rescue experiments, we demonstrated that SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095 and concomitant activation of Wnt/β-catenin signaling pathway.miR-5095 mimics inhibited the luciferase activity of A172 and U87 cells transduced with wild type SNHG7 plasmid,while mutations of the putative miR-5095 binding sites in SNHG7 abrogated this effect	MI0018001	Biochem Biophys Res Commun 2018 Feb 5 496, 712-718 doi:10.1016/j.bbrc.2018.01.109 PMID:29360452
1610	LncRNA	SNHG8	miR-152	c-Met	Ishikawa,Japan, Hec1-A, Hec1-B, An3Ca, Rl95-2,Ec Tissue	Endometrial Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29630089	LncRNA SNHG8 participates in the development of endometrial carcinoma through regulating c-MET expression by miR-152	SNHG8 expression in endometrial carcinoma tissue was significantly higher than that in normal endometrium.After transfection with SNHG8 siRNA,the cell viability of AN3CA cells decreased, whereas the activity of Ishikawa was increased after transfection with SNHG8 overexpression plasmid.SNHG8 was bound to miR-152 and miR-152 targeted on c-MET. In addition, miR-152 mimics inhibited the expression of c-MET, and the inhibitory effect was reversed after SNHG8 overexpression. Silencing SNHG8 reduced c-MET expression, and c-MET expression was reversed after addition of miR-152 inhibitor. 	MI0000462	Eur Rev Med Pharmacol Sci 2018 Mar 22, 1629-1637 doi:10.26355/eurrev_201803_14698 PMID:29630089
1611	LncRNA	SOX2OT	miR-200a	Sox2	Bxpc-3, Capan-1, Hs766T And Hpde	Pancreatic Cancer	Homo sapiens (human)	Microarray,RIP etc	29643475	Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA  in pancreatic ductal adenocarcinoma.	We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC.We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells,exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. Finally,we observed a decreased exosomal Sox2ot expression in postoperative blood samples of PDAC patients. The exosomal lncRNA Sox2ot plays important roles in tumor progression and may be a useful maker for pancreatic cancer prognosis. 	MI0000737	Oncogene 2018 Jul 37, 3822-3838 doi:10.1038/s41388-018-0237-9 PMID:29643475
1612	LncRNA	SOX2OT	miR-200b	Sox2	Bxpc-3, Capan-1, Hs766T And Hpde	Pancreatic Cancer	Homo sapiens (human)	Microarray,RIP etc	29643475	Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA  in pancreatic ductal adenocarcinoma.	We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC.We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells,exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. Finally,we observed a decreased exosomal Sox2ot expression in postoperative blood samples of PDAC patients. The exosomal lncRNA Sox2ot plays important roles in tumor progression and may be a useful maker for pancreatic cancer prognosis. 	MI0000342	Oncogene 2018 Jul 37, 3822-3838 doi:10.1038/s41388-018-0237-9 PMID:29643475
1613	LncRNA	SOX2OT	miR-200c	Sox2	Bxpc-3, Capan-1, Hs766T And Hpde	Pancreatic Cancer	Homo sapiens (human)	Microarray,RIP etc	29643475	Tumor-derived exosomal lnc-Sox2ot promotes EMT and stemness by acting as a ceRNA  in pancreatic ductal adenocarcinoma.	We identified a lncRNA-Sox2ot from exosomes of highly invasive PDAC cells, and analyzed the expression of Sox2ot in the plasma samples and found that the plasma exosomal Sox2ot expression was high and correlated with TNM stage and overall survival rate of PDAC patients. Further research showed that Sox2ot promotes epithelial-mesenchymal transition (EMT) and stem cell like properties by regulating Sox2 expression. Sox2ot competitively binds to the miR-200 family to regulate the expression of Sox2, thus promoting invasion and metastasis of PDAC.We also confirmed the transmission of the exosomes from producer cells to recipient PDAC cells,exosomal Sox2ot can promote tumor invasion and metastasis in vitro and in vivo. We further confirmed tumor generated exosomes could excrete to tumor cell or blood circulation in vivo condition. Finally,we observed a decreased exosomal Sox2ot expression in postoperative blood samples of PDAC patients. The exosomal lncRNA Sox2ot plays important roles in tumor progression and may be a useful maker for pancreatic cancer prognosis. 	MI0000650	Oncogene 2018 Jul 37, 3822-3838 doi:10.1038/s41388-018-0237-9 PMID:29643475
1614	LncRNA	SPRY4-IT1	miR-101-3p	EZH2	Hibec, Cclp-1, Hucct1, Huh-28, Kmbc And Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29642935	SP1-induced upregulation of lncRNA SPRY4-IT1 exerts oncogenic properties by scaffolding EZH2/LSD1/DNMT1 and sponging miR-101-3p in cholangiocarcinoma.	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally,SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore,SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the  epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold.Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p. 	MIMAT0000099	J Exp Clin Cancer Res 2018 Apr 11 37, 81 doi:10.1186/s13046-018-0747-x PMID:29642935
1615	LncRNA	SPRY4-IT1	miR-101-3p	EZH2	Lovo, Rko, Sw620 And Sw480 	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28720069	Long non-coding RNA SPRY4-IT1 promotes proliferation and invasion by acting as a ceRNA of miR-101-3p in colorectal cancer cells.	SPRY4-IT1 was upregulated in human primary colorectal carcinoma tissues.Knockdown of SPRY4-IT1 inhibited colorectal carcinoma cell proliferation,migration,and invasion.Moreover,we confirmed that the expression of epithelial-mesenchymal transition-related genes was modulated through alteration of SPRY4-IT1 expression. SPRY4-IT1 could negatively regulate the expression of miR-101-3p in colorectal carcinoma cells.The bioinformatics prediction revealed putative miR-101-3p binding sites within SPRY4-IT1 transcripts. 	MIMAT0000099	Tumour Biol 2017 Jul 39, 1010428317716250 doi:10.1177/1010428317716250 PMID:28720069
1616	LncRNA	TINCR	miR-7	SP1	Mda-Mb-231,Mda-Mb-435, Mda-Mb-453, Mda-Mb-468,Mcf-7, Breast Cancer Tissue	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29614984	Up-regulation of ceRNA TINCR by SP1 contributes to tumorigenesis in breast cancer. 	TINCR was aberrantly up-regulated by SP1,which in turn stimulated cell proliferation,anchorage-independent growth and suppressed cell apoptosis in breast cancer.TINCR silencing significantly suppressed migration and invasion in vitro and xenograft tumor growth in vivo.Mechanistically, TINCR modulated KLF4 expression via competing with miR-7, which consequently contributed to its oncogenic potential.MiR-7 inhibition severely compromised TINCR silencing-elicited tumor repressive effects	MI0008947	BMC Cancer 2018 Apr 3 18, 367 doi:10.1186/s12885-018-4255-3 PMID:29614984
1617	LncRNA	TINCR	miR-544a	FBXW7	A549, H322, H460, Glc-82, Spc-A1,Lung Cancer Tumor Tissues	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP etc	29324317	TINCR suppresses proliferation and invasion through regulating miR-544a/FBXW7 axis in lung cancer. 	INCR overexpression suppressed proliferation and invasion in lung cancer cells.TINCR was confirmed as a molecular sponge of miR-544a. We further validated that miR-544a facilitated proliferation and invasion, and miR-544a could reverse TINCR-mediated anti-proliferation and anti-invasion effect in lung cancer cells. TINCR acted as a competing endogenous RNA (ceRNA) to sequester miR-544a from its target gene FBXW7. FBXW7 suppressed proliferation and invasion,and FBXW7 knockdown abolished the inhibition of TINCR on proliferation and invasion in lung cancer cells. 	MI0003515	Biomed Pharmacother 2018 Mar 99, 9-17 doi:10.1016/j.biopha.2018.01.049 PMID:29324317
1618	LncRNA	TP53TG	miR-18a	PTEN	Hbe, A549,Nsclc Tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay,RIP,in vitro knockdown etc	29588850	TP53TG1 enhances cisplatin sensitivity of non-small cell lung cancer cells through regulating miR-18a/PTEN axis.	TP53TG1 level was downregulated in NSCLC tissues and cell lines. Upregulated TP53TG1 enhanced cisplatin sensitivity and apoptosis of A549/DDP cells, while TP53TG1 depletion inhibited cisplatin sensitivity and apoptosis of A549 cells.TP53TG1 suppressed miR-18a expression in A549 cells. Moreover,TP53TG1-mediated enhancement effect on cisplatin sensitivity was abated following the restoration of miR-18a expression in A549/DDP cells, while si-TP53TG1-induced decrease of cisplatin sensitivity and apoptosis was counteracted by miR-18a inhibitor in A549 cells. Furthermore, TP53TG1 promoted PTEN expression via inhibiting miR-18a.Finally,TP53TG1 sensitized NSCLC cells to cisplatin in vivo.TP53TG1 increased the sensitivity of NSCLC cells to cisplatin by modulating miR-18a/PTEN axis, elucidating a novel approach to boost the effectiveness of chemotherapy for NSCLC.  	MI0000072	Cell Biosci 2018  8, 23 doi:10.1186/s13578-018-0221-7 PMID:29588850
1619	LncRNA	TP73-AS1	miR-142	HMGB1	U118, U251, Snb119, Ln229,Shg-44, Brain Glioma Tissues	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	28379612	The Long Non-Coding RNA TP73-AS1 Interacted With miR-142 to Modulate Brain Glioma Growth Through HMGB1/RAGE Pathway	P73 antisense RNA 1T, also known as TP73-AS1 or PDAM, is a long non-coding RNA which may regulate apoptosis via regulation of p53-dependent anti-apoptotic genes.TP73-AS1 was specifically upregulated in brain glioma tissues and cell lines,and was associated with poorer prognosis in patients with glioma. TP73-AS1 knocking down suppressed human brain glioma cell proliferation and invasion in vitro, as well as HMGB1 protein.MiR-142 has been reported to play a pivotal role in cancers,here we observed that TP73-AS1 and miR-142 could negatively regulate each other. Results from luciferase assays suggested that TP73-AS1 might compete with HMGB1 for miR-142 binding.Further,HMGB1/RAGE was involved in TP73-AS1/miR-142 regulation of glioma cell proliferation and invasion. In glioma tissues, TP73-AS1 and HMGB1 expression was up-regulated, whereas miR-142 expression was down-regulated. Data from the present study revealed that TP73-AS1 promoted the brain glioma growth and invasion through acting as a competing endogenous RNA (ceRNA) to promote HMGB1 expression by sponging miR-142. 	MI0000458	J Cell Biochem 2018 Apr 119, 3007-3016 doi:10.1002/jcb.26021 PMID:28379612
1620	LncRNA	TP73-AS1	miR-124	p53	Ptbe Tissues, Human Brain Glioma Cells 	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29412778	The Long Noncoding RNA TP73-AS1 Interacted with miR-124 to Modulate Glioma Growth by Targeting Inhibitor of Apoptosis-Stimulating Protein of p53.	TP73-AS1 was specifically upregulated in brain glioma cell lines and promoted glioma cell growth through targeting miR-124. TP73-AS1 knocking down suppressed human brain glioma cell proliferation, invasion, and metastasis in vitro.The inhibitory effect of TP73-AS1 knocking down on glioma cell proliferation and invasion could partly be restored by miR-124 inhibition.In addition, miR-124-dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in TP73-AS1-induced brain glioma cell growth.	MI0000443	DNA Cell Biol 2018 Feb 37, 117-125 doi:10.1089/dna.2017.3941 PMID:29412778
1621	LncRNA	TUG1	miR-129-5p	AEG1	A375, Wm35,Sk-Mel-5,Sk-Mel-2,Malignant Melanoma Tissues	Melanoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29543785	Long Noncoding RNA Taurine-Upregulated Gene1 (TUG1) Promotes Tumor Growth and Metastasis Through TUG1/Mir-129-5p/Astrocyte-Elevated Gene-1 (AEG-1) Axis in Malignant Melanoma.	Downregulation of either TUG1 or AEG1 suppressed cell growth and metastasis.miR-129-5p can bind directly to AEG1 and TUG1 can directly sponge miR-129-5p.Inhibition of TUG1 expression suppressed the expression of Bcl-2, MMP-9, and cyclin D1, and raised the level of cleaved caspase3 by modulating AEG1 level in melanoma cells. Inhibition of TUG1 reduced the growth of tumors in vivo and improved the chemosensitivity of A375 cells to cisplatin and 5-FU.Reduction of TUG1 level suppressed cell growth and metastasis by regulating AEG1 expression mediated by targeting miR-129-5p.	MIMAT0000242	Med Sci Monit 2018 Mar 15 24, 1547-1559 doi:10.12659/msm.906616 PMID:29543785
1622	LncRNA	TUG1	miR-145	KLF4	Ags1, Mgc803, Sgc7901, And Mkn53,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	MALAT1 synchronize the expression level of KLF4 and miR-145 and MALAT1 had a strong impact than TUG1 in regulating KLF4 through sponging miR-145.	MI0000461	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
1623	LncRNA	TUG1	miR-132-3p	SOX4	U2Os, Mg-63, Saos-2, And 143B And The Human Normal Osteoblastic Cell Line 	Osteosarcoma	Homo sapiens (human)	RT-qPCR, Western blot, Luciferase reporter assay, in vitro knockdown	29436190	Long Non-Coding RNA TUG1 Promotes Proliferation and Inhibits Apoptosis of Osteosarcoma Cells by Sponging miR-132-3p and Upregulating SOX4 Expression.	TUG1 was highly expressed in human OS tissues,OS cell lines,and primary OS cells.TUG1 knockdown hindered proliferation and induced apoptosis in human OS cell lines and primary OS cells.Moreover, TUG1 inhibited miR-132-3p expression by direct interaction,and introduction of miR-132-3p inhibitor partly abrogated the effect of TUG1 knockdown on the proliferation and apoptosis of OS cells.Furthermore, SOX4 was validated as a target of miR-132-3p.Further functional analyses revealed that miR-132-3p inhibited proliferation and induced apoptosis of OS cells, while this effect was greatly abated following SOX4 overexpression.Moreover, TUG1 knockdown suppressed proliferation and promoted apoptosis by upregulating miR-132-3p and downregulating SOX4 in primary OS cells.	MIMAT0000426	Yonsei Med J 2018 Mar 59, 226-235 doi:10.3349/ymj.2018.59.2.226 PMID:29436190
1624	LncRNA	TUG1	miR-29c	NA	Control And Bc Cell Lines 	Bladder Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,in vitro knockdown	29321088	Upregulation of long non-coding RNA TUG1 promotes bladder cancer cell 5 proliferation, migration and invasion by inhibiting miR-29c.	TUG1 was upregulated and microRNA-29c(miR-29c) was downregulated in BC tissues and cell lines.Furthermore, TUG1 knockdown markedly increased the expression of miR-29c in vitro.On the contrary, overexpression of TUG1 remarkably decreased the expression of miR-29c.Transfection with plasmids containing mutant TUG1 has no effect on the expression of miR-29c. There were direct interactions between miR-29c and the binding sites of TUG1.In addition,the inhibitory effects of small interfering RNA specific for TUG1 on BC cell proliferation,migration and invasion were reversed by downregulation of miR-29c.  	MI0000735	Oncol Res 2018 Aug 23 26, 1083-1091 doi:10.3727/096504018x15152085755247 PMID:29321088
1625	LncRNA	TUNAR	miR-200a	Rac1	Shg44, U251, Gl15,U87,	Glioma	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay etc	29540255	Long non-coding RNA TUNAR represses growth, migration and invasion of human glioma cells through regulating miR-200a and Rac1.	TUNAR was confirmed to positively regulate miR-200a,and knockdown of miR-200a reversed TUNAR-induced inhibitory effects on glioma cells. Further, Rac1 was negatively regulated by miR-200a.Rac1 overexpression abolished miR-200a overexpression-induced inhibition of viability,migration, and invasion, as well as increase of apoptosis.Besides,Rac1 knockdown inhibited glioma by inactivating the Wnt/β-catenin and NF-κB signal pathways.TUNAR played an anti-cancer role in glioma cells by upregulating miR-200a and inhibiting Rac1,thereby might represent a potential therapeutic target for the treatment of human glioma. 	MI0000737	Oncol Res 2018 Dec 27 27, 107-115 doi:10.3727/096504018x15205622257163 PMID:29540255
1626	LncRNA	TUSC7	miR-10a	MDR1	U87,Gbm Tissues	Glioblastoma	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown etc	29397407	Long non-coding RNA TUSC7 inhibits temozolomide resistance by targeting miR-10a in glioblastoma. 	Low expression of TUSC7 in GBM cells and tissues resistant to TMZ.Upregulation of TUSC7 suppressed both TMZ resistance and expression of multidrug resistance protein 1 (MDR1) in U87TR cells.TUSC7 acted by directly targeting and silencing expression of miR-10a gene,and miR-10a mediated TUSC7-induced inhibition on TMZ resistance in U87TR cells. 	MI0000266	Cancer Chemother Pharmacol 2018 Apr 81, 671-678 doi:10.1007/s00280-018-3522-y PMID:29397407
1627	LncRNA	TUSC7	miR-224	DESC1	Te-13, Kyse140, Ec9706, Kyse30,Het-1A,Escc Tissues 	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,luciferase reporter assays	29530057	LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1.	TUSC7 was downregulated in ESCC tissues and cells,and low TUSC7 indicated worse overall survival.TUSC7 specifically bound to miR-224, and we proved miR-224 was upregulated in ESCC and negatively correlated with TUSC7 expression.Overexpression of TUSC7/inhibition of miR-224 suppressed cell proliferation,colony formation and chemotherapy resistance of ESCC cells,and promoted cell apoptosis.TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224.TUSC7 suppressed chemotherapy resistance of ESCC by downregulating miR-224 to modulate DESC1/EGFR/AKT pathway. 	MI0000301	J Exp Clin Cancer Res 2018 Mar 12 37, 56 doi:10.1186/s13046-018-0724-4 PMID:29530057
1628	LncRNA	TUSC7	miR-224	EGFR	Te-13, Kyse140, Ec9706, Kyse30,Het-1A,Escc Tissues 	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,luciferase reporter assays	29530057	LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1.	TUSC7 was downregulated in ESCC tissues and cells,and low TUSC7 indicated worse overall survival.TUSC7 specifically bound to miR-224, and we proved miR-224 was upregulated in ESCC and negatively correlated with TUSC7 expression.Overexpression of TUSC7/inhibition of miR-224 suppressed cell proliferation,colony formation and chemotherapy resistance of ESCC cells,and promoted cell apoptosis.TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224.TUSC7 suppressed chemotherapy resistance of ESCC by downregulating miR-224 to modulate DESC1/EGFR/AKT pathway. 	MI0000301	J Exp Clin Cancer Res 2018 Mar 12 37, 56 doi:10.1186/s13046-018-0724-4 PMID:29530057
1629	LncRNA	TUSC7	miR-224	AKT	Te-13, Kyse140, Ec9706, Kyse30,Het-1A,Escc Tissues 	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,luciferase reporter assays	29530057	LncRNA-TUSC7/miR-224 affected chemotherapy resistance of esophageal squamous cell carcinoma by competitively regulating DESC1.	TUSC7 was downregulated in ESCC tissues and cells,and low TUSC7 indicated worse overall survival.TUSC7 specifically bound to miR-224, and we proved miR-224 was upregulated in ESCC and negatively correlated with TUSC7 expression.Overexpression of TUSC7/inhibition of miR-224 suppressed cell proliferation,colony formation and chemotherapy resistance of ESCC cells,and promoted cell apoptosis.TUSC7 suppressed the proliferation and chemotherapy resistance of ESCC cells by increasing DESC1 expression via inhibiting miR-224.TUSC7 suppressed chemotherapy resistance of ESCC by downregulating miR-224 to modulate DESC1/EGFR/AKT pathway. 	MI0000301	J Exp Clin Cancer Res 2018 Mar 12 37, 56 doi:10.1186/s13046-018-0724-4 PMID:29530057
1630	LncRNA	UCA1	miR-126	PI3K	K562, Hl60,  Mg63, Hhfob1.19Hek293	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29762824	Long noncoding RNA UCA1 promotes cell proliferation, migration and invasion of human leukemia cells via sponging miR-126	lncRNA UCA1 was upregulated in ML cell lines.Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion,and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126,and the anti-ML actions of miR-126 were abolished by RAC1 overexpression.Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression.	MI0000471	Eur Rev Med Pharmacol Sci 2018 Apr 22, 2233-2245 doi:10.26355/eurrev_201804_14809 PMID:29762824
1631	LncRNA	UCA1	miR-126	AKT	K562, Hl60,  Mg63, Hhfob1.19Hek293	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29762824	Long noncoding RNA UCA1 promotes cell proliferation, migration and invasion of human leukemia cells via sponging miR-126	lncRNA UCA1 was upregulated in ML cell lines.Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion,and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126,and the anti-ML actions of miR-126 were abolished by RAC1 overexpression.Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression.	MI0000471	Eur Rev Med Pharmacol Sci 2018 Apr 22, 2233-2245 doi:10.26355/eurrev_201804_14809 PMID:29762824
1632	LncRNA	UCA1	miR-126	JAK	K562, Hl60,  Mg63, Hhfob1.19Hek293	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29762824	Long noncoding RNA UCA1 promotes cell proliferation, migration and invasion of human leukemia cells via sponging miR-126	lncRNA UCA1 was upregulated in ML cell lines.Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion,and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126,and the anti-ML actions of miR-126 were abolished by RAC1 overexpression.Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression.	MI0000471	Eur Rev Med Pharmacol Sci 2018 Apr 22, 2233-2245 doi:10.26355/eurrev_201804_14809 PMID:29762824
1633	LncRNA	UCA1	miR-126	STAT	K562, Hl60,  Mg63, Hhfob1.19Hek293	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29762824	Long noncoding RNA UCA1 promotes cell proliferation, migration and invasion of human leukemia cells via sponging miR-126	lncRNA UCA1 was upregulated in ML cell lines.Knockdown of lncRNA UCA1 inhibited cell viability, migration, invasion,and prompted apoptosis of ML cells in vitro. LncRNA UCA1 could bind with miR-126 and downregulate miR-126 expression. Simultaneously, the anti-growth and anti-metastasis actions of lncRNA UCA1 knockdown on ML cells were reversed by miR-126 suppression. RAC1 was a target gene of miR-126,and the anti-ML actions of miR-126 were abolished by RAC1 overexpression.Moreover, PI3K/AKT and JAK/STAT signaling pathways were blocked by miR-126 overexpression while were activated by RAC1 overexpression.	MI0000471	Eur Rev Med Pharmacol Sci 2018 Apr 22, 2233-2245 doi:10.26355/eurrev_201804_14809 PMID:29762824
1634	LncRNA	UCA1	miR-206	VEGF	Sibcb,Cervical Cancer Tissues	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29523226	Downregulation of lncRNA UCA1 inhibits proliferation and invasion of cervical cancer cells through miR-206 expression.  	Interference of lncRNA UCA1 inhibited cell proliferation,migration,invasion,and viability. Results of the luciferase reporter assay revealed a binding site between lncRNA UCA1 and miR-206. Knockdown of lncRNA UCA1 could directly upregulate miR-206 expression. VEGF downregulation was also observed after knockdown of lncRNA UCA1.	MIMAT0000462	Oncol Res 2018 Mar 9, 10.3727/096504018x15185714083446 doi:10.3727/096504018x15185714083446 PMID:29523226
1635	LncRNA	UCA1	miR-182	PFKFB2	U251 And U87Mg	Glioblastoma	Homo sapiens (human)	qPCR etc	29655792	Long non-coding RNA UCA1/miR-182/PFKFB2 axis modulates glioblastoma-associated stromal cells-mediated glycolysis and invasion of glioma cells.	lncRNA UCA1/miR-182 axis has been regarded as a nodal driver of glioma invasion mediated by GB-associated stromal cells (GASCs) and GASC-secreted chemokine CXCL14.In clinical specimens, CXCL14 upregulation in GASCs also correlated with poor prognosis. Notably, CXCL14-high GASCs mediated lncRNA UCA1 upregulation and miR-182 downregulation in glioma cells. Moreover, miR-182 directly bound to the fructose-2,6-biphosphatase PFKFB2.UCA1/miR-182 axis thereby modulated GASC-induced glycolysis in glioma cells. Overall, UCA1/miR-182/PFKFB2 axis modulates chemokine CXCL14 secretion, glycolysis and invasion of glioma cells in GASCs. 	MI0000272	Biochem Biophys Res Commun 2018 Jun 7 500, 569-576 doi:10.1016/j.bbrc.2018.04.091 PMID:29655792
1636	LncRNA	UCA1	miR-1	COX6B2	Cervical Cancer tissues	Cervical Cancer	Homo sapiens (human)	qPCR etc	29620291	Integrated analysis of long noncoding RNA competing interactions revealed potential biomarkers in cervical cancer: Based on a public database.	HOTAIR and UCA1 both were significantly higher expressed in GC tumor tissues than adjacent non-tumor tissues.The results from the qRT-PCR validation in 82 newly diagnosed GC patients and the above bioinformatics results were 100% in agreement.To further analyze the association between  the 2 key lncRNAs and clinicopathological characteristics of 82 GC patients,we found that HOTAIR was significantly associated with tumor size and lymphatic metastasis,and UCA1 was significantly associated with tumor size, TNM stage and  lymphatic metastasis. HOTAIR and UCA1 were found to be significantly associated with overall survival.The miR-1was downexpressed when lncRNA UCA1 was overexpressed in glioma cells.mRNA XIRP1 was found to interact with miRNA miR-133a-3p.Key miRNA miR-133a-3p was predicted to target key lncRNA HOTAIR.	MI0000651	Mol Med Rep 2018 Jun 17, 7845-7858 doi:10.3892/mmr.2018.8846 PMID:29620291
1637	LncRNA	UCA1	miR-7-5p	EGFR	Mgc-803  And  Bgc-823	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot RIP etc	29723509	Long non-coding RNA UCA1 upregulation promotes the migration of hypoxia-resistant gastric cancer cells through the miR-7-5p/EGFR axis.	UCA1 was upregulated in HRGC cells, which promoted their migration.miR-7-5p could bind to specific sites of UCA1 to regulate the target EGFR through competitive endogenous RNA function.UCA1 directly interacted with miR-7-5p and decreased the binding of miR-7-5p to the EGFR 3'-untranslated region,which suppressed the degradation of EGFR mRNA by miR-7-5p.Therefore,long-term hypoxia induced UCA1 to promote cell migration by enhancing the expression of EGFR.This study thus reveals a new mechanism by which a hypoxic microenvironment promotes tumor metastasis, and highlights UCA1 as a potential biomarker for predicting the metastasis of gastric cancer to guide clinical treatment. 	MIMAT0000252	Exp Cell Res 2018 Jul 15 368, 194-201 doi:10.1016/j.yexcr.2018.04.030 PMID:29723509
1638	LncRNA	UCA1	miR-129	SOX4	769P, 786O, Achn, A498, Caki2	Renal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29760557	UCA1 promotes cell proliferation and invasion and inhibits apoptosis through regulation of the miR129-SOX4 pathway in renal cell carcinoma.	UCA1 expression was upregulated in RCC tissue and cells, and higher UCA1 expression was associated with advanced pathogenic status and poor prognosis of RCC patients. UCA1 knockdown suppressed proliferation and invasion and induced apoptosis in RCC cells. UCA1 inhibited miR129 expression by direct interaction in RCC cells. miR129 overexpression inhibited cell proliferation and invasion and promoted apoptosis. Moreover, miR129 downregulation abrogated UCA1 knockdown-mediated antiproliferation, anti-invasion, and proapoptosis effects in RCC cells. Furthermore, UCA1 acted as a ceRNA of miR129 to enhance target-gene SOX4 expression in RCC cells. UCA1 promoted cell proliferation and invasion and inhibited apoptosis by regulating SOX4 via miR129 in RCC, offering a promising therapeutic target and prognosis marker for RCC patients. 	MIMAT0000242	Onco Targets Ther 2018  11, 2475-2487 doi:10.2147/ott.S160192 PMID:29760557
1639	LncRNA	UCA1	miR-122-5p	IMP1	Mda-Mb-231, T47D And Mcf7	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc	29669595	IMP1 regulates UCA1-mediated cell invasion through facilitating UCA1 decay and decreasing the sponge effect of UCA1 for miR-122-5p.	In breast cancer cells,IMP1 interacts with UCA1 via the "ACACCC" motifs within UCA1 and destabilizes UCA1 through the recruitment of CCR4-NOT1 deadenylase complex.Meanwhile,binding of IMP1 prevents the association of miR-122-5p with UCA1,thereby shifting the availability of miR-122-5p from UCA1 to the target mRNAs and reducing the UCA1-mediated cell invasion.Accordingly, either IMP1 silencing or UCA1 overexpression resulted in reduced levels of free miR-122-5p within the cytoplasm, affecting miR-122-5p in regulating its target mRNAs.Our study provides initial evidence that interaction between IMP1 and UCA1 enhances UCA1 decay and competes for miR-122-5p binding,leading to the liberation of miR-122-5p activity and the reduction of cell invasiveness. 	MIMAT0000421	Breast Cancer Res 2018 Apr 18 20, 32 doi:10.1186/s13058-018-0959-1 PMID:29669595
1640	LncRNA	UCA1	miR-125a	HK2	Hl60 And Hs-5	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29663500	Knockdown of LncRNA-UCA1 suppresses chemoresistance of pediatric AML by inhibiting glycolysis through the microRNA-125a/hexokinase 2 pathway.	UCA1 expression was upregulated following ADR-based chemotherapy.Knockdown of UCA1 increased the cytotoxic effect of ADR and inhibited HIF-1α-dependent glycolysis in ADR-resistant AML cells. Additionally, UCA1 functioned as a ceRNA of miR-125a by directly binding to miR-125a. HK2,a target of miR-125a,was positively regulated by UCA1 in HL60 and HL60/ADR cells.More notably, UCA1 overexpression overturned miR-125-mediated inhibition on HIF-1α-dependent glycolysis in HL60 and HL60/ADR cells.Furthermore, 2-deoxy-glucose (2-DG) exposure inhibited HIF-1α-dependent glycolysis,and attenuated UCA1-induced increase of chemoresistance in HL60 and HL60/ADR cells.We conclude that knockdown of UCA1 plays a positive role in overcoming the chemoresistance of pediatric AML,through suppressing glycolysis by the miR-125a/HK2 pathway, contributing to a better understanding of the molecular mechanism of chemoresistance in AML. 	MI0000469	J Cell Biochem 2018 Jul 119, 6296-6308 doi:10.1002/jcb.26899 PMID:29663500
1641	LncRNA	UCA1	miR-18a	YAP1	Skbr-3	Breast Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29408336	Long non-coding RNA UCA1 desensitizes breast cancer cells to trastuzumab by impeding miR-18a repression of Yes-associated protein 1.	UCA1 knockdown upregulated miR-18a and promoted miR-18a repression of Yes-associated protein 1 (YAP1).A luciferase reporter assay confirmed the association of miR-18a with wild-type UCA1 but not with UCA1 mutated at the predicted miR-18a-binding site. The direct targeting of YAP1 by miR-18a was verified by the observation that miR-18a mimic suppressed luciferase expression from a construct containing the YAP1 3' untranslated region.Meanwhile,reciprocal repression of UCA1 and miR-18a were found to be Argonaute 2-dependent. Knockdown of YAP1 recapitulated the effect of UCA1 silencing by reducing the viability of trastuzumab-treated breast cancer cells, whereas inhibition of miR-18a abrogated UCA1 knockdown-induced improvement of trastuzumab sensitivity in breast cancer cells.	MI0000072	Biochem Biophys Res Commun 2018 Feb 19 496, 1308-1313 doi:10.1016/j.bbrc.2018.02.006 PMID:29408336
1642	LncRNA	UCA1	miR-193a	HMGB1	H520, Skmes1	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown, RNAi	29355524	Long non-coding RNA UCA1 promotes lung cancer cell proliferation and migration via microRNA-193a/HMGB1 axis.	UCA1 down-regulation inhibited cell proliferation and migration in both SKMES-1 and H520 lung cancer cells.Then we demonstrated that repressed UCA1 promoted the miR-193a expression and miR-193a could bind to the predicted binding site of UCA1. We then dissected the role of miR-193a in lung cancer and proved the anti-tumor role of miR-193a. Furthermore,miR-193a displayed its role in lung cancer via modulating the HMGB1 expression. In addition, over-expression of HMGB1 could restore the UCA1 knockdown induced repression of cell proliferation and migration.	MI0000487	Biochem Biophys Res Commun 2018 Feb 5 496, 738-745 doi:10.1016/j.bbrc.2018.01.097 PMID:29355524
1643	LncRNA	UCA1	miR-590-3p	CREB1	Ags, Mkn-28, Sgc-7901,Mkn-45,Ges-1, Gc Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29516678	UCA1 promotes cell proliferation and invasion of gastric cancer by targeting CREB1 sponging to miR-590-3p.   	UCA1 is significantly higher in GC tissues and cells compared with adjacent normal tissues and a gastric epithelium cell line, respectively. Higher UCA1 expression was associated with lymph node metastasis, TNM stage, and poor overall survival (OS) in GC patients. In vitro functional studies confirmed that UCA1 promotes cell proliferation,colony formation ability,and cell invasion in GC cells. We demonstrated that knockdown of UCA1 inhibits tumor growth in vivo. The double luciferase reporter,RNA-binding protein immunoprecipitation assay,and RNA pull down assay demonstrated that miR-590-3p serves as a target for UCA1. UCA1 promoted cell proliferation and invasion by negatively regulating miR-590-3p expression. Moreover,we demonstrated that CREB1 is a downstream target of miR-590-3p and UCA1 activates CREB1 expression by sponging to miR-590-3p. Thus, these results showed that UCA1 functions as an oncogene in GC and may be a target for treatment of GC.	MIMAT0004801	Cancer Med 2018 Apr 7, 1253-1263 doi:10.1002/cam4.1310 PMID:29516678
1644	LncRNA	UCA1	miR-96	FOXO3	PANC-1, SW1990, AsPC-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29500870	LncRNA UCA1 impacts cell proliferation, invasion, and migration of pancreatic cancer through regulating miR-96/FOXO3.	The colocalization relationship between lncRNA UCA1 and miR-96 was detected by RNA FISH. Whether UCA1 could target miR-96 and whether miR-96 could target FOXO3 3'UTR were verified by dual-luciferase reporter gene assay. High expression of lncRNA UCA1 and FOXO3 and low expression of miR-96 were shown in pancreatic cancer. Inhibition of UCA1 suppressed pancreatic tumor cell proliferation, colony formation, and metastasis, while inhibition of miR-96 promoted pancreatic cancer cell progression. FOXO3 was the downstream target gene of miR-96 and showed the opposite effects. LncRNA UCA1 promoted cell proliferation, invasion, migration and inhibited cell apoptosis of pancreatic cancer through down-regulating miR-96  and up-regulating FOXO3	MI0000098	IUBMB Life 2018 Apr 70, 276-290 doi:10.1002/iub.1699 PMID:29500870
1645	LncRNA	UCA1	miR-301a	CXCR4	Mhcc97,Mg63,Hfob1.19,Os-732 ,Neuroblastoma Tissues 	Liver Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown	29523218	Knockdown of urothelial carcinoma associated 1 suppressed cell growth and migration through regulating miR-301a and CXCR4 in osteosarcoma MHCC97 cells.	Knockdown of UCA1 reduced cell viability, inhibited migration and invasion, and promoted cell apoptosis.However,the effect of UCA1  knockdown on cell growth and migration was blocked by miR-301a overexpression,whose expression was regulated by UCA1. We also found that miR-301a positively regulated the CXCR4 expression. CXCR4 inhibition reversed the effect of miR-301a overexpression on cell growth and migration.Moreover,miR-301a activated the Wnt/-catenin and NF-B pathways via regulating CXCR4.	MI0000745	Oncol Res 2018 Dec 27 27, 55-64 doi:10.3727/096504018x15201143705855 PMID:29523218
1646	LncRNA	XIST	miR-185	TGFB1	Mgc803, Bgc823, Sgc-7901,Ags ,Katoiii	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,etc	29053187	XIST promotes gastric cancer (GC) progression through TGF-β1 via targeting miR-185. 	A negative correlation was indicated between XIST and miR-185 in GC cells.In addition,TGF-β1 was predicted as a target gene of miR-185. miR-185 can modulate TGF-β1 expression negatively in vitro.Moreover, we found that sh-XIST inhibited GC development via decreasing TGF-β1 by upregulating miR-185 in vitro.Therefore,we speculated that XIST can act as a competing endogenous lncRNA (ceRNA) to regulate TGF-β1 by sponging miR-185 in GC.Taken these together,it was indicated that XIST/miR-185/TGF-β1 axis participated in the development of GC. XIST could act as a potential prognostic biomarker in GC development.  	MI0000482	J Cell Biochem 2018 Mar 119, 2787-2796 doi:10.1002/jcb.26447 PMID:29053187
1647	LncRNA	XIST	miR-367	ZEB2	A549 , H226 ,Nsclc Tissues	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown,RNAi,RIP etc	29339211	Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer.  	lncRNA XIST and ZEB2 mRNA in metastatic NSCLC tissues.Knockdown of lncRNA XIST inhibited ZEB2 expression,and repressed TGF-β-induced EMT and NSCLC cell migration and invasion. Being in consistent with the in vitro findings, the in vivo experiment of metastasis showed that knockdown of lncRNA XIST inhibited pulmonary metastasis of NSCLC cells in mice. In addition, knockdown of ZEB2 expression can inhibit TGF-β-induced EMT and NSCLC cell migration and invasion. Mechanistically, lncRNA XIST and ZEB2 were targets of miR-367 and miR-141.Furthermore, both miR-367 and  miR-141 expression can be upregulated by knockdown of lncRNA XIST. Taken together, our study reveals that lncRNA XIST can promote TGF-β-induced EMT and cell invasion and metastasis by regulating miR-367/miR-141-ZEB2 axis in NSCLC. 	MI0000775	Cancer Lett 2018 Apr 1 418, 185-195 doi:10.1016/j.canlet.2018.01.036 PMID:29339211
1648	LncRNA	XIST	miR-141	ZEB2	A549 , H226 ,Nsclc Tissues	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown,RNAi,RIP etc	29339211	Long non-coding RNA XIST promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-367/141-ZEB2 axis in non-small-cell lung cancer.  	lncRNA XIST and ZEB2 mRNA in metastatic NSCLC tissues.Knockdown of lncRNA XIST inhibited ZEB2 expression,and repressed TGF-β-induced EMT and NSCLC cell migration and invasion. Being in consistent with the in vitro findings, the in vivo experiment of metastasis showed that knockdown of lncRNA XIST inhibited pulmonary metastasis of NSCLC cells in mice. In addition, knockdown of ZEB2 expression can inhibit TGF-β-induced EMT and NSCLC cell migration and invasion. Mechanistically, lncRNA XIST and ZEB2 were targets of miR-367 and miR-141. Furthermore, both miR-367 and  miR-141 expression can be upregulated by knockdown of lncRNA XIST. Taken together, our study reveals that lncRNA XIST can promote TGF-β-induced EMT and cell invasion and metastasis by regulating miR-367/miR-141-ZEB2 axis in NSCLC. 	MI0000457	Cancer Lett 2018 Apr 1 418, 185-195 doi:10.1016/j.canlet.2018.01.036 PMID:29339211
1649	LncRNA	XIST	miR-200c	ZEB2	 5637,T24	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29559853	LncRNA XIST/miR-200c regulates the stemness properties and tumourigenicity of human bladder cancer stem cell-like cells. 	lncRNA XIST possesses the reverse function in bladder cancer cells.miR-200c overexpression and XIST knockdown could inhibit cell clone formation,self-renewal ability and EMT in BCSC-like cells. miR-200c knockdown could restore the tumour growth inhibition caused by XIST knockdown.	MI0000650	Cancer Cell Int 2018  18, 41 doi:10.1186/s12935-018-0540-0 PMID:29559853
1650	LncRNA	XIST	miR-194-5p	MAPK1	Mhcc97L, Mhcc97H, Hepg2, Smmc7221, Huh7, Bel-7402	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29227532	LncRNA XIST functions as a molecular sponge of miR-194-5p to regulate MAPK1 expression in hepatocellular carcinoma cell.	XIST was significantly upregulated in HCC tissues and associated with tumor size and vascular invasion.Gain- and loss-of-function of XIST further presented that XIST promoted the progression of HCC cells, including proliferation, migration,and invasion. Moreover, silencing of XIST could inhibit tumor growth in vivo.XIST could target miR-194-5p and thus decrease miR-194-5p expression.Besides that,restoring XIST could reverse the inhibitory effect of miR-194-5p on the proliferation and invasion of HCC cells.We further elucidated such rescue role might through derepressing MAPK1 expression,the target of miR-194-5p.We pinpointed that LncRNA XIST can act as a ceRNA for MAPK1 mRNA through miR-194-5p. These results deepen our understanding of the role of XIST in HCC.	MIMAT0000460	J Cell Biochem 2018 Jun 119, 4458-4468 doi:10.1002/jcb.26540 PMID:29227532
1651	LncRNA	XIST	miR-137	PXN	A549, H450, 95D, H1299, Spc-A-1 And H522 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29337100	Knockdown of long non-coding RNA XIST inhibits cell viability and invasion by regulating miR-137/PXN axis in non-small cell lung cancer.	XIST was substantially upregulated and miR-137 was aberrantly downregulated in NSCLC tissues and cells. XIST was identified to function as a competitive endogenous RNA (ceRNA) for miR-137 to promote NSCLC cell viability and invasion. Additionally, our results suggested that miR-137 targeted the 3'UTR of paxillin (PXN) to suppress NSCLC cell viability and invasion. Meanwhile, miR-137 was negatively correlated with PXN expression while XIST was positively correlated with PXN expression.More importantly, XIST positively regulated PXN levels by sponging miR-137 in vitro and in vivo. 	MI0000454	Int J Biol Macromol 2018 May 111, 623-631 doi:10.1016/j.ijbiomac.2018.01.022 PMID:29337100
1652	LncRNA	XIST	miR-491-5p	NA	Cne1, Cne2, Sune-1 And C666-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot etc	29219216	Knockdown of long non-coding RNA XIST suppresses nasopharyngeal carcinoma progression by activating miR-491-5p.	XIST expression was significantly upregulated in NPC tissues and cell lines.Knockdown of XIST inhibited NPC cell proliferation and invasion and induced apoptosis in vitro,as well as suppressed NPC tumor growth in vivo.Further analysis revealed that XIST and miR-491-5p interact with and repress each other. XIST may function as an endogenous miR-491-5p sponge to regulate the target gene of miR-491-5p. 	MIMAT0002807	J Cell Biochem 2018 May 119, 3936-3944 doi:10.1002/jcb.26535 PMID:29219216
1653	LncRNA	XIST	miR-34a	WNT1	Ncm460, Lovo, Sw480, Hct116 And Ht29 	Colon Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29679755	Long non-coding RNA XIST sponges miR-34a to promotes colon cancer progression via Wnt/β-catenin signaling pathway.	XIST expression level was upregulated in colon cancer tissues and cell lines.In addition,the growth rate of cells transfected with si-XIST was significantly decreased compared to that with si-NC, which was reversed by miR-34a targeted with 3'-UTR. Moreover,miR-34a suppressed the expression of WNT1 by binding with the 3'-UTR, which interact with WNT1 to inhibit the proliferation of cells.Furthermore, miR-34a inhibitor rescued the dysregulation of WNT1, β-catenin,cyclinD1,c-Myc and MMP-7 by si-XIST.Besides, XIST knockdown inhibited tumor growth in vivo. In short, the current study suggests XIST plays as an important role in colon cancer progression targeted by miR-34a via Wnt/β-catenin signaling pathway,providing a novel insight for the pathogenesis and underlying therapeutic target for colon cancer. 	MI0000268	Gene 2018 Jul 30 665, 141-148 doi:10.1016/j.gene.2018.04.014 PMID:29679755
1654	LncRNA	XIST	miR-155	CDX1	Mcf-7, Zr-75-1, Hcc-1937, Mda-Mb-231, Mda-Mb-468 And Mda-Mb-453	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29550489	Long non-coding RNA XIST inhibited breast cancer cell growth, migration, and invasion via miR-155/CDX1 axis.	XIST was significantly down-regulated in breast cancer tissues and cell lines. Further functional analysis indicated that overexpression of XIST remarkably inhibited breast cancer cell growth, migration, and invasion.The results of luciferase reporter assays verified that miR-155 was a direct target of XIST in breast cancer. Moreover,caudal-type homeobox 1 (CDX1) was identified as a direct target of miR-155 and miR-155/CDX1 rescued the effects of XIST in breast cancer cells.Taken together,XIST is down-regulated in breast cancer and suppresses breast cancer cell growth, migration, and invasion via the miR-155/CDX1 axis. 	MI0000681	Biochem Biophys Res Commun 2018 Apr 15 498, 1002-1008 doi:10.1016/j.bbrc.2018.03.104 PMID:29550489
1655	LncRNA	XIST	miR-195-5p	YAP	Mg-63, 143B, Mhm And Sjsa1, Osteoblast Cell Line, 	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29384226	The expression of LncRNA RP11-87C12.5 is high in newly diagnosed ALL group and low in complete remission ALL group. In B-ALL, the expression of IncRNA RP11-87C12.5 significantly enhances in cCD79a low expression group. In newly diagnosed ALL group, compared with low expression group, lncRNA RP11-87C12.5 high expression group have higer remission rate and relapse rate, but the difference was not statistically significant.Long non-coding RNA XIST promotes osteosarcoma progression by targeting YAP via miR-195-5p.	XIST expression was significantly upregulated in OS tissues and cell lines and negatively correlated with clinical prognosis.XIST knockdown inhibited cancer cell proliferation and invasion in vitro, inhibited the EMT of OS cells in vitro, and suppressed subcutaneous tumor growth in vivo. Further analysis demonstrated that XIST regulated YAP expression by functioning as a competing endogenous RNA that sponged miR-195-5p in OS cells. XIST directly interacted with miR-195-5p and decreased the binding of miR-195-5p to the YAP 3'UTR, which suppressed the degradation of YAP mRNA by miR-195-5p.	MIMAT0000461	J Cell Biochem 2018 Jul 119, 5646-5656 doi:10.1002/jcb.26743 PMID:29384226
1656	LncRNA	XIST	miR-34a-5p	NA	Panc-1, Aspc-1, Mia Paca-2,Hpac, Cfapc-1,Bxpc-3,Pc Tissues 	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,in vitro knockdown,Luciferase reporter assay etc	29393501	Long non-coding RNA XIST exerts oncogenic functions in pancreatic cancer via miR-34a-5p.	Overexpression of XIST significantly promoted the proliferation,migration and invasion, and suppressed cell apoptosis of BxPC-3 cells;knockdown of XIST significantly inhibited the proliferation,migration and invasion,and accelerated cell apoptosis of PANC-1 cells. Furthermore, BxPC-3 and PANC-1 cells transfected with different vectors were injected subcutaneously into nude mice to explore tumor formation. We found that XIST promoted tumor formation in vivo.Subsequently, we found that microRNA-34a-5p (miR34a-5p) was downregulated in PC tissues,and predicted a poor prognosis in PC patients. In addition, the results  indicated that miR-34a-5p is a target gene of XIST and was significantly negatively correlated with XIST. More importantly,miR-34a-5p rescued the facilitation of malignant behavior mediated by XIST. These results indicated that XIST and miR-34a-5p may be potential effective therapeutic targets for PC. 	MIMAT0000255	Oncol Rep 2018 Apr 39, 1591-1600 doi:10.3892/or.2018.6245 PMID:29393501
1657	LncRNA	ZEB1	miR-205-5p	ADPGK-AS1	Hek-293T, Panc-1 And Sw-1991	Pancreatic Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot etc	29667486	LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB2-mediated epithelial-mesenchymal transition.	MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal.ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR.The expression of MiR-205-5p was negatively correlated with proliferation,migration and invasion, and positively correlated with apoptosis rate of PC cells,while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1.ADPGK-AS1 strongly promoted the tumorigenesis via downregulating miR-205-5p expression and induced the EMT process in vivo.ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT. 	MIMAT0000266	Cancer Biol Ther 2018 Jul 3 19, 573-583 doi:10.1080/15384047.2018.1423912 PMID:29667486
1658	LncRNA	ZEB1	miR-205-5p	ADPGK-AS1	Hek-293T, Panc-1 And Sw-1991	Pancreatic Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot etc	29667486	LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB2-mediated epithelial-mesenchymal transition.	MiR-205-5p was low-expressed while ZEB1 and ADPGK-AS1 were high-expressed in PC tissues and cells compared with the normal.ADPGK-AS1 could directly target miR-205-5p and miR-205-5p could directly target ZEB1 3'UTR.The expression of MiR-205-5p was negatively correlated with proliferation,migration and invasion, and positively correlated with apoptosis rate of PC cells,while ZEB1 and ADPGK-AS1 had an inversed effect. Further in vitro and in vivo investigation indicated that epithelial-mesenchymal transition (EMT) could be restrained by miR-205-5p through targeting ZEB1.ADPGK-AS1 strongly promoted the tumorigenesis via downregulating miR-205-5p expression and induced the EMT process in vivo.ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT. 	MIMAT0000266	Cancer Biol Ther 2018 Jul 3 19, 573-583 doi:10.1080/15384047.2018.1423912 PMID:29667486
1659	LncRNA	ZEB1-AS1	miR-101	ZEB1	Sw480, Dld-1, Hct116, Sw620, And Ht29, A Normal Colonic Cell Line 	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29511455	Interplay between long noncoding RNA ZEB1-AS1 and miR-101/ZEB1 axis regulates proliferation and migration of colorectal cancer cells.	ZEB1-AS1 was upregulated in CRC tissues and cells. MiR-101 was downregulated in CRC tissues and negatively correlated with ZEB1-AS1 and ZEB1 expression levels in CRC. Functional experiments showed that, consistent with ZEB1-AS1 depletion, miR-101 overexpression and ZEB1 depletion inhibited the proliferation and migration of CRC cells. Overexpression of miR-101 partially abolished the effects of ZEB1-AS1 on the proliferation and migration of these cells. Moreover, combined ZEB1-AS1 depletion and miR-101 overexpression significantly inhibited cell proliferation and migration of the CRC cells. Hence, ZEB1-AS1 functioned as a molecular sponge for miR-101 and relieved the inhibition of ZEB1 caused by miR-101.	MI0000103	Am J Transl Res 2018  10, 605-617,  PMID:29511455
1660	LncRNA	ZEB2-AS1	miR-204	HMGB1	AsPC-1, HPAC, Cfpac-1, and Panc-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	29753015	LncRNA ZEB2-AS1 promotes pancreatic cancer cell growth and invasion through regulating the miR-204/HMGB1 axis.	the expression level of ZEB2-AS1 was elevated in pancreatic cancer cell lines and tissues.ZEB2-AS1 inhibition decreased cell growth and invasion in pancreatic cancer.Mechanismly,ZEB2-AS1 exerted as a ceRNA and negatively regulated miR-204 expression.In addition, HMGB1 was identified as a down-stream target of miR-204. The miR-204/HMGB1 axis mediated ZEB2-AS1's effect on pancreatic cancer.lncRNA ZEB2-AS1 may be a candidate prognostic biomarker and a target for new therapies in pancreatic cancer patients. 	MI0000284	Int J Biol Macromol 2018 Sep 116, 545-551 doi:10.1016/j.ijbiomac.2018.05.044 PMID:29753015
1661	LncRNA	ZFAS1	miR-329	NA	T24, Rt4, 5637, Sw780, Se780 And Um-Uc-3	Bladder Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay etc	29653362	The long noncoding RNA ZFAS1 facilitates bladder cancer tumorigenesis by sponging miR-329.	ZFAS1 expression was significantly upregulated in bladder cancer tissues and cell lines.Furthermore, Kaplan-Meier analysis revealed that high ZFAS1 expression was significantly associated with unfavorable progression free survival (PFS) and overall survival(OS) of bladder cancer patients.Moreover, silencing of ZFAS1 expression could markedly suppress bladder cancer cells proliferation and colony formation, arrest cell cycle, promote cell apoptosis and inhibit cell migration in vitro. In addition, bioinformatics analysis, luciferase reporter assay,and pull down assay revealed that ZFAS1 straightly interacted with miR-329.Lastly, rescue experiments confirmed that miR-329 inhibitor reversed the tumor suppressing roles of ZFAS1 knockdown on bladder cancer cells.Collectively, our results illuminated that ZFAS1 could serve as an oncogene in the tumorigenesis of bladder cancer,and discovered the functional regulatory network of ZFAS1 sponging miR-329. 	MI0001725	Biomed Pharmacother 2018 Jul 103, 174-181 doi:10.1016/j.biopha.2018.04.031 PMID:29653362
1662	LncRNA	LINC00319	miR-32	AURKA	Paa,Agi Y-83A,A549,Hbe,Anip-973	Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28800794	Long Intergenic Noncoding RNA 319 (linc00319) Promotes Cell Proliferation and Invasion in Lung Cancer Cells by Directly Downregulating the Tumor Suppressor MiR-32.	linc00319 increased the proliferation and invasion of A549 cells,and suppressed cell apoptosis.linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32. High level of HOTAIR was demonstrated to be correlated with invasion, metastasis,and poor survival in lung cancer patients.	MI0000090	Oncol Res 2017 Aug 11, 10.3727/096504017x15016337254650 doi:10.3727/096504017x15016337254650 PMID:28800794
1663	LncRNA	LINC00319	miR-32	SOX9	Paa,Agi Y-83A,A549,Hbe,Anip-973	Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28800794	Long Intergenic Noncoding RNA 319 (linc00319) Promotes Cell Proliferation and Invasion in Lung Cancer Cells by Directly Downregulating the Tumor Suppressor MiR-32.	linc00319 increased the proliferation and invasion of A549 cells,and suppressed cell apoptosis.linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32. High level of HOTAIR was demonstrated to be correlated with invasion, metastasis,and poor survival in lung cancer patients.	MI0000090	Oncol Res 2017 Aug 11, 10.3727/096504017x15016337254650 doi:10.3727/096504017x15016337254650 PMID:28800794
1664	LncRNA	LINC00319	miR-32	TWIST1	Paa,Agi Y-83A,A549,Hbe,Anip-973	Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28800794	Long Intergenic Noncoding RNA 319 (linc00319) Promotes Cell Proliferation and Invasion in Lung Cancer Cells by Directly Downregulating the Tumor Suppressor MiR-32.	linc00319 increased the proliferation and invasion of A549 cells,and suppressed cell apoptosis.linc00319 promotes cell proliferation and invasion in lung cancer cells by directly binding with and downregulating the tumor suppressor miR-32. High level of HOTAIR was demonstrated to be correlated with invasion, metastasis,and poor survival in lung cancer patients.	MI0000090	Oncol Res 2017 Aug 11, 10.3727/096504017x15016337254650 doi:10.3727/096504017x15016337254650 PMID:28800794
1665	LncRNA	C2DAT1	miR-34a-5p	Sirt1	Mg63,Os-732,Hfob1.19	Osteosarcoma	Homo sapiens (human)	Luciferase Reporter Assay,qPCR,Western blot,etc.	28810936	LncRNA C2dat1 Promotes Cell Proliferation, Migration, and Invasion by Targeting MiR-34a-5p in Osteosarcoma Cells.	C2dat1 suppression reduced cell viability,invasion and migration,while increased cell apoptosis in OS-732 cells. MiR-34a-5p was a target of C2dat1.	MIMAT0000255	Oncol Res 2018 Jun 11 26, 753-764 doi:10.3727/096504017x15024946480113 PMID:28810936
1666	LncRNA	AC023115.3	miR-26a	GSK3b-Mcl1	U87Mg And U251Mg	Glioblastoma	Homo sapiens (human)	qPCR,westen blot,microarray etc.	28499919	Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy	AC023115.3 was preferentially enriched in the Ago2-containing microRNA ribonucleoprotein complexes (miRNPs) compared with the immunoprecipitates with control IgG,indicating that AC023115.3 is present in the Ago2-containing miRNPs likely through an association with microRNAs.AC023115.3 was induced by cisplatin and suppressed glioma chemoresistance.AC023115.3 inhibited cisplatin-induced autophagy.AC023115.3 promoted cisplatin-induced apoptosis via decreasing autophagy. AC023115.3 acted as a miR-26a sponge and inhibited its activity.AC023115.3 sensitized glioma cell to cisplatin-induced apoptosis through regulation of the miR-26a-GSK3β-Mcl1 signalling.	MI0000083	Biochim Biophys Acta Mol Cell Res 2017 Aug 1864, 1393-1404 doi:10.1016/j.bbamcr.2017.05.008 PMID:28499919
1667	LncRNA	AF113014	miR-20a	Egr2	Smmc7721, Hepg2, Sk-Hep1 And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28542387	LncRNA-AF113014 promotes the expression of Egr2 by interaction with miR-20a to inhibit proliferation of hepatocellular carcinoma cells	AF113014 is differentially expressed between HCC cell lines and normal hepatocytes.Furthermore,we discovered that AF113014 up-regulated Egr2 expression through interacting with miR-20a.	MI0000076	PLoS One 2017  12, e0177843 doi:10.1371/journal.pone.0177843 PMID:28542387
1668	LncRNA	AF119895	miR-6508-3p	NXF3	L02 And Hcc Cell Lines 	Hepatocellular Carcinoma	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29274323	AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p.	AF119895 promoted migration and invasion of HCC cells both in vitro and in vivo.Furthermore,we identified that NXF3 was a downstream target of AF119895.NXF3 depletion could decrease HCC cells migration and invasion.In addition,AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3'UTR.	MIMAT0025473	Exp Cell Res 2018 Feb 1 363, 129-139 doi:10.1016/j.yexcr.2017.12.016 PMID:29274323
1669	LncRNA	AGER1	miR-185	AGER	I.E., Pc9, L78, A549, Glc-82, Sbc-5, 95D, Nci-H460, Nci-H292 And Nci- H1395	Lung Cancer	Homo sapiens (human)	qRT-PCR,western blotting,Luciferase reporter assay	29068471	Long non-coding RNA AGER-1 functionally upregulates the innate immunity gene AGER and approximates its anti-tumor effect in lung cancer.	LncAGER expression was moderately correlated with AGER expression underlying a mechanism that lncAGER upregulates AGER by competitively binding to miRNA-185. LncAGER was significantly down-regulated in 76.4% of lung cancer tissues compared to adjacent normal tissues due to promoter hypermethylation.Over-expression of the lncRNA resulted in significant decreases in proliferation rate, migration ability,colony formation efficiency of lung cancer cells and tumor growth in nude mice.	MI0000482	Mol Carcinog 2018 Mar 57, 305-318 doi:10.1002/mc.22756 PMID:29068471
1670	LncRNA	AK027145	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
1671	LncRNA	ANRIL	miR-323	BRI3	Mb Daoy	Medulloblastoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28513871	Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on Proliferation and Migration by Targeting miR-323.	ANRIL was up-regulated in MB and its silence significantly lowered cell viability and migration but promoted cell apoptosis.ANRIL acted as a sponge of miR-323 and its silence functioned through up-regulating miR-323.BRI3 and CDK6 were target genes of miR-323 and the effect of BRI3 on DAOY cells was the same as ANRIL.ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3.ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR-323-mediated regulation of BRI3,which could activate p38 MAPK,ERK,and AKT as well as Wnt signaling pathway.	MI0000807	J Cell Biochem 2017 Dec 118, 4735-4744 doi:10.1002/jcb.26141 PMID:28513871
1672	LncRNA	ANRIL	miR-323	CDK6	Mb Daoy	Medulloblastoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28513871	Potential Role of Long Non-Coding RNA ANRIL in Pediatric Medulloblastoma Through Promotion on Proliferation and Migration by Targeting miR-323.	ANRIL was up-regulated in MB and its silence significantly lowered cell viability and migration but promoted cell apoptosis.ANRIL acted as a sponge of miR-323 and its silence functioned through up-regulating miR-323.BRI3 and CDK6 were target genes of miR-323 and the effect of BRI3 on DAOY cells was the same as ANRIL.ANRIL suppression could reduce phosphorylated levels of p38 MAPK, ERK and AKT, and inhibit Wnt signaling pathway through positively regulating BRI3.ANRIL inhibition repressed cell proliferation and migration but promoted cell apoptosis through miR-323-mediated regulation of BRI3,which could activate p38 MAPK,ERK,and AKT as well as Wnt signaling pathway.	MI0000807	J Cell Biochem 2017 Dec 118, 4735-4744 doi:10.1002/jcb.26141 PMID:28513871
1673	LncRNA	ANRIL	miR-199a	NA	Mda-Mb-231, Mda-Mb-468, Mda-Mb-453,Tb-549,Mcf-7 And Td-47	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	28961506	Long non-coding RNA ANRIL promotes carcinogenesis via sponging miR-199a in triple-negative breast cancer.	Expression level of ANRIL was up-regulated in TNBC tumor tissue and cell lines compared to noncancerous tissue and non-TNBC cells.the up-regulated ANRIL expression was closely correlated to poor prognosis.ANRIL knockdown interfered by interference oligonucleotide could markedly suppress TNBC cells proliferation and enhance apoptosis. ANRIL overexpression modulated TNBC tumorigenesis through acting as molecular 'sponge' for miR-199a.	MI0000242	Biomed Pharmacother 2017 Dec 96, 14-21 doi:10.1016/j.biopha.2017.09.107 PMID:28961506
1674	LncRNA	ANRIL	miR-34a	Sirt1	U251	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29057547	Knockdown of long non-coding RNA ANRIL inhibits proliferation, migration, and invasion but promotes apoptosis of human glioma cells by upregulation of miR-34a. 	ANRIL was upregulated in glioma cells and its suppression inhibited cell proliferation, migration and invasion but promoted cell apoptosis. ANRIL acted as a sponge of miR-34a,and Sirt1 is a target of miR-34a.Then, Sirt1 was proved to function through activation of the PI3K/AKT and mTOR signaling pathways. In conclusion, ANRIL was upregulated in glioma, and its inhibition could repress cell proliferation, migration and invasion but inhibit cell apoptosis through miR-34a-mediated downregulation of Sirt1,involving the inactivation of the PI3K/AKT and mTOR pathways.  	MI0000268	J Cell Biochem 2018 Mar 119, 2708-2718 doi:10.1002/jcb.26437 PMID:29057547
1675	LncRNA	ANRIL	let-7a	NA	Cne1, Cne2, S18, Hone1, And 5-8F	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,MTT assay etc.	28117929	Downregulation of lncRNA ANRIL represses tumorigenicity and enhances cisplatin-induced cytotoxicity via regulating microRNA let-7a in nasopharyngeal carcinoma.	ANRIL was highly expressed and let-7a was downregulated in NPC tissues and cells.ANRIL could negatively regulate miR-let-7a expression. ANRIL knockdown inhibited NPC cell proliferation and induced apoptosis, while anti-let-7a reversed these effects. Combination treatment of si-ANRIL and DDP led to a lower viability, a more DNA strand breaks damage and a higher comet tail length compared with any single treatment, whereas let-7a inhibitor abolished these effects.Furthermore,depletion of ANRIL exacerbated DDP-induced cytotoxicity in NPC cells in vivo.	MI0000060	J Biochem Mol Toxicol 2017 Jul 31 doi:10.1002/jbt.21904 PMID:28117929
1676	LncRNA	ANRIL	miR-125a	NA	5-8F, Cne1, Cne2 And Hone1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assays	28402230	Downregulation of lncRNA ANRIL inhibits proliferation, induces apoptosis, and enhances radiosensitivity in nasopharyngeal carcinoma cells through regulating miR-125a	The expression of lncRNA ANRIL was upregulated in NPC tissues and cells. Moreover, knockdown of ANRIL repressed proliferation,promoted apoptosis, and improved radiosensitivity in NPC via functioning as a miR-125a sponge.	MI0000469	Cancer Biol Ther 2017 May 4 18, 331-338 doi:10.1080/15384047.2017.1310348 PMID:28402230
1677	LncRNA	ANRIL	miR-186	NA	Hela, Caski, Siha, Ht-3, And C33A	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase Reporter Assay	28550682	Long Noncoding RNA ANRIL Promotes Cervical Cancer Development by Acting as a Sponge of miR-186	ANRIL expression was significantly upregulated in cervical cancer tumors and cell lines.The bioinformatics prediction program and miR-186 directly targeted ANRIL. The expression level of miR-186 was downregulated in cervical cancer tumors and cell lines and was negatively correlated to that of ANRIL.	MI0000483	Oncol Res 2018 Apr 10 26, 345-352 doi:10.3727/096504017x14953948675449 PMID:28550682
1678	LncRNA	ANRIL	miR-122-5p	NA	Smmc772, Huh7, Hep3B, And Hepg2 And Normal Hepatic Cell Line 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,in vitro knockdown,RIP	29127494	Knockdown of LncRNA ANRIL suppresses cell proliferation, metastasis, and invasion via regulating miR-122-5p expression in hepatocellular carcinoma.	ANRIL was upregulated and miR-122-5p was downregulated in HCC tissues and cells.ANRIL was negatively correlated with miR-122-5p expression in HCC tissues.Knockdown of ANRIL or miR-122-5p overexpression suppressed HCC cell viability, colony formation ability, metastasis, and invasion.ANRIL was demonstrated to directly bind to miR-122-5p and inhibit its expression.Forced expression of ANRIL abolished the inhibitory effect of miR-122-5p overexpression on HCC progression. In vivo experiment demonstrated that ANRIL knockdown impeded tumor growth in vivo and increased miR-122-5p expression.	MIMAT0000421	J Cancer Res Clin Oncol 2018 Feb 144, 205-214 doi:10.1007/s00432-017-2543-y PMID:29127494
1679	LncRNA	ASLNC02525	miR-489-3p	TWIST1	Hepg2, Qgy-7701, Smmc-7721,L-02	Hepatocellular Carcinoma	Homo sapiens (human)	Luciferase reporter experiment,qPCR,etc.	28713968	Inhibition of proliferation and invasion of hepatocellular carcinoma cells by lncRNA-ASLNC02525 silencing and the mechanism.	ASLNC02525, as an RNA sponge, broke the negative regulation of twist1 by hsa-miRNA-489-3p,and once ASLNC02525 was silenced,the highly expressed hsa-miRNA489-3p regained its regulation on twist1 and inhibited the proliferation and invasion. 	MIMAT0002805	Int J Oncol 2017 Sep 51, 851-858 doi:10.3892/ijo.2017.4069 PMID:28713968
1680	LncRNA	ATB	miR-200b	Kindlin-2	Kyse150, Kyse140, Kyse410, Kyse520, Kyse510, Ec109, Ec9706 And Kyse30 W	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP etc	28640252	Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis.	Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo.Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2.Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2.Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC.Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients. The results showed that the median overall survival of patients with high lnc-ATB expression was 20 months,whereas the median overall survival for patients with low lnc-ATB expression was 51 months.	MI0000342	Cell Death Dis 2017 Jun 22 8, e2888 doi:10.1038/cddis.2017.245 PMID:28640252
1681	LncRNA	ATB	miR-200a	ZEB1	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000737	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1682	LncRNA	ATB	miR-200a	ZEB2	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000737	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1683	LncRNA	ATB	miR-200b	ZEB1	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000342	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1684	LncRNA	ATB	miR-200b	ZEB2	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000342	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1685	LncRNA	ATB	miR-200c	ZEB1	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000650	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1686	LncRNA	ATB	miR-200c	ZEB2	Mg63, U2Os, Saos2, And Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28469952	Long noncoding RNA ATB promotes osteosarcoma cell proliferation, migration and invasion by suppressing miR-200s	LncRNA-ATB is also upregulated in osteosarcoma tissues and cell lines,and positively associated with Enneking stage, metastasis and recurrence.Increased lncRNA-ATB level indicates poor recurrence-free survival and overall survival. Mechanistically, we found that lncRNA-ATB inhibits miR-200s, and upregulates miR-200s target genes ZEB1 and ZEB2.	MI0000650	Am J Cancer Res 2017  7, 770-783,  PMID:28469952
1687	LncRNA	ATB	miR-200a	NA	Ihh-4, Tpc-1, K1, Hth83, Nthy-Ori 3-1	Thyroid Cancer	Homo sapiens (human)	qPCR etc.	28770959	The expression and function of long noncoding RNA lncRNA-ATB in papillary thyroid cancer.	ATB is upregulated in PTC tissues compared with noncancerous tissues.ATB is upregulated and functions as an oncogene in PTC.Furthermore, lncRNA-ATB may serve as a diagnostic biomarker and therapeutic target for PTC.High-expression of lncRNA-ATB is associated with large tumor size and lymph node metastasis.LncRNA-ATB has been reported to promote cancer metastasis via binding and negatively regulating miR-200 family,and then inducing epithelial-mesenchymal transition22.	MI0000737	Eur Rev Med Pharmacol Sci 2017 Jul 21, 3239-3246,  PMID:28770959
1688	LncRNA	ATB	miR-200b	NA	Ihh-4, Tpc-1, K1, Hth83, Nthy-Ori 3-1	Thyroid Cancer	Homo sapiens (human)	qPCR etc.	28770959	The expression and function of long noncoding RNA lncRNA-ATB in papillary thyroid cancer.	ATB is upregulated in PTC tissues compared with noncancerous tissues.ATB is upregulated and functions as an oncogene in PTC.Furthermore, lncRNA-ATB may serve as a diagnostic biomarker and therapeutic target for PTC.High-expression of lncRNA-ATB is associated with large tumor size and lymph node metastasis.LncRNA-ATB has been reported to promote cancer metastasis via binding and negatively regulating miR-200 family,and then inducing epithelial-mesenchymal transition22.	MI0000342	Eur Rev Med Pharmacol Sci 2017 Jul 21, 3239-3246,  PMID:28770959
1689	LncRNA	ATB	miR-200c	NA	Ihh-4, Tpc-1, K1, Hth83, Nthy-Ori 3-1	Thyroid Cancer	Homo sapiens (human)	qPCR etc.	28770959	The expression and function of long noncoding RNA lncRNA-ATB in papillary thyroid cancer.	ATB is upregulated in PTC tissues compared with noncancerous tissues.ATB is upregulated and functions as an oncogene in PTC.Furthermore, lncRNA-ATB may serve as a diagnostic biomarker and therapeutic target for PTC.High-expression of lncRNA-ATB is associated with large tumor size and lymph node metastasis.LncRNA-ATB has been reported to promote cancer metastasis via binding and negatively regulating miR-200 family,and then inducing epithelial-mesenchymal transition22.	MI0000650	Eur Rev Med Pharmacol Sci 2017 Jul 21, 3239-3246,  PMID:28770959
1690	LncRNA	BANCR	miR-204	Notch2	A375, A875 And M14, And Human Epidermal Melanocytes	Melanoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29075789	BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR204.	the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines.Knockdown of BANCR inhibited melanoma cell proliferation and invasion,and induced cell apoptosis.the inhibitory effect of BANCR siRNA in cell growth and migration.miR204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR204.BANCR may promote melanoma cell growth through inhibition of miR204,leading to the activation of Notch2 pathway. BANCR knockdown inhibited tumor growth in vivo.   	MI0000284	Int J Oncol 2017 Dec 51, 1941-1951 doi:10.3892/ijo.2017.4173 PMID:29075789
1691	LncRNA	CAMTA1	miR-20b	VEGF	Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28550685	Long Noncoding RNA CAMTA1 Promotes Proliferation and Mobility of Human Breast Cancer Cell Line MDA- MB-231 Via Targeting miR-20b	LncCAMTA1 might promote proliferation and mobility of human breast cancer cell via binding with miR-20b.And VEGF was directly target of miR-20b and regulated activation of MAPK/ERK and JAK/STAT3 signal pathways.	MI0001519	Oncol Res 2018 May 7 26, 625-635 doi:10.3727/096504017x14953948675395 PMID:28550685
1692	LncRNA	CASC2	miR-181a	PTEN	U251, U373, Snb19, U118, And Ln229	Glioma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,MTT assay etc.	28121023	LncRNA CASC2 Interacts With miR-181a to Modulate Glioma Growth and Resistance to TMZ Through PTEN Pathway.	CASC2 expression was down-regulated in glioma tissues and cell lines.Exogenous CACS2 alone was sufficient to inhibit glioma cells' proliferation and amplified TMZ-induced repression of cell proliferation, while CACS2 knockdown could reverse this process. CASC2 up-regulates PTEN through direct inhibiting miR-181a and plays an important role in glioma sensitivity to TMZ and may serve as a potential target for cancer diagnosis and treatment.	MI0000269	J Cell Biochem 2017 Jul 118, 1889-1899 doi:10.1002/jcb.25910 PMID:28121023
1693	LncRNA	CASC2	miR-24-3p	SOX7	Hepg2, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	29091305	LncRNA CASC2 inhibited the viability and induced the apoptosis of hepatocellular carcinoma cells through regulating miR-24-3p	lncRNA CASC2,acting as an onco-suppressor, was involved in the pathogenesis and progression of HCC, and its possible mechanism was induced the growth inhibition on HCC through miR-24-3p/SOX7 axis.Our results revealed a possible regulatory mechanism in HCC pathogenesis and warranted that lncRNA CASC2 was an important regulator in HCC.	MIMAT0000080	J Cell Biochem 2018 Aug 119, 6391-6397 doi:10.1002/jcb.26479 PMID:29091305
1694	LncRNA	CASC2	miR-181a	RASSF6	Mg- 63, Sw1353, Saos- 2, Sosp-9607 And U2Os And Human Osteoblasts Hfob	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Western blot	29194827	Downregulation of lncRNA CASC2 facilitates osteosarcoma growth and invasion through miR-181a.	CASC2 expression was downregulated in osteosarcoma samples and cell lines. Moreover, we showed that downregulated expression of CASC2 was correlated with advanced TNM stage.Furthermore,overexpression of CASC2 inhibited osteosarcoma cell proliferation,colony formation, and invasion. In addition, we indicated that ectopic expression of CASC2 suppressed miR-181a expression and enhanced the expression of Ras association domain family member 6 (RASSF6),PTEN and ATM in osteosarcoma cell,which were the direct target gene of miR-181a.Moreover,we indicated that RASSF6 expression was downregulated in osteosarcoma samples and cell lines and downregulated expression of RASSF6 was correlated with advanced TNM stage. We found that the expression of RASSF6 was positively correlated with the expression of CASC2 in osteosarcoma tissues. Ectopic expression of CASC2 suppressed the osteosarcoma cell proliferation, colony formation and invasion through regulating RASSF6 expression.	MI0000269	Cell Prolif 2018 Feb 51 doi:10.1111/cpr.12409 PMID:29194827
1695	LncRNA	CASC2	miR-367	FBXW7	Mhcc-97L, Hep-3B, Hepg2, Huh7, Smmc-7721, Mhcc-97H And Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28716020	Long non-coding RNA CASC2 suppresses epithelial-mesenchymal transition of hepatocellular carcinoma cells through CASC2/miR-367/FBXW7 axis.	CASC2 expression was markedly downregulated in aggressive HCC tissues compared with non-aggressive HCCs.the CASC2/miR-367/FBXW7 axis may be a ponderable and promising therapeutic target for HCC. CASC2 low-expressing and miR-367 high-expressing HCC patients showed the poorest clinical outcome. CASC2 was recognized as a competing endogenous RNA (ceRNA) for miR-367 and could exert its anti-metastatic effects on cell migration, invasion and EMT progression through CASC2/miR-367/FBXW7 axis, which might inject some new vitalities into the development therapeutic targets for HCC.	MI0000775	Mol Cancer 2017 Jul 17 16, 123 doi:10.1186/s12943-017-0702-z PMID:28716020
1696	LncRNA	CASC2	miR-18a-5p	PTEN	Het-1A,Ec,Ec9706, Eca109, Ec-1, Kyse30, And Kyse150	Esophageal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28964779	The long noncoding RNA CASC2 inhibits tumorigenesis through modulating the expression of PTEN by targeting miR-18a-5p in esophageal carcinoma.	the expression of CASC2 to be significantly downregulated in EC tissues and EC cell lines;low expression of CACS2 was associated with advanced TNM stage and lymph node metastases.upregulation of CASC2 significantly inhibited the proliferation of EC cells.CASC2,acting as a competing endogenous RNAs (ceRNAs) of miR-18a-5p, exerts its biological effects by modulating the expression of PTEN.The expression level of PTEN is related to a patient's clinicopathologic characteristic and overall survival 	MIMAT0000072	Exp Cell Res 2017 Dec 1 361, 30-38 doi:10.1016/j.yexcr.2017.09.037 PMID:28964779
1697	LncRNA	CASC2c	miR-101	CPEB1	U251 And U87	Astrocytoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,Cell migration and invasion assay,ISH etc.	28252647	CASC2c as an unfavorable prognosis factor interacts with miR-101 to mediate astrocytoma tumorigenesis.	High CASC2c was positively correlated with astrocytoma progression, and an unfavorable prognosis factor for patients.Knockdown CASC2c inhibited proliferation and tumorgenesis. Overexpression of CASC2c promotes the malignant characteristic of astrocytoma cells.CASC2c directly bound miR-101 and mediated pre-miR-101 processing into mature miR-101, and functions as a competitor of miR-101 target genes such as CPEB1.	MI0000103	Cell Death Dis 2017 Mar 2 8, e2639 doi:10.1038/cddis.2017.11 PMID:28252647
1698	LncRNA	CASC7	miR-21	ING3	Sw480, Hct-116	Colon Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot etc.	28954383	Long non-coding RNA CASC7 inhibits the proliferation and migration of colon cancer cells via inhibiting microRNA-21	CASC7 overexpression could inhibit cell viability, migration and invasion, and promote apoptosis in CRC cells.CASC7 and ING3 were both a target of miR-21 in CRC cells,and CASC7 could control ING3 expression by regulating miR-21.Moreover, we have found that CASC7 inhibited colon cancer cell proliferation and migration via miR- 21/ING3 axis.These observations suggested that CASC7 played an important role in CRC pathogenesis and may be considered as a novel diagnostic marker of CRC.	MI0000077	Biomed Pharmacother 2017 Nov 95, 1644-1653 doi:10.1016/j.biopha.2017.09.052 PMID:28954383
1699	LncRNA	CCAT1	miR-33a	NA	M21, B16F10, Melanoma200, Mel-Rm, A375, A2058	Melanoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown	28409554	The lncRNA CCAT1 Upregulates Proliferation and Invasion in Melanoma Cells via Suppressing miR-33a.	Expression of CCAT1 was significantly upregulated in melanoma tissue and cell lines. CCAT1 knockdown observably suppressed the proliferation, migration, and invasion abilities.CCAT1 acts as an oncogenic factor in the genesis of melanoma and exerts tumor-promoting roles via sponging miR-33a, providing a novel insight for competing endogenous RNA (ceRNA) in the tumorigenesis of melanoma. 	MI0000091	Oncol Res 2018 Mar 5 26, 201-208 doi:10.3727/096504017x14920318811749 PMID:28409554
1700	LncRNA	CCAT1	miR-181a-5p	HOXA1	Rpmi-8226, U266, Mm.1S, Km3 And H929,Npcs	Multiple Myeloma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29228867	Long non-coding RNA CCAT1 promotes multiple myeloma progression by acting as a molecular sponge of miR-181a-5p to modulate HOXA1 expression.	the relative expression levels of CCAT1 were significantly upregulated in MM tissues and cell lines compared with healthy donors and normal plasma cells (nPCs).High expression of CCAT1 was correlated shorter overall survival of MM patients. CCAT1 knockdown significantly inhibited cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis in vitro, and suppressed tumor growth in vivo. MiR-181a-5p was a direct target of CCAT1, and repression of miR-181a-5p could rescue the inhibition of CCAT1 knockdown on MM progression. In addition,CCAT1 positively regulated HOXA1 expression through sponging miR-181a-5p in MM cells.lncRNA CCAT1 exerted an oncogenic role in MM by acting as a ceRNA of miR-181a-5p. These results suggest that CCAT1 may serve as a novel diagnostic marker and therapeutic target for MM.	MIMAT0000256	Cell Cycle 2018  17, 319-329 doi:10.1080/15384101.2017.1407893 PMID:29228867
1701	LncRNA	CCAT1	miR-181b	FGFR3	U87,Ln229,Hek293T	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	28475287	lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR-181b.	CCAT1 expression was significantly increased, while miR-181b decreased,in glioma tissues.Interestingly, miR-181b expression was negatively correlated with the CCAT1 level in glioma samples. Knockdown of CCAT1 notably suppressed proliferation, migration and the epithelial-mesenchymal transition (EMT) process, and promoted the apoptosis of U87 and LN229 glioma cells, which could be enhanced by transfection with miR-181b mimic while it was abolished by anti-miR-181b.CCAT1 may act as a competing endogenous RNA (ceRNA) for miR-181b, regulating the de-repression of FGFR3 and PDGFRα.	MI0000270	J Cell Biochem 2017 Dec 118, 4548-4557 doi:10.1002/jcb.26116 PMID:28475287
1702	LncRNA	CCAT1	miR-7	HOXB13	Eca-109 And Te-1	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Cell proliferation assay etc.	27956498	H3K27 acetylation activated-long non-coding RNA CCAT1 affects cell proliferation and migration by regulating SPRY4 and HOXB13 expression in esophageal squamous cell carcinoma.	lncRNA CCAT1, whose expression is significantly increased and is correlated with outcomes in Esophageal Squamous Cell Carcinoma.Further experiments revealed that CCAT1 knockdown significantly repressed the proliferation and migration both in vitro and in vivo. In cytoplasm, CCAT1 regulates HOXB13 as a molecular decoy for miR-7, a microRNA that targets both CCAT1 and HOXB13, thus facilitating cell growth and migration.	MI0008947	Nucleic Acids Res 2017 Apr 7 45, 3086-3101 doi:10.1093/nar/gkw1247 PMID:27956498
1703	LncRNA	CCAT1	miR-218-5p	CDC2	So-Rb50, Y79 And Weri-Rb1	Retinoblastoma	Homo sapiens (human)	qPCR,RNAi,Western blot,Cell migration and invasion assay etc.	28088735	Long non-coding RNA CCAT1 promotes human retinoblastoma SO-RB50 and Y79 cells through negative regulation of miR-218-5p.	The expression of lncRNA CCAT1 in RB tissues was significantly increased compared with normal tissues. It was also shown that lncRNA CCAT1 in RB SORB50, Y79 and WERI-RB1 cells was significantly higher than that in normal podiatric retina. LncRNA CCAT1 promotes the proliferation migration and invasion, and reduces cell apoptosis of SO-RB50 and Y79 cells, probably through negative modulation of miR-218-5p.	MIMAT0000275	Biomed Pharmacother 2017 Mar 87, 683-691 doi:10.1016/j.biopha.2017.01.004 PMID:28088735
1704	LncRNA	CCAT1	miR-410	ITPKB	Hct-116/Hct-8 	Colorectal Cancer	Homo sapiens (human)	qPCR etc.	29190961	Long noncoding RNA CCAT1 functions as a ceRNA to antagonize the effect of miR-410 on the down-regulation of ITPKB in human HCT-116 and HCT-8 cells	The effect of lnc CCAT1 on human HCT-116/HCT-8 cells and its potential mechanism were investigated.In present study, differential expression of CCAT1, miR-410 and ITPKB were detected in colon cancer tissues and adjacent parts. Then the prediction programs were applied to predict the target genes of miR-410.The complementary bindings of miR-410 with lnc CCAT1 and ITPKB were assessed by luciferase assays. The interaction between LncRNA CCAT1 and miR-410 was analyzed. In addition, the mRNA and protein of ITPKB and apoptosis factors were examined in cells after miR-410 overexpression or silencing. Meanwhile, MTT and flow cytometer were used to detect the cells proliferation and apoptosis level. Results showed that CCAT1 and miR-410 were up-regulated in colon cancer tissues, but ITPKB was down-regulated. Lnc CCAT1 and ITPKB were predicted to be the targets of miR-410 and the prediction were verified by luciferase assays. The expression of lnc CCAT1 and ITPKB were inhibited by miR-410 in human HCT-116/ HCT-8 cells. Meanwhile, lnc CCAT1 could lead to a decrease of miR-410. Furthermore, miR-410 overexpression could promote cell proliferation and reduce apoptosis. In summary, these data demonstrated that miR-410 could promote cell proliferation and reduce apoptosis by inhibiting ITPKB expression and the expression of lnc CCAT1 antagonized the effect of miR-410.	MI0002465	Oncotarget 2017 Nov 3 8, 92855-92863 doi:10.18632/oncotarget.21612 PMID:29190961
1705	LncRNA	CCAT1	miR-490-3p	Cyclin-D1	Mhcc97H, Mhcc97L, Hep3B, And Smcc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RNAi,Luciferase reporter assay	28381168	Long non-coding RNA colon cancer–associated transcript 1 functions as a competing endogenous RNA to regulate cyclin-dependent kinase 1 expression by sponging miR-490-3p in hepatocellular carcinoma progression	the long non-coding RNA colon cancer–associated transcript 1 was upregulated in hepatocellular carcinoma tissues,and high colon cancer–associated transcript 1 expression level was positively associated with tumor volume and American Joint Committee on Cancer stage in hepatocellular carcinoma patients.These data demonstrated that the colon cancer–associated transcript 1/miR-490-3p/cyclin-dependent kinase 1 regulatory pathway promotes the progression of hepatocellular carcinoma.	MIMAT0002806	Tumour Biol 2017 Apr 39, 1010428317697572 doi:10.1177/1010428317697572 PMID:28381168
1706	LncRNA	CCAT1	miR-218	ZFX	Amc-Hn-8 And Tu212	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR,western blot,Luciferase reporter assays etc.	28631575	Long non-coding RNA CCAT1/miR-218/ZFX axis modulates the progression of laryngeal squamous cell cancer	expressions of colon cancer–associated transcript-1 and zinc finger protein, X-linked were significantly higher while microRNA-218 expression was significantly lower in the laryngeal squamous cell cancer tissues than those in the adjacent normal tissues.Moreover, a novel CCAT1-miR-218-ZFX regulatory axis was demonstrated in the proliferation and invasion of LSCC cells in vitro and in vivo.	MI0000294	Tumour Biol 2017 Jun 39, 1010428317699417 doi:10.1177/1010428317699417 PMID:28631575
1707	LncRNA	CCAT1	miR-148a	PIK3IP1	143B, Khos, Mg-63, And U2Os	Osteosarcoma	Homo sapiens (human)	qPCR,RNAi etc.	28549102	Long non-coding RNA CCAT1/miR-148a axis promotes osteosarcoma proliferation and migration through regulating PIK3IP1	CCAT1 was upregulated in osteosarcoma tissues and cells, and was involved in the proliferation and migration of osteosarcoma via regulating miR-148a/phosphatidyl inositol 3-kinase interacting protein 1 (PIK3IP1) signal pathway.	MI0000253	Acta Biochim Biophys Sin (Shanghai) 2017 Jun 1 49, 503-512 doi:10.1093/abbs/gmx041 PMID:28549102
1708	LncRNA	CCAT1	miR-148b	caspase3	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,RIP	29024383	Down-regulation of LncRNA CCAT1 enhances radiosensitivity via regulating miR-148b in breast cancer.	CCAT1 was up-regulated and miR-148b was down-regulated in radioresistant breast cancer tissues compared with radiosensitive breast cancer tissues.CCAT1 down-regulation reduced colony formation rates and caspase3 activity in breast cancer cells under irradiation.Moreover, CCAT1 could negatively regulate miR-148b expression. Furthermore, overexpression of miR-148b suppressed colony survival fraction and caspase3 expression under irradiation in breast cancer cells,which was exacerbated by CCAT1 knockdown.	MI0000811	Cell Biol Int 2018 Feb 42, 227-236 doi:10.1002/cbin.10890 PMID:29024383
1709	LncRNA	CCAT2	miR-424	NA	Skov3, Omc685, A2780 And Ho8910,Ose386,Eoc Tissue	Ovarian Cancer	Homo sapiens (human)	Western blot,Luciferase reporter assay,in vitro knockdown	28550684	Long Noncoding RNA CCAT2 Knockdown Suppresses Tumorous Progression by Sponging miR-424 in Epithelial Ovarian Cancer.   	CCAT2 acts as competing endogenous RNA (ceRNA) or sponge via negatively targeting miR-424, providing a novel diagnostic marker and therapeutic target for EOC. 	MI0001446	Oncol Res 2018 Mar 5 26, 241-247 doi:10.3727/096504017x14953948675412 PMID:28550684
1710	LncRNA	CCAT2	miR-216b	BCL-2	Hec-1-A And Rl95-2	Endometrial Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29036788	Knockdown of lncRNA CCAT2 inhibits endometrial cancer cells growth and metastasis via sponging miR-216b.	Knockdown of CCAT2 inhibited HEC-1-A and RL95-2 cells viability, migration, invasion, but induced apoptosis.CCAT2 was an endogenous sponge by competing for miR-216b, and miR-216b suppression alleviated  CCAT2 silence-diminished cell growth and metastasis. miR-216b negatively regulated Bcl-2 and Bcl-2 could further active PTEN/PI3K/AKT and mTOR signaling pathways.patients with elevated expression of CCAT2 are prone to developing distant metastasis,and have poorer over all survival and progression-free survival.	MI0005569	Cancer Biomark 2017 Dec 12 21, 123-133 doi:10.3233/cbm-170388 PMID:29036788
1711	LncRNA	CCAT2	miR-34a	FOXM1	Smmc-7721, Plc/Prf/5, Huh7, Sk-Hep-1, And Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay,RIP,ChIP etc.	28744394	A positive feedback loop of long noncoding RNA CCAT2 and FOXM0 promotes hepatocellular carcinoma growth.	a significant upregulation of CCAT2 in HCC tissues as compared to non-tumor tissues.CCAT2 functions as a competitive endogenous RNA (ceRNA) of FOXM1 through competitive interaction with miR-34a. a positive correlation between the tumorous CCAT2 expression and a significantly reduced overall survival(OS). 	MI0000268	Am J Cancer Res 2017  7, 1423-1434,  PMID:28744394
1712	LncRNA	CRNDE	miR-384	IRS1	Sw1990, Panc-1,Capan-1,Jf305 And Bxpc-3,Hpde6-C7,Hek293T	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28940804	Long non-coding RNA CRNDE sponges miR-384 to promote proliferation and metastasis of pancreatic cancer cells through upregulating IRS1.	Upregulation of the expression of CRNDE was found in pancreatic cancer tissues as well as cell lines,in comparison with the adjacent non-tumour tissues and human pancreatic duct epithelial cells.High expression of CRNDE was correlated with poor clinicpathological characteristics and shorter overall survival.We identified miR-384 as a direct target for CRNDE.Moreover,the CRNDE knockdown considerably inhibited pancreatic cancer cell proliferation, migration and invasion not only in vitro but also in vivo.In addition, CRNDE positively regulated IRS1 expression through sponging miR-384. 	MIMAT0001075	Cell Prolif 2017 Dec 50 doi:10.1111/cpr.12389 PMID:28940804
1713	LncRNA	CRNDE	miR-181a-5p	TCF4	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,FISH,MTT assay etc.	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/β-catenin signaling.	The expression levels of the CRNDE were upregulated in CRC clinical tissue samples.Significantly, we found that the repression of cell proliferation,the reduction of chemoresistance,and the inhibition of Wnt/β-catenin signaling induced by CRNDE knockdown would require the increased expression of miR-181a-5p.	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
1714	LncRNA	CRNDE	miR-181a-5p	CTNNB1	Hct116 And Sw480	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,FISH,MTT assay etc.	28086904	The lncRNA CRNDE promotes colorectal cancer cell proliferation and chemoresistance via miR-181a-5p-mediated regulation of Wnt/β-catenin signaling.	The expression levels of the CRNDE were upregulated in CRC clinical tissue samples.Significantly, we found that the repression of cell proliferation,the reduction of chemoresistance,and the inhibition of Wnt/β-catenin signaling induced by CRNDE knockdown would require the increased expression of miR-181a-5p.	MIMAT0000256	Mol Cancer 2017 Jan 13 16, 9 doi:10.1186/s12943-017-0583-1 PMID:28086904
1715	LncRNA	CRNDE	miR-136	E2F1	Sw480, Hct116 And Ht-29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,Cell migration and invasion assay etc.	28115855	Long noncoding RNA CRNDE functions as a competing endogenous RNA to promote metastasis and oxaliplatin resistance by sponging miR-136 in colorectal cancer.	We confirmed the upregulation of CRNDE in both primary specimens from colorectal cancer patients and colorectal cancer cell lines.Overexpression of CRNDE promoted the migration and invasion potency of colorectal cancer cells. Knockdown of CRNDE with OXA treatment decreased cell viability and promoted DNA damage and cell apoptosis.Further in-depth mechanistic studies revealed that CRNDE functioned as a competing endogenous RNA for miR-136, led to the de-repression of its endogenous target,E2F transcription factor 1(E2F1).	MI0000475	Onco Targets Ther 2017  10, 205-216 doi:10.2147/ott.S116178 PMID:28115855
1716	LncRNA	CRNDE	miR-451	NA	Mm1.S, Ncih929, U266, Rpmi8226	Multiple Myeloma	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,Cell proliferation assay etc.	28276319	Long Non-coding RNA CRNDE Promotes Multiple Myeloma Cell Growth By Suppressing MiR-451.	CRNDE expression level,in MM sample and cell lines,is higher than control. Knockdown of CRNDE significantly inhibits the proliferative vitality of MM cells and induces cell cycle arrest in G0/G1 phase and apoptosis-promoting. Subsequently, miR-451 inhibitor rescues the tumorigenesis inhibition induced by CRNDE knockdown.	MI0001729	Oncol Res 2017 Aug 7 25, 1207-1214 doi:10.3727/096504017x14886679715637 PMID:28276319
1717	LncRNA	CRNDE	miR-136-5p	BCL-2	U87 and U251	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	29152149	The long non-coding RNA CRNDE acts as a ceRNA and promotes glioma malignancy by preventing miR-136-5p-mediated downregulation of Bcl-2 and Wnt2	we confirmed high CRNDE expression in clinical glioma specimens and observed through experiments in human glioma cell lines a novel molecular mechanism by which CRNDE may contribute to glioma pathogenesis. By inducing or silencing CRNDE expression, we detected a positive correlation between CRNDE levels and the proliferative,migratory, and invasive capacities of glioma cells, which were concomitant with a decreased apoptosis rate. Our experiments also suggest that these effects are mediated by downregulation of miR-136-5p,which correlated with the glioma WHO grade. Based on predicted CRNDE/miR-136-5p/mRNA interactions, both the mRNA and protein expression analyses suggested that miR-136-5p-mediated repression of Bcl-2 and Wnt2 underlies the pro-tumoral actions of CRNDE.We therefore propose that CRNDE functions as a competing endogenous RNA (ceRNA) that binds to and negatively regulates miR-136-5p, thereby protecting Bcl-2 and Wnt2 from miR-136-5p-mediated inhibition in glioma.	MIMAT0000448	Oncotarget 2017 Oct 20 8, 88163-88178 doi:10.18632/oncotarget.21513 PMID:29152149
1718	LncRNA	CRNDE	miR-136-5p	Wnt2	U87 and U251	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	29152149	The long non-coding RNA CRNDE acts as a ceRNA and promotes glioma malignancy by preventing miR-136-5p-mediated downregulation of Bcl-2 and Wnt2	we confirmed high CRNDE expression in clinical glioma specimens and observed through experiments in human glioma cell lines a novel molecular mechanism by which CRNDE may contribute to glioma pathogenesis. By inducing or silencing CRNDE expression, we detected a positive correlation between CRNDE levels and the proliferative,migratory, and invasive capacities of glioma cells, which were concomitant with a decreased apoptosis rate. Our experiments also suggest that these effects are mediated by downregulation of miR-136-5p,which correlated with the glioma WHO grade. Based on predicted CRNDE/miR-136-5p/mRNA interactions, both the mRNA and protein expression analyses suggested that miR-136-5p-mediated repression of Bcl-2 and Wnt2 underlies the pro-tumoral actions of CRNDE.We therefore propose that CRNDE functions as a competing endogenous RNA (ceRNA) that binds to and negatively regulates miR-136-5p, thereby protecting Bcl-2 and Wnt2 from miR-136-5p-mediated inhibition in glioma.	MIMAT0000448	Oncotarget 2017 Oct 20 8, 88163-88178 doi:10.18632/oncotarget.21513 PMID:29152149
1719	LncRNA	CRNDE	miR-145	E2F3	Sgc7901, Bgc823, Mgc803, Ags	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi,Luciferase reporter assay	28490034	Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145	CRNDE was highly expressed in GC cell lines and tissues.Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145. 	MI0000461	Cell Physiol Biochem 2017  42, 13-21 doi:10.1159/000477107 PMID:28490034
1720	LncRNA	CRNDE	miR-136	c-Myc	Mcf-7, Mda-Mb-231, Mda-Mb-468 And Bt-549	Breast Cancer	Homo sapiens (human)	qPCR	28469804	Long noncoding RNA CRNDE activates Wnt/β-catenin signaling pathway through acting as a molecular sponge of microRNA-136 in human breast cancer	CRNDE expression is remarkably up-regulated in BC tissue specimens and cell lines in comparison to corresponding normal tissues and normal human breast epithelial cells. Up-regulated CRNDE expression was greatly associated with larger tumor size, advanced TNM stage and unfavorable prognosis of BC patients. We uncovered that miR-136 is a bona fide binding target of CRNDE, and that up-regulation of CRNDE promoted the mRNA and protein expressions of β-catenin, c-myc and cyclinD1.	MI0000475	Am J Transl Res 2017  9, 1977-1989,  PMID:28469804
1721	LncRNA	CRNDE	miR-217	TCF7L2	Ht-29, Sw480, Hct-116, Sw620, Lovo, Sw48, Dld-1, Caco2 And Ht-15 	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28472810	The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway	high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression.	MIMAT0000274	Cell Physiol Biochem 2017  41, 2489-2502 doi:10.1159/000475941 PMID:28472810
1722	LncRNA	CRNDE-p	miR-217	NA	Ncm460, Ht-29, Sw480, Hct-116, Sw620, Lovo, Sw48, Dld-1, Caco2 And Ht-15	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29137379	Diagnostic potential of serum exosomal colorectal neoplasia differentially expressed long non-coding RNA (CRNDE-p) and microRNA-217 expression in colorectal carcinoma.	High CRNDE-p and low miR-217 levels in exosomes released from CRC cells than in exosomes released from the control NCM460 cells. serum exosomal CRNDE-p and miR-217 levels show diagnostic and prognostic potential for CRC patients.	MIMAT0000274	Oncotarget 2017 Oct 13 8, 83745-83753 doi:10.18632/oncotarget.19407 PMID:29137379
1723	LncRNA	CTA	miR-210	DOX	Saos-2, U-2Os And Mg-63	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,MIT,Luciferase reporter assays	28415557	Long non-coding RNA CTA sensitizes osteosarcoma cells to doxorubicin through inhibition of autophagy	lncRNA CTA was markedly downregulated in OS tissues compared to their matched non-tumor tissues.In addition, OS patients with low lncRNA CTA levels showed a worse prognosis when compared with those with high expression of lncRNA CTA. LncRNA CTA could be activated by doxorubicin (DOX), and could promote OS cell apoptosis by competitively binding miR-210, while inhibit cell autophagy. 	MI0000286	Oncotarget 2017 May 9 8, 31465-31477 doi:10.18632/oncotarget.16356 PMID:28415557
1724	LncRNA	DANCR	miR-496	mTOR	A549, H1299,H358,Hbe,Lung Adc Tissue	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown,RNAi,RIP etc	29266795	LncRNA-DANCR contributes to lung adenocarcinoma progression by sponging miR-496 to modulate mTOR expression.    	Differentiation antagonizing non-protein coding RNA (DANCR) was up-regulated in lung adenocarcinoma (ADC) and that the knockdown of DANCR inhibited tumour cell proliferation, migration and invasion and restored cell apoptosis rescued;cotransfection with a miR-496 inhibitor reversed these effects. 	MI0003136	J Cell Mol Med 2018 Mar 22, 1527-1537 doi:10.1111/jcmm.13420 PMID:29266795
1725	LncRNA	DANCR	miR-33a-5p	AXL	Mg63, U2Os, Saos2, Hos, 143B	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28642170	lncRNA DANCR promotes tumor progression and cancer stemness features in osteosarcoma by upregulating AXL via miR-33a-5p Q2 inhibition	DANCR promoted osteosarcoma progression by mediating cancer stem cells (CSC) features. Moreover,DANCR upregulated expression of the receptor tyrosine kinase AXL by competitively binding to miR-33a-5p. Furthermore, DANCR enhanced the expression of proteins downstream of the AXL-Akt pathway. DANCR was consistently significantly increased in osteosarcoma tissues, and its expression was positively correlated with tumor size and metastasis as an independent poor prognostic factor. Furthermore, both in patient tumors and xenograft tumors, DANCR expression was positively related to AXL and negatively related to miR-33a-5p. Taken together, our results suggest that DANCR is a crucial upregulator of osteosarcoma and an independent predictor of prognosis. DANCR increases CSC function by upregulating AXL via competitively binding to miR-33a-5p,and this function is sequentially performed through the PI3K-Akt signaling pathway	MIMAT0000091	Cancer Lett 2017 Oct 1 405, 46-55 doi:10.1016/j.canlet.2017.06.009 PMID:28642170
1726	LncRNA	DGCR5	miR-1180	AKT	Beas-2B, H520, H157, Skmes1, H460, A549, H1299, Hek293T 	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28744397	Long non-coding RNA DGCR5 is involved in the regulation of proliferation, migration and invasion of lung cancer by targeting miR-1180.	DGCR5 was downregulated and miR-1180 was upregulated in the sera and tissues of LC patients and was correlated with poor prognosis. a negative correlation between the expression of DGCR5 and miR-1180 in LC tissues and sera. DGCR5 negatively regulated miR-1180 expression. DGCR5 suppressed the proliferation, migration and invasion of LC cells by targeting miR-1180. Recently, a novel lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) was found to be downregulated in hepatocellular carcinoma (HCC), and low expression of DGCR5 was closely associated with poor five-year survival rate.	MI0006273	Am J Cancer Res 2017  7, 1463-1475,  PMID:28744397
1727	LncRNA	DLX6-AS1	miR-26a	PTEN	A498, Achn, Caki-1, Caki2, 786-O And G401	Renal Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assays etc	28881158	Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis	In this study, we identified an upregulated lncRNA, DLX6-AS1, in RCC tumor tissues compared with normal kidney tissues. Our data suggested that DLX6-AS1 promoted RCC cell growth and tumorigenesis via targeting miR-26a.	MI0000083	Cell Cycle 2017  16, 2212-2219 doi:10.1080/15384101.2017.1361072 PMID:28881158
1728	LncRNA	ENST00000535511	miR-133b	UBD	CRC tissues	Colorectal Cancer	Homo sapiens (human)	microarray,qPCR etc.	28177879	Comprehensive analysis of differentially expressed profiles of lncRNAs and construction of miR-133b mediated ceRNA network in colorectal cancer.	qRT-PCR was performed to assess their expression levels in 14 pairs of matched colorectal tumor/non-tumor sample. This analysis revealed that miR-133b was significantly downregulated in CRC tumor samples, while UBD and lncRNA ENST00000535511 were significantly upregulated in CRC tumor samples. A significantly positive correlation between UBD and lncRNA ENST00000535511 was also observed.	MIMAT0000770	Oncotarget 2017 Mar 28 8, 21095-21105 doi:10.18632/oncotarget.15045 PMID:28177879
1729	LncRNA	FBXL19-AS1	miR-203	NA	Lovo,Ht29,Hct116,Sw620	Colorectal Cancer	Homo sapiens (human)	microarray,qPCR,Luciferase reporter assay etc.	28479250	Long non-coding RNA FBXL19-AS1 plays oncogenic role in colorectal cancer by sponging miR-203	FBXL19-AS1 was the most significantly upregulated lncRNA in metastatic tumors. Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development.	MI0000283	Biochem Biophys Res Commun 2017 Jun 17 488, 67-73 doi:10.1016/j.bbrc.2017.05.008 PMID:28479250
1730	LncRNA	FER1L4	miR-106a-5p	PTEN	Hepg2, Huh7, Hep3B, And Hccm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28759956	Long non-coding RNA Fer-1-like protein 4 acts as a tumor suppressor via miR-106a-5p and predicts good prognosis in hepatocellular carcinoma.	FER1L4 was lowly expressed in HCC tissue specimens as well as in malignant HCC cell lines, while the situation is opposite in miR-106a-5p. FER1L4 could exert a tumor suppressive impact on HCC, which at least, in part, through suppressing miR-106a-5p expression. FER1L4, as well as miR-106a-5p, can predict the clinical prognosis of HCC alone or combined, which may be a novel therapeutic target for treating HCC. lncRNA FER1L4 and miR-106a-5p functioned as competing endogenous RNA (ceRNA) that miR-106a-5p could regulate the expression of FER1L4 by targeting PTEN in human gastric cancer.	MIMAT0000103	Cancer Biomark 2017 Jul 19 20, 55-65 doi:10.3233/cbm-170090 PMID:28759956
1731	LncRNA	FOXD2-AS1	miR-363-5p	S100A1	Sune-1, Cne-1, Hne-1, Cne-2, C666-1,Hone-1,Npc Tissues	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown etc	29248577	Long non-coding RNA FOXD2-AS1 aggravates nasopharyngeal carcinoma carcinogenesis  by modulating miR-363-5p/S100A1 pathway	The aberrant overexpression of FOXD2-AS1 indicated the poor prognosis of NPC patients. Silence of FOXD2-AS1 was able to repress NPC cell growth in vitro while overexpression of FOXD2-AS1 inversed this process. 	MIMAT0003385	Gene 2018 Mar 1 645, 76-84 doi:10.1016/j.gene.2017.12.026 PMID:29248577
1732	LncRNA	FTH1P3	miR-224-5p	FZD5	Scc1, Scc25, Tu183, Hsu3, Fadu, Oec-M1, Snu1041 Etc.	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,RNA pull-down assay etc.	28093311	Long non-coding RNA FTH1P3 facilitates oral squamous cell carcinoma progression by acting as a molecular sponge of miR-224-5p to modulate fizzled 5 expression.	FTH1P3 was over-expressed in OSCC and decreased the survival rate of OSCC patients.Ectopic expression of FTH1P3 facilitates cell proliferation and colony formation in OSCC cells.Moreover, FTH1P3 acted as a ceRNA, effectively becoming sponge for miR-224-5p and thereby modulating the expression of fizzled 5. Importantly, expression analysis revealed that both FTH1P3 and fizzled 5 were up-regulated in OSCC cell lines and tissues, and over-expression of fizzled 5 also functioned as an oncogene in OSCC cells.	MIMAT0000281	Gene 2017 Apr 5 607, 47-55 doi:10.1016/j.gene.2017.01.009 PMID:28093311
1733	LncRNA	FTH1P3	miR-224-5p	RAC1	Ocm-1A, Mum-2C, C918, Mum-2B	Uveal Melanoma	Homo sapiens (human)	qPCR,Western blot etc.	29095823	Long non-coding RNA FTH1P3 facilitates uveal melanoma cell growth and invasion through miR-224-5p	lncRNA FTH1P3 was commonly up-regulated in uveal melanoma cell lines and tissues and acted as an oncogene in uveal melanoma progression by inhibiting miR-224-5p expression. These results suggest that lncRNA FTH1P3 plays a crucial role in uveal melanoma and investigation of the underlying mechanism may be a target for the treatment of uveal melanoma.	MIMAT0000281	PLoS One 2017  12, e0184746 doi:10.1371/journal.pone.0184746 PMID:29095823
1734	LncRNA	FTX	miR-342-3p	AEG-1	U87Mg And Ln18	Glioma	Homo sapiens (human)	qPCR,Cell transfection,Western blot,MTT assay etc.	28112756	Long noncoding RNA FTX is upregulated in gliomas and promotes proliferation and invasion of glioma cells by negatively regulating miR-342-3p.	the expression of FTX and miR-342-3p was associated with progression of gliomas. FTX directly inhibited the expression of miR-342-3p, which subsequently regulates the expression of AEG-1. Collectively, FTX is critical for proliferation and invasion of glioma cells by regulating miR-342-3p and AEG-1.	MIMAT0000753	Lab Invest 2017 Apr 97, 447-457 doi:10.1038/labinvest.2016.152 PMID:28112756
1735	LncRNA	GAPLINC	miR-34a	c-Met	Hct116,Crc Tissue 	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29427222	Long Noncoding RNA GAPLINC Promotes Cells Migration and Invasion in Colorectal Cancer Cell by Regulating miR-34a/c-MET Signal Pathway.	GAPLINC expression was obviously increased in CRC tissues.In HCT116, silencing of GAPLINC weakened cell migration and invasion, while overexpression of GAPLINC significantly promoted cell migration and invasion. Through dual-luciferase, RNA pull-down, and Transwell assays, we verified that miR-34a was the downstream molecule of GAPLINC and that miR-34a negatively regulated the migration and invasion of HCT116 cell.Furthermore, we found that GAPLINC positively regulated the miR-34a target gene c-MET in CRC tissues. 	MI0000268	Dig Dis Sci 2018 Apr 63, 890-899 doi:10.1007/s10620-018-4915-9 PMID:29427222
1736	LncRNA	GAS5	miR-221	ARHI	Khos, 143B, Saos-2, U2Os,Mg-63,Hfob 1.19, Hek-293T	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	28519068	Long Noncoding RNA GAS5 Suppresses Cell Growth and Epithelial-Mesenchymal Transition in Osteosarcoma by Regulating the miR-221/ARHI Pathway.	GAS5 and ARHI levels were significantly reduced, while miR-221 increased, both in osteosarcoma tissues and cells. Overexpression of GAS5 suppressed the proliferation, migration, and epithelial-mesenchymal transition (EMT) of osteosarcoma cells.GAS5 could directly bind to miR-221 to decrease miR-221 expression and enhance ARHI expression. The effect of GAS5 overexpression on the proliferation, migration and EMT was reversed by miR-221 mimics or ARHI siRNA in osteosarcoma cells.GAS5 suppressed tumor volume, Ki-67 and PCNA staining, and EMT process in the development of osteosarcoma in vivo.Taken together, lncRNA GAS5 functions as a competing endogenous RNA for miR-221 to suppress cell growth and EMT in osteosarcoma by regulating the miR-221/ARHI pathway.  	MI0000298	J Cell Biochem 2017 Dec 118, 4772-4781 doi:10.1002/jcb.26145 PMID:28519068
1737	LncRNA	GAS5	miR-222-3p	PTEN	 Bhp5-16, Tpc, K1 And Bhp2-7, Nthy-Ori 3-1	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29423063	LncRNA Gas5 acts as a ceRNA to regulate PTEN expression by sponging miR-222-3p in papillary thyroid carcinoma.	Over-expression of Gas5 remarkably suppressed PTC cells proliferation in vitro and inhibited the growth of tumor cells in vivo likewise. Gas5 was identified as a target of miR-222-3p which was aberrantly high in PTC cells.Enhanced expression of miR-222-3p promoted the proliferation of PTC cells while knocking down miR-222-3p could inhibit it. The advanced effects of miR-222-3p on the proliferation of PTC cells could be partly reversed by the upregulation of Gas5 expression.Gas5 increased the protein level of the PTEN,one of miR-222-3p's targets, which further activated PTEN/AKT pathway.	MIMAT0000279	Oncotarget 2018 Jan 9 9, 3519-3530 doi:10.18632/oncotarget.23336 PMID:29423063
1738	LncRNA	GAS5	miR-135b	NA	A549 And H1975	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,MTT assay etc.	28117028	LncRNA GAS5 Inhibits Tumorigenesis and Enhances Radiosensitivity By Suppressing miR-135b Expression in Non-Small Cell Lung Cancer.	GAS5 was down-regulated and miR-135b was up-regulated in NSCLC tissues and cells. The expressions of GAS5 and miR-135b changed inversely in response to irradiation. Gain of function experiments revealed that GAS5 overexpresion and miR-135b downregulation significantly suppressed tumorigenesis by repressing cell proliferation, invasion and enhanced radiosensitivity of NSCLC cells by reducing colony formation rates. Moreover, rescue experiments demonstrated that miR-135b upregulation markedly abolished GAS5 overexpression-induced tumorigenesis inhibition and radiosensitivity improvement.	MI0000810	Oncol Res 2017 Sep 21 25, 1305-1316 doi:10.3727/096504017x14850182723737 PMID:28117028
1739	LncRNA	GAS5	miR-23a	NA	A549, H838, H157, Hcc827	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,luciferase reporter assay,MTT assay etc.	28059053	Long noncoding RNA GAS5 suppresses tumorigenesis by inhibiting miR-23a 5 expression in non-small cell lung cancer.	GAS5 was down-regulated in NSCLC tissues and cells and was negatively correlated with miR-23a expression.GAS5 directly interacted with miR-23a and reversely regulate its expression. miR-23a overexpression markedly promoted NSCLC cell proliferation and invasion, while GAS5 overexpression dramatically inhibited NSCLC cell proliferation, invasion and promoted apoptosis.	MI0000079	Oncol Res 2017 Jul 5 25, 1027-1037 doi:10.3727/096504016x14822800040451 PMID:28059053
1740	LncRNA	GAS5	miR-196a	FOXG1	Siha, Ht-3, Sw756 And Me-180	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	28671039	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.	GAS5 expression was decreased in cervical cancer tissues and cells.GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression.Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA-mediated clinical therapy against this disease. 	MI0000238	Tumour Biol 2017 Jul 39, 1010428317711315 doi:10.1177/1010428317711315 PMID:28671039
1741	LncRNA	GAS5	miR-205	FOXG1	Siha, Ht-3, Sw756 And Me-180	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	28671039	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.	GAS5 expression was decreased in cervical cancer tissues and cells.GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression.Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA-mediated clinical therapy against this disease. 	MI0000285	Tumour Biol 2017 Jul 39, 1010428317711315 doi:10.1177/1010428317711315 PMID:28671039
1742	LncRNA	GAS5	miR-196a	PTEN	Siha, Ht-3, Sw756 And Me-180	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	28671039	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.	GAS5 expression was decreased in cervical cancer tissues and cells.GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression.Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA-mediated clinical therapy against this disease. 	MI0000238	Tumour Biol 2017 Jul 39, 1010428317711315 doi:10.1177/1010428317711315 PMID:28671039
1743	LncRNA	GAS5	miR-205	PTEN	Siha, Ht-3, Sw756 And Me-180	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc	28671039	LncRNA GAS5 suppresses the tumorigenesis of cervical cancer by downregulating miR-196a and miR-205.	GAS5 expression was decreased in cervical cancer tissues and cells.GAS5 overexpression suppressed cervical cancer cell proliferation, invasion, and apoptosis. GAS5 was able to directly bind to miR-196a and miR-205 to downregulate their expression.Moreover, GAS5 induced forkhead box protein O1 and phosphatase and tensin homolog expression by repressing miR-196a and miR-205, respectively. Exogenous expression of GAS5 hindered tumor growth in vivo by downregulating miR-196a and miR-205. Upregulation of GAS5 suppressed cell proliferation, invasion, and apoptosis of cervical cancer cells by downregulating miR-196a and miR-205, contributing to our understanding the pathogenesis of cervical cancer and development of long non-coding RNA-mediated clinical therapy against this disease. 	MI0000285	Tumour Biol 2017 Jul 39, 1010428317711315 doi:10.1177/1010428317711315 PMID:28671039
1744	LncRNA	GAS5	miR-137	NA	A2058, B16, M21, Mm200, Mel-Rm And A375	Melanoma	Homo sapiens (human)	qPCR	28386376	Long non-coding RNA GAS5 inhibits tumorigenesis via miR-137 in melanoma	The expression of GAS5 was down-regulated in melanoma tissues compared to adjacent normal tissues. Finally, we suggested that GAS5 inhibited the growth of melanoma through miR-137 in vivo.	MIMAT0000429	Am J Transl Res 2017  9, 1509-1520,  PMID:28386376
1745	LncRNA	Gm15290	miR-615-5p	IGF2	Sk-Mes-1, A549, Nci-H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28474572	LncRNA Gm15290 Promotes Cell Proliferation and Invasion in Non-Small Cell Lung Cancer Through Directly Interacting With and Suppressing the Tumor Suppressor miR-615-5p	First,lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively.The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. 	MIMAT0004804	Oncol Res 2017 May 5, 10.3727/096504017x14930316817366 doi:10.3727/096504017x14930316817366 PMID:28474572
1746	LncRNA	Gm15290	miR-615-5p	AKT2	Sk-Mes-1, A549, Nci-H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28474572	LncRNA Gm15290 Promotes Cell Proliferation and Invasion in Non-Small Cell Lung Cancer Through Directly Interacting With and Suppressing the Tumor Suppressor miR-615-5p	First,lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively.The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. 	MIMAT0004804	Oncol Res 2017 May 5, 10.3727/096504017x14930316817366 doi:10.3727/096504017x14930316817366 PMID:28474572
1747	LncRNA	Gm15290	miR-615-5p	SHMT2	Sk-Mes-1, A549, Nci-H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot	28474572	LncRNA Gm15290 Promotes Cell Proliferation and Invasion in Non-Small Cell Lung Cancer Through Directly Interacting With and Suppressing the Tumor Suppressor miR-615-5p	First,lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively.The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. 	MIMAT0004804	Oncol Res 2017 May 5, 10.3727/096504017x14930316817366 doi:10.3727/096504017x14930316817366 PMID:28474572
1748	LncRNA	H19	miR-17	p21	Weri-Rb-1, So-Rb50, And Y7,Arpe-19,Retinoblastoma Tissues	Retinoblastoma	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,RIP etc	29143996	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.	H19 is downregulated in retinoblastoma tissues and cell lines.Gain-of-function and loss-of-function assays showed that H19 inhibits retinoblastoma cell proliferation, induces retinoblastoma cell cycle arrest and cell apoptosis.Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In addition, functional assays demonstrated that the mutation of miR-17-92 cluster binding sites on H19 abolished the proliferation inhibiting, cell cycle arrest and cell apoptosis inducing roles of H19 in retinoblastoma. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	MI0000071	J Cell Biochem 2018 Apr 119, 3497-3509 doi:10.1002/jcb.26521 PMID:29143996
1749	LncRNA	H19	miR-18a	p21	Weri-Rb-1, So-Rb50, And Y7,Arpe-19,Retinoblastoma Tissues	Retinoblastoma	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,RIP etc	29143996	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.	H19 is downregulated in retinoblastoma tissues and cell lines.Gain-of-function and loss-of-function assays showed that H19 inhibits retinoblastoma cell proliferation, induces retinoblastoma cell cycle arrest and cell apoptosis.Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In addition, functional assays demonstrated that the mutation of miR-17-92 cluster binding sites on H19 abolished the proliferation inhibiting, cell cycle arrest and cell apoptosis inducing roles of H19 in retinoblastoma. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	MI0000072	J Cell Biochem 2018 Apr 119, 3497-3509 doi:10.1002/jcb.26521 PMID:29143996
1750	LncRNA	H19	miR-19a	p21	Weri-Rb-1, So-Rb50, And Y7,Arpe-19,Retinoblastoma Tissues	Retinoblastoma	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,RIP etc	29143996	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.	H19 is downregulated in retinoblastoma tissues and cell lines.Gain-of-function and loss-of-function assays showed that H19 inhibits retinoblastoma cell proliferation, induces retinoblastoma cell cycle arrest and cell apoptosis.Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In addition, functional assays demonstrated that the mutation of miR-17-92 cluster binding sites on H19 abolished the proliferation inhibiting, cell cycle arrest and cell apoptosis inducing roles of H19 in retinoblastoma. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	MI0000073	J Cell Biochem 2018 Apr 119, 3497-3509 doi:10.1002/jcb.26521 PMID:29143996
1751	LncRNA	H19	miR-19b	p21	Weri-Rb-1, So-Rb50, And Y7,Arpe-19,Retinoblastoma Tissues	Retinoblastoma	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,RIP etc	29143996	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.	H19 is downregulated in retinoblastoma tissues and cell lines.Gain-of-function and loss-of-function assays showed that H19 inhibits retinoblastoma cell proliferation, induces retinoblastoma cell cycle arrest and cell apoptosis.Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In addition, functional assays demonstrated that the mutation of miR-17-92 cluster binding sites on H19 abolished the proliferation inhibiting, cell cycle arrest and cell apoptosis inducing roles of H19 in retinoblastoma. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	MI0000074	J Cell Biochem 2018 Apr 119, 3497-3509 doi:10.1002/jcb.26521 PMID:29143996
1752	LncRNA	H19	miR-20a	p21	Weri-Rb-1, So-Rb50, And Y7,Arpe-19,Retinoblastoma Tissues	Retinoblastoma	Homo sapiens (human)	Western blot,qPCR,in vitro knockdown,RIP etc	29143996	Long non-coding RNA H19 suppresses retinoblastoma progression via counteracting miR-17-92 cluster.	H19 is downregulated in retinoblastoma tissues and cell lines.Gain-of-function and loss-of-function assays showed that H19 inhibits retinoblastoma cell proliferation, induces retinoblastoma cell cycle arrest and cell apoptosis.Mechanistically, we identified seven miR-17-92 cluster binding sites on H19, and found that H19 directly bound to miR-17-92 cluster via these seven binding sites. Through binding to miR-17-92 cluster, H19 relieves the suppressing roles of miR-17-92 cluster on p21. Furthermore, H19 represses STAT3 activation induced by miR-17-92 cluster. Hence, our results revealed that H19 upregulates p21 expression,inhibits STAT3 phosphorylation, and downregulates the expression of STAT3 target genes BCL2, BCL2L1, and BIRC5. In addition, functional assays demonstrated that the mutation of miR-17-92 cluster binding sites on H19 abolished the proliferation inhibiting, cell cycle arrest and cell apoptosis inducing roles of H19 in retinoblastoma. In conclusion, our data suggested that H19 inhibits retinoblastoma progression via counteracting the roles of miR-17-92 cluster, and implied that enhancing the action of H19 may be a promising therapeutic strategy for retinoblastoma.  	MI0000076	J Cell Biochem 2018 Apr 119, 3497-3509 doi:10.1002/jcb.26521 PMID:29143996
1753	LncRNA	H19	miR-29a-3p	E2F1	786-O	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP,RNAi	29214011	Long non-coding RNA H19 regulates E2F1 expression by competitively sponging endogenous miR-29a-3p in clear cell renal cell carcinoma.	lncRNA-H19 was high expressed and negatively correlated with miR-29a-3p in ccRCC.miR-29a-3p was identified as a direct target of lncRNA-H19. down-regulated lncRNA-H19 could affect the expression of miR-29a-3p targeting E2F1 with competitively binding miR-29a-3p.lncRNA-H19 knockdown inhibited cells migration and invasion, but this effect was attenuated by co-transfection of lncRNA-H19 siRNA and miR-29a-3p inhibitor. Over expression of E2F1 could rescue lncRNA-H19 siRNA induced suppression on cell migration and invasion in ccRCC cells.These results show a possible competing endogenous RNAs regulatory network involving lncRNA-H19 regulates E2F1 expression by competitively sponging  endogenous miR-29a-3p in ccRCC.  	MIMAT0000086	Cell Biosci 2017  7, 65 doi:10.1186/s13578-017-0193-z PMID:29214011
1754	LncRNA	H19	let-7	LIN28	Mda-Mb-231, Sk-Br-3 And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,ISH etc.	28102845	H19/let-7/LIN28 reciprocal negative regulatory circuit promotes breast cancer stem cell maintenance.	BCSCs express high levels of H19, and ectopic overexpression of H19 significantly promotes breast cancer cell clonogenicity, migration and mammosphere-forming ability. Conversely, silencing of H19 represses these BCSC properties. In concordance, knockdown of H19 markedly inhibits tumor growth and suppresses tumorigenesis in nude mice. Mechanistically, we found that H19 functions as a competing endogenous RNA to sponge miRNA let-7, leading to an increase in expression of a let-7 target, the core pluripotency factor LIN28, which is enriched in BCSC populations and breast patient samples.	MI0000060	Cell Death Dis 2017 Jan 19 8, e2569 doi:10.1038/cddis.2016.438 PMID:28102845
1755	LncRNA	H19	miR-675-5p	VDR	Ht-29 And Dld-1	Colon Cancer	Homo sapiens (human)	qPCR,Cell transfection,Western blot,ChIP,Luciferase reporter assay,MTT assay etc.	28189050	H19 Overexpression Induces Resistance to 1,25(OH)2D3 by Targeting VDR Through miR-675-5p in Colon Cancer Cells.	VDR signaling was able to inhibit the expression of H19 through regulating C-Myc/Mad-1 network.H19, on the other hand, was able to inhibit the expression of VDR through micro RNA 675-5p (miR-675-5p). Furthermore, H19 overexpression induced resistance to the treatment with 1,25(OH)2D3 both in vitro and in vivo.	MIMAT0004284	Neoplasia 2017 Mar 19, 226-236 doi:10.1016/j.neo.2016.10.007 PMID:28189050
1756	LncRNA	H19	miR-200a	b-catenin	Hct116, Sw480, 293Tn	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28164117	The lncRNA H19 Promotes Cell Proliferation by Competitively Binding to miR-200a and Derepressing β-Catenin Expression in Colorectal Cancer.	H19 expression was upregulated in CRC tissues compared with adjacent noncancerous tissues. H19 overexpression facilitated colon cancer cell proliferation, whereas H19 knockdown inhibited cell proliferation. miR-200a bound to H19 and inhibited its expression, thereby decreasing CRC cell proliferation. H19 promotes cell proliferation by competitively binding to miR-200a and derepressing β-catenin in CRC.	MI0000737	Biomed Res Int 2017  2017, 2767484 doi:10.1155/2017/2767484 PMID:28164117
1757	LncRNA	H19	miR-200b	GIT2	C13-Pt, C13-Pb, C13-Lm	Breast Cancer	Homo sapiens (human)	qPCR,microarray,RIP,Western blotting etc.	28611183	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b	H19 might be exploited as a biomarker for metastatic cells within breast tumors and perhaps as a therapeutic target to prevent metastasis.	MI0000342	Sci Signal 2017 Jun 13 10 doi:10.1126/scisignal.aak9557 PMID:28611183
1758	LncRNA	H19	miR-200c	GIT2	C13-Pt, C13-Pb, C13-Lm	Breast Cancer	Homo sapiens (human)	qPCR,microarray,RIP,Western blotting etc.	28611183	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b	H19 might be exploited as a biomarker for metastatic cells within breast tumors and perhaps as a therapeutic target to prevent metastasis.	MI0000650	Sci Signal 2017 Jun 13 10 doi:10.1126/scisignal.aak9557 PMID:28611183
1759	LncRNA	H19	let-7b	GIT2	C13-Pt, C13-Pb, C13-Lm	Breast Cancer	Homo sapiens (human)	qPCR,microarray,RIP,Western blotting etc.	28611183	The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b	H19 might be exploited as a biomarker for metastatic cells within breast tumors and perhaps as a therapeutic target to prevent metastasis.	MI0000063	Sci Signal 2017 Jun 13 10 doi:10.1126/scisignal.aak9557 PMID:28611183
1760	LncRNA	H19	miR-138	HMGA1	Sw480, Ht-29, Colon26, Hct-8, And Rko	Colon Cancer	Homo sapiens (human)	qPCR,western blot,luciferase reporter assay	28358427	H19 promotes the migration and invasion of colon cancer by sponging miR-138 to upregulate the expression of HMGA1	H19 shRNA strongly reduced the tumor growth and tumor volume. H19 shRNA also inhibited metastasis via suppressing hepatic metastases and the expression of metastasis-related proteins. Taken together, our research indicated an H19-miR138-HMGA1 pathway in regulating the migration and invasion of colon cancer, 	MI0000455	Int J Oncol 2017 May 50, 1801-1809 doi:10.3892/ijo.2017.3941 PMID:28358427
1761	LncRNA	H19	let-7	PDK	Mda-Mb-231,Mcf-7, Sk-Br-3 And Hek293T	Breast Cancer	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29106390	Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia.	lncRNA H19 is responsible for glycolysis and BCSC maintenance.Furthermore,H19 knockdown decreases PDK1 xpression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo.Reprogramming is referred to as the conversion of differentiated cells to a stem-like state. Ectopic expression of four transcription factors (Oct4, Klf4, Sox2 and c-Myc) reprograms various types of somatic cells to induced pluripotent stem cells. Accordingly, H19 and PDK1 expression exhibits strong correlations in primary breast carcinomas. H19 acting as a competitive endogenous RNA sequesters miRNA let-7 to release Hypoxia-inducible factor 1α, leading to an increase in PDK1 expression. Lastly, aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. 	MI0000060	Oncogene 2018 Feb 22 37, 1062-1074 doi:10.1038/onc.2017.368 PMID:29106390
1762	LncRNA	H19	let-7c	HER2	Bgc823 And Sgc7901, And The Normal Gastric Epithelial Cell Line 	Gastric Cancer	Homo sapiens (human)	RT-qPCR,Western blot	29207111	H19 functions as a competing endogenous RNA to regulate human epidermal growth factor receptor expression by sequestering let7c in gastric cancer.	the expression levels of H19 lncRNA in GC tissue samples were significantly higher when compared with that in matched benign adjacent tissue samples.H19 silenced GC cells exhibited significantly increased let-7c expression and decreased HER2 protein expression levels.	MI0000064	Mol Med Rep 2018 Feb 17, 2600-2606 doi:10.3892/mmr.2017.8184 PMID:29207111
1763	LncRNA	H19	miR-19a	ID2	Hl-60,Hek-193T	Acute Myeloid Leukemia	Homo sapiens (human)	Western blot,luciferase reporter assay,etc.	28765931	LncRNA H19 regulates ID2 expression through competitive binding to hsa-miR-19a/b in acute myelocytic leukemia.	it was demonstrated that the knockdown of lncRNA H19 resulted in increased expression of hsa-microRNA-19a/b and decreased expression of inhibitor of DNA binding 2 (ID2) in AML cells.	MI0000073	Mol Med Rep 2017 Sep 16, 3687-3693 doi:10.3892/mmr.2017.7029 PMID:28765931
1764	LncRNA	H19	miR-19b	ID2	Hl-60,Hek-193T	Acute Myeloid Leukemia	Homo sapiens (human)	Western blot,luciferase reporter assay,etc.	28765931	LncRNA H19 regulates ID2 expression through competitive binding to hsa-miR-19a/b in acute myelocytic leukemia.	it was demonstrated that the knockdown of lncRNA H19 resulted in increased expression of hsa-microRNA-19a/b and decreased expression of inhibitor of DNA binding 2 (ID2) in AML cells.	MI0000074	Mol Med Rep 2017 Sep 16, 3687-3693 doi:10.3892/mmr.2017.7029 PMID:28765931
1765	LncRNA	H19	miR-21	NA	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	28799568	Association of long non-coding RNA H19 and microRNA-21 expression with the biological features and prognosis of non-small cell lung cancer.	H19 and miR-21 expression was measured in tumor tissues and corresponding non-tumor lung tissues from 200 patients by quantitative reverse transcription polymerase chain reaction. Expression of both H19 and miR-21 was significantly higher in lung tissues from patients with NSCLC than in normal lung tissues. Increased expression of H19 and miR-21 was positively correlated with advanced tumor-node-metastasis stage and tumor size. miR-21 expression was highest in stage I and II NSCLC, whereas H19 expression was highest in stage III and IV NSCLC. The results show that H19 may mainly contributes to the progression of NSCLC, and its expression levels can reflect the invasive and metastatic status to some extent. New H19 and miR-targeting anticancer drugs will soon enter the clinical stage of development and ultimately become available for the treatment of patients with lung cancer.	MI0000077	Cancer Gene Ther 2017 Aug 24, 317-324 doi:10.1038/cgt.2017.20 PMID:28799568
1766	LncRNA	H19	let-7a	NA	Thyroid Cancer tissues	Thyroid Cancer	Homo sapiens (human)	qPCR etc.	28655518	Effects of long non-coding RNA H19 and microRNA let7a expression on thyroid cancer prognosis.	TC patients with a lower 5-year survival rate showed upregulated levels of lncRNA H19 expression and,downregulated levels of miRNA let7a expression.This study aims to explore the effects of long non-coding RNA H19 (lncRNA H19) and microRNA let7a (miRNA let7a) expression on the prognosis of thyroid cancer.TC patients with a lower 5-year survival rate showed upregulated levels of lncRNA H19 expression and, downregulated levels of miRNA let7a expression.LncRNA H19 and miRNA let7a expression, tumor diameter,TNM stage and lymph node metastasis were independent prognostic factors of TC.increased lncRNA H19 and decreased miRNA let7a expression levels are associated with poor prognosis in TC patients.	MI0000060	Exp Mol Pathol 2017 Aug 103, 71-77 doi:10.1016/j.yexmp.2017.06.004 PMID:28655518
1767	LncRNA	H19	miR-138	ZEB1	Hct-116 And Sw-481	Colon Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28781681	Overexpression of long non-coding RNA H20 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells.	overexpression of H20 is associated with decreased recurrence free survival and overall survival rates in patients with colorectal cancer,and increased viability and migration in colon cancer cells.H19 may function as a competing endogenous RNA for miR-138 and miR-200a,antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin,zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2,all of which were associated with the EMT process.	MI0000455	Oncol Lett 2017 Aug 14, 2446-2452 doi:10.3892/ol.2017.6390 PMID:28781681
1768	LncRNA	H19	miR-200a	ZEB2	Hct-116 And Sw-481	Colon Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28781681	Overexpression of long non-coding RNA H20 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells.	overexpression of H20 is associated with decreased recurrence free survival and overall survival rates in patients with colorectal cancer,and increased viability and migration in colon cancer cells.H19 may function as a competing endogenous RNA for miR-138 and miR-200a,antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin,zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2,all of which were associated with the EMT process.	MI0000737	Oncol Lett 2017 Aug 14, 2446-2452 doi:10.3892/ol.2017.6390 PMID:28781681
1769	LncRNA	H19	miR-138	ZEB1	Hct-116 And Sw-481	Colon Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28781681	Overexpression of long non-coding RNA H20 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells.	overexpression of H20 is associated with decreased recurrence free survival and overall survival rates in patients with colorectal cancer,and increased viability and migration in colon cancer cells.H19 may function as a competing endogenous RNA for miR-138 and miR-200a,antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin,zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2,all of which were associated with the EMT process.	MI0000455	Oncol Lett 2017 Aug 14, 2446-2452 doi:10.3892/ol.2017.6390 PMID:28781681
1770	LncRNA	H19	miR-200a	ZEB2	Hct-116 And Sw-481	Colon Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28781681	Overexpression of long non-coding RNA H20 is associated with unfavorable prognosis in patients with colorectal cancer and increased proliferation and migration in colon cancer cells.	overexpression of H20 is associated with decreased recurrence free survival and overall survival rates in patients with colorectal cancer,and increased viability and migration in colon cancer cells.H19 may function as a competing endogenous RNA for miR-138 and miR-200a,antagonizing their functions and thus leading to the derepression of their endogenous targets vimentin,zinc finger E-box-binding homeobox (ZEB) OL-9705-NPS 1 and ZEB2,all of which were associated with the EMT process.	MI0000737	Oncol Lett 2017 Aug 14, 2446-2452 doi:10.3892/ol.2017.6390 PMID:28781681
1771	LncRNA	H19	miR-29b-3p	DNMT3B	Biu, 5673, Ej, T24	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28779971	lncRNA H19 regulates epithelial–mesench mal transition and metastasis of bladder cancer by miR-29b-3p as competing endogenous RNA	up-regulating H19 antagonized miR-29b-3p-mediated proliferation, migration and EMT suppression in BC cells. Furthermore,H19 knockdown partially reversed the function of miR-29b-3p inhibitor on DNMT3B and facilitated miR-29b-3p-induced MET. Taken together, we demonstrated for the first time that H19 might function as ceRNA (competing endogenous RNA) for miR-29b-3p and relieve the suppression for DNMT3B, which led to EMT and metastasis of BC. Our findings highlight a novel mechanism of H19 in progression of BC and provide H19/miR-29b-3p/ DNMT3B axis as a promising therapeutic target for BC.	MIMAT0000100	Biochim Biophys Acta Mol Cell Res 2017 Oct 1864, 1887-1899 doi:10.1016/j.bbamcr.2017.08.001 PMID:28779971
1772	LncRNA	HCAL	miR-15a	LAPTM4B	Lo2, Hepg2, Plc/Prf/5, Sk-Hep-1, Huh-7, And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	29246322	Long Noncoding RNA HCAL Facilitates the Growth and Metastasis of Hepatocellular Carcinoma by Acting as a ceRNA of LAPTM4B.	HCAL that was highly expressed in HCC tissues.HCAL upregulation was clinically associated with poor differentiation, intravascular cancer embolus,and decreased survival of patients with HCC.HCAL silencing significantly inhibited the growth and metastasis of HCC cells both in vitro and in vivo.HCAL directly interacted with and functioned as a sponge for microRNAs such as miR-15a, miR-196a, and miR-196b to modulate LAPTM4B expression.the presence of a novel lncRNA-miRNA-mRNA regulatory network, the HCAL-miR-15a/miR-196a/miR-196b-LAPTM4B network,in HCC and indicate that HCAL may be a potential target for treating HCC. 	MI0000069	Mol Ther Nucleic Acids 2017 Dec 15 9, 440-451 doi:10.1016/j.omtn.2017.10.018 PMID:29246322
1773	LncRNA	HCAL	miR-196a	LAPTM4B	Lo2, Hepg2, Plc/Prf/5, Sk-Hep-1, Huh-7, And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	29246322	Long Noncoding RNA HCAL Facilitates the Growth and Metastasis of Hepatocellular Carcinoma by Acting as a ceRNA of LAPTM4B.	HCAL that was highly expressed in HCC tissues.HCAL upregulation was clinically associated with poor differentiation, intravascular cancer embolus,and decreased survival of patients with HCC.HCAL silencing significantly inhibited the growth and metastasis of HCC cells both in vitro and in vivo.HCAL directly interacted with and functioned as a sponge for microRNAs such as miR-15a, miR-196a, and miR-196b to modulate LAPTM4B expression.the presence of a novel lncRNA-miRNA-mRNA regulatory network, the HCAL-miR-15a/miR-196a/miR-196b-LAPTM4B network,in HCC and indicate that HCAL may be a potential target for treating HCC. 	MIMAT0000226	Mol Ther Nucleic Acids 2017 Dec 15 9, 440-451 doi:10.1016/j.omtn.2017.10.018 PMID:29246322
1774	LncRNA	HCAL	miR-196b	LAPTM4B	Lo2, Hepg2, Plc/Prf/5, Sk-Hep-1, Huh-7, And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	29246322	Long Noncoding RNA HCAL Facilitates the Growth and Metastasis of Hepatocellular Carcinoma by Acting as a ceRNA of LAPTM4B.	HCAL that was highly expressed in HCC tissues.HCAL upregulation was clinically associated with poor differentiation, intravascular cancer embolus,and decreased survival of patients with HCC.HCAL silencing significantly inhibited the growth and metastasis of HCC cells both in vitro and in vivo.HCAL directly interacted with and functioned as a sponge for microRNAs such as miR-15a, miR-196a, and miR-196b to modulate LAPTM4B expression.the presence of a novel lncRNA-miRNA-mRNA regulatory network, the HCAL-miR-15a/miR-196a/miR-196b-LAPTM4B network,in HCC and indicate that HCAL may be a potential target for treating HCC. 	MI0001150	Mol Ther Nucleic Acids 2017 Dec 15 9, 440-451 doi:10.1016/j.omtn.2017.10.018 PMID:29246322
1775	LncRNA	HEIH	miR-200b	EZH2	Hema-Lp, Sk-Mel-28, A375, A2058, Sk-Mel-2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc	28487474	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429.	lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients.Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation,migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription. The expression of miR-200b is inversely associated  with lncRNA-HEIH in melanoma tissues.Furthermore,overexpression of miR-200b/a/429 abrogates melanoma cell proliferation, migration and invasion enhanced by lncRNA-HEIH. In conclusion,we identified lncRNA-HEIH as a key oncogene in melanoma via transcriptional inhibition of miR-200b/a/429 Our data suggested that lncRNA-HEIH may serve as a promising prognostic biomarker and therapeutic target for melanoma. 	MI0000342	Biosci Rep 2017 Jun 30 37 doi:10.1042/bsr20170682 PMID:28487474
1776	LncRNA	HEIH	miR-200a	EZH2	Hema-Lp, Sk-Mel-28, A375, A2058, Sk-Mel-2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc	28487474	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429.	lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients.Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation,migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription. The expression of miR-200b is inversely associated  with lncRNA-HEIH in melanoma tissues.Furthermore,overexpression of miR-200b/a/429 abrogates melanoma cell proliferation, migration and invasion enhanced by lncRNA-HEIH. In conclusion,we identified lncRNA-HEIH as a key oncogene in melanoma via transcriptional inhibition of miR-200b/a/429 Our data suggested that lncRNA-HEIH may serve as a promising prognostic biomarker and therapeutic target for melanoma. 	MI0000737	Biosci Rep 2017 Jun 30 37 doi:10.1042/bsr20170682 PMID:28487474
1777	LncRNA	HEIH	miR-429	EZH2	Hema-Lp, Sk-Mel-28, A375, A2058, Sk-Mel-2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc	28487474	Long noncoding RNA HEIH promotes melanoma cell proliferation, migration and invasion via inhibition of miR-200b/a/429.	lncRNA-HEIH is highly expressed in melanoma tissues and cell lines, associated with advanced clinical stages, and predicts poor outcomes in melanoma patients.Functional assays showed that ectopic expression of lncRNA-HEIH promotes melanoma cell proliferation, migration and invasion. Knockdown of lncRNA-HEIH inhibits melanoma cell proliferation,migration and invasion. Mechanistically, we revealed that lncRNA-HEIH directly binds to miR-200b/a/429 promoter and represses miR-200b/a/429 transcription. The expression of miR-200b is inversely associated  with lncRNA-HEIH in melanoma tissues.Furthermore,overexpression of miR-200b/a/429 abrogates melanoma cell proliferation, migration and invasion enhanced by lncRNA-HEIH. In conclusion,we identified lncRNA-HEIH as a key oncogene in melanoma via transcriptional inhibition of miR-200b/a/429 Our data suggested that lncRNA-HEIH may serve as a promising prognostic biomarker and therapeutic target for melanoma. 	MIMAT0001536	Biosci Rep 2017 Jun 30 37 doi:10.1042/bsr20170682 PMID:28487474
1778	LncRNA	HERG	miR-940	TWIST1	U87, U251, Ln229	Glioblastoma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	29296221	Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma	LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend.In conclusion,our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma.	MIMAT0004983	Oncotarget 2017 Dec 8 8, 108031-108041 doi:10.18632/oncotarget.22446 PMID:29296221
1779	LncRNA	HERG	miR-940	SNAIL	U87, U251, Ln229	Glioblastoma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	29296221	Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma	LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend.In conclusion,our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma.	MIMAT0004983	Oncotarget 2017 Dec 8 8, 108031-108041 doi:10.18632/oncotarget.22446 PMID:29296221
1780	LncRNA	HERG	miR-940	MMP9	U87, U251, Ln229	Glioblastoma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	29296221	Long noncoding RNA lncHERG promotes cell proliferation, migration and invasion in glioblastoma	LncHERG knockdown impaired cell proliferation, migration and invasion while inhibition of miR-940 in the meantime reversed this trend.In conclusion,our study highlights the essential role of lncHERG in glioblastoma by acting as a competing endogenous RNA of miR-940, which may serve as a new prognostic biomarker in glioblastoma.	MIMAT0004983	Oncotarget 2017 Dec 8 8, 108031-108041 doi:10.18632/oncotarget.22446 PMID:29296221
1781	LncRNA	HIF1A-AS2	miR-129-5p	DNMT3A	Sw620, Dld-1, Ht-29, Hct116, Normal Cells 	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RIP	29278853	LncRNA HIF1A-AS2 positively affects the progression and EMT formation of colorectal cancer through regulating miR-129-5p and DNMT3A.	immunofluorescence, all those assays reflected a fact that as a ceRNA, HIF1A-AS2 could directly bind with miR-129-5p, and could positively affect cell proliferation, invasion and EMT formation by regulation of the expression of miR-129-5p and DNMT3A.	MIMAT0000242	Biomed Pharmacother 2018 Feb 98, 433-439 doi:10.1016/j.biopha.2017.12.058 PMID:29278853
1782	LncRNA	HIX0023999	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
1783	LncRNA	HNF1A-AS1	miR-34a	p53	Sw480, Caco2, Rko, Hct8, Hct116, Sw620,Fhc	Colon Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	28943452	Long non-coding RNA HNF1A-AS1 mediated repression of miR-34a/SIRT1/p53 feedback loop promotes the metastatic progression of colon cancer by functioning as a competing endogenous RNA.	HNF1A-AS1 was frequently upregulated in colon cancer tissues and associated with poor prognosis.Upregulated HNF1A-AS1 promoted colon cancer cell viability, migration and invasion both in vitro and in vivo.HNF1A-AS1 silencing impaired tumor growth and metastasis.HNF1A-AS1 functioned as an oncogene in metastasis of colon cancer in part through serving as a competing endogenous RNA to modulate miRNA-34a expression, subsequently with repression of  miR-34a/SIRT1/p53 feedback loop and activation of canonical Wnt signaling pathway.  	MI0000268	Cancer Lett 2017 Dec 1 410, 50-62 doi:10.1016/j.canlet.2017.09.012 PMID:28943452
1784	LncRNA	HNF1A-AS1	miR-17-5p	NA	H1299, H1650, A549, And Pc9 And Human Bronchial Epithelial Cell Line 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	29289833	Long non-coding RNA HNF1A-AS1 promotes cell proliferation and invasion via regulating miR-17-5p in non-small cell lung cancer.	HNF1A-AS1 was upregulation in NSCLC tissues and cell lines.High HNF1A-AS1 expression was associated with patients' advanced TNM stage and lymph node metastasis. Reduced HNF1A-AS1 expression inhibited lung cancer cells proliferation, invasion and increased cells apoptosis rate. Bioinformatics analysis and luciferase reporter assay revealed that HNF1A-AS1 interacted with miR-17-5p by directly targeting it. Rescue experiments showed that miR-17-5p suppression reversed the tumor-suppressing role of HNF1A-AS1 knockdown on NSCLC progression.	MIMAT0000070	Biomed Pharmacother 2018 Feb 98, 594-599 doi:10.1016/j.biopha.2017.12.080 PMID:29289833
1785	LncRNA	HNF1A-AS1	miR-214	SOX-4	Kyse70, Kyse450, Ec109 And Ec970 	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28656277	HNF1A-AS1 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging miR214 to upregulate the expression of SOX-4.	upregulated expression of HAS1 was detected in ESCC tissues and four human ESCC cell lines (KYSE70, KYSE450, EC109 and EC970) compared with normal tissues and cell lines.HAS1-siRNA counteracted the effect of miR-214 inhibitor on cell viability and mobility in EC109 cells. HAS1-siRNA abated the role of miR-214 inhibitor in promoting tumor growth and metastasis. HAS1-miR-214-SOX-4 pathway in regulating the growth and metastasis of ESCC, providing a promising target for ESCC therapy.	MI0000290	Int J Oncol 2017 Aug 51, 657-667 doi:10.3892/ijo.2017.4034 PMID:28656277
1786	LncRNA	HOTAIR	miR-34a	EZH2	Bxpc3, Capan2, Cfpac1, Panc04.03, Panc1, Sw1990 And Hek293T	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,ChIP,MTT assay etc.	27594424	EZH2 coupled with HOTAIR to silence MicroRNA-34a by the induction of heterochromatin formation in human pancreatic ductal adenocarcinoma.	we studied the effect of ectopic EZH2 expression to the silencing of miR-34a, and identified HOTAIR as an interacting partner to induce heterochromatin formation during miR-34a repression.We then showed that HOTAIR played a critical role in EZH2-mediated repression of miR-34a, as knockdown of HOTAIR attenuated the miR-34a inhibition effect in EZH2-overexpressing HPDE cells.HOTAIR physically interacted with miR-34a promoter,and the EZH2-interacting region located at 5' HOTAIR RNA was essential in repressing miR-34a and promoting cell proliferation.	MI0000268	Int J Cancer 2017 Jan 1 140, 120-129 doi:10.1002/ijc.30414 PMID:27594424
1787	LncRNA	HOTAIR	miR-454-3p	STAT3	Hc-A, Sw1353, Oums-27, Hcs-2/8, Jj012	Chondrosarcoma	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,CCK-8 assay etc.	28182000	Knockdown of long non-coding RNA HOTAIR increases miR-454-3p by targeting Stat3 and Atg12 to inhibit chondrosarcoma growth.	HOTAIR expression was upregulated in chondrosarcoma tissues and cell lines. Functional experiments reveal that HOTAIR knockdown leads to growth inhibition of human chondrosarcoma cells in vitro and in vivo. In addition to cycle arrest and apoptosis, knockdown of HOTAIR inhibits autophagy, which favors cell death. Mechanistically, we demonstrated that HOTAIR induced DNA methylation of miR-454-3p by recruiting EZH2 and DNMT1 to the miR-454-3p promoter regions,which markedly silences miR-454-3p expression. Further analysis revealed that STAT3 and ATG12 are targets of miR-454-3p,initiate HOTAIR deficiency-induced apoptosis and reduce autophagy.	MIMAT0003885	Cell Death Dis 2017 Feb 9 8, e2605 doi:10.1038/cddis.2017.31 PMID:28182000
1788	LncRNA	HOTAIR	miR-613	PCNA	H1299, H23, H292, A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	29187267	LncRNA-HOTAIR affects tumorigenesis and metastasis of non-small cell lung cancer by up-regulating miR-613	Down-regulation of HOTAIR suppressed tumorigenesis and metastasis of NSCLC via up-regulating the expression of miR-613.	MIMAT0003281	Oncol Res 2018 Jun 11 26, 725-734 doi:10.3727/096504017x15119467381615 PMID:29187267
1789	LncRNA	HOTAIR	miR-613	VEGF	H1299, H23, H292, A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	29187267	LncRNA-HOTAIR affects tumorigenesis and metastasis of non-small cell lung cancer by up-regulating miR-613	Down-regulation of HOTAIR suppressed tumorigenesis and metastasis of NSCLC via up-regulating the expression of miR-613.	MIMAT0003281	Oncol Res 2018 Jun 11 26, 725-734 doi:10.3727/096504017x15119467381615 PMID:29187267
1790	LncRNA	HOTAIR	miR-197	FUS1	Hct116, Sw480, Lovo, Ht29, Fhc	Colorectal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	29137688	The long noncoding RNA HOTAIR promotes colorectal cancer progression by sponging miR-197	HOTAIR knockdown promoted apoptosis and inhibited cell proliferation, migration and invasion in vitro and in vivo.Moreover, HOTAIR modulated the progression of colorectal cancer by competitively binding miR-197.Taken together, our study has identified a novel pathway through which HOTAIR exerts its oncogenic role,and provided a molecular basis for potential applications of HOTAIR in the prognosis and treatment of colorectal cancer.	MI0000239	Oncol Res 2018 Apr 10 26, 473-481 doi:10.3727/096504017x15105708598531 PMID:29137688
1791	LncRNA	HOTAIR	miR-217	AXL	769-P And Achn	Renal Cancer	Homo sapiens (human)	qPCR,Western blot,RIP	28492542	LncRNA HOTAIR regulates HIF-1α/AXL signaling through inhibition of miR-217 in renal cell carcinoma	HOTAIR expression was upregulated, which was correlated with tumor progression, and miR-217 downregulated in Rcc tissues and cells.Importantly,HOTAIR expression was negatively correlated with miR-217 expression in Rcc tissues.	MIMAT0000274	Cell Death Dis 2017 May 11 8, e2772 doi:10.1038/cddis.2017.181 PMID:28492542
1792	LncRNA	HOTAIR	miR-613	Notch3	Bxpc3, Cfpac-1, Panc-1 And L3.6Pl	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28415631	LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer	The long non-coding RNA,HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines,and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA.	MIMAT0003281	Oncotarget 2017 May 16 8, 32905-32917 doi:10.18632/oncotarget.16462 PMID:28415631
1793	LncRNA	HOTAIR	miR-148a	Snail2	Kyse30, Kyse150, Te-1, Eca-1, Eca-109	Esophageal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28441714	Long non-coding RNA HOTAIR functions as miRNA sponge to promote the epithelial to mesenchymal transition in esophageal cancer	High lncRNA-HOTAIR expression was associated with significantly poorer overall survival in EC. Mechanistic investigations revealed lncRNA-HOTAIR promotes the EMT by acting as a miR-148a sponge to positively regulate Snail2 expression	MI0000253	Biomed Pharmacother 2017 Jun 90, 888-896 doi:10.1016/j.biopha.2017.03.103 PMID:28441714
1794	LncRNA	HOTAIR	miR-218	NFKB	Ht29, Sw480, , Fhc	Colorectal Cancer	Homo sapiens (human)	qPCR,RIP,Western Blot,etc.	28918035	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal Cancer.	HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-κB signaling in CRC. Thus, HOTAIR may serve as a promising therapeutic target for CRC patients.siVOPP1-1 inactivated NF-κB signaling, including the suppression of pathways involved in cell survival (p65-NF-κB, pAkt, pERK) and the cell cycle (E2F1 and TS). HOTAIR was reported to act as a prognostic circulating marker and potential therapeutic target in patients with tumor diseases,while its chemotherapeutic value has rarely been discussed in clinical research. Previous research has found that HOTAIR negatively regulated the expression of miRNAs mainly by functioning as a competing endogenous RNA (ceRNA) sponge, such as miR-145 and miR-331-3p in breast and gastric cancer, respectively.	MI0000294	Mol Ther Nucleic Acids 2017 Sep 15 8, 356-369 doi:10.1016/j.omtn.2017.07.007 PMID:28918035
1795	LncRNA	HOTAIR	miR-218	TYMS	Ht29, Sw480, , Fhc	Colorectal Cancer	Homo sapiens (human)	qPCR,RIP,Western Blot,etc.	28918035	lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal Cancer.	HOTAIR contributes to 5FU resistance through suppressing miR-218 and activating NF-κB signaling in CRC. Thus, HOTAIR may serve as a promising therapeutic target for CRC patients.siVOPP1-1 inactivated NF-κB signaling, including the suppression of pathways involved in cell survival (p65-NF-κB, pAkt, pERK) and the cell cycle (E2F1 and TS). HOTAIR was reported to act as a prognostic circulating marker and potential therapeutic target in patients with tumor diseases,while its chemotherapeutic value has rarely been discussed in clinical research. Previous research has found that HOTAIR negatively regulated the expression of miRNAs mainly by functioning as a competing endogenous RNA (ceRNA) sponge, such as miR-145 and miR-331-3p in breast and gastric cancer, respectively.	MI0000294	Mol Ther Nucleic Acids 2017 Sep 15 8, 356-369 doi:10.1016/j.omtn.2017.07.007 PMID:28918035
1796	LncRNA	HOTAIR	miR-152-3p	MET	A375 And A875	Melanoma	Homo sapiens (human)	qPCR,Western blot,RIP,RNA pull-down assay etc.	29156728	Long non-coding RNA HOTAIR acts as a competing endogenous RNA to promote malignant melanoma progression by sponging miR-152-3p.	HOTAIR is overexpressed in melanoma tissues and cells, especially in metastatic melanoma. High HOTAIR levels correlate with poor prognosis in melanoma patients. We also determined that HOTAIR functions as a competing endogenous RNA (ceRNA) for miR-152-3p. miR-152-3p was decreased and acted as a tumor suppressor in melanoma, and c-MET was the functional target of miR-152-3p. Furthermore, HOTAIR promotes the growth and metastasis of melanoma cells by competitively binding miR-152-3p, which functionally liberates c-MET mRNA and results in the activation of the downstream PI3k/Akt/mTOR signaling pathway. We determined that HOTAIR acts as a ceRNA to promote malignant melanoma progression by sponging miR-152-3p. This finding elucidates a new mechanism for HOTAIR in melanoma development and provides a potential therapeutic target for melanoma patients.	MIMAT0000438	Oncotarget 2017 Oct 17 8, 85401-85414 doi:10.18632/oncotarget.19910 PMID:29156728
1797	LncRNA	HOTAIR	miR-331-3p	NA	Cervical cancer cell lines	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase Assay etc.	28745272	Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer Interacting with MicroRNA-17-5p.	HOTAIR expression was significantly upregulated in both cervical cancer tissues and cell lines. HOTAIR could regulate tumorigenesis of gastric cancer in vivo and in vitro through acting as a competing endogenous RNA to sequester miR-331-3p28. the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer.	MI0000812	Oncol Res 2018 Apr 10 26, 353-361 doi:10.3727/096504017x15002869385155 PMID:28745272
1798	LncRNA	HOTAIR	miR-17-5p	NA	Cervical cancer cell lines	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase Assay etc.	28745272	Long Noncoding RNA HOTAIR: An Oncogene in Human Cervical Cancer Interacting with MicroRNA-17-5p.	HOTAIR expression was significantly upregulated in both cervical cancer tissues and cell lines. HOTAIR could regulate tumorigenesis of gastric cancer in vivo and in vitro through acting as a competing endogenous RNA to sequester miR-331-3p28. the tumor-promoting role of HOTAIR in cervical cancer via sponging miR-17-5p, providing a novel therapeutic target for future treatment of cervical cancer.	MIMAT0000070	Oncol Res 2018 Apr 10 26, 353-361 doi:10.3727/096504017x15002869385155 PMID:28745272
1799	LncRNA	HOTAIR	miR-545	EGFR	Sw480 And Lovo	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28364379	MicroR-545 mediates colorectal cancer cells proliferation through up-regulating epidermal growth factor receptor expression in HOTAIR long non-coding RNA dependent.	HOTAIR expression was significantly up-regulated in colorectal tissues compared with normal tissues. miR-545 expression was suppressed by HOTAIR overexpression whereas enhanced by HOTAIR silence. Suppression of EGFR expression by miR-545 mimic was abrogated by HOTAIR overexpression. HOTAIR long non-coding RNA mediates microR-545 regulating colorectal cancer cells proliferation.Although therapeutic advantage has been raised in surgery with radiation and chemotherapy, patients still face a big challenge for improving the survival rate and quality of life.	MI0003516	Mol Cell Biochem 2017 Jul 431, 45-54 doi:10.1007/s11010-017-2974-4 PMID:28364379
1800	LncRNA	HOTTIP	miR-101	ZEB1	U87, U251	Malignant Glioma	Homo sapiens (human)	qPCR,luciferase reporter assay etc.	28886531	Long non-coding RNA HOTTIP promotes hypoxia-induced epithelialmesenchymal transition of malignant glioma by regulating the miR-101/ZEB1 axis	HOTTIP was the most upregulated lncRNA in glioma cells treated by hypoxia. High levels of HOTTIP and HIF-1α were correlated with glioma metastasis and poor patient prognosis. Knockdown of HIF-1α and HOTTIP blocked hypoxia-induced EMT, and suppressed invasion and migration of glioma cells. Finally, HOTTIP sponged endogenous miR-101 and inhibited its activity, which resulted in increased ZEB1 expression and promoted process of EMT. HIF-1α/HOTTIP/miR-101/ZEB1 axis plays essential role in hypoxia-induced EMT and metastasis of glioma, and HOTTIP may serve as a therapeutic target to reverse EMT and prevent glioma progression.	MI0000103	Biomed Pharmacother 2017 Nov 95, 711-720 doi:10.1016/j.biopha.2017.08.133 PMID:28886531
1801	LncRNA	HOTTIP	miR-574-5p	EZH1	H69, H446, H146, H446Ar, H69Ar	Small Cell Lung Cancer	Homo sapiens (human)	mcroarray,qPCR,Western blot ,RIP,Luciferase reporter assay etc.	29041935	A long non-coding RNA HOTTIP expression is associated with disease progression and predicts outcome in small cell lung cancer patients	HOTTIP was overexpressed in SCLC tissues, and its expression was correlated with the clinical stage and the shorter survival time of SCLC patients. Moreover, HOTTIP knockdown could impair cell proliferation, affect the cell cycle and inhibit tumor growth of mice, while HOTTIP overexpression might enhance cell proliferation and cell cycle in vitro and in vivo. Mechanistic investigations showed that HOTTIP functions as an oncogene in SCLC progression by sponging miR-574-5p and affecting the expression of polycomb group protein EZH1.	MIMAT0004795	Mol Cancer 2017 Oct 17 16, 162 doi:10.1186/s12943-017-0729-1 PMID:29041935
1802	LncRNA	HOTTIP	miR-30b	HOXA13	Eca-109, Kyse-30, Kyse-150,Kyse-180, Kyse-410, Kyse-450, Kyse-510, Te-10 And Te-13 	Esophageal Squamous Cancer	Homo sapiens (human)	Western blot,RIP,ChIP,qPCR,etc.	28534516	Transcriptional and posttranscriptional regulation of HOXA13 by lncRNA HOTTIP facilitates tumorigenesis and metastasis in esophageal squamous carcinoma cells	HOTTIP modulated HOXA13 at both the transcriptional and posttranscriptional levels in ESCC cells and HOTTIP-miR-30b-HOXA13 axis may serve as potential diagnostic markers or drug targets for ESCC therapies.	MI0000441	Oncogene 2017 Sep 21 36, 5392-5406 doi:10.1038/onc.2017.133 PMID:28534516
1803	LncRNA	HOXA11-AS	miR-214-3p	EZH2	U251, U87, Ln229, Shg-44, A172	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assays,Western blot etc.	28946213	Regulation of HOXA11-AS/miR-214-3p/EZH2 axis on the growth, migration and invasion of glioma cells	HOXA11-AS was up-regulated in glioma tissues and cell lines, and related to overall survival.High expression of HOXA11-AS was correlated with shorter overall survival in patients with glioma. Knockdown of HOXA11-AS inhibited glioma cell proliferation, migration and invasion in vitro, and tumor growth in vivo. In addition, we demonstrated that HOXA11-AS functioned as a competing endogenous RNA (ceRNA) for miR-214-3p, which in turn positively regulated the expression of its direct target EZH2.	MIMAT0000271	Biomed Pharmacother 2017 Nov 95, 1504-1513 doi:10.1016/j.biopha.2017.08.097 PMID:28946213
1804	LncRNA	HOXA11-AS	miR-124	p21	Ocm-1A, Mum-2C, C918, Mum-2B, D78 	Uveal Melanoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28749709	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma	The aim of this study was to explore the critical role of lncRNA HOXA11-AS in uveal melanoma (UM) progression.Briefly, we found that HOXA11-AS is overexpressed in UM tissues and cells; HOXA11-AS could regulate UM cell growth, invasion, and apoptosis. Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression. In addition, we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS. Collectively, our findings reveal an oncogenic role for HOXA11-AS in UM tumorigenesis.	MI0000443	DNA Cell Biol 2017 Oct 36, 837-844 doi:10.1089/dna.2017.3808 PMID:28749709
1805	LncRNA	HOXA11-AS	miR-124	EZH2	Ocm-1A, Mum-2C, C918, Mum-2B, D78 	Uveal Melanoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28749709	LncRNA HOXA11-AS Exerts Oncogenic Functions by Repressing p21 and miR-124 in Uveal Melanoma	The aim of this study was to explore the critical role of lncRNA HOXA11-AS in uveal melanoma (UM) progression.Briefly, we found that HOXA11-AS is overexpressed in UM tissues and cells; HOXA11-AS could regulate UM cell growth, invasion, and apoptosis. Mechanistically, RNA immunoprecipitation demonstrated that HOXA11-AS could simultaneously interact with enhancer of zeste homolog 2 (EZH2) to suppress its target p21 protein expression. In addition, we demonstrated that HOXA11-AS functioned as a molecular sponge for miR-124, and overexpression of miR-124 attenuated the proliferation and invasion-promoting effect of HOXA11-AS. Collectively, our findings reveal an oncogenic role for HOXA11-AS in UM tumorigenesis.	MI0000443	DNA Cell Biol 2017 Oct 36, 837-844 doi:10.1089/dna.2017.3808 PMID:28749709
1806	LncRNA	HOXA11-AS	miR-124	Sp1	A549,H1299, H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,etc.	29034803	LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non–small cell lung cancer cells	HOXA11-AS expression was upregulated in non-small cell lung cancer tissues and cell lines. High levels of HOXA11-AS expression were correlated with larger tumor size and lymph node metastasis. Functional analysis revealed that HOXA11-AS promotes non–small cell lung cancer cell proliferation and invasion. In particular, HOXA11-AS functions as a competing endogenous RNA to regulate transcriptional factor Sp1 expression via sponging miR-124. Collectively, our findings reveal an oncogenic role for HOXA11-AS in non–small cell lung cancer tumorigenesis.	MI0000443	Tumour Biol 2017 Oct 39, 1010428317721440 doi:10.1177/1010428317721440 PMID:29034803
1807	LncRNA	HOXA11-AS	miR-200b	ZEB1	A549, H1299, 95D	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,RIP,Western blotting etc.	28615992	Overexpression of lncRNA HOXA11-AS promotes cell epithelial–mesenchymal transition by repressing miR-200b in non-small cell lung cancer	upregulation of lncRNA HOXA11-AS predicted a poor prognosis and lncRNA HOXA11-AS promoted cell epithelial-mesenchymal transition (EMT) by inhibiting miR-200b expression in NSCLC.	MI0000342	Cancer Cell Int 2017  17, 64 doi:10.1186/s12935-017-0433-7 PMID:28615992
1808	LncRNA	HOXA11-AS	miR-124-3p	ROCK1	U2Os, Mg-63 And Khos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc.	28558357	Long non-coding RNA HOXA11-AS functions as a competing endogenous RNA to regulate ROCK1 expression by sponging miR-124-3p in osteosarcoma.	the expression of HOXA11-AS was upregulated in OS tissues and cell lines.The high expression of HOXA11-AS was associated with advanced clinical stage, distant metastasis and poor overall survival of OS. HOXA11-AS silencing suppressed OS cells proliferation, invasion and induced cell arrest in G0/G1 phase. HOXA11-AS acts as an endogenous sponge by directly binding miR-124-3p,and decreasing the xpression of miR-124-3p.HOXA11-AS may regulate tumor progression by affecting miR-124-3p targets, and ROCK1 expression.	MIMAT0000422	Biomed Pharmacother 2017 Aug 92, 437-444 doi:10.1016/j.biopha.2017.05.081 PMID:28558357
1809	LncRNA	HOXA11-AS	miR-1297	EZH2	A549, H460, 1299, Pc9	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	28717185	Clinical Significance and Effect of lncRNA HOXA11-AS in NSCLC: A Study Based on Bioinformatics, In Vitro and in Vivo Verification.	an up-regulated trend in HOXA11-AS level in NSCLC tissues was found compared to corresponding non-cancerous lung tissues based on qRT-PCR.Additionally, Sun39 et al. investigated the potential mechanism of HOXA11-AS in gastric cancer cells, and they found that HOXA11-AS could play an oncogenic role through the EZH2/HOXA11-AS/LSD1 complex or HOXA11-AS/miR-1297/EZH2 crosstalk. Richards43 et al. NSCLC accounts for approximately 80% of lung cancer, and currently, it still has an unsatisfactory prognosis despite the advances made in its treatments, with an overall 5-year survival rate of less than 16%5,6,7.	MIMAT0005886	Sci Rep 2017 Jul 17 7, 5567 doi:10.1038/s41598-017-05856-2 PMID:28717185
1810	LncRNA	HOXA11-AS	miR-1297	LSD1	A549, H460, 1299, Pc9	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	28717185	Clinical Significance and Effect of lncRNA HOXA11-AS in NSCLC: A Study Based on Bioinformatics, In Vitro and in Vivo Verification.	an up-regulated trend in HOXA11-AS level in NSCLC tissues was found compared to corresponding non-cancerous lung tissues based on qRT-PCR.Additionally, Sun39 et al. investigated the potential mechanism of HOXA11-AS in gastric cancer cells, and they found that HOXA11-AS could play an oncogenic role through the EZH2/HOXA11-AS/LSD1 complex or HOXA11-AS/miR-1297/EZH2 crosstalk. Richards43 et al. NSCLC accounts for approximately 80% of lung cancer, and currently, it still has an unsatisfactory prognosis despite the advances made in its treatments, with an overall 5-year survival rate of less than 16%5,6,7.	MIMAT0005886	Sci Rep 2017 Jul 17 7, 5567 doi:10.1038/s41598-017-05856-2 PMID:28717185
1811	LncRNA	HOXA11-AS	miR-125a-5p	PADI2	Colo205, Hct116, Lovo, Sw620, Caco-2, And Sw480	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29050308	The lncRNA HOXA11-AS functions as a competing endogenous RNA to regulate PADI2 expression by sponging miR-125a-5p in liver metastasis of colorectal cancer.	We previously described the potential involvement of HOMEOBOX A11 (HOXA11) antisense RNA (HOXA11-AS), miR-125a-5p, and peptidyl arginine deiminase 2 (PADI2) in promoting liver metastasis in CRC patients. In the present study, we verified the significant upregulation of HOXA11-AS and PADI2, as well as the downregulation of miR-125a-5p, in CRC patients with liver metastasis. Overexpression and knockdown studies of HOXA11-AS or PADI2, as well as gain-/loss-of-function studies of miR-125a-5p, revealed a positive correlation between HOXA11-AS and PADI2 and a negative correlation with miR-125a-5p in the regulation of liver metastasis in CRC cell lines. Overall, we conclude that HOXA11-AS promotes liver metastasis in CRC by functioning as a miR-125a-5p sponge and describe a novel HOXA11-AS-miR-125a-5p-PADI2 regulatory network involved in CRC liver metastasis. In this study, HOXA11-AS expression was up-regulated in the tissues of CRC patients with liver metastasis. The knockdown and overexpression of HOXA11-AS inhibited and promoted the migration and invasion of colon cancer cells, respectively. Moreover, we confirmed that HOXA11-AS functions as a ceRNA to regulate PADI2 expression by sponging miR-125a-5p. The HOXA11-AS/miR-125a-5p/PADI2 regulatory network may represent a novel therapeutic target for liver metastasis of CRC.	MIMAT0000443	Oncotarget 2017 Sep 19 8, 70642-70652 doi:10.18632/oncotarget.19956 PMID:29050308
1812	LncRNA	HOXA-AS2	miR-520c-3p	TGFBR2	Mcf-10A, Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase report assay etc.	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	HOXA-AS2 was up-regulated in human breast cancer tissues and cell lines and associated with clinicopathological characteristics. HOXA-AS2 may be a potential prognostic and therapeutic target in breast cancer. HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
1813	LncRNA	HOXA-AS2	miR-520c-3p	RELA	Mcf-10A, Mda-Mb-231, Mda-Mb-453, And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase report assay etc.	28545023	Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge.	HOXA-AS2 was up-regulated in human breast cancer tissues and cell lines and associated with clinicopathological characteristics. HOXA-AS2 may be a potential prognostic and therapeutic target in breast cancer. HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. 	MIMAT0002846	Oncotarget 2017 Jul 11 8, 46090-46103 doi:10.18632/oncotarget.17552 PMID:28545023
1814	LncRNA	HOXD-AS1	miR-147a	pRB	A549, H1703, Sk-Mes-1, Nci-H1299	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,etc.	29033588	hOXD-as1 functions as an oncogenic cerna to promote nsclc cell progression by sequestering mir-147a	HOXD-AS1 could negatively regulate the expression of miR-147a. miR-147a inhibition abrogated the effect of HOXD-AS1 knockdown on the proliferation and apoptosis of NSCLC cells. Furthermore, HOXD-AS1 positively regulated the expression of pRB (a tumor suppressor protein) in NSCLC cells. Taken together, our data indicated that HOXD-AS1 might be an oncogenic lncRNA that promotes proliferation of NSCLC and could be a therapeutic target in NSCLC.	MI0000262	Onco Targets Ther 2017  10, 4753-4763 doi:10.2147/ott.S143787 PMID:29033588
1815	LncRNA	HOXD-AS1	miR-130a-3p	EZH2	Snu449, Huh28, Smmc-7721, Huh7, Hep3B,Human Embryonic Kidney Cell Line	Liver Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,In vitro assays,Luciferase reporter assay	28810927	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4.	In the current study, using gene expression profiling analysis we discovered a lncRNA HOXD-AS1 was upregulated in HCC and significantly correlated with poor prognosis of HCC patients. Meanwhile, we demonstrated that HOXD-AS1 promoted HCC metastasis by acting as a ceRNA to upregulate the expression of SOX4 and activated the expression of EZH2 and MMP2, two direct target genes of SOX4.In this study, we found that HOXD-AS1 was significantly upregulated in HCC tissues. Clinical investigation demonstrated high expression level of HOXD-AS1 was associated with poor prognosis and high tumor node metastasis stage of HCC patients, and was an independent risk factor for survival. lncRNAs also can function as competing endogenous RNAs (ceRNAs) by competitively binding miRNAs, thereby modulating the derepression of miRNAs targets. 	MIMAT0000427	Mol Cancer 2017 Aug 14 16, 136 doi:10.1186/s12943-017-0680-1 PMID:28810927
1816	LncRNA	HOXD-AS1	miR-130a-3p	MMP2	Snu449, Huh28, Smmc-7721, Huh7, Hep3B,Human Embryonic Kidney Cell Line	Liver Cancer	Homo sapiens (human)	Microarray,qPCR,Western blot,In vitro assays,Luciferase reporter assay	28810927	STAT3-mediated upregulation of lncRNA HOXD-AS1 as a ceRNA facilitates liver cancer metastasis by regulating SOX4.	In the current study, using gene expression profiling analysis we discovered a lncRNA HOXD-AS1 was upregulated in HCC and significantly correlated with poor prognosis of HCC patients. Meanwhile, we demonstrated that HOXD-AS1 promoted HCC metastasis by acting as a ceRNA to upregulate the expression of SOX4 and activated the expression of EZH2 and MMP2, two direct target genes of SOX4.In this study, we found that HOXD-AS1 was significantly upregulated in HCC tissues. Clinical investigation demonstrated high expression level of HOXD-AS1 was associated with poor prognosis and high tumor node metastasis stage of HCC patients, and was an independent risk factor for survival. lncRNAs also can function as competing endogenous RNAs (ceRNAs) by competitively binding miRNAs, thereby modulating the derepression of miRNAs targets. 	MIMAT0000427	Mol Cancer 2017 Aug 14 16, 136 doi:10.1186/s12943-017-0680-1 PMID:28810927
1817	LncRNA	HOXD-AS1	miR-19a	ARHGAP11A	Hcclm3, Mhcc97H, Mhcc97L, Smmc7721 And L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	28724429	The noncoding RNA HOXD-AS1 is a critical regulator of the metastasis and apoptosis phenotype in human hepatocellular carcinoma.	remarkable overexpression of HOXD-AS1 in metastatic cancer tissues.In vitro and in vivo gain- or loss-of-function studies re-affirmed that HOXD-AS1 is able to facilitate cancer metastasis and inhibit apoptosis. HOXD-AS1 is an oncogenic lncRNA that promotes HCC metastasis and that its pro-metastatic phenotype can partially be attributed to the HOXD-AS1/miR19a/ARHGAP11A signaling axis. downregulated by ectopic HOXD-AS1 overexpression, leading to a remarkably reduced apoptotic effect. OXD-AS1 functions as a competing endogenous RNA (ceRNA) by “sponging” miR19a during HCC metastasis/recurrence.	MI0000073	Mol Cancer 2017 Jul 19 16, 125 doi:10.1186/s12943-017-0676-x PMID:28724429
1818	LncRNA	HULC	miR-122	PI3K	Mg63,Hfob1.19,Os-732	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28688193	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma.	Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G.high levels of HULC were associated with low survival rates in osteosarcoma patients.	MI0000442	J Cell Biochem 2018 Jan 119, 1050-1061 doi:10.1002/jcb.26273 PMID:28688193
1819	LncRNA	HULC	miR-122	AKT	Mg63,Hfob1.19,Os-732	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28688193	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma.	Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G.high levels of HULC were associated with low survival rates in osteosarcoma patients.	MI0000442	J Cell Biochem 2018 Jan 119, 1050-1061 doi:10.1002/jcb.26273 PMID:28688193
1820	LncRNA	HULC	miR-122	STAT	Mg63,Hfob1.19,Os-732	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28688193	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma.	Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G.high levels of HULC were associated with low survival rates in osteosarcoma patients.	MI0000442	J Cell Biochem 2018 Jan 119, 1050-1061 doi:10.1002/jcb.26273 PMID:28688193
1821	LncRNA	HULC	miR-122	JAK	Mg63,Hfob1.19,Os-732	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28688193	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma.	Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G.high levels of HULC were associated with low survival rates in osteosarcoma patients.	MI0000442	J Cell Biochem 2018 Jan 119, 1050-1061 doi:10.1002/jcb.26273 PMID:28688193
1822	LncRNA	HULC	miR-122	HNF4G	Mg63,Hfob1.19,Os-732	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28688193	Knockdown of lncRNA HULC inhibits proliferation, migration, invasion, and promotes apoptosis by sponging miR-122 in osteosarcoma.	Suppression of HULC in osteosarcoma cells inhibited cell viability,migration,invasion, and promoted apoptosis. HULC functioned as an endogenous sponge for miR-122,and its silence functioned through upregulating miR-122.Furthermore,overexpression of miR-122 inactivated PI3K/AKT, JAK/STAT, and Notch pathways by downregulation of HNF4G.high levels of HULC were associated with low survival rates in osteosarcoma patients.	MI0000442	J Cell Biochem 2018 Jan 119, 1050-1061 doi:10.1002/jcb.26273 PMID:28688193
1823	LncRNA	HULC	miR-6825-5p	COX-2	Hepg2, Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP,etc.	28634076	lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein.	HULC promoted the growth of HCC cells through elevating COX-2 protein. knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells.HULC promoted the survival of HepG2 and Hep3B cells in a dosedependent manner.We previous revealed that three miRNAs (miR-6825e5p, miR-6845e5p and miR-6886e3p) were involved in HULC mediated USP22 and Sirt1 upregulation	MIMAT0027550	Biochem Biophys Res Commun 2017 Aug 26 490, 693-699 doi:10.1016/j.bbrc.2017.06.103 PMID:28634076
1824	LncRNA	HULC	miR-6845-5p	COX-2	Hepg2, Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP,etc.	28634076	lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein.	HULC promoted the growth of HCC cells through elevating COX-2 protein. knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells.HULC promoted the survival of HepG2 and Hep3B cells in a dosedependent manner.We previous revealed that three miRNAs (miR-6825e5p, miR-6845e5p and miR-6886e3p) were involved in HULC mediated USP22 and Sirt1 upregulation	MIMAT0027590	Biochem Biophys Res Commun 2017 Aug 26 490, 693-699 doi:10.1016/j.bbrc.2017.06.103 PMID:28634076
1825	LncRNA	HULC	miR-6886-3p	COX-2	Hepg2, Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP,etc.	28634076	lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein.	HULC promoted the growth of HCC cells through elevating COX-2 protein. knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells.HULC promoted the survival of HepG2 and Hep3B cells in a dosedependent manner.We previous revealed that three miRNAs (miR-6825e5p, miR-6845e5p and miR-6886e3p) were involved in HULC mediated USP22 and Sirt1 upregulation	MIMAT0027673	Biochem Biophys Res Commun 2017 Aug 26 490, 693-699 doi:10.1016/j.bbrc.2017.06.103 PMID:28634076
1826	LncRNA	ILF3-AS1	miR-200b	EZH2	SK-MEL-2, SK-MEL-28 and A375	Melanoma	Homo sapiens (human)	qPCR,RIP etc.	28935763	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration and invasion via negatively regulating miR-200b/a/429 in melanoma	lncRNA ILF3-AS1 is upregulated in melanoma tissues and cell lines, and correlated with poor prognosis of melanoma patients. Functional experiments showed that knockdown of ILF3-AS1 inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues.Moreover,inhibition of miR-200b/a/429 abrogates the biological roles of ILF3-AS1 knockdown on melanoma cell proliferation, migration and invasion. 	MI0000342	Biosci Rep 2017 Dec 22 37 doi:10.1042/bsr20171031 PMID:28935763
1827	LncRNA	ILF3-AS1	miR-200a	EZH2	SK-MEL-2, SK-MEL-28 and A375	Melanoma	Homo sapiens (human)	qPCR,RIP etc.	28935763	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration and invasion via negatively regulating miR-200b/a/429 in melanoma	lncRNA ILF3-AS1 is upregulated in melanoma tissues and cell lines, and correlated with poor prognosis of melanoma patients. Functional experiments showed that knockdown of ILF3-AS1 inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues.Moreover,inhibition of miR-200b/a/429 abrogates the biological roles of ILF3-AS1 knockdown on melanoma cell proliferation, migration and invasion. 	MI0000737	Biosci Rep 2017 Dec 22 37 doi:10.1042/bsr20171031 PMID:28935763
1828	LncRNA	ILF3-AS1	miR-429	EZH2	SK-MEL-2, SK-MEL-28 and A375	Melanoma	Homo sapiens (human)	qPCR,RIP etc.	28935763	Long noncoding RNA ILF3-AS1 promotes cell proliferation, migration and invasion via negatively regulating miR-200b/a/429 in melanoma	lncRNA ILF3-AS1 is upregulated in melanoma tissues and cell lines, and correlated with poor prognosis of melanoma patients. Functional experiments showed that knockdown of ILF3-AS1 inhibits melanoma cell proliferation, migration and invasion. Mechanistically, we found that ILF3-AS1 interacts with EZH2, promotes the binding of EZH2 to the miR-200b/a/429 promoter, and represses miR-200b/a/429 expression. The expression of ILF3-AS1 is negatively correlated with that of miR-200b/a/429 in melanoma tissues.Moreover,inhibition of miR-200b/a/429 abrogates the biological roles of ILF3-AS1 knockdown on melanoma cell proliferation, migration and invasion. 	MIMAT0001536	Biosci Rep 2017 Dec 22 37 doi:10.1042/bsr20171031 PMID:28935763
1829	LncRNA	KCNQ1OT1	miR-370	CCNE2	U87, U251	Glioma	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assay	28381990	Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells’ Malignancy by Activating miR-370/CCNE2 Axis	KCNQ1OT1 expression was up-regulated in glioma tissues and cells.These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.	MI0000778	Front Cell Neurosci 2017  11, 84 doi:10.3389/fncel.2017.00084 PMID:28381990
1830	LncRNA	LET	miR-145	TGFb1	T24, 5637, J82, Sw780, Biu87, Scaber And Umuc3	Bladder Cancer	Homo sapiens (human)	qPCR,RIP,western blot etc.	28839463	TGFβ1 Promotes Gemcitabine Resistance through Regulating the LncRNA-LET/NF90/miR-145 Signaling Axis in Bladder Cancer	LET was the only lncRNA that was downregulated more than 2 folds in GEM-treated xenografts derived from both T24 and 5637 cells. The array results were further validated in these cell lines treated with or without GEM. reduced lncRNA-LET increased the NF90 protein stability, which in turn repressed biogenesis of miR-145 and subsequently resulted in accumulation of CSCs evidenced by the elevated levels of stemness markers HMGA2 and KLF4. UBC patients which displayed lower expression levels of lncRNA-LET and miR-145 had a reduced survival rate, whereas TGFβ1 expression level did not show significant difference in clinical outcome.	MI0000461	Theranostics 2017  7, 3053-3067 doi:10.7150/thno.19542 PMID:28839463
1831	LncRNA	LeXis	miR-199a	CTNNB1	Nhost, Khos, 143B, Lm7, U2Os, And Mg-63 	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc.	28744406	Long noncoding RNA LeXis promotes osteosarcoma growth through upregulation of CTNNB1 expression.	LeXis expression was upregulated in OS tissues. Increased LeXis expression was significantly correlated with high tumor stage, large tumor size, and poor prognosis. LeXis increased CTNNB1 expression by functioning as a ceRNA of CTNNB1 against miR-199a.Moreover, LeXis increased CTNNB1 expression by functioning as a ceRNA of CTNNB1 against miR-199a. The 5-year survival rate of patients with OS having distant metastases is approximately 30% .	MI0000242	Am J Cancer Res 2017  7, 1577-1587,  PMID:28744406
1832	LncRNA	LINC00052	miR-452-5P	EPB41L3	L02, Smmc7721, Sk-Hep1, Huh7, Hepg2   	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP etc	28969024	LINC00052 upregulates EPB41L3 to inhibit migration and invasion of hepatocellular carcinoma by binding miR-452-5p.	We found that overexpression of LINC00052 could upregulate the EPB41L3 expression and it might serve as a tumor suppressor gene in HCC. Database analysis showed that miR-452-5P could target LINC00052. The binding regions between LINC00052 and miR-452-5P were confirmed by luciferase assays. Moreover, LINC00052 inhibited cell malignant behavior by increasing miR-452-5P expression, suggesting that LINC00052 was negatively regulated by miR-452-5P.In addition, overexpression of  miR-452-5P resulted in a decrease of EPB41L3 expression, suggesting that EPB41L3  was as a target of miR-452-5P. In conclusion, these results demonstrated that a novel pathway was mediated by LINC00052 in HCC. 	MIMAT0001635	Oncotarget 2017 Sep 8 8, 63724-63737 doi:10.18632/oncotarget.18892 PMID:28969024
1833	LncRNA	LINC00152	miR-138	HIF-1a	Gbc-Sd And H69	Gallbladder Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	28077595	Long non-coding RNA LINC00152 promotes gallbladder cancer metastasis and epithelial-mesenchymal transition by regulating HIF-1α via miR-138.	LINC00152 is overexpressed in gallbladder cancer (GBC) tissue samples and cell lines.Functionally, LINC00152 dramatically promoted cell migration,invasion and epithelial-mesenchymal transition (EMT) progression in vitro. In vivo, LINC00152 overexpression significantly promoted tumour peritoneal spreading and metastasis. LINC00152 functions as a molecular sponge for miR-138, which directly suppresses the expression of HIF-1α.We revealed that miR-138 is a suppressor of GBC cell metastasis and EMT progression, and a similar phenomenon was observed in HIF-1α knockdown NOZ cells.	MI0000455	Open Biol 2017 Jan 7 doi:10.1098/rsob.160247 PMID:28077595
1834	LncRNA	LINC00152	miR-205	P16	Achn, Caki-1, Caki-2 And 786-O	Renal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,ChIP,Luciferase reporter assay,Flow cytometry assay etc.	28337379	Long intergenic non-coding RNA 00152 promotes renal cell carcinoma progression by epigenetically suppressing P16 and negatively regulates miR-205.	LINC00152 expression was up-regulated in RCC tissues compared with adjacent normal tissues.Furthermore, knockdown of LINC00152 inhibited RCC cell proliferation and S phase cell proportion in vitro. Mechanistically,LINC00152 may contribute to RCC progression by epigenetically repressing P16 expression and interacted with miR-205.	MI0000285	Am J Cancer Res 2017  7, 312-322,  PMID:28337379
1835	LncRNA	LINC00152	miR-103a-3p	FEZF1	U87, U251 And Hek	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28651608	Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway.	Linc00152 was up-regulated in glioma tissues as well as in GSCs. Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs  by binding to miR-103a-3p, which functions as a tumor suppressor.In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1),a direct target of miR-103a-3p which played an oncogenic role in GSCs.FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A).CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.Linc00152 knockdown combined with over-expressed miR-103a-3p suppressed tumor growth and manifested high survival in nude mice.	MIMAT0000101	Mol Cancer 2017 Jun 26 16, 110 doi:10.1186/s12943-017-0677-9 PMID:28651608
1836	LncRNA	LINC00152	miR-103a-3p	CDC25A	U87, U251 And Hek	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28651608	Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway.	Linc00152 was up-regulated in glioma tissues as well as in GSCs. Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs  by binding to miR-103a-3p, which functions as a tumor suppressor.In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1),a direct target of miR-103a-3p which played an oncogenic role in GSCs.FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A).CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.Linc00152 knockdown combined with over-expressed miR-103a-3p suppressed tumor growth and manifested high survival in nude mice.	MIMAT0000101	Mol Cancer 2017 Jun 26 16, 110 doi:10.1186/s12943-017-0677-9 PMID:28651608
1837	LncRNA	LINC00152	miR-138	HIF1	Hct-116	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	29345294	Hypoxia stimulates the cytoplasmic localization of oncogenic long noncoding RNA LINC00152 in colorectal cancer.	A cell culture under hypoxic conditions revealed several lncRNAs,such as LINC00152, whose levels were increased in the cytoplasm of colorectal cancer cells.A database study indicated that LINC00152 shares microRNA-binding sites, such as miR-138 and miR-193, with HIF1,thus suggesting that LINC00152 could possibly function as a competing endogenous RNA that can augment Hif1 translation in the cytoplasm of hypoxic colorectal cancer cells. 	MI0000455	Int J Oncol 2018 Feb 52, 453-460 doi:10.3892/ijo.2017.4218 PMID:29345294
1838	LncRNA	LINC00176	miR-9	Myc	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000466	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1839	LncRNA	LINC00176	miR-9	Max	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000466	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1840	LncRNA	LINC00176	miR-9	AP-4	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000466	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1841	LncRNA	LINC00176	miR-185	Myc	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000482	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1842	LncRNA	LINC00176	miR-185	Max	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000482	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1843	LncRNA	LINC00176	miR-185	AP-4	Huh7 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	RNA-seq,Microarray,qRT–PCR	28869604	Myc target gene, long intergenic noncoding RNA, Linc00176 in hepatocellular carcinoma regulates cell cycle and cell survival by titrating tumor suppressor microRNAs.	Linc00176 regulates expression of more than 200 genes by the sponge function for tumor suppressor miRNAs, miR-9 and miR-185. Linc00176 is expressed at a high level only in HCC, and is activated by Myc, Max and AP-4 transcription regulators. Myc also upregulates miR-9 and miR-185. In Linc00176-depleted HCC, these miRNAs were released from Linc00176 and downregulated their target mRNAs.	MI0000482	Oncogene 2018 Jan 4 37, 75-85 doi:10.1038/onc.2017.312 PMID:28869604
1844	LncRNA	LINC00339	miR-539-5p	MMP-2	U87,U251,Glioma Tissues	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29499931	Long Non-coding RNA LINC00339 Stimulates Glioma Vasculogenic Mimicry Formation by Regulating the miR-539-5p/TWIST1/MMPs Axis.  	Knockdown of LINC00339 inhibited glioma cell proliferation, migration, invasion, and tube formation,meanwhile downregulating the expression of VM-related molecular MMP-2 and MMP-14.TWIST1 upregulated the promoter activities of MMP-2 and MMP-14.  	MIMAT0003163	Mol Ther Nucleic Acids 2018 Mar 2 10, 170-186 doi:10.1016/j.omtn.2017.11.011 PMID:29499931
1845	LncRNA	LINC00339	miR-539-5p	MMP-14	U87,U251,Glioma Tissues	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29499931	Long Non-coding RNA LINC00339 Stimulates Glioma Vasculogenic Mimicry Formation by Regulating the miR-539-5p/TWIST1/MMPs Axis.  	Knockdown of LINC00339 inhibited glioma cell proliferation, migration, invasion, and tube formation,meanwhile downregulating the expression of VM-related molecular MMP-2 and MMP-14.TWIST1 upregulated the promoter activities of MMP-2 and MMP-14.  	MIMAT0003163	Mol Ther Nucleic Acids 2018 Mar 2 10, 170-186 doi:10.1016/j.omtn.2017.11.011 PMID:29499931
1846	LncRNA	LINC00460	miR-149-5p	IL6	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1, Immortalized Nasopharyngeal Epithelial Cell Line 	Nasopharyngeal Cancer	Homo sapiens (human)	RNA-seq,qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	28987345	LncRNA-LINC00460 facilitates nasopharyngeal carcinoma tumorigenesis through sponging miR-149-5p to up-regulate IL6.	LINC00460 was markedly increased in NPC tissues and cells compared to their corresponding controls. Silencing LINC00460 was able to suppress NPC cell growth in vitro while overexpressing LINC00460 reversed this process. LINC00460 contributed to the progression of NPC through regulating miR-149-5p/IL6 signal pathway. 	MIMAT0000450	Gene 2018 Jan 10 639, 77-84 doi:10.1016/j.gene.2017.10.006 PMID:28987345
1847	LncRNA	LINC00473	miR-195	IKKa	Sk- Nep- 1	Wilms Tumor	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	29159834	LINC00473 antagonizes the tumour suppressor miR-195 to mediate the pathogenesis of Wilms tumour via IKKα.	the expression of LINC00473 was elevated in tumour tissues than that in relative normal tissues. Higher LINC00473 levels correlated to higher stage and unfavourable histology Wilms tumour. Mechanistically, knockdown of LINC00473 inhibited cell vitality and induced Bcl-2-dependent apoptosis and G1/S arrest via CDK2 and cyclin D1.Moreover,LINC00473 harboured binding sites for miR-195 and limited miR-195 availability in a dose-dependent manner.Forced expression of miR-195 impaired tumour survival and metastasis, which, however,could be restored by LINC00473. Furthermore, IKKα was the downstream of LINC00473/miR-195 signals and could be directly targeted by miR-195 to participate LINC00473-induced tumour progression. Loss-of-function of LINC00473 in vivo effectively promoted the regression of Wilms tumour via miR-195/IKKα-mediated growth inhibition.	MI0000489	Cell Prolif 2018 Feb 51 doi:10.1111/cpr.12416 PMID:29159834
1848	LncRNA	LINC00511	miR-29b-3p	VEGFA	Panc-1, Mia Paca-2, Capan-2, Sw1990, Aspc-1, Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	28984028	Linc00511 acts as a competing endogenous RNA to regulate VEGFA expression through sponging hsa-miR-29b-3p in pancreatic ductal adenocarcinoma.	The aberrant up-regulation of linc00511 was detected in PDAC cell lines and patient specimens compared with controls.An increase in linc00511 expression indicates the adverse clinical pathological characteristics and poor prognosis. linc00511 depletion in PDAC cells decreased proliferation,migration, invasion and endothelial tube formation.linc00511 could up-regulate VEGFA via its competing endogenous RNA (ceRNA) activity on hsa-miR-29b-3p.	MIMAT0000100	J Cell Mol Med 2018 Jan 22, 655-667 doi:10.1111/jcmm.13351 PMID:28984028
1849	LncRNA	LINC00657	miR-106a-5p	PTEN	Hepg2, Huh7, Hep3B, Bel-7402, Smmc-7721, Hccm3 	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28919047	Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression	The expression level of LINC00657 was downregulated in HCC tissues and HCC cell lines.Moreover,we illustrated the role of LINC00657 in suppressing the growth, invasion, migration of HCC in vitro.In addition, we found that LINC00657 can act as a ceRNA for PTEN mRNA through miR-106a-5p.Finally, we confirmed the role of LINC00657 in vivo.These results deepen our understanding of the role of LINC00657 in HCC.	MIMAT0000103	Int J Biochem Cell Biol 2017 Nov 92, 34-42 doi:10.1016/j.biocel.2017.09.008 PMID:28919047
1850	LncRNA	LINC00668	miR-297	VEGFA	Scc4, Scc9, Scc1, Scc25, Tu183, Hsu3, Fadu, Oec-M1, Snu1041, And Scc15	Oral Squamous Cell Cancer	Homo sapiens (human)	RNAi,Western blot,qPCR,Luciferase reporter assays,RNA pull-down assays	28564590	Long intergenic non-coding RNA 668 regulates VEGFA signaling through inhibition of miR-297 in oral squamous cell carcinoma.	LINC00668 is up-regulated in human primary OSCC tissues.We first demonstrated that LINC00668 expression was up-regulated, which was correlated with tumor progression, and miR-297 down-regulated in OSCC tissues and cells. Importantly, LINC00668 expression was negatively correlated with miR-297 expression in OSCC tissues. Loss-of-function of LINC00668 revealed that LINC00668 functioned as a ceRNA for miR-297 to facilitate VEGFA expression, promoting OSCC progression. Finally, we confirmed that LINC00668 promoted OSCC activity through VEGFA signaling.In conclusion, these results suggest that LINC00668 promotes OSCC tumorigenesis via miR-297/VEGFA axis, which may provide a new target for the diagnosis and therapy of OSCC disease.	MIMAT0004450	Biochem Biophys Res Commun 2017 Aug 5 489, 404-412 doi:10.1016/j.bbrc.2017.05.155 PMID:28564590
1851	LncRNA	LINC00673	miR-150-5p	ZEB1	Beas-2B, A549, H1975, H596, H520, H1650, H1703 And Hek-293	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28697764	Long non-coding RNA linc00673 regulated non-small cell lung cancer proliferation, migration, invasion and epithelial mesenchymal transition by sponging miR-150-5p.	high linc00673 expression was associated with poor prognosis of NSCLC patients.Linc00673 acted as a ceRNA by sponging miR-150-5p and regulated ZEB1 expression indirectly. linc00673 modulated cell proliferation, migration, invasion and EMT by sponging miR-150-5p and regulating ZEB1 expression indirectly. the inhibition of linc00673 significantly attenuated the tumorigenesis ability of A549 cells in vivo. Linc00673 is associated with poor survival in NSCLC patients.	MIMAT0000451	Mol Cancer 2017 Jul 11 16, 118 doi:10.1186/s12943-017-0685-9 PMID:28697764
1852	LncRNA	LINC00858	miR-422a	KLK4	A549, Sk-Mes-1, H1299, 95D, H460, H520, H1975, H157, Sk-Lu-1, And Spc-A-1	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,RNA pull-down assay,CCK-8 assay etc.	28177876	Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer.	LINC00858 levels were remarkably higher in NSCLC tissues and cell lines. Ectopic expression of LINC00858 in NSCLC cells promoted cell proliferation and induced cell migration and invasion. Moreover, LINC00858 functioned as a competitive endogenous RNA (ceRNA),effectively becoming sponge for miR-422a and thereby modulating the expression of kallikrein-related peptidase 4 (KLK4). In NSCLC patients, high expression of LINC00858 closely correlated with tumor progression.	MIMAT0001339	Aging (Albany NY) 2017 Feb 6 9, 475-486 doi:10.18632/aging.101171 PMID:28177876
1853	LncRNA	LINC0086	miR-214	NA	C666-1 And Hk-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Cell transfection,Luciferase reporter assay,Flow cytometry assay,CCK-8 assay etc.	28245169	Long Non-Coding RNA LINC0086 Functions as a Tumor Suppressor in Nasopharyngeal Carcinoma By Targeting miR-214.	LINC0086 decreased in NPC patient serum samples and tissues.Upregulation of LINC0086 inhibited cancer cell proliferation and promoted apoptosis. In addition, Upregulation of LINC0086 dramatically decreased the expression of miR-214 in C666-1 and HK-1 cells.We also validated that both miR-214 and LINC0086 presented in the RISC complex, demonstrating that LINC0086 could decrease miR-214 expression by directly interacting with miR-214. Furthermore, the suppressive effects of LINC0086 on NPC cell growth were reversed by overexpression miR-214 expression in vitro and in vivo.	MI0000290	Oncol Res 2017 Aug 7 25, 1189-1197 doi:10.3727/096504017x14865126670075 PMID:28245169
1854	LncRNA	LINC01133	miR-422a	NA	Mg63, Saos-2, Hos, And U2-Os	Osteosarcoma	Homo sapiens (human)	qPCR	28390115	Long Noncoding RNA LINC01133 Functions as an miR-422a Sponge to Aggravate the Tumorigenesis of Human Osteosarcoma	we found that the expression level of LINC01133 was statistically upregulated in OS tumor tissue and cell lines compared to noncancerous tissues and a normal human osteoplastic cell line. In summary, our study discovered that lncRNA LINC01133 aggravates the proliferation, migration, and invasion of OS by sponging miR-422a, which provides a novel insight in the tumorigenesis of OS. 	MIMAT0001339	Oncol Res 2018 Apr 10 26, 335-343 doi:10.3727/096504017x14907375885605 PMID:28390115
1855	LncRNA	LINC01296	miR-122	MMP-9	Sgc-7901, Bgc-823, Mgc-803, And Mkn-45,Ges-1 	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot	29091895	Long intergenic noncoding RNA 01296 aggravates gastric cancer cells progress through miR-122/MMP-9.	LINC01296 was up-regulated in GC tissue and  correlated with poor prognosis.LINC01296 knockdown significantly inhibited GC tumor growth. LINC01296 sponged miR-122,LINC01296 was positively correlated with MMP-9 expression, while miR-122 was negatively correlated to it. Overall,results indicate that LINC01296 acts as oncogenic lncRNA in GC carcinogenesis, suggesting the LINC01296/miR-122/MMP-9 regulatory pathway in GC tumorigenesis.GC patients with high LINC01296 levels had poor overall survivals than that with low LINC01296 level. 	MI0000442	Biomed Pharmacother 2018 Jan 97, 450-457 doi:10.1016/j.biopha.2017.10.066 PMID:29091895
1856	LncRNA	lincRNA-ROR	miR-145	p53	Sw480, Sw1116, Ls174T, Hct116 And Lovo	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	27696511	The long noncoding RNA-ROR promotes the resistance of radiotherapy for human colorectal cancer cells by targeting the p53/miR-145 pathway.	lincRNA-ROR was upregulated in CRC cell lines and tissue samples. We further showed that knockdown of lincRNA-ROR enhanced the sensitivity to radiotherapy for CRC by inhibiting cell viability and promoting apoptosis. Activity of the p53/miR-145 pathway may help explain the role of lincRNA-ROR for stress-induced regulation in CRC therapy.Combined specific knockdown of lincRNA-ROR and radiotherapy treatment in xenograft model resulted in a significant reduction in the tumor growth.	MI0000461	J Gastroenterol Hepatol 2017 Apr 32, 837-845 doi:10.1111/jgh.13606 PMID:27696511
1857	LncRNA	ATB	miR-141-3p	TGFB	Bgc823 And Sgc7901	Gastric Cancer	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Flow cytometry assay,Cell proliferation assay etc.	28115163	Lnc-ATB contributes to gastric cancer growth through a MiR-141-3p/TGFβ2 feedback loop.	lnc-ATB was significantly upregulated in GC tissues compared to lnc-ATB expression in ANTs.These high lnc-ATB expression levels predicted poor prognosis in GC patients. Low levels of lnc-ATB inhibited GC cell proliferation and cell cycle arrest in vitro. Lnc-ATB was found to directly bind miR-141-3p.Moreover, TGF-β actives lnc-ATB and TGF-β2 directly binds mir-141-3p.Finally, we demonstrated that lnc-ATB fulfilled its oncogenic roles in a ceRNA-mediated manner.	MIMAT0000432	Biochem Biophys Res Commun 2017 Mar 11 484, 514-521 doi:10.1016/j.bbrc.2017.01.094 PMID:28115163
1858	LncRNA	LOC100129148	miR-539-5p	KLF12	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,CCK-8 assay etc.	28328537	Long non-coding RNA LOC100129148 functions as an oncogene in human nasopharyngeal carcinoma by targeting miR-539-5p.	LOC100129148 was up-regulated in NPC tissues and cell lines, and higher expression of LOC100129148 resulted in a markedly poorer survival time.Over-expressed LOC100129148 favored, but silenced LOC100129148 hampered cell proliferation in NPC cells. Additionally, LOC100129148 enhanced the KLF12 expression through functioning as a competitive 'sponge' for miR-539-5p.	MIMAT0003163	Aging (Albany NY) 2017 Mar 21 9, 999-1011 doi:10.18632/aging.101205 PMID:28328537
1859	LncRNA	LOC101927497	miR-574-5p	NA	Mkn28 And Mgc-803	Gastric Cancer	Homo sapiens (human)	RNA-seq,qRT-PCR,in vitro knockdown	29223541	Functional role of lncRNA LOC101927497 in N-methyl-N'-nitro-N-nitrosoguanidine-induced malignantly transformed human gastric epithelial cells.	LncRNA LOC101927497 functions as a suppressor by interacting with miR-574-5p, thus inhibiting the malignant phenotype of GES-1-T cells.	MIMAT0004795	Life Sci 2018 Jan 15 193, 93-103 doi:10.1016/j.lfs.2017.12.007 PMID:29223541
1860	LncRNA	LUCAT1	miR-200c	ABCB1	Mg-63,U2Os,Hos,Saos-2,Hfob,Mg63/Mtx, Hos/Mtx,U2Os/Mtx  	Osteosarcoma	Homo sapiens (human)	RNAi,qPCR,Western blot，Luciferase reporter assay	29170124	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis	LUCAT1 was up-regulated in MTX-resistant cells (MG63/MTX, HOS/MTX) compared to that in parental cells. LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. In vitro and vivo, LUCAT1 knockdown decreased the expression levels drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion and tumor growth of osteosarcoma cells.the modulation of LUCAT1 on ABCB1 through sponging miR-200c.	MI0000650	Biochem Biophys Res Commun 2018 Jan 1 495, 947-953 doi:10.1016/j.bbrc.2017.11.121 PMID:29170124
1861	LncRNA	LUCAT1	miR-200c	MDR1	Mg-63,U2Os,Hos,Saos-2,Hfob,Mg63/Mtx, Hos/Mtx,U2Os/Mtx  	Osteosarcoma	Homo sapiens (human)	RNAi,qPCR,Western blot，Luciferase reporter assay	29170124	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis	LUCAT1 was up-regulated in MTX-resistant cells (MG63/MTX, HOS/MTX) compared to that in parental cells. LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. In vitro and vivo, LUCAT1 knockdown decreased the expression levels drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion and tumor growth of osteosarcoma cells.the modulation of LUCAT1 on ABCB1 through sponging miR-200c.	MI0000650	Biochem Biophys Res Commun 2018 Jan 1 495, 947-953 doi:10.1016/j.bbrc.2017.11.121 PMID:29170124
1862	LncRNA	LUCAT1	miR-200c	MRP5	Mg-63,U2Os,Hos,Saos-2,Hfob,Mg63/Mtx, Hos/Mtx,U2Os/Mtx  	Osteosarcoma	Homo sapiens (human)	RNAi,qPCR,Western blot，Luciferase reporter assay	29170124	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis	LUCAT1 was up-regulated in MTX-resistant cells (MG63/MTX, HOS/MTX) compared to that in parental cells. LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. In vitro and vivo, LUCAT1 knockdown decreased the expression levels drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion and tumor growth of osteosarcoma cells.the modulation of LUCAT1 on ABCB1 through sponging miR-200c.	MI0000650	Biochem Biophys Res Commun 2018 Jan 1 495, 947-953 doi:10.1016/j.bbrc.2017.11.121 PMID:29170124
1863	LncRNA	LUCAT1	miR-200c	LRP1	Mg-63,U2Os,Hos,Saos-2,Hfob,Mg63/Mtx, Hos/Mtx,U2Os/Mtx  	Osteosarcoma	Homo sapiens (human)	RNAi,qPCR,Western blot，Luciferase reporter assay	29170124	Long non-coding RNA LUCAT1 modulates methotrexate resistance in osteosarcoma via miR-200c/ABCB1 axis	LUCAT1 was up-regulated in MTX-resistant cells (MG63/MTX, HOS/MTX) compared to that in parental cells. LncRNA LUCAT1 and ABCB1 protein expression levels were both up-regulated when induced by different concentration of methotrexate. In vitro and vivo, LUCAT1 knockdown decreased the expression levels drug resistance related genes (MDR1, MRP5, LRP1), proliferation, invasion and tumor growth of osteosarcoma cells.the modulation of LUCAT1 on ABCB1 through sponging miR-200c.	MI0000650	Biochem Biophys Res Commun 2018 Jan 1 495, 947-953 doi:10.1016/j.bbrc.2017.11.121 PMID:29170124
1864	LncRNA	LUCAT1	miR-375	NA	Ln229, U251, Snb19,U87, H4,Glioma Tissues	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29089067	Knockdown of Long Noncoding RNA LUCAT1 Inhibits Cell Viability and Invasion by Regulating miR-375 in Glioma.	LUCAT1 was substantially upregulated in glioma tissues and cells.LUCAT1 inhibition significantly suppressed the proliferation and invasion of glioma cells. The lncRNA LUCAT1 was critical for the  proliferation and invasion of glioma cells by regulating miR-375. 	MIMAT0000728	Oncol Res 2018 Mar 5 26, 307-313 doi:10.3727/096504017x15088061795756 PMID:29089067
1865	LncRNA	M18204.1	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
1866	LncRNA	MALAT1	miR-124	STAT3	A549, H23, H522, H1299, H460, 16Hbe And Hek-293T	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29215698	The lncRNA MALAT1 contributes to non-small cell lung cancer development via modulating miR-124/STAT3 axis.	MALAT1 was significantly upregulated in five human NSCLC cells.On the contrary,miR-124 was remarkably downregulated, which indicated a potential negative correlation between miR-124 and MALAT1.MALAT1can act as a competing endogenous lncRNA (ceRNA) to modulate miR-124/STAT3 in NSCLC. MALAT1/miR-124/STAT3 was involved in NSCLC development.MALAT1 can have interactions with estrogen receptor and indicate poor survival of breast cancer.	MI0000443	J Cell Physiol 2018 Sep 233, 6679-6688 doi:10.1002/jcp.26325 PMID:29215698
1867	LncRNA	MALAT1	miR-101-3p	MCL1	A549, H1299,H469, Spc-A1 And A549/Ddp, Nhbe	Lung Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29484127	MALAT1/miR-101-3p/MCL1 axis mediates cisplatin resistance in lung cancer.	Lung cancer patients with high MALAT1 levels were associated with cisplatin resistance and low overall survival.MALAT1 knockdown in lung cancer cells resulted in miR-101-3p upregulation and increased cisplatin sensitivity.miR-101-3p decreased myeloid cell leukemia 1(MCL1) expression by binding to the 3'-untranslated region (3'-UTR) of its mRNA. MALAT1/miR-101-3p/MCL1 signaling underlies cisplatin resistance in lung cancer.   	MIMAT0000099	Oncotarget 2018 Jan 26 9, 7501-7512 doi:10.18632/oncotarget.23483 PMID:29484127
1868	LncRNA	MALAT1	miR-143-3p	ZEB1	Huh-6, Hepg2, Smmc-7721, Bel-7402,Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28543721	Long Non-Coding RNA MALAT1 Regulates ZEB1 Expression by Sponging miR-143-3p and Promotes Hepatocellular Carcinoma Progression.	MALAT1 was upregulated in HCC tissues. ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1.The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p.MALAT1 may regulate ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression.the patients with higher MALAT1 expression had poor overall survival.	MIMAT0000435	J Cell Biochem 2017 Dec 118, 4836-4843 doi:10.1002/jcb.26158 PMID:28543721
1869	LncRNA	MALAT1	miR-129-5p	HMGB1	Lovo, Hct116, Sw480, Ht29,Hiec	Colon Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29226325	LncRNA MALAT1 induces colon cancer development by regulating miR-129-5p/HMGB1 axis.	miR-129-5p mimics were able to restrain the progression of colon cancer cells. In addition, high motility group box protein 1 (HMGB1), was predicted as a mRNA target of miR-129-5p. Furthermore, we found that MALAT1 exerted its biological functions through regulating HMGB1 by sponging miR-129-5p in vitro. Silencing MALAT1 greatly inhibited HMGB1 expression which can be reversed by miR-129-5p inhibitors.MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer.	MIMAT0000242	J Cell Physiol 2018 Sep 233, 6750-6757 doi:10.1002/jcp.26383 PMID:29226325
1870	LncRNA	MALAT1	miR-129-5p	HMGB1	 Lovo, Hct116,Sw480, Ht29,Hiec	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29130936	JAK2-binding long noncoding RNA promotes breast cancer brain metastasis.	MALAT1 was upregulated in human colon cancer cell lines.miR-129-5p was downregulated in colon cancer cells with a significant increase of HMGB1 expression.miR-129-5p was identified and confirmed as a direct regulator of MALAT1 and miR-129-5p mimics were able to restrain the progression of colon cancer cells. In addition, high motility group box protein 1 (HMGB1), was predicted as a mRNA target of miR-129-5p. Furthermore, we found that MALAT1 exerted its biological functions through regulating HMGB1 by sponging miR-129-5p in vitro. Silencing MALAT1 greatly inhibited HMGB1 expression which can be reversed by miR-129-5p inhibitors.MALAT1 may serve as a competing endogenous lncRNA (ceRNA) to mediate HMGB1 by sponging miR-129-5p in colon cancer.	MIMAT0000242	J Clin Invest 2017 Dec 1 127, 4498-4515 doi:10.1172/jci91553 PMID:29130936
1871	LncRNA	MALAT1	miR-143	E-cadherin	Hela	Cervical Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,MTT assay etc.	28252165	Effects of miRNA-143 and the non-coding RNA MALAT1 on the pathogenesis and metastasis of HeLa cells.	The levels of MALAT1 were also significantly higher in the MALAT1 transfection group compared to the control group. Low levels of miRNA-143 and high levels of MALAT1 could potentiate proliferation of the cervical cancer cell line HeLa, and accelerate its invasion and migration via enhancement of vimentin and reduction of E-cadherin levels, respectively.	MI0000459	Genet Mol Res 2017 Feb 23 16 doi:10.4238/gmr16019269 PMID:28252165
1872	LncRNA	MALAT1	miR-202	Gli2	Mkn28, Mkn45 And Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,Cell proliferation assay etc.	27887846	Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression.	MALAT1 was upregulated in GC tissues and higher MALAT1 expression was correlated with larger tumor size, lymph node metastasis, and TNM stage. Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202. In addition, knockdown of Malat1 inhibited GC cells proliferation, S-phase cell number, and induced cell apoptosis via negatively regulating miR-202 in vitro.	MI0003130	Biomed Pharmacother 2017 Jan 85, 264-271 doi:10.1016/j.biopha.2016.11.014 PMID:27887846
1873	LncRNA	MALAT1	miR-203	TYMS	U87 And U251	Glioblastoma	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28187000	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.	Four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues. Only MALAT1 was significantly desregulated in serum. LncRNA MALAT1 inhibition re-sensitized TMZ resistant cells through up-regulating miR-203 and down-regulating TS expression. On the other hand, MALAT1 overexpression promoted resistance by suppressing miR-203 and promoting TS expression.	MI0000283	Oncotarget 2017 Apr 4 8, 22783-22799 doi:10.18632/oncotarget.15199 PMID:28187000
1874	LncRNA	MALAT1	miR-204	CXCR4	Hibepic, Rbe, Huh28, Frh0201, Qbc939, Snu-1196	Hilar Cholangiocarcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28059437	Long Non-Coding RNA MALAT1 Interacted with miR-204 to Modulates Human Hilar Cholangiocarcinoma Proliferation, Migration and Invasion by Targeting CXCR4.	lncRNA-MALAT1 was specifically upregulated in HCCA tissues and cell lines,and was associated with pathological T stage, a larger tumor size and perineural invasion. Knockdown of MALAT1 inhibited the proliferation, migration and invasion of human HCCA cell. In addition, chemokine receptor-4 (CXCR4) was involved in MALAT1 induced human HCCA growth, migration and invasion.	MI0000284	J Cell Biochem 2017 Nov 118, 3643-3653 doi:10.1002/jcb.25862 PMID:28059437
1875	LncRNA	MALAT1	miR-142-3p	HMGB1	Saos2, Mg63, U2Os, Sw1353, Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Flow cytometry assay,MTT assay etc.	28346809	MALAT1 promotes osteosarcoma development by regulation of HMGB1 via miR-142-3p and miR-129-5p.	MALAT1 and HMGB1 were significantly increased in human OS cell lines and knockdown of MALAT1 reduced HMGB1 expression. Moreover, knockdown of MALAT1 decreased HMGB1 expression, inhibited OS cell growth and promoted apoptosis, while miR-142-3p and miR-129-5p inhibitor partly restored the inhibitory effect of MALAT1 knockdown on HMGB1 expression, OS cell growth and the promotion of apoptosis.	MIMAT0000434	Cell Cycle 2017 Mar 19 16, 578-587 doi:10.1080/15384101.2017.1288324 PMID:28346809
1876	LncRNA	MALAT1	miR-216a	p21	Panc-1, Bxpc3, Aspc-1, Sw1990 And Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Flow cytometry assay etc.	28034748	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells.	We confirmed significantly higher MALAT1 expression in PDAC tissues than in the normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase.	MI0000292	Biochem Biophys Res Commun 2017 Feb 5 483, 816-822 doi:10.1016/j.bbrc.2016.12.167 PMID:28034748
1877	LncRNA	MALAT1	miR-216a	B-MYB	Panc-1, Bxpc3, Aspc-1, Sw1990 And Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Flow cytometry assay etc.	28034748	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells.	We confirmed significantly higher MALAT1 expression in PDAC tissues than in the normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase.	MI0000292	Biochem Biophys Res Commun 2017 Feb 5 483, 816-822 doi:10.1016/j.bbrc.2016.12.167 PMID:28034748
1878	LncRNA	MALAT1	miR-216a	RAF1	Panc-1, Bxpc3, Aspc-1, Sw1990 And Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Flow cytometry assay etc.	28034748	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells.	We confirmed significantly higher MALAT1 expression in PDAC tissues than in the normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase.	MI0000292	Biochem Biophys Res Commun 2017 Feb 5 483, 816-822 doi:10.1016/j.bbrc.2016.12.167 PMID:28034748
1879	LncRNA	MALAT1	miR-216a	PCNA1	Panc-1, Bxpc3, Aspc-1, Sw1990 And Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Flow cytometry assay etc.	28034748	MiR-216a decreases MALAT1 expression, induces G2/M arrest and apoptosis in pancreatic cancer cells.	We confirmed significantly higher MALAT1 expression in PDAC tissues than in the normal tissues. The following in vitro cell assay further confirmed a direct binding between miR-216a and MALAT1 and the suppressive effect of miR-216a on MALAT1 expression. MiR-216a overexpression had similar effects as MALAT1 siRNA on restoring p21 and p27 expression and inhibiting B-MYB, RAF1 and PCNA1 expression in both PANC-1 and BxPC3 cells. MiR-216a overexpression and MALAT1 knockdown induced cell cycle arrest at G2/M phase.	MI0000292	Biochem Biophys Res Commun 2017 Feb 5 483, 816-822 doi:10.1016/j.bbrc.2016.12.167 PMID:28034748
1880	LncRNA	MALAT1	miR-124	JAG1	Cal-27, Scc-9, Scc-4, Scc-15 And Scc-25	Tongue Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,MTT assay etc.	28260102	Long non-coding RNA MALAT1 interacts with miR-124 and modulates tongue cancer growth by targeting JAG1.	MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth.	MI0000443	Oncol Rep 2017 Apr 37, 2087-2094 doi:10.3892/or.2017.5445 PMID:28260102
1881	LncRNA	MALAT1	miR-140	Slug	Mum-2C, Ocm-1A, Mum-2B And C918	Uveal Melanoma	Homo sapiens (human)	qPCR,Western blot,Cell proliferation assay,Cell migration and invasion assay etc.	27725873	Long noncoding RNA MALAT1 promotes uveal melanoma cell growth and invasion by silencing of miR-140.	The expression of MALAT1 was upregulated in the uveal melanoma tissues compared to normal tissues. Among them, MALAT1 was upregulated in 72% uveal melanoma tissues compared to their paired normal tissues. Knockdown of MALAT1 suppressed uveal melanoma cell proliferation, colony information, invasion and migration. Moreover, we showed that knockdown of MALAT1 promoted miR-140 expression and suppressed Slug and ADAM10 expression in the MUM-2C cell. In addition, we demonstrated that miR-140 was downregulated in the uveal melanoma tissues compared to normal tissues and cell lines. The expression level of MALAT1 was inversely correlated with the expression level of miR-140 in uveal melanoma tissues.	MI0000456	Am J Transl Res 2016  8, 3939-3946,  PMID:27725873
1882	LncRNA	MALAT1	miR-140	ADAM10	Mum-2C, Ocm-1A, Mum-2B And C918	Uveal Melanoma	Homo sapiens (human)	qPCR,Western blot,Cell proliferation assay,Cell migration and invasion assay etc.	27725873	Long noncoding RNA MALAT1 promotes uveal melanoma cell growth and invasion by silencing of miR-140.	The expression of MALAT1 was upregulated in the uveal melanoma tissues compared to normal tissues. Among them, MALAT1 was upregulated in 72% uveal melanoma tissues compared to their paired normal tissues. Knockdown of MALAT1 suppressed uveal melanoma cell proliferation, colony information, invasion and migration. Moreover, we showed that knockdown of MALAT1 promoted miR-140 expression and suppressed Slug and ADAM10 expression in the MUM-2C cell. In addition, we demonstrated that miR-140 was downregulated in the uveal melanoma tissues compared to normal tissues and cell lines. The expression level of MALAT1 was inversely correlated with the expression level of miR-140 in uveal melanoma tissues.	MI0000456	Am J Transl Res 2016  8, 3939-3946,  PMID:27725873
1883	LncRNA	MALAT1	miR-204	ZEB2	Mcf-10A	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28675122	MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial-mesenchymal transition in breast cancer.	This study provided evidence that long non-coding RNA MALAT1 was up-regulated in breast cancer tissues and cell lines. MALAT1 promoted cancer cell invasion through inducing epithelial-mesenchymal transition. Interestingly, we revealed there was a reciprocal repression between MALAT1 and miR-204. ZEB2 was identified as a downstream target of miR-204 and MALAT1 exerted its function mainly through the miR-204/ZEB2 axis. Our findings suggested that MALAT1 may serve as a new diagnostic biomarker and therapy target for breast cancer. Patients with higher levels of MALAT1 expression had poorer overall survival than those with lower levels of MALAT1 expression. 	MI0000284	Tumour Biol 2017 Jul 39, 1010428317690998 doi:10.1177/1010428317690998 PMID:28675122
1884	LncRNA	MALAT1	miR-23b-3p	ATG12	Sgc7901, Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29162158	Long noncoding RNA MALAT1 regulates autophagy associated chemoresistance via miR-23b-3p sequestration in gastric cancer	Chemoresistant GC cells had higher levels of MALAT1 and increased autophagy compared with parental cells. Silencing of MALAT1 inhibited chemo-induced autophagy, whereas MALAT1 promoted autophagy in gastric cancer cells. Knockdown of MALAT1 sensitized GC cells to chemotherapeutics. MALAT1 acts as a competing endogenous RNA for miR-23b-3p and attenuates the inhibitory effect of miR-23b-3p on ATG12, leading to chemo-induced autophagy and chemoresistance in GC cells.	MIMAT0000418	Mol Cancer 2017 Nov 21 16, 174 doi:10.1186/s12943-017-0743-3 PMID:29162158
1885	LncRNA	MALAT1	miR-509-5p	FOXP1	Mm.1S, Opm-2, Nci-H929, U266, Rpmi-8226 	Multiple Myeloma	Homo sapiens (human)	qPCR,Luciferase reporter assays,Western blot,RIP etc.	29254219	LncRNA MALAT1 acts as an oncogene in multiple myeloma through sponging miR-509-5p to modulate FOXP1 expression	MALAT1 expression was upregulated in MM samples and cell lines. In function assays, we confirmed that MALAT1 inhibition significantly suppressed cells proliferation, induced cells apoptosis, arrested cells in G1/S phase, and inhibited MM cells growth in vivo. Furthermore, MALAT1 was identified to function as a competitive endogenous RNA (ceRNA) for miR-509-5p to promote MM cell viability. Additionally, our results suggested that miR-509-5p targeted the 3’-UTR of FOXP1 to suppress MM cells progression. Meanwhile, our results showed that miR-509-5p inhibitors significantly abrogated the decreased expression of FOXP1 induced by MALAT1 suppression, indicating that MALAT1 could positively regulate FOXP1 expression by sponging miR-509-5p. Our findings suggested that MALAT1/miR-509-5p/FOXP1 axis was one of the key signalings in mediating MM cell growth, and further indicated that MALAT1 could act as a novel diagnostic marker and therapeutic target for the treatment of MM.	MIMAT0004779	Oncotarget 2017 Nov 24 8, 101984-101993 doi:10.18632/oncotarget.21957 PMID:29254219
1886	LncRNA	MALAT1	miR-125b	BCL-2	T24, 5637	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29151968	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells	MALAT1 is capable of suppressing mature miR-125b and increasing the expression of its target genes (Bcl-2 and MMP-13), but has no effect on pri-miR-125b and pre-miR-125b.We observe that the biotin-labeled MALAT1–RNA probe is able to pull down Ago2 and miR-125b and that the negative regulation of miR-125b by MALAT1 is dependent on Ago2. Importantly, the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes. All together, these data suggest that the “MALAT1-miR-125b-Bcl-2 / MMP-13” axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	MI0000446	J Cancer 2017  8, 3803-3811 doi:10.7150/jca.21228 PMID:29151968
1887	LncRNA	MALAT1	miR-125b	MMP-13	T24, 5637	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29151968	LncRNA MALAT1 Inhibits Apoptosis and Promotes Invasion by Antagonizing miR-125b in Bladder Cancer Cells	MALAT1 is capable of suppressing mature miR-125b and increasing the expression of its target genes (Bcl-2 and MMP-13), but has no effect on pri-miR-125b and pre-miR-125b.We observe that the biotin-labeled MALAT1–RNA probe is able to pull down Ago2 and miR-125b and that the negative regulation of miR-125b by MALAT1 is dependent on Ago2. Importantly, the results of flow cytometry assay and transwell assay reveal that the MALAT1-mediated cancer progression is in part due to specific suppression of miR-125b and activation of its two target genes. All together, these data suggest that the “MALAT1-miR-125b-Bcl-2 / MMP-13” axis plays an important role in the progression of BCa, thereby may provide a potential therapeutic strategy for the treatment of human BCa.	MI0000446	J Cancer 2017  8, 3803-3811 doi:10.7150/jca.21228 PMID:29151968
1888	LncRNA	MALAT1	miR-124	Capn4	Hnepc, 5-8F, Cne-2, C666-1, Hone-1 	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28857668	MALAT1/miR-124/Capn4 axis regulates proliferation, invasion and EMT in nasopharyngeal carcinoma cells	MALAT1 and Capn4 were upregulated while miR-124 expression was downregulated in NPC cell lines.MALAT1 knockdown inhibited proliferation, invasion and EMT of NPC cells. Moreover, MALAT1 improved Capn4 expression by sponging miR-124. MALAT1 upregulation abated miR-124-induced repression on NPC cell proliferation, invasion and EMT. Furthermore, Capn4 overexpression reversed the inhibitory effect of MALAT1 silencing on proliferation, invasion and EMT of NPC cells.	MI0000443	Cancer Biol Ther 2017 Oct 3 18, 792-800 doi:10.1080/15384047.2017.1373214 PMID:28857668
1889	LncRNA	MALAT1	miR-183	ITGB1	A375, C32, Edmel3, G361, Hbl, Wm1115, Sk-Mel-1, M14, Mv3, A875, M21	Melanoma	Homo sapiens (human)	qPCR,Western blot	27966454	Deregulation of miR-183 promotes melanoma development via lncRNA MALAT1 regulation and ITGB1 signal activation	We further found that the expression and function of miR-183 were suppressed by MALAT1. We also illustrated that MALAT1 may function as a sponge competitive endogenous RNA (ceRNA) for miR-183, and thus regulate the molecular expression of ITGB1.	MI0000273	Oncotarget 2017 Jan 10 8, 3509-3518 doi:10.18632/oncotarget.13862 PMID:27966454
1890	LncRNA	MALAT1	miR-1297	HMGB2	Mkn45, Mkn28, Bgc-823, And Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28396617	Long non-coding RNA MALAT1 drives gastric cancer progression by regulating HMGB2 modulating the miR-1297	In this study, we demonstrated MALAT1 was up-regulation in GC tissues compared with adjacent normal tissues and higher MALAT1 expression was correlated with local invasion, lymph node metastasis and TNM stage. Patients with higher MALAT1 expression predicted a shorter survival and poor prognosis. Mechanistically, our results demonstrated that MALAT1 was negatively correlation with miR-1297 and functioned as a molecular sponging miR-1297, antagonizing its ability to suppress HMGB2 expression.	MIMAT0005886	Cancer Cell Int 2017  17, 44 doi:10.1186/s12935-017-0408-8 PMID:28396617
1891	LncRNA	MALAT1	miR-146b-5p	AKT	Mhcc97-H, Smmc-7721, Hep3B And Hepg2 	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,luciferase reporter assay	28404923	Down-regulation of miR-146b-5p by long noncoding RNA MALAT1 in hepatocellular carcinoma promotes cancer growth and metastasis	TNF receptor associated factor 6 (TRAF6) was confirmed as a direct target of miR-146b-5p in HCC and miR-146b-5p exerted the tumor suppression roles through inhibiting the phosphorylation of Akt mediated by TRAF6. Furthermore, we identified long non-coding RNA MALAT1 as a molecular sponge of miR-146b-5p to down-regulate its expression in HCC. In general, our results indicate that miR-146b-5p inhibits tumor growth and metastasis of HCC by targeting TRAF6 mediated Akt phosphorylation.	MIMAT0002809	Oncotarget 2017 Apr 25 8, 28683-28695 doi:10.18632/oncotarget.15640 PMID:28404923
1892	LncRNA	MALAT1	miR-124	ERK	Y79	Retinoblastoma	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28550678	Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promoted Apoptosis By Targeting miR-124 in Retinoblastoma	Results showed that the expression of MALAT1 was significantly higher in Y79 cell line than ARPE-19 cell line.MiR-124 was up-regulated by MALAT1 silence and hence was identified as a target of MALAT1. 	MI0000443	Oncol Res 2018 May 7 26, 581-591 doi:10.3727/096504017x14953948675403 PMID:28550678
1893	LncRNA	MALAT1	miR-124	MAPK	Y79	Retinoblastoma	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28550678	Knockdown of Long Noncoding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Inhibits Proliferation, Migration, and Invasion and Promoted Apoptosis By Targeting miR-124 in Retinoblastoma	Results showed that the expression of MALAT1 was significantly higher in Y79 cell line than ARPE-19 cell line.MiR-124 was up-regulated by MALAT1 silence and hence was identified as a target of MALAT1. 	MI0000443	Oncol Res 2018 May 7 26, 581-591 doi:10.3727/096504017x14953948675403 PMID:28550678
1894	LncRNA	MALAT1	miR-195	EGFR	L-02 And Qsg-7701, And Hcc Cell Lines 	Hepatocellular Carcinoma	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay	28722813	Knockdown of long non-coding RNA MALAT1 inhibits growth and motility of human hepatoma cells via modulation of miR-195.	MALAT1 was highly expressed in HCC cell lines when compared to normal liver cells. Malat1 silence suppressed HCC cells viability, migration and invasion, induced apoptosis, and arrested more cells in G0/G1 phase. Malat1 acted as a circular endogenous RNA (ceRNA) for miR-195. Malat1 silence could not suppress HCC cell growth and motility when miR-195 was knocked down. EGFR was a direct target of miR-195. miR-195 overexpression could not suppress HCC cell growth and motility when the 3'UTR site of EGFR was overexpressed. Furthermore, Malat1 silence blocked the activation of PI3K/AKT and JAK/STAT pathways, while EGFR overexpression activated them.	MI0000489	J Cell Biochem 2018 Feb 119, 1368-1380 doi:10.1002/jcb.26297 PMID:28722813
1895	LncRNA	MALAT1	miR-101	Rap1B	U251 And U87	Glioma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assays etc.	28551849	Long non-coding RNA MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101.	MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101.The present study elucidates a novel MALAT1-miR-101-Rap1B regulatory axis in glioma, contributing to a better understanding of the glioma pathogenesis and providing a promising therapeutic target for glioma patients. MALAT1 was found to be upregulated in glioma tissues and correlated with the progression of glioma.Although enormous efforts have been made to improve therapeutic strategies, the mortality of malignant glioma remains high and the median survival is less than 14 months.At present, the main treatment methods of glioma include surgical techniques, radiotherapy and chemotherapy, however, these traditional treatments obtain a poor prognosis due to the highly invasive nature and resistance to radiation and chemotherapy of glioma.	MI0000103	J Neurooncol 2017 Aug 134, 19-28 doi:10.1007/s11060-017-2498-5 PMID:28551849
1896	LncRNA	MALAT1	miR-144-3p	ROCK1	Mg-63, U2Os, Mnng/Hos, Hfob 1.19	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc.	28938647	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.	MALAT1 was up-regulated and functioned as an oncogene in osteosarcoma via RhoA and its downstream ROCKs.we confirmed that MALAT1 could regulate ROCK1/ROCK2 and their mediated metastasis and proliferation by working as a ceRNA mechanism via miR-144-3p.an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p.	MIMAT0000436	Oncotarget 2017 Aug 29 8, 59417-59434 doi:10.18632/oncotarget.19727 PMID:28938647
1897	LncRNA	MALAT1	miR-144-3p	ROCK2	Mg-63, U2Os, Mnng/Hos, Hfob 1.19	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot etc.	28938647	Long non-coding RNA MALAT1 for promoting metastasis and proliferation by acting as a ceRNA of miR-144-3p in osteosarcoma cells.	MALAT1 was up-regulated and functioned as an oncogene in osteosarcoma via RhoA and its downstream ROCKs.we confirmed that MALAT1 could regulate ROCK1/ROCK2 and their mediated metastasis and proliferation by working as a ceRNA mechanism via miR-144-3p.an overexpression of MALAT1 inhibited ROCK1/ROCK2 expression and its mediated metastasis and proliferation by working as a competitive endogenous RNA (ceRNA) via miR-144-3p.	MIMAT0000436	Oncotarget 2017 Aug 29 8, 59417-59434 doi:10.18632/oncotarget.19727 PMID:28938647
1898	LncRNA	MALAT1	miR-217	KRAS	Panc-1, Aspc-1, Mia Paca-2 And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase report assay etc.	28701723	The lncRNA MALAT1 acts as a competing endogenous RNA to regulate KRAS expression by sponging miR-217 in pancreatic ductal adenocarcinoma.	MALAT1 is expressed at higher levels in pancreatic ductal adenocarcinoma (PDAC) tissues than in nontumour tissues and in metastatic PDAC than in localized tumours. Plasma levels of MALAT1-derived fragments are significantly elevated in patients with prostate cancer compared with those without prostate cance. MALAT1 regulates KRAS expression by influencing the spatial distribution of miR-217. MALAT1 inhibits the translocation of miR-217 from the nucleus to the cytoplasm. Patients with PDAC and high MALAT1 expression levels have shorter overall survival than patients with PDAC and low MALAT1 expression levels. Resistance to KRAS inhibition has been observed experimentally in studies regarding pancreatic cancer treatment34; thus, targeting MALAT1 may be another way to achieve KRAS/MAPK pathway inactivation.	MI0000293	Sci Rep 2017 Jul 12 7, 5186 doi:10.1038/s41598-017-05274-4 PMID:28701723
1899	LncRNA	MALAT1	miR-217	MAPK	Panc-1, Aspc-1, Mia Paca-2 And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase report assay etc.	28701723	The lncRNA MALAT1 acts as a competing endogenous RNA to regulate KRAS expression by sponging miR-217 in pancreatic ductal adenocarcinoma.	MALAT1 is expressed at higher levels in pancreatic ductal adenocarcinoma (PDAC) tissues than in nontumour tissues and in metastatic PDAC than in localized tumours. Plasma levels of MALAT1-derived fragments are significantly elevated in patients with prostate cancer compared with those without prostate cance. MALAT1 regulates KRAS expression by influencing the spatial distribution of miR-217. MALAT1 inhibits the translocation of miR-217 from the nucleus to the cytoplasm. Patients with PDAC and high MALAT1 expression levels have shorter overall survival than patients with PDAC and low MALAT1 expression levels. Resistance to KRAS inhibition has been observed experimentally in studies regarding pancreatic cancer treatment34; thus, targeting MALAT1 may be another way to achieve KRAS/MAPK pathway inactivation.	MI0000293	Sci Rep 2017 Jul 12 7, 5186 doi:10.1038/s41598-017-05274-4 PMID:28701723
1900	LncRNA	MEG3	miR-21	MRP1	K562	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28190319	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.	MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells.	MI0000077	Biomol Ther (Seoul) 2017 Sep 1 25, 490-496 doi:10.4062/biomolther.2016.162 PMID:28190319
1901	LncRNA	MEG3	miR-21	MDR1	K562	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28190319	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.	MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells.	MI0000077	Biomol Ther (Seoul) 2017 Sep 1 25, 490-496 doi:10.4062/biomolther.2016.162 PMID:28190319
1902	LncRNA	MEG3	miR-21	ABCG2	K562	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28190319	LncRNA MEG3 Regulates Imatinib Resistance in Chronic Myeloid Leukemia via Suppressing MicroRNA-21.	MEG3 was significantly decreased in imatinib-resistant CML patients and imatinib-resistant K562 cells.Overexpression of MEG3 in imatinib-resistant K562 cells markedly decreased cell proliferation, increased cell apoptosis, reversed imatinib resistance, and reduced the expression of MRP1, MDR1, and ABCG2. Interestingly, MEG3 binds to miR-21. MEG3 and miR-21 were negatively correlated in CML patients. In addition, miR-21 mimics reversed the phenotype of MEG3-overexpression in imatinib-resistant K562 cells.	MI0000077	Biomol Ther (Seoul) 2017 Sep 1 25, 490-496 doi:10.4062/biomolther.2016.162 PMID:28190319
1903	LncRNA	MEG3	miR-214	NA	Evs, A2780, A2780Cp, Ovcar-3 And Skov3	Ovarian Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,Flow cytometry assay,CCK-8 assay etc.	28175963	Curcumin suppresses cisplatin resistance development partly via modulating extracellular vesicle-mediated transfer of MEG3 and miR-214 in ovarian cancer.	Curcumin weakened the EVs-N's capability to induce drug resistance and induced significant changes of lncRNAs in the EVs. MEG3 is one of the most upregulated lncRNAs. Curcumin led to demethylation in the promoter region of MEG3 and 5-AZA-dC treatment restored MEG3 expression in a dose dependent manner. MEG3 restoration by curcumin significantly reduced miR-214 in cells and in EVs. Functionally, miR-214 inhibition weakened the EVs-N's capability to enhance chemoresistance, while miR-214 overexpression increased the capability of EVs-CU in inducing chemoresistance.	MI0000290	Cancer Chemother Pharmacol 2017 Mar 79, 479-487 doi:10.1007/s00280-017-3238-4 PMID:28175963
1904	LncRNA	MEG3	miR-203	TYMS	U87R and U251R	Glioblastoma	Homo sapiens (human)	qPCR etc.	28187000	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.	Firstly, RT-qPCR was performed to verify the 10 lncRNAs using 90 GBM tissues from patients showing response to TMZ and 90 from patients showing no response. Among these, four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues.	MI0000283	Oncotarget 2017 Apr 4 8, 22783-22799 doi:10.18632/oncotarget.15199 PMID:28187000
1905	LncRNA	MEG3	miR-770	NA	Mkn45, Sgc7901, Bgc823, And Ags	Gastric Cancer	Homo sapiens (human)	qPCR,Cell transfection,Cell proliferation assay etc.	28345805	Promoter hypermethylation-mediated downregulation of miR-770 and its host gene MEG3, a long non-coding RNA, in the development of gastric cardia adenocarcinoma.	MEG3 and miR-770 was significantly downregulated in GCA patients and cell lines. Overexpression of MEG3 and miR-770 inhibited gastric cancer cell proliferation and invasion in vitro. Furthermore, the expression level of MEG3 and miR-770 was significantly increased in cancer cells after treated with 5-Aza-dC. The aberrant hypermethylation of proximal promoter and enhancer region of MEG3 was detected in GCA tissues.	MI0005118	Mol Carcinog 2017 Aug 56, 1924-1934 doi:10.1002/mc.22650 PMID:28345805
1906	LncRNA	MEG3	miR-19a	PTEN	U251, U87, Nha	Glioma	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28276316	Long Noncoding RNA MEG3 Suppresses Glioma Cell Proliferation, Migration, and Invasion By Acting As Competing Endogenous RNA of MiR-19a.	MEG3 was down-regulated and miR-19a was up-regulated in malignant glioma tissues and cell lines. MiR-19a represses the expression of PTEN and promotes glioma cell proliferation, migration and invasion. However, MEG3 could directly bind to miR-19a and effectively act as a competing endogenous RNA (ceRNA) for miR-19a to suppress tumorigenesis.	MI0000073	Oncol Res 2017 Nov 2 25, 1471-1478 doi:10.3727/096504017x14886689179993 PMID:28276316
1907	LncRNA	MEG3	miR-664	ADH4	Huh7, 7721, Hepg2, 7402, Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot etc.	28374914	Overexpression of long non-coding RNA MEG3 inhibits proliferation of hepatocellular carcinoma Huh7 cells via negative modulation of miRNA-664	MEG3 over-expression imposes another level of post-transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR-664 target gene, ADH4, through competitive ‘sponging’ miR-664. In addition,NF-κB may affect transcription of MEG3 by directly binding to the promoter region. Our data revealed that NF-κB may affect the transcript of MEG3. MEG3 overexpression inhibited the proliferation of HCC cells, at least in part by affecting miR-664mediated regulation of ADH4. Together, these results suggest that MEG3 is a suppressor of tumor which acts in part through ‘sponging’ miR-664. 	MI0006442	J Cell Biochem 2017 Nov 118, 3713-3721 doi:10.1002/jcb.26018 PMID:28374914
1908	LncRNA	MEG3	miR-183	p38	Bon1, Qgp-1	Pancreatic Neuroendocrine Tumor	Homo sapiens (human)	qPCR,Western blot	29132136	MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183	MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells.	MI0000273	Cell Physiol Biochem 2017  44, 345-356 doi:10.1159/000484906 PMID:29132136
1909	LncRNA	MEG3	miR-183	ERK	Bon1, Qgp-1	Pancreatic Neuroendocrine Tumor	Homo sapiens (human)	qPCR,Western blot	29132136	MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183	MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells.	MI0000273	Cell Physiol Biochem 2017  44, 345-356 doi:10.1159/000484906 PMID:29132136
1910	LncRNA	MEG3	miR-183	AKT	Bon1, Qgp-1	Pancreatic Neuroendocrine Tumor	Homo sapiens (human)	qPCR,Western blot	29132136	MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183	MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells.	MI0000273	Cell Physiol Biochem 2017  44, 345-356 doi:10.1159/000484906 PMID:29132136
1911	LncRNA	MEG3	miR-22-5p	TET2	K562	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR	29029424	microRNA-22 can regulate expression of the long non-coding RNA MEG3 in acute myeloid leukemia	The lower expression of MEG3 and TET2 in AML cell lines was detected by RT-qPCR.The stable MEG3, TET2 overexpression cell pools in K562 cells was successful established.After transfection, MTT assay revealed that cell growth was significantly increased in AML cell lines transfected with TET2 compared with controls.	MI0000078	Oncotarget 2017 Sep 12 8, 65211-65217 doi:10.18632/oncotarget.18059 PMID:29029424
1912	LncRNA	MEG3	miR-22-3p	TET2	K562	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR	29029424	microRNA-22 can regulate expression of the long non-coding RNA MEG3 in acute myeloid leukemia	The lower expression of MEG3 and TET2 in AML cell lines was detected by RT-qPCR.The stable MEG3, TET2 overexpression cell pools in K562 cells was successful established.After transfection, MTT assay revealed that cell growth was significantly increased in AML cell lines transfected with TET2 compared with controls.	MI0000078	Oncotarget 2017 Sep 12 8, 65211-65217 doi:10.18632/oncotarget.18059 PMID:29029424
1913	LncRNA	MEG3	miR-664a	NA	Hfob 1.19,U-2 Os	Osteosarcoma	Homo sapiens (human)	qPCR	28669734	Inhibition of miR-664a interferes with the migration of osteosarcoma cells via modulation of MEG3.	the expression level of MEG3 gene was increased while the expression level of miR-664a was decreased.In addition, changes in expression level of MEG3 and miR-644a interferes with the migration of osteosarcoma cells migration speed of osteosarcoma cells.As a result of this study, it was shown that the upregulated expression of miR-664a could have an inhibitory effect on MEG3 gene expression and migration of osteosarcoma cells.	MI0006442	Biochem Biophys Res Commun 2017 Aug 26 490, 1100-1105 doi:10.1016/j.bbrc.2017.06.174 PMID:28669734
1914	LncRNA	MEG3	miR-421	E-cadherin	Mda-Mb-231, Mcf-7, Skbr3, Mcf-10A 	Breast Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28463794	LncRNA MEG3 inhibits cell epithelial-mesenchymal transition by sponging miR-421 targeting E-cadherin in breast cancer.	MEG3 was significantly down-regulated in breast cancer tissues compared to adjacent normal tissues.MEG3/miR-421/E-cadherin regulatory axis may be a novel therapeutic target for breast cancer.endogenous miR-421 expression was negatively regulated by MEG3 in breast cancer cells and MEG3 regulated E-cadherin expression by sponging to miR-421 in breast cancer cells.Survival analysis showed that lower MEG3 predicted a poor DFS and OS for patients. Down-regulation of MEG3 enhances cisplatin resistance of lung cancer cells through activation of the WNT/b-catenin signaling pathway.	MIMAT0003339	Biomed Pharmacother 2017 Jul 91, 312-319 doi:10.1016/j.biopha.2017.04.085 PMID:28463794
1915	LncRNA	MEG3	miR-214	AIFM2	Ccrf-Cem, Jurkat, Sup-T1, H9	T Cell Lymphoblastic Lymphoma	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28534937	The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma.	Down-regulated level of MEG3 was also found in three T-LBL cell lines (CCRF-CEM, Jurkat and SUP-T1) compared with human T-cell line H9. MEG3 worked as an anti-oncogene in T-LBL, and the MEG3-miR-214-AIFM2 pathway regulated the growth of T-LBL, providing potential prognosis markers as well as new potential targets for T-LBL treatment. MEG3 effectively suppressed tumor growth and the expression of proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA). 	MI0000290	Int J Oncol 2017 Jul 51, 316-326 doi:10.3892/ijo.2017.4006 PMID:28534937
1916	LncRNA	MEG3	miR-214	PCNA	Ccrf-Cem, Jurkat, Sup-T1, H9	T Cell Lymphoblastic Lymphoma	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28534937	The inhibitory effect of MEG3/miR-214/AIFM2 axis on the growth of T-cell lymphoblastic lymphoma.	Down-regulated level of MEG3 was also found in three T-LBL cell lines (CCRF-CEM, Jurkat and SUP-T1) compared with human T-cell line H9. MEG3 worked as an anti-oncogene in T-LBL, and the MEG3-miR-214-AIFM2 pathway regulated the growth of T-LBL, providing potential prognosis markers as well as new potential targets for T-LBL treatment. MEG3 effectively suppressed tumor growth and the expression of proliferation markers Ki-67 and proliferating cell nuclear antigen (PCNA). 	MI0000290	Int J Oncol 2017 Jul 51, 316-326 doi:10.3892/ijo.2017.4006 PMID:28534937
1917	LncRNA	MEG3	miR-9	FOXO1	Te1, Te13, Eca109, Yes2, T.Tn, Heepic	Esophageal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28539329	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer.	Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Upregulation of MEG3 led to the inhibition of proliferation and invasiveness of the cancer cells. The aberrant promoter hypermethylation of MEG3 indicates silencing of its expression. Furthermore, MEG3 acts as a ceRNA to regulate the expression of E-cadherin and FOXO1 by binding hsa-miR-9. downregulation and hypermethylation of MEG3 was associated with ESCC patients' survival.	MI0000466	Mol Cancer Res 2017 Jul 15, 800-810 doi:10.1158/1541-7786.Mcr-16-0385 PMID:28539329
1918	LncRNA	MEG3	miR-9	E-cadherin	Te1, Te13, Eca109, Yes2, T.Tn, Heepic	Esophageal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28539329	Aberrant Methylation-Mediated Silencing of lncRNA MEG3 Functions as a ceRNA in Esophageal Cancer.	Significant downregulation of MEG3 was detected in esophageal cancer cells and ESCC tissues and the expression level of MEG3 was significantly increased in cancer cells after treated with the DNA methyltransferase inhibitor 5-Aza-dC. Upregulation of MEG3 led to the inhibition of proliferation and invasiveness of the cancer cells. The aberrant promoter hypermethylation of MEG3 indicates silencing of its expression. Furthermore, MEG3 acts as a ceRNA to regulate the expression of E-cadherin and FOXO1 by binding hsa-miR-9. downregulation and hypermethylation of MEG3 was associated with ESCC patients' survival.	MI0000466	Mol Cancer Res 2017 Jul 15, 800-810 doi:10.1158/1541-7786.Mcr-16-0385 PMID:28539329
1919	LncRNA	MEG3	miR-93	PCNA	U-251, M059J	Glioma	Homo sapiens (human)	qPCR,Western blot,etc.	28791407	Long non-coding RNA MEG3 inhibits cell growth of gliomas by targeting miR-93 and inactivating PI3K/AKT pathway	MEG3 was then overexpressed by ligating to a lentiviral vector.Overexpressed MEG3 inhibited the proliferation of U-251 cells, and restrained the expression of proliferation marker proteins Ki67 and proliferating cell nuclear antigen (PCNA). However, cell apoptosis rate of U-251 cells and the expression of apoptosis marker proteins were elevated by MEG3. Furthermore, miR-93 was predicted a direct target of lncRNA-MEG3 by bioinformatics analysis. Overexpressed MEG3 counteracted the role of miR-93 in facilitating proliferation and inhibiting apoptosis in U-251 cells. Moreover, MEG3 restained the activation of phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) pathway by reducing cytomembrane translocation of AKT. Finally, the in vivo experiment revealed that MEG3 strongly reduced tumor growth, tumor volume and the expression of Ki67 and PCNA. lncRNA-MEG3 also inhibited the level of miR-93 and the expression of PI3K/AKT pathway related proteins in vivo. Taken together, our research indicated a MEG3-miR- 93-PI3K-AKT pathway in regulating the growth of glioma, providing a promising therapy for glioma.	MI0000095	Oncol Rep 2017 Oct 38, 2408-2416 doi:10.3892/or.2017.5871 PMID:28791407
1920	LncRNA	MIAT	miR-150	ZEB1	A549, L78, H226	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,luciferase reporter assay etc.	28843520	The long non-coding RNA MIAT regulates zinc finger E-box binding homeobox 1 expression by sponging miR-150 and promoteing cell invasion in non-small-cell lung cancer	MIAT indirectly regulated ZEB1 expression through sponging and suppressing microRNA (miR)-150, which represses ZEB1 and interacts with MIAT in a sequence-specific manner. Thus, MIAT may inhibit ZEB1 expression and promote cell invasion of NSCLC cells via the miR-150/ ZEB1 pathway. Taken together, our findings suggested that MIAT plays an oncogenic role in NSCLC through the ZEB1 signaling pathway by sponging miR-150, and MIAT may therefore serve as a valuable prognostic biomarker and therapeutic target for NSCLC.	MI0000479	Gene 2017 Oct 30 633, 61-65 doi:10.1016/j.gene.2017.08.009 PMID:28843520
1921	LncRNA	MIAT	miR-155-5p	DUSP7	Mcf-10A, Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	29100300	Long non-coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p.	MIAT expression was upregulated in breast cancer cell lines and tissues.MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients.MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer. MIAT was specifically up-regulated in the plasma and aqueous humor of cataract patients.	MIMAT0000646	Oncotarget 2017 Sep 29 8, 76153-76164 doi:10.18632/oncotarget.19190 PMID:29100300
1922	LncRNA	MIR100HG	miR-100	GATA6	NCI-H508, Caco-2, SW403, SW948, HT29 and etc.	Colorectal Cancer	Homo sapiens (human)	qPCR etc.	29035371	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/β-catenin signaling	MIR100HG,miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/β-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG,but this repression is relieved by miR-125b targeting of GATA6.These findings identify a clinically actionable, epigenetic cause of cetuximab resistance.	MI0000102	Nat Med 2017 Nov 23, 1331-1341 doi:10.1038/nm.4424 PMID:29035371
1923	LncRNA	MIR100HG	miR-125b	GATA6	NCI-H508, Caco-2, SW403, SW948, HT29 and etc.	Colorectal Cancer	Homo sapiens (human)	qPCR etc.	29035371	lncRNA MIR100HG-derived miR-100 and miR-125b mediate cetuximab resistance via Wnt/β-catenin signaling	MIR100HG,miR-100 and miR-125b overexpression was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab. miR-100 and miR-125b coordinately repressed five Wnt/β-catenin negative regulators, resulting in increased Wnt signaling, and Wnt inhibition in cetuximab-resistant cells restored cetuximab responsiveness. Our results describe a double-negative feedback loop between MIR100HG and the transcription factor GATA6, whereby GATA6 represses MIR100HG,but this repression is relieved by miR-125b targeting of GATA6.These findings identify a clinically actionable, epigenetic cause of cetuximab resistance.	MI0000446	Nat Med 2017 Nov 23, 1331-1341 doi:10.1038/nm.4424 PMID:29035371
1924	LncRNA	miR210HG	miR-503	N-cadherin	U2Os, Saos-2, Hos,Mg-63, And 143B,Nhost,Fob	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28972855	Long Noncoding RNA miR210HG Sponges miR-503 to Facilitate Osteosarcoma Cell Invasion and Metastasis.	miR210HG expression level was significantly upregulated in 55 cases of osteosarcoma tissue samples compared to adjacent normal tissue.the aberrantly enhanced miR210HG expression predicted poor prognosis and lower survival rate.miR210HG knockdown suppressed the osteosarcoma cell proliferation, invasion, and epithelial-mesenchymal transition-related marker(N-cadherin and vimentin) expression.miR210HG silencing decreased the tumor growth. miR-503 was verified to be the target miRNA of miR210HG.miR-503 could reverse the role of miR210HG on osteosarcoma cells.miR210HG sponges miR-503 to facilitate osteosarcoma cell invasion and metastasis,revealing the oncogenic role of miR210HG on osteosarcoma cells. 	MI0003188	DNA Cell Biol 2017 Dec 36, 1117-1125 doi:10.1089/dna.2017.3888 PMID:28972855
1925	LncRNA	miR210HG	miR-503	vimentin	U2Os, Saos-2, Hos,Mg-63, And 143B,Nhost,Fob	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28972855	Long Noncoding RNA miR210HG Sponges miR-503 to Facilitate Osteosarcoma Cell Invasion and Metastasis.	miR210HG expression level was significantly upregulated in 55 cases of osteosarcoma tissue samples compared to adjacent normal tissue.the aberrantly enhanced miR210HG expression predicted poor prognosis and lower survival rate.miR210HG knockdown suppressed the osteosarcoma cell proliferation, invasion, and epithelial-mesenchymal transition-related marker(N-cadherin and vimentin) expression.miR210HG silencing decreased the tumor growth. miR-503 was verified to be the target miRNA of miR210HG.miR-503 could reverse the role of miR210HG on osteosarcoma cells.miR210HG sponges miR-503 to facilitate osteosarcoma cell invasion and metastasis,revealing the oncogenic role of miR210HG on osteosarcoma cells. 	MI0003188	DNA Cell Biol 2017 Dec 36, 1117-1125 doi:10.1089/dna.2017.3888 PMID:28972855
1926	LncRNA	MSTO2P	miR-335	MSTOP2	Nci-N87, Snu-1, Snu-16, Ags, And Kato-Iii	Gastric Cancer	Homo sapiens (human)	qPCR etc.	28618927	Long non-coding RNA MSTO2P promotes the proliferation and colony formation in gastric cancer by indirectly regulating miR-335 expression	The expression levels of misato family member 2, pseudogene were significantly associated with lymphatic metastasis and distal metastasis in 80 paired gastric cancer tissues using real-time quantitative reverse transcription polymerase chain reaction experiments. Long non-coding RNA misato family member 2, pseudogene influenced biologic functions in gastric cancer cells via indirectly regulating the activation of miR-335. 	MI0000816	Tumour Biol 2017 Jun 39, 1010428317705506 doi:10.1177/1010428317705506 PMID:28618927
1927	LncRNA	n340790	miR-1254	NFKB	Sw579	Thyroid Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28559970	The lncRNA n340790 accelerates carcinogenesis of thyroid cancer by regulating miR-1254	Here, we found that the lncRNA n340790 was highly expressed in human thyroid cancer tissues and was strongly correlated with the clinical characteristics of patients. There was a good prognostic value of n340790 for thyroid cancer. Furthermore, we discovered that n340790 could act as an endogenous sponge by directly binding to miR-1254 and downregulating miR-1254 expression.	MIMAT0005905	Am J Transl Res 2017  9, 2181-2194,  PMID:28559970
1928	LncRNA	NBAT1	miR-21	PTEN	Mg63, U2Os, 143B, Lm7, Khos, Nhost 	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,etc.	29119050	Long noncoding RNA NBAT1 negatively modulates growth and metastasis of osteosarcoma cells through suppression of miR-21	NBAT1 functions as a tumor suppressor in some cancers. However, the expression pattern,the biological function and the mechanisms of NBAT1 in OS progress have not been elucidated. In this study, for the frst time, we found that NBAT1 expression is downregulated in OS tissues and cell lines and is associated with clinical stage, distant metastasis and poor prognosis. Loss- and gain-of-function assays showed that NBAT1 played a negative regulatory role in OS growth and metastasis in vitro and in vivo. Further investigation demonstrated that NBAT1 physically interacted with miR-21 and then suppressed its expression. NBAT1 also regulated downstream genes targeted by miR-21, including PTEN, PDCD4, TPM1 and RECK. These fndings may extend the function of NBAT1 in tumor progression and provide a novel target for OS treatment.	MI0000077	Am J Cancer Res 2017  7, 2009-2019,  PMID:29119050
1929	LncRNA	NEAT1	miR-485	STAT3	Huh7, Hep3B, Hepg2, Bel-7404, Sk-Hep1, Lo2 And Hek-293T	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29219178	The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR-485 and enhancing the expression of the STAT3.	miR-485 was significantly downregulated in HCC cells.miR-485 was increased by sh-NEAT1 and miR-485 can modulate NEAT1 expression negatively. miR-485 was confirmed as a interacting target of NEAT1.STAT3 was recognized as a direct target of miR-485 and miR-485 mimics can inhibit STAT3 expression.NEAT1 can act as a competing endogenous lncRNA (ceRNA) to regulated STAT3 by sponging miR-485 in HCC. Taken these together, NEAT1 can be used as an important biomarker in HCC diagnosis and treatment.STAT3 can regulate various genes which can control proliferation, survival, and invasion process.	MI0002469	J Cell Physiol 2018 Sep 233, 6733-6741 doi:10.1002/jcp.26371 PMID:29219178
1930	LncRNA	NEAT1	miR-211	HMGA2	Mcf-10A, Mcf-7,Mda-Mb-231,T-47-D And Zr-75-1	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28720546	The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer.	lncRNA NEAT1 was up-regulated in breast cancer cell lines and tissues.NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance.the EMT-inducer HMGA2 was identified as a down-stream target of miR-211.LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis.breast cancer patients with low levels of NEAT1 expression had better overall survival time than those with high levels. 	MI0000287	Int J Biol Macromol 2017 Dec 105, 346-353 doi:10.1016/j.ijbiomac.2017.07.053 PMID:28720546
1931	LncRNA	NEAT1	miR-193a	MCL1	Rpmi8226, Jjn-3, U266, Anbl6, Opm-2, Mm1S, And Mm1R	Multiple Myeloma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29205703	LncRNA NEAT1 promotes dexamethasone resistance in multiple myeloma by targeting miR-193a/MCL1 pathway.	upregulation of NEAT1 was tightly linked to poor prognosis. knockdown of NEAT1, the DEX-induced sensitivity was enhanced in the resistant cells.Meanwhile, overexpression of NEAT1 increased the DEX-induced resistance in the sensitive cells.the NEAT1/miR-193a/MCL1 pathway is closely associated with the development of DEX resistance in myeloma cells,and knockdown of NEAT1 can significantly improve DEX sensitivity in MM.Patientswith elevatedNEAT1 expression showed reduced survival times compared with patients with low levels of NEAT1 expression.	MI0000487	J Biochem Mol Toxicol 2018 Jan 32 doi:10.1002/jbt.22008 PMID:29205703
1932	LncRNA	NEAT1	miR-193b-3p	CCND1	Hela And Siha	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29416780	LncRNA NEAT1 enhances the radio-resistance of cervical cancer via miR-193b-3p/CCND1 axis.	the overexpression of NEAT1 accelerated proliferation,The effect of NEAT1 on cell proliferation was dependent on the dose of ionizing radiation. And the silence of NEAT1 also caused cell cycle arrest in G0/G1 phase, and triggered more apoptosis.NEAT1 could function as a ceRNA to regulate cyclin D1 through sponging miR-193b-3p in cervical cancer. miR-193b-3p and cyclin D1 could inhibit NEAT1-mediated suppressive effect on proliferation, and its stimulative effect on cell cycle arrest and apoptosis. NEAT1 could facilitate the radio-resistance of cervical cancer via competitively binding miR-193b-3p to up-regulate the expression of cyclin D1. And the overexpression of NEAT1 improved the survival rate in an ionizing radiation-dependent manner, while the silence of NEAT1 decreased the survival rate in the ionizing radiation-mediated way.	MIMAT0002819	Oncotarget 2018 Jan 5 9, 2395-2409 doi:10.18632/oncotarget.23416 PMID:29416780
1933	LncRNA	NEAT1	miR-101	EZH2	Mcf-7, Skbr3, Mda-Mb-453, T-47D And Du4475	Breast Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,MTT assay etc.	28034643	The long non-coding RNA NEAT1 interacted with miR-101 modulates breast cancer growth by targeting EZH2.	lncRNA-NEAT1 was specifically upregulated in BC cell lines and promoted BC cell growth through targeting miR-101. Knockdown of NEAT1 inhibited the proliferation and DNA synthesis of human BC cell in vitro. In addition, the regulation of EZH2 by miR-101 was required in NEAT1 induced BC cell growth. These findings indicated that NEAT1 might suppress the tumor growth via miR-101 dependent EZH2 regulation.	MI0000103	Arch Biochem Biophys 2017 Feb 1 615, 1-9 doi:10.1016/j.abb.2016.12.011 PMID:28034643
1934	LncRNA	NEAT1	miR-107	CDK6	Cd133+ U87	Glioma	Homo sapiens (human)	qPCR etc.	27878295	Silencing of the long non-coding RNA NEAT1 suppresses glioma stem-like properties through modulation of the miR-107/CDK6 pathway.	We found higher NEAT1 RNA expression in CD133+ human glioma primary culture stem cells and CD133+ U87 cells via RT-PCR. Moreover, NEAT1 knockdown in the CD133+ U87 cells resulted in decreased colony formation, increased G1 cell cycle arrest and apoptosis. In addition, these effects were accompanied by miR-107 activation and inactivation of CDK6 protein.	MI0000114	Oncol Rep 2017 Jan 37, 555-562 doi:10.3892/or.2016.5266 PMID:27878295
1935	LncRNA	NEAT1	miR-181d-5p	SOX5	U87 Mg , U251Mg And Hek 293T	Glioma	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28185956	Long non-coding RNA NEAT1 regulates permeability of the blood-tumor barrier via miR-181d-5p-mediated expression changes in ZO-1, occludin, and claudin-5.	NEAT1 was remarkably up-regulated in glioma endothelial cells (GECs). Knockdown of NEAT1 impaired the integrity and increased the permeability of the BTB, accompanied by downregulation of expression of the tight junction proteins ZO-1, occludin and claudin-5 in GECs. Knockdown of NEAT1 also down-regulated the expression of sex determining region Y-box protein 5 (SOX5), which was defined as a direct and functional downstream target of miR-181d-5p. SOX5 interacts with the promoter region of ZO-1, occludin and claudin-5 in GECs.	MIMAT0002821	Biochim Biophys Acta Mol Basis Dis 2017 Sep 1863, 2240-2254 doi:10.1016/j.bbadis.2017.02.005 PMID:28185956
1936	LncRNA	NEAT1	miR-194	ZEB1	Skov3, Heya-8	Ovarian Cancer	Homo sapiens (human)	qPCR,luciferase reporter assay,Western blot etc.	29180871	lncrna NEAT1 contributes to paclitaxel resistance of ovarian cancer cells by regulating ZeB1 expression via mir-194	NEAT1 was upregulated, and miR-194 was downregulated in PTX-resistant ovarian cancer tissues and cells.Functionally, NEAT1 knockdown enhanced cell sensitivity to PTX via promoting PTX-induced apoptosis in vitro. NEAT1 was identifed as a molecular sponge of miR-194 to upregulate ZEB1 expression. Mechanistically, NEAT1-knockdown-induced PTX sensitivity was mediated by miR-194/ZEB1 axis.Moreover, NEAT1 knockdown improved PTX sensitivity of ovarian cancer in vivo.	MI0000488	<U+FEFF>Onco Targets Ther 2017  10, 5377-5390 doi:10.2147/ott.S147586 PMID:29180871
1937	LncRNA	NEAT1	miR-98-5p	MAPK6	A549, H1299, H460, H1975	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Luciferase activity assay,Western blot etc.	29095526	NEAT1/has-mir-98-5p/MAPK6 axis is involved in non-small-cell lung cancer (NSCLC) development	NEAT1 was upregulated while hsa-mir-98-5p was downregulated respectively in NSCLC cell lines compared to human normal lung epithelial BES-2B cells. Inhibition of NEAT1 can suppress the progression of NSCLC cells and hsa-mir-98-5p can reverse this phenomenon. Bioinformatics search was used to elucidate the correlation between NEAT1 and hsa-mir-98-5p. Additionally, a novel mRNA target of hsa-mir-98-5p, MAPK6, was predicted. Overexpression and knockdown studies were conducted to verify whether NEAT1 exhibits its biological functions through regulating hsa-mir-98-5p and MAPK6 in vitro. NEAT1 was able to increase MAPK6 expression and hsa-mir-98-5p mimics can inhibit MAPK6 via downregulating NEAT1 levels. We speculated that NEAT1 may act as a competing endogenous lncRNA (ceRNA) to upregulate MAPK6 by attaching hsa-mir-98-5p in lung cancers. Taken these together, NEAT1/has-mir-98-5p/MAPK6 is involved in the development and progress in NSCLC. NEAT1 could be recommended as a prognostic biomarker and therapeutic indicator in NSCLC diagnosis and treatment. 	MIMAT0000096 	J Cell Biochem 2019 Mar 120, 2836-2846 doi:10.1002/jcb.26442 PMID:29095526
1938	LncRNA	NEAT1	miR-613	NA	Mhcc97H, Mhcc97L, Smcc7721, Huh7 	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28783584	NEAT1 promotes cell proliferation and invasion in hepatocellular carcinoma by negative regulating miR-613 expression	NEAT1 was notably upregulated in HCC tissues and cells. Higher NEAT1 expression associated with larger tumor size and vascular invasion of HCC patients.Knockdown of NEAT1 significantly suppressed HCC cell proliferation, colony formation and cell invasion. Interestingly, lower miR-613 expression negatively associated with the NEAT1 expression in HCC tissues and was regulated by NEAT1. Additionally, we demonstrated that NEAT1 promoted HCC cell proliferation and invasion by regulating miR-613 expression.	MI0003626	Biomed Pharmacother 2017 Oct 94, 612-618 doi:10.1016/j.biopha.2017.07.111 PMID:28783584
1939	LncRNA	NEAT1	miR-377-3p	E2F3	A549, Spc-A1, H1299, 95D, Sk-Mes-1, Nci-H520	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,etc.	29085511	Long non-coding RNA NEAT1 regulates E2F3 expression by competitively binding to miR377 in Non small cell lung cancer	NEAT1 was highly expressed in NSCLC,and high NEAT1 expression was associated with a shorter overall survival.NEAT1 promoted NSCLC cell growth and affected the cell cycle process in vitro. Furthermore, NEAT1 was observed to bind hsa-miR-377-3p, functioning as a competing endogenous RNA, which resulted in de-repression of its target gene E2F transcription factor 3 (E2F3). E2F3, as an oncogene, may promote NSCLC progression.These results suggested that NEAT1 may promote the development of NSCLC through the miR-377-3p-E2F3 pathway.	MIMAT0000730	Oncol Lett 2017 Oct 14, 4983-4988 doi:10.3892/ol.2017.6769 PMID:29085511
1940	LncRNA	NEAT1	miR-129	CTBP2	Ec109, Ec9706	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assay	29147064	LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis	NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells.Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129.	MIMAT0000730	Dis Markers 2017  2017, 5314649 doi:10.1155/2017/5314649 PMID:29147064
1941	LncRNA	NEAT1	miR-34a	c-Met	Achn, 786-O, A498, And Caki-1	Renal Cancer	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown	28968960	The long non-coding RNA NEAT1 enhances epithelial-to-mesenchymal transition and chemoresistance via the miR-34a/c-Met axis in renal cell carcinoma	NEAT1 is up-regulated in RCC tissue compared to corresponding non-tumor tissue.High NEAT1 expression was associated with tumor progression and poor survival in RCC patients.Mechanistic analysis revealed that NEAT1 acts as a competitive sponge for miR-34a, which prevents inhibition of c-Met. Thus, NEAT1 promotes RCC progression through the miR-34a/c-Met axis.	MI0000268	Oncotarget 2017 Sep 8 8, 62927-62938 doi:10.18632/oncotarget.17757 PMID:28968960
1942	LncRNA	NEAT1	miR-101	Fos	Siha, Caski, Hela	Cervical Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown	29207151	Long non-coding nuclear paraspeckle assembly transcript 1 acts as prognosis biomarker and increases cell growth and invasion in cervical cancer by sequestering microRNA101.	the expression of NEAT1 was higher in cervical cancer cells/tissues compared with that in normal human keratinocytes/tissues.downregulation of NEAT1 inhibited colony formation, cell migration and invasion. Further investigation using the luciferase reporter assay revealed that the expression of mircoRNA101 (miR101) target gene Fos was positively associated with NEAT1 expression due to NEAT1competitive molecular sequestering of miR101 via base pairing. Furthermore, reduction of miR101 expression by inhibitor transfection reversed the effect of NEAT1 siRNA on cervical cancer cells.	MI0000103	Mol Med Rep 2018 Feb 17, 2771-2777 doi:10.3892/mmr.2017.8186 PMID:29207151
1943	LncRNA	NEAT1	miR-218	NA	Mcf-7 , Sk-Br-3 , An Immortalized Breast Epithelial Cell Line 	Breast Cancer	Homo sapiens (human)	qPCR,luciferase assay,etc.	28946559	NEAT1 negatively regulates miR-218 expression and promotes breast cancer progression.	NEAT1 expression was significantly up-regulated in breast cancer tissues compared to adjacent normal tissues, and higher NEAT1 was positively associated with lymph node metastasis and TNM stage. Patients with higher NEAT1 had a poor prognosis. Furthermore, miR-218 was shown to be a direct target of NEAT1 in breast cancer cells. In addition, NEAT1 promoted cell invasion and proliferation  by negatively regulating miR-218 in breast cancer. MiR-218 is a direct target of NEAT1.Kaplan-Meier analysis and the log-rank test were used to establish the relationship between NEAT1 and overall survival. Recent studies have shown that lncRNAs play a crucial effect in multiple processes in cells by acting as competing endogenous (ceRNAs) to regulate miRNAs. 	MI0000294	Cancer Biomark 2017 Sep 7 20, 247-254 doi:10.3233/cbm-170027 PMID:28946559
1944	LncRNA	NEAT1	miR-129-5p	VCP	Hepg2, L02, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28526689	Long non-coding RNA NEAT1 promotes hepatocellular carcinoma cell proliferation through the regulation of miR-129-5p-VCP-IκB.	the expression of NEAT1 was significantly increased in the HCC tissues and cell lines.Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased. Additionally, it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. In the present study, it was concluded that the expression of NEAT1 was significantly increased in the HCC tissues and cell lines. Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased.Additionally,it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. The study concluded that the overexpression of NEAT1 inhibited the expression of miR-129-5p by regulating VCP/IκB, thereby promoting the proliferation of HCC cells. This study provides new insights into the pathogenesis of HCC, as well as identifying new target genes for diagnosis and treatment.	MIMAT0000242	Am J Physiol Gastrointest Liver Physiol 2017 Aug 1 313, G150-g156 doi:10.1152/ajpgi.00426.2016 PMID:28526689
1945	LncRNA	NEAT1	miR-101-3p	EMP2	5-8F, Cne1, Cne2, S26, Hne1, Sune1, Hone1, Np69	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29050268	Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism.	NEAT1 is down-regulated in NPC tissues and is associated with poor prognosis. NEAT1 antagonized miR-101-3p through a competing endogenous RNA (ceRNA) mechanism and that the interaction between NEAT1 and EMP2 was miR-101-3p dependent. a novel connection of NEAT1, miR-101-3p and EMP2 in NPC migration and radiation resistance. NPC patients with high NEAT1 expression levels had longer overall survival than patients with low and negative NEAT1 expression levels.	MIMAT0000099	Oncotarget 2017 Sep 19 8, 70156-70171 doi:10.18632/oncotarget.19596 PMID:29050268
1946	LncRNA	NEAT1	miR-181a-5p	HMGB2	A549, H1299, H446, H460,Nci-H1650,Nsclc Tissues	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	28762332	Long Noncoding RNA NEAT1 Promotes Proliferation and Invasion via Targeting miR-181a-5p in Non-Small Cell Lung Cancer. 	NEAT1 was detected to be significantly upregulated in NSCLC tissues and closely associated with advanced TNM stages,lymph node metastasis, distant metastasis, and poor prognosis.Further experiments revealed that lncRNA NEAT1 silencing inhibited cell proliferation and invasion in vitro. In addition, mechanistic analysis showed that lncRNA NEAT1 upregulated the miR-181a-5p-targeted gene HMGB2 through acting as a competitive "sponge" of miR-181a-5p.	MIMAT0000256	Oncol Res 2018 Mar 5 26, 289-296 doi:10.3727/096504017x15009404458675 PMID:28762332
1947	LncRNA	NNT-AS1	miR-363	CDK6	MHCC97L, HepG2, HCCLM3, Hep3B and Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP,etc.	29179477	Long noncoding RNA NNT-AS1 promotes hepatocellular carcinoma progression and metastasis through miR-363/CDK6 axis	In present study, our team identified the up-regulated expression of NNT-AS1 in HCC tissue and cell lines compared with adjacent noncancerous tissue and normal cells. Moreover, HCC patients with high NNT-AS1 levels had poor prognosis than that with low NNT-AS1 level.In vitro, gain- and loss-of-function experiments revealed that enhanced NNT-AS1 expression promoted the proliferation ability and alleviated the cycle arrest and apoptosis, while NNT-AS1 knockdown suppressed the proliferation and induced G0/G1 phase arrest and apoptosis.In vivo, NNT-AS1 knockdown inhibited the HCC neoplastic tumor volume and weight. Bioinformatics analysis and luciferase reporter assay validated that miR-363 targeted NNT-AS1 and CDK6 3’-UTR. MiR-363 was down-regulated in HCC tissue and cells. NNT-AS1 competed with CDK6 for miR-363 binding and could increase CDK6 expression. 	MI0000764	Oncotarget 2017 Oct 24 8, 88804-88814 doi:10.18632/oncotarget.21321 PMID:29179477
1948	LncRNA	BLACAT1	miR-144	N-cadherin	A549, Sk-Mes-1, H1299, Calu-3	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28885863	Long Noncoding RNA Bladder Cancer Associated Transcript 1 Promotes the Proliferation, Migration, and Invasion of Non small cell lung cancer Through Sponging miR-144	In NSCLC cells, BLACAT1 expression was also upregulated. Both in vivo and in vitro, BLACAT1 silencing transfected with si-BLACAT1 could suppress proliferation, migration, and invasion, and induce G0/G1 phase arrest. Bioinformatics methods and luciferase reporter assay revealed the close link within miR-144 and BLACAT1 3-untranslated region (UTR). Furthermore, combining experiments of miR-144 and BLACAT1 indicated that miR-144 could reverse the function of BLACAT1 on NSCLC cells’ phenotype. Overall, this study reveals the overexpression of BLACAT1 in NSCLC tissue and cells, and discovers the oncogenic role of BLACAT1 in NSCLC genesis through sponging miR-144, providing a potential biomarker for early detection and prognosis prediction of NSCLC.	MI0000460	DNA Cell Biol 2017 Oct 36, 845-852 doi:10.1089/dna.2017.3854 PMID:28885863
1949	LncRNA	BLACAT1	miR-144	Vimentin	A549, Sk-Mes-1, H1299, Calu-3	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28885863	Long Noncoding RNA Bladder Cancer Associated Transcript 1 Promotes the Proliferation, Migration, and Invasion of Non small cell lung cancer Through Sponging miR-144	In NSCLC cells, BLACAT1 expression was also upregulated. Both in vivo and in vitro, BLACAT1 silencing transfected with si-BLACAT1 could suppress proliferation, migration, and invasion, and induce G0/G1 phase arrest. Bioinformatics methods and luciferase reporter assay revealed the close link within miR-144 and BLACAT1 3-untranslated region (UTR). Furthermore, combining experiments of miR-144 and BLACAT1 indicated that miR-144 could reverse the function of BLACAT1 on NSCLC cells’ phenotype. Overall, this study reveals the overexpression of BLACAT1 in NSCLC tissue and cells, and discovers the oncogenic role of BLACAT1 in NSCLC genesis through sponging miR-144, providing a potential biomarker for early detection and prognosis prediction of NSCLC.	MI0000460	DNA Cell Biol 2017 Oct 36, 845-852 doi:10.1089/dna.2017.3854 PMID:28885863
1950	LncRNA	ODRUL	miR-3182	MMP2	Saos2, Hos, U2-Os, Mg63, 143B	Osteosarcoma	Homo sapiens (human)	qPCR,microarray,Western blot,Luciferase reporter assay etc.	28750740	LncRNA ODRUL Contributes to Osteosarcoma Progression through the miR-3182/MMP2 Axis	ODRUL is upregulated in OS tissues and cell lines and correlates with poor prognosis. ODRUL knockdown significantly inhibits OS cell proliferation, migration, invasion, and tumor growth in vitro and in vivo by decreasing matrix metalloproteinase (MMP) expression. A microarray screen combined with online database analysis showed that miR-3182 is upregulated and MMP2 is downregulated in sh-ODRUL-expressing MG63 cells and that miR-3182 harbors potential binding sites for ODRUL and the 30 UTR of MMP2 mRNA. In addition, miR-3182 expression and function are inversely correlated with ODRUL expression in vitro and in vivo.A luciferase reporter assay demonstrated that ODRUL could directly interact with miR-3182 and upregulate MMP2 expression via its competing endogenous RNA activity on miR-3182 at the posttranscriptional level. Taken together, our study has elucidated the role of oncogenic ODRUL in OS progression and may provide a new target in OS therapy.	MIMAT0015062	Mol Ther 2017 Oct 4 25, 2383-2393 doi:10.1016/j.ymthe.2017.06.027 PMID:28750740
1951	LncRNA	OIP5-AS1	miR-448	BCL-2	H1975 And Hcc827	Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RIP	29247949	Long non-coding RNA OIP5-AS1 functions as an oncogene in lung adenocarcinoma through targeting miR-448/Bcl-2.	the expression of OIP5-AS1 was definitely high in lung adenocarcinoma tissues and cells, while miR-448 was sluggishly expressed in lung adenocarcinoma. OIP5-AS1 and miR-448 was negatively related to each other, the result was obtained from Pearson correlation analysis. We discovered a fact that OIP5-AS1 could directly sponge miR-448 through using dual luciferase reporter assay, RIP assay and RNA pull-down assay. Cell proliferation, migration and invasion were restrained after we disrupted the expression of OIP5-AS1 in lung adenocarcinoma. We also certified that OIP5-AS1 could sponge and regulate miR-448 to affect cell function in lung adenocarcinoma. MiR-448 could target Bcl-2 and affect the expression of Bcl-2. Then, we discovered that the expression of OIP5-AS1 and Bcl-2 was positively related.	MIMAT0001532	Biomed Pharmacother 2018 Feb 98, 102-110 doi:10.1016/j.biopha.2017.12.031 PMID:29247949
1952	LncRNA	p21	miR-9	E-cadherin	L02, Hepg2, Smmc7721, Hep3B, Mhcc97H And Sk-Hep1 	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	28721075	LincRNA-p21 inhibits invasion and metastasis of hepatocellular carcinoma through miR-9/E-cadherin cascade signaling pathway molecular mechanism.	The effects of miR-9 on HCC cells were studied by using miR-9 inhibitor in vitro. Luciferase assay was used to validate  the target of miR-9. The results showed that lincRNA-p21 was downregulated in human HCC tissues and cell lines. LincRNA-p21 overexpression significantly inhibited HCC cell migration and invasion in vitro. Besides, lincRNA-p21 negatively regulated miR-9 expression level, and miR-9 was upregulated in human HCC tissues and cells. MiR-9 knockdown inhibited HCC cell migration and invasion in vitro. Finally,E-cadherin was a direct target of miR-9. The expression level of E-cadherin was found to be regulated by lincRNA-p21 and miR-9. Altogether, the results suggested that lincRNA-p21 inhibits migration and invasion of HCC cells through regulating miR-9-mediated E-cadherin cascade signaling pathway. 	MI0000466	Onco Targets Ther 2017  10, 3241-3247 doi:10.2147/ott.S134910 PMID:28721075
1953	LncRNA	PART1	miR-143	DNMT3A	Lovo,Sw620	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase reporter assay 	28619512	PART-1 functions as a competitive endogenous RNA for promoting tumor progression by sponging miR-143 in colorectal cancer.	In the present study, we revealed that prostrate androgen-regulated transcript1 (PART-1) was highly expressed in colorectal cancer cells and tissues , and knockdown of PART-1 suppressed cell proliferation and metastasis, both in vitro and in vivo. In addition, PART-1 functioned as a ceRNA of DNMT3A,by sponging miR-143. Finally,PART-1 induced tumor progression by regulating DNMT3A. The Kaplan-Meier log-rank test was used to compare survival curves.Several studies have reported that miR-143 could regulate tumor progression through direct interaction with DNMT3A. As an enzyme modulating DNA methylation, DNMT3A can exert diverse epigenetic regulations. 	MI0000459	Biochem Biophys Res Commun 2017 Aug 19 490, 317-323 doi:10.1016/j.bbrc.2017.06.042 PMID:28619512
1954	LncRNA	PCAT1	miR-122	WNT1	Qbc939, Kmbc, Hibec 	Cholangiocarcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,etc.	28753454	Long noncoding RNA PCAT1 regulates extrahepatic cholangiocarcinoma progression via the Wnt/b-catenin-signaling pathway	PCAT1 is up-regulated in both ECC tissue samples and cell lines. Here, we showed that downregulation of PCAT1 following transfection with silencing RNA reduced ECC cell growth and increased cell apoptosis. Additionally, PCAT1 suppression inhibited ECC cell migration and invasion as determined by transwell assay. Furthermore, we determined that PCAT1 is a competing endogenous for microRNA (miR)-122, with bioinformatics analysis and luciferase-reporter assay results demonstrating that PCAT1 regulated WNT1 expression via miR-122. Moreover, PCAT1 downregulation increased levels of glycogen synthase kinase 3b and significantly decreased b-catenin levels in whole cell lysates and nuclear fractions, indicating that PCAT1 silencing inhibited the Wnt/b-catenin-signaling pathway. We also observed that exogenous expression of WNT1 reversed PCAT1-silencing-induced inhibition of ECC cell growth inhibition. These results indicated that PCAT1 silencing inhibited ECC progression by reducing Wnt/b-catenin signaling through miR-122 repression and WNT1 expression. Our findings revealed an important role of PCAT1 in ECC and suggested that PCAT1 might be a potential ECC-related therapeutic target.	MI0000442	Biomed Pharmacother 2017 Oct 94, 55-62 doi:10.1016/j.biopha.2017.07.025 PMID:28753454
1955	LncRNA	PCAT-1	miR-129-5p	HMGB1	Mhcc-97H, Smmc-7721, Huh7,Hepg2, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,western blot etc.	28931210	Long noncoding RNA PCAT-1 promotes invasion and metastasis via the miR-129-5p-HMGB1 signaling pathway in hepatocellular carcinoma	PCAT-1 could act as an endogenous RNA by directly binding to miR-129-5p. In addition, Luciferase reporter assay and western blotting analyses showed that PCAT-1 repressed inhibitory effect of miR-129-5p and reverse high mobility group box 1 (HMGB1) expression, a target gene of miR-129-5p. PCAT-1 functions as competing endogenous RNA (ceRNA) to provide a better understanding for HCC metastasis, and serves as a potential diagnostic and therapeutic target via PCAT-1/miR-129-5p/HMGB1 regulatory crosstalk for the deadly disease.	MIMAT0000242	Biomed Pharmacother 2017 Nov 95, 1187-1193 doi:10.1016/j.biopha.2017.09.045 PMID:28931210
1956	LncRNA	PCAT-1	miR-215	CRKL	Smmc7721, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,luciferase reporter assays etc.	28887306	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma	Here, we report how miRNAs regulate PCAT-1 expression and also investigate the biological significance of this regulation in hepatocellular carcinoma (HCC). We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays. We also found that posttranscriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 upregulated PCAT-1 expression and promoted cell viability. The tumor-suppressing role of miR-215 was further confirmed in an in vivo mouse HCC xenograft model. Of note, gene profiling assays suggested that the kinase CRKlike proto-oncogene, adaptor protein (CRKL) is a potential downstream target of the miR-215- PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation. Taken together and considering the essential role of CRKL in cancer cells, we propose that the TP53-miR-215-PCAT-1-CRKL axis might represent an important regulatory pathway in HCC.	MI0000291	J Biol Chem 2017 Oct 27 292, 17939-17949 doi:10.1074/jbc.M116.773978 PMID:28887306
1957	LncRNA	PCAT-1	miR-215	TP53	Smmc7721, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,luciferase reporter assays etc.	28887306	The long noncoding RNA PCAT-1 links the microRNA miR-215 to oncogene CRKL-mediated signaling in hepatocellular carcinoma	Here, we report how miRNAs regulate PCAT-1 expression and also investigate the biological significance of this regulation in hepatocellular carcinoma (HCC). We found that miR-215, a P53-inducible miRNA, is a key regulator of PCAT-1 expression in HCC and identified an interaction between miR-215 and PCAT-1 in dual luciferase reporter gene assays. We also found that posttranscriptional silencing of PCAT-1 by miR-215 or PCAT-1 siRNAs significantly inhibited proliferation of HCC cells and, conversely, that inhibition of endogenous miR-215 upregulated PCAT-1 expression and promoted cell viability. The tumor-suppressing role of miR-215 was further confirmed in an in vivo mouse HCC xenograft model. Of note, gene profiling assays suggested that the kinase CRKlike proto-oncogene, adaptor protein (CRKL) is a potential downstream target of the miR-215- PCAT-1 axis in HCC, and we demonstrated that CRKL silencing significantly suppresses cell proliferation. Taken together and considering the essential role of CRKL in cancer cells, we propose that the TP53-miR-215-PCAT-1-CRKL axis might represent an important regulatory pathway in HCC.	MI0000291	J Biol Chem 2017 Oct 27 292, 17939-17949 doi:10.1074/jbc.M116.773978 PMID:28887306
1958	LncRNA	PCAT-1	miR-34a	cMyc	Breast Cancer tissues	Breast Cancer	Homo sapiens (human)	qPCR etc.	28989584	Expression Analysis of Long Non-Coding PCAT-1 in Breast Cancer.	over-expression of PCAT-1 in 12/47 (25.5%) of tumoral tissues compared with their corresponding ANCTs. PCAT-1 is possibly involved in the pathogenesis of fraction of breast cancers. Future studies are needed to evaluate its precise function in breast cancer.In other words, PCAT-1 has a protective effect on cMyc by disruption of MYC regulation by miR-34a. 	MI0000268	Int J Hematol Oncol Stem Cell Res 2017 Jul 1 11, 185-191,  PMID:28989584
1959	LncRNA	PCAT14	miR-372	ATAD2	Huh7, Hcclm3, Hepg2, Smmc7721, Plc5, And Qgy7701	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28415780	Long noncoding RNA PCAT-14 induces proliferation and invasion by hepatocellular carcinoma cells by inducing methylation of miR-372	the lncRNA PCAT-14 is overexpressed in patients with hepatocellular carcinoma (HCC), and is associated with a poor prognosis after surgery. In addition, PCAT-14 inhibits miR-372 expression by inducing methylation of the miR-372 promoter. 	MI0000780	Oncotarget 2017 May 23 8, 34429-34441 doi:10.18632/oncotarget.16260 PMID:28415780
1960	LncRNA	PCAT7	miR-134-5p	ELF2	Sune-1, Cne-1, Hne-1, Cne2, C666-1, Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28728844	Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma.	Relative expression of PCAT7 expression in NPC cell lines and normal oral epidermal cell.Here, we discovered the novel LncRNA, prostate cancer associated transcript 7 (PCAT7), which was overexpressed and associated with worse prognosis in NPC. Decreased PCAT7 expression was found to significantly suppress tumor cell proliferation in vitro, and inhibited tumor growth and reduced the expression of proliferation antigen Ki67 in vivo. Rescue assay was performed to further confirm that PCAT7 contributed to the progression of NPC through regulating miR-134-5p/ELF2 signal pathway.The Kaplan-Meier survival analysis indicated that PCAT7 high expression has a worse overall survival compared to the low expression subgroup hese results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p. 	MIMAT0000447	Biochem Biophys Res Commun 2017 Sep 16 491, 374-381 doi:10.1016/j.bbrc.2017.07.093 PMID:28728844
1961	LncRNA	PCAT7	miR-134-5p	ELF2	Sune-1, Cne-1, Hne-1, Cne2, C666-1, Hone-1.Nasopharyngeal Carcinoma Tissues	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RNAi,etc.	28728844	Long non-coding RNA PCAT7 regulates ELF2 signaling through inhibition of miR-134-5p in nasopharyngeal carcinoma.	Decreased PCAT7 expression was found to significantly suppress tumor cell proliferation in vitro, and inhibited tumor growth and reduced the expression of proliferation antigen Ki67 in vivo. Rescue assay was performed to further confirm that PCAT7 contributed to the progression of NPC through regulating miR-134-5p/ELF2 signal pathway.The Kaplan-Meier survival analysis indicated that PCAT7 high expression has a worse overall survival compared to the low expression subgroup. These results indicated that PCAT7 might contribute to the tumor progression in NPC by functioning as a ceRNA to sponge miR-134-5p.To explore the interaction between PCAT7 and targeted miRNA, we predicted the miRNAs that might interact with PCAT7 using miRDB. 	MIMAT0000447	Biochem Biophys Res Commun 2017 Sep 16 491, 374-381 doi:10.1016/j.bbrc.2017.07.093 PMID:28728844
1962	LncRNA	PDIA3P	miR-185-5p	CCND2	Scc4, Scc9, Scc1, Scc25, Tu183, Hsu3,Fadu, Oec-M1, Snu1041,Scc15 And The Nhok	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,RNAi	29246288	The lncRNA PDIA3P Interacts with miR-185-5p to Modulate Oral Squamous Cell Carcinoma Progression by Targeting Cyclin D2.	PDIA3P was overexpressed in oral squamous cell carcinoma (OSCC) and decreased the survival rate of OSCC patients.silencing PDIA3P by small interfering RNA (siRNA) inhibited OSCC cell proliferation and repressed tumor growth and reduced the expression of proliferation antigen Ki-67 invivo. PDIA3P negatively regulated miR-185-5p in OSCC cells.silencing PDIA3P by siRNA suppressed proliferation via miR-185-5p in OSCC cells.silencing PDIA3P by siRNA inhibited CCND2 protein (no influence on mRNA levels) expression via miR-185-5p in OSCC cells, and CCND2 facilitated cell proliferation of SCC4 and SCC15 cells induced by sh-PDIA3P1.   	MIMAT0000455	Mol Ther Nucleic Acids 2017 Dec 15 9, 100-110 doi:10.1016/j.omtn.2017.08.015 PMID:29246288
1963	LncRNA	PRINS	miR-491-5p	PMAIP1	Ht-29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,FISH etc.	28149533	TFF3-dependent resistance of human colorectal adenocarcinoma cells HT-29/B6 to apoptosis is mediated by miR-491-5p regulation of lncRNA PRINS.	RNA interference-based gain- and loss-of-function experiments examined miR-491-PRINS axis to exert the TFF3-mediated phenotype. Chemical inhibition of selected pathways showed that phosphatidylinositol 3-kinase/AKT accounts for TFF3-mediated downregulation of miR-491-5p and accumulation of PRINS. Moreover, we showed that PRINS colocalises with PMAIP1 (NOXA) in nuclei of HT-29/B6 possessing inhibitory effects.	MIMAT0002807	Cell Death Discov 2017  3, 16106 doi:10.1038/cddiscovery.2016.106 PMID:28149533
1964	LncRNA	PRNCR1	miR-203	TYMS	U87 and U251	Glioblastoma	Homo sapiens (human)	qPCR etc.	28187000	MALAT1 is a prognostic factor in glioblastoma multiforme and induces chemoresistance to temozolomide through suppressing miR-203 and promoting thymidylate synthase expression.	Firstly, RT-qPCR was performed to verify the 10 lncRNAs using 90 GBM tissues from patients showing response to TMZ and 90 from patients showing no response. Among these, four lncRNAs (MALAT1, LOC100506474, MEG3 and PRNCR1) were found significantly dysregulated in responding tissues compared with non-responding tissues.	MI0000283	Oncotarget 2017 Apr 4 8, 22783-22799 doi:10.18632/oncotarget.15199 PMID:28187000
1965	LncRNA	PTENP1	miR-106b	PTEN	Ges-1, Ags, Sgc7901, Mgc803 And Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,Cell transfection,Luciferase reporter assay,Cell migration and invasion assay etc.	28212532	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.	PTENP1 and PTEN were concurrently downregulated in GC samples. PTENP1 overexpression inhibited cell growth and induced apoptosis in GC cells. We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay.	MIMAT0000680	Oncotarget 2017 Apr 18 8, 26079-26089 doi:10.18632/oncotarget.15317 PMID:28212532
1966	LncRNA	PTENP1	miR-93	PTEN	Ges-1, Ags, Sgc7901, Mgc803 And Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,Cell transfection,Luciferase reporter assay,Cell migration and invasion assay etc.	28212532	Long non-coding RNA PTENP1 functions as a ceRNA to modulate PTEN level by decoying miR-106b and miR-93 in gastric cancer.	PTENP1 and PTEN were concurrently downregulated in GC samples. PTENP1 overexpression inhibited cell growth and induced apoptosis in GC cells. We further demonstrated that PTENP1 could act as a ceRNA to sponge miR-106b and miR-93 from targeting PTEN for downregulation using a novel ceRNA in vitro gradient assay.	MI0000095	Oncotarget 2017 Apr 18 8, 26079-26089 doi:10.18632/oncotarget.15317 PMID:28212532
1967	LncRNA	PTENP1	miR-193a-3p	PTEN	Sk-Hep-1, Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	Western blots,qPCR,Luciferase reporter assay,RIP etc.	29296207	Long non-coding RNA PTENP1 interacts with miR-193a-3p to suppress cell migration and invasion through the PTEN pathway in hepatocellular carcinoma	PTENP1 level in the HCC tissues was significantly lower compared with those in the adjacent normal tissues. And PTENP1 was able to repress cell invasion, metastasis, and proliferation capacity in HCC cell lines. The overexpression of PTENP1 inhibited HCC growth both in vitro and in vivo. There were a binding sequence and direct interaction between PTENP1 and miR-193a-3p. PTENP1 as an endogenous sponge interacted with miR-193a-3p, leading to regulate the downstream PTEN/Akt pathway.	MIMAT0000459	Oncotarget 2017 Dec 8 8, 107859-107869 doi:10.18632/oncotarget.22305 PMID:29296207
1968	LncRNA	PVT1	miR-199a-5p	HIF1a	A549 And Spca-1	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot	29115513	LncRNA PVT1 regulate expression of HIF1α via functioning as ceRNA for miR-199a-5p in Non small cell lung cancer under hypoxia.	PVT1 was overexpressed in the hypoxic lung cancer cells.PVT1 functioned as competing endogenous (ceRNA) for miR199a5p, upregulated expression of its endogenous targets HIF1α and inhibited its function.	MIMAT0000231	Mol Med Rep 2018 Jan 17, 1105-1110 doi:10.3892/mmr.2017.7962 PMID:29115513
1969	LncRNA	PVT1	miR-200c	EZH2	A-375 ,Sk-Mel-5,Pig1, Melanoma Tissue	Melanoma	Homo sapiens (human)	qPCR,RIP etc 	29286144	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma.    	PVT1 was highly expressed in the melanoma tissues and cells. Silencing of PVT1 significantly inhibited cell proliferation, migration and invasion, and arrested  the cell cycle at the G0/G1 stage. Additionally, PVT1 silencing significantly decreased the cyclin D1 expression in the melanoma cells. 	MI0000650	Int J Mol Med 2018 Mar 41, 1275-1282 doi:10.3892/ijmm.2017.3335 PMID:29286144
1970	LncRNA	PVT1	miR-195	EZH2	Hpv-16- Positive Caski And Siha	Cervical Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,ChIP,Dual-luciferase reporter assay, RNA pull-down assay,Cell proliferation assay etc.	28296507	LncRNA PVT1 epigenetically silences miR-195 and modulates EMT and chemoresistance in cervical cancer cells.	PVT1 directly interacts with EZH2 and the complex anchors in the promoter region of miR-195. PVT1 overexpression resulted in increased H3K27me3 levels in the miR-195 promoter region, while PVT1 knockdown decreased H3K27me3 levels in the promoter region. In addition, PVT1 could competitively bind with miR-195. MiR-195 overexpression suppressed PVT1 expression in the cancer cells. Both PVT1 and miR-195 could inhibit paclitaxel (PTX) induced epithelial-to-mesenchymal transition (EMT) and also sensitize CaSki cells to PTX. 	MI0000489	J Drug Target 2017 Aug 25, 637-644 doi:10.1080/1061186x.2017.1307379 PMID:28296507
1971	LncRNA	PVT1	miR-424	NA	Hela, Siha, Ect1/E6E7	Cervical Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,Cell proliferation assay etc.	28276314	Long Non-Coding RNA PVT1 Facilitates Cervical Cancer Progression Via Negative Regulating of miR-424.	PVT1 was up-regulated in cervical cancer tissue and cell lines. After transfecting PVT1 siRNA, the proliferation, migration and invasion of cervical cancer cells were markedly decreased. Bioinformatics analysis revealed that miR-424 was potentially targeted by PVT1, which was confirmed by dual-luciferase reporter assay. Finally, miR-424 lower-expression could recover the tumor-suppressive effects of PVT1 knockdown in cervical cancer cell lines.	MI0001446	Oncol Res 2017 Sep 21 25, 1391-1398 doi:10.3727/096504017x14881559833562 PMID:28276314
1972	LncRNA	PVT1	miR-152	CD151	Sgc7901 And Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28258379	Long Noncoding RNA PVT1 Acts as a Sponge to Inhibit microRNA-152 in Gastric Cancer Cells.	PVT1 was up-regulated in GC tissues. MiR-152 was negatively associated with PVT1 expression in GC tissues. We found that PVT1 have three binding sequences for miR-152. Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues.	MI0000462	Dig Dis Sci 2017 Nov 62, 3021-3028 doi:10.1007/s10620-017-4508-z PMID:28258379
1973	LncRNA	PVT1	miR-152	FGF2	Sgc7901 And Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28258379	Long Noncoding RNA PVT1 Acts as a Sponge to Inhibit microRNA-152 in Gastric Cancer Cells.	PVT1 was up-regulated in GC tissues. MiR-152 was negatively associated with PVT1 expression in GC tissues. We found that PVT1 have three binding sequences for miR-152. Moreover, PVT1 might inhibit the expression of miR-152 and increased the expression of CD151 and FGF2 through regulating miR-152. PVT1 was positively associated with CD151 and FGF2 expression in GC tissues.	MI0000462	Dig Dis Sci 2017 Nov 62, 3021-3028 doi:10.1007/s10620-017-4508-z PMID:28258379
1974	LncRNA	PVT1	miR-186	HIF-1a	Sgc-7921, Ags And Bgc-823	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,MTT assay etc.	28122299	The long noncoding RNA PVT1 functions as a competing endogenous RNA by sponging miR-186 in gastric cancer.	PVT1 expression was markedly upregulated in GC tissues and cell lines, and high expression levels of PVT1 were obviously correlated with advanced tumor stage and lymph node metastasis. Further functional experiments indicated up-regulation of PVT1 promoted the GC cell proliferation and invasion, while down-regulation of PVT1 inhibited cell proliferation and invasion. In addition, PVT1 could directly interact with miR-186 in GC cells and this interaction lead to the inhibition of downstream of HIF-1α expression.	MI0000483	Biomed Pharmacother 2017 Apr 88, 302-308 doi:10.1016/j.biopha.2017.01.049 PMID:28122299
1975	LncRNA	PVT1	miR-195	NA	A549, H157, Hcc827, H838	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28848163	Knockdown of Lncrna PVT1 Enhances Radiosensitivity in Non-Small Cell Lung Cancer by Sponging Mir-195	PVT1 was negatively correlated with miR-195 expression in NSCLC tissues and associated with poor prognosis of NSCLC patients. Knockdown of PVT1 enhances radiosensitivity of NSCLC by sponging miR-195, providing a novel therapeutic target to improve radiotherapy efficiency in NSCLC.	MI0000489	Cell Physiol Biochem 2017  42, 2453-2466 doi:10.1159/000480209 PMID:28848163
1976	LncRNA	PVT1	miR-186	Atg7	hCMEC/D3	Glioma	Homo sapiens (human)	qPCR,Western blot	28351322	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186	The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.	MI0000483	Tumour Biol 2017 Mar 39, 1010428317694326 doi:10.1177/1010428317694326 PMID:28351322
1977	LncRNA	PVT1	miR-186	Beclin1	hCMEC/D3	Glioma	Homo sapiens (human)	qPCR,Western blot	28351322	PVT1 affects growth of glioma microvascular endothelial cells by negatively regulating miR-186	The long non-coding RNA PVT1 was found to be highly expressed in glioma vascular endothelial cells. PVT1 overexpression increased the expression of Atg7 and Beclin1 by targeting miR-186, which induced protective autophagy, thus promoting glioma vascular endothelial cell proliferation, migration, and angiogenesis.	MI0000483	Tumour Biol 2017 Mar 39, 1010428317694326 doi:10.1177/1010428317694326 PMID:28351322
1978	LncRNA	PVT1	miR-203	LASP1	Kyse30, Kyse410, Kyse520, Kyse510, Kyse140, And Kyse150	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot, luciferase reporter assay	28404954	Upregulation of the long non-coding RNA PVT1 promotes esophageal squamous cell carcinoma progression by acting as a molecular sponge of miR-203 and LASP1	PVT1 expression is significantly up-regulated in ESCC tumor samples compared with their normal counterparts.PVT1 promote ESCC progression via functioning as a molecular sponge for miR-203 and LASP1 and provide the first evidence of dysregulated PVT1/miR-203/LASP1 axis in ESCC.	MI0000283	Oncotarget 2017 May 23 8, 34164-34176 doi:10.18632/oncotarget.15878 PMID:28404954
1979	LncRNA	PVT1	miR-186-5p	YAP1	Hepg2, Hep3B, Huh-7, Hcclm9, Sk-Hep1, And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,RIP	28656879	Long non-coding RNA PVT1 serves as a competing endogenous RNA for miR-186-5p to promote the tumorigenesis and metastasis of hepatocellular carcinoma	It was determined that plasmacytoma variant translocation 1 was significantly higher, while miR-186-5p was statistically lower in the hepatocellular carcinoma tissues than that in the adjacent normal tissues.	MIMAT0000456	Tumour Biol 2017 Jun 39, 1010428317705338 doi:10.1177/1010428317705338 PMID:28656879
1980	LncRNA	PVT1	miR-26b	NA	M21, B16F10, Mm200, Mel-Rm, A375, A2058	Melanoma	Homo sapiens (human)	qPCR	28409552	Long Noncoding RNA PVT1 Promotes Melanoma Progression Via Endogenous Sponging MiR-26b	Expression of PVT1 was significantly up-regulated in melanoma tissue and associated with poor prognosis.Overall,our study demonstrates the oncogenic role of PVT1 as a miR-26b sponge, possibly providing a novel therapeutic target for melanoma	MI0000084	Oncol Res 2018 Jun 11 26, 675-681 doi:10.3727/096504017x14920318811730 PMID:28409552
1981	LncRNA	PVT1	miR-200a	MMP9	Nci-H1650, A549, Sk-Mes-1, Ncih1975,95D	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase assays	28731781	lncRNA-PVT1 Facilitates Invasion Through Upregulation of MMP9 in Non small cell lung cancer Cell	Taken together,lncRNA-PVT1 functions as a competitive endogenous RNA to regulate MMP9 expression through competitively binding the common microRNAs, miR-200a and miR-200b. These findings suggest that lncRNA-PVT1 could predispose NSCLC patients to metastases and may serve as a promising target for antimetastatic therapies.	MI0000737	DNA Cell Biol 2017 Sep 36, 787-793 doi:10.1089/dna.2017.3725 PMID:28731781
1982	LncRNA	PVT1	miR-200b	MMP9	Nci-H1650, A549, Sk-Mes-1, Ncih1975,95D	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,luciferase assays	28731781	lncRNA-PVT1 Facilitates Invasion Through Upregulation of MMP9 in Non small cell lung cancer Cell	Taken together,lncRNA-PVT1 functions as a competitive endogenous RNA to regulate MMP9 expression through competitively binding the common microRNAs, miR-200a and miR-200b. These findings suggest that lncRNA-PVT1 could predispose NSCLC patients to metastases and may serve as a promising target for antimetastatic therapies.	MI0000342	DNA Cell Biol 2017 Sep 36, 787-793 doi:10.1089/dna.2017.3725 PMID:28731781
1983	LncRNA	PVT1	miR-200b	BMI1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000342	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1984	LncRNA	PVT1	miR-200b	ZEB1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000342	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1985	LncRNA	PVT1	miR-200b	ZEB2	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000342	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1986	LncRNA	PVT1	miR-200a	BMI1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000737	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1987	LncRNA	PVT1	miR-200a	ZEB1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000737	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1988	LncRNA	PVT1	miR-200a	ZEB2	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000737	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1989	LncRNA	PVT1	miR-200c	BMI1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000650	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1990	LncRNA	PVT1	miR-200c	ZEB1	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000650	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1991	LncRNA	PVT1	miR-200c	ZEB2	293T, Achn And Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase assays etc.	29156724	lncRNA PVT1 and its splicing variant function as competing endogenous RNA to regulate clear cell renal cell carcinoma progression.	Plasmacytoma variant translocation 1 (PVT1),was shown to be upregulated in clear cell renal cell carcinoma (ccRCC) in our study, while Kaplan-Meier curve and Cox regression analysis showed that high expression of PVT1 was associated with poor overall survival (OS) and disease free survival (DFS) in ccRCC patients.PVT1 could function as an oncogenic transcript partly through sponging miR-200s to regulate BMI1, ZEB1 and ZEB2 expression.	MI0000650	Oncotarget 2017 Oct 17 8, 85353-85367 doi:10.18632/oncotarget.19743 PMID:29156724
1992	LncRNA	PVT1-5	miR-126	SLC7A5	Besa-2B And Four Lung Cancer Cell Lines 	Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown	29277611	Long non-coding RNA PVT1-5 promotes cell proliferation by regulating miR-126/SLC7A5 axis in lung cancer.	PVT1-5 expression was significantly increased in lung cancer tissues and cell lines.miR-126 was associated with lncRNA-PVT1-5. Furthermore, knockdown of lncRNA-PVT1-5 in cells could down-regulate the expression of SLC7A5, the target of oncogenic miR-126, resulting in the cell proliferation. Conversely, inhibiting the expression of miR-126 markedly increased the expression of SLC7A5 and alleviated cell proliferation inhibition.	MI0000471	Biochem Biophys Res Commun 2018 Jan 15 495, 2350-2355 doi:10.1016/j.bbrc.2017.12.114 PMID:29277611
1993	LncRNA	RNPC1	miR-181a	CASC2	A549,Nsclc Tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,in vitro knockdown etc	29288351	RNPC1 inhibits non-small cell lung cancer progression via regulating miR-181a/CASC2 axis. 	RNPC1 and long non-coding RNA CASC2 expression levels were significantly downregulated in lung cancer tissues compared with normal adjacent tissues, and their expression levels were positively correlated. Functionally, overexpression of RNPC1 or CASC2 inhibited non-small cell lung cancer cells proliferation, migration and invasion, and promoted cells apoptosis. Mechanistically, RNPC1 was found to harbor binding sites on CASC2 and directly bound to CASC2, and increased CASC2 mRNA stability and expression. Notably, the promotive effects of RNPC1 on CASC2 expression were attenuated by miR-181a overexpression. Moreover, CASC2 3'UTR with mutated miR-181a binding sites did not respond to RNPC1 alteration. Finally, the inhibitory effects of RNPC1 overexpression were attenuated or even reversed by CASC2 knockdown or miR-181a overexpression. 	MI0000269	Biotechnol Lett 2018 Mar 40, 543-550 doi:10.1007/s10529-017-2504-1 PMID:29288351
1994	LncRNA	lincRNA-ROR	miR-145	OCT4	Du145, 22Rv1	Prostate Cancer	Homo sapiens (human)	qPCR,microarray, etc.	28843521	Curcumin suppresses proliferation and in vitro invasion of human prostate cancer stem cells by ceRNA effect of miR-145 and lncRNA-ROR	lncRNA-ROR and Oct4 mRNA both contain miR-145 binding sites, and Oct4 and lncRNA-ROR directly compete for microRNA binding. Curcumin induced high miR-145 expression and inhibited the expression of lncRNA-ROR. The tumorigenicity of curcumin- treated HuPCaSCs in nude mice was significantly reduced. In summary, reducing the expression of endogenous lncRNA-ROR could effectively increase the available concentration of miR-145 in HuPCaSCs, where miR-145 prevents cell proliferation by decreasing Oct4 expression. In particular, we hypothesized that lncRNA-ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Oct4. Thus, curcumin suppresses the proliferation, in vitro invasion, and tumorigenicity of HuPCaSCs through ceRNA effect of miR-145 and lncRNA-ROR caused.	MI0000461	Gene 2017 Oct 5 631, 29-38 doi:10.1016/j.gene.2017.08.008 PMID:28843521
1995	LncRNA	lincRNA-ROR	miR-145-5p	c-Myc	Oral Cancer tissues	Oral Cancer	Homo sapiens (human)	qPCR	28443494	Expression profiling of long non-coding RNA identifies linc-RoR as a prognostic biomarker in oral cancer	In oral squamous cell carcinomas, for the first time, we observed linc-RoR overexpression, downregulation of miR-145-5p, and overexpression of c-Myc, Klf4, Oct4, and Sox2, suggesting the existence of linc-RoR-mediated competing endogenous RNA network in undifferentiated tumors.	MIMAT0000437	Tumour Biol 2017 Apr 39, 1010428317698366 doi:10.1177/1010428317698366 PMID:28443494
1996	LncRNA	lincRNA-ROR	miR-145-5p	Klf4	Oral Cancer tissues	Oral Cancer	Homo sapiens (human)	qPCR	28443494	Expression profiling of long non-coding RNA identifies linc-RoR as a prognostic biomarker in oral cancer	In oral squamous cell carcinomas, for the first time, we observed linc-RoR overexpression, downregulation of miR-145-5p, and overexpression of c-Myc, Klf4, Oct4, and Sox2, suggesting the existence of linc-RoR-mediated competing endogenous RNA network in undifferentiated tumors.	MIMAT0000437	Tumour Biol 2017 Apr 39, 1010428317698366 doi:10.1177/1010428317698366 PMID:28443494
1997	LncRNA	lincRNA-ROR	miR-145-5p	OCT4	Oral Cancer tissues	Oral Cancer	Homo sapiens (human)	qPCR	28443494	Expression profiling of long non-coding RNA identifies linc-RoR as a prognostic biomarker in oral cancer	In oral squamous cell carcinomas, for the first time, we observed linc-RoR overexpression, downregulation of miR-145-5p, and overexpression of c-Myc, Klf4, Oct4, and Sox2, suggesting the existence of linc-RoR-mediated competing endogenous RNA network in undifferentiated tumors.	MIMAT0000437	Tumour Biol 2017 Apr 39, 1010428317698366 doi:10.1177/1010428317698366 PMID:28443494
1998	LncRNA	lincRNA-ROR	miR-145-5p	Sox2	Oral Cancer tissues	Oral Cancer	Homo sapiens (human)	qPCR	28443494	Expression profiling of long non-coding RNA identifies linc-RoR as a prognostic biomarker in oral cancer	In oral squamous cell carcinomas, for the first time, we observed linc-RoR overexpression, downregulation of miR-145-5p, and overexpression of c-Myc, Klf4, Oct4, and Sox2, suggesting the existence of linc-RoR-mediated competing endogenous RNA network in undifferentiated tumors.	MIMAT0000437	Tumour Biol 2017 Apr 39, 1010428317698366 doi:10.1177/1010428317698366 PMID:28443494
1999	LncRNA	lincRNA-ROR	miR-145	FSCN1	Spc-A1 And H1299	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,RIP etc.	28388536	Long noncoding RNA ROR regulates chemoresistance in docetaxel-resistant lung adenocarcinoma cells via epithelial mesenchymal transition pathway	Long intergenic non-protein coding RNA, regulator of reprogramming (linc-ROR), was first discovered in induced pluripotent stem cells (iPSCs) and was upregulated in docetaxel-resistant LAD cells. The function of linc-ROR exerted in LAD cells depended on the sponging of miR-145, therefore, releasing the miR-145 target FSCN1, and thus contributing to the acquisition of chemoresistance and EMT phenotypes of docetaxel-resistant LAD cells.	MI0000461	Oncotarget 2017 May 16 8, 33144-33158 doi:10.18632/oncotarget.16562 PMID:28388536
2000	LncRNA	lincRNA-ROR	let-7i-5p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000415	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2001	LncRNA	lincRNA-ROR	let-7b-5p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000063	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2002	LncRNA	lincRNA-ROR	let-7e-5p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000066	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2003	LncRNA	lincRNA-ROR	let-7e-3p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0004485	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2004	LncRNA	lincRNA-ROR	let-7b-3p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0004482	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2005	LncRNA	lincRNA-ROR	let-7c-3p	Sox2	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0026472	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2006	LncRNA	lincRNA-ROR	let-7i-5p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000415	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2007	LncRNA	lincRNA-ROR	let-7b-5p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000063	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2008	LncRNA	lincRNA-ROR	let-7e-5p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0000066	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2009	LncRNA	lincRNA-ROR	let-7e-3p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0004485	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2010	LncRNA	lincRNA-ROR	let-7b-3p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0004482	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2011	LncRNA	lincRNA-ROR	let-7c-3p	Nanog	Panc-1, Sw1990	Pancreatic Cancer	Homo sapiens (human)	qPCR,RIP etc.	28580169	Endogenous miRNA Sponge LincRNA-ROR promotes proliferation, invasion and stem cell-like phenotype of pancreatic cancer cells	linc-ROR was up-regulated in PDAC tissues and related to poor prognosis.Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family.	MIMAT0026472	Cell Death Discov 2017  3, 17004 doi:10.1038/cddiscovery.2017.4 PMID:28580169
2012	LncRNA	lincRNA-ROR	miR-145	Nanog	Breast Cancer tissues	Breast Cancer	Homo sapiens (human)	qPCR	28869448	Large intergenic non-coding RNA-ROR as a potential biomarker for the diagnosis and dynamic monitoring of breast cancer	Among lncRNAs, large intergenic non-coding RNA regulator of reprogramming (lincRNA-ROR or linc-ROR) is a member of subvariety of lncRNAs, was first discovered in induced pluripotent stem cells (iPSCs), and plays a central role in promoting survival in iPSCs and embryonic stem cells (ESCs) through preventing the activation of cellular stress pathways.And linc-ROR also acts as a ceRNA to increase stemness gene Nanog expression by sponging miR-145 in cancer cells.	MI0000461	Cancer Biomark 2017 Aug 23 20, 165-173 doi:10.3233/cbm-170064 PMID:28869448
2013	LncRNA	lincRNA-ROR	miR-145	ZEB2	Hh, Hcclm3, Mhcc97-H, Hepg2 And Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28680141	The lincRNA-ROR/miR-145 axis promotes invasion and metastasis in hepatocellular carcinoma via induction of epithelial-mesenchymal transition by targeting ZEB2.	linc-ROR was upregulated in HCC tissues and high linc-ROR expression level predicted poor prognosis.ROR was upregulated in HCC tissues and high linc-ROR expression level predicted poor prognosis. ROR and ZEB2 interact with miR-145 by functioning as competing endogenous RNAs (ceRNAs).The disease-free survival (DFS) and over survival (OS) curves were plotted using the Kaplan-Meier method. 	MI0000461	Sci Rep 2017 Jul 5 7, 4637 doi:10.1038/s41598-017-04113-w PMID:28680141
2014	LncRNA	lincRNA-ROR	miR-145	TGFB	Tpc1, Ffpe Tissue	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR,in vitro knockdown wtc	29280051	Long Non-coding RNA Linc-ROR Is Upregulated in Papillary Thyroid Carcinoma.  	ROR was shown to exert regulatory effect in proliferation, invasion, and stemness of gastricc arcinoma stem cells and in breast cancer,pancreatic cancer, hepatocellular cancer, endometrial cancer, and naso- pharyngeal carcinomas.ROR lncRNA had a negative regulatory on miR-145.SiRNA experiments with ROR also led to increased expression of miR-145, supporting the role of ROR as an endogenous miR-145 sponge.There was upregulation of miR-145 after ROR silencing with a specific siRNA.	MI0000461	Endocr Pathol 2018 Mar 29, 1-8 doi:10.1007/s12022-017-9507-2 PMID:29280051
2015	LncRNA	RP11-436H11.5	miR-335-5p	BCL-W	A498, 786-O, Osrc-2	Renal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot etc.	29070041	LncRNA RP11-436H11.5, functioning as a competitive endogenous RNA, upregulates BCL-W expression by sponging miR-335-5p and promotes proliferation and invasion in renal cell carcinoma	The results of survival analysis indicated that patients in the high lncRNA RP11-436H11.5 group presented significantly worse outcomes compared with those in the low lncRNA RP11-436H11.5 group. Downregulation of lncRNA RP11-436H11.5 suppressed RCC cell proliferation and invasion in vitro and in vivo. Luciferase reporter assay results demonstrated that lncRNA RP11-436H11.5 enhanced BCL-W expression by regulating miR-335-5p expression. LncRNA RP11-436H11.5 could function as a miR-335-5p decoy to derepress expression of BCL-W. LncRNA RP11-436H11.5 could function as a competing endogenous RNA to promote RCC cell proliferation and invasion, which might serve as a therapeutic application to suppress RCC progression.lncRNA RP11-436H11.5 can function as a miR-335-5p decoy to derepress BCL-W and promote RCC cell proliferation and invasion. An orthotopic xenograft mouse model indicated that lncRNA RP11-436H11.5 could participate in miR-335-BCL-W-mediated RCC cell proliferation and invasion. LncRNA RP11-436H11.5 may be a novel therapeutic target and prognostic marker in RCC.	MIMAT0000765	Mol Cancer 2017 Oct 25 16, 166 doi:10.1186/s12943-017-0735-3 PMID:29070041
2016	LncRNA	RPPH1	miR-122	DAM10	Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR etc.	29200969	Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression.	RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer.	MI0000442	Cancer Cell Int 2017  17, 109 doi:10.1186/s12935-017-0480-0 PMID:29200969
2017	LncRNA	RPPH1	miR-122	PKM2	Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR etc.	29200969	Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression.	RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer.	MI0000442	Cancer Cell Int 2017  17, 109 doi:10.1186/s12935-017-0480-0 PMID:29200969
2018	LncRNA	RPPH1	miR-122	NOD2	Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR etc.	29200969	Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression.	RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer.	MI0000442	Cancer Cell Int 2017  17, 109 doi:10.1186/s12935-017-0480-0 PMID:29200969
2019	LncRNA	RPPH1	miR-122	IGF1R	Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR etc.	29200969	Inhibition of breast cancer cell proliferation and tumorigenesis by long non-coding RNA RPPH1 down-regulation of miR-122 expression.	RPPH1 functions as a tumour promoter and plays an important role in advancing tumorigenesis by targeting miR-122 and may serve as a novel and potential therapeutic, diagnostic or prognostic target in breast cancer.	MI0000442	Cancer Cell Int 2017  17, 109 doi:10.1186/s12935-017-0480-0 PMID:29200969
2020	LncRNA	SNHG1	miR-145	p70S6k	Lovo And Hct116	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot	29416759	SNHG1 promotes cell proliferation by acting as a sponge of miR-145 in colorectal cancer.	SNHG1 expression was correlated with advanced colorectal cancer stage and tumor recurrence.SNHG1 promoted cell proliferation by acting as a sponge of miR-145, a well known tumor suppressor of colorectal cancer.colorectal cancer patients with higher expression of SNHG1 had a worse prognosis.SNHG1 may act as a potential therapeutic target for the treatment of colorectal cancer. 	MI0000461	Oncotarget 2018 Jan 5 9, 2128-2139 doi:10.18632/oncotarget.23255 PMID:29416759
2021	LncRNA	SNHG1	miR-145	E2F3	Lovo And Hct116	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot	29416759	SNHG1 promotes cell proliferation by acting as a sponge of miR-145 in colorectal cancer.	SNHG1 expression was correlated with advanced colorectal cancer stage and tumor recurrence.SNHG1 promoted cell proliferation by acting as a sponge of miR-145, a well known tumor suppressor of colorectal cancer.colorectal cancer patients with higher expression of SNHG1 had a worse prognosis.SNHG1 may act as a potential therapeutic target for the treatment of colorectal cancer. 	MI0000461	Oncotarget 2018 Jan 5 9, 2128-2139 doi:10.18632/oncotarget.23255 PMID:29416759
2022	LncRNA	SNHG1	miR-326	NOB1	Mg-63, U2Os,Saos-2,Sosp-9607, Hfob 1.19	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29115574	Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma.	high SNHG1 expression predicts poor overall survival of OS patients.Knockdown of SNHG1 inhibited cell growth and metastasis of OS invitro and invivo.there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues.SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. 	MI0000808	Int J Oncol 2018 Jan 52, 77-88 doi:10.3892/ijo.2017.4187 PMID:29115574
2023	LncRNA	SNHG1	miR-101-3p	SOX9	A549, Spc-A1, H23 And Nci-H520	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28147312	Upregulated lncRNA SNHG1 contributes to progression of non-small cell lung cancer through inhibition of miR-101-3p and activation of Wnt/β-catenin signaling pathway.	SNHG1 was up-regulated in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore,SNHG1 inhibition suppressed NSCLC cell proliferation both in vitro and in vivo. We also found that miR-101-3p could act as a target of SNHG1 in NSCLC and the inhibition of NSCLC progression induced by SNHG1 knockdown required the activity of miR-101-3p.In addition,we identified that SOX9 acted as a target of miR-101-3p,and SOX9 played the oncogenic role in NSCLC by activating Wnt/β-catenin signaling pathway.	MIMAT0000099	Oncotarget 2017 Mar 14 8, 17785-17794 doi:10.18632/oncotarget.14854 PMID:28147312
2024	LncRNA	SNHG1	miR-199a-3p	CDK7	Pc3, Du145, Lncap, Rwpe-1 And Hek293T	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28400279	SNHG1 lncRNA negatively regulates miR-199a-3p to enhance CDK7 expression and promote cell proliferation in prostate cancer	In this study,we demonstrated that a lncRNA, Small Nucleolar RNA Host Gene 1 (SNHG1), as a ceRNA for miR-199a-3p, played a critical role in prostate cancer cell proliferation. We found that SNHG1 was aberrantly up-regulated in prostate carcinoma tissues; while, miR-199a-3p was abnormally down-regulated.	MIMAT0000232	Biochem Biophys Res Commun 2017 May 20 487, 146-152 doi:10.1016/j.bbrc.2017.03.169 PMID:28400279
2025	LncRNA	SNHG1	miR-195	p53	U251 And U87	Glioma	Homo sapiens (human)	qPCR etc.	28501778	Upregulation of the long non-coding RNA SNHG1 predicts poor prognosis, promotes cell proliferation and invasion, and reduces apoptosis in glioma.	SNHG1 expression was measured in glioma tissues and cell lines.The association between SNHG1 expression in tissues and clinicopathological characteristics and prognosis in glioma patients was also explored. SNHG1 was highly expressed in glioma tissues, and its upregulation was closely related to old age.ectopic expression of SNHG1 enhanced cell proliferation and cell invasion and reduced cell apoptosis in vitro, while SNHG1 knockdown reversed these effects. Taken together, our findings indicate that SNHG1 functions as an oncogene in glioma and may serve as a novel therapeutic target in future treatments.High expression of SNHG1 correlates with large tumor size, poor differentiation,aggressive BCLC stage and poor prognosis of HCC patients.High expression of SNHG1 also exacerbates HCC cell proliferation, invasion, and migration in vitro via suppression of miR-195 and p53.SNHG1 promoted cell proliferation via proto-oncogene CST3 upregulation by acting as a non-degradable sponge for the tumor suppressor miR-338 in esophageal cancer cells. 	MI0000489	Biomed Pharmacother 2017 Jul 91, 906-911 doi:10.1016/j.biopha.2017.05.014 PMID:28501778
2026	LncRNA	SNHG1	miR-338	p53	U251 And U87	Glioma	Homo sapiens (human)	qPCR etc.	28501778	Upregulation of the long non-coding RNA SNHG1 predicts poor prognosis, promotes cell proliferation and invasion, and reduces apoptosis in glioma.	SNHG1 expression was measured in glioma tissues and cell lines.The association between SNHG1 expression in tissues and clinicopathological characteristics and prognosis in glioma patients was also explored. SNHG1 was highly expressed in glioma tissues, and its upregulation was closely related to old age.ectopic expression of SNHG1 enhanced cell proliferation and cell invasion and reduced cell apoptosis in vitro, while SNHG1 knockdown reversed these effects. Taken together, our findings indicate that SNHG1 functions as an oncogene in glioma and may serve as a novel therapeutic target in future treatments.High expression of SNHG1 correlates with large tumor size, poor differentiation,aggressive BCLC stage and poor prognosis of HCC patients.High expression of SNHG1 also exacerbates HCC cell proliferation, invasion, and migration in vitro via suppression of miR-195 and p53.SNHG1 promoted cell proliferation via proto-oncogene CST3 upregulation by acting as a non-degradable sponge for the tumor suppressor miR-338 in esophageal cancer cells. 	MI0000814	Biomed Pharmacother 2017 Jul 91, 906-911 doi:10.1016/j.biopha.2017.05.014 PMID:28501778
2027	LncRNA	SNHG12	miR-195	SOX5	U87,U251,Glioma Tissues	Glioma	Homo sapiens (human)	Microarray,qPCR,Western blot,in vitro knockdown,RIP	29499929	Inhibition of TDP43-Mediated SNHG12-miR-195-SOX5 Feedback Loop Impeded Malignant  Biological Behaviors of Glioma Cells.	Long non-coding RNA (lncRNA) dysregulation is involved in tumorigenesis and regulation of diverse cellular processes in gliomas.SNHG12 significantly inhibited malignant biological behaviors of glioma cells. miR-195, downregulated in glioma tissues and cells, significantly impaired the malignant progression of glioma cells.TDP43 upregulated miR-195 in an SNHG12-dependent manner. SNHG12 and miR-195 were in an RNA-induced silencing complex (RISC).Inhibition of SNHG12 combined with restoration of miR-195 robustly reduced tumor growth in vivo. SOX5 was overexpressed in glioma tissues and cells.miR-195 targeted SOX5 3' UTR in a sequence-specific manner. Gelsolin was activated by SOX5. More importantly, SOX5 activated SNHG12 promoter and upregulated its expression, forming a feedback loop. 	MI0000489	Mol Ther Nucleic Acids 2018 Mar 2 10, 142-158 doi:10.1016/j.omtn.2017.12.001 PMID:29499929
2028	LncRNA	SNHG12	miR-199a	MLK3	Sk-Hep1	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,Flow cytometry assay,Cell proliferation assay etc.	28073380	Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma.	SNHG12 was significantly higher in the HCC tissues than that in the adjacent normal tissues. There were direct interactions between miR-199a/b-5p and the binding site of SNHG12. SNHG12 functioned as an endogenous sponge for miR-199a/b-5p to regulate the expression of MLK3 and affect the NF-κB pathway.	MI0000242	J Exp Clin Cancer Res 2017 Jan 10 36, 11 doi:10.1186/s13046-016-0486-9 PMID:28073380
2029	LncRNA	SNHG12	miR-320	CRKL	Sgc7901, Nci-N87 And Ags  And Normal Gastric Epithelial Cell Line 	Gastric Cancer	Homo sapiens (human)	RT-qPCR,Western blot,Luciferase reporter assay,in vitro knockdown	29207106	LncRNA SNHG12 regulates gastric cancer progression by acting as a molecular sponge of miR320.	SNHG12 was significantly overexpressed in GC and its expression level was highly associated with tumor size, tumornodemetastasis stage, distant metastasis, lymphatic metastasis.Additionally, inhibition of SNHG12 in GC cell lines SGC7901 and AGS suppressed cell growth, colony formation, proliferation and invasion. MicroRNA (miR)320,a putative target gene of SNHG12, was inversely correlated with SNHG12 expression in GC tissues and cell lines. In addition,the present study determined that miR320 was directly regulated by SNHG12 and suppression of miR320 expression reversed the inhibitory effects of SNHG12 siRNA on GC cell proliferation and invasion.	MI0000542	Mol Med Rep 2018 Feb 17, 2743-2749 doi:10.3892/mmr.2017.8143 PMID:29207106
2030	LncRNA	SNHG12	miR-195-5p	Notch2	143B, U2Os, Mg63 And Hos And Normal Human Osteoblast Cell Line 	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29229388	LncRNA SNHG12 promotes tumorigenesis and metastasis in osteosarcoma by upregulating Notch2 by sponging miR-195-5p.	SNHG12 was significantly upregulated in both osteosarcoma tissues and cell lines and osteosarcoma patients with high levels of SNHG12 tended to have a poor prognosis. Dual-luciferase reporter and RIP assays were conducted to confirm that SNHG12 functioned as a ceRNA, modulating the expression of Notch2 by sponging miR-195-5p in osteosarcoma. 	MIMAT0000461	Biochem Biophys Res Commun 2018 Jan 8 495, 1822-1832 doi:10.1016/j.bbrc.2017.12.047 PMID:29229388
2031	LncRNA	SNHG14	miR-203	N-WASP	A-498, 786-O,Caki-2, Caki-1,Hk-2	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29312804	SP1-induced up-regulation of lncRNA SNHG14 as a ceRNA promotes migration and invasion of clear cell renal cell carcinoma by regulating N-WASP.	SNHG14 was significantly up-regulated in ccRCC cell lines.the transcription factor SP1 can bind to the promoter region of SNHG14, resulting in the overexpression of SNHG14 in ccRCC. enhanced expression of lncRNA SNHG14 promoted cell migration and invasion through promoting N-WASP protein level. SNHG14 functioned as ceRNA to regulate N-WASP expression and cell motility ability via a miR-203-dependent manner.SNHG14 is a critical lncRNA that promotes ccRCC migration and invasion via sponging miR-203 and elevating N-WASP. 	MI0000283	Am J Cancer Res 2017  7, 2515-2525,  PMID:29312804
2032	LncRNA	SNHG15	miR-153	VEGFA	Hcmecs/D3	Glioma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	29048682	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153	SNHG15 is highly expressed in glioma-induced endothelial cells while miR-153 is lowly expressed in glioma-induced endothelial cells.SNHG15 negatively regulates the expression of miR-153 and miR-153 negatively regulates the expression of VEGFA and Cdc42, which in turn affects glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Therefore, we suggest that SNHG15 and miR-153 are novel targets for glioma anti-angiogenesis therapy.	MI0000463	Oncol Rep 2017 Nov 38, 3265-3277 doi:10.3892/or.2017.5985 PMID:29048682
2033	LncRNA	SNHG15	miR-153	Cdc4	Hcmecs/D3	Glioma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	29048682	SNHG15 affects the growth of glioma microvascular endothelial cells by negatively regulating miR-153	SNHG15 is highly expressed in glioma-induced endothelial cells while miR-153 is lowly expressed in glioma-induced endothelial cells.SNHG15 negatively regulates the expression of miR-153 and miR-153 negatively regulates the expression of VEGFA and Cdc42, which in turn affects glioma vascular endothelial cell proliferation, migration and tube formation in vitro. Therefore, we suggest that SNHG15 and miR-153 are novel targets for glioma anti-angiogenesis therapy.	MI0000463	Oncol Rep 2017 Nov 38, 3265-3277 doi:10.3892/or.2017.5985 PMID:29048682
2034	LncRNA	SNHG15	miR-211-3p	NA	Mcf-7, Bt-20, Zr-75-1, Mda-Mb-231 And An Immortalized Breast Epithelial Cell Line 	Breast Cancer	Homo sapiens (human)	RT-PC,Western blot,Luciferase reporter assay,in vitro knockdown	29217194	Long noncoding RNA SNHG15 promotes human breast cancer proliferation, migration and invasion by sponging miR-211-3p.	SNHG15 downregulation suppressed cell migration and invasion in MCF-7 and BT-20 cells, and inhibited  epithelial-mesenchymal transition (EMT).In mechanism, we found that SNHG15 acted as a competing endogenous RNA to sponge miR-211-3p, which was downregulated in breast cancers and inhibited cell proliferation and migration. Our results showed that there was a negative correlation between SNHG15 and miR-211-3p expression in breast cancer patients.	MIMAT0022694	Biochem Biophys Res Commun 2018 Jan 8 495, 1594-1600 doi:10.1016/j.bbrc.2017.12.013 PMID:29217194
2035	LncRNA	SNHG15	miR-141	NA	143B, U2Os, Hos, Mg63, And Saos2	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	28720111	LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141.	up-regulation of SNHG15 was inversely correlated with miR-141 expression in OS tissues. SNHG15 could directly interact with miR-141 and regulate its expression.SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141, providing a new potential target and prognostic biomarker for the treatment of OS.	MI0000457	J Biomed Sci 2017 Jul 18 24, 46 doi:10.1186/s12929-017-0353-9 PMID:28720111
2036	LncRNA	SNHG16	miR-140-5p	ZEB1	Eca109, Ec9706, Te1, Kyse-30 And Kyse-70	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RIP	29416674	SNHG16/miR-140-5p axis promotes esophagus cancer cell proliferation, migration and EMT formation through regulating ZEB1.	miR-140-5p could interact with SNHG16 and the level of miR-140-5p was inverse correlated with SNHG16 in ESCC specimens.SNHG16 directly targets miR-140-5p by binding with microRNA binding site harboring in the SNHG16 sequence. SNHG16 could act as an oncogenic lncRNA that promotes tumor progression through acting as an endogenous 'sponge' by competing with miR-140-5p, thereby regulating target ZEB1.	MIMAT0000431	Oncotarget 2018 Jan 2 9, 1028-1040 doi:10.18632/oncotarget.23178 PMID:29416674
2037	LncRNA	SNHG16	miR-216-5p	ZEB1	Hela, Caski, Siha, And C33A And The Normal Cervical Epithelial Cell Line H8	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,in vitro knockdown,RIP	29126969	SNHG16/miR-216-5p/ZEB1 signal pathway contributes to the tumorigenesis of cervical cancer cells.	miR-216-5p could interact with SNHG16 and there existed a negative correlation between the expression levels of miR-216-5p and SNHG16 in cervical cancer specimens. SNHG16 directly targeted miR-216-5p by harboring the binding sites of microRNA in the SNHG16 sequence.Additionally, bioinformatics analysis provided an evidence that ZEB1 was a potential target of miR-216-5p.	MIMAT0000273	Arch Biochem Biophys 2018 Jan 1 637, 1-8 doi:10.1016/j.abb.2017.11.003 PMID:29126969
2038	LncRNA	SNHG16	miR-98	E2F5	Mda-Mb-231, Mcf-7, Mda-Mb-468 And Hek293T	Breast Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	28232182	SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5.	Expression levels of SNHG16 were found to be frequently higher in breast cancer tissues than in the paired noncancerous tissues.Gain- and loss-of-function studies proved that SNHG16 significantly promoted breast cancer cell migration. In addition, we identified a positive correlation between SNHG16 and E2F5 in breast cancer tissues.Furthermore,we demonstrated that forced expression of miR-98 could partially abrogate SNHG16-mediated increase of breast cancer cells migration,suggesting that SNHG16 promoted cell migration in a miR-98 dependent manner.	MI0000100	Biochem Biophys Res Commun 2017 Apr 1 485, 272-278 doi:10.1016/j.bbrc.2017.02.094 PMID:28232182
2039	LncRNA	SNHG3	miR-182-5p	c-Myc	Ht29, Hct116, Sw480, Lovo	Colorectal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP,Western blot	28731158	The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer.	SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes.The results confirmed that SNHG3 was markedly upregulated in CRC.Notably, Kaplan-Meier analysis and log-rank test demonstrated that patients with overexpression of SNHG3 had poorer overall survival time than those with low expression of SNHG3.HOTAIR expression levels were significantly positively correlated with hepatocellular carcinoma (HCC) recurrence and metastasis and with the overall survival time of patients with HCC.	MIMAT0000259	Oncol Rep 2017 Sep 38, 1402-1410 doi:10.3892/or.2017.5837 PMID:28731158
2040	LncRNA	SNHG5	miR-32	AGO2	Sgc-7901 And Mgc-803	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	27871067	The lncRNA SNHG5/miR-32 axis regulates gastric cancer cell proliferation and migration by targeting KLF4.	SNHG5 contains a putative miR-32-binding site and that deletion of this site abolishes the responsiveness to miR-32. Suppression of SNHG5 expression by miR-32 was found to be Argonaute (Ago)2-dependent. Immunoprecipitation showed that SNHG5 could be pulled down from the Ago-2 complex with miR-32.	MI0000090	Faseb j 2017 Mar 31, 893-903 doi:10.1096/fj.201600994R PMID:27871067
2041	LncRNA	SNHG5	miR-205-5p	ABCC2	K562	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR,Western blot etc.	28861326	LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p.	SNHG5 and ABCC2 expressions were up-regulated in the isolated peripheral blood cells of the CML patients when compared with healthy controls, and SNHG5 expression levels was positively correlated with ABCC2 in CML patients.In vitro studies showed that the expressions of SNHG5 and ABCC2 were up-regulated in imatinib resistant cells (K562-R) when compared to K562 cells. Bioinformatics analysis showed the interaction between SNHG5 and miR-205-5p.Overexpression of SNHG5 suppressed the expression of miR-205-5p and the expression of SNHG5 was negatively correlated with the miR-205-5p expression in CML patients. In addition, ABCC2 was predicted as a downstream target of miR-205-5p, and overexpression of miR-205-5p suppressed the expression of ABCC2 in K562-R cells.overexpression of SNHG5 in K562 cells increased imatinib resistance and knock-down of SNHG5 reduced the imatinib resistance in K562-R cells. Further experiments showed that SNHG5 promotes imatinib resistance through regulating ABCC2. Taken together, SNHG5 promotes imatinib resistance in CML via acting as a competing endogenous RNA against miR-205-5p.The results demonstrated the expression levels of SNHG5 and ABCC2 from peripheral blood cells of CML patients were significantly higher than that from healthy donors.	MIMAT0000266	Am J Cancer Res 2017  7, 1704-1713,  PMID:28861326
2042	LncRNA	SNHG6	miR-101-3p	ZEB1	Mgc-803, Ags, Sgc-7901, Bgc-823	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28683446	LncRNA SNHG6 is Associated with Poor Prognosis of Gastric Cancer and Promotes Cell Proliferation and EMT through Epigenetically Silencing p27 and Sponging miR-101-3p	SNHG6 was overexpressed in gastric cancer tissues and cell lines.In summary,our findings demonstrated that SNHG6 acted as an oncogene in gastric cancer cells through regulating miR-101-3p/ZEB1 at a post-transcriptional level and silencing expression at a transcriptional level by recruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p27. High expression levels of SNHG6 wereassociated with invasion depth, lymph node metastasis, distant metastasis and tumor/node/metastasis (TNM) stage, and predicted poor prognosis. 	MIMAT0000099	Cell Physiol Biochem 2017  42, 999-1012 doi:10.1159/000478682 PMID:28683446
2043	LncRNA	SNHG6	miR-26a	TAK1	Bel-7402, Smmc-7721, Mhcc-97H, Sk-Hep-1, Huh7 And Hcc-Lm3	Hepatocellular Carcinoma	Homo sapiens (human)	microarray,qPCR,RNAi etc.	27530352	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.	We found that five SNHG6 transcripts were differentially expressed in HCC tissues while only the SNHG6-003 had an oncogenic function.Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis.Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-β-activated kinase 1 (TAK1).Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern.	MI0000083	Oncogene 2017 Feb 23 36, 1112-1122 doi:10.1038/onc.2016.278 PMID:27530352
2044	LncRNA	SNHG6	miR-26b	TAK1	Bel-7402, Smmc-7721, Mhcc-97H, Sk-Hep-1, Huh7 And Hcc-Lm3	Hepatocellular Carcinoma	Homo sapiens (human)	microarray,qPCR,RNAi etc.	27530352	The long non-coding RNA, SNHG6-003, functions as a competing endogenous RNA to promote the progression of hepatocellular carcinoma.	We found that five SNHG6 transcripts were differentially expressed in HCC tissues while only the SNHG6-003 had an oncogenic function.Ectopic expression of SNHG6-003 in HCC cells promoted cell proliferation and induced drug resistance, whereas SNHG6-003 knockdown promoted apoptosis.Moreover, SNHG6-003 functioned as a competitive endogenous RNA (ceRNA), effectively becoming sponge for miR-26a/b and thereby modulating the expression of transforming growth factor-β-activated kinase 1 (TAK1).Importantly, expression analysis revealed that both SNHG6-003 and TAK1 were upregulated in human cancers, exhibiting a co-expression pattern.	MI0000084	Oncogene 2017 Feb 23 36, 1112-1122 doi:10.1038/onc.2016.278 PMID:27530352
2045	LncRNA	SNHG7	miR-193b	FAIM2	H125, 95D, A549, Normal Lung Epithelial Cells 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	29131440	miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer.	We reported that oncogene SNHG7 predicted a poor clinical outcome and functioned as competitive endogenous RNA (ceRNA) antagonized microRNA-193b (miR-193b) to up-regulate the FAIM2 level in NSCLC	MI0003137	Cell Prolif 2018 Feb 51 doi:10.1111/cpr.12406 PMID:29131440
2046	LncRNA	SOX21-AS1	miR-145	MYO6	Ht29, Hct8, Ls513, Sw620 And Hct116,Fhc	Colorectal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,RIP	29217166	Long non-coding RNA SOX21-AS1 sponges miR-145 to promote the tumorigenesis of colorectal cancer by targeting MYO6.	lncRNA SOX21-AS1 expression was significantly over-expressed in CRC tissue samples and cells. The aberrant over-expression of SOX21-AS1 indicated poor prognosis of CRC patients. SOX21-AS1 silencing inhibited the proliferation, invasion, and decreased the tumor growth of CRC cells.miR-145 was proved to be the target of SOX21-AS1,besides, myosin VI (MYO6) was found to be one of the targets of miR-145.the tumorigenic effect of lncRNA SOX21-AS1 in CRC cells via targeting miR-145/MYO6, providing a novel insight for CRC carcinogenesis. 	MI0000461	Biomed Pharmacother 2017 Dec 96, 953-959 doi:10.1016/j.biopha.2017.11.145 PMID:29217166
2047	LncRNA	SOX2OT	miR-194-5p	TDGF-1	U87, U251	Glioblastoma	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown,Luciferase reporter assay etc.	29132362	Knockdown of SOX2OT inhibits the malignant biological behaviors of glioblastoma stem cells via up-regulating the expression of miR-194-5p and miR-122	Knockdown of SOX2OT significantly increased the expression of miR-194-5p and miR-122 in GSCs.SOX2OT bound to both miR-194-5p and miR-122. SOX3 and TDGF-1 were up-regulated in human glioma tissues and GSCs. Knockdown of SOX3 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and decreased TDGF-1 mRNA and protein expression through direct binding to the TDGF-1 promoter. Over-expression of miR-194-5p and miR-122 decreased the mRNA and protein expression of SOX3 by targeting its 3’UTR. Knockdown of TDGF-1 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and inhibited the JAK/STAT signaling pathway. Furthermore, SOX3 knockdown also inhibited the SOX2OT expression through direct binding to the SOX2OT promoter and formed a positive feedback loop.	MIMAT0000460	Mol Cancer 2017 Nov 13 16, 171 doi:10.1186/s12943-017-0737-1 PMID:29132362
2048	LncRNA	SOX2OT	miR-122	TDGF-1	U87, U251	Glioblastoma	Homo sapiens (human)	qPCR,Western blot,in vitro knockdown,Luciferase reporter assay etc.	29132362	Knockdown of SOX2OT inhibits the malignant biological behaviors of glioblastoma stem cells via up-regulating the expression of miR-194-5p and miR-122	Knockdown of SOX2OT significantly increased the expression of miR-194-5p and miR-122 in GSCs.SOX2OT bound to both miR-194-5p and miR-122. SOX3 and TDGF-1 were up-regulated in human glioma tissues and GSCs. Knockdown of SOX3 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and decreased TDGF-1 mRNA and protein expression through direct binding to the TDGF-1 promoter. Over-expression of miR-194-5p and miR-122 decreased the mRNA and protein expression of SOX3 by targeting its 3’UTR. Knockdown of TDGF-1 inhibited the proliferation, migration and invasion of GSCs, promoted GSCs apoptosis, and inhibited the JAK/STAT signaling pathway. Furthermore, SOX3 knockdown also inhibited the SOX2OT expression through direct binding to the SOX2OT promoter and formed a positive feedback loop.	MI0000442	Mol Cancer 2017 Nov 13 16, 171 doi:10.1186/s12943-017-0737-1 PMID:29132362
2049	LncRNA	SPRY4-IT1	miR-101-3p	EZH2	Ej, Umuc3, T24T	Bladder Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Cell cycle assay,Cell apoptosis assay etc.	27998761	LncRNA SPRY4-IT1 sponges miR-101-3p to promote proliferation and metastasis of bladder cancer cells through up-regulating EZH2.	SPRY4-IT1 knockdown induced inhibition of cell proliferation, cell migration and invasion ability,and caused promotion of apoptosis in bladder cancer both in vitro and in vivo.Mechanistically, knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression.	MIMAT0000099	Cancer Lett 2017 Mar 1 388, 281-291 doi:10.1016/j.canlet.2016.12.005 PMID:27998761
2050	LncRNA	STARD13	miR-340	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000802	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2051	LncRNA	STARD13	miR-448	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MIMAT0001532	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2052	LncRNA	STARD13	miR-374	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000782	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2053	LncRNA	STARD13	miR-203	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000283	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2054	LncRNA	STARD13	let-7	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000060	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2055	LncRNA	STARD13	miR-216b	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0005569	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2056	LncRNA	STARD13	miR-316	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	NA	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2057	LncRNA	STARD13	miR-23	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000079	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2058	LncRNA	STARD13	miR-153	FAS	Hepg2, Huh7, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27844181	STARD13 promotes hepatocellular carcinoma apoptosis by acting as a ceRNA for Fas.	STARD13 and Fas expression levels were significantly decreased and positively correlated in HCC tissues. Patients with higher STARD13 or Fas expression levels had longer overall survival. Additionally, STARD13 3'-UTR enhanced cellular apoptosis and the 3'-UTRs of STARD13 and Fas were predicted to harbor nine similar miRNA binding sites. And STARD13 3'-UTR promoted Fas expression in a 3'-UTR- and miRNA-dependent way and increased the sensitivity of HCC cells to chemotherapy.	MI0000463	Biotechnol Lett 2017 Feb 39, 207-217 doi:10.1007/s10529-016-2253-6 PMID:27844181
2059	LncRNA	TALNEC2	miR-21	STAT3	A172, U87	Glioma	Homo sapiens (human)	qPCR,Western blot etc.	28423669	The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells	TALNEC2 was highly expressed in GBM with poor prognosis, in GBM specimens derived from short-term survivors and in glioma cells and glioma stem cells. Two of the downregulated miRNAs,miR-21 and miR-191, mediated some of TALNEC2 effects on the stemness and mesenchymal transformation of GSCs. 	MI0000077	Oncotarget 2017 May 9 8, 31785-31801 doi:10.18632/oncotarget.15991 PMID:28423669
2060	LncRNA	TALNEC2	miR-191	STAT3	A172, U87	Glioma	Homo sapiens (human)	qPCR,Western blot etc.	28423669	The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells	TALNEC2 was highly expressed in GBM with poor prognosis, in GBM specimens derived from short-term survivors and in glioma cells and glioma stem cells.Two of the downregulated miRNAs,miR-21 and miR-191, mediated some of TALNEC2 effects on the stemness and mesenchymal transformation of GSCs. 	MI0000465	Oncotarget 2017 May 9 8, 31785-31801 doi:10.18632/oncotarget.15991 PMID:28423669
2061	LncRNA	TINCR	miR-137	NA	Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28546230	TINCR expression is associated with unfavorable prognosis in patients with hepatocellular carcinoma.	TINCR was significantly up-regulated in HCC. the associations of TINCR with clinicopathological characteristics, disease-free survival (DFS) and overall survival (OS) of patients were further evaluated. high TINCR expression was significantly correlated with tumor size,tumor differentiation status, TNM stage, and vascular invasion. TINCR was demonstrated as a direct target of miR-137 and miR-133a, and was suppressed by miR-137/miR-133a.	MIMAT0000429	Biosci Rep 2017 Aug 31 37 doi:10.1042/bsr20170301 PMID:28546230
2062	LncRNA	TINCR	miR-133a	NA	Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28546230	TINCR expression is associated with unfavorable prognosis in patients with hepatocellular carcinoma.	TINCR was significantly up-regulated in HCC. the associations of TINCR with clinicopathological characteristics, disease-free survival (DFS) and overall survival (OS) of patients were further evaluated.  high TINCR expression was significantly correlated with tumor size,tumor differentiation status, TNM stage, and vascular invasion. TINCR was demonstrated as a direct target of miR-137 and miR-133a, and was suppressed by miR-137/miR-133a.	MI0000159	Biosci Rep 2017 Aug 31 37 doi:10.1042/bsr20170301 PMID:28546230
2063	LncRNA	TINCR	miR-375	PDK1	Kato Iii, Nci-N87, Hgc-27, And Snu-1	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase report assay etc.	28744139	The long noncoding RNA, TINCR, functions as a competing endogenous RNA to regulate PDK1 expression by sponging miR-375 in gastric cancer.	miR-375 level decreased and TINCR level increased in tumor tissues.TINCR was a target of miR-375 and inhibited its expression in GC cells.Furthermore,the low expression of TINCR increased cell apoptosis and inhibited the proliferation of GC cells,while the downregulation of miR-375 reversed the function.In particular,TINCR could negatively regulate the miR-375 expression and increased the PDK1 expression in GC cells.Finally,tumor growth suppression was retarded with miR-375 downregulated in TINCR knockdown of GC cell xenografts. 	MIMAT0000728	Onco Targets Ther 2017  10, 3353-3362 doi:10.2147/ott.S137726 PMID:28744139
2064	LncRNA	TP73-AS1	miR-200a	TFAM	Hs578Bst, Bt474, Mda-Mb-231, T47D, Mcf-7, And Mda-Mb-453	Breast Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	28639399	TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition.	TP73-AS1 was specifically upregulated in BC tissues and BC cell lines and was correlated to a poorer prognosis in patients with BC. TP73-AS1 could regulate miR-200a through direct targeting. Moreover, TP73-AS1 might compete with TFAM for miR-200a binding thus to promote TFAM expression.TP73-AS1 promoted BC cell proliferation through acting as a competing endogenous RNA (ceRNA) by sponging miR-200a. High TP73-AS1 expression in BC was related with poorer clinicopathological parameters and shorter overall survival.	MI0000737	J Cell Biochem 2018 Jan 119, 680-690 doi:10.1002/jcb.26231 PMID:28639399
2065	LncRNA	TP73-AS1	miR-200a	HMGB1	Hcclm3, Mhcc97L, Smmc7722, Hep3B And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28403886	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation	TP73-AS1 was upregulated in HCC tissues and cell lines. High TP73-AS1 expression was correlated with worse clinicopathological features, poorer prognosis and shorter survival. In HCC tissues, miR-200a was down-regulated while HMGB1 and RAGE were up-regulated; TP73-AS1 was inversely correlated with miR-200a, while positively correlated with HMGB1 and RAGE, respectively. 	MI0000737	J Exp Clin Cancer Res 2017 Apr 12 36, 51 doi:10.1186/s13046-017-0519-z PMID:28403886
2066	LncRNA	TP73-AS1	miR-200a	RAGE	Hcclm3, Mhcc97L, Smmc7722, Hep3B And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28403886	The long non-coding RNA TP73-AS1 modulates HCC cell proliferation through miR-200a-dependent HMGB1/RAGE regulation	TP73-AS1 was upregulated in HCC tissues and cell lines. High TP73-AS1 expression was correlated with worse clinicopathological features, poorer prognosis and shorter survival. In HCC tissues, miR-200a was down-regulated while HMGB1 and RAGE were up-regulated; TP73-AS1 was inversely correlated with miR-200a, while positively correlated with HMGB1 and RAGE, respectively. 	MI0000737	J Exp Clin Cancer Res 2017 Apr 12 36, 51 doi:10.1186/s13046-017-0519-z PMID:28403886
2067	LncRNA	TTN-AS1	miR-133b	FSCN1	Eca-109, Kyse 30, Kyse 150, Kyse180, Kyse410, Kyse450, Kyse510, Te-10 And Te-13	Esophageal Squamous Cancer	Homo sapiens (human)	Microarray,qRT-PCR,Western blot,Luciferase reporter assayin vitro knockdown,RNAi,RIP	29101304	Functional Role of a Novel Long Noncoding RNA TTN-AS1 in Esophageal Squamous Cell Carcinoma Progression and Metastasis.	lncRNA-TTN-AS1 as an oncogene is highly expressed in ESCC tissues and cell lines, and promotes ESCC cell proliferation and metastasis. Mechanistically, lncRNA-TTN-AS1 promotes expression of transcription factor Snail1 by competitively binding miR-133b, resulting in the epithelial-mesenchymal transition (EMT) cascade.Moreover,lncRNA-TTN-AS1 also induces FSCN1 expression by sponging miR-133b and upregulation of mRNA-stabilizing protein HuR,which further promotes ESCC invasion cascades.	MIMAT0000770	Clin Cancer Res 2018 Jan 15 24, 486-498 doi:10.1158/1078-0432.Ccr-17-1851 PMID:29101304
2068	LncRNA	TUBB2A	miR-596	CLDN4	AGS, HGC-27, and SGC-7901	Gastric Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot,RNA-seq	28819095	Non-coding RNAs participate in the regulatory network of CLDN4 via ceRNA mediated miRNA evasion.	non-coding RNAs play important roles in the regulatory network of Claudin-4. As such, non-coding RNAs should be considered as potential biomarkers and therapeutic targets against gastric cancer.During the complex process of metastasis, primary cancer cells undergo a sequential series of events including local dissemination, intravasation into the vascular system, survival in the circulatory system, extravasation out of the vascular system,and regrowth at distant sites3,4,5.Among these ncRNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) have appealed to a large group of researchers and become a main focus of attention.Kaplan–Meier analysis of the correlation between CLDN4 expression levels and overall survival. 	MIMAT0003264	Nat Commun 2017 Aug 18 8, 289 doi:10.1038/s41467-017-00304-1 PMID:28819095
2069	LncRNA	TUG1	miR-145-5p	NA	Bgc-823 And Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,Cell proliferation assay etc.	27983921	Long Noncoding RNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation and Invasion in Gastric Cancer via Negatively Modulating miRNA-145-5p.	TUG1 was significantly overexpressed and miR-145-5p was dramatically downregulated in GC cell lines.TUG1 knockdown strikingly inhibited cell proliferation and invasion in vitro and markedly suppressed tumor growth in vivo. Furthermore, TUG1 could directly bind to miR-145-5p and repress miR-145-5p expression.TUG1 overexpression significantly relieved the inhibition on GC cell proliferation and invasion in vitro and tumor growth in vivo, mediated by miR-145-5p overexpression.	MIMAT0000437	Oncol Res 2017 May 24 25, 789-798 doi:10.3727/096504016x14783677992682 PMID:27983921
2070	LncRNA	TUG1	miR-186	CPEB2	Ht-29-P/Ht-29-R Cell And Hct-8	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,Flow cytometry assay,MTT assay etc.	28302487	TUG1 mediates methotrexate resistance in colorectal cancer via miR-186/CPEB2 axis.	Here, we observed lncRNA TUG1 was associated to the MTX resistant in colorectal cancer cells.Firstly, quantitative analysis indicated that TUG1 was significantly increased in tumors which were resistant to MTX treatment.TUG1 knockdown re-sensitized the MTX resistance in colorectal cancer cells, which were MTX-resistant colorectal cell line. 	MI0000483	Biochem Biophys Res Commun 2017 Sep 16 491, 552-557 doi:10.1016/j.bbrc.2017.03.042 PMID:28302487
2071	LncRNA	TUG1	miR-300	TGb1	Eh-Gb1, Gbc-Sd, Noz, Sgc-996	Gallbladder Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,Cell proliferation assay etc.	28178615	Long non-coding RNA TUG1 promotes cell proliferation and metastasis by negatively regulating miR-300 in gallbladder carcinoma.	TUG1 expression was significantly overexpressed in GBC tissues.Functionally, this study demonstrated that knockdown of TUG1 significantly inhibited GBC cell proliferation, metastasis.Mechanically, we found that TUG1 is upregulated by TGF-β1, and knockdown of TUG1 inhibited GBC cell EMT.Furthermore, we identified that miR-300, which has been reported as a suppressor in other types of cancer, is negatively regulated by TUG1	MI0005525	Biomed Pharmacother 2017 Apr 88, 863-869 doi:10.1016/j.biopha.2017.01.150 PMID:28178615
2072	LncRNA	TUG1	miR-335-5p	ROCK1	Mg-63, U2Os And Mnng/Hos	Osteosarcoma	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay etc.	28205334	Long non-coding RNA TUG1 promotes migration and invasion by acting as a ceRNA of miR-335-5p in osteosarcoma cells.	TUG1 was elevated and correlated with a poor prognosis in osteosarcoma patients.Decreased TUG1 could remarkably inhibit osteosarcoma cell migration and invasion. Furthermore, the results of a real-time quantitative PCR showed that TUG1 and miR-335-5p could affect each other's expression.respectively. Finally, we affirmed that TUG1 affected ROCK1 expression and ROCK1-mediated migration/invasion by working as a competitive endogenous RNA (ceRNA) via miR-335-5p.	MIMAT0000765	Cancer Sci 2017 May 108, 859-867 doi:10.1111/cas.13201 PMID:28205334
2073	LncRNA	TUG1	miR-145	Sirt3	Huh28, Hucct1, Rbe, Hccc-9810	Intrahepatic Cholangiocarcinoma	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29371936	LncRNA TUG1 sponges miR-145 to promote cancer progression and regulate glutamine metabolism via Sirt3/GDH axis	In this study, we investigated the role of TUG1 in the pathogenesis of intrahepatic cholangiocarcinoma (ICC).TUG1 is upregulated in ICC samples, which correlates with poor prognosis and adverse clinical pathological characteristics. Knockdown of TUG1 inhibited the proliferation, motility, and invasiveness of cultured ICC cells, and decreased tumor burden in a xenograft mouse model. When we explored the mechanisms underlying these effects, we found that TUG1 acts as an endogenous competing RNA (ceRNA) that ‘sponges’ miR-145, thereby preventing the degradation of Sirt3 mRNA and increasing expression of Sirt3 and GDH proteins. Accordingly, glutamine consumption, α-KG production, and ATP levels were dramatically decreased by TUG1 knockdown in ICC cells, and this effect was reversed by miR-145 inhibition. These findings indicate that the TUG1/miR-145/Sirt3/GDH regulatory network may provide a novel therapeutic strategy for treatment of ICC.	MI0000461	Oncotarget 2017 Dec 26 8, 113650-113661 doi:10.18632/oncotarget.21922 PMID:29371936
2074	LncRNA	TUG1	miR-382	EZH2	Panc-1, Aspc-1, Hek 293T 	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RIP	28813705	The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation, Migration and EMT Phenotype Formation Through Sponging Mir-382	TUG1 was overexpressed in PC tissues and cell lines, and high expression of TUG1 predicted poor prognosis. at least partially, by functioning as an endogenous ‘sponge’ and competing for miR-382 binding to the miRNA target EZH2.	MI0000790	Cell Physiol Biochem 2017  42, 2145-2158 doi:10.1159/000479990 PMID:28813705
2075	LncRNA	TUG1	miR-142	ZEB2	T24 And Biu-87	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,MIT	28503069	Downregulation of long noncoding RNA TUG1 inhibits proliferation and induces apoptosis through the TUG1/miR-142/ZEB2 axis in bladder cancer cells	The levels of TUG1 and ZEB2 were significantly increased in bladder cancer tissues and cells. Moreover, ZEB2 was verified as a direct target of miR-142 and miR-142 could specially bind to TUG1.	MI0000458	Onco Targets Ther 2017  10, 2461-2471 doi:10.2147/ott.S124595 PMID:28503069
2076	LncRNA	TUG1	miR-138-5p	SIRT1	Hela, Caski	Cervical Cancer	Homo sapiens (human)	qPCR,Western blot etc.	29029428	Long non-coding RNA TUG1 promotes cervical cancer progression by regulating the miR-138-5p-SIRT1 axis	TUG1 expression was upregulated in cervical cancer tissues and correlated with advanced clinical features and poor overall survival.In addition, our results indicated that TUG1 could act as an endogenous sponge by directly binding to miR-138-5p and suppressed miR-138-5p expression.	MIMAT0000430	Oncotarget 2017 Sep 12 8, 65253-65264 doi:10.18632/oncotarget.18224 PMID:29029428
2077	LncRNA	TUG1	miR-153	ZEB2	Mg63 And U2-Os 	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase Reporter Assays,RIP	28411362	Knockdown of Long Noncoding RNA TUG1 Inhibits the Proliferation and Cellular Invasion of Osteosarcoma Cells By Sponging MiR-153	TUG1 was overexpressed and miR-153 was downregulated in osteosarcoma tissues and cell lines.  Moreover, TUG1 was confirmed to be a miR-153 sponge. 	MI0000463	Oncol Res 2018 Jun 11 26, 665-673 doi:10.3727/096504017x14908298412505 PMID:28411362
2078	LncRNA	TUG1	miR-381	SOX4	Ges-1, Bgastric Cancer-823, Mgastric Cancer-803, Sgastric Cancer-7901,Mkn28	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,etc.	28927144	MiR-381 inhibits migration and invasion in human gastric carcinoma through downregulatedting SOX4	downregulation of miR-381 by lncRNA-TUG1 promoted the metastasis of GC cells by inhibiting SOX4.	MI0000789	Oncol Lett 2017 Sep 14, 3760-3766 doi:10.3892/ol.2017.6637 PMID:28927144
2079	LncRNA	TUG1	miR-145	ZEB1	Atc, Sw1736, Kat18, Ftc, Ftc133, Hgc-27	Thyroid Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28645161	LncRNA TUG1 influences papillary thyroid cancer cell proliferation, migration and EMT formation through targeting miR-145.	TUG1 contributes to the progression of thyroid cancer cells through regulating miR-145/ZEB1 signal pathway.LncRNA TUG1 was found to be up-regulated in thyroid cancer tissues and thyroid cancer cells compared with that in the human normal breast epithelial cell HGC-27.Increased lncRNA TUG1 expression was found to significantly promote tumor cell proliferation,and facilitate cell invasion,while down-regulated TUG1 could obviously inhibit cell proliferation,migration/invasion and reverse EMT to MET.These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145,and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells.	MI0000461	Acta Biochim Biophys Sin (Shanghai) 2017 Jul 1 49, 588-597 doi:10.1093/abbs/gmx047 PMID:28645161
2080	LncRNA	TUSC7	miR-211-3p	CDK6	M5, Dld1, Hct116, Sw480, Sw620, And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,CCK-8 assay etc.	28214867	The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer.	TUSC7 was significantly downregulated in CRC tissues. Ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p.	MIMAT0022694	Cell Physiol Biochem 2017  41, 635-644 doi:10.1159/000457938 PMID:28214867
2081	LncRNA	TUSC7	miR-23b	NA	HEC1A/CR	Endometrial Cancer	Homo sapiens (human)	qPCR	28653877	Long non-coding RNA tumor suppressor candidate 7 advances chemotherapy sensitivity of endometrial carcinoma through targeted silencing of miR-23b	In this study, the low expression of TUSC7 was confirmed in endometrial carcinoma tissues and was associated with high pathological stages of endometrial carcinoma, which revealed that TUSC7 might be involved in tumorigenesis and progression of endometrial carcinoma. Moreover, the expression of TUSC7 in endometrial carcinoma tissues and cell lines resistant to CDDP and Taxol was lower than that in sensitive endometrial carcinoma tissues and cell lines, which indicated that the TUSC7 expression level was positively correlated with the response of endometrial carcinoma patients to chemotherapy with CDDP and Taxol. MiR-23b upregulation mostly reversed the TUSC7-induced regulatory effects on HEC1A/CR cell line.	MI0000439	Tumour Biol 2017 Jun 39, 1010428317707883 doi:10.1177/1010428317707883 PMID:28653877
2082	LncRNA	UCA1	miR-184	SF1	Tca8113, Tscca, Cal-27,Scc-9,Nhok	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot	29125238	LncRNA UCA1 promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by sunppressing miR-184 expression.	UCA1 expression was upregulated in OSCC tissues, cell lines, and CDDP resistant OSCC cells. UCA1 facilitated proliferation, enhanced CDDP chemoresistance, and suppressed apoptosis in OSCC cells.UCA1 could interact with miR-184 to repress its expression. downregulation of miR-184 partly reversed the tumor suppression effect and CDDP chemosensitivity of UCA1 knockdown in CDDP-resistant OSCC cells.UCA1 could perform as a miR-184 sponge to modulate SF1 expression.depletion of UCA1 further boosted CDDP-mediated repression effect on tumor growth. UCA1 accelerated proliferation, increased CDDP chemoresistance and restrained apoptosis partly through modulating SF1 via sponging miR-184 in OSCC cells. 	MI0000481	Cancer Med 2017 Dec 6, 2897-2908 doi:10.1002/cam4.1253 PMID:29125238
2083	LncRNA	UCA1	miR-16	MDR1	K562	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	27854515	lnclncRNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.RNA UCA1 Contributes to Imatinib Resistance by Acting as a ceRNA Against miR-16 in Chronic Myeloid Leukemia Cells.	UCA1 was significantly upregulated in K562/IM and K562/IM-R cells compared with K562 cells, and UCA1 in K562/IM cells was higher than that in K562/IM-R cells. Overexpression of UCA1 increased MDR1 expression to promote IM resistance of CML cells. Furthermore, for the first time, we demonstrated that UCA1 functions as a competitive endogenous (ceRNA) of MDR1 through completely binding the common miR-16.	MI0000070	DNA Cell Biol 2017 Jan 36, 18-25 doi:10.1089/dna.2016.3533 PMID:27854515
2084	LncRNA	UCA1	miR-182	p53	U373Mg, T98Mg, Swo38, U251 And Shg44	Glioma	Homo sapiens (human)	qPCR,RNAi,Western blot,Luciferase reporter assay,MTT assay etc.	28137422	The lncRNA UCA1 interacts with miR-182 to modulate glioma proliferation and migration by targeting iASPP.	Upregulation of lncRNA-UCA1 in glioma tissues and cell lines could promote glioma cell proliferation and migration through interaction with miR-182, and knockdown of UCA1 inhibited the proliferation and migration of human glioma cell. In addition, miR-182 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) was required in the regulation of UCA1 induced glioma cell proliferation.	MI0000272	Arch Biochem Biophys 2017 Jun 1 623-624, 1-8 doi:10.1016/j.abb.2017.01.013 PMID:28137422
2085	LncRNA	UCA1	miR-203	Snail2	Mhcc97L, Huh7, Mhcc97H And Sk-Hep1	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,Cell proliferation assay etc.	28271214	Long non-coding RNA UCA1 regulates the expression of Snail2 by miR-203 to promote hepatocellular carcinoma progression.	UCA1 was markedly upregulated in HCC tissues. Furthermore, gain-of-function and loss-of-function analysis showed that UCA1 knockdown inhibited HCC cells proliferation and invasion in vitro and xenograft tumour growth in vivo. Moreover, UCA1 overexpression promoted cell epithelial-mesenchymal transition (EMT) in HCC via effectively sponging to miR-203 and thereby activating the expression of transcription factor Snail2.	MI0000283	J Cancer Res Clin Oncol 2017 Jun 143, 981-990 doi:10.1007/s00432-017-2370-1 PMID:28271214
2086	LncRNA	UCA1	miR-135a	NA	Sw1990，Bxpc-3, Miapaca-2, Panc-1, Capan-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,RNAi,Northern blot,Luciferase reporter assay,Flow cytometry assay etc.	28315290	UCA1 Regulates the Growth and Metastasis of Pancreatic Cancer By Sponging MiR-135a.	UCA1 was overexpressed in PC tissues and cell lines. The proliferation of PC cells was inhibited after UCA1 was suppressed by a lentiviral vector. Cell apoptosis rate was largely promoted by down-regulating UCA1. Luciferase activity assay further comfirmed the targeting relationship between UCA1 and miR-135a. Moreover, miRNA-135a reversed the effect of UCA1 on cell apoptosis rate and cell viability in SW1990 cells. The migration and invasion capacity of PC cells suppressed by UCA1 siRNA was then enhanced by miR-135a inhibitor.	MI0000161	Oncol Res 2017 Nov 2 25, 1529-1541 doi:10.3727/096504017x14888987683152 PMID:28315290
2087	LncRNA	UCA1	miR-143	HMGB1	T24, 5637, J82, Rt4, Ht1376	Bladder Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot etc.	29113184	LncRNA UCA1 promotes the invasion and EMT of bladder cancer cells by regulating the miR143/HMGB1 pathway	UCA1 negatively regulated miR-143 expression in a dose-dependent manner in bladder cancer cells. In addition,UCA1 and HMGB1 were upregulated and miR-143 was downregulated in bladder cancer specimens. Overall, the data suggested that UCA1 may promote the invasion and EMT of bladder cancer cells by regulating the miR-143/HMGB1 pathway, which exhibits an important regulatory role in the pathology of bladder cancer.	MI0000459	Oncol Lett 2017 Nov 14, 5556-5562 doi:10.3892/ol.2017.6886 PMID:29113184
2088	LncRNA	UCA1	miR-195	ARL2	5637, Umuc2	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,RIP	29130995	LncRNA UCA1 Promotes Mitochondrial Function of Bladder Cancer via the MiR-195/ARL2 Signaling Pathway	UCA1 enhances mitochondrial function in bladder cancer cells.These data suggest that UCA1 enhanced mitochondrial function and cell viability through the UCA1/miR-195/ARL2 axis in vitro and in vivo. 	MI0000489	Cell Physiol Biochem 2017  43, 2548-2561 doi:10.1159/000484507 PMID:29130995
2089	LncRNA	UCA1	miR-184	BCL-2	Du145 And Lncap	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assay	28209917	Artesunate suppresses the viability and mobility of prostate cancer cells through UCA1, the sponge of miR-184	UCA1 was up-regulated in prostate cancer tissues compared to hyperplastic prostatic tissues,and a higher UCA1 level predicted poor prognosis in PCa patients.Then we determined that the miR-184/Bcl-2 axis might be the downstream signaling pathway of UCA1 upon ART treatment. UCA1 binds to miR-184 through its seed sequences and may function as a sponge for miR-184.	MI0000481	Oncotarget 2017 Mar 14 8, 18260-18270 doi:10.18632/oncotarget.15353 PMID:28209917
2090	LncRNA	UCA1	miR-495	p21	786-O, Achn, Caki-1, And Caki-2	Renal Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay,RNAi	28466784	LncRNA UCA1 promotes renal cell carcinoma proliferation through epigenetically repressing p21 expression and negatively regulating miR-495	In this study, we found that urothelial carcinoma-associated 1 was overexpressed in renal cell carcinoma tissues compared with the adjacent normal tissues, and higher urothelial carcinoma-associated 1 expression levels were positively associated with advanced tumor stage and poor survival time in renal cell carcinoma patients. Moreover, urothelial carcinoma-associated 1 was found to be associated with enhancer of zeste homolog 2, which suppressed p21 expression through histone methylation (H3K27me3) on p21 promoter. These findings illuminated that urothelial carcinoma–associated 1 promoted renal cell carcinoma progression through enhancer of zeste homolog 2 and interacted with miR-495. 	MI0003135	Tumour Biol 2017 May 39, 1010428317701632 doi:10.1177/1010428317701632 PMID:28466784
2091	LncRNA	UCA1	miR-122	NA	Shg44, U87, U251, And A172 Normal Human Astrocytes 	Glioma	Homo sapiens (human)	RT-PCR,Luciferase reporter assay,in vitro knockdown	28548636	Long Noncoding RNA UCA1 Targets miR-122 to Promote Proliferation, Migration, and Invasion of Glioma Cells.	UCA1 was upregulated in glioma tissue and indicated a poor prognosis. UCA1 knockdown induced by si-UCA1 significantly suppressed the proliferative, migrative, and invasive activities of glioma cell lines (U87 and U251).the complementary binding within UCA1 and  miR-122 at the 3'-UTR. Functional experiments revealed that UCA1 acted as an miR-122 "sponge" to modulate glioma cell proliferation, migration, and invasion via downregulation of miR-122.	MI0000442	Oncol Res 2018 Jan 19 26, 103-110 doi:10.3727/096504017x14934860122864 PMID:28548636
2092	LncRNA	UCA1	miR-144	EGFR	Wi-38, Hel-1	Lung Cancer	Homo sapiens (human)	luciferase reporter assay,qPCR,western blot etc.	28762326	Long Noncoding RNA Urothelial Carcinoma Associated 1 Promotes the Proliferation and Metastasis of Human Lung Tumor Cells by Regulating MicroRNA-144	This result indicated that the up-regulated expression of lncRNA UCA1 was involved in the canceration of normal lung cells. These findings will be helpful for understanding the critical roles of lncRNA UCA1 and miRNA-144 in lung cancer cells, and provide new therapeutic strategy for lung cancer therapy.The experimental study from Cheng et al. demonstrated that lncRNA UCA1 promoted non-T790M cells acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) by activating the AKT/mammalian target of rapamycin (mTOR) pathway in EGFR-mutant NSCLC.	MI0000460	Oncol Res 2018 May 7 26, 537-546 doi:10.3727/096504017x15009792179602 PMID:28762326
2093	LncRNA	UCC	miR-143	KRAS	Sw480, Sw620, Hct116, Caco-2, Dld-1, And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,RIP	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143	A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’stage, and patient outcomes. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA.	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
2094	LncRNA	UCC	miR-143	IGF1R	Sw480, Sw620, Hct116, Caco-2, Dld-1, And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,RIP	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143	A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’stage, and patient outcomes. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA.	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
2095	LncRNA	UCC	miR-143	BCL-2	Sw480, Sw620, Hct116, Caco-2, Dld-1, And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,RIP	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143	A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’stage, and patient outcomes. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA.	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
2096	LncRNA	UCC	miR-143	HK2	Sw480, Sw620, Hct116, Caco-2, Dld-1, And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,RNAi,RIP	28492554	The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143	A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines. UCC levels correlated with lymph node metastasis, Dukes’stage, and patient outcomes. Moreover, mechanistic investigations showed that UCC may act as an endogenous sponge by competing for miR-143, thereby regulating the targets of this miRNA.	MI0000459	Cell Death Dis 2017 May 11 8, e2778 doi:10.1038/cddis.2017.191 PMID:28492554
2097	LncRNA	UICLM	miR-215	ZEB2	Sw620, Sw480, Lovo, Ht-29, Hct116, Dld-1, Rko	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blotting,RIP etc.	29187907	Long non-coding RNA UICLM promotes colorectal cancer liver metastasis by acting as a ceRNA for microRNA-215 to regulate ZEB2 expression	lncRNA UICLM (up-regulated in colorectal cancer liver metastasis) was significantly up-regulated in cases of CRC with liver metastasis.Moreover, UICLM expression was higher in CRC tissues than in normal tissues, and UICLM expression was associated with poor patient survival. Knockdown of UICLM inhibited CRC cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and CRC stem cell formation in vitro as well as tumor growth and liver metastasis in vivo. Ectopic expression of UICLM promoted CRC cell proliferation and invasion. Mechanistic investigations revealed that UICLM induced its biological effects by regulating ZEB2, as the oncogenesis facilitated by UICLM was inhibited by ZEB2 depletion. Further study indicated that UICLM acted as a competing endogenous RNA (ceRNA) for miR-215 to regulate ZEB2 expression.	MI0000291	Theranostics 2017  7, 4836-4849 doi:10.7150/thno.20942 PMID:29187907
2098	LncRNA	USP16	miR-21	PTEN	Mhcc97H, Mhcc97L, Hepg2, Smmc-7721, And Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot	29179215	Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression	Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p.	MI0000077	Cell Physiol Biochem 2017  44, 1188-1198 doi:10.1159/000485449 PMID:29179215
2099	LncRNA	USP16	miR-590-5p	PTEN	Mhcc97H, Mhcc97L, Hepg2, Smmc-7721, And Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot	29179215	Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression	Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p.	MIMAT0003258	Cell Physiol Biochem 2017  44, 1188-1198 doi:10.1159/000485449 PMID:29179215
2100	LncRNA	XIST	miR-137	FOXC1	Hcmec/D3, U87Mg, U118Mg, Hek293T	Glioma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,ChIP,Cell proliferation assay,Cell migration assay etc.	28287613	Knockdown of long non-coding RNA XIST increases blood-tumor barrier permeability and inhibits glioma angiogenesis by targeting miR-137.	lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited glioma angiogenesis. The analysis of the mechanism of action revealed that the reduction of XIST inhibited the expression of the transcription factor forkhead box C1 (FOXC1) and zonula occludens 2 (ZO-2) by upregulating miR-137. FOXC1 decreased BTB permeability by increasing the promoter activity and expression of ZO-1 and occludin, and promoted glioma angiogenesis by increasing the promoter activity and expression of chemokine (C-X-C motif) receptor 7b (CXCR7).	MIMAT0000429	Oncogenesis 2017 Mar 13 6, e303 doi:10.1038/oncsis.2017.7 PMID:28287613
2101	LncRNA	XIST	miR-497	MACC1	Sgc-7901, Bgc-823, Hgc-27 And Mkn-28	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay,MTT assay etc.	27911852	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer.	XIST expression was significantly increased in GC tissues and cell lines. LncRNA XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to GC cell growth. LncRNA XIST also contributed to GC cell invasion both in vitro and in vivo. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis.	MI0003138	Oncotarget 2017 Jan 17 8, 4125-4135 doi:10.18632/oncotarget.13670 PMID:27911852
2102	LncRNA	XIST	miR-139-5p	PDK1	Hepg2, Hep3B, Plc, Huh7, Smmc7721 And L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,RNAi,Western blot,RIP,Luciferase reporter assay etc.	28231734	Long non-coding RNA XIST promotes cell growth by regulating miR-139-5p/PDK1/AKT axis in hepatocellular carcinoma.	XIST expression was significantly increased in hepatocellular carcinoma tissues and cell lines. XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to hepatocellular carcinoma cell growth. In addition, we revealed that there was reciprocal repression between XIST and miR-139-5p. PDK1 was identified as a direct target of miR-139-5p.	MIMAT0000250	Tumour Biol 2017 Feb 39, 1010428317690999 doi:10.1177/1010428317690999 PMID:28231734
2103	LncRNA	XIST	miR-449a	BCL-2	Nl9980, Nci-H1299, Nci-H460, Spc-A-1, And A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,RNAi,Western blot,Cell migration and invasion assay,CCK-8 assay etc.	28248928	The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer.	The expression levels of XIST were significantly elevated. Knockdown of XIST significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis. Furthermore, XIST knockdown elevated the expression of E-cadherin, and suppressed the expression of Bcl-2. We further identified reciprocal repression between XIST and miR-449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2.	MI0001648	Acta Pharmacol Sin 2017 Mar 38, 371-381 doi:10.1038/aps.2016.133 PMID:28248928
2104	LncRNA	XIST	miR-133a	EGFR	Patu8988, Sw1990, Bxpc-3, Aspc-1, Cfpac-1 And Panc-1	Pancreatic Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Cell proliferation assay,MTT assay etc.	28295543	LncRNA XIST Promotes Pancreatic Cancer Proliferation through miR-133a/EGFR.	lncRNA-XIST was specifically upregulated in PC tissues and cell lines, and high XIST expression in PC was related to poorer prognosis (larger tumor size, perineural invasion, lymph node micrometastases and shorter overall survival). XIST augmented PC cell proliferation. In the present study, XIST and miR-133a reciprocally inhibited each other in PC cells. Exogenous miR-133a expression significantly inhibited PC cell proliferation. Moreover, as exhibited by luciferase reporter gene assays, miR-133a bound to XIST and the 3'UTR of EGFR by direct targeting. In PC tissues, miR-133a expression was down-regulated and EGFR expression was up-regulated; miR-133a was inversely correlated with EGFR and XIST, respectively; XIST was positively correlated with EGFR. Taken together, these findings will shed light on the role and mechanism of XIST/miR-133a/EGFR in regulating PC cells proliferation.	MI0000159	J Cell Biochem 2017 Oct 118, 3349-3358 doi:10.1002/jcb.25988 PMID:28295543
2105	LncRNA	XIST	miR-101	EZH2	Kyse30, Kyse510, Kyse410, Kyse520, Kyse140 And Kyse150	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc	29100288	Long noncoding RNA XIST promotes malignancies of esophageal squamous cell carcinoma via regulation of miR-101/EZH2.	XIST was significantly upregulated in esophageal squamous cancerous tissues and cancer cell lines,as compared with that in the corresponding non-cancerous tissues and immortalized normal squamous epithelial cells. High XIST expression predicted poor prognosis of esophageal squamous cancer patients. Lentivirus mediated knockdown of XIST inhibited proliferation, migration and invasion of esophageal squamous cancer cells in vitro and suppressed tumor growth in vivo. Knockdown of XIST resulted in elevated expression of miR-101 and decreased expression of EZH2. Further analysis showed that XIST functioned as the competitive endogenous RNA of miR-101 to regulate EZH2 expression.Moreover, enforced expression of EZH2 significantly attenuated the anti-proliferation activity upon XIST knockdown. Conclusively, XIST plays an important role in malignant progression of ESCC via modulation of miR-101/EZH2 axis. Our results showed that patients with high XIST level had a significantly shortened overall survival as well as disease-free survival than those with low XIST level. 	MI0000103	Oncotarget 2017 Sep 29 8, 76015-76028 doi:10.18632/oncotarget.18638 PMID:29100288
2106	LncRNA	XIST	miR-140	iASPP	Aspc-1, Bxpc3, Sw1990,Panc-1, Capan-1, Capan-2	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	29371940	The lncRNA XIST interacts with miR-140/miR-124/iASPP axisto promote pancreatic carcinoma growth	XIST might be an oncogenic lncRNA that promoted proliferation of PC cell line through inhibiting miR- 140/miR-124 expression and promoting cell cycle-related factor expression, and could be regarded as a therapeutic target in human pancreatic carcinoma.XIST is highly expressed in PC tissues and cell line and related with clinicopathologic features.	MI0000456	Oncotarget 2017 Dec 26 8, 113701-113718 doi:10.18632/oncotarget.22555 PMID:29371940
2107	LncRNA	XIST	miR-124	iASPP	Aspc-1, Bxpc3, Sw1990,Panc-1, Capan-1, Capan-2	Pancreatic Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay etc.	29371940	The lncRNA XIST interacts with miR-140/miR-124/iASPP axisto promote pancreatic carcinoma growth	XIST might be an oncogenic lncRNA that promoted proliferation of PC cell line through inhibiting miR- 140/miR-124 expression and promoting cell cycle-related factor expression, and could be regarded as a therapeutic target in human pancreatic carcinoma.XIST is highly expressed in PC tissues and cell line and related with clinicopathologic features.	MI0000443	Oncotarget 2017 Dec 26 8, 113701-113718 doi:10.18632/oncotarget.22555 PMID:29371940
2108	LncRNA	XIST	miR-429	NA	A172，U251	Glioma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	29187887	Long Non-coding RNA XIST Promotes Glioma Tumorigenicity and Angiogenesis by Acting as a Molecular Sponge of miR-429	lncRNA XIST expression inversely correlated with miR-429 expression in glioma cells; miR-429 modulated XIST expression by directly targeting the XIST gene sequence.In addition, miR-429 inhibitor restored metastatic and pro-angiogenic ability of gliomas abolished by silencing XIST.	MIMAT0001536	J Cancer 2017  8, 4106-4116 doi:10.7150/jca.21024 PMID:29187887
2109	LncRNA	XIST	miR-21-5p	PDCD4	Mg63, U2Os, Saos2, Hos, Sosp-9697, Sv40	Osteosarcoma	Homo sapiens (human)	qPCR,Western blotting,Luciferase reporter assay etc.	29048648	Long non-coding RNA XIST regulates PDCD4 expression by interacting with miR-21-5p and inhibits osteosarcoma cell growth and metastasis	XIST regulated PDCD4 expression by competitively binding to miR-21-5p. XIST inhibited cell proliferation and cell mobility by competitively binding to miR-21-5p and upregulating PDCD4 in OS. Our study demonstrated that lncRNA-XIST,which acts as a miRNA sponge, impedes miR-21-5p to maintain the expression of PDCD4, which contributes to the progression of OS. Our fndings suggest that the newly identifed XIST/miR-21-5p/PDCD4 axis could be a potential biomarker or therapeutic target for OS.	MIMAT0000076	Int J Oncol 2017 Nov 51, 1460-1470 doi:10.3892/ijo.2017.4127 PMID:29048648
2110	LncRNA	XIST	miR-497	MACC1	Sgc-7901, Bgc-823,Hgc-27, Mkn-28	Gastric Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assay etc.	29212249	Long non-coding RNA XIST promotes cell growth and invasion through regulating miR-497/MACC1 axis in gastric cancer	LncRNA XIST promoted cell cycle progression from the G1 phase to the S phase and protected cells from apoptosis, which contributed to GC cell growth. LncRNA XIST also contributed to GC cell invasion both in vitro and in vivo. We revealed that XIST functioned as competing endogenous RNA to repress miR-497, which controlled its down-stream target MACC1. We proposed that XIST was responsible for GC cell proliferation and invasion and XIST exerted its function through the miR-497/MACC1 axis. Our fndings suggested that lncRNA XIST may be a candidate prognostic biomarker and a target for new therapies in GC patients.	MI0003138	Oncotarget 2017 Nov 7 8, 94554-94568 doi:10.18632/oncotarget.21791 PMID:29212249
2111	LncRNA	XIST	miR-23a	RKIP	Pc3, Du145, Lncap	Prostate Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assays,Western blot etc.	29212233	LncRNA XIST acts as a tumor suppressor in prostate cancer through sponging miR-23a to modulate RKIP expression	XIST was down-regulated in prostate cancer specimens and cell lines. Low expression of XIST was correlated with poor prognosis and advanced tumor stage in prostate cancer patients.XIST negatively regulates the expression of miR-23a and subsequently promotes RKIP expression at post-transcriptional level. Consequently, we investigated the correlation between XIST and miR-23a, and identified miR-23a as a direct target of XIST. In addition, over-expression of miR-23a efficiently abrogated the up-regulation of RKIP induced by XIST, suggesting that XIST positively regulates the expression of RKIP by competitively binding to miR-23a. Taken together, our study indicated that lncRNA XIST acts as a tumor suppressor in prostate cancer, and this regulatory effect of XIST will shed new light on epigenetic diagnostics and therapeutics in prostate cancer.	MI0000079	Oncotarget 2017 Nov 7 8, 94358-94370 doi:10.18632/oncotarget.21719 PMID:29212233
2112	LncRNA	XIST	miR-29c	NA	Cne-1, Cne-2	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,Western blot etc.	28985197	Downregulation of lncRNA X Inactive Specifc Transcript (XIST) Suppresses Cell Proliferation and Enhances Radiosensitivity by Upregulating mir-29c in Nasopharyngeal Carcinoma Cells	XIST was upregulated and miR-29c was downregulated in NPC cells.The expressions of XIST and miR-29c changed reversely in response to irradiation. Knockdown of XIST and miR-29c overexpression both resulted in a dramatic suppression of cell proliferation, a marked enhancement of radiosensitivity, and an obvious increase of g-H2AX foci formation in NPC cells. Luciferase reporter assay and qRT-PCR analysis demonstrated that XIST interacts with miR-29c and negatively regulates its expression. Moreover, miR-29c inhibition abrogated XIST knockdown-induced cell proliferation inhibition and radiosensitivity increase in NPC cells.	MI0000735	Med Sci Monit 2017 Oct 6 23, 4798-4807 doi:10.12659/msm.905370 PMID:28985197
2113	LncRNA	XIST	miR-186-5p	NA	A549, H1299, Sk-Mes-1, Calu-3	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi,Luciferase reporter assay	28448993	The Long Non-Coding RNA XIST Controls Non-Small Cell Lung Cancer Proliferation and Invasion by Modulating miR-186-5p	XIST was upregulated in NSCLC cell lines and tissues. Functionally, XIST knockdown inhibited cancer cell proliferation and invasion, and induced apoptosis in vitro, and suppressed subcutaneous tumor growth in vivo. Mechanistic investigations revealed a reciprocal repressive interaction between XIST and miR-186-5p.	MIMAT0000456	Cell Physiol Biochem 2017  41, 2221-2229 doi:10.1159/000475637 PMID:28448993
2114	LncRNA	XIST	miR-124	AR	Tcc-Sup, Ej, Sw780 And Um-Uc-3	Bladder Cancer	Homo sapiens (human)	qPCR,Western blot,Luciferase reporter assay	28869948	The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)	XIST and AR were upregulated in bladder cancer tissues and positively correlated. These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.	MI0000443	Cell Physiol Biochem 2017  43, 405-418 doi:10.1159/000480419 PMID:28869948
2115	LncRNA	XIST	miR-181a	PTEN	Hcclm3, Hepg2, Hep3B, Smmc-7721, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR,Western blot etc.	28388883	Long non-coding RNA XIST regulates PTEN expression by sponging miR-181a and promotes hepatocellular carcinoma progression	MiR-181a had multiple binding sites with the long non-coding RNA (lncRNA) XIST. The regulation of miR-181a on PTEN was mediated by lncRNA XIST. The proliferation and invasion of cells with siXIST were significantly enhanced compared with those of control cells, while knockdown of miR-181a abolished the enhancing effects.	MI0000269	BMC Cancer 2017 Apr 7 17, 248 doi:10.1186/s12885-017-3216-6 PMID:28388883
2116	LncRNA	XIST	miR-132-3p	MAPK1	Lovo, Hct116, Sw620, Sw480 And Ht29	Colorectal Cancer	Homo sapiens (human)	qPCR,Western blot etc.	28730777	Long non-coding RNA XIST functions as an oncogene in human colorectal cancer by targeting miR-132-3p	The expression level of XIST was significantly increased in both CRC tissues sample and CRC cells.XIST promoted CRC cell proliferation by affecting the cell cycle.In addition,XIST and miR-132-3p were inhibited by each other reciprocally. 	MIMAT0000426	J buon 2017 May-Jun 22, 696-703,  PMID:28730777
2117	LncRNA	XIST	let-7i	BAG-1	A549, A549/Ddp 	Lung Cancer	Homo sapiens (human)	qPCR,Western blot,RNAi,Luciferase reporter assays etc	28961027	LncRNA XIST promotes human lung adenocarcinoma cells to cisplatin resistance via let-7i/BAG-1 axis	LncRNA XIST expression was markedly increased in cisplatin-resistant A549/DDP cells compared with parental A549 cells as shown by qRT-PCR. LncRNA XIST overexpression in A549 cells increased their chemosensitivity to cisplatin both in vitro and in vivo by protecting cells from apoptosis and promoting cell proliferation. We revealed that XIST functioned as competing endogenous RNA to repress let-7i, which controlled its down-stream target BAG-1. We proposed that XIST was responsible for cisplatin resistance of LAD cells and XIST exerted its function through the let-7i/BAG-1 axis.	MI0000434	Cell Cycle 2017  16, 2100-2107 doi:10.1080/15384101.2017.1361071 PMID:28961027
2118	LncRNA	XIST	miR-320b	RAP2B	U2Os, Saos-2, Mg63, And Mnng/Hos	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,Luciferase Reporter Assays	28409547	Long Non-Coding RNA XIST Promotes Osteosarcoma Progression by Targeting Ras-Related Protein RAP2B via miR-320b 	XIST expression was significantly increased in osteosarcoma tissues and cell lines by LncRNA Profiler and qRT-PCR.The competing relationship between XIST and miR-320b was confirmed by Luciferase report assay.	MIMAT0005792	Oncol Res 2018 Jul 5 26, 837-846 doi:10.3727/096504017x14920318811721 PMID:28409547
2119	LncRNA	XLOC_000983	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
2120	LncRNA	XLOC_005104	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
2121	LncRNA	XLOC_006324	miR-148b	NA	Sgc-7901, Sgc-7901, Ags	Gastric Cancer	Homo sapiens (human)	microarray,qPCR etc.	28043146	Microarray analysis of long non-coding RNAs related to microRNA-148b in gastric cancer.	To confirm the microarray results, we randomly selected two up-regulated lncRNAs (XLOC_000983, XLOC_005104) and six down-regulated lncRNAs (M18204.1, ENST00000548900.1, XLOC_006324, ENST00000420902.1, AK027145, HIX0023999) with log foldchanges > 2 to perform real-time PCR. The results of real-time PCR indicated a consistency of 87.5% between the real-time PCR results and the microarray results in SGC-7901 cells, these also showed a same result between PCR and microarray in AGS cells.	MI0000811	Neoplasma 2017  64, 199-208 doi:10.4149/neo_2017_205 PMID:28043146
2122	LncRNA	XLOC_008466	miR-874	MMP2	A549, H460	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,RIP,Luciferase reporter assay etc	28501870	Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874	Up-regulation of XLOC_008466 in NSCLC patients was related to lymph node metastasis and the TNM stage.Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression 	MI0005532	Cell Physiol Biochem 2017  42, 126-136 doi:10.1159/000477121 PMID:28501870
2123	LncRNA	ZFAS1	miR-150-5p	Sp1	Ovcar3, Caov3, Ovca429, Skov3, A2780, And Cov644	Ovarian Cancer	Homo sapiens (human)	qPCR,Cell transfection,Western blot,Luciferase reporter assay,MTT assay etc.	28099946	Long non-coding RNA ZFAS1 interacts with miR-150-5p to regulate Sp1 expression and ovarian cancer cell malignancy.	ZFAS1 was upregulated in epithelial ovarian cancer tissues, and was negatively correlated to the overall survival rate of patients.While depletion of ZFAS1 inhibited proliferation, migration, and development of chemoresistance, overexpression of ZFAS1 exhibited an even higher proliferation rate, migration activity, and chemoresistance in EOC cell lines. We further found miR-150-5p was a potential target of ZFAS1, which was downregulated in epithelial ovarian cancer tissue.MiR-150-5p subsequently inhibited expression of transcription factor Sp1,as evidence by luciferase assays. Inhibition of miR-150-5p rescued the suppressed proliferation and migration induced by depletion of ZFAS1 in epithelial ovarian cancer cells,at least in part. 	MIMAT0000451	Oncotarget 2017 Mar 21 8, 19534-19546 doi:10.18632/oncotarget.14663 PMID:28099946
2124	LncRNA	ZFAS1	miR-486	NA	U2Os, Saos-2, Hos, Mg-63	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assays,RIP etc.	29262629	Long non-coding RNA ZFAS1 sponges miR-486 to promote osteosarcoma cells progression and metastasis in vitro and vivo	Furthermore,the up-regulated expression of ZFAS1 was closely related to poor prognosis. In vitro, loss-of-function experiments showed that ZFAS1 knockdown significantly suppressed the proliferation, induced cycle arrest at G0/G1 phase and enhance apoptosis. In vivo, ZFAS1 knockdown inhibited the tumor growth. Bioinformatics online programs predicted that ZFAS1 sponge miR-486 at 3’-UTR with complementary binding sites, which was validated using luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Rescue experiments confirmed that miR-486 could reverse the functions of ZFAS1 on osteosarcoma genesis. In conclusion, our results demonstrate that ZFAS1 act as competing endogenous RNA (ceRNA) for miR- 486, and act as oncogene in osteosarcoma tumorigenesis, and discover the functional regulatory pathway of ZFAS1 sponging miR-486.	MIMAT0004762	Oncotarget 2017 Nov 28 8, 104160-104170 doi:10.18632/oncotarget.22032 PMID:29262629
2125	LncRNA	ZFAS1	miR-150	SP1	Esophageal Squamous Cancer tissues	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR etc.	28938617	Development and validation of nomogram based on lncRNA ZFAS1 for predicting survival in lymph node-negative esophageal squamous cell carcinoma patients	ZFAS1 expression was significantly higher in ESCC tissues compared with the corresponding adjacent normal tissues.clinicopathological factors and ZFAS1 expression,can accurately predict the prognosis of lymph node-negative ESCC patients without preoperative chemoradiotherapy.ZFAS1 was found to act as a competing endogenous RNA (ceRNA) in liver cancer by binding to miR-150 and inhibiting the tumor suppressor function of miR-150.ZFAS1 promoted the increased expression of SP1 in ovarian cancer by competitive antagonism against miR-150 to enhance the ability of cell proliferation and chemotherapy resistance for ovarian cancer cells.ZFAS1 acts as an oncogene in colorectal cancer.ZFAS1 was found to promote gastric cancer cell proliferation by inhibiting KLF2 and NKD2 expression.	MI0000479	Oncotarget 2017 Aug 29 8, 59048-59057 doi:10.18632/oncotarget.19937 PMID:28938617
2126	LncRNA	ZFAS1	miR-150	KLF2	Esophageal Squamous Cancer tissues	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR etc.	28938617	Development and validation of nomogram based on lncRNA ZFAS1 for predicting survival in lymph node-negative esophageal squamous cell carcinoma patients	ZFAS1 expression was significantly higher in ESCC tissues compared with the corresponding adjacent normal tissues.clinicopathological factors and ZFAS1 expression,can accurately predict the prognosis of lymph node-negative ESCC patients without preoperative chemoradiotherapy.ZFAS1 was found to act as a competing endogenous RNA (ceRNA) in liver cancer by binding to miR-150 and inhibiting the tumor suppressor function of miR-150.ZFAS1 promoted the increased expression of SP1 in ovarian cancer by competitive antagonism against miR-150 to enhance the ability of cell proliferation and chemotherapy resistance for ovarian cancer cells.ZFAS1 acts as an oncogene in colorectal cancer.ZFAS1 was found to promote gastric cancer cell proliferation by inhibiting KLF2 and NKD2 expression.	MI0000479	Oncotarget 2017 Aug 29 8, 59048-59057 doi:10.18632/oncotarget.19937 PMID:28938617
2127	LncRNA	ZFAS1	miR-150	NKD2	Esophageal Squamous Cancer tissues	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR etc.	28938617	Development and validation of nomogram based on lncRNA ZFAS1 for predicting survival in lymph node-negative esophageal squamous cell carcinoma patients	ZFAS1 expression was significantly higher in ESCC tissues compared with the corresponding adjacent normal tissues.clinicopathological factors and ZFAS1 expression,can accurately predict the prognosis of lymph node-negative ESCC patients without preoperative chemoradiotherapy.ZFAS1 was found to act as a competing endogenous RNA (ceRNA) in liver cancer by binding to miR-150 and inhibiting the tumor suppressor function of miR-150.ZFAS1 promoted the increased expression of SP1 in ovarian cancer by competitive antagonism against miR-150 to enhance the ability of cell proliferation and chemotherapy resistance for ovarian cancer cells.ZFAS1 acts as an oncogene in colorectal cancer.ZFAS1 was found to promote gastric cancer cell proliferation by inhibiting KLF2 and NKD2 expression.	MI0000479	Oncotarget 2017 Aug 29 8, 59048-59057 doi:10.18632/oncotarget.19937 PMID:28938617
2128	LncRNA	ZFAS1	miR-200b	BMI1	Khos, 143B, Lm7, U2Os, Mg-63, Nhost	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	28744396	LncRNA ZFAS1 promotes growth and metastasis by regulating BMI1 and ZEB2 in osteosarcoma.	a functional role of ZFAS1 on OS growth and metastasis.The expression of ZFAS1 was signifiantly overex- pressed in OS samples and cell lines, and upregulation of ZFAS1 is signifiantly associated with unfavorable prognosis of OS patients. Functional assays also demonstrated that ZFAS1 enhanced the growth and metastatic ability of OS cells in vitro and in vivo.Mechanistically, we found that ZFAS1 positively regulated malignant phenotypes by competitively binding the miR-200b and miR-200c and upregulating BMI1.ZFAS1 also interacted with ZEB2 and regulated ZEB2 protein stability. Furthermore, we demonstrated that SP1 functions as an upstream activated factor of ZFAS1.ZFAS1 may be a potential therapeutic target for OS tumorigenesis and progression. 	MI0000342	Am J Cancer Res 2017  7, 1450-1462,  PMID:28744396
2129	LncRNA	ZFAS1	miR-200b	BMI1	Khos, 143B, Lm7, U2Os, Mg-63, Nhost	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	28744396	LncRNA ZFAS1 promotes growth and metastasis by regulating BMI1 and ZEB2 in osteosarcoma.	a functional role of ZFAS1 on OS growth and metastasis.The expression of ZFAS1 was signifiantly overex- pressed in OS samples and cell lines, and upregulation of ZFAS1 is signifiantly associated with unfavorable prognosis of OS patients. Functional assays also demonstrated that ZFAS1 enhanced the growth and metastatic ability of OS cells in vitro and in vivo.Mechanistically, we found that ZFAS1 positively regulated malignant phenotypes by competitively binding the miR-200b and miR-200c and upregulating BMI1.ZFAS1 also interacted with ZEB2 and regulated ZEB2 protein stability. Furthermore, we demonstrated that SP1 functions as an upstream activated factor of ZFAS1.ZFAS1 may be a potential therapeutic target for OS tumorigenesis and progression. 	MI0000342	Am J Cancer Res 2017  7, 1450-1462,  PMID:28744396
2130	LncRNA	ZFAS1	miR-200c	ZEB2	Khos, 143B, Lm7, U2Os, Mg-63, Nhost	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	28744396	LncRNA ZFAS1 promotes growth and metastasis by regulating BMI1 and ZEB2 in osteosarcoma.	a functional role of ZFAS1 on OS growth and metastasis.The expression of ZFAS1 was signifiantly overex- pressed in OS samples and cell lines, and upregulation of ZFAS1 is signifiantly associated with unfavorable prognosis of OS patients. Functional assays also demonstrated that ZFAS1 enhanced the growth and metastatic ability of OS cells in vitro and in vivo.Mechanistically, we found that ZFAS1 positively regulated malignant phenotypes by competitively binding the miR-200b and miR-200c and upregulating BMI1.ZFAS1 also interacted with ZEB2 and regulated ZEB2 protein stability. Furthermore, we demonstrated that SP1 functions as an upstream activated factor of ZFAS1.ZFAS1 may be a potential therapeutic target for OS tumorigenesis and progression. 	MI0000650	Am J Cancer Res 2017  7, 1450-1462,  PMID:28744396
2131	LncRNA	ZFAS1	miR-200c	ZEB2	Khos, 143B, Lm7, U2Os, Mg-63, Nhost	Osteosarcoma	Homo sapiens (human)	qPCR,Western blot,RIP etc.	28744396	LncRNA ZFAS1 promotes growth and metastasis by regulating BMI1 and ZEB2 in osteosarcoma.	a functional role of ZFAS1 on OS growth and metastasis.The expression of ZFAS1 was signifiantly overex- pressed in OS samples and cell lines, and upregulation of ZFAS1 is signifiantly associated with unfavorable prognosis of OS patients. Functional assays also demonstrated that ZFAS1 enhanced the growth and metastatic ability of OS cells in vitro and in vivo.Mechanistically, we found that ZFAS1 positively regulated malignant phenotypes by competitively binding the miR-200b and miR-200c and upregulating BMI1.ZFAS1 also interacted with ZEB2 and regulated ZEB2 protein stability. Furthermore, we demonstrated that SP1 functions as an upstream activated factor of ZFAS1.ZFAS1 may be a potential therapeutic target for OS tumorigenesis and progression. 	MI0000650	Am J Cancer Res 2017  7, 1450-1462,  PMID:28744396
2132	LncRNA	ZFAS1	miR-150	NA	Hl-60, Kg-1, Ml-1 And Skno-1	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR etc.	28672980	Overexpression of long non-coding RNA zinc finger antisense 1 in acute myeloid leukemia cell lines influences cell growth and apoptosis.	ZFAS1 mRNA were significantly increased in all human four AML cell lines compared with the T lymphocytic leukemia cell line or Burkitt's lymphoma cell line. ZFAS1 promoted the proliferation and inhibited the apoptosis of AML cells. Li et al identified that ZFAS1 functions as an oncogene in hepatocellular carcinoma progression by binding miR-150 and abrogating its tumor-suppressive function. molecular abnormalities and outcome in older patients with cytogenetically normal AML and revealed that patients with an unfavorable lncRNA score had a shorter overall survival and disease-free survival rate than those with a favorable lncRNA score. 	MI0000479	Exp Ther Med 2017 Jul 14, 647-651 doi:10.3892/etm.2017.4535 PMID:28672980
2133	LncRNA	AC130710	miR-129-5p	NA	Ags, Bgc-823, Mgc-803, Sgc-7901 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR etc.	24969565	lncRNA-AC130710 targeting by miR-129-5p is upregulated in gastric cancer and associates with poor prognosis.	AC130710 in gastric cancer was significantly higher. Its expression level was significantly associated with tumor size, tumor-node-metastasis (TNM) stages, and distal metastasis. miR-129-5p may play an important role in the downregulation of AC130710 in gastric cancer cells. These results indicated that lncRNA-AC130710 may be a potential tumor marker for gastric cancer prognosis.	MIMAT0000242	Tumour Biol 2014 Oct 35, 9701-6 doi:10.1007/s13277-014-2274-5 PMID:24969565
2134	LncRNA	CASC2	miR-21	NA	786-O, A498	Renal Cancer	Homo sapiens (human)	qPCR, Cell transfection, Dual-luciferase reporter assay, Cell proliferation assay etc.	27222255	Downregulation of lncRNA CASC2 by microRNA-21 increases the proliferation and migration of renal cell carcinoma cells.	The present study confirmed that CASC2 was downregulated in human RCC tissues and human RCC cell lines (786-O and A498). Restoration of CASC2 expression via transfection with a pcDNA3.1(+)-CASC2 vector was able to inhibit cell proliferation and migration in 786-O and A498 cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed that CASC2 was a direct target gene of miR-21. miR-21 was able to decrease the expression of CASC2 in 786-O and A498 cells. Furthermore, overexpression of miR-21 partly abrogated CASC2-mediated inhibition of 786-O and A498 cell proliferation and migration.	MI0000077	Mol Med Rep 2016 Jul 14, 1019-25 doi:10.3892/mmr.2016.5337 PMID:27222255
2135	LncRNA	CASC2	miR-21	NA	U251, U87	Glioma	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25446261	Long non-coding RNA CASC2 suppresses malignancy in human gliomas by miR-21.	In this study, we confirmed that CASC2 was lowly expressed in glioma tissues as well as in U251 and U87 glioma cell lines. Overexpression of CASC2 inhibited the malignancy of glioma cells, including proliferation, migration, and invasion, and promoted cell apoptosis. We found that up-regulated CASC2 decreased the expression of miR-21 significantly and there is a reciprocal repression between CASC2 and miR-21 in an Argonaute2-dependent manner.	MI0000077	Cell Signal 2015 Feb 27, 275-82 doi:10.1016/j.cellsig.2014.11.011 PMID:25446261
2136	LncRNA	CCAT1	let-7	Myc	Hep-2	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR, Western blot	27830017	CCAT1 promotes laryngeal squamous cell carcinoma cell proliferation and invasion	CCAT1 expression was upregulated in LSCC tissues compared with the normal adjacent tissues. We also demonstrated that CCAT1 overexpression suppressed the expression of let-7 and enhanced the expression of HMGA2 and Myc, the direct target genes of let-7. 	MI0000060	Am J Transl Res 2016  8, 4338-4345,  PMID:27830017
2137	LncRNA	CRNDE	miR-384	NF-kB	Mhcc97H, Hep3B, Mhcc97L, Bel-7402, Qgy-7703, Hccc9810, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	27822419	LncRNA CRNDE promotes hepatic carcinoma cell proliferation, migration and invasion by suppressing miR-384.	Herein, we found that the expression of CRNDE was increased in human hepatic carcinoma (HCC) tissues and cell lines. At the same time, CRNDE promotes HCC cell proliferation, migration, and invasion in vitro. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was significantly downregulated in HCC tissues. Moreover, we indicated CRNDE negatively regulated miR-384 expression in HCC.	MI0001145	Am J Cancer Res 2016  6, 2299-2309,  PMID:27822419
2138	LncRNA	CRNDE	miR-384	p-AKT	Mhcc97H, Hep3B, Mhcc97L, Bel-7402, Qgy-7703, Hccc9810, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	27822419	LncRNA CRNDE promotes hepatic carcinoma cell proliferation, migration and invasion by suppressing miR-384.	Herein, we found that the expression of CRNDE was increased in human hepatic carcinoma (HCC) tissues and cell lines. At the same time, CRNDE promotes HCC cell proliferation, migration, and invasion in vitro. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was significantly downregulated in HCC tissues. Moreover, we indicated CRNDE negatively regulated miR-384 expression in HCC.	MI0001145	Am J Cancer Res 2016  6, 2299-2309,  PMID:27822419
2139	LncRNA	CTBP	miR-21-5p	LAMP2	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc.	27113935	Evaluation of Circulatory RNA-Based Biomarker Panel in Hepatocellular Carcinoma.	We examined RNA-based biomarker panel expression level in 20 paired HCC tissues and adjacent non-tumor tissues by qRT-PCR. In tumor tissues, lncRNA-CTBP, miR-16-2, miR-21-5p expression were at a level higher than that of non-tumor tissues, with the median ratio of 421, 0.26; 12.7, 0.24; and 13.02, 0.28, respectively, compared with normal counterparts.	MIMAT0000076	Mol Diagn Ther 2016 Jun 20, 265-77 doi:10.1007/s40291-016-0200-9 PMID:27113935
2140	LncRNA	CTBP	miR-16-2	LAMP2	Hepatocellular Carcinoma tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc.	27113935	Evaluation of Circulatory RNA-Based Biomarker Panel in Hepatocellular Carcinoma.	We examined RNA-based biomarker panel expression level in 20 paired HCC tissues and adjacent non-tumor tissues by qRT-PCR. In tumor tissues, lncRNA-CTBP, miR-16-2, miR-21-5p expression were at a level higher than that of non-tumor tissues, with the median ratio of 421, 0.26; 12.7, 0.24; and 13.02, 0.28, respectively, compared with normal counterparts.	MI0000115	Mol Diagn Ther 2016 Jun 20, 265-77 doi:10.1007/s40291-016-0200-9 PMID:27113935
2141	LncRNA	DLEU2	miR-16-1	CCND1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	Here, we demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2142	LncRNA	DLEU2	miR-16-1	CCND2	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	Here, we demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2143	LncRNA	DLEU2	miR-16-1	CCND3	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2144	LncRNA	DLEU2	miR-16-1	CCNE1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2145	LncRNA	DLEU2	miR-16-1	CDK4	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2146	LncRNA	DLEU2	miR-16-1	CDK6	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2147	LncRNA	DLEU2	miR-16-1	CHK1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2148	LncRNA	DLEU2	miR-16-1	MCM5	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000070	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2149	LncRNA	DLEU2	miR-15a	CCND1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2150	LncRNA	DLEU2	miR-15a	CCND2	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2151	LncRNA	DLEU2	miR-15a	CCND3	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2152	LncRNA	DLEU2	miR-15a	CCNE1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2153	LncRNA	DLEU2	miR-15a	CDK4	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2154	LncRNA	DLEU2	miR-15a	CDK6	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2155	LncRNA	DLEU2	miR-15a	CHK1	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2156	LncRNA	DLEU2	miR-15a	MCM5	null mice	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Northern blot etc.	20060366	The DLEU2/miR-15a/16-1 cluster controls B cell proliferation and its deletion leads to chronic lymphocytic leukemia.	We demonstrate that deletion in mice of the 13q14-minimal deleted region (MDR), which encodes the DLEU2/miR-15a/16-1 cluster, causes development of indolent B cell-autonomous, clonal lymphoproliferative disorders, recapitulating the spectrum of CLL-associated phenotypes observed in humans. miR-15a/16-1-deletion accelerates the proliferation of both human and mouse B cells by modulating the expression of genes controlling cell-cycle progression.	MI0000069	Cancer Cell 2010 Jan 19 17, 28-40 doi:10.1016/j.ccr.2009.11.019 PMID:20060366
2157	LncRNA	DLEU2	miR-16-1	BCL-2	Chronic lymphocytic leukemia cells	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR etc.	19347735	Chronic lymphocytic leukemia and 13q14: miRs and more.	We propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 	MI0000070	Leuk Lymphoma 2009 Mar 50, 502-5 doi:10.1080/10428190902763509 PMID:19347735
2158	LncRNA	DLEU2	miR-15a	BCL-2	Chronic lymphocytic leukemia cells	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR etc.	19347735	Chronic lymphocytic leukemia and 13q14: miRs and more.	We propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 	MI0000069	Leuk Lymphoma 2009 Mar 50, 502-5 doi:10.1080/10428190902763509 PMID:19347735
2159	LncRNA	DLEU2	miR-16-1	CCND1	Chronic lymphocytic leukemia cells	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR etc.	19347735	Chronic lymphocytic leukemia and 13q14: miRs and more.	We propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 	MI0000070	Leuk Lymphoma 2009 Mar 50, 502-5 doi:10.1080/10428190902763509 PMID:19347735
2160	LncRNA	DLEU2	miR-15a	CCND1	Chronic lymphocytic leukemia cells	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR etc.	19347735	Chronic lymphocytic leukemia and 13q14: miRs and more.	We propose a model of a multigenic pathomechanism in 13q14.3, where several tumor suppressor genes, including the miRNA genes miR-16-1 and miR-15a, are co-regulated by the two long non-coding RNA genes DLEU1 and DLEU2 that span the critical region. 	MI0000069	Leuk Lymphoma 2009 Mar 50, 502-5 doi:10.1080/10428190902763509 PMID:19347735
2161	LncRNA	DLEU2	miR-15a	Cyclin-E1	Hek293, U2Os Etc.	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2162	LncRNA	DLEU2	miR-16-1	Cyclin-E1	Hek293, U2Os Etc.	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2163	LncRNA	DLEU2	miR-15a	Cyclin-E1	Hek293, U2Os Etc.	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-2.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2164	LncRNA	DLEU2	miR-16-1	Cyclin-E1	Hek293, U2Os Etc.	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-2.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2165	LncRNA	DLEU2	miR-15a	Cyclin-E1	Hek293, U2Os Etc.	Myeloma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-3.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2166	LncRNA	DLEU2	miR-16-1	Cyclin-E1	Hek293, U2Os Etc.	Myeloma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-3.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2167	LncRNA	DLEU2	miR-15a	Cyclin-D1	Hek293, U2Os Etc.	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2168	LncRNA	DLEU2	miR-16-1	Cyclin-D1	Hek293, U2Os Etc.	Chronic Lymphocytic Leukemia	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-1.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2169	LncRNA	DLEU2	miR-15a	Cyclin-D1	Hek293, U2Os Etc.	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-2.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2170	LncRNA	DLEU2	miR-16-1	Cyclin-D1	Hek293, U2Os Etc.	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-2.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2171	LncRNA	DLEU2	miR-15a	Cyclin-D1	Hek293, U2Os Etc.	Myeloma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-3.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000069	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2172	LncRNA	DLEU2	miR-16-1	Cyclin-D1	Hek293, U2Os Etc.	Myeloma	Homo sapiens (human)	qPCR, Western blot, Northern blot, Luciferase reporter assay etc.	19591824	DLEU2, frequently deleted in malignancy, functions as a critical host gene of the cell cycle inhibitory microRNAs miR-15a and miR-16-3.	The microRNAs miR-15a and miR-16-1 are downregulated in multiple tumor types and are frequently deleted in chronic lymphocytic leukemia (CLL), myeloma and mantle cell lymphoma. DLEU2 negatively regulates the G1 Cyclins E1 and D1 through miR-15a/miR-16-1 and provide evidence that these oncoproteins are subject to miR-15a/miR-16-1-mediated repression under normal conditions. We also demonstrate that DLEU2 overexpression blocks cellular proliferation and inhibits the colony-forming ability of tumor cell lines in a miR-15a/miR-16-1-dependent way.	MI0000070	Exp Cell Res 2009 Oct 15 315, 2941-52 doi:10.1016/j.yexcr.2009.07.001 PMID:19591824
2173	LncRNA	DNM3OS	miR-199a	PTEN	Type I, Type Ii Etc.	Ovarian Cancer	Homo sapiens (human)	qPCR etc.	20400975	TWISTing stemness, inflammation and proliferation of epithelial ovarian cancer cells through MIR199A2/214.	The characterization of Twist1 as a regulator of a unique miRNA cluster responsible for the regulation of the IKKb/NFkB and PTEN/AKT pathways and its association of ovarian CSC differentiation. Our data suggest that Twist1 may be an important regulator of 'stemness' in EOC cells. The regulation of MIR199A2/214 expression may be used as a potential therapeutic approach in EOC patients.	MI0000281	Oncogene 2010 Jun 17 29, 3545-53 doi:10.1038/onc.2010.111 PMID:20400975
2174	LncRNA	DNM3OS	miR-214	PTEN	Type I, Type Ii Etc.	Ovarian Cancer	Homo sapiens (human)	qPCR etc.	20400975	TWISTing stemness, inflammation and proliferation of epithelial ovarian cancer cells through MIR199A2/214.	The characterization of Twist1 as a regulator of a unique miRNA cluster responsible for the regulation of the IKKb/NFkB and PTEN/AKT pathways and its association of ovarian CSC differentiation. Our data suggest that Twist1 may be an important regulator of 'stemness' in EOC cells. The regulation of MIR199A2/214 expression may be used as a potential therapeutic approach in EOC patients.	MI0000290	Oncogene 2010 Jun 17 29, 3545-53 doi:10.1038/onc.2010.111 PMID:20400975
2175	LncRNA	ENST00000515084	miR-370	NA	Mcf-7 And Bcap-37	Breast Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay, Cell viability assay, Transient transfection etc.	24879036	A polymorphism rs12325489C>T in the lincRNA-ENST00000515084 exon was found to modulate breast cancer risk via GWAS-based association analyses.	We found that the C allele of the rs12325489C>T polymorphism in the exonic regions of lincRNA-ENST00000515084 was associated with a significantly increased risk of breast cancer, compared with the rs12325489TT genotype. Biochemical analysis demonstrated that the C to T base change at rs12325489C>T disrupts the binding site for miRNA-370, thereby influencing the transcriptional activity of lincRNA-ENST00000515084 in vitro and in vivo, and affecting cell proliferation and tumor growth.	MI0000778	PLoS One 2014  9, e98251 doi:10.1371/journal.pone.0098251 PMID:24879036
2176	LncRNA	FER1L4	miR-106a-5p	NA	Ncm460, Rko, Lovo, Hct116, Sw480 And Sw620	Colon Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc.	26224446	Long non-coding RNA Fer-1-like protein 4 suppresses oncogenesis and exhibits prognostic value by associating with miR-106a-5p in colon cancer.	The results showed the aberrant expression of FER1L4 and miR-106a-5p in colon cancer tissues. In addition, significant negative correlation between FER1L4 and miR-106a-5p expression levels was observed. Among the colon cancer cell lines, FER1L4 levels were relatively lower, with concurrent high levels of miR-106a-5p. Restoration of FER1L4 decreased the expression of miR-106a-5p, and had a significant influence on colon cancer cell proliferation, migration and invasion. The FER1L4 expression was correlated with depth of tumor invasion, lymph node metastasis, vascular invasion and clinical stage. Circulating FER1L4 and miR-106a-5p levels were decreased and increased, respectively, in colon cancer patients after surgery.	MIMAT0000103	Cancer Sci 2015 Oct 106, 1323-32 doi:10.1111/cas.12759 PMID:26224446
2177	LncRNA	GAS5	miR-21	PTEN	Bel-7402, Smmc-7721, Hcclm3 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	26404135	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21.	The levels of GAS5 and miR-21 were correlated with the clinicopathological characteristics of HCC. HCC patients with higher levels of GAS5 or with the lower levels of miR-21 have longer survival times. There are lower levels of GAS5 and higher levels of miR-21 in HCC cell lines (Be7402, SMMC-7721, and HCCLM3) than in normal liver L-02 cells, and the levels correlate with the aggression of the HCC cell lines. Knockdown of GAS5 upregulates miR-21 levels in Bel-7402 cells (weakly aggressive); in contrast, there are opposite changes in HCCLM3 cells (highly aggressive). Moreover, GAS5 that upregulated or downregulated the expression of PDCD4 and PTEN was reversed by inhibiting or overexpressing miR-21 level in Bel-7402 and HCCLM3 cells. Then, overexpression of GAS5 suppresses the migration and invasion of HCC cells and high expression of miR-21 largely eliminates GAS5-mediated suppression of HCC cell migration and invasion.	MI0000077	Tumour Biol 2016 Feb 37, 2691-702 doi:10.1007/s13277-015-4111-x PMID:26404135
2178	LncRNA	GAS5	miR-21	NA	Mcf-7 And Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ISH, MTT assay etc.	23933812	Negative regulation of lncRNA GAS5 by miR-21.	This negative correlation between miR-21 and GAS5 is also seen in breast tumor specimens. Of interest, GAS5 can also repress miR-21 expression. Whereas ectopic expression of GAS5 suppresses, GAS5-siRNA increases miR-21 expression. Experiments with in vitro cell culture and xenograft mouse model suggest that GAS5 functions as a tumor suppressor.	MI0000077	Cell Death Differ 2013 Nov 20, 1558-68 doi:10.1038/cdd.2013.110 PMID:23933812
2179	LncRNA	H19	miR-141	caspase3	Hfob1.19	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, MTT assay etc.	27186302	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.	Both H19 and miR-675 levels in hFOB1.19 cells were significantly decreased by overexpression of miR-141 than that in control group, but their expression were reversed by miR-141 inhibitor. In addition, expression of H19 and miR-675 in adjacent tissues were both significantly higher than that in tumor tissues. However, cell viability was significantly decreased by co-transfection of siRNA-H19/miR-675 inhibitor and miR-141 inhibitor compared with the miR-141 inhibitor group with time increasing, suggesting that the promote role of miR-141 inhibitor on cell proliferation may be suppressed by silencing H19 or miR-675 inhibitor.	MI0000460	Am J Transl Res 2016  8, 1780-8,  PMID:27186302
2180	LncRNA	H19	miR-141	BCL-2	Hfob1.19	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, MTT assay etc.	27186302	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.	Both H19 and miR-675 levels in hFOB1.19 cells were significantly decreased by overexpression of miR-141 than that in control group, but their expression were reversed by miR-141 inhibitor. In addition, expression of H19 and miR-675 in adjacent tissues were both significantly higher than that in tumor tissues. However, cell viability was significantly decreased by co-transfection of siRNA-H19/miR-675 inhibitor and miR-141 inhibitor compared with the miR-141 inhibitor group with time increasing, suggesting that the promote role of miR-141 inhibitor on cell proliferation may be suppressed by silencing H19 or miR-675 inhibitor.	MI0000460	Am J Transl Res 2016  8, 1780-8,  PMID:27186302
2181	LncRNA	H19	miR-675	VEGF	Hfob1.19	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, MTT assay etc.	27186302	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.	Both H19 and miR-675 levels in hFOB1.19 cells were significantly decreased by overexpression of miR-141 than that in control group, but their expression were reversed by miR-141 inhibitor. In addition, expression of H19 and miR-675 in adjacent tissues were both significantly higher than that in tumor tissues. However, cell viability was significantly decreased by co-transfection of siRNA-H19/miR-675 inhibitor and miR-141 inhibitor compared with the miR-141 inhibitor group with time increasing, suggesting that the promote role of miR-141 inhibitor on cell proliferation may be suppressed by silencing H19 or miR-675 inhibitor.	MI0005416	Am J Transl Res 2016  8, 1780-8,  PMID:27186302
2182	LncRNA	H19	miR-675	IGF2	Hfob1.19	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, MTT assay etc.	27186302	miR-141 modulates osteoblastic cell proliferation by regulating the target gene of lncRNA H19 and lncRNA H19-derived miR-675.	Both H19 and miR-675 levels in hFOB1.19 cells were significantly decreased by overexpression of miR-141 than that in control group, but their expression were reversed by miR-141 inhibitor. In addition, expression of H19 and miR-675 in adjacent tissues were both significantly higher than that in tumor tissues. However, cell viability was significantly decreased by co-transfection of siRNA-H19/miR-675 inhibitor and miR-141 inhibitor compared with the miR-141 inhibitor group with time increasing, suggesting that the promote role of miR-141 inhibitor on cell proliferation may be suppressed by silencing H19 or miR-675 inhibitor.	MI0005416	Am J Transl Res 2016  8, 1780-8,  PMID:27186302
2183	LncRNA	H19	miR-29a	VASH2	Hek293	Glioma	Homo sapiens (human)	qPCR, Cell transfection, Western blot etc.	27543358	Long non-coding RNA H19 regulates glioma angiogenesis and the biological behavior of glioma-associated endothelial cells by inhibiting microRNA-29a.	H19 was up-regulated in microvessels from glioma tissues and glioma-associated endothelial cells (GEC) cultured in glioma conditioned medium. Knockdown of H19 suppressed glioma-induced endothelial cell proliferation, migration and tube formation in vitro and meanwhile up-regulated the expression of miR-29a. Bioinformatics analysis and luciferase reporter assay defined that H19 mediated the above effects via directly binding to miR-29a.	MI0000087	Cancer Lett 2016 Oct 28 381, 359-69 doi:10.1016/j.canlet.2016.08.009 PMID:27543358
2184	LncRNA	H19	miR-675	NA	Hep-2, Inoe	Head And Neck Squamous Carcinoma	Homo sapiens (human)	qPCR, Cell transfection, Cell proliferation assay, Cell migration and invasion assay etc.	27994496	Overexpression of lncRNA H19/miR-675 promotes tumorigenesis in head and neck squamous cell carcinoma.	We observed that both H19 and miR-675 were significantly overexpressed in a cohort of 65 primary tumor samples and two HNSCC cell lines. Importantly, when paired with patient follow-up data, higher expression of either H19 or miR-675 was significantly correlated with higher risk of patient relapse, and associated with worse overall survival and poor disease-free survival. Knockdown miR-675 caused significant reduction of cell viability, migratory and invasive capabilities.	MI0005416	Int J Med Sci 2016  13, 914-922 doi:10.7150/ijms.16571 PMID:27994496
2185	LncRNA	H19	miR-107	c-Myc	A549, L78, H460, 16Hbe	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, RNAi, ChIP, Luciferase reporter assay, Flow cytometry assay etc.	26722426	c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer.	The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively. The number of cells in G2/M stage decreased significantly with the knockdown of H19 and miR-107 compared with the control group.	MIMAT0000104	Int J Clin Exp Pathol 2015  8, 12400-9,  PMID:26722426
2186	LncRNA	H19	miR-675	CDH13	U87, U251 Etc.	Glioma	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Luciferase reporter assay etc.	24466011	Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675.	By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression.	MI0005416	PLoS One 2014  9, e86295 doi:10.1371/journal.pone.0086295 PMID:24466011
2187	LncRNA	HOST2	let-7b	STAT3	Ovcar3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25292198	LncRNA-HOST2 regulates cell biological behaviors in epithelial ovarian cancer through a mechanism involving microRNA let-7b.	The data showed that HOST2 was obviously upregulated in an EOCderived cell line, OVCAR-3, compared with the other tested cell lines, including MKN28, Huh-7, HepG2, McF-7,DU145, A357, MG63, Hep-2, ARK2 and Hela. HOST2 promotes tumor cell migration, invasion and proliferation in epithelial ovarian cancer by working in key aspetcs of biological behaviors.	MI0000063	Hum Mol Genet 2015 Feb 1 24, 841-52 doi:10.1093/hmg/ddu502 PMID:25292198
2188	LncRNA	HOTAIR	miR-125a-5p	caspase2	A549	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay etc.	26962687	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis.	MIMAT0000443	Cell Death Dis 2016 Mar 10 7, e2137 doi:10.1038/cddis.2016.41 PMID:26962687
2189	LncRNA	HOTAIR	miR-125a-5p	caspase2	Du145	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay etc.	26962687	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis.	MIMAT0000443	Cell Death Dis 2016 Mar 10 7, e2137 doi:10.1038/cddis.2016.41 PMID:26962687
2190	LncRNA	HOTAIR	miR-125a-5p	caspase2	Hela	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay etc.	26962687	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis.	MIMAT0000443	Cell Death Dis 2016 Mar 10 7, e2137 doi:10.1038/cddis.2016.41 PMID:26962687
2191	LncRNA	HOTAIR	miR-125a-5p	caspase2	Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay etc.	26962687	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis.	MIMAT0000443	Cell Death Dis 2016 Mar 10 7, e2137 doi:10.1038/cddis.2016.41 PMID:26962687
2192	LncRNA	HOTAIR	miR-125a-5p	caspase2	Hct116	Colon Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay etc.	26962687	MiR-125a-5p decreases after long non-coding RNA HOTAIR knockdown to promote cancer cell apoptosis by releasing caspase 2.	In 80 clinical colon cancer tissues, HOTAIR and miR-125a-5p levels were higher than adjacent tissues, whereas caspase 2 was lower. RNA sequencing detected that miR-125a-5p was decreased after HOTAIR knockdown and miR-125a-5p mimics could rescue the apoptosis induced by HOTAIR deficiency. In order to find out whether HOTAIR is essential for cancer cell survival, we transfected a specific siRNA targeting HOTAIR (siHOT1) or scrambled siRNA (siNC) into HCT116, HeLa, HepG2, A549 and DU145 cells. Each siRNA depleted HOTAIR and led to concomitant apoptosis.	MIMAT0000443	Cell Death Dis 2016 Mar 10 7, e2137 doi:10.1038/cddis.2016.41 PMID:26962687
2193	LncRNA	AF147447	miR-34c	MUC2	7901 And Mkn45	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, Western blot, Luciferase reporter assay etc.	27835575	Helicobacter pylori infection related long noncoding RNA (lncRNA) AF147447 inhibits gastric cancer proliferation and invasion by targeting MUC2 and up-regulating miR-34c.	We identified an lncRNA-AF147447 decreased expressed by H. pylori infection, which can inhibit GC proliferation and invasion in vitro and in vivo, act as a tumor suppressor in the development of H. pylori induced GC. LncRNA AF147447 could repress MUC2 expression by direct binding or increasing miR-34c expression. We also found that transcription factor E2F1 could be recruited to lncRNA AF147447 promoter by RNA immunoprecipatation and RNA pull down assays.	MI0000743	Oncotarget 2016 Dec 13 7, 82770-82782 doi:10.18632/oncotarget.13165 PMID:27835575
2194	LncRNA	AKR7L	miR-23b	DRD5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2195	LncRNA	AKR7L	miR-23b	GDF5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2196	LncRNA	ANRIL	miR-99a	PRC2	Sgc7901, Bgc823, Mgc803	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP etc.	24810364	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.	Higher expression of ANRIL was significantly correlated with a higher TNM stage and tumor size. Further experiments revealed that ANRIL knockdown significantly repressed the proliferation both in vitro and in vivo. We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.	MI0000101	Oncotarget 2014 Apr 30 5, 2276-92 doi:10.18632/oncotarget.1902 PMID:24810364
2197	LncRNA	ANRIL	miR-449a	PRC2	Sgc7901, Bgc823, Mgc803	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP etc.	24810364	Long noncoding RNA ANRIL indicates a poor prognosis of gastric cancer and promotes tumor growth by epigenetically silencing of miR-99a/miR-449a.	Higher expression of ANRIL was significantly correlated with a higher TNM stage and tumor size. Further experiments revealed that ANRIL knockdown significantly repressed the proliferation both in vitro and in vivo. We also showed that E2F1 could induce ANRIL and ANRIL-mediated growth promotion is in part due to epigenetic repression of miR-99a/miR-449a in Trans by binding to PRC2, thus forming a positive feedback loop, continuing to promote GC cell proliferation.	MIMAT0001541	Oncotarget 2014 Apr 30 5, 2276-92 doi:10.18632/oncotarget.1902 PMID:24810364
2198	LncRNA	ATB	miR-200a	TGFB	U251 And A172	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc.	27267902	Long non-coding RNA ATB promotes glioma malignancy by negatively regulating miR-200a.	ATB is abnormally up-regulated both in glioma tissues and cell lines compared with normal brain tissues, and glioma patients with high ATB expression had shorter overall survival time. Knockdown of ATB significantly inhibits glioma malignancy, including cell proliferation, colony formation, migration, invasion in vitro, and the xenograft tumor formation in vivo. In addition, ATB was confirmed to target miR-200a, and miR-200a inhibition reversed the malignant characteristics of ATB knockdown on glioma cells. In particular, ATB may act as a ceRNA, effectively becoming a sink for miR-200a, thereby modulating the derepression of TGF-2.	MI0000737	J Exp Clin Cancer Res 2016 Jun 6 35, 90 doi:10.1186/s13046-016-0367-2 PMID:27267902
2199	LncRNA	ATB	miR-200c	ZEB1	Skbr-3	Breast Cancer	Homo sapiens (human)	microarray, qPCR, Western blot, Luciferase reporter assay, MTT assay etc.	25871474	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.	We identified long noncoding RNA activated by TGF-2 (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. In addition, we also found that the high level of lnc-ATB was correlated with trastuzumab resistance of breast cancer patients.	MI0000650	Oncotarget 2015 May 10 6, 11652-63 doi:10.18632/oncotarget.3457 PMID:25871474
2200	LncRNA	ATB	miR-200c	ZNF-217	Skbr-3	Breast Cancer	Homo sapiens (human)	microarray, qPCR, Western blot, Luciferase reporter assay, MTT assay etc.	25871474	LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.	We identified long noncoding RNA activated by TGF-2 (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. In addition, we also found that the high level of lnc-ATB was correlated with trastuzumab resistance of breast cancer patients.	MI0000650	Oncotarget 2015 May 10 6, 11652-63 doi:10.18632/oncotarget.3457 PMID:25871474
2201	LncRNA	ATB	miR-200a	ZEB1	Mkn1, Mkn7, Mkn28, Mkn45, Mkn74 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR etc.	25986864	A Long Non-coding RNA Activated by Transforming Growth Factor-汕 is an Independent Prognostic Marker of Gastric Cancer.	The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGFb/miR-200s/ZEB axis, resulting in a poor prognosis in GC.LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients.	MI0000737	Ann Surg Oncol 2015 Dec 22 Suppl 3, S915-22 doi:10.1245/s10434-015-4554-8 PMID:25986864
2202	LncRNA	ATB	miR-200b	ZEB1	Mkn1, Mkn7, Mkn28, Mkn45, Mkn74 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR etc.	25986864	A Long Non-coding RNA Activated by Transforming Growth Factor-汕 is an Independent Prognostic Marker of Gastric Cancer.	The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGFb/miR-200s/ZEB axis, resulting in a poor prognosis in GC.LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients.	MI0000342	Ann Surg Oncol 2015 Dec 22 Suppl 3, S915-22 doi:10.1245/s10434-015-4554-8 PMID:25986864
2203	LncRNA	ATB	miR-200c	ZEB1	Mkn1, Mkn7, Mkn28, Mkn45, Mkn74 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR etc.	25986864	A Long Non-coding RNA Activated by Transforming Growth Factor-汕 is an Independent Prognostic Marker of Gastric Cancer.	The high lncRNA-ATB group experienced a lower overall survival rate compared with the low lncRNA-ATB group, and multivariate analysis indicated that lncRNA-ATB was an independent prognostic factor.LncRNA-ATB plays an important role in EMT to promote invasion and metastasis through the TGFb/miR-200s/ZEB axis, resulting in a poor prognosis in GC.LncRNA-ATB is a novel biomarker of lncRNA, indicative of a poor prognosis in GC patients.	MI0000650	Ann Surg Oncol 2015 Dec 22 Suppl 3, S915-22 doi:10.1245/s10434-015-4554-8 PMID:25986864
2204	LncRNA	ATB	miR-200a	ZEB1	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000737	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2205	LncRNA	ATB	miR-200a	ZEB2	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000737	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2206	LncRNA	ATB	miR-200b	ZEB1	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000342	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2207	LncRNA	ATB	miR-200b	ZEB2	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000342	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2208	LncRNA	ATB	miR-200c	ZEB1	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000650	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2209	LncRNA	ATB	miR-200c	ZEB2	Smmc-7721	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	24768205	A long noncoding RNA activated by TGF汕1-promotes the invasion-metastasis cascade in hepatocellular carcinoma.	In this study, we observed that the lncRNA-activated by TGFb1 (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL-11 mRNA, autocrine induction of IL-11, and triggering STAT3 signaling. 	MI0000650	Cancer Cell 2014 May 12 25, 666-81 doi:10.1016/j.ccr.2014.03.010 PMID:24768205
2210	LncRNA	BANCR	miR-9	NFkB1	Bgc823, Sgc7901	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, MTT assay etc.	26248136	BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-κB1.	BANCR expression was significantly up-regulated in gastric tumor tissues and gastric cell lines. Down-regulation of BANCR inhibited gastric cancer cell growth and promoted cell apoptosis, and it also contributed to a significant decrease of NF-κB1 (P50/105) expression and 3'UTR of NF-κB1 activity. Overexpression of NF-κB1 reversed the effect of BANCR on cancer cell growth and apoptosis. MiroRNA-9 (miR-9) targeted NF-κB1, and miR-9 inhibitor also reversed the effects of BANCR on gastric cancer cell growth and apoptosis.	MI0000466	Biochem Biophys Res Commun 2015 Sep 18 465, 225-31 doi:10.1016/j.bbrc.2015.07.158 PMID:26248136
2211	LncRNA	BC032469	miR-1207-5p	hTERT	Kato-Iii, Sgc-7901, Mkn28, Ags, Mkn45	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, Western blot, Luciferase reporter assay etc.	26549025	Long noncoding RNA BC032469, a novel competing endogenous RNA, upregulates hTERT expression by sponging miR-1207-5p and promotes proliferation in gastric cancer.	Here, we report that BC032469, a novel lncRNA, expressed highly in gastric cancer tissues, and the upregulation was clinically associated with larger tumor size, poor differentiation and shorter survival of gastric cancer patients. Mechanistically, BC032469 could directly bind to miR-1207-5p and effectively functioned as a sponge for miR-1207-5p to modulate the derepression of hTERT. Thus, BC032469 may function as a ceRNA to impair miR-1207-5p-dependent hTERT downregulation, suggesting that it may be clinically valuable as a poor prognostic biomarker of gastric cancer.	MIMAT0005871	Oncogene 2016 Jul 7 35, 3524-34 doi:10.1038/onc.2015.413 PMID:26549025
2212	LncRNA	BC040587	miR-23b	DRD5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2213	LncRNA	BC040587	miR-23b	GDF5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2214	LncRNA	CASC2	miR-18a	PIAS3	Caco2, Sw480, Sw620, Hct-116, Ht-29 Etc.	Colorectal Cancer	Homo sapiens (human)	qPCR, Flow cytometry assay, Cell proliferation assay etc.	27198161	The long noncoding RNA CASC2 functions as a competing endogenous RNA by sponging miR-18a in colorectal cancer.	In this study, CASC2 expression was significantly decreased in CRC tissues and CRC cell lines, and decreased expression was significantly more frequent in patients with advanced tumor-node-metastasis stage disease (TNM III and IV). Further functional experiments indicate that CASC2 could directly upregulate PIAS3 expression by functioning as a competing endogenous RNA (ceRNA) for miR-18a. This interactions leads to the de-repression of genes downstream of STAT3 and consequentially inhibition of CRC cell proliferation and tumor growth in vitro and in vivo by extending the G0/G1-S phase transition.	MI0000072	Sci Rep 2016 May 20 6, 26524 doi:10.1038/srep26524 PMID:27198161
2215	LncRNA	CCAT1	miR-155	c-Myc	Hl-60	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay etc.	26923190	Long Non-Coding RNA CCAT1 Acts as a Competing Endogenous RNA to Regulate Cell Growth and Differentiation in Acute Myeloid Leukemia	the aberrant upregulation of CCAT1 was detected in French-American-British M4 and M5 subtypes of adult AML patients. By gain- and loss-of-function analysis, we determined that CCAT1 repressed monocytic differentiation and promoted cell growth of HL-60 by sequestering tumor suppressive miR-155. Accordingly, a significant decrease in miR-155 level was detected in AML patients. Re-introduction of miR-155 into HL-60 cells restored monocytic maturation and repressed cell proliferation. Furthermore, CCAT1 could up-regulated c-Myc via its competing endogenous RNA (ceRNA) activity on miR-155. In conclusion, these results revealed new mechanism of lncRNA CCAT1 in AML development, and suggested that the manipulation of CCAT1 expression could serve as a potential strategy in AML therapy.	MI0000681	Mol Cells 2016 Apr 30 39, 330-6 doi:10.14348/molcells.2016.2308 PMID:26923190
2216	LncRNA	CCAT1	miR-490	hnRNPA1	Mgc-803, Sgc-7901, Ags Etc.	Colon Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26825578	The long noncoding RNA colon cancer-associated transcript-1/miR-490 axis regulates gastric cancer cell migration by targeting hnRNPA1	we provide the first evidence that CCAT1 regulates miR-490 in gastric cancer (GC) cells. Interestingly, miR-490 can also repress CCAT1 expression. CCAT1 expression was significantly upregulated, and miR-490 expression was downregulated in GC. The negative correlation between miR-490 and CCAT1 expression was observed in GC tissues. Importantly, CCAT1 contains a putative miR-490-binding site, and deletion of this binding site abolishes their miR-490 responsiveness. Post-transcriptional CCAT1 silencing by miR-490 significantly suppressed GC cell migration. Furthermore, miR-490 directly bound to the hnRNPA1 mRNA 3'-UTR to repress its translation. Inhibition of miR-490 rescued CCAT1 siRNA-mediated suppression of cell migration. hnRNPA1 expression was significantly upregulated in GC specimens, and there was a negative correlation between miR-490 and hnRNPA1 expression and also a positive correlation between hnRNAP1 expression level and CCAT1 level	MI0003125	IUBMB Life 2016 Mar 68, 201-10 doi:10.1002/iub.1474 PMID:26825578
2217	LncRNA	CCAT1	miR-218-5p	Bmi1	GBC tissues, GBC-SD, SGC-996, NOZ and EH-GB2 cell lines	Gallbladder Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	25569100	Long non-coding RNA CCAT1 promotes gallbladder cancer development via negative modulation of miRNA-218-5p.	In this study, we demonstrated that CCAT1 was upregulated in gallbladder cancer (GBC) tissues. CCAT1 silencing downregulated, whereas CCAT1 overexpression enhanced the expression of miRNA-218-5p target gene Bmi1 through competitively 'spongeing' miRNA-218-5p. Our data revealed that CCAT1 knockdown impaired the proliferation and invasiveness of GBC cells, at least in part through affetcing miRNA-218-5p-mediated regulation of Bmi1. Moreover, CCAT1 transcript level was correlated with Bmi1 mRNA level in GBC tissues.	MIMAT0000275	Cell Death Dis 2015 Jan 8 6, e1583 doi:10.1038/cddis.2014.541 PMID:25569100
2218	LncRNA	CRNDE	miR-384	PIWIL4	U87, U251 Etc.	Glioma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27049681	CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis	Herein, the function and potential molecular mechanisms of CRNDE and miR-384 were illustrated in glioma cells. CRNDE overexpression facilitated cell proliferation, migration, and invasion, while inhibited glioma cells apoptosis. Quantitative real-time polymerase chain reaction (PCR) demonstrated that miR-384 was downregulated in human glioma tissues and glioma cell lines. Moreover, restoration of miR-384 exerted tumor-suppressive functions. In addition, the expression of miR-384 was negatively correlated with CRNDE expression. A binding region between CRNDE and miR-384 was confirmed using luciferase assays. Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression. At the molecular level, treatment by CRNDE knockdown or miR-384 overexpression resulted in a decrease of piwi-like RNA-mediated gene silencing 4 (PIWIL4) protein. Besides, PIWIL4 was identified as a target of miR-384 and plays an oncogenic role in glioma. Similarly, downstream proteins of PIWIL4 such as STAT3, cyclin D1, VEGFA, SLUG, MMP-9, caspase 3, Bcl-2, and bcl-xL were modulated when treated with miR-384 and PIWIL4. Remarkably, CRNDE knockdown combined with miR-384 overexpression led to tumor regression in vivo.	MIMAT0001075	J Invest Dermatol 2016 Aug 136, 1701-1710 doi:10.1016/j.jid.2016.03.028 PMID:27049681
2219	LncRNA	CRNDE	miR-186	XIAP	HEK293T	Glioma	Homo sapiens (human)	qPCR, Cell proliferation assay, Cell migration and invasion assay etc.	26231038	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.	We found that CRNDE expression was up-regulated while miR-186 expression was down-regulated in GSCs. Overexpression of CRNDE could promote the cellular proliferation, migration, invasion and inhibit the apoptosis in GSCs. Overexpression of miR-186 exerted functions of inhibiting the proliferation, migration and invasion of GSCs and promoting apoptosis. And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2.	MI0000483	Oncotarget 2015 Sep 22 6, 25339-55 doi:10.18632/oncotarget.4509 PMID:26231038
2220	LncRNA	CRNDE	miR-186	PAK7	HEK293T	Glioma	Homo sapiens (human)	qPCR, Cell proliferation assay, Cell migration and invasion assay etc.	26231038	CRNDE affects the malignant biological characteristics of human glioma stem cells by negatively regulating miR-186.	We found that CRNDE expression was up-regulated while miR-186 expression was down-regulated in GSCs. Overexpression of CRNDE could promote the cellular proliferation, migration, invasion and inhibit the apoptosis in GSCs. Overexpression of miR-186 exerted functions of inhibiting the proliferation, migration and invasion of GSCs and promoting apoptosis. And CRNDE decreased the expression levels of XIAP and PAK7 by binding to miR-186 and negatively regulating it. In addition, miR-186 binded to XIAP and PAK7 3'UTR region, and decrease the expression of them, thus regulating the expression levels of downstream target proteins such as caspase 3, BAD, cyclin D1 and MARK2.	MI0000483	Oncotarget 2015 Sep 22 6, 25339-55 doi:10.18632/oncotarget.4509 PMID:26231038
2221	LncRNA	DQ192290	miR-23b	DRD5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2222	LncRNA	DQ192290	miR-23b	GDF5	AGS and MKN-45 cells	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2223	LncRNA	EWSAT1	miR-326	Cyclin-D1	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Luciferase reporter assay, RNA pull-down assay etc.	27816050	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	We identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters. 	MIMAT0000756	Aging (Albany NY) 2016 Nov 3 8, 2948-2960 doi:10.18632/aging.101103 PMID:27816050
2224	LncRNA	EWSAT1	miR-330-5p	Cyclin-D1	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Luciferase reporter assay, RNA pull-down assay etc.	27816050	Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p.	We identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive 'sponge' of miR-326/330-5p clusters. 	MIMAT0004693	Aging (Albany NY) 2016 Nov 3 8, 2948-2960 doi:10.18632/aging.101103 PMID:27816050
2225	LncRNA	FER1L4	miR-106a-5p	PTEN	Ags, Mgc-803, Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	26306906	Long noncoding RNA FER1L4 suppresses cancer cell growth by acting as a competing endogenous RNA and regulating PTEN expression.	We observed that FER1L4 was downregulated in gastric cancer and that its level corresponded with that of PTEN mRNA. Both FER1L4 and PTEN mRNA were targets of miR-106a-5p. Further experiments demonstrated that FER1L4 downregulation liberates miR-106a-5p and decreases the abundances of PTEN mRNA and protein. More importantly, FER1L4 downregulation accelerated cell proliferation by promoting the G0/G1 to S phase transition.	MIMAT0000103	Sci Rep 2015 Aug 26 5, 13445 doi:10.1038/srep13445 PMID:26306906
2226	LncRNA	FER1L4	miR-106a-5p	RB1	Ges-1, Ags, Mgc-803, Sgc-7901 Etc.	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25124853	Long noncoding RNA associated-competing endogenous RNAs in gastric cancer.	RB1 is one of miR-106a-5p's targets, and has been validated by dual luciferase reporter assay25. In this study, the interaction between FER1L4 and miR-106a-5p was first predicted by miRcode. Then dual luciferase reporter assay showed that the luciferase activity of the mutant FER1L4 plasmid was about 56% higher than that of the wild-type plasmid. This indicated that the mutations introduced in the seed matches impair the ability of miR-106a-5p to bind to FER1L4. qRT-PCR analysis revealed that transfection of small interfering RNA (siRNA) against FER1L4 not only reduced FER1L4 levels in GES-1, AGS, MGC-803 and SGC-7901, but also reduced RB1 levels in all cells tested.	MIMAT0000103	Sci Rep 2014 Aug 15 4, 6088 doi:10.1038/srep06088 PMID:25124853
2227	LncRNA	FTX	miR-374a	MCM2	Smmc-7721, Hcclm3, Hep3B, Hepg2, Huh7, 97H And Gsg7701	Hepatocellular Carcinoma	Homo sapiens (human)	RIP etc.	27065331	Long noncoding RNA FTX inhibits hepatocellular carcinoma proliferation and metastasis by binding MCM2 and miR-374a	lnc-FTX is expressed at higher levels in female livers than in male livers and is significantly downregulated in HCC tissues compared with normal liver tissues. Patients with higher lnc-FTX expression exhibited longer survival, suggesting that lnc-FTX is a useful prognostic factor for HCC patients. lnc-FTX inhibits HCC cell growth and metastasis both in vitro and in vivo. Mechanistically, lnc-FTX represses Wnt/汕-catenin signaling activity by competitively sponging miR-374a and inhibits HCC cell epithelial-mesenchymal transition and invasion. In addition, lnc-FTX binds to the DNA replication licensing factor MCM2, thereby impeding DNA replication and inhibiting proliferation in HCC cells.	MI0000782	Oncogene 2016 Oct 13 35, 5422-5434 doi:10.1038/onc.2016.80 PMID:27065331
2228	LncRNA	GAS5	miR-21	PTEN	Skbr-3	Breast Cancer	Homo sapiens (human)	microarray, qPCR etc.	27034004	Downregulation of LncRNA GAS5 causes trastuzumab resistance in breast cancer	Expression of the lncRNA GAS5 was decreased in SKBR-3/Tr cells and in breast cancer tissue from trastuzumab-treated patients. Inhibition of GAS5 promoted SKBR-3 cell proliferation, and GAS5 knockdown partially reversed lapatinib-induced inhibition of SKBR-3/Tr cell proliferation. GAS5 suppresses cancer proliferation by acting as a molecular sponge for miR-21, leading to the de-repression of phosphatase and tensin homologs (PTEN), the endogenous target of miR-21. Moreover, mTOR activation associated with reduced GAS5 expression was required to suppress PTEN.	MI0000077	Oncotarget 2016 May 10 7, 27778-86 doi:10.18632/oncotarget.8413 PMID:27034004
2229	LncRNA	GAS5	miR-23a	MT2A	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27827524	Long non-coding RNA GAS5 acts as a molecular sponge to regulate miR-23a in gastric cancer.	We showed that GAS5 expression was decreased in GC tissue and inversed correlated with up-regulated expression of miR-23a. GAS5 negatively regulated miR-23a expression in GC cells. The bio-informatics prediction showed putative miR-23a binding sites within GAS5 transcripts. Furthermore, our data indicated the positive regulation of GAS5 on the miR-23a target, MT2A, wherein GAS5 suppressed the negative regulation of miR-23a on MT2A by binding its 3'UTR. Additionally, the expression of MT2A was also decreased in GC tissues, showing a positive or negative correlation with GAS5 or miR-23a, respectively.	MI0000079	Minerva Med 2016 Nov 9,   PMID:27827524
2230	LncRNA	GAS5	miR-222	BMF	Mcf-7, T47D, Mda-Mb-231	Glioma	Homo sapiens (human)	qPCR, Lentiviral infection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc.	26370254	Gas5 Exerts Tumor-suppressive Functions in Human Glioma Cells by Targeting miR-222.	Here, Gas5 is found to be downregulated in glioma specimens and U87 and U251 glioma cell lines. We showed that the introduction of Gas5 by plasmid transfection increased the expression of tumor suppressor Bcl-2-modifying factor (bmf) and Plexin C1 via directly targeting and reducing the expression of miR-222. Downregulated expression of miR-222 inhibited U87 and U251 cell proliferation and promoted the apoptosis by upregulating bmf.	MI0000299	Mol Ther 2015 Dec 23, 1899-911 doi:10.1038/mt.2015.170 PMID:26370254
2231	LncRNA	GAS5	miR-103	PTEN	Hhua, Jec	Endometrial Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc.	26511107	LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells.	We identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells. In summary, we demonstrate that GAS5 acts as an tumor suppressor lncRNA in endometrial cancer. Through inhibiting the expression of miR-103, GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis, and, thus, could be an important mediator in the pathogenesis of endometrial cancer.	MIMAT0000101	J Biomed Sci 2015 Oct 29 22, 100 doi:10.1186/s12929-015-0213-4 PMID:26511107
2232	LncRNA	GIHCG	miR-200b	EZH2	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MI0000342	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2233	LncRNA	GIHCG	miR-200a	EZH2	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MI0000737	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2234	LncRNA	GIHCG	miR-429	EZH2	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MIMAT0001536	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2235	LncRNA	GIHCG	miR-200b	DNMT1	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MI0000342	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2236	LncRNA	GIHCG	miR-200a	DNMT1	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MI0000737	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2237	LncRNA	GIHCG	miR-429	DNMT1	L02, Qsg7701, Smmc7721, Hep3B, Huh7, And Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, RIP, ChIP, RNA pull-down assay, Cell proliferation assay etc.	27380494	Long noncoding RNA GIHCG promotes hepatocellular carcinoma progression through epigenetically regulating miR-200b/a/429.	Our results further revealed that GIHCG is upregulated in HCC tissues in comparison with adjacent non-tumor tissues. High GIHCG expression is correlated with large tumor size, microvascular invasion, advanced BCLC stage, and poor survival of HCC patients. Functional experiments showed that GIHCG promotes HCC cells proliferation, migration, and invasion in vitro, and promotes xenografts growth and metastasis in vivo. Mechanistically, we demonstrated that GIHCG physically associates with EZH2 and the promoter of miR-200b/a/429, recruits EZH2 and DNMT1 to the miR-200b/a/429 promoter regions, upregulates histone H3K27 trimethylation and DNA methylation levels on the miR-200b/a/429 promoter, and dramatically silences miR-200b/a/429 expression.	MIMAT0001536	J Mol Med (Berl) 2016 Nov 94, 1281-1296 doi:10.1007/s00109-016-1442-z PMID:27380494
2238	LncRNA	H19	miR-630	EZH2	Np69, Npc, Cne2	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	27040767	Long noncoding RNA H19 regulates EZH2 expression by interacting with miR-630 and promotes cell invasion in nasopharyngeal carcinoma	Herein, we found that H19 was overexpressed in NPC tissues and poorly differentiated cell lines. Knockdown of H19 significantly inhibited the invasive ability of NPC cells. Moreover, H19 affected the expression of enhancer of zeste homolog 2 (EZH2), which has also been observed to be up-regulated in NPC and to promote cell invasion. Rather than direct interaction, H19 regulated EZH2 expression by suppressing the activity of miR-630, which is a repressor of EZH2 and interacts with H19 in a sequence-specific manner. Furthermore, H19 inhibited E-cadherin expression and promoted cell invasion of NPC cells via the miR-630/EZH2 pathway	MIMAT0003299	Biochem Biophys Res Commun 2016 May 13 473, 913-919 doi:10.1016/j.bbrc.2016.03.150 PMID:27040767
2239	LncRNA	H19	miR-675	RUNX1	Ags And Ges-1	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26931432	Long Noncoding RNA H19-Derived miR-675 Enhances Proliferation and Invasion via RUNX1 in Gastric Cancer Cells	we found that H19 depended on miR-675 to enhance the proliferation and invasion of gastric cancer AGS cells, and the expression of miR-675 was positively correlated with H19 in patients with gastric cancer. Subsequently, the tumor-suppressor runt domain transcription factor 1 (RUNX1) was confirmed to be a downstream molecule of H19/miR-675 axis, since overexpression of H19 or miR-675 significantly decreased RUNX1 expression in AGS cells, and knockdown of H19 or miR-675 enhanced RUNX1 expression. More importantly, a series of assays further demonstrated that introduction of RUNX1 abrogated H19/miR-675-induced Akt/mTOR pathway activation and the following cellular proliferation and invasion of AGS cells	MI0005416	Oncol Res 2016  23, 99-107 doi:10.3727/096504015x14496932933575 PMID:26931432
2240	LncRNA	H19	miR-342-3p	FOXM1	Gbc-Sd, Ehgb-1 And Noz	Gallbladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27716361	Long non-coding RNA H19 regulates FOXM1 expression by competitively binding endogenous miR-342-3p in gallbladder cancer.	We demonstrated H19 was overexpressed and negatively correlated with miR-342-3p in GBC. H19 silencing down-regulated, whereas over-expression enhanced the expression of miR-342-3p targeting FOXM1 through competitively 'sponging' miR-342-3p. Furthermore, H19 knockdown inhibited both cells invasion and proliferation, but this effects was attenuated by co-transfection of siRNA-H19 and miR-342-3p inhibitor in GBC cells.	MIMAT0000753	J Exp Clin Cancer Res 2016 Oct 3 35, 160 doi:10.1186/s13046-016-0436-6 PMID:27716361
2241	LncRNA	H19	miR-194-5p	AKT2	Gbc-Sd, Eh-Gb1, And Noz	Gallbladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay etc.	26803515	Long noncoding RNA H19 contributes to gallbladder cancer cell proliferation by modulated miR-194-5p targeting AKT2.	The expression of H19 and AKT2 were significantly elevated in GBC tissues, and the level of miR-194-5p is markedly decreased. Moreover, H19 elevation was significantly associated with tumor size. In addition, overexpression of H19 in GBC-SD cells downregulated miR-194-5p and markedly increased AKT2 expression, and miR-194-5p mimic reversed these effects. Eventually, GBC cells were arrested in G0/G1-phase after H19 knockdown, inhibition of miR-194-5p markedly promoted cells into S-phase and co-transfection of siH19, and miR-194-5p inhibitor exerted mutually counter-regulated effects on cell cycle.	MIMAT0000460	Tumour Biol 2016 Jul 37, 9721-30 doi:10.1007/s13277-016-4852-1 PMID:26803515
2242	LncRNA	H19	miR-148a-3p	DNMT1	Hep-2	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26872375	Regulation of laryngeal squamous cell cancer progression by the lncRNA H19/miR-148a-3p/DNMT1 axis	We identified microRNA miR-148a-3p as an inhibitory target for H19. Overexpression of miR-148a-3p reduced LSCC migration, invasion and proliferation cell, while inhibition of miR-148a-3p did the opposite. The inhibition of LSCC progression induced by H19 knockdown required the activity of miR-148a-3p. We also identified DNA methyltransferase enzyme DNMT1 as a target of miR-148a-3p. Cellular DNA methylation levels were inhibited by both miR-148a-3p overexpression and H19 knockdown	MIMAT0000243	Oncotarget 2016 Mar 8 7, 11553-66 doi:10.18632/oncotarget.7270 PMID:26872375
2243	LncRNA	H19	miR-140	iASPP	U373, A172, U251, T98G And U87Mg	Glioma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay, MTT assay etc.	27693036	The lncRNA H19 interacts with miR-140 to modulate glioma growth by targeting iASPP.	lncRNA-H19 was specifically upregulated in glioma cell lines and promoted glioma cell growth through targeting miR-140. Knockdown of H19 inhibited the proliferation and invasion of human glioma cell and suppressed its metastasis in vitro and in vivo. In addition, miR-140 dependent inhibitor of apoptosis-stimulating protein of p53 (iASPP) regulation was required in H19 induced glioma cell growth. These findings indicated that H19 might regulate the tumor growth and metastasis via miR-140 dependent iASPP regulation.	MI0000456	Arch Biochem Biophys 2016 Nov 15 610, 1-7 doi:10.1016/j.abb.2016.09.014 PMID:27693036
2244	LncRNA	H19	miR-17-5p	YES1	Tpc-1, Nim, Nthy-Ori 3-1 And Bcpap	Thyroid Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27093644	Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer	Our results suggest that H19 functions as a competitive endogenous RNA (ceRNA) by acting as a sink for miR-17-5p, revealing a potential ceRNA regulatory network involving H19 and miR-17-5p with a role in the modulation of YES1 expression. This mechanism may contribute to a better understanding of thyroid cancer pathogenesis and provide new insights into the treatment of this disease.	MIMAT0000070	Febs j 2016 Jun 283, 2326-39 doi:10.1111/febs.13741 PMID:27093644
2245	LncRNA	H19	miR-372	CXCR4	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000780	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2246	LncRNA	H19	miR-373	CXCR4	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H19 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4.	MI0000781	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2247	LncRNA	H19	miR-675	EGR1	Hep3B And Hepg2	Liver Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ChIP, Dual-luciferase reporter assay, Cell proliferation assay etc.	26376677	miR675 upregulates long noncoding RNA H19 through activating EGR1 in human liver cancer.	Herein, we demonstrate miR675 overexpression promotes and silencing miR675 attenuated liver cancer cell growth in vitro and in vivo. Mechanistically, miR675 inhibits the heterochromatin1 isoform HP1汐 expression in human liver cancer cells which causes a dramatically decrease of the total histone H3 lysine 9 trimethylation (H3K9me3) , histone H3 lysine 27 trimethylation (H3K27me3) and a increase of histone H3 lysine 27 acetylation(H3K27Ac).Notably, a significant reduction of the H3K9me3 and H3K27me3 and the increment of H3K27Ac occupancy on the promoter region of EGR1 triggers EGR1 transcription, translation, sumoylation and activation which upregulates lincRNA H19. Strikingly, H19 may induce and activate tumor-specific pyruvate kinase M2 (PKM2) which is essential for the Warburg effect in its dimer and for gene expression in its teramer during tumorigenesis.	MI0005416	Oncotarget 2015 Oct 13 6, 31958-84 doi:10.18632/oncotarget.5579 PMID:26376677
2248	LncRNA	H19	miR-675	c-Cbl	U87 And U252	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc.	26353930	H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b.	We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested.	MI0005416	Oncotarget 2015 Oct 6 6, 29209-23 doi:10.18632/oncotarget.4976 PMID:26353930
2249	LncRNA	H19	miR-675	Cbl-b	U87 And U252	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay, Cell proliferation assay etc.	26353930	H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b.	We showed that overexpression of H19/miR-675 enhanced the aggressive phenotype of breast cancer cells including increased cell proliferation and migration in vitro, and increased tumor growth and metastasis in vivo. Moreover, we identified ubiquitin ligase E3 family (c-Cbl and Cbl-b) as direct targets of miR-675 in breast cancer cells. Using a luciferase assay, we demonstrated that H19, through its microRNA, decreased both c-Cbl and Cbl-b expression in all breast cancer cell lines tested.	MI0005416	Oncotarget 2015 Oct 6 6, 29209-23 doi:10.18632/oncotarget.4976 PMID:26353930
2250	LncRNA	H19	miR-675	RUNX1	Ags, Mgc803 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24388988	The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1.	The expression levels of H19 and miR-675 in five gastric cancer cell lines were correlated with each other. We next assessed the correlation of miR-675 and H19 expression in 24 human gastric cancer tissues. The expression of H19 and miR-675 in gastric cancer tissues was correlated with each other.	MI0005416	Biochem Biophys Res Commun 2014 Jun 6 448, 315-22 doi:10.1016/j.bbrc.2013.12.126 PMID:24388988
2251	LncRNA	H19	miR-675	ISM1	Sgc7901, Mkn45, Mkn-28 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	24810858	Overexpression of lncRNA H19 enhances carcinogenesis and metastasis of gastric cancer.	The results showed that overexpression of H19 promoted the features of GC including proliferation, migration, invasion and metastasis. H19 and its associated miR-675 act as oncogenes by promoting cell growth and malignant transformation in human gastric cancer. The upregulation of H19 and miR-675 in GC suggests that both H19 and miR-675 are important factors in GC tumorigenesis and metastasis. Furthermore, we showed that H19 plays additional roles mediated by separate pathways and interaction with its target gene ISM1.	MI0005416	Oncotarget 2014 Apr 30 5, 2318-29 doi:10.18632/oncotarget.1913 PMID:24810858
2252	LncRNA	H19	let-7	HMGA2	Panc-1, Sw1990, Aspc-1, Bxpc-3, Cfpac-1 Etc.	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24920070	H19 promotes pancreatic cancer metastasis by derepressing let-7's suppression on its target HMGA2-mediated EMT.	The levels of H19 was overexpressed in PDAC and was upregulated remarkably in primary tumors which subsequently metastasized, compared to those did not metastasis. H19 promoted PDAC cell invasion and migration. An important role of H19 in regulating metastasis of PDAC and provides some clues for elucidating the lncRNAmiRNA functional network in cancer.	MI0000060	Tumour Biol 2014 Sep 35, 9163-9 doi:10.1007/s13277-014-2185-5 PMID:24920070
2253	LncRNA	H19	miR-200a	hnRNP	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000737	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2254	LncRNA	H19	miR-200b	hnRNP	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000342	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2255	LncRNA	H19	miR-200c	hnRNP	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0004657	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2256	LncRNA	H19	miR-141	hnRNP	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000457	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2257	LncRNA	H19	miR-429	hnRNP	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0001536	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2258	LncRNA	H19	miR-200a	ZEB1	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000737	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2259	LncRNA	H19	miR-200b	ZEB1	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000342	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2260	LncRNA	H19	miR-200c	ZEB1	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0004657	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2261	LncRNA	H19	miR-141	ZEB1	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000457	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2262	LncRNA	H19	miR-429	ZEB1	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0001536	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2263	LncRNA	H19	miR-200a	ZEB2	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000737	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2264	LncRNA	H19	miR-200b	ZEB2	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000342	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2265	LncRNA	H19	miR-200c	ZEB2	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0004657	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2266	LncRNA	H19	miR-141	ZEB2	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MI0000457	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2267	LncRNA	H19	miR-429	ZEB2	Smmc7721, Hcclm3	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, in vitro knockdown etc.	23222811	Epigenetic activation of the MiR-200 family contributes to H19-mediated metastasis suppression in hepatocellular carcinoma.	In this study, we show that H19 was underexpressed in intratumoral HCC tissues (T), as compared with peritumoral tissues (L). Additionally, low T/L ratio of H19 predicted poor prognosis. H19 suppressed HCC progression metastasis and the expression of markers of epithelial-to-mesenchymal transition. Furthermore, H19 associated with the protein complex hnRNP U/PCAF/RNAPol II, activating miR-200 family by increasing histone acetylation.	MIMAT0001536	Carcinogenesis 2013 Mar 34, 577-86 doi:10.1093/carcin/bgs381 PMID:23222811
2268	LncRNA	H19	miR-675	RB	Colon Cancer tissues	Colon Cancer	Homo sapiens (human)	qPCR, Northern blot, ISH etc.	19926638	Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer.	By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent non-cancerous tissues. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy.	MI0005416	Carcinogenesis 2010 Mar 31, 350-8 doi:10.1093/carcin/bgp181 PMID:19926638
2269	LncRNA	H19	miR-675	RB	Colorectal Cancer tissues	Colorectal Cancer	Homo sapiens (human)	qPCR, Northern blot, ISH etc.	19926638	Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer.	By quantitative reverse transcription-polymerase chain reaction, both H19 and miR-675 were found to be upregulated in human colon cancer cell lines and primary human colorectal cancer (CRC) tissues compared with adjacent non-cancerous tissues. Our findings demonstrate that H19-derived miR-675, through downregulation of its target RB, regulates the CRC development and thus may serve as a potential target for CRC therapy.	MI0005416	Carcinogenesis 2010 Mar 31, 350-8 doi:10.1093/carcin/bgp181 PMID:19926638
2270	LncRNA	HNF1A-AS1	miR-30b	BCL-2	Hepg2, Smmc-7721, Plc/Prf/5, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	27084450	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p	First, we revealed: HNF1A-AS1 was frequently overexpressed in HCC tissues and cell lines and its relative high expression was closely related to larger tumor size, multiple tumor lesions, poor differentiation and advanced TNM stage. Then we found: HNF1A-AS1 functioned as an oncogene in tumor growth and apoptosis through sponging tumor-suppressive hsa-miR-30b-5p (miR-30b) and de-repressing Bcl-2. Further experiments identified: HNF1A-AS1-miR-30b axis significantly promoted autophagy under starvation and ATG5 was first proved to be a target of miR-30b.	MI0000441	Biochem Biophys Res Commun 2016 May 13 473, 1268-1275 doi:10.1016/j.bbrc.2016.04.054 PMID:27084450
2271	LncRNA	HOTAIR	miR-326	Phox2a	A549, 95D, Nci-H460, Hlamp And H838	Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Flow cytometry assay etc.	27186394	MiR-326 regulates cell proliferation and migration in lung cancer by targeting phox2a and is regulated by HOTAIR.	By using siRNAs and luciferase assays, we also demonstrated that Phox2a is a functional target of miR-326, and that miR-326 is regulated by long non-coding RNA HOTAIR through silencing HOTAIR. Enforced expression of miR-326 inhibited cell proliferation and migration in vitro and tumor growth in nude mice, decreased proportion of cells in S phase and increased cell apoptosis in both A549 and H838 cells. In addition, we found miR-326 bound to 3'UTR of Phox2a but not KLF3, and enforced expression of miR-326 decreased accumulation of Phox2a in both A549 and H838. Moreover, exogenous expression of Phox2a compromised inhibitory effects of miR-326 on cell proliferation and migration. We also found silencing of HOTAIR caused increased expression of miR-326.	MIMAT0000756	Am J Cancer Res 2016  6, 173-86,  PMID:27186394
2272	LncRNA	HOTAIR	miR-214	PIK3R3	Skov3, Ovcar3, And A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay etc.	26826873	HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3.	The expression of HOTAIR and PIK3R3 in ovarian SKOV3 and OVCAR3 was increased compared with A2780 cells. The mRNA level of HOTAIR and PIK3R3 in ovarian cancer SKOV3 cells was decreased when transected with miR-214 or miR-217 compared to negative control. The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced. The proliferation, migration and invasion was decreased in ovarian SKOV3 when HOTAIR or PIK3R3 was silenced.	MI0000290	Med Sci Monit 2016 Jan 31 22, 325-31 doi:10.12659/msm.894913 PMID:26826873
2273	LncRNA	HOTAIR	miR-217	PIK3R3	Skov3, Ovcar3, And A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay etc.	26826873	HOTAIR Promotes Proliferation, Migration, and Invasion of Ovarian Cancer SKOV3 Cells Through Regulating PIK3R3.	The expression of HOTAIR and PIK3R3 in ovarian SKOV3 and OVCAR3 was increased compared with A2780 cells. The mRNA level of HOTAIR and PIK3R3 in ovarian cancer SKOV3 cells was decreased when transected with miR-214 or miR-217 compared to negative control. The mRNA and protein level of PIK3R3 was decreased when HOTAIR was silenced and the mRNA level of HOTAIR was decreased when PIK3R3 was silenced. The proliferation, migration and invasion was decreased in ovarian SKOV3 when HOTAIR or PIK3R3 was silenced.	MIMAT0000274	Med Sci Monit 2016 Jan 31 22, 325-31 doi:10.12659/msm.894913 PMID:26826873
2274	LncRNA	HOTAIR	miR-148a	HLA-G	Hela, Me-180, Siha And Caski	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	27574106	Long non-coding RNA HOTAIR modulates HLA-G expression by absorbing miR-148a in human cervical cancer.	HOTAIR expression was obviously increased in cervical cancer tissue. HOTAIR upregulation was associated with advanced pathological stage, histology, lymph node invasion and lymphatic metastasis, and also correlated with shorter overall survival of cervical cancer patients. Furthermore, HOTAIR overexpression promoted the proliferation, migration and invasion of cervical cancer cells, while HOTAIR knockdown inhibited cell invasion and cell viability, induced apoptosis and inhibited growth in vitro and in vivo. Moreover, HOTAIR modulated human leucocyte antigen-G (HLA-G) expression by competitively binding miR-148a.	MI0000253	Int J Oncol 2016 Sep 49, 943-52 doi:10.3892/ijo.2016.3589 PMID:27574106
2275	LncRNA	HOTAIR	miR-1	CCND1	Kyse30, Kyse140, Kyse150, Kyse180, Kyse410, And Kyse510	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc.	27816685	Long Noncoding RNA HOTAIR Controls Cell Cycle by Functioning as a Competing Endogenous RNA in Esophageal Squamous Cell Carcinoma.	We found that HOTAIR was aberrantly upregulated in ESCC cells and that HOTAIR depletion inhibited proliferation and led to G1 cell cycle arrest in ESCC cells. Besides, we found that HOTAIR acted as an endogenous sponge to downregulate miR-1 expression by directly binding to miR-1. Furthermore, HOTAIR overturned the effect of miR-1 on the proliferation and cell cycle profile in ESCC cells, which involved the derepression of cyclin D1 (CCND1) expression, a target of miR-1. Taken together, our study elucidated a novel HOTAIR /miR-1/CCND1 regulatory axis in which HOTAIR acted as a competing endogenous RNA by sponging miR-1 and upregulated CCND1 expression, thereby facilitating the tumorigenesis of ESCC. 	MI0000651	Transl Oncol 2016 Dec 9, 489-497 doi:10.1016/j.tranon.2016.09.005 PMID:27816685
2276	LncRNA	HOTAIR	miR-126	VEGFA	Sgc-7901 And Bgc-823	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc.	27900563	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes.	HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway.	MI0000471	Tumour Biol 2016 Nov 30, 10.1007/s13277-016-5448-5 doi:10.1007/s13277-016-5448-5 PMID:27900563
2277	LncRNA	HOTAIR	miR-126	PIK3R2	Sgc-7901 And Bgc-823	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc.	27900563	LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes.	HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway.	MI0000471	Tumour Biol 2016 Nov 30, 10.1007/s13277-016-5448-5 doi:10.1007/s13277-016-5448-5 PMID:27900563
2278	LncRNA	HOTAIR	miR-148b-3p	NA	Ha1800, A172	Glioma	Homo sapiens (human)	qPCR, RNAi, Luciferase reporter assay, Flow cytometry assay etc.	27446363	miR-148b-3p inhibits malignant biological behaviors of human glioma cells induced by high HOTAIR expression.	The results confirmed that HOTAIR mRNA expression was inversely correlated with miR-148b-3p expression in A172 glioma cells. The results showed that HOTAIR promotes factors associated with malignancy, including cell proliferation, cell cycle progression and invasion, whereas miR-148b-3p suppresses malignancy. Bioinformatics and luciferase reporter assays showed that miR-148b-3p modulates HOTAIR expression by directly targeting the HOTAIR gene sequence.	MIMAT0000759	Oncol Lett 2016 Aug 12, 879-886 doi:10.3892/ol.2016.4743 PMID:27446363
2279	LncRNA	H19	miR-21	EGFR	Ags1, Mgc803, Sgc7901, And Mkn55,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	We performed bioinformatic screening of miRNAs that share common miRNA response elements (MREs) with lncRNAs and their downstream mRNA targets. The prediction identified three microRNAs (miR-21, miR-145 and miR-148a) and five gastric cancer-specific target genes (EGFR, KLF4, DNMT1 and AGO4) which also showed strong correlation with lncRNAs in regression analysis. Finally, we constructed an integrated lncRNA-miRNA-mRNA interaction network of the candidate genes to understand the post-transcriptional gene regulation. The ceRNA network analysis revealed that the differentially regulated miR-21 and miR-148a were playing as central candidates coordinating sponging activity of the lncRNAs analyzed (H19, TUG1 and MALAT1) in this study and the overexpression of H19 and miR-21 could be a signature event of gastric tumorigenesis that could serve as prognostic indicators and therapeutic targets.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
2280	LncRNA	H19	miR-21	KLF4	Ags1, Mgc803, Sgc7901, And Mkn55,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	We performed bioinformatic screening of miRNAs that share common miRNA response elements (MREs) with lncRNAs and their downstream mRNA targets. The prediction identified three microRNAs (miR-21, miR-145 and miR-148a) and five gastric cancer-specific target genes (EGFR, KLF4, DNMT1 and AGO4) which also showed strong correlation with lncRNAs in regression analysis. Finally, we constructed an integrated lncRNA-miRNA-mRNA interaction network of the candidate genes to understand the post-transcriptional gene regulation. The ceRNA network analysis revealed that the differentially regulated miR-21 and miR-148a were playing as central candidates coordinating sponging activity of the lncRNAs analyzed (H19, TUG1 and MALAT1) in this study and the overexpression of H19 and miR-21 could be a signature event of gastric tumorigenesis that could serve as prognostic indicators and therapeutic targets.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
2281	LncRNA	H19	miR-21	DNMT1	Ags1, Mgc803, Sgc7901, And Mkn55,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	We performed bioinformatic screening of miRNAs that share common miRNA response elements (MREs) with lncRNAs and their downstream mRNA targets. The prediction identified three microRNAs (miR-21, miR-145 and miR-148a) and five gastric cancer-specific target genes (EGFR, KLF4, DNMT1 and AGO4) which also showed strong correlation with lncRNAs in regression analysis. Finally, we constructed an integrated lncRNA-miRNA-mRNA interaction network of the candidate genes to understand the post-transcriptional gene regulation. The ceRNA network analysis revealed that the differentially regulated miR-21 and miR-148a were playing as central candidates coordinating sponging activity of the lncRNAs analyzed (H19, TUG1 and MALAT1) in this study and the overexpression of H19 and miR-21 could be a signature event of gastric tumorigenesis that could serve as prognostic indicators and therapeutic targets.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
2282	LncRNA	H19	miR-21	AGO4	Ags1, Mgc803, Sgc7901, And Mkn55,Gastric Adenocarcinomas Tissues	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi etc	29719612	Comprehensive analysis of aberrantly expressed lncRNAs and construction of ceRNA  network in gastric cancer.  	We performed bioinformatic screening of miRNAs that share common miRNA response elements (MREs) with lncRNAs and their downstream mRNA targets. The prediction identified three microRNAs (miR-21, miR-145 and miR-148a) and five gastric cancer-specific target genes (EGFR, KLF4, DNMT1 and AGO4) which also showed strong correlation with lncRNAs in regression analysis. Finally, we constructed an integrated lncRNA-miRNA-mRNA interaction network of the candidate genes to understand the post-transcriptional gene regulation. The ceRNA network analysis revealed that the differentially regulated miR-21 and miR-148a were playing as central candidates coordinating sponging activity of the lncRNAs analyzed (H19, TUG1 and MALAT1) in this study and the overexpression of H19 and miR-21 could be a signature event of gastric tumorigenesis that could serve as prognostic indicators and therapeutic targets.	MI0000077	Oncotarget 2018 Apr 6 9, 18386-18399 doi:10.18632/oncotarget.24841 PMID:29719612
2283	LncRNA	CTNNAP1	miR-141	CTNNA1	Sw480 And Sw620	Colorectal Cancer	Homo sapiens (human)	qPCR, Cell transfection, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc.	27487124	Downregulated pseudogene CTNNAP1 promote tumor growth in human cancer by downregulating its cognate gene CTNNA1 expression.	The result showed that the expression of CTNNAP1 was downregulated in 70% tumor samples (39/56) compared to adjacent normal samples. The mechanistic experiments revealed that pseudogene CTNNAP1 played a pivotal role in the regulation of its cognate gene CTNNA1 by competition for microRNA-141. Moreover, gain-of-function approaches showed that overexpression of CTNNAP1 or CTNNA1 significantly inhibited cell proliferation and tumor growth in vitro and in vivo by inducing G0/G1 cell cycle arrest.	MI0000457	Oncotarget 2016 Aug 23 7, 55518-55528 doi:10.18632/oncotarget.10833 PMID:27487124
2284	LncRNA	ENST00000518554	miR-15a	PPP3CA	Glioblastoma tissues	Glioblastoma	Homo sapiens (human)	microarray, qPCR etc.	27600337	Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme.	In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM.	MI0000069	Oncol Rep 2016 Nov 36, 2911-2925 doi:10.3892/or.2016.5070 PMID:27600337
2285	LncRNA	ENST00000520186	miR-21	PPP3CA	Glioblastoma tissues	Glioblastoma	Homo sapiens (human)	microarray, qPCR etc.	27600337	Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme.	In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM.	MI0000077	Oncol Rep 2016 Nov 36, 2911-2925 doi:10.3892/or.2016.5070 PMID:27600337
2286	LncRNA	ENST00000547415	miR-29b	PPP3CA	Glioblastoma tissues	Glioblastoma	Homo sapiens (human)	microarray, qPCR etc.	27600337	Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme.	In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM.	MI0000105	Oncol Rep 2016 Nov 36, 2911-2925 doi:10.3892/or.2016.5070 PMID:27600337
2287	LncRNA	ENST00000559981	miR-29c	PPP3CA	Glioblastoma tissues	Glioblastoma	Homo sapiens (human)	microarray, qPCR etc.	27600337	Identification and functional characterization of lncRNAs acting as ceRNA involved in the malignant progression of glioblastoma multiforme.	In our expression profling analysis, the lncRNA ENST00000520186, ENST00000559981, ENST00000547415 and ENST00000518554 were separately considered as the ceRNA of miR-15a, miR-21, miR-29b and miR-29c in GBM. So far, these ceRNAs have not been reported implicated in GBM. Four mRNAs may be regulated by these miRNAs and lncRNAs, the PPP3CA have been reported to be aberrantly expressed in other tumors, but have not been studied in GBM.	MI0000735	Oncol Rep 2016 Nov 36, 2911-2925 doi:10.3892/or.2016.5070 PMID:27600337
2288	LncRNA	FGFR3-AS	miR-374a	P21	Smmc-7721, Bel-7404 	Hepatocellular Carcinoma	Homo sapiens (human)	RT-qPCR, Western blot, in vitro knockdown	29463348	Long non-coding RNA FGFR3-AS1 promotes hepatocellular carcinoma carcinogenesis via modulating PI3K/AKT pathway.	FGFR3-AS1 knockdown significantly inhibited cell proliferation but induced apoptosis.Moreover,FGFR3-AS1 knockdown led to more HCC cells arrested in G0 stage. Besides, FGFR3-AS1 knockdown significantly inhibited cell migration and invasion. Additionally,we found that FGFR3-AS1 silence dramatically delayed tumor growth in vivo.In mechanism, we found FGFR3-AS1 silence decreased the activation of PI3K/AKT signaling pathway.LncRNAs could regulate cell proliferation,apoptosis, migration and invasion by sponging miRNAs or interacting with specific proteins.Furthermore, western blot (WB) results indicated that FGFR3-AS1 knockdown promoted the expression of P21 but inhibited CYCLIN D1 expression.	MI0000782	Oncol Res 2018 Sep 14 26, 1257-1265 doi:10.3727/096504018x15172756878992 PMID:29463348
2289	LncRNA	FGFR3-AS	miR-374a	Cyclin-D1	Smmc-7721, Bel-7404 	Hepatocellular Carcinoma	Homo sapiens (human)	RT-qPCR, Western blot, in vitro knockdown	29463348	Long non-coding RNA FGFR3-AS1 promotes hepatocellular carcinoma carcinogenesis via modulating PI3K/AKT pathway.	FGFR3-AS1 knockdown significantly inhibited cell proliferation but induced apoptosis.Moreover,FGFR3-AS1 knockdown led to more HCC cells arrested in G0 stage. Besides, FGFR3-AS1 knockdown significantly inhibited cell migration and invasion. Additionally,we found that FGFR3-AS1 silence dramatically delayed tumor growth in vivo.In mechanism, we found FGFR3-AS1 silence decreased the activation of PI3K/AKT signaling pathway.LncRNAs could regulate cell proliferation,apoptosis, migration and invasion by sponging miRNAs or interacting with specific proteins.Furthermore, western blot (WB) results indicated that FGFR3-AS1 knockdown promoted the expression of P21 but inhibited CYCLIN D1 expression.	MI0000782	Oncol Res 2018 Sep 14 26, 1257-1265 doi:10.3727/096504018x15172756878992 PMID:29463348
2290	LncRNA	FTX	miR-545	RIG-I	Hepg2, Hep3B, Huh7, Smmc-7721 And Bel-7402	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay, MTT assay etc.	26992218	Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.	The results showed that the expression of lncRNA Ftx and miR-545 in HCC tissues were significantly higher than that in the non-tumor tissues and correlated with each other. Further results confirmed that lncRNA Ftx and miR-545 were upregulated in a panel of HCC cell lines compared with that in non-transformed LO2 hepatic cell line. LncRNA Ftx and miR-545 functions to enhance proliferation, tumorigenicity and cell cycle progression of HCC cells.	MI0003516	Oncotarget 2016 May 3 7, 25350-65 doi:10.18632/oncotarget.8129 PMID:26992218
2291	LncRNA	GAS5	miR-103	AKT	Pc3, Du145, And Lncap	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay, Cell proliferation assay, ISH etc.	27743383	LncRNA GAS5 inhibits proliferation and progression of prostate cancer by targeting miR-103 through AKT/mTOR signaling pathway.	The lncRNA GAS5 levels were reduced significantly in the PCa tissues and cell lines. A low exposure of lncRNA GAS5 caused AKT/mTOR signaling pathway activation in PC3 cells. In addition, over-exposure of lncRNA GAS5 was proven to significantly decelerate PCa cell progression in vitro and tumor growth in vivo through inactivating the AKT/mTOR signaling pathway.In this research, the exposure levels of the main components of the AKT/mTOR signaling pathway, including AKT, mTOR, and S6K1, all of which are tumorrelated genes, were assessed at total and at phosphorylation protein levels in vitro and in vivo.	MI0000109	Tumour Biol 2016 Oct 14, 10.1007/s13277-016-5429-8 doi:10.1007/s13277-016-5429-8 PMID:27743383
2292	LncRNA	GAS5	miR-103	mTOR	Pc3, Du145, And Lncap	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay, Cell proliferation assay, ISH etc.	27743383	LncRNA GAS5 inhibits proliferation and progression of prostate cancer by targeting miR-103 through AKT/mTOR signaling pathway.	The lncRNA GAS5 levels were reduced significantly in the PCa tissues and cell lines. A low exposure of lncRNA GAS5 caused AKT/mTOR signaling pathway activation in PC3 cells. In addition, over-exposure of lncRNA GAS5 was proven to significantly decelerate PCa cell progression in vitro and tumor growth in vivo through inactivating the AKT/mTOR signaling pathway.In this research, the exposure levels of the main components of the AKT/mTOR signaling pathway, including AKT, mTOR, and S6K1, all of which are tumorrelated genes, were assessed at total and at phosphorylation protein levels in vitro and in vivo.	MI0000109	Tumour Biol 2016 Oct 14, 10.1007/s13277-016-5429-8 doi:10.1007/s13277-016-5429-8 PMID:27743383
2293	LncRNA	GAS5	miR-103	S6K1	Pc3, Du145, And Lncap	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay, Cell proliferation assay, ISH etc.	27743383	LncRNA GAS5 inhibits proliferation and progression of prostate cancer by targeting miR-103 through AKT/mTOR signaling pathway.	The lncRNA GAS5 levels were reduced significantly in the PCa tissues and cell lines. A low exposure of lncRNA GAS5 caused AKT/mTOR signaling pathway activation in PC3 cells. In addition, over-exposure of lncRNA GAS5 was proven to significantly decelerate PCa cell progression in vitro and tumor growth in vivo through inactivating the AKT/mTOR signaling pathway.In this research, the exposure levels of the main components of the AKT/mTOR signaling pathway, including AKT, mTOR, and S6K1, all of which are tumorrelated genes, were assessed at total and at phosphorylation protein levels in vitro and in vivo.	MI0000109	Tumour Biol 2016 Oct 14, 10.1007/s13277-016-5429-8 doi:10.1007/s13277-016-5429-8 PMID:27743383
2294	LncRNA	GCASPC	miR-17-3p	PC	Gbc-Sd, Sgc-996, Noz And Ocug-1	Gallbladder Cancer	Homo sapiens (human)	qPCR, RIP, RNA pull-down assay, Mass Spetcrometry etc.	27450454	Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase-Dependent Cell Proliferation in Gallbladder Cancer.	GCASPC levels were significantly lower in gallbladder cancer than adjacent nontumor tissues and were associated with tumor size, American Joint Committee on Cancer tumor stage, and patient outcomes. GCASPC overexpression suppressed cell proliferation in vitro and in vivo, whereas GCASPC silencing had opposite effects. By RNA pull-down and mass spectrometry, we identified pyruvate carboxylase as an RNA-binding protein that associated with GCASPC. 	MIMAT0000071	Cancer Res 2016 Sep 15 76, 5361-71 doi:10.1158/0008-5472.Can-15-3047 PMID:27450454
2295	LncRNA	H19	miR-675	p53	Rt4, Ht-1376, 5637, 253J, Tccsup, T24,And J82	Bladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	26198047	H19-derived miR-675 contributes to bladder cancer cell proliferation by regulating p53 activation	We found that miR-675 expression levels were remarkably increased in bladder cancer tissues as compared with adjacent noncancerous tissues or normal bladder tissue from health donors; moreover, enhanced miR-675 expression was also observed in bladder cancer cell lines. Ectopic expression of H19 significantly increased bladder cancer cell proliferation and miR-675 expression in vitro	MI0005416	Tumour Biol 2016 Jan 37, 263-70 doi:10.1007/s13277-015-3779-2 PMID:26198047
2296	LncRNA	H19	miR-138	ZEB1	Sw620, Hct-116	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer.	H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets. Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. 	MI0000455	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
2297	LncRNA	H19	miR-138	ZEB1	Sw620, Hct-116	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer.	H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets. Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. 	MI0000455	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
2298	LncRNA	H19	miR-200a	ZEB2	Sw620, Hct-116	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer.	H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets. Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. 	MI0000737	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
2299	LncRNA	H19	miR-200a	ZEB2	Sw620, Hct-116	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26068968	The LncRNA H19 promotes epithelial to mesenchymal transition by functioning as MiRNA sponges in colorectal cancer.	H19 functioned as a competing endogenous RNA (ceRNA) for miR-138 and miR-200a, antagonized their functions and led to the de-repression of their endogenous targets. Vimentin, ZEB1, and ZEB2, all of which were core marker genes for mesenchymal cells. 	MI0000737	Oncotarget 2015 Sep 8 6, 22513-25 doi:10.18632/oncotarget.4154 PMID:26068968
2300	LncRNA	H19	miR-675	AKT	Huh-7, Mhcc-97H, Hepg2 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24939300	Downregulation of LncRNAH19 and MiR-675 promotes migration and invasion of human hepatocellular carcinoma cells through AKT/GSK-3汕/Cdc25A signaling pathway.	The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells as compared with the control group. Inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3汕/Cdc25A signaling pathway. 	MI0005416	J Huazhong Univ Sci Technolog Med Sci 2014 Jun 34, 363-369 doi:10.1007/s11596-014-1284-2 PMID:24939300
2301	LncRNA	H19	miR-675	GSK-3b	Huh-7, Mhcc-97H, Hepg2 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24939300	Downregulation of LncRNAH19 and MiR-675 promotes migration and invasion of human hepatocellular carcinoma cells through AKT/GSK-3汕/Cdc25A signaling pathway.	The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells as compared with the control group. Inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3汕/Cdc25A signaling pathway. 	MI0005416	J Huazhong Univ Sci Technolog Med Sci 2014 Jun 34, 363-369 doi:10.1007/s11596-014-1284-2 PMID:24939300
2302	LncRNA	H19	miR-675	Cdc25A	Huh-7, Mhcc-97H, Hepg2 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24939300	Downregulation of LncRNAH19 and MiR-675 promotes migration and invasion of human hepatocellular carcinoma cells through AKT/GSK-3汕/Cdc25A signaling pathway.	The expression levels of LncRNAH19 and miR-675 were higher in MHCC-97H cells than in L02, Huh-7 and HepG2 cells. Transwell migration assay revealed that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the migration of HCC cells as compared with the control group. Transwell invasion assay demonstrated that the miR-675 inhibitor and LncRNAH19siRNA could significantly increase the invasion of HCC cells as compared with the control group. Inhibition of LncRNAH19 and miR-675 expression can promote migration and invasion of HCC cells via AKT/GSK-3汕/Cdc25A signaling pathway. 	MI0005416	J Huazhong Univ Sci Technolog Med Sci 2014 Jun 34, 363-369 doi:10.1007/s11596-014-1284-2 PMID:24939300
2303	LncRNA	H19	miR-675	TGFBI	P69, M12	Prostate Cancer	Homo sapiens (human)	qPCR, Western blot etc.	24988946	lncRNA H19/miR-675 axis represses prostate cancer metastasis by targeting TGFBI.	In this study, we found that long non-coding RNA H19 (H19) and H19-derived microRNA-675 (miR-675) were significantly downregulated in the metastatic prostate cancer cell line M12 compared with the non-metastatic prostate epithelial cell line P69. Upregulation of H19 in P69 and PC3 cells significantly increased the level of miR-675 and repressed cell migration; however, ectopic expression of H19 in M12 cells could not increase the level of miR-675 and therefore had no effect on cell migration.	MI0005416	Febs j 2014 Aug 281, 3766-75 doi:10.1111/febs.12902 PMID:24988946
2304	LncRNA	CRNDE	miR-384	PIWIL4	U87, U251, Hek 293T	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc.	27058823	CRNDE Promotes Malignant Progression of Glioma by Attenuating miR-384/PIWIL4/STAT3 Axis.	CRNDE overexpression facilitated cell proliferation, migration, and invasion, while inhibited glioma cells apoptosis. Moreover, CRNDE promoted cell malignant behavior by decreasing miR-384 expression. Knockdown of CRNDE combined with overexpression of miR-384 restrained tumor growth and exhibit high survival in nude mice.	MIMAT0001075	Mol Ther 2016 Aug 24, 1199-215 doi:10.1038/mt.2016.71 PMID:27058823
2305	LncRNA	MIR155HG	miR-155	BIC	Ramos, Jy25, Cb33, U266, Jurkat, K562, Hl60 Etc.	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qPCR, Northern blot etc.	15738415	Accumulation of miR-155 and BIC RNA in human B cell lymphomas.	Relative to the control B cells, BIC RNA levels were elevated from 2- to 10-fold in DLBCL cells, with one sample showing an increase of >20-fold. 	MI0000681	Proc Natl Acad Sci U S A 2005 Mar 8 102, 3627-32 doi:10.1073/pnas.0500613102 PMID:15738415
2306	LncRNA	NEAT1	miR-98-5p	CTR1	A549, H460, H1299	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Dual-luciferase reporter assay etc.	27270317	NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells.	In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it.	MIMAT0000096	Oncotarget 2016 Jul 12 7, 43337-43351 doi:10.18632/oncotarget.9712 PMID:27270317
2307	LncRNA	NEAT1	miR-214	bcatenin	Cbms, Tams, Bmdms, Raw 264.7	Thyroid Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RNA pull-down assay, Cell migration and invasion assay etc.	28000845	Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214.	NEAT1 was highly expressed in patients with thyroid cancer. NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced β-catenin (a direct target of miRNA-214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA-214, presenting a reciprocal repression correlation.	MI0000290	Int J Oncol 2017 Feb 50, 708-716 doi:10.3892/ijo.2016.3803 PMID:28000845
2308	LncRNA	NEAT1	miR-204	ZEB1	Cne-2, Hone-1, 5-8F, Sune-1 Etc.	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27020592	The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma	We found that lncRNA NEAT1 was significantly upregulated in NPC cell lines and tissues. Knockdown of NEAT1 could sensitize NPC cells to radiation in vitro. Further investigation found that NEAT1 regulated radioresistance by modulating EMT phenotype. Furthermore, we found that there was reciprocal repression between NEAT1 and miR-204. ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.	MI0000284	Tumour Biol 2016 Sep 37, 11733-11741 doi:10.1007/s13277-015-4773-4 PMID:27020592
2309	LncRNA	NEAT1	miR-548	FUS	Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR, RNAi etc.	27147820	NEAT1 is Required for Survival of Breast Cancer Cells Through FUS and miR-548	we demonstrated that downregulating the expression of the lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in breast cancer cells inhibited cell growth and induced cell apoptosis. In addition, the RNA-binding protein fused in sarcoma/translocated in liposarcoma (FUS/TLS) physically interacted with NEAT1, and reducing the expression of FUS/TLS also induced cell apoptosis. Multiple miRNAs were identified as regulators of NEAT1, but only overexpression of miR-548ar was able to decrease NEAT1 expression and promote apoptosis	MI0003593	Gene Regul Syst Bio 2016  10, 11-7 doi:10.4137/grsb.S29414 PMID:27147820
2310	LncRNA	NEAT1	miR-129-5p	WNT4	Mcf10A, Mcf7 And Hcc1937	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, ChIP etc.	27556296	Dysregulation of the BRCA1/long non-coding RNA NEAT1 signaling axis contributes to breast tumorigenesis.	Our studies show that NEAT1 upregulation resulting from BRCA1 deficiency stimulates in vitro and in vivo breast tumorigenicity. NEAT1 epigenetically silences miR-129-5p expression by promoting the DNA methylation of the CpG island in the miR-129 gene. Silencing of miR-129-5p expression by NEAT1 results in upregulation of WNT4 expression, a target of miR-129-5p, which leads to activation of oncogenic WNT signaling. Our functional studies indicate that this NEAT1/miR-129-5p/WNT4 axis contributes to the tumorigenic effects of BRCA1 deficiency. Finally our in silico expression correlation analysis suggests the existence of the BRCA1/NEAT1/miR-129-5p axis in breast cancer.	MIMAT0000242	Oncotarget 2016 Oct 4 7, 65067-65089 doi:10.18632/oncotarget.11364 PMID:27556296
2311	LncRNA	NEAT1	let-7e	NRAS	U87, T98G, U251, A272 And U373	Glioma	Homo sapiens (human)	qPCR, Cell transfection, Western blot, RIP, Dual-luciferase reporter assay, Cell migration and invasion assay etc.	27556696	Knockdown of NEAT1 restrained the malignant progression of glioma stem cells by activating microRNA let-7e.	Quantitative real-time PCR demonstrated that NEAT1 was upregulated in GSCs. NEAT1 knockdown inhibited GSC cell proliferation, migration and invasion and promoted GSC apoptosis. A potential binding region between NEAT1 and microRNA let-7e was confirmed by dual-luciferase assays. Upregulation of NEAT1 reduced the expression of let-7e, and there was reciprocal repression between NEAT1 and let-7e in an Argonaute 2-dependent manner. Let-7e expression was lower expression in glioblastoma tissues and GSCs than in normal brain tissues and cells. Restoration of let-7e suppressed tumor function by inhibiting proliferation, migration and invasion while promoting apoptosis in GSCs.	MI0000066	Oncotarget 2016 Sep 20 7, 62208-62223 doi:10.18632/oncotarget.11403 PMID:27556696
2312	LncRNA	NEAT1	miR-449b-5p	c-Met	U87, U373, And U251	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc.	26242266	Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis.	We suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. RNA immunoprecipitation assay combined with luciferase reporter assay confirmed miR-449b-5p-specific binding to NEAT1. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met.	MIMAT0003327	Tumour Biol 2016 Jan 37, 673-83 doi:10.1007/s13277-015-3843-y PMID:26242266
2313	LncRNA	NEAT1	miR-107	CDK6	Hep-2	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26822763	Long noncoding RNA NEAT1 promotes laryngeal squamous cell cancer through regulating miR-107/CDK6 pathway	NEAT1 level was significantly higher in LSCC than in corresponding adjacent non-neoplastic tissues, and patients with neck nodal metastasis or advanced clinical stage had higher NEAT1 expression. Moreover, siRNA mediated NEAT1 knockdown significantly inhibited the proliferation and induced apoptosis and cell cycle arrest at G1 phase in LSCC cells. The growth of LSCC xenografts was significantly suppressed by the injection of NEAT1 siRNA lentivirus. Furthermore, NEAT1 regulated CDK6 expression in LSCC cells which was mediated by miR-107	MIMAT0000104	J Exp Clin Cancer Res 2016 Jan 29 35, 22 doi:10.1186/s13046-016-0297-z PMID:26822763
2314	LncRNA	NEAT1	miR-377-3p	E2F3	A549, Spc-A1, H1299, 95D, Sk-Mes-1, Nci-H520 Etc.	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RNA pull-down assay etc.	27351135	Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.	We identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression.	MIMAT0000730	Oncotarget 2016 Aug 9 7, 51784-51814 doi:10.18632/oncotarget.10108 PMID:27351135
2315	LncRNA	NEAT1	miR-124-3p	HuR	OVCAR3 cell line and ovarian cancer tissues	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27075229	HuR-regulated lncRNA NEAT1 stability in tumorigenesis and progression of ovarian cancer	In this study, we identified that NEAT1 was up-regulated in OC patients and cell lines, and its expression was associated with the FIGO stage and lymph node metastasis. Furthermore, the ectopic expression of NEAT1_1 in OVCAR-3 cell lines promoted cell proliferation and invasion, whereas knockdown of NEAT1_1 did the opposite. Furthermore, NEAT1_1 was stabilized by an RNA-binding protein HuR, but suppressed by miR-124-3p in OC cells. Accordingly, the increased HuR mRNA and decreased miR-124-3p levels were observed in OC patients.	MIMAT0000422	Cancer Med 2016 Jul 5, 1588-98 doi:10.1002/cam4.710 PMID:27075229
2316	LncRNA	NEAT1	miR-506-3p	NA	Aspc-1, Bxpc-3, Sw1990 And Panc-1	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc.	27888106	Long non-coding RNA NEAT1 facilitates pancreatic cancer progression through negative modulation of miR-506-3p.	Here, we found that the expression level of NEAT1 was higher in PC tissues compared to the corresponding non-tumor tissues. Besides, our findings indicate that high NEAT1 expression level is closely correlated with tumor progression and poor survival in PC patients. Furthermore, we also found that knockdown of NEAT1 remarkably suppressed cell proliferation by inducing cell cycle arrest and apoptosis promotion in PC cells. Moreover, bioinformatics analysis and luciferase reporter assay revealed that NEAT1 directly bound to the miR-506-3p, which has been reported to act as a tumor suppressor in diverse cancers.	MIMAT0002878	Biochem Biophys Res Commun 2017 Jan 22 482, 828-834 doi:10.1016/j.bbrc.2016.11.120 PMID:27888106
2317	LncRNA	NEAT1	miR-449a	NOTCH1	A549	Lung Cancer	Homo sapiens (human)	qPCR, RNAi etc.	25818739	MicroRNA-449a inhibits cell growth in lung cancer and regulates long noncoding RNA nuclear enriched abundant transcript 1.	Our result showed that, the level of NEAT1 was up-regulated when the knockdown of miR-449a; on the contrary, the expression of NEAT1 was down-regulated when miR-449a was the overexpression.	MI0001648	Indian J Cancer 2014 Mar 51 Suppl 3, e77-81 doi:10.4103/0019-509x.154055 PMID:25818739
2318	LncRNA	NeD125	miR-125b-1	BCL-2	Neuroblastoma cells	Neuroblastoma	Homo sapiens (human)	qPCR, Cell transfection, Western blot, ChIP, RNA pull-down assay etc.	26480000	Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells.	Linc-NeD125 represents the host gene for miR-125b-1, a microRNA with an established role as negative regulator of human neuroblastoma cell proliferation. Here, we demonstrate that these two overlapping non coding RNAs are coordinately induced during in vitro neuronal differentiation, and that their expression is regulated by different mechanisms. While the production of miR-125b-1 relies on transcriptional regulation, linc-NeD125 is controlled at the post-transcriptional level, through modulation of its stability.	MI0000446	RNA Biol 2015  12, 1323-37 doi:10.1080/15476286.2015.1096488 PMID:26480000
2319	LncRNA	NLC1-C	miR-320a	ARPP-19	Ntera-2, Nccit, Hek293 T Cell	Testicular Embryonal Carcinoma	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc.	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MIMAT0000510	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
2320	LncRNA	NLC1-C	miR-320a	ERRR	Ntera-2, Nccit, Hek293 T Cell	Testicular Embryonal Carcinoma	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc.	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MIMAT0000510	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
2321	LncRNA	NLC1-C	miR-383	Cyclin-D1	Ntera-2, Nccit, Hek293 T Cell	Testicular Embryonal Carcinoma	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc.	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MI0000791	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
2322	LncRNA	NLC1-C	miR-383	IRF1	Ntera-2, Nccit, Hek293 T Cell	Testicular Embryonal Carcinoma	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Northern blot, RIP, RNA pull-down assay etc.	26539909	Downregulation of miR-320a/383-sponge-like long non-coding RNA NLC1-C (narcolepsy candidate-region 1 genes) is associated with male infertility and promotes testicular embryonal carcinoma cell proliferation.	NLC1-C, also known as long intergenic non-protein-coding RNA162 (LINC00162), was down-regulated in the cytoplasm and accumulated in the nucleus of spermatogonia and primary spermatocytes in the testes of infertile men with mixed patterns of MA compared with normal control. The accumulation of NLC1-C in the nucleus repressed miR-320a and miR-383 transcript and promoted testicular embryonal carcinoma cell proliferation by binding to Nucleolin.	MI0000791	Cell Death Dis 2015 Nov 5 6, e1960 doi:10.1038/cddis.2015.267 PMID:26539909
2323	LncRNA	NR_024015	miR-526-3p	NA	Te1, Te13, T.Tn, Yes-2, And Eca109	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR, Cell proliferation assay etc.	27583835	A genetic polymorphism at miR-526b binding-site in the lincRNA-NR_024015 exon confers risk of esophageal squamous cell carcinoma in a population of North China.	The expression level of lincRNA-NR_024015 in ESCC tumor tissues was significantly higher than that in corresponding normal tissues and rs8506 genotype has a genotype-specific effect on lincRNA-NR_024015 expression. Furthermore, rs8506 G to A variant might influence lincRNA-NR_024015 expression and function by disrupting the binding of hsa-miR-526b to the site. High expression level of lincRNA-NR_024015 and rs8506 A allele were associated with poor ESCC patients' survival.	MI0003150	Mol Carcinog 2017 Mar 56, 960-971 doi:10.1002/mc.22549 PMID:27583835
2324	LncRNA	NUTF2P3-001	miR-3923	KRAS	Panc-1 And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc.	26755660	Hypoxia-induced lncRNA-NUTF2P3-001 contributes to tumorigenesis of pancreatic cancer by derepressing the miR-3923/KRAS pathway.	lncRNA-NUTF2P3-001 is upregulated in pancreatic cancer cells under hypoxia and CoCl2 treatment, which is attributed to the binding of hypoxia-inducible factor-1α (HIF-1α) to hypoxia response elements (HREs) in the upstream of KRAS promoter. Data from pancreatic cancer patients show a positive correlation between lncRNA-NUTF2P3-001 and KRAS, which is associated with advanced tumor stage and worse prognosis. Hence, our data provide a new lncRNA-mediated regulatory mechanism for the tumor oncogene KRAS and implicate that lncRNA-NUTF2P3-001 and miR-3923 can be applied as novel predictors and therapeutic targets for pancreatic cancer.	MI0016430	Oncotarget 2016 Feb 2 7, 6000-14 doi:10.18632/oncotarget.6830 PMID:26755660
2325	LncRNA	p21	miR-146b-5p	b-catenin	U87 and glioma tissues	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27166258	MiR-146b-5p overexpression attenuates stemness and radioresistance of glioma stem cells by targeting HuR/lincRNA-p21/β-catenin pathway	we found that lincRNA-p21 negatively regulated the expression and activity of β-catenin in GSCs. Downregulation of lincRNA-p21 in GSCs was resulted from upregulation of Hu antigen R (HuR) expression caused by miR-146b-5p downregulation. MiR-146b-5p overexpression increased apoptosis and radiosensitivity, decreased cell viability, neurosphere formation capacity and stem cell marker expression, and induced differentiation in GSCs. Moreover, knock-down lincRNA-p21 or HuR and β-catenin overexpression could rescue the phenotypic changes resulted from miR-146b-5p overexpression in GSCs	MIMAT0002809	Oncotarget 2016 Jul 5 7, 41505-41526 doi:10.18632/oncotarget.9214 PMID:27166258
2326	LncRNA	PCA3	miR-1261	PRKD3	Rwpe-1, Lncap	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc.	27743381	Snail-activated long non-coding RNA PCA3 up-regulates PRKD3 expression by miR-1261 sponging, thereby promotes invasion and migration of prostate cancer cells.	In the present study, the level of PCA3 expression in prostate cancer cells was reduced by small interfering RNA (siRNA). Subsequently, the ability of LNCaP cell proliferation, invasion, and migration of PCa was compromised both in vivo and in vitro with the occurrence of cell autophagy. The transcription factor, Snail, activated the expression of lncRNA PCA3, which could inhibit the translation of PRKD3 protein via competitive miR-1261 sponging, and thus high expression of PRKD3 further promoted invasion and migration of prostate cancer.	MI0006396	Tumour Biol 2016 Oct 14, 10.1007/s13277-016-5450-y doi:10.1007/s13277-016-5450-y PMID:27743381
2327	LncRNA	PCAT-1	miR-34a	cMyc	Lncap	Prostate Cancer	Homo sapiens (human)	qPCR, RNAi, Luciferase reporter assay etc.	25425964	The Long Non-Coding RNA PCAT-1 Promotes Prostate Cancer Cell Proliferation through cMyc.	We show that PCAT-1 promotes prostate cell proliferation and that this phenotype is mediated through up-regulation of the cMyc protein (encoded by the MYC gene). Antagonism of cMyc is able to reverse PCAT-1mediated cell proliferation. We show that PCAT-1 regulates cMyc post-transcriptionally through the MYC 3' untranslated region (UTR). Further, we find a protetcive effetc of PCAT-1 on cMyc by interfering with the regulation of MYC by miR-34a.	MI0000268	Neoplasia 2014 Nov 16, 900-8 doi:10.1016/j.neo.2014.09.001 PMID:25425964
2328	LncRNA	PlncRNA-1	miR-34c	AR	22Rv1, Lncap, Pc3, Du145	Prostate Cancer	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, ChIP, Flow cytometry assay etc.	26808578	A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression.	In this study, we demonstrated that long non-coding RNA PlncRNA-1, whose expression is promoted by Androgen Receptor (AR), protects AR from microRNA-mediated suppression in PCa cells. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. Together, the data generated in this study indicate that PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa.	MI0000743	Cancer Lett 2016 Apr 28 374, 62-74 doi:10.1016/j.canlet.2016.01.033 PMID:26808578
2329	LncRNA	PlncRNA-1	miR-297	AR	22Rv1, Lncap, Pc3, Du145	Prostate Cancer	Homo sapiens (human)	qPCR, Western blot, Northern blot, RIP, ChIP, Flow cytometry assay etc.	26808578	A feed-forward regulatory loop between androgen receptor and PlncRNA-1 promotes prostate cancer progression.	In this study, we demonstrated that long non-coding RNA PlncRNA-1, whose expression is promoted by Androgen Receptor (AR), protects AR from microRNA-mediated suppression in PCa cells. PlncRNA-1 knockdown resulted in the up-regulation of a series of AR-targeting microRNAs, among which miR-34c and miR-297 were found to regulate both AR and PlncRNA-1 expression at the post-transcriptional level. Together, the data generated in this study indicate that PlncRNA-1 sponges AR-targeting microRNAs to protect AR from microRNA-mediated down-regulation and that these events form a regulatory feed-forward loop in the development of PCa.	MI0005775	Cancer Lett 2016 Apr 28 374, 62-74 doi:10.1016/j.canlet.2016.01.033 PMID:26808578
2330	LncRNA	PTCSC3	miR-574-5p	NA	Bcpap, Ftc133, 8505C Etc.	Thyroid Cancer	Homo sapiens (human)	qPCR etc.	23599737	A long non-coding RNA, PTCSC3, as a tumor suppressor and a target of miRNAs in thyroid cancer cells.	Following transfection with PTCSC3, all three thyroid cancer cells originating from various pathological types of thyroid cancers demonstrated significant growth inhibition, cell cycle arrest and increased apoptosis. So PTCSC3 as a tumor suppressor was investigated as a competing endogenous RNA for miR-574-5p.	MIMAT0004795	Exp Ther Med 2013 Apr 5, 1143-1146 doi:10.3892/etm.2013.933 PMID:23599737
2331	LncRNA	PTENP1	miR-17	PTEN	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2332	LncRNA	PTENP1	miR-17	PHLPP	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2333	LncRNA	PTENP1	miR-17	ULK1	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2334	LncRNA	PTENP1	miR-17	ATG7	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2335	LncRNA	PTENP1	miR-17	p62	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2336	LncRNA	PTENP1	miR-19b	PTEN	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2337	LncRNA	PTENP1	miR-19b	PHLPP	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2338	LncRNA	PTENP1	miR-19b	ULK1	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2339	LncRNA	PTENP1	miR-19b	ATG7	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2340	LncRNA	PTENP1	miR-19b	p62	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2341	LncRNA	PTENP1	miR-20a	PTEN	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2342	LncRNA	PTENP1	miR-20a	PHLPP	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2343	LncRNA	PTENP1	miR-20a	ULK1	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2344	LncRNA	PTENP1	miR-20a	ATG7	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2345	LncRNA	PTENP1	miR-20a	p62	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	25617127	Suppression of hepatocellular carcinoma by baculovirus-mediated expression of long non-coding RNA PTENP1 and MicroRNA regulation.	Here we confirmed that PTENP1 and PTEN were downregulated in several HCC cells.These data colletcively unveiled the molecular mechanisms of how PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vetcor for PTENP1 lncRNA modulation and HCC therapy.PTENP1 repressed the tumorigenic properties of HCC cells and demonstrated the potential of the SB-BV hybrid vector for PTENP1 lncRNA modulation and HCC therapy. The overexpressed PTENP1 decoyed oncomirs miR-17, miR-19b and miR-20a, which would otherwise target PTEN, PHLPP (a negative AKT regulator) and such autophagy genes as ULK1, ATG7 and p62, indicating that PTENP1 modulated the HCC cell behavior and gene networks by miRNA regulation.	MI0000076	Biomaterials 2015 Mar 44, 71-81 doi:10.1016/j.biomaterials.2014.12.023 PMID:25617127
2346	LncRNA	PVT1	miR-1207-5p	TGFB	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2347	LncRNA	PVT1	miR-1207-5p	CTNNB1	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2348	LncRNA	PVT1	miR-1207-5p	MMP2	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2349	LncRNA	PVT1	miR-1207-5p	Slug	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2350	LncRNA	PVT1	miR-1207-5p	Snail	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2351	LncRNA	PVT1	miR-1207-5p	Vimentin	Ht-29, Hct-116 Etc.	Colorectal Cancer	Homo sapiens (human)	microarray, qPCR etc.	26990997	Role of cancer stem cells in racial disparity in colorectal cancer.	This increase in AA was associated with a marked rise in lncRNA PVT1 (plasmacytoma variant translocation 1), a host gene of miR-1207-5p	MIMAT0005871	Cancer Med 2016 Jun 5, 1268-78 doi:10.1002/cam4.690 PMID:26990997
2352	LncRNA	PVT1	miR-200b	EZH2	Siha And Hela	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, ChIP, RNA pull-down assay etc.	27272214	Long noncoding RNA PVT1 promotes cervical cancer progression through epigenetically silencing miR-200b.	Our results revealed that PVT1 is upregulated in cervical cancer tissues. Overexpression of PVT1 promotes cervical cancer cells proliferation, cell cycle progression and migration, and depletion of PVT1 inhibits cervical cancer cell proliferation, cell cycle progression, and migration. Mechanistically, we verified that PVT1 binds to EZH2, recruits EZH2 to the miR-200b promoter, increases histone H3K27 trimethylation level on the miR-200b promoter, and inhibits miR-200b expression.	MI0000342	Apmis 2016 Aug 124, 649-58 doi:10.1111/apm.12555 PMID:27272214
2353	LncRNA	PVT1	miR-146a	EGFR	Lncap, Pc-3 And Du145	Prostate Cancer	Homo sapiens (human)	qPCR, MSP-PCR, RNAi etc.	27794184	LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a.	Our results showed that miR-146a was downregulated and negatively correlated with PVT1 level in prostate cancer. PVT1 mediated miR-146a expression by inducing the methylation of CpG Island in its promoter. miR-146a overexpression eliminated the effects of PVT1 knockdown on prostate cancer cells. PVT1 regulated prostate cancer cell viability and apoptosis depending on miR-146a.	MI0000477	Cancer Med 2016 Dec 5, 3512-3519 doi:10.1002/cam4.900 PMID:27794184
2354	LncRNA	RMRP	miR-206	Cyclin-D2	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay etc.	27192121	LncRNA-RMRP promotes carcinogenesis by acting as a miR-206 sponge and is used as a novel biomarker for gastric cancer.	RMRP levels in tissue, plasma and gastric juices from patients with gastric cancer were significantly different from those from controls. Its levels were significantly associated with Borrmann type and metastasis. Plasma and gastric juice RMRP had higher sensitivity and specificity than commonly used markers (such as carcinoembryonic antigen and carbohydrate antigen 19-9). Knockdown of RMRP significantly inhibited cell proliferation in vitro and in vivo, whereas overexpression of RMRP promoted cell growth. Acting as a miR-206 sponge, RMRP modulated cell cycle by regulating Cyclin D2 expression. 	MIMAT0000462	Oncotarget 2016 Jun 21 7, 37812-37824 doi:10.18632/oncotarget.9336 PMID:27192121
2355	LncRNA	RMRP	miR-206	KRAS	A549, Spc-A1, H1299 And H23	Lung Cancer	Homo sapiens (human)	qPCR, Cell transfection, Western blot etc.	27906963	LncRNA-RMRP Acts as an Oncogene in Lung Cancer.	RMRP expression was upregulated in 25 cases compared to the adjacent normal tissues. We also showed that RMRP expression was upregulated in lung adenocarcinoma cell lines compared to the bronchial epithelial cell line. Ectopic expression of RMRP promoted lung adenocarcinoma cell proliferation, colony formation and invasion. In addition, overexpression of RMRP inhibited the miR-206 expression in the H1299 cell and increased the KRAS, FMNL2 and SOX9 expression, which were the target genes of miR-206. Re-expression of miR-206 reversed the RMRP-induced the H1299 cell proliferation and migration.	MIMAT0000462	PLoS One 2016  11, e0164845 doi:10.1371/journal.pone.0164845 PMID:27906963
2356	LncRNA	lincRNA-ROR	miR-34a	BCL-2	Mda-Mb-231, Mcf10A	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ChIP, Flow cytometry assay etc.	27449099	Large intergenic non-coding RNA-ROR reverses gemcitabine-induced autophagy and apoptosis in breast cancer cells.	Untreated MDA-MB-231 cell lines strongly expressed linc-ROR, but linc-ROR knockdown decreased cell viability and expression of p62 and p53 while increasing apoptosis. Linc-ROR knockdown also increased LC3-II/β-actin, Beclin 1, NOTCH1, and Bcl-2 expression, as well as the number of autophagic vesicles in MDA-MB-231 cells. Linc-ROR negatively regulated miR-34a expression by inhibiting histone H3 acetylation in the miR-34a promoter.	MI0000268	Oncotarget 2016 Sep 13 7, 59604-59617 doi:10.18632/oncotarget.10730 PMID:27449099
2357	LncRNA	lincRNA-ROR	miR-145	NA	Ncm460, Rko, Caco2, Hct8, Sw480 And Sw620	Colon Cancer	Homo sapiens (human)	qPCR etc.	27071407	Long Non-Coding RNA lincRNA-ROR Promotes the Progression of Colon Cancer and Holds Prognostic Value by Associating with miR-145	In the present study, qRT-PCR was performed to measure the expression levels of lincRNA-ROR in colon cancer tissues and cell lines. Then, the clinicopathological significance and prognostic value of lincRNA-ROR were analyzed. LincRNA-ROR expression correlated with pT stage, pN stage, AJCC stage and vascular invasion. Knockdown of lincRNA-ROR restored the expression of miR-145, and had a significant influence on colon cancer cell proliferation, migration and invasion. Patients of the high lincRNA-ROR/low miR-145 group had significantly poorer outcomes than those of the low lincRNA-ROR/high miR-145 group.	MI0000461	Pathol Oncol Res 2016 Oct 22, 733-40 doi:10.1007/s12253-016-0061-x PMID:27071407
2358	LncRNA	lincRNA-ROR	miR-145	Nanog	pancreatic cancer stem cells	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, Flow cytometry assay, FISH etc.	26636540	ROR functions as a ceRNA to regulate Nanog expression by sponging miR-145 and predicts poor prognosis in pancreatic cancer.	Compared with adjacent non-tumor tissues, ROR was up-regulated in most tumor tissues. Knockdown of ROR by RNA interference in PCSCs inhibited proliferation, induced apoptosis and decreased migration. Moreover, ROR silencing resulted in significantly decreased tumourigenicity of PCSCs in nude mice than controls. In particular, ROR may act as a ceRNA, effectively becoming a sink for miR-145, thereby activating the derepression of core transcription factors Nanog.	MI0000461	Oncotarget 2016 Jan 12 7, 1608-18 doi:10.18632/oncotarget.6450 PMID:26636540
2359	LncRNA	lincRNA-ROR	miR-205	OCT4	HEK293T	Breast Cancer	Homo sapiens (human)	qPCR, RIP, in vivo knockdown etc.	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.	linc-ROR was upregulated in breast tumor and ectopic overexpression of linc-ROR in immortalized human mammary epithelial cells induced an epithelial-to-mesenchymal transition (EMT) program. Moreover,linc-ROR enhanced breast cancer cell migration and invasion. Linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205. linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs.	MI00002850	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
2360	LncRNA	lincRNA-ROR	miR-205	Nanog	HEK293T	Breast Cancer	Homo sapiens (human)	qPCR, RIP, in vivo knockdown etc.	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.	linc-ROR was upregulated in breast tumor and ectopic overexpression of linc-ROR in immortalized human mammary epithelial cells induced an epithelial-to-mesenchymal transition (EMT) program. Moreover,linc-ROR enhanced breast cancer cell migration and invasion. Linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205. linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs.	MI0000285	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
2361	LncRNA	lincRNA-ROR	miR-205	Sox2	HEK293T	Breast Cancer	Homo sapiens (human)	qPCR, RIP, in vivo knockdown etc.	24922071	LincRNA-ROR induces epithelial-to-mesenchymal transition and contributes to breast cancer tumorigenesis and metastasis.	linc-ROR was upregulated in breast tumor and ectopic overexpression of linc-ROR in immortalized human mammary epithelial cells induced an epithelial-to-mesenchymal transition (EMT) program. Moreover,linc-ROR enhanced breast cancer cell migration and invasion. Linc-ROR was associated with miRNPs and functioned as a competing endogenous RNA to mi-205. linc-ROR functions as an important regulator of EMT and can promote breast cancer progression and metastasis through regulation of miRNAs.	MI0000285	Cell Death Dis 2014 Jun 12 5, e1287 doi:10.1038/cddis.2014.249 PMID:24922071
2362	LncRNA	lincRNA-ROR	miR-145	TNBC	Hek293T, Mcf-7, Hs578T, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	microarray, qPCR, Western blot etc.	25253741	lincRNA-ROR and miR-145 Regulate Invasion in Triple-negative Breast Cancer via Targeting ARF6.	lincRNA-ROR was significant upregulated in DCIS and IDC tumor tissues, showing the highest expression in invasive tumor tissues. Overexpression of the long non-coding RNA, lincRNA-ROR, functions as a competitive endogenous RNA sponge in TNBC. Interestingly, lincRNA-ROR is dramatically upregulated in TNBC and in metastatic disease and knockdown restores miR-145 expression.	MI0000461	Mol Cancer Res 2015 Feb 13, 330-8 doi:10.1158/1541-7786.Mcr-14-0251 PMID:25253741
2363	LncRNA	lincRNA-ROR	miR-145	OCT4	HEK293T	Endometrial Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay, FISH etc.	24589415	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 	MI0000461	Gynecol Oncol 2014 May 133, 333-9 doi:10.1016/j.ygyno.2014.02.033 PMID:24589415
2364	LncRNA	lincRNA-ROR	miR-145	Nanog	HEK293T	Endometrial Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay, FISH etc.	24589415	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 	MI0000461	Gynecol Oncol 2014 May 133, 333-9 doi:10.1016/j.ygyno.2014.02.033 PMID:24589415
2365	LncRNA	lincRNA-ROR	miR-145	Sox2	HEK293T	Endometrial Cancer	Homo sapiens (human)	qPCR, RNAi, Flow cytometry assay, FISH etc.	24589415	Linc-RNA-RoR acts as a sponge against mediation of the differentiation of endometrial cancer stem cells by microRNA-145.	We began by assessing the expression of linc-RoR in ECSC growing under tumorsphere conditions and differentiated conditions (removal of bFGF). In qRT-PCR analyses, a marked reduction of linc-RoR and core TFs was observed in all differentiated tumorspheres. This finding suggested that linc-RoR expression was positively correlated with levels of undifferentiated tumorspheres. The effects of miR-145 could be eliminated after increasing the expression of linc-RoR in ETs or mutated targeted sequences in linc-RoR. 	MI0000461	Gynecol Oncol 2014 May 133, 333-9 doi:10.1016/j.ygyno.2014.02.033 PMID:24589415
2366	LncRNA	RP11-838N2.4	miR-10a	EphA8	U87, U251	Glioblastoma	Homo sapiens (human)	qPCR, Western blot, RIP etc.	27270310	Long noncoding RNA RP11-838N2.4 enhances the cytotoxic effects of temozolomide by inhibiting the functions of miR-10a in glioblastoma cell lines	We found that the level of the lncRNA RP11-838N2.4 was lower in TMZ-resistant GBM cells (U87TR, U251TR) compared to the parental, non-resistant GBM cells (U87, U251).In GBM patients, the decreased level of lncRNA RP11-838N2.4 correlated with higher risk of GBM relapse, as well as shorter postoperative survival times.Moreover, lncRNA RP11-838N2.4 acts as an endogenous sponge, suppressing the function of miR-10a through conserved sequences and increasing the expression of EphA8 that enhanced the rate of cell apoptosis, thereby intensified sensitivity of GBM cells to TMZ.	MI0000266	Oncotarget 2016 Jul 12 7, 43835-43851 doi:10.18632/oncotarget.9699 PMID:27270310
2367	LncRNA	RSU1P2	let-7a	N-myc	Smmc-7721 And Hepg3	Cervical Cancer	Homo sapiens (human)	qPCR, Western blot, Flow cytometry assay, Cell migration and invasion assay etc.	27487126	LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells.	Here, we found that the lncRNA RSU1P2 is upregulateded in cervical cancer tissues and has a tumour-promoting role. We revealed that RSU1P2 acts as a ceRNA through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity.	MI0000060	Oncotarget 2017 Jul 4 8, 43768-43781 doi:10.18632/oncotarget.10844 PMID:27487126
2368	LncRNA	SIRT1-AS	miR-29c	SIRT1	Hcc-9903	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot etc.	26324025	A novel mutation in SIRT1-AS leading to a decreased risk of HCC	SIRT1-AS overexpression promoted the proliferation of the human HCC cell lines by upregulating the SIRT1 protein level. The mechanism was that SIRT1-AS bound to SIRT1 mRNA at 3'UTR, masked the miR-29c binding site and stabilized SIRT1 mRNA.	MI0000735	Oncol Rep 2015 Nov 34, 2343-50 doi:10.3892/or.2015.4205 PMID:26324025
2369	LncRNA	MEG3	miR-3163	SKP2	Atcc, Rockville, Md, Usa	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26482610	Skp2 regulates non-small cell lung cancer cell growth by Meg3 and miR-3163	These data suggest that the Skp2 may be regulated by Meg3 at post-transcriptional level. Bioinformatics analyses showed that miR-3163 bound to 3'-UTR of Skp2 mRNA in NSCLC cells to inhibit its translation, which was supported by luciferase reporter assay. Meg3 augmented the effects of miR-3163 on Skp2 mRNA, possibly through binding-induced function enhancement, which was supported by the double fluorescent in situ hybridization showing co-localized intracellular Meg3 and miR-3163 signals in NSCLC cells. The miR-3163 levels in NSCLC were not different from in NT, suggesting that the regulation of Skp2 in NSCLC by miR-3163 may require coordination of Meg3	MIMAT0015037	Tumour Biol 2016 Mar 37, 3925-31 doi:10.1007/s13277-015-4151-2 PMID:26482610
2370	LncRNA	SNHG1	miR-195	NA	Hepg2, L02	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Cell transfection, Luciferase reporter assay, Cell proliferation assay, ISH etc.	27932778	Expression of Long Non-Coding RNA (lncRNA) Small Nucleolar RNA Host Gene 1 (SNHG1) Exacerbates Hepatocellular Carcinoma Through Suppressing miR-195.	The expression level of lncRNA SNHG1 was remarkably upregulated in HCC tissues and cell lines compared with normal tissues and cell lines. High expression of lncRNA SNHG1 contributed to the downregulation of miR-195 in HepG2 cells. Also, lncRNA SNHG1 exacerbated HCC cell proliferation, invasion, and migration in vitro through the inhibition of miR-195.	MI0000489	Med Sci Monit 2016 Dec 9 22, 4820-4829 doi:10.12659/msm.898574 PMID:27932778
2371	LncRNA	SOX2OT	miR-211	SOX2	Nt-2	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR etc.	26862518	Down-Regulatory Effects of miR-211 on Long Non-Coding RNA SOX2OT and SOX2 Genes in Esophageal Squamous Cell Carcinoma	Compared with mock-transfected cells, overexpression of miR-211 caused a significant down-regulation of both genes. Furthermore, flow-cytometry assay revealed a significant elevation in sub-G1 cell population following ectopic expression of miR-211 in NT-2 cells. Considering the vital role of SOX2OT and SOX2 genes in pluripotency and tumorigenesis, our data suggest an important and inhibitory role for miR-211 in the aforementioned processes.	MI0000287	Cell J 2016 Winter 17, 593-600 doi:10.22074/cellj.2016.3811 PMID:26862518
2372	LncRNA	treRNA	miR-190a	SNAIL1	Hepg2, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	26608035	miR-190a inhibits epithelial-mesenchymal transition of hepatoma cells via targeting the long non-coding RNA treRNA.	We further examined the expression profile of treRNA and miR-190a in 24 pairs of HCC tissues and adjacent normal tissues. miR-190a exhibited a significantly low expression in HCC tissues compared to adjacent normal tissues. Meanwhile, an elevated expression of treRNA was observed in HCC tissue compared to adjacent normal tissue.	MI0000486	FEBS Lett 2015 Dec 21 589, 4079-87 doi:10.1016/j.febslet.2015.11.024 PMID:26608035
2373	LncRNA	treRNA	miR-190a	Vimentin	Hepg2, Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	26608035	miR-190a inhibits epithelial-mesenchymal transition of hepatoma cells via targeting the long non-coding RNA treRNA.	We further examined the expression profile of treRNA and miR-190a in 24 pairs of HCC tissues and adjacent normal tissues. miR-190a exhibited a significantly low expression in HCC tissues compared to adjacent normal tissues. Meanwhile, an elevated expression of treRNA was observed in HCC tissue compared to adjacent normal tissue.	MI0000486	FEBS Lett 2015 Dec 21 589, 4079-87 doi:10.1016/j.febslet.2015.11.024 PMID:26608035
2374	LncRNA	TUG1	miR-9	MTHFD2	Bt474, Mcf-7, Mda-Mb-231, And T47D	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay, Flow cytometry assay, MTT assay etc.	28053623	LncRNA Taurine-Upregulated Gene 1 Promotes Cell Proliferation by Inhibiting MicroRNA-9 in MCF-7 Cells.	Higher expression of TUG1 was observed in breast cancer tissues and cell lines than in the corresponding controls. TUG1 knockdown reduced proliferation, suppressed cell cycle progression, and promoted apoptosis of MCF-7 cells. The dual luciferase reporter assay showed that TUG1 could negatively regulate the expression of miR-9. MiR-9 inhibition abrogated the effect of TUG1 knockdown on the proliferation, cell cycle progression, and apoptosis of MCF-7 cells. TUG1 positively regulated the expression of MTHFD2 in breast cancer cells.	MI0000466	J Breast Cancer 2016 Dec 19, 349-357 doi:10.4048/jbc.2016.19.4.349 PMID:28053623
2375	LncRNA	TUG1	miR-9-5p	POU2F1	U2Os, Saos-2, Mg63, And Mnng/Hos	Osteosarcoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	27658774	Long non-coding RNA TUG1 contributes to tumorigenesis of human osteosarcoma by sponging miR-9-5p and regulating POU2F1 expression.	TUG1 knockdown inhibited cell proliferation and colony formation, and induced G0/G1 cell cycle arrest and apoptosis in vitro, and suppressed tumor growth in vivo. Besides, we found that TUG1 acted as an endogenous sponge to directly bind to miR-9-5p and downregulated miR-9-5p expression. Moreover, TUG1 overturned the effect of miR-9-5p on the proliferation, colony formation, cell cycle arrest, and apoptosis in osteosarcoma cells. 	MIMAT0000441	Tumour Biol 2016 Nov 37, 15031-15041 doi:10.1007/s13277-016-5391-5 PMID:27658774
2376	LncRNA	TUG1	miR-144	c-Met	Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	27261864	Inhibition of long non-coding RNA TUG1 on gastric cancer cell transference and invasion through regulating and controlling the expression of miR-144/c-Met axis.	The expression level of lncRNA-TUG1 in GC tissue was significant higher than that in para-C tissue and the high expression level of lncRNA-TUG1 in GC tissue was significantly correlated with tumor lymph nodes metastasis and advance TNM phasing. The transferring and invading capacity of SGC-7901 cells was highly inhibited after being transfected by lncRNA-TUG1 specific siRNA. The results of qRT-PCR and western-blot proved that the expression of microRNA-144 was significantly boosted and the expression level of c-Met mRNA and protein was inhibited after lncRNA-TUG1 was silenced.	MI0000460	Asian Pac J Trop Med 2016 May 9, 508-12 doi:10.1016/j.apjtm.2016.03.026 PMID:27261864
2377	LncRNA	TUG1	miR-299	VEGF	U251 Mg, U87Mg	Glioblastoma	Homo sapiens (human)	qPCR, RNAi etc.	27345398	Long non-coding RNA taurine upregulated 1 enhances tumor-induced angiogenesis through inhibiting microRNA-299 in human glioblastoma.	Here we demonstrated that TUG1 was up-expressed in human glioblastoma tissues and glioblastoma cell lines. Knockdown of TUG1 remarkably suppressed tumor-induced endothelial cell proliferation, migration and tube formation as well as reducing spheroid-based angiogenesis ability in vitro, which are the critical steps for tumor angiogenesis. Overall, the results demonstrated that TUG1 enhances tumor-induced angiogenesis and VEGF expression through inhibiting miR-299. 	MI0000744	Oncogene 2017 Jan 19 36, 318-331 doi:10.1038/onc.2016.212 PMID:27345398
2378	LncRNA	TUG1	miR-26a	PTEN	U251, Shg-44	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27363339	Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells.	TUG1 expression was confirmed to be upregulated in glioma tissues, and showed an inverse correlation with downregulated miR-26a. TUG1 could negatively regulate the expression of miR-26a in glioma cells. Further experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3'UTR. Additionally, the expression of PTEN was also upregulated in glioma tissues, showing a positive or negative correlation with TUG1 or miR-26a, respectively.	MI0000083	Biochem Biophys Res Commun 2016 Sep 2 477, 743-748 doi:10.1016/j.bbrc.2016.06.129 PMID:27363339
2379	LncRNA	TUG1	miR-34a-5p	VEGFA	Hepg2, Huh-6, And Smmc-7221	Hepatoblastoma	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	27362796	Targeting long non-coding RNA-TUG1 inhibits tumor growth and angiogenesis in hepatoblastoma.	We show that TUG1 is significantly upregulated in human hepatoblastoma specimens and metastatic hepatoblastoma cell lines. TUG1 knockdown inhibits tumor growth and angiogenesis in vivo, and decreases hepatoblastoma cell viability, proliferation, migration, and invasion in vitro. TUG1, miR-34a-5p, and VEGFA constitutes to a regulatory network, and participates in regulating hepatoblastoma cell function, tumor progression, and tumor angiogenesis. 	MIMAT0000255	Cell Death Dis 2016 Jun 30 7, e2278 doi:10.1038/cddis.2016.143 PMID:27362796
2380	LncRNA	TUG1	miR-145	ZEB2	Bladder Cancer tissues	Bladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay etc.	26318860	Double-negative feedback loop between long non-coding RNA TUG1 and miR-145 promotes epithelial to mesenchymal transition and radioresistance in human bladder cancer cells.	We confirmed that TUG1 was overexpressed in bladder cancer tissues and established cell lines. Knockdown of TUG1 inhibited bladder cancer cell metastasis both in vitro and in vivo. Furthermore, we found that TUG1 promoted cancer cell invasion and radioresistance through inducing epithelial-to-mesenchymal transition (EMT). Interestingly, TUG1 decreased the expression of miR-145 and there was a reciprocal repression between TUG1 and miR-145 in an Argonaute2-dependent manner. ZEB2 was identified as a down-stream target of miR-145 and TUG1 exerted its function through the miR-145/ZEB2 axis.	MI0000461	FEBS Lett 2015 Oct 7 589, 3175-81 doi:10.1016/j.febslet.2015.08.020 PMID:26318860
2381	LncRNA	TUG1	miR-144	HSF2	Hcmec/D3, Astrocytes, Brain Vascular Pericytes	Glioma	Homo sapiens (human)	qPCR, Lentiviral infection, Western blot, RIP, ChIP etc.	26078353	The long noncoding RNA TUG1 regulates blood-tumor barrier permeability by targeting miR-144.	LncRNA TUG1 (taurine upregulated gene 1) was highly expressed in glioma vascular endothelial cells from glioma tissues. It also upregulated in glioma co-cultured endothelial cells (GEC) from BTB model in vitro. Knockdown of TUG1 increased BTB permeability, and meanwhile down-regulated the expression of the tight junction proteins ZO-1, occludin, and claudin-5. TUG1 increased BTB permeability via binding to miR-144 and then reducing EC tight junction protein expression by targeting HSF2.	MI0000460	Oncotarget 2015 Aug 14 6, 19759-79 doi:10.18632/oncotarget.4331 PMID:26078353
2382	LncRNA	TUSC7	miR-23b	NA	U251, U87 And Hek 293T	Glioma	Homo sapiens (human)	qPCR, RIP, Luciferase reporter assay, RNA pull-down assay, Cell proliferation assay etc.	27766072	Long Non-coding RNA TUSC7, a Target of miR-23b, Plays Tumor-Suppressing Roles in Human Gliomas.	TUSC7 was poorly expressed in tissues and cell lines of glioma, and the lower expression was correlated with glioma of the worse histological grade. Moreover, TUSC7 is a prognostic biomarker of glioma patients. Up-regulation of TUSC7 suppressed cellular proliferation and invasion of glioma cells, and accelerated cellular apoptosis. TUSC7 inhibited the proliferation, migration and invasion of glioma cells and promoted cellular apoptosis largely bypassing miR-23b.	MI0000439	Front Cell Neurosci 2016  10, 235 doi:10.3389/fncel.2016.00235 PMID:27766072
2383	LncRNA	TUSC7	miR-10a	EphA4	Hepg2, Mhcc97L, Hep3B, Smmc-7721, Mhcc97H, And Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay etc.	27002617	Long non-coding RNA TUSC7 acts a molecular sponge for miR-10a and suppresses EMT in hepatocellular carcinoma.	In this study, we observed that the expression of TUSC7 was immensely decreased in HCC. Clinically, the lower expression of TUSC7 predicted poorer survival and may be an independent risk factor for HCC patients. Moreover, TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis.	MI0000266	Tumour Biol 2016 Aug 37, 11429-41 doi:10.1007/s13277-016-4892-6 PMID:27002617
2384	LncRNA	TUSC7	miR-23b	p53	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	The results indicated that TUSC7 was downregulated in GC samples and was an independent prognostic indicator of disease-free survival (DFS) and disease-specific survival (DSS) in GC patients.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2385	LncRNA	UCA1	miR-196a-5p	p27Kip1	5637 And Umuc-2	Bladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27591936	Long non-coding RNA UCA1 promotes cisplatin/gemcitabine resistance through CREB modulating miR-196a-5p in bladder cancer cells.	In the present study, knockdown of UCA1 decreased chemosensitivity to cisplatin/gemcitabine by suppressing cell proliferation and inducing apoptosis, while overexpression of UCA1 increased chemosensitivity in bladder cancer cells. Moreover, UCA1 activated transcription factor CREB which led to miR-196a-5p expression by binding with its promoter. miR-196a-5p induction is involved in UCA1 inhibition of apoptosis induced by cisplatin/gemcitabine via targeting p27Kip1.	MIMAT0000226	Cancer Lett 2016 Nov 1 382, 64-76 doi:10.1016/j.canlet.2016.08.015 PMID:27591936
2386	LncRNA	UCA1	miR-18a	HIF1a	Mcf-7, Bt474, Lcc2, And Lcc9	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, Dual-luciferase reporter assay, Flow cytometry assay etc.	27629141	Long non-coding RNA UCA1 enhances tamoxifen resistance in breast cancer cells through a miR-18a-HIF1α feedback regulatory loop.	Our findings reveal that tamoxifen induces UCA1 upregulation in ER-positive breast cancer cells in a HIF1α-dependent manner. UCA1 upregulation results in significantly enhanced tamoxifen resistance. The upregulated UCA1 sponges miR-18a, which is a negative regulator of HIF1α. Therefore, UCA1 upregulation is further enhanced through a miR-18a-HIF1α feedback loop.	MI0000072	Tumour Biol 2016 Nov 37, 14733-14743 doi:10.1007/s13277-016-5348-8 PMID:27629141
2387	LncRNA	UCA1	miR-204	sox4	Ec9706 And Kyse	Esophageal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc.	27667646	lncRNA-UCA1 enhances cell proliferation through functioning as a ceRNA of Sox4 in esophageal cancer.	UCA1 was significantly upregulated in EC tissues and associated with poor prognosis. Overexpression of UCA1 promoted the proliferation of EC cells, while silence of UCA1 inhibited EC cells growth. Furthermore, we found that Sox4 was a direct target gene of UCA1. UCA1 regulated Sox4 expression through functioning as a competing endogenous RNA (ceRNA). UCA1 directly interacted with miR-204 and decreased the binding of miR-204 to Sox4 3'UTR, which suppressed the degradation of Sox4 mRNA by miR-204.	MI0000284	Oncol Rep 2016 Nov 36, 2960-2966 doi:10.3892/or.2016.5121 PMID:27667646
2388	LncRNA	UCA1	miR-27b	BCL-2	Sgc-7901	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, Flow cytometry assay etc.	27694794	Long Non-Coding RNA (LncRNA) Urothelial Carcinoma Associated 1 (UCA1) Increases Multi-Drug Resistance of Gastric Cancer via Downregulating miR-27b.	UCA1 was significantly upregulated in the cancerous tissues and its expression was negatively correlated with miR-27b expression level. Inhibition of UCA1 significantly restored miR-27b expression in MDR gastric cancer cells. UCA1 knockdown and miR-27b overexpression reduced IC50 of ADR, DDP, and 5-FU in SGC-7901/ADR cells and increased ADR induced cell apoptosis.	MI0000440	Med Sci Monit 2016 Oct 1 22, 3506-3513 doi:10.12659/msm.900688 PMID:27694794
2389	LncRNA	UCA1	miR-507	FOXM1	A375 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Cell proliferation assay etc.	27389544	LncRNA UCA1-miR-507-FOXM1 axis is involved in cell proliferation, invasion and G0/G1 cell cycle arrest in melanoma.	In our experiments, UCA1 expression was discovered to be upregulated in melanoma tissues and cells, while the depletion of UCA1 led to the inhibition of cell proliferation, invasion and cell cycle arrest. To further our understanding of the mechanisms of UCA1, a system of experiments was built. We found that miR-507 could directly bind to UCA1 at the miRNA recognition site, and that there was a negative correlation between miR-507 and UCA1. Additionally, FOXM1 is a target of miR-507 and can be downregulated by either miR-507 overexpression or UCA1 depletion. Downregulated FOXM1 was analogous to the depletion of UCA1 and the overexpression of miR-507.	MI0003194	Med Oncol 2016 Aug 33, 88 doi:10.1007/s12032-016-0804-2 PMID:27389544
2390	LncRNA	UCA1	miR-204-5p	CREB1	Hek-293T, Hct8, Hct116, Ht29, Lovo	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	27046651	LncRNA—UCA1 enhances cell proliferation and 5-fluorouracil resistance in colorectal cancer by inhibiting miR-204-5p	We found that UCA1 was up-regulated in CRCs and negatively correlated with survival time in two CRC cohorts. Functional assays revealed the in vitro and in vivo growth-promoting function of UCA1 and revealed that UCA1 can decrease the sensitivity of CRC cells to 5-FU by attenuating apoptosis. Further mechanistic studies revealed that UCA1 could sponge endogenous miR-204-5p and inhibit its activity. We also identified CREB1 as a new target of miR-204-5p. The protein levels of CREB1 were significantly up-regulated in CRCs, negatively associated with survival time and positively correlated with the UCA1 expression.	MIMAT0000265	Sci Rep 2016 Apr 5 6, 23892 doi:10.1038/srep23892 PMID:27046651
2391	LncRNA	UCA1	miR-145	FSCN1	5637, T24, Umuc2	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26544536	Long noncoding RNA UCA1 promotes bladder cancer cell migration and invasion via hsa-miR-145/ ZEB1/2 /FSCN1 pathway.	Here, we demonstrated that overexpression of lncRNA-UCA1 could induce epithelial to mesenchymal transition (EMT) and increase the migratory and invasive abilities of bladder cancer cells. Mechanistically, lncRNA-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1).	MI0000461	Cancer Sci 2016 Jan 107, 18-27 doi:10.1111/cas.12844 PMID:26544536
2392	LncRNA	UCA1	miR-16	GLS2	Umuc2, 5637	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26373319	Long non-coding RNA UCA1 promotes glutamine metabolism by targeting miR-16 in human bladder cancer.	Real-time reverse transcriptase-polymerase chain reaction demonstrated that the RNA level of urothelial carcinoma-associated 1 and GLS2 was positively correlated in bladder cancer tissues and cell lines. Furthermore, luciferase reporter assays indicated that there was a miR-16 binding site in urothelial carcinoma-associated 1, and it showed appreciable levels of sponge effects on miR-16 as readouts in a dose-dependent manner.	MI0000070	Jpn J Clin Oncol 2015 Nov 45, 1055-63 doi:10.1093/jjco/hyv132 PMID:26373319
2393	LncRNA	UCA1	miR-143	RISC	Mda-Mb-231	Breast Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, ISH etc.	26439035	Long noncoding RNA UCA1 modulates breast cancer cell growth and apoptosis through decreasing tumor suppressive miR-143	UC1 was significantly upregulated, while miR-143 was significantly downregulated in the tumor tissues than in the adjacent normal tissues. There are direct interactions between miR-143 and the miRNA recognition sites of UCA1. UCA1 is present in Ago2-containing RNA-induced silencing complex (RISC), through association with miR-143. Through downregulating miR-143, UCA1 can modulate breast cancer cell growth and apoptosis	MI0000459	Eur Rev Med Pharmacol Sci 2015 Sep 19, 3403-11,  PMID:26439035
2394	LncRNA	UCA1	miR-216b	FGFR1	Mhcc97L, Smmc7721, Mhcc97H, Hepg2, Sk-Hep1 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP etc.	25760077	Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway.	Herein, we found that UCA1 was aberrantly upregulated in HCC tissues and associated with TNM stage, metastasis and postoperative survival. UCA1 depletion inhibited the growth and metastasis of HCC cell lines in vitro and in vivo. the present study elucidates a novel lncRNA- miRNA-mRNA regulatory network that is UCA1-miR-216b-FGFR1-ERK signaling pathway in HCC, which may help to lead a better understanding the pathogenesis of HCC and probe the feasibility of lncRNA-directed diagnosis and therapy for this deadly disease.	MI0005569	Oncotarget 2015 Apr 10 6, 7899-917 doi:10.18632/oncotarget.3219 PMID:25760077
2395	LncRNA	UCA1	miR-193a-3p	ERBB4	A549, H1299, H446, H460, Ncih1650, Beas-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26655272	LncRNA-UCA1 exerts oncogenic functions in non-small cell lung cancer by targeting miR-193a-3p	UCA1 overexpression enhanced, whereas UCA1 silencing impaired the proliferation and colony formation of NSCLC cells. Moreover, mechanistic investigations showed that UCA1 upregulated the expression of miR-193a-3p target gene ERBB4 through competitively 'spongeing' miR-193a-3p. Overall, we concluded that UCA1 functions as an oncogene in NSCLC, acting mechanistically by upregulating ERBB4 in part through 'spongeing' miR-193a-3p	MIMAT0000459	Cancer Lett 2016 Feb 1 371, 99-106 doi:10.1016/j.canlet.2015.11.024 PMID:26655272
2396	LncRNA	UCA1	miR-143	mTOR	Bladder Cancer tissues	Bladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24890811	Long non-coding RNA UCA1 promotes glycolysis by upregulating hexokinase 2 through the mTOR-STAT3/microRNA143 pathway.	In this study, we show that lncRNA UCA1 promotes glycolysis in bladder cancer cells, and that UCA1-induced hexokinase 2 (HK2) functions as an important mediator in this process. We further show that UCA1 activates mTOR to regulate HK2 through both activation of STAT3 and repression of microRNA143. 	MI0000459	Cancer Sci 2014 Aug 105, 951-5 doi:10.1111/cas.12461 PMID:24890811
2397	LncRNA	UCA1	miR-1	Ago2	Bladder Cancer tissues	Bladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	25015192	Hsa-miR-1 downregulates long non-coding RNA urothelial cancer associated 1 in bladder cancer.	Here, we report that downregulated hsa-miR-1 and upregulated lncRNA urothelial cancer associated 1 (UCA1) were inversely expressed in bladder cancer. Hsa-miR-1 decreased the expression of UCA1 in bladder cancer cells in an Ago2-slicer-dependent manner. The binding site between UCA1 and hsa-miR-1 was confirmed. Overexpression of hsa-miR-1 inhibited bladder cancer cell growth, induced apoptosis, and decreased cell motility. hsamiR-1 to play tumor suppressive roles via downregulating lncRNA UCA1 in bladder cancer, which may have potential therapeutic significance.	MI0000651	Tumour Biol 2014 Oct 35, 10075-84 doi:10.1007/s13277-014-2321-2 PMID:25015192
2398	LncRNA	ucoo2kmd.1	miR-211-3p	CD44	Hct116, Sw480	Colorectal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	26974151	Long Non-Coding RNA ucoo2kmd.1 Regulates CD44-Dependent Cell Growth by Competing for miR-211-3p in Colorectal Cancer	We found that lncRNA-uc002kmd.1 expression was usually highly expressed in carcinoma compared with the tissue adjacent to the carcinoma. Through a series of experiments, the results showed that lncRNA-uc002kmd.1 regulates CD44 as a molecular decoy for miR211-3p. Our data indicated that the overexpression of lncRNA-uc002kmd.1 enhanced cell proliferation in CRC	MIMAT0022694	PLoS One 2016  11, e0151287 doi:10.1371/journal.pone.0151287 PMID:26974151
2399	LncRNA	UFC1	miR-34a	HuR	Bel-7402, Sk-Hep1, Huh7, Mhcc-97H	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR, in vitro knockdown etc.	25449213	The Long Intergenic Noncoding RNA UFC1, A Target of MicroRNA 34a, Interacts With the mRNA Stabilizing Protein HuR to Increase Levels of β-Catenin in HCC Cells.	Levels of the lincRNA-UFC1 were increased in HCC tissues compared with controls, and associated with tumor size, Barcelona Clinic Liver Cancer stage, and patient outcomes. Transgenic expression of the lincRNA-UFC1 in HCC cells promoted their proliferation and cell-cycle progression and inhibited apoptosis, whereas short hairpin RNA knockdown of lincRNA-UFC1 had opposite effetcs. Levels of lincRNA-UFC1 correlated with those of b-catenin in HCC tissues. In contrast, there was a negative correlation between levels of microRNA 34a and lincRNA-UFC1 in HCC tissues; microRNA 34a reduced the stability of lincRNA-UFC1	MI0000268	Gastroenterology 2015 Feb 148, 415-26.e18 doi:10.1053/j.gastro.2014.10.012 PMID:25449213
2400	LncRNA	Unigene56159	miR-140-5p	Slug	Smmc-7721 And Hepg2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell migration and invasion assay, MTT assay etc.	27597739	Long non-coding RNA Unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells.	We identified a novel lncRNA, lncRNA-Unigene56159, which is highly expressed in HBV-related HCC tissues, and further analysis showed that this lncRNA was induced by HBV in vitro. Functionally, Unigene56159 significantly promoted cell migration/invasion and epithelial-mesenchymal transition (EMT) in HCC. Mechanistically, Unigene56159 could directly bind to miR-140-5p and effectively act as a competing endogenous RNA (ceRNA) for miR-140-5p to de-repress the expression of the target gene Slug.	MIMAT0000431	Cancer Lett 2016 Nov 28 382, 166-175 doi:10.1016/j.canlet.2016.08.029 PMID:27597739
2401	LncRNA	XIST	miR-92b	Smad7	Qsg-7701, Smmc-7721, Huh-6, Huh-7, Hepg2, Hcclm3 And Qgy-7703	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc.	27100897	MicroRNA-92b promotes hepatocellular carcinoma progression by targeting Smad7 and is mediated by long non-coding RNA XIST	we showed that miR-92b was significantly upregulated in tumor tissue and plasma of HCC patients, and its expression level was highly correlated with gender and microvascular invasion. Functionally, miR-92b could promote cell proliferation and metastasis of HCC in vitro and in vivo. Mechanistic investigations suggested that Smad7, which exhibited an inverse relationship with miR-92b expression in HCC, was a direct target of miR-92b and could reverse its effects on HCC tumorigenesis. Furthermore, long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and miR-92b could directly interact with and repress each other, and XIST could inhibit HCC cell proliferation and metastasis by targeting miR-92b	MI0003560	Cell Death Dis 2016 Apr 21 7, e2203 doi:10.1038/cddis.2016.100 PMID:27100897
2402	LncRNA	XIST	miR-101	EZH2	Sgc7901, Hgc27, Bgc823, Mkn45, Mkn28, And Ags	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Cell proliferation assay etc.	27620004	Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression.	lncRNA XIST was significantly up-regulated in gastric cancer tissues and cell lines. Overexpression of lncRNA XIST was markedly associated with larger tumor size, lymph node invasion, distant metastasis and TNM stage in gastric cancer patients. Functionally, knockdown of lncRNA XIST exerted tumor-suppressive effects by inhibiting cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo. Furthermore, an inverse relationship between lncRNA XIST and miR-101 was found. Polycomb group protein enhancer of zeste homolog 2 (EZH2), a direct target of miR-101, could mediated the biological effects that lncRNA XIST exerted.	MI0000103	J Exp Clin Cancer Res 2016 Sep 13 35, 142 doi:10.1186/s13046-016-0420-1 PMID:27620004
2403	LncRNA	XIST	miR-34a-5p	E2F3	Sune-1, Cne-1, Hne-1, Cne-2, C666-1 And Hone-1	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27461945	Long non-coding RNA XIST exerts oncogenic functions in human nasopharyngeal carcinoma by targeting miR-34a-5p.	Here, we discovered that XIST was up-regulated in NPC tissues and higher expression of XIST contributed to a markedly poorer survival time. In addition, multivariate analysis demonstrated XIST was an independent risk factor for prognosis. XIST over-expression enhanced, while XIST silencing hampered the cell growth in NPC. Additionally, mechanistic analysis revealed that XIST up-regulated the expression of miR-34a-5p targeted gene E2F3 through acting as a competitive 'sponge' of miR-34a-5p.	MIMAT0000255	Gene 2016 Oct 30 592, 8-14 doi:10.1016/j.gene.2016.07.055 PMID:27461945
2404	LncRNA	XIST	miR-152	RISC	Glioblastoma tissues	Glioblastoma	Homo sapiens (human)	qPCR, RIP, Luciferase reporter assay etc.	25578780	Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152.	Our results proved that XIST expression was up-regulated in glioma tissues and GSCs. Functionally, knockdown of XIST exerted tumor-suppressive functions by reducing cell proliferation, migration and invasion as well as inducing apoptosis. Mechanistic investigations defined the direct binding ability of the predicted miR-152 binding site on the XIST. In addition, XIST and miR-152 are probably in the same RNA induced silencing complex (RISC).	MI0000462	Cancer Lett 2015 Apr 1 359, 75-86 doi:10.1016/j.canlet.2014.12.051 PMID:25578780
2405	LncRNA	ZFAS1	miR-150	ZEB1	Huh7, Hepg2, Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RIP, Luciferase reporter assay etc.	26069248	Amplification of long non-coding RNA ZFAS1 promotes metastasis in hepatocellular carcinoma.	ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14 and MMP16 expression, inhibiting these effects of miR-150.	MI0000479	Cancer Res 2015 Aug 1 75, 3181-91 doi:10.1158/0008-5472.Can-14-3721 PMID:26069248
2406	LncRNA	ZFAS1	miR-150	MMP14	Huh7, Hepg2, Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RIP, Luciferase reporter assay etc.	26069248	Amplification of long non-coding RNA ZFAS1 promotes metastasis in hepatocellular carcinoma.	ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14 and MMP16 expression, inhibiting these effects of miR-150.	MI0000479	Cancer Res 2015 Aug 1 75, 3181-91 doi:10.1158/0008-5472.Can-14-3721 PMID:26069248
2407	LncRNA	ZFAS1	miR-150	MMP16	Huh7, Hepg2, Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RIP, Luciferase reporter assay etc.	26069248	Amplification of long non-coding RNA ZFAS1 promotes metastasis in hepatocellular carcinoma.	ZFAS1 functions as an oncogene in HCC progression by binding miR-150 and abrogating its tumor suppressive function in this setting. miR-150 repressed HCC cell invasion by inhibiting ZEB1 and the matrix metalloproteinases MMP14 and MMP16. Conversely, ZFAS1 activated ZEB1, MMP14 and MMP16 expression, inhibiting these effects of miR-150.	MI0000479	Cancer Res 2015 Aug 1 75, 3181-91 doi:10.1158/0008-5472.Can-14-3721 PMID:26069248
2408	LncRNA	ZNFX1-AS1	miR-9	ZNFX1	Hepg2, Hep3B, Snu449, Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay, Cell apoptosis assay etc.	27574442	Long noncoding RNA ZNFX1-AS1 suppresses growth of hepatocellular carcinoma cells by regulating the methylation of miR-9.	Our results suggest that ZNFX1-AS1 was markedly downregulated in HCC samples and cell lines. Overexpression of ZNFX1-AS1 inhibited the cell proliferation and colony formation in HCC cell lines and also induced HCC cell apoptosis. Additionally, miR-9 was lowly expressed in HCC tissues and positively correlated with ZNFX1-AS1 expression. Meanwhile, significant upregulation of miR-9 and downregulation of the methylation of miR-9 promoter CpG island were observed when ZNFX1-AS1 was overexpressed.	MI0000466	Onco Targets Ther 2016  9, 5005-14 doi:10.2147/ott.S103329 PMID:27574442
2409	LncRNA	HOTAIR	miR-1	FOXC1	Hepg2 And Lo2	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, ChIP, Luciferase reporter assay etc.	27895772	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma.	The relative levels of FOXC1 and HOTAIR expression in HCC tissues and HepG2 cells were significantly higher than those in normal liver LO2 cells and adjacent carcinoma tissues. Overexpression of HOTAIR promoted HCC cell proliferation and progression of tumor xenografts. The present authors have demonstrated that FOXC1 binds to the upstream region of HOTAIR in HCC cells and that FOXC1 activates lncRNA HOTAIR expression in HCC HepG2 cells.	MI0000651	Oncol Lett 2016 Nov 12, 4061-4067 doi:10.3892/ol.2016.5127 PMID:27895772
2410	LncRNA	HOTAIR	miR-7	HuR	Scc25, Hn4, Cal27, Scc4, Hn30, Hn12, Hn13 And Fadu	Head And Neck Squamous Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell migration and invasion assay etc.	27941336	A Feed-Forward Regulatory Loop between HuR and the Long Noncoding RNA HOTAIR Promotes Head and Neck Squamous Cell Carcinoma Progression and Metastasis.	Knockdown of HOTAIR and HuR decreased cell viability, cellular migration and invasion. Moreover, HuR interacted and stabilized HOTAIR stability and thus promoted HOTAIR expression. Notably, HOTAIR acted as a miRNA sponge for HuR. HuR also reinforced HOTAIR sponge activity through miRNA recruitment, thus enhancing HuR expression in turn. Finally, HuR and HOTAIR levels were positively correlated and significantly up-regulated in tumours samples.	MI0008947	Cell Physiol Biochem 2016  40, 1039-1051 doi:10.1159/000453160 PMID:27941336
2411	LncRNA	HOTAIR	miR-326	SP1	A549/Cddp	Lung Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc.	27460077	miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1.	Our results showed that HOTAIR was significantly upregulated in A549/CDDP cells compared with parental A549 cells. The results showed that si-HOTAIR increased miR-326 expression (Fig. 6b) and synergistically reduced SP1 expression (Fig. 6c), ultimately enhanced sensitivity to cisplatin in A549/CDDP cells. In contrast to si-HOTAIR, pcDNA/HOTAIR vector inhibited miR-326 expression and synergistically enhanced SP1 expression in A549 cells	MI0000808	Tumour Biol 2016 Oct 37, 13287-13294 doi:10.1007/s13277-016-5244-2 PMID:27460077
2412	LncRNA	HOTAIR	miR-373	Rab22a	Skov3, A2780 And Cp70	Ovarian Cancer	Homo sapiens (human)	qPCR, RNAi, Cell migration assay etc.	27484896	LncRNA HOTAIR controls the expression of Rab22a by sponging miR-373 in ovarian cancer.	HOTAIR was significantly upregulated. Furthermore, the upregulation of HOTAIR increased the proliferation, migration and invasion of ovarian cancer cells. By contrast, the knockdown of HOTAIR repressed cell invasion and viability. HOTAIR functioned as a ceRNA, and acted as a sink for miR-373, thereby regulating the expression of Rab22a. The upregulation of HOTAIR contributed to the malignant progression of ovarian cancer cells.	MI0000781	Mol Med Rep 2016 Sep 14, 2465-72 doi:10.3892/mmr.2016.5572 PMID:27484896
2413	LncRNA	HOTAIR	miR-663b	IGF2	Bxpc3, Cfpac-1, Panc-1 And L3.6Pl	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27895308	Epigenetic inhibition of miR-663b by long non-coding RNA HOTAIR promotes pancreatic cancer cell proliferation via up-regulation of insulin-like growth factor 2.	The long non-coding RNA, HOTAIR, was up-regulated in both pancreatic cancer cells and tissues, and HOTAIR suppressed the expression of miR-663b in pancreatic cancer by histone modification on H3K4me3 and H3K27me3 on miR-663b promoter. Further in vivo studies demonstrated that the stable overexpression of miR-663b or knock-down of HOTAIR inhibited tumor growth and was associated with IGF2 expression.	MI0006336	Oncotarget 2016 Dec 27 7, 86857-86870 doi:10.18632/oncotarget.13490 PMID:27895308
2414	LncRNA	HOTAIR	miR-148a	GPER	Mda-Mb-231And Bt549	Breast Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25928008	Estradiol induces HOTAIR levels via GPER-mediated miR-148a inhibition in breast cancer	we found that HOTAIR was increased in the peripheral blood mononuclear cells and cancer tissues from breast cancer patients, and was especially higher in patients with metastatic breast cancer. In addition, we found that estrogen promoted HOTAIR through its receptor GPER and estrogen-induced breast cancer cell migration was reversed by deleting HOTAIR in TN breast cancer cells MDA-MB-231and BT549. Furthermore, we identified that E2-GPER induces the level of HOTAIR through the suppression of miR-148a. miR-148a level was negatively correlated with HOTAIR level in breast cancer patients. After the mutation of the predicted miR-148a binding sites in HOTAIR, miR-148a had no effect on HOTAIR	MI0000253	J Transl Med 2015 Apr 25 13, 131 doi:10.1186/s12967-015-0489-x PMID:25928008
2415	LncRNA	HOTAIR	miR-193a	c-KIT	Acute Myeloid Leukemia tissues	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP etc.	25979172	Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia	We report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a.	MI0000487	FEBS Lett 2015 Jul 8 589, 1981-7 doi:10.1016/j.febslet.2015.04.061 PMID:25979172
2416	LncRNA	HOTAIR	miR-218	EZH2	Hepg2, Bel7404, Plc5, Huh7 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot etc.	26024833	Hotair Mediates Hepatocarcinogenesis through Suppressing MiRNA-218 Expression and Activating P14 and P16 Signaling.	We found that Hotair was increased in HCC tissues compared to their adjacent non-tumor tissues and the normal liver tissues. Increased Hotair negatively regulated miR-218 expression in HCC, which might be mediated through an EZH2-targeting-miR-218-2 promoter regulatory axis. Further investigation revealed that Hotair knockdown dramatically inhibited cell viability and induced G1-phase arrest in vitro and suppressed tumorigenicity in vivo by promoting miR-218 expression.	MI0000294	J Hepatol 2015 Oct 63, 886-95 doi:10.1016/j.jhep.2015.05.016 PMID:26024833
2417	LncRNA	HOTAIR	miR-1	MAPK1	Skov3, Es-2, Ovcar3, A2780, And Coc1	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion	In this study, we report that HOTAIR may function as a ceRNA to regulate the expression of MAPK1 through competition for miR-1, miR-214-3p, or miR-330-5p in ovarian SKOV3 cells, providing a new insight in the treatment of ovarian cancer.	MI0000651	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
2418	LncRNA	HOTAIR	miR-214-3p	MAPK1	Skov3, Es-2, Ovcar3, A2780, And Coc1	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion	In this study, we report that HOTAIR may function as a ceRNA to regulate the expression of MAPK1 through competition for miR-1, miR-214-3p, or miR-330-5p in ovarian SKOV3 cells, providing a new insight in the treatment of ovarian cancer.	MIMAT0000271	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
2419	LncRNA	HOTAIR	miR-330-5p	MAPK1	Skov3, Es-2, Ovcar3, A2780, And Coc1	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26117268	HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion	In this study, we report that HOTAIR may function as a ceRNA to regulate the expression of MAPK1 through competition for miR-1, miR-214-3p, or miR-330-5p in ovarian SKOV3 cells, providing a new insight in the treatment of ovarian cancer.	MIMAT0004693	Med Sci Monit 2015 Jun 28 21, 1856-63 doi:10.12659/msm.893528 PMID:26117268
2420	LncRNA	HOTAIR	miR-205	Cyclin-J	Hcv29, 5637, T24, J82, Sw780	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, Northern blot etc.	26469956	Long non-coding RNA HOTAIR regulates cyclin J via inhibition of microRNA-205 expression in bladder cancer	We have identified cyclin J (CCNJ) gene, which is involved in cell cycle regulation, as a novel target for miR-205. Furthermore, a long non-coding RNA HOTAIR (HOX transcript antisense RNA) was observed to participate in the silencing of miR-205 in bladder cancer cells by breaking the balance of histone modification between H3K4me3 (histone H3 at lysine 4 methylation) and H3K27me3 on miR-205 promoter.	MI0000285	Cell Death Dis 2015 Oct 15 6, e1907 doi:10.1038/cddis.2015.269 PMID:26469956
2421	LncRNA	HOTAIR	miR-34a	c-Met	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	26136075	LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer	we found that HOTAIR was more highly expressed in diffuse-type GC than in intestinal type. In the diffuse type, there is significant relationship between HOTAIR expression and DFS. CDH1 was downregulated in diffuse-type GC tissues and showed a negative relationship with HOTAIR. In addition, HOTAIR knockdown significantly repressed migration, invasion and metastasis both in vitro and vivo and reversed the epithelial-to-mesenchymal transition in GC cells. We also showed that HOTAIR recruiting and binding to PRC2 epigenetically represses miR34a, which controls the targets C-Met (HGF/C-Met/Snail pathway) and Snail, thus contributing to GC cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with microRNAs during epigenetic regulation.	MI0000268	Cell Death Dis 2015 Jul 2 6, e1802 doi:10.1038/cddis.2015.150 PMID:26136075
2422	LncRNA	HOTAIR	miR-34a	Snail	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	26136075	LincHOTAIR epigenetically silences miR34a by binding to PRC2 to promote the epithelial-to-mesenchymal transition in human gastric cancer	we found that HOTAIR was more highly expressed in diffuse-type GC than in intestinal type. In the diffuse type, there is significant relationship between HOTAIR expression and DFS. CDH1 was downregulated in diffuse-type GC tissues and showed a negative relationship with HOTAIR. In addition, HOTAIR knockdown significantly repressed migration, invasion and metastasis both in vitro and vivo and reversed the epithelial-to-mesenchymal transition in GC cells. We also showed that HOTAIR recruiting and binding to PRC2 epigenetically represses miR34a, which controls the targets C-Met (HGF/C-Met/Snail pathway) and Snail, thus contributing to GC cell-EMT process and accelerating tumor metastasis. Moreover, it is demonstrated that HOTAIR crosstalk with microRNAs during epigenetic regulation.	MI0000268	Cell Death Dis 2015 Jul 2 6, e1802 doi:10.1038/cddis.2015.150 PMID:26136075
2423	LncRNA	HOTAIR	miR-152	HLA-G	Sgc7901, Mgc-803	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Luciferase reporter assay, ELISA etc.	26187665	Long non-coding RNA HOTAIR promotes HLA-G expression via inhibiting miR-152 in gastric cancer cells.	Significant HOTAIR overexpression was observed in GC tissues, as well as strong positive correlations with HLA-G levels in both tissue and peripheral blood samples. HOTAIR overexpression might also get involved in tumor escape mechanisms, involving HLA-G upregulation via inhibiting miR-152.	MI0000462	Biochem Biophys Res Commun 2015 Aug 28 464, 807-13 doi:10.1016/j.bbrc.2015.07.040 PMID:26187665
2424	LncRNA	HOTAIR	miR-326	FGF1	U87, U251, Hek 293T	Glioma	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc.	26183397	Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326.	Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways.	MI0000808	Oncotarget 2015 Sep 8 6, 21934-49 doi:10.18632/oncotarget.4290 PMID:26183397
2425	LncRNA	HOTAIR	miR-21	NA	Serum	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25099764	Combined detection of serum exosomal miR-21 and HOTAIR as diagnostic and prognostic biomarkers for laryngeal squamous cell carcinoma.	The expression of exosomal miR-21 and HOTAIR was significantly higher in patients with LSCC than those with vocal cord polyps. There were significant differences of serum exosomal miR-21 and HOTAIR expressions between the advanced T classifications (T3/T4) or clinical stages (III/IV) and the early stages. The patients with lymph node metastasis had higher serum exosomal miR-21 and HOTAIR expressions than those without.	MI0000077	Med Oncol 2014 Sep 31, 148 doi:10.1007/s12032-014-0148-8 PMID:25099764
2426	LncRNA	HOTAIR	miR-141	AGO2	86-O, Achn	Renal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	24616104	Long non-coding RNA HOTAIR is targeted and regulated by miR-141 in human cancer cells.	We found that HOTAIR expression is inversely correlated to miR-141 expression in renal carcinoma cells. HOTAIR promotes malignancy, including proliferation and invasion, whereas miR-141 suppresses malignancy in human cancer cells. miR-141 binds to HOTAIR in a sequence-specific manner and suppresses HOTAIR expression and functions, including proliferation and invasion.	MI0000457	J Biol Chem 2014 May 2 289, 12550-65 doi:10.1074/jbc.M113.488593 PMID:24616104
2427	LncRNA	HOTAIR	miR-7	HoxD10	Mda-Mb-231 And Mcf-7	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, CHIP-PCR, Dual-luciferase reporter assay etc.	25070049	MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway.	To explore why miR-7 expression was downregulated in breast cancer cells and BCSCs, we examined HOTAIR expression and found that the downregulation of miR-7 was closely related to the high level of HOTAIR expression in breast cancer patients. HOTAIR inhibits many tumor suppression genes including HoxD10 in MDA-MB-231 cells. We downregulated the expression of HOTAIR by RNA interference in MDA-MB-231 cells and found that the expression of HoxD10 along with miR-7 were enhanced.	MI0008947	Stem Cells 2014 Nov 32, 2858-68 doi:10.1002/stem.1795 PMID:25070049
2428	LncRNA	HOTAIR	miR-130a	c-Myc	Gbc-Sd, Sgc-996,Noz, Eh-Gb2 Etc.	Gallbladder Cancer	Homo sapiens (human)	qPCR, Northern blot, RIP, in vitro knockdown etc.	24953832	Long non-coding RNA HOTAIR, a c-Myc activated driver of malignancy, negatively regulates miRNA-130a in gallbladder cancer.	The HOTAIR transcripts were expressed at higher levels in the tumor tissues compared with adjacent normal tissues, indicating that HOTAIR was frequently up-regulated in GBC.A positive correlation between c-Myc and HOTAIR mRNA levels was observed in gallbladder cancer tissues. HOTAIR is a c-Myc-activated driver of malignancy, which acts in part through repression of miRNA-130a. 	MI0000448	Mol Cancer 2014 Jun 23 13, 156 doi:10.1186/1476-4598-13-156 PMID:24953832
2429	LncRNA	HOTAIR	miR-331-3p	HER2	Mgc-803, Sgc-7901, Bgc-823, Ags	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	24775712	Lnc RNA HOTAIR functions as a competing endogenous RNA to regulate HER2 expression by sponging miR-331-3p in gastric cancer.	HOTAIR upregulation was associated with larger tumor size, advanced pathological stage and extensive metastasis, and also correlated with shorter overall survival of gastric cancer patients. In particular, HOTAIR may act as a ceRNA, effectively becoming a sink for miR-331-3p, thereby modulating the derepression of HER2 and imposing an additional level of post-transcriptional regulation.	MIMAT0000760	Mol Cancer 2014 Apr 28 13, 92 doi:10.1186/1476-4598-13-92 PMID:24775712
2430	LncRNA	HOTAIR	miR-34a	HDAC1	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2431	LncRNA	HOTAIR	miR-34a	PIAS3	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2432	LncRNA	HOTAIR	miR-34a	TPM3	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2433	LncRNA	HOTAIR	miR-34a	TCF7L2	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2434	LncRNA	HOTAIR	miR-34a	ARNT2	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2435	LncRNA	HOTAIR	miR-34a	CREBBP	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2436	LncRNA	HOTAIR	miR-34a	JUP	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2437	LncRNA	HOTAIR	miR-34a	AKT2	Lncap, Pc3, Du145, Rwpe-1 Etc.	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	23936419	Genistein inhibits prostate cancer cell growth by targeting miR-34a and oncogenic HOTAIR.	LncRNA profiling showed that HOTAIR was highly regulated by genistein and its expression was higher in castration-resistant PCa cell lines than in normal prostate cells. Knockdown (siRNA) of HOTAIR decreased PCa cell proliferation, migration and invasion and induced apoptosis and cell cycle arrest. miR-34a was also up-regulated by genistein and may directly target HOTAIR in both PC3 and DU145 PCa cells. Our results indicated that genistein inhibited PCa cell growth through down-regulation of oncogenic HOTAIR that is also targeted by tumor suppressor miR-34a. These findings enhance understanding of how genistein regulates lncRNA HOTAIR and miR-34a in PCa.	MI0000268	PLoS One 2013  8, e70372 doi:10.1371/journal.pone.0070372 PMID:23936419
2438	LncRNA	HOTAIR	miR-196a	HOXB8	Gastrointestinal Stromal Tumor tissues	Gastrointestinal Stromal Tumor	Homo sapiens (human)	qPCR etc.	22258453	Upregulation of miR-196a and HOTAIR drive malignant character in gastrointestinal stromal tumors.	In this study, we identified frequent upregulation of miR-196a and lincRNA HOTAIR in high-risk gastrointestinal stromal tumors (GIST). In like manner, overexpression of HOTAIR was also strongly associated with high-risk grade and metastasis among GIST specimens. RNA interference-mediated knockdown of HOTAIR altered the expression of reported HOTAIR target genes and suppressed GIST cell invasiveness. 	MI0000238	Cancer Res 2012 Mar 1 72, 1126-36 doi:10.1158/0008-5472.Can-11-1803 PMID:22258453
2439	LncRNA	HOTAIRM1	miR-196b	HOXA	AML tissues	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR etc.	26436590	The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature.	Interestingly, HOTAIRM1 was overexpressed in NPM1-mutated AML (P < 0.001) and within this group retained its prognostic value (OR: 2.21; P = 0.01). Moreover, HOTAIRM1 expression was associated with a specific 33- microRNA signature that included miR-196b (P < 0.001). miR-196b is located in the HOX genomic region and has previously been reported to have an independent prognostic value in AML.	MI0001150	Oncotarget 2015 Oct 13 6, 31613-27 doi:10.18632/oncotarget.5148 PMID:26436590
2440	LncRNA	HOTAIRM1	miR-196b	HOXA	AML tissues	Acute Promyelocytic Leukemia	Homo sapiens (human)	qPCR etc.	26436590	The lincRNA HOTAIRM1, located in the HOXA genomic region, is expressed in acute myeloid leukemia, impacts prognosis in patients in the intermediate-risk cytogenetic category, and is associated with a distinctive microRNA signature.	The lowest HOTAIRM1 levels were observed in APL patients, whereas the highest levels were in patients with t(6;9) AML.	MI0001150	Oncotarget 2015 Oct 13 6, 31613-27 doi:10.18632/oncotarget.5148 PMID:26436590
2441	LncRNA	HOTTIP	miR-192	AGO2	Smmc7721, Hepg2 And Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc.	26710269	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.	In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. Consistent with this notion, a significant negative correlation between these miRNAs and HOTTIP exists in HCC tissue specimens. Interestingly, the dysregulation of the three ncRNAs was associated with overall survival of HCC patients. In addition, the posttranscriptional silencing of HOTTIP by miR-192, miR-204 or HOTTIP siRNAs could significantly suppress viability of HCC cells. On the contrary, antagonizing endogenous miR-192 or miR-204 led to increased HOTTIP expression and stimulated cell proliferation.	MI0000234	PLoS Genet 2015 Dec 11, e1005726 doi:10.1371/journal.pgen.1005726 PMID:26710269
2442	LncRNA	HOTTIP	miR-204	AGO2	Smmc7721, Hepg2 And Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Dual-luciferase reporter assay, Cell proliferation assay etc.	26710269	MiRNA-192 [corrected] and miRNA-204 Directly Suppress lncRNA HOTTIP and Interrupt GLS1-Mediated Glutaminolysis in Hepatocellular Carcinoma.	In the current study, we identified miR-192 and miR-204 as two microRNAs (miRNAs) suppressing HOTTIP expression via the Argonaute 2 (AGO2)-mediated RNA interference (RNAi) pathway in HCC. Interaction between miR-192 or miR-204 and HOTTIP were further confirmed using dual luciferase reporter gene assays. Consistent with this notion, a significant negative correlation between these miRNAs and HOTTIP exists in HCC tissue specimens. Interestingly, the dysregulation of the three ncRNAs was associated with overall survival of HCC patients. In addition, the posttranscriptional silencing of HOTTIP by miR-192, miR-204 or HOTTIP siRNAs could significantly suppress viability of HCC cells. On the contrary, antagonizing endogenous miR-192 or miR-204 led to increased HOTTIP expression and stimulated cell proliferation.	MI0000284	PLoS Genet 2015 Dec 11, e1005726 doi:10.1371/journal.pgen.1005726 PMID:26710269
2443	LncRNA	HOTTIP	miR-125b	HOXA	Bel7402, Mhcc97H, Mhcc97H-Luc	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25424744	Long non-coding RNA HOTTIP is frequently up-regulated in hepatocellular carcinoma and is targeted by tumor suppressive miR-125b.	In our profiling study, HOTTIP was identified as the most significantly up-regulated lncRNA in human HCCs, even in early stage of HCC formation. HOTTIP is a novel oncogenic lncRNA, which negatively regulated by miR-125b. Overexpression of HOTTIP contributes to hepatocarcinogenesis by regulating the expression of its neighboring protein-coding genes.Knock-down of HOTTIP significantly suppressed the expression of a number of HOXA genes. 	MI0000446	Liver Int 2015 May 35, 1597-606 doi:10.1111/liv.12746 PMID:25424744
2444	LncRNA	HOXA11-AS	miR-1297	EZH2	Gastric Cancer tissues	Gastric Cancer	Homo sapiens (human)	RNA-seq, microarray, qPCR, Cell transfection, Western blot, RIP, ChIP, Luciferase reporter assay etc.	27651312	LncRNA HOXA11-AS Promotes Proliferation and Invasion of Gastric Cancer by Scaffolding the Chromatin Modification Factors PRC2, LSD1, and DNMT1.	In vitro and in vivo assays of HOXA11-AS alterations revealed a complex integrated phenotype affecting cell growth, migration, invasion, and apoptosis. Mechanistically, EZH2 along with the histone demethylase LSD1 or DNMT1 were recruited by HOXA11-AS, which functioned as a scaffold. HOXA11-AS also functioned as a molecular sponge for miR-1297, antagonizing its ability to repress EZH2 protein translation. In addition, we found that E2F1 was involved in HOXA11-AS activation in gastric cancer cells.	MI0006358	Cancer Res 2016 Nov 1 76, 6299-6310 doi:10.1158/0008-5472.Can-16-0356 PMID:27651312
2445	LncRNA	HULC	miR-200a-3p	ZEB1	Huh-6, Huh-7, Hepg2, Bel-7402, Mhcc-97H, Sk-Hep1, Smmc-7721 Etc.	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	27285757	LncRNA HULC enhances epithelial-mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1 signaling pathway.	We found that HULC was aberrantly up-regulated in HCC tissues and associated with TNM stage, intrahepatic metastases, HCC recurrence, and postoperative survival. HULC depletion inhibited the growth and metastasis of HCC cell lines in vitro and in vivo. Moreover, HULC contributes to ZEB1-induced epithelial-mesenchymal transition (EMT), a requirement for tumor invasion and metastasis that plays a key role in cancer progression.	MIMAT0000682	Oncotarget 2016 Jul 5 7, 42431-42446 doi:10.18632/oncotarget.9883 PMID:27285757
2446	LncRNA	HULC	miR-203	ADAM9	Plc, Hepg2, Smmc-7721, Huh7 And Bel-7402	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Luciferase reporter assay, Flow cytometry assay, Cell proliferation assay etc.	26179263	miR-203 suppresses the proliferation and metastasis of hepatocellular carcinoma by targeting oncogene ADAM9 and oncogenic long non-coding RNA HULC.	We also confirmed that miR-203 and oncogene ADAM9 (a disintegrin and metalloproteinase 9)/oncogenic long non-coding RNA HULC (highly up-regulated in liver cancer) were inversely expressed in hepatocellular carcinoma (HCC) tissues or cell lines. More intriguingly, up-regulation of miR-203 diminished the expression of ADAM9 and HULC in HCC cancer cells. Over-expression of miR-203 could markedly inhibit cell proliferation, invasion and induce cell apoptosis. Furthermore, we identified that miR-203 modulated ADAM9 and HULC in a novel post-transcriptional regulatory mechanism. Over-expression of HULC partly rescued the miR-203-mediated antitumor effects.	MI0000283	Anticancer Agents Med Chem 2016  16, 414-23 doi:10.2174/1871520615666150716105955 PMID:26179263
2447	LncRNA	HULC	miR-372	IL-6	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H29 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	MI0000780	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2448	LncRNA	HULC	miR-372	IL-6	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H29 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	MI0000780	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2449	LncRNA	HULC	miR-373	CXCR4	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H29 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	MI0000781	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2450	LncRNA	HULC	miR-373	CXCR4	Qbc939	Cholangiocarcinoma	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay	27809873	LncRNAs H29 and HULC, activated by oxidative stress, promote cell migration and invasion in cholangiocarcinoma through a ceRNA manner	We identified that two lncRNAs, H19 and HULC, were differentially expressed among all the samples under the treatment of hypoxic or inflammatory factors, and they were shown to be stimulated by short-term oxidative stress responses to H2O2 and glucose oxidase in CCA cell lines. H19 and HULC functioned as competing endogenous RNAs (ceRNAs) by sponging let-7a/let-7b and miR-372/miR-373, respectively, which activate pivotal inflammation cytokine IL-6 and chemokine receptor CXCR4. Our study revealed that H19 and HULC, up-regulated by oxidative stress, regulate CCA cell migration and invasion by targeting IL-6 and CXCR4 via ceRNA patterns of sponging let-7a/let-7b and miR-372/miR-373, respectively.	MI0000781	J Hematol Oncol 2016 Nov 3 9, 117 doi:10.1186/s13045-016-0348-0 PMID:27809873
2451	LncRNA	HULC	miR-107	E2F1	Hepg2, Huh7, Hepg2.2.15 Etc.	Liver Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc.	26540633	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).	Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo. Taken together, we conclude that HULC promotes tumor angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling.	MI0000114	Oncotarget 2016 Jan 5 7, 241-54 doi:10.18632/oncotarget.6280 PMID:26540633
2452	LncRNA	HULC	miR-107	SPHK1	Hepg2, Huh7, Hepg2.2.15 Etc.	Liver Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, ChIP, Luciferase reporter assay etc.	26540633	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1).	Levels of HULC were positively correlated with levels of SPHK1 and its product, sphingosine-1-phosphate (S1P), in patients HCC samples. HULC increased SPHK1 in hepatoma cells. Mechanistically, HULC activated the promoter of SPHK1 in hepatoma cells through the transcription factor E2F1. Chromatin immunoprecipitation (ChIP) and electrophoretic mobility shift assay (EMSA) further showed that E2F1 was capable of binding to the E2F1 element in the SPHK1 promoter. HULC increased the expression of E2F1 in hepatoma cells and levels of HULC were positively correlated with those of E2F1 in HCC tissues. Intriguingly, HULC sequestered miR-107, which targeted E2F1 mRNA 3'UTR, by complementary base pairing. Functionally, si-SPHK1 remarkably abolished the HULC-enhanced tumor angiogenesis in vitro and in vivo. Taken together, we conclude that HULC promotes tumor angiogenesis in liver cancer through miR-107/E2F1/SPHK1 signaling.	MI0000114	Oncotarget 2016 Jan 5 7, 241-54 doi:10.18632/oncotarget.6280 PMID:26540633
2453	LncRNA	HULC	miR-9	PPARA	H7402, Huh7, Hepg2, And Hepg2.2.15	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR etc.	25592151	Long noncoding RNA HULC modulates abnormal lipid metabolism in hepatoma cells through an miR-9-mediated RXRA signaling pathway.	HULC modulated the deregulation of lipid metabolism in HCC by activating the acyl-CoA synthetase subunit ACSL1. Moreover, HULC mRNA levels correlated positively with ACSL1 levels in 60 HCC cases according to real-time PCR analysis. Mechanistic investigations showed that HULC upregulated the transcriptional factor PPARA, which activated the ACSL1 promoter in hepatoma cells. HULC also suppressed miR-9 targeting of PPARA mRNA by eliciting methylation of CpG islands in the miR-9 promoter. We documented the ability of HULC to promote lipogenesis, thereby stimulating accumulation of intracellular triglycerides and cholesterol in vitro and in vivo.	MI0000466	Cancer Res 2015 Mar 1 75, 846-57 doi:10.1158/0008-5472.Can-14-1192 PMID:25592151
2454	LncRNA	HULC	miR-372	CREB	Creb, Hulc, Prkacb Etc.	Liver Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	20423907	CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer.	The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it's inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.	MI0000780	Nucleic Acids Res 2010 Sep 38, 5366-83 doi:10.1093/nar/gkq285 PMID:20423907
2455	LncRNA	KLKP1	miR-125b	NA	Prostate cancer cells	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	27556357	Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer.	Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions.	MI0000446	Oncotarget 2016 Sep 13 7, 60503-60518 doi:10.18632/oncotarget.11391 PMID:27556357
2456	LncRNA	LINC00152	miR-128	NTRK3	Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	27351280	LINC00052 regulates the expression of NTRK3 by miR-128 and miR-485-3p to strengthen HCC cells invasion and migration.	We found one LncRNA which called intergenic non-protein coding RNA 52 (LINC00052) has the ability to inhibit invasion and migration of hepatocarcinoma cells. We found that invasion, migration and proliferation abilities in SMMC7721 cell were inhibited after up-expressing LINC00052. We identified that NTRK3 was the target gene of LINC00052. Down-expression of NTRK3 could increase SMMC7721 cell invasion, migration and proliferation. Meanwhile, we discovered that LINC00052 could regulate NTRK3 expression by forming complementary base pairing with miR-128 and miR-485-3p to reduce the luciferase activity of NTRK3 3'UTR. 	MI0000447	Oncotarget 2016 Jul 26 7, 47593-47608 doi:10.18632/oncotarget.10250 PMID:27351280
2457	LncRNA	LINC00152	miR-485-3p	NTRK3	Smmc7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	27351280	LINC00052 regulates the expression of NTRK3 by miR-128 and miR-485-3p to strengthen HCC cells invasion and migration.	We found one LncRNA which called intergenic non-protein coding RNA 52 (LINC00052) has the ability to inhibit invasion and migration of hepatocarcinoma cells. We found that invasion, migration and proliferation abilities in SMMC7721 cell were inhibited after up-expressing LINC00052. We identified that NTRK3 was the target gene of LINC00052. Down-expression of NTRK3 could increase SMMC7721 cell invasion, migration and proliferation. Meanwhile, we discovered that LINC00052 could regulate NTRK3 expression by forming complementary base pairing with miR-128 and miR-485-3p to reduce the luciferase activity of NTRK3 3'UTR. 	MIMAT0002176	Oncotarget 2016 Jul 26 7, 47593-47608 doi:10.18632/oncotarget.10250 PMID:27351280
2458	LncRNA	LINC00152	miR-193a-3p	ERBB4	Sw480, Caco2, Sw620 And Ht29	Colon Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay, Cell proliferation assay etc.	27633443	Linc00152 Functions as a Competing Endogenous RNA to Confer Oxaliplatin Resistance and Holds Prognostic Values in Colon Cancer.	Elevated expression of Linc00152 was observed by using qRT-PCR in colon cancer tissues when compared with adjacent normal mucosa. Linc00152 as a candidate prognostic indicator of outcome and drug responsiveness in colon cancer patients, and the involvement of competing endogenous RNAs mechanism in Linc00152/miR-193a-3p/ERBB4/AKT signaling axis may provide a novel choice in the investigation of drug resistance.	MIMAT0000459	Mol Ther 2016 Dec 24, 2064-2077 doi:10.1038/mt.2016.180 PMID:27633443
2459	LncRNA	LINC00152	miR-802	TCF4	Pancreatic Cancer tissues	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	25910082	Next-generation sequencing reveals novel differentially regulated mRNAs, lncRNAs, miRNAs, sdRNAs and a piRNA in pancreatic cancer.	The upregulation of LINC00152 (MACE log2fc: 2.3, qPCR: 1.5) and downregulation of LINC00261 (MACE log2fc: 5.3, qPCR: 4.4) in PDAC tissues was confirmed by qPCR.In silico target analysis of miR-802 revealed potential binding sites in the 3′ UTR of TCF4, encoding a transcription factor that controls Wnt-signalling genes. Overexpression of miR-802 in MiaPaCa pancreatic cancer cells reduced TCF4 protein levels. 	MI0003906	Mol Cancer 2015 Apr 25 14, 94 doi:10.1186/s12943-015-0358-5 PMID:25910082
2460	LncRNA	LINC00161	miR-645	IFIT2	Mg-63 And U2Os	Osteosarcoma	Homo sapiens (human)	microarray, qPCR, RNAi, RIP, Dual-luciferase reporter assay etc.	27609068	Long non-coding RNA LINC00161 sensitises osteosarcoma cells to cisplatin-induced apoptosis by regulating the miR-645-IFIT2 axis.	Here, we found that lncRNA LINC00161 was induced by cisplatin in osteosarcoma cells. Elevated LINC00161 increased cisplatin-induced apoptosis and reversed the cisplatin-resistant phenotype of osteosarcoma cells by upregulating IFIT2. Further mechanistic studies revealed that LINC00161 could sponge endogenous miR-645 and inhibit its activity leading to IFIT2 increase. In addition, we identified that LINC00161 enhanced cisplatin-induced apoptosis through regulation of the miR-645-IFIT2 pathway.	MI0003660	Cancer Lett 2016 Nov 28 382, 137-146 doi:10.1016/j.canlet.2016.08.024 PMID:27609068
2461	LncRNA	LINC00261	miR-802	TCF4	Pancreatic Cancer tissues	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	25910082	Next-generation sequencing reveals novel differentially regulated mRNAs, lncRNAs, miRNAs, sdRNAs and a piRNA in pancreatic cancer.	The upregulation of LINC00152 (MACE log2fc: 2.3, qPCR: 1.5) and downregulation of LINC00261 (MACE log2fc: 5.3, qPCR: 4.4) in PDAC tissues was confirmed by qPCR.In silico target analysis of miR-802 revealed potential binding sites in the 3′ UTR of TCF4, encoding a transcription factor that controls Wnt-signalling genes. Overexpression of miR-802 in MiaPaCa pancreatic cancer cells reduced TCF4 protein levels. 	MI0003906	Mol Cancer 2015 Apr 25 14, 94 doi:10.1186/s12943-015-0358-5 PMID:25910082
2462	LncRNA	LINC00673	miR-1231	PTPN11	Bxpc-3 And Cfpac-1	Pancreatic Cancer	Homo sapiens (human)	qPCR, Flow cytometry assay etc.	27213290	Pancreatic cancer risk variant in LINC00673 creates a miR-1231 binding site and interferes with PTPN11 degradation.	Flow cytometry analysis indicated that LINC00673 overexpression resulted in a substantial accumulation of PDAC cells in G0/G1 phase, accompanied by a substantial decrease in the number of cells in S phase. LINC00673 is able to reinforce the interaction of PTPN11 with PRPF19, an E3 ubiquitin ligase, and promote PTPN11 degradation through ubiquitination, which causes diminished SRC-ERK oncogenic signaling and enhanced activation of the STAT1-dependent antitumor response. A G>A change at rs11655237 in exon 4 of LINC00673 creates a target site for miR-1231 binding, which diminishes the effect of LINC00673 in an allele-specific manner and thus confers susceptibility to tumorigenesis.	MI0006321	Nat Genet 2016 Jul 48, 747-57 doi:10.1038/ng.3568 PMID:27213290
2463	LncRNA	LINC00969	miR-125b	KLKP1	Lncap	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	27556357	Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer.	Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions.	MI0000446	Oncotarget 2016 Sep 13 7, 60503-60518 doi:10.18632/oncotarget.11391 PMID:27556357
2464	LncRNA	LINC01021	miR-486	p53	Sw480	Colorectal Cancer	Homo sapiens (human)	RNA-seq, qPCR, Western blot, Luciferase reporter assay, pSILAC etc.	26183718	p53-regulated networks of protein, mRNA, miRNA and lncRNA expression revealed by integrated pSILAC and NGS analyses.	Ectopic LINC01021 expression inhibited proliferation in SW480 cells. We confirmed upregulation of the novel direct p53 target genes LINC01021, MDFI, ST14 and miR-486 and showed that ectopic LINC01021 expression inhibited proliferation in SW480 cells.	MI0002470	Mol Cell Proteomics 2015 Oct 14, 2609-29 doi:10.1074/mcp.M115.050237 PMID:26183718
2465	LncRNA	LINC01138	miR-125b	KLKP1	Lncap	Prostate Cancer	Homo sapiens (human)	microarray, qPCR etc.	27556357	Identification of androgen-responsive lncRNAs as diagnostic and prognostic markers for prostate cancer.	Five lncRNAs, RP1-4514.2, SUZ12P1, SNHG5, LINC01138, and SNHG1, were down-regulated under DHT treatment. Five lncRNAs, KLKP1, LINC00969, LINC-PINT, TUG1 and MIR17HG, were up-regulated under DHT treatment. Notably, RP1-4514.2 and LINC01138 were induced and KLKP1 was reduced over 2 fold after AR silenced, suggesting the involvement of AR in androgen-mediated regulation of these lncRNAs expressions.	MI0000446	Oncotarget 2016 Sep 13 7, 60503-60518 doi:10.18632/oncotarget.11391 PMID:27556357
2466	LncRNA	linc-223	miR-125-5p	IRF4	Hl-60, K562	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR, Luciferase reporter assay, in vitro knockdown	27517498	The miR-223 host non-coding transcript linc-223 induces IRF4 expression in acute myeloid leukemia by acting as a competing endogenous RNA	we show that linc-223 directly binds to miR-125-5p and that its knockdown increases the repressing activity of miR-125-5p resulting in the downregulation of its target interferon regulatory factor 4 (IRF4), which it was previously shown to inhibit the oncogenic activity of miR-125-5p in vivo. Furthermore, data from primary AML samples show significant downregulation of linc-223 in different AML subtypes	MIMAT0000443	Oncotarget 2016 Sep 13 7, 60155-60168 doi:10.18632/oncotarget.11165 PMID:27517498
2467	LncRNA	lnc34a	miR-34a	p53	Colo205, Sw480, Ht29, Sw620, Ls174T, Dld1 Etc.	Colon Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	27077950	A long non-coding RNA targets microRNA miR-34a to regulate colon cancer stem cell asymmetric division	Here we report a novel LncRNA, Lnc34a, that is enriched in colon cancer stem cells (CCSCs) and initiates asymmetric division by directly targeting the microRNA miR-34a to cause its spatial imbalance. Lnc34a recruits Dnmt3a via PHB2 and HDAC1 to methylate and deacetylate the miR-34a promoter simultaneously, hence epigenetically silencing miR-34a expression independent of its upstream regulator, p53. Lnc34a levels affect CCSC self-renewal and colorectal cancer (CRC) growth in xenograft models. Lnc34a is upregulated in late-stage CRCs, contributing to epigenetic miR-34a silencing and CRC proliferation.	MI0000268	Elife 2016 Apr 14 5 doi:10.7554/eLife.14620 PMID:27077950
2468	LncRNA	lncARSR	miR-34	AXL	786-O And Achn	Renal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, ChIP, Luciferase reporter assay, ISH etc.	27117758	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA.	Compared with matched pre-therapy tumors, lncARSR was abundant in sunitinib-resistant RCC. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	MI0000268	Cancer Cell 2016 May 9 29, 653-668 doi:10.1016/j.ccell.2016.03.004 PMID:27117758
2469	LncRNA	lncARSR	miR-34	c-Met	786-O And Achn	Renal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, ChIP, Luciferase reporter assay, ISH etc.	27117758	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA.	Compared with matched pre-therapy tumors, lncARSR was abundant in sunitinib-resistant RCC. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	MI0000268	Cancer Cell 2016 May 9 29, 653-668 doi:10.1016/j.ccell.2016.03.004 PMID:27117758
2470	LncRNA	lncARSR	miR-449	AXL	786-O And Achn	Renal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, ChIP, Luciferase reporter assay, ISH etc.	27117758	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA.	Compared with matched pre-therapy tumors, lncARSR was abundant in sunitinib-resistant RCC. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	MI0001648	Cancer Cell 2016 May 9 29, 653-668 doi:10.1016/j.ccell.2016.03.004 PMID:27117758
2471	LncRNA	lncARSR	miR-449	c-Met	786-O And Achn	Renal Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Northern blot, ChIP, Luciferase reporter assay, ISH etc.	27117758	Exosome-Transmitted lncARSR Promotes Sunitinib Resistance in Renal Cancer by Acting as a Competing Endogenous RNA.	Compared with matched pre-therapy tumors, lncARSR was abundant in sunitinib-resistant RCC. lncARSR promoted sunitinib resistance via competitively binding miR-34/miR-449 to facilitate AXL and c-MET expression in RCC cells. Furthermore, bioactive lncARSR could be incorporated into exosomes and transmitted to sensitive cells, thus disseminating sunitinib resistance. Treatment of sunitinib-resistant RCC with locked nucleic acids targeting lncARSR or an AXL/c-MET inhibitor restored sunitinib response.	MI0001648	Cancer Cell 2016 May 9 29, 653-668 doi:10.1016/j.ccell.2016.03.004 PMID:27117758
2472	LncRNA	LOC150622	miR-23b	TUSC7	HEK-293T and MKN-45	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2473	LncRNA	LOC553103	miR-BART6-3p	CDH2	Ags	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2474	LncRNA	LOC553103	miR-BART6-3p	CDH2	5-8F And Hne2	Nasopharyngeal Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2475	LncRNA	LOC553103	miR-BART6-3p	CDH2	Ags	Gastric Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2476	LncRNA	LOC553103	miR-BART6-3p	CDH2	5-8F And Hne2	Nasopharyngeal Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2477	LncRNA	LOC553103	miR-BART6-3p	SNAL1	Ags	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2478	LncRNA	LOC553103	miR-BART6-3p	SNAL1	5-8F And Hne2	Nasopharyngeal Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2479	LncRNA	LOC553103	miR-BART6-3p	SNAL1	Ags	Gastric Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2480	LncRNA	LOC553103	miR-BART6-3p	SNAL1	5-8F And Hne2	Nasopharyngeal Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2481	LncRNA	LOC553103	miR-BART6-3p	MMP2	5-8F, HNE2, AGS and C666-1	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2482	LncRNA	LOC553103	miR-BART6-3p	MMP2	5-8F, HNE2, AGS and C666-1	Nasopharyngeal Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2483	LncRNA	LOC553103	miR-BART6-3p	MMP2	5-8F, HNE2, AGS and C666-1	Gastric Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2484	LncRNA	LOC553103	miR-BART6-3p	MMP2	5-8F, HNE2, AGS and C666-1	Nasopharyngeal Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2485	LncRNA	LOC553103	miR-BART6-3p	MMP9	5-8F, HNE2, AGS and C666-1	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2486	LncRNA	LOC553103	miR-BART6-3p	MMP9	5-8F, HNE2, AGS and C666-1	Nasopharyngeal Cancer	Homo sapiens (human)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2487	LncRNA	LOC553103	miR-BART6-3p	MMP9	5-8F, HNE2, AGS and C666-1	Gastric Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2488	LncRNA	LOC553103	miR-BART6-3p	MMP9	5-8F, HNE2, AGS and C666-1	Nasopharyngeal Cancer	Epstein-Barr virus (EBV)	microarray, qPCR, RNAi, Luciferase reporter assay etc.	27584792	Epstein-Barr virus-encoded miR-BART6-3p inhibits cancer cell metastasis and invasion by targeting long non-coding RNA LOC553103.	We identified and validated that a novel long non-coding RNA (lncRNA) LOC553103 was downregulated by EBV-miR-BART6-3p, and LOC553103 knockdown by specific siRNAs phenocopied the effect of EBV-miR-BART6-3p, while LOC553103 overexpression promoted cancer cell migration and invasion to facilitate EMT.	MIMAT0003415	Cell Death Dis 2016 Sep 1 7, e2353 doi:10.1038/cddis.2016.253 PMID:27584792
2489	LncRNA	M59227	miR-23b	TUSC7	HEK-293T and MKN-45	Gastric Cancer	Homo sapiens (human)	microarray, qPCR, RNAi etc.	25765901	Reciprocal repression between TUSC7 and miR-23b in gastric cancer.	LncRNA M59227 and 3 mRNAs, PLK1, PTTG1 and VCAN, were overexpressed in GC. In contrast, the expression of 4 lncRNAs, LOC150622, AKR7 L, DQ192290 and BC040587, and 2 mRNAs, DRD5 and GDF5, were downregulated in GC.The results indicated that TUSC7 is a p53-regulated tumour suppressor that acts in part by repressing miR-23b and that TUSC7 may be a key regulatory hub in GC.	MI0000439	Int J Cancer 2015 Sep 15 137, 1269-78 doi:10.1002/ijc.29516 PMID:25765901
2490	LncRNA	MALAT1	miR-448	KDM5B	Mda-Mb-231, Mda-Mb-453, Hs578T, T47D, Au565 And Skbr3	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	26917489	Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448.	KDM5B induces the expression of MALAT1 and its effector metastasis- associated genes in triple negative breast carcinoma cells. KDM5B interacts with MALAT1 to modulate its expression in triple negative breast carcinoma cells and consequently facilitate invasion and associated metastatic activities.	MI0001637	BMC Cancer 2016 Feb 25 16, 160 doi:10.1186/s12885-016-2108-5 PMID:26917489
2491	LncRNA	MALAT1	miR-26b	p62	Bel-7402, Bel-7402/5-Fu	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	27524242	The HIF-2α-MALAT1-miR-216b axis regulates multi-drug resistance of hepatocellular carcinoma cells via modulating autophagy.	The results showed that MALAT1 was over two times higher in BEL-7402/5-FU cells than in BEL-7402 cells. It was HIF-2α, but not HIF-1α induced MALAT1 upregulation in HCC cells. Dual luciferase assay demonstrated that there were at least two binding sites of miR-26b in MALAT1. Therefore, we infer that there is a HIF-2α-MALAT1-miR-216b axis in HCC cells. Cell viability assay showed that both MALAT1 siRNA and miR-216b mimics reduced IC50 of 5-FU, ADR and MMC in BEL-7402/5-FU cells. MALAT1 siRNA and miR-216b mimics showed similar effect as 3-MA on reducing LC3-II levels, inhibiting p62 degradation and suppressing GFP-LC3 puncta formation in BEL-7402/5-FU cells. Flow cytometric analysis showed that 3-MA treatment, MALAT1 siRNA and miR-216b mimics all promoted 5-FU induced apoptosis in BEL-7402/5-FU cells.	MI0000084	Biochem Biophys Res Commun 2016 Sep 23 478, 1067-73 doi:10.1016/j.bbrc.2016.08.065 PMID:27524242
2492	LncRNA	MALAT1	miR-1	CDC42	Hbl-100, Mcf-7, Mda-Mb-231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay, Immunofluorescent assay etc.	26926567	MALAT1 induced migration and invasion of human breast cancer cells by competitively binding miR-1 with cdc42	In this study we identified long non-coding RNA (lncRNA) MALAT1 can function as a ceRNA of cell division cycle 42 (cdc42) 3'UTR in inducing migration and invasion of breast cancer cells via miR-1. We found that miR-1 bound both MALAT1 and cdc42 3'UTR directly. Further study showed that MALAT1 induced migration and invasion of breast cancer cells while reduced the level of cdc42. 	MI0000651	Biochem Biophys Res Commun 2016 Mar 25 472, 262-9 doi:10.1016/j.bbrc.2016.02.102 PMID:26926567
2493	LncRNA	MALAT1	miR-375	DNMT1	Siha And Caski	Cervical Cancer	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Dual-luciferase reporter assay, Flow cytometry assay etc.	27658300	MiR-375 Is Epigenetically Downregulated by HPV-16 E6 Mediated DNMT1 Upregulation and Modulates EMT of Cervical Cancer Cells by Suppressing lncRNA MALAT1.	MiR-375 overexpression or MALAT1 siRNA partly restored E-cadherin expression and also significantly reduced N-cadherin. Following immunofluorescent staining confirmed these trends. Since EMT is an important mechanism of enhanced tumor cell invasion and metastasis, we further detected how miR-375 and MALAT1 modulate invasion capacity of SiHa cells. Transwell assay showed that both miR-375 overexpression and MALAT1 knockdown significantly reduced invasion capacity of SiHa cells.	MI0000783	PLoS One 2016  11, e0163460 doi:10.1371/journal.pone.0163460 PMID:27658300
2494	LncRNA	MALAT1	miR-200c	TGFB	Rl-952, Hec-1-B And Jec	Endometrial Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Luciferase reporter assay, Cell proliferation assay etc.	27693631	Disrupting MALAT1/miR-200c sponge decreases invasion and migration in endometrioid endometrial carcinoma.	In the present study, we first showed that miR-200c levels were higher in most EEC specimens than in non-tumor tissues, while MALAT1 levels were lower. Moreover, we found that miR-200c bound directly to MALAT1 using luciferase reporter and qRT-PCR assays. MALAT1 and miR-200c are reciprocally repressed, and TGF-β increased MALAT1 expression by inhibiting miR-200c. When the interaction between miR-200c/MALAT1 was interrupted, the invasive capacity of EEC cells was decreased and EMT markers expression were altered in vitro.	MI0000650	Cancer Lett 2016 Dec 1 383, 28-40 doi:10.1016/j.canlet.2016.09.019 PMID:27693631
2495	LncRNA	MALAT1	miR-206	ANXA2	Gbc-Sd, Sgc-996 Etc.	Gallbladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. The high Malat1 levels correlated positively with tumor size and lymphatic metastasis, and correlated negatively with overall survival. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206.Furthermore, in agreement with in vitro results, IHC data demonstrate that the levels of ANXA2 and KRAS are lower in the shRNA-Malat1 group than in the control group (Figure 7C and 7D). This suggests that Malat1, ANXA2 and KRAS are oncogenic in in vivo GBC subcutaneous tumors.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
2496	LncRNA	MALAT1	miR-206	KRAS	Gbc-Sd, Sgc-996 Etc.	Gallbladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	27191262	Long non-coding RNA Malat1 promotes gallbladder cancer development by acting as a molecular sponge to regulate miR-206.	In this study, we show that Malat1 is overexpressed in gallbladder cancer (GBC) tissue and cells. The high Malat1 levels correlated positively with tumor size and lymphatic metastasis, and correlated negatively with overall survival. We also show that Malat1 functions as a competing endogenous RNA (ceRNA) for miR-206.Furthermore, in agreement with in vitro results, IHC data demonstrate that the levels of ANXA2 and KRAS are lower in the shRNA-Malat1 group than in the control group (Figure 7C and 7D). This suggests that Malat1, ANXA2 and KRAS are oncogenic in in vivo GBC subcutaneous tumors.	MI0000490	Oncotarget 2016 Jun 21 7, 37857-37867 doi:10.18632/oncotarget.9347 PMID:27191262
2497	LncRNA	LINC00152	miR-376c-3p	Ki-67	Caco2, Hct-116, Ht-29, Sw480, And Sw620	Colorectal Cancer	Homo sapiens (human)	qPCR, Flow cytometry assay, CCK-8 assay etc.	28078002	LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.	We found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Overexpression of LINC00152 resulted in decreased cell viability and increased apoptosis in CSC cell lines. Interestingly, miR-376c-3p down-regulated the expression of LINC00152 in CSC cells. In addition, miR-376c-3p suppressed the effect of LINC00152 on the viability and apoptosis of CSC cells.	MIMAT0000720	Am J Transl Res 2016  8, 5286-5297,  PMID:28078002
2498	LncRNA	LINC00152	miR-376c-3p	BCL-2	Caco2, Hct-116, Ht-29, Sw480, And Sw620	Colorectal Cancer	Homo sapiens (human)	qPCR, Flow cytometry assay, CCK-8 assay etc.	28078002	LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.	We found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Overexpression of LINC00152 resulted in decreased cell viability and increased apoptosis in CSC cell lines. Interestingly, miR-376c-3p down-regulated the expression of LINC00152 in CSC cells. In addition, miR-376c-3p suppressed the effect of LINC00152 on the viability and apoptosis of CSC cells.	MIMAT0000720	Am J Transl Res 2016  8, 5286-5297,  PMID:28078002
2499	LncRNA	LINC00152	miR-376c-3p	Fas	Caco2, Hct-116, Ht-29, Sw480, And Sw620	Colorectal Cancer	Homo sapiens (human)	qPCR, Flow cytometry assay, CCK-8 assay etc.	28078002	LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.	We found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines. Overexpression of LINC00152 resulted in decreased cell viability and increased apoptosis in CSC cell lines. Interestingly, miR-376c-3p down-regulated the expression of LINC00152 in CSC cells. In addition, miR-376c-3p suppressed the effect of LINC00152 on the viability and apoptosis of CSC cells.	MIMAT0000720	Am J Transl Res 2016  8, 5286-5297,  PMID:28078002
2500	LncRNA	LINC00312	miR-197-3p	TIMP2	T24, Biu87, And 5637	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot etc.	27631965	LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p.	qRT-PCR indicated that LINC00312 expression was lower but miR-197-3p expression was higher in BC tissues compared with adjacent tissues; LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion.	MIMAT0000227	Tumour Biol 2016 Nov 37, 14553-14563 doi:10.1007/s13277-016-5303-8 PMID:27631965
2501	LncRNA	LINC00312	miR-197-3p	MMP2	T24, Biu87, And 5637	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot etc.	27631965	LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p.	qRT-PCR indicated that LINC00312 expression was lower but miR-197-3p expression was higher in BC tissues compared with adjacent tissues; LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion.	MIMAT0000227	Tumour Biol 2016 Nov 37, 14553-14563 doi:10.1007/s13277-016-5303-8 PMID:27631965
2502	LncRNA	LINC00312	miR-197-3p	MMP9	T24, Biu87, And 5637	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot etc.	27631965	LINC00312 inhibits the migration and invasion of bladder cancer cells by targeting miR-197-3p.	qRT-PCR indicated that LINC00312 expression was lower but miR-197-3p expression was higher in BC tissues compared with adjacent tissues; LINC00312 was negatively correlated with miR-197-3p. The migration test revealed that the downregulation of miR-197-3p and overexpression of LINC00312 inhibited cell migration and invasion abilities, while the overexpression of miR-197-3p and the upregulation of LINC00312 promoted cell migration and invasion.	MIMAT0000227	Tumour Biol 2016 Nov 37, 14553-14563 doi:10.1007/s13277-016-5303-8 PMID:27631965
2503	LncRNA	LOC554202	miR-31	RhoA	CF7, SKBr3 and T47D	Breast Cancer	Homo sapiens (human)	qPCR etc.	22289355	miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer.	Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes.	MI0000089	Mol Cancer 2012 Jan 30 11, 5 doi:10.1186/1476-4598-11-5 PMID:22289355
2504	LncRNA	LOC554202	miR-31	WAVE3	CF7, SKBr3 and T47D	Breast Cancer	Homo sapiens (human)	qPCR etc.	22289355	miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer.	Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes.	MI0000089	Mol Cancer 2012 Jan 30 11, 5 doi:10.1186/1476-4598-11-5 PMID:22289355
2505	LncRNA	MALAT1	miR-124	E2F1	Mcf-7, Bcap-37 And Mdamb-435S	Breast Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Dual-luciferase reporter assay etc.	26918449	miR-124 downregulation leads to breast cancer progression via LncRNA-MALAT1 regulation and CDK4/E2F1 signal activation.	We also found that MALAT1 was increased in most breast cancer cells. In contrast, miR-124 was downregulated in the MCF-7 cells with MALAT1 overexpression. We found that MALAT1 expression had no effect in breast cancer cells treated with the miR-124 mimic or miR-124 inhibitor. Taken together, our results reveal that MALAT1 may act as an endogenous potent regulator that reduces miR-124 expression.	MI0000443	Oncotarget 2016 Mar 29 7, 16205-16 doi:10.18632/oncotarget.7578 PMID:26918449
2506	LncRNA	MALAT1	miR-122	IGF1R	Sgc7901, Mkn45 And Bgc823	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Cell proliferation assay etc.	27486823	The lncRNA MALAT1 is a novel biomarker for gastric cancer metastasis.	Here, we reported that the tissue and plasma MALAT1 levels were significantly higher in gastric cancer patients with distant metastasis than patients without distant metastasis and the healthy controls. In addition, high levels of plasma MALAT1 independently correlated to a poor prognosis for gastric cancer patients. Functional studies revealed that knockdown of MALAT1 could inhibit cell proliferation, cell cycle progression, migration and invasion, and promote apoptosis in gastric cancer cells. Furthermore, the miR-122-IGF-1R signaling correlated with the dysregulated MALAT1 expression in gastric cancer.	MI0000442	Oncotarget 2016 Aug 30 7, 56209-56218 doi:10.18632/oncotarget.10941 PMID:27486823
2507	LncRNA	MALAT1	miR-363-3p	MCL-1	Sgc-996, Noz	Gallbladder Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Flow cytometry assay, Cell proliferation assay etc.	27420766	The lncRNA MALAT1 functions as a competing endogenous RNA to regulate MCL-1 expression by sponging miR-363-3p in gallbladder cancer.	n this study, we found that MALAT1 expression was up-regulated in GBC tissues. Luciferase reporter assays and RNA pull down assays showed that MALAT1 is a target of miR-363-3p. Real-time quantitative PCR and Western blot analysis indicated that MALAT1 regulated Myeloid cell leukaemia-1 (MCL-1) expression as a competing endogenous RNA (ceRNA) for miR-363-3p in GBC cells. Furthermore, MALAT1 silencing decreased GBC cell proliferation and the S phase cell population and induced apoptosis in vitro.	MIMAT0000707	J Cell Mol Med 2016 Dec 20, 2299-2308 doi:10.1111/jcmm.12920 PMID:27420766
2508	LncRNA	MALAT1	miR-155	FBXW7	U87 And Shg139	Glioma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay etc.	27904771	Tumor-suppressive function of long noncoding RNA MALAT1 in glioma cells by suppressing miR-155 expression and activating FBXW7 function.	The expression of MALAT1 was significantly decreased in glioma specimens than in noncancerous brain tissues. In addition, MALAT1 expression was significantly correlated with tumor size, WHO grade and Karnofsky Performance Status (KPS), and was an independent prognostic factor for survival of glioma patients. Further, MALAT1 suppresses cell viability by down-regulating miR-155. FBXW7 mRNA was identified as a direct target of miR-155 in glioma. Finally, we found that MALAT1 positively regulated FBXW7 expression, which was responsible for glioma progression mediated by MALAT1-miR-155 pathway.	MI0000681	Am J Cancer Res 2016  6, 2561-2574,  PMID:27904771
2509	LncRNA	MALAT1	miR-204	SLUG	A549, H1299, H460, H446 Etc.	Lung Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	27294002	LncRNA MALAT1 exerts oncogenic functions in lung adenocarcinoma by targeting miR-204.	In this study, we found that MALAT1 upregulation was associated with larger tumor size and lymph-node metastasis, and also correlated with shorter overall survival of lung adenocarcinoma patients. Furthermore, MALAT1 promotes EMT and metastasis of lung adenocarcinoma cells in vitro and in vivo. In particular, MALAT1 upregulated the expression of miR-204 target gene SLUG through competitively 'spongeing' miR-204. In summary we unveil a branch of the MALAT1/miR-204/SLUG pathway that regulates the progression of lung adenocarcinoma.	MI0000284	Am J Cancer Res 2016  6, 1099-107,  PMID:27294002
2510	LncRNA	MALAT1	miR-376a	TGFA	Saos2, Mg63, U2Os, Sw1353, Hfob	Osteosarcoma	Homo sapiens (human)	qPCR, Cell transfection, Western blot, Luciferase reporter assay, MTT assay etc.	27458156	MALAT1 promotes osteosarcoma development by targeting TGFA via MIR376A.	Here, we showed that MALAT1 was increased in human OS cell lines and tissues and promoted OS cell growth, while MALAT1 knockdown suppressed OS cell growth. TGFA expression was positively correlated with MALAT1 expression, and both were negatively correlated with MIR376A expression. There was a direct interaction between MIR376A and MALAT1 via a putative MIR376A binding site within the MALAT1 3'-untranslated region (3'-UTR). There was also a direct interaction between MIR376A and the TGFA 3'-UTR. Thus, MALAT1 may promote OS cell growth through inhibition of MIR376A, leading to increased expression of TGFA.	MI0000784	Oncotarget 2016 Aug 23 7, 54733-54743 doi:10.18632/oncotarget.10752 PMID:27458156
2511	LncRNA	MALAT1	miR-506	iASPP	Skov3, A2780, Ho8910, And Caov3	Ovarian Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, MTT assay etc.	28031721	Long noncoding RNA MALAT1-regulated microRNA 506 modulates ovarian cancer growth by targeting iASPP.	lncRNA-MALAT1 was specifically upregulated in ovarian cancer cell lines and promoted ovarian cancer-cell growth through targeting microRNA (miR)-506. Knockdown of MALAT1 inhibited the proliferation and DNA synthesis of human ovarian cancer cell in vitro. In addition, miR-506-dependent iASPP regulation was required in MALAT1-induced ovarian cancer-cell growth.	MI0003193	Onco Targets Ther 2017  10, 35-46 doi:10.2147/ott.S112686 PMID:28031721
2512	LncRNA	MALAT1	miR-22	MMP14	A375, Sk-Mel-5 And Sk-Mel-2	Melanoma	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Cell migration and invasion assay etc.	27564100	Long non-coding RNA MALAT1 acts as a competing endogenous RNA to promote malignant melanoma growth and metastasis by sponging miR-22.	In this study, the aberrant up-regulation of MALAT1 was detected in melanoma. We determined that MALAT1 promotes melanoma cells proliferation, invasion and migration by sponging miR-22. MiR-22 was decreased and acted as a tumor suppressor in melanoma, and MMP14 and Snail were the functional targets of miR-22. Furthermore, MALAT1 could modulate MMP14 and Snail by operating as a competing endogenous RNA (ceRNA) for miR-22.	MI0000078	Oncotarget 2016 Sep 27 7, 63901-63912 doi:10.18632/oncotarget.11564 PMID:27564100
2513	LncRNA	MALAT1	miR-25	RBM24	Nasopharyngeal Cancer tissues	Nasopharyngeal Cancer	Homo sapiens (human)	microarray, qPCR, Luciferase reporter assay, Cell migration and invasion assay etc.	27584791	RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma.	In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). The restoration of RBM24 expression suppressed NPC cellular proliferation, migration and invasion and impeded metastatic colonization in mouse models. Microarray analyses revealed that miR-25 expression was upregulated by RBM24 expression in NPC cells. Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells.	MI0000082	Cell Death Dis 2016 Sep 1 7, e2352 doi:10.1038/cddis.2016.252 PMID:27584791
2514	LncRNA	MALAT1	miR-1	KRAS	Breast Cancer tissues	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	26275461	Hsa-miR-1 suppresses breast cancer development by down-regulating K-ras and long non-coding RNA MALAT1	The effects of up-regulation of miR-1 were similar to that of silencing K-RAS and MALAT1 in breast cancer cells	MI0000651	Int J Biol Macromol 2015 Nov 81, 491-7 doi:10.1016/j.ijbiomac.2015.08.016 PMID:26275461
2515	LncRNA	MALAT1	miR-1	Slug	Breast Cancer tissues	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26676637	Reciprocal regulation of Hsa-miR-1 and long noncoding RNA MALAT1 promotes triple-negative breast cancer development	We reported that MALAT1 was upregulated in triple-negative breast cancer (TNBC) tissues. Knockdown of MALAT1 inhibited proliferation, motility, and increased apoptosis in vitro. In vivo study indicated that knockdown of MALAT1 inhibited tumor growth and metastasis. Patients with high MALAT1 expression had poorer overall survival time than those with low MALAT1 expression. In addition, our findings demonstrate a reciprocal negative control relationship between MALAT1 and miR-1: downregulation of MALAT1 increased expression of microRNA-1 (miR-1), while overexpression of miR-1 decreased MALAT1 expression. Slug was identified as a direct target of miR-1. 	MI0000651	Tumour Biol 2016 Jun 37, 7383-94 doi:10.1007/s13277-015-4605-6 PMID:26676637
2516	LncRNA	MALAT1	miR-9	ERa	Mg-63	Osteosarcoma	Homo sapiens (human)	qPCR, Cell proliferation assay etc.	25592968	17β-estradiol regulates cell proliferation, colony formation, migration, invasion and promotes apoptosis by upregulating miR-9 and thus degrades MALAT-1 in osteosarcoma cell MG-63 in an estrogen receptor-independent manner	Consistent with a previous study, high dose of E2 treatment dramatically downregulated expressing level of long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT-1). The observation of upregulation of miR-9 after a high dose of E2 treatment indicated the cause of MALAT-1 reduction. Downregulation of MALAT-1 promoted the combination of SFPQ/PTBP2 complex. Furthermore, the abolishment of the effects on these physiological processes caused by ectopic expression of miR-9 ASOs suggested the necessity of miR-9 in MALAT-1 regulation.	MI0000466	Biochem Biophys Res Commun 2015 Feb 20 457, 500-6 doi:10.1016/j.bbrc.2014.12.114 PMID:25592968
2517	LncRNA	MALAT1	miR-200c	ZEB2	ACHN, 786-O, SN12-PM6 and HK-2	Renal Cancer	Homo sapiens (human)	qPCR etc.	26461224	LncRNA MALAT1 functions as a competing endogenous RNA to regulate ZEB2 expression by sponging miR-200s in clear cell kidney carcinoma	We found that MALAT1 exist a higher fold change (Tumor/Normal) in clear cell kidney carcinoma (KIRC) from The Cancer Genome Atlas (TCGA) Data Portal and a negative correlation with miR-200s family. We further demonstrated MALAT1 promote KIRC proliferation and metastasis through sponging miR-200s in vitro and in vivo. In addition, miR-200c can partly reverse the MALAT1's stimulation on proliferation and metastasis in KIRC. In summary we unveil a branch of the MALAT1/miR-200s/ZEB2 pathway that regulates the progression of KIRC.	MI0000650	Oncotarget 2015 Nov 10 6, 38005-15 doi:10.18632/oncotarget.5357 PMID:26461224
2518	LncRNA	MALAT1	miR-140	CCAAT	Hcmec/D3, Ecs	Glioma	Homo sapiens (human)	qPCR, Western blot, RIP, ChIP, Luciferase reporter assay etc.	26619802	Knockdown of long non-coding RNA MALAT1 increases the blood-tumor barrier permeability by up-regulating miR-140	Our results proved that MALAT1 expression was up-regulated in brain microvessels of human glioma and glioma endothelial cells (GECs) which were obtained by co-culturing endothelial cells with glioma cells. Functionally, knockdown of MALAT1 resulted in an impairment and increased the permeability of BTB as well as decreased the expression of ZO-1, occludin and claudin-5 in GECs. Further, there was reciprocal repression between MALAT1 and miR-140, and miR-140 mediated the effects that MALAT1 knockdown exerted. Mechanistic investigations defined that nuclear factor YA (NFYA), a CCAAT box-binding transcription factor, was a direct and functional downstream target of miR-140, which was involved in the MALAT1 knockdown induced regulation of BTB function. Furthermore, NFYA could up-regulate the promoter activities and bind to the promoters of ZO-1, occludin and claudin-5 in GECs.	MI0000456	Biochim Biophys Acta 2016 Feb 1859, 324-38 doi:10.1016/j.bbagrm.2015.11.008 PMID:26619802
2519	LncRNA	MALAT1	miR-145	Ago2	Hela, Caski	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, RIP, Flow cytometry assay, RNA pull-down assay etc.	26311052	Long non-coding RNA MALAT1 modulates radiosensitivity of HR-HPV+ cervical cancer via sponging miR-145.	We found MALAT1 expression was significantly higher in radioresistant than in radiosensitive cancer cases. In addition, MALAT1 and miR-145 expression inversely changed in response to irradiation in HR-HPV+ cervical cancer cells. We found CaSki and Hela cells with knockdown of MALAT1 had significantly lower colony formation, higher ratio of G2/M phase block and higher ratio of cell apoptosis. Next, we confirmed that miR-145 and MALAT1 were in the same Ago2 complex and there was a reciprocal repression between them. Then, we explored the function of MALAT1-miR-145 in radiosensitivity of cervical cancers cells and demonstrated that si-MALAT1 and miR-145 had some level of synergic effect in reducing cancer cell colony formation, cell cycle regulation, and inducing apoptosis.	MI0000461	Tumour Biol 2016 Feb 37, 1683-91 doi:10.1007/s13277-015-3946-5 PMID:26311052
2520	LncRNA	MALAT1	miR-124	RBG2	Hela, Caski, Siha	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, Flow cytometry assay etc.	26242259	MALAT1-miR-124-RBG2 axis is involved in growth and invasion of HR-HPV-positive cervical cancer cells.	Findings of this study confirmed higher MALAT1 expression in HR-HPV (+) cervical cancer. Knockdown of endogenous MALAT1 significantly reduced cell growth rate and invasion and increased cell apoptosis of Hela and siHa cells. Besides, knockdown of MALAT1 increased the expression of miRNA-124, while ectopic expression of miR-124 decreased MALAT1 expression. MALAT1 can indirectly modulate GRB2 expression via competing miR-124. Knockdown of GRB2 reduced cell invasion and increased cell apoptosis. In conclusion, MALAT1 can promote HR-HPV (+) cancer cell growth and invasion at least partially through the MALAT1-miR-124-RBG2 axis.	MI0000443	Tumour Biol 2016 Jan 37, 633-40 doi:10.1007/s13277-015-3732-4 PMID:26242259
2521	LncRNA	MALAT1	miR-1	slug	5-8F, Cne-2, Hone-1, Sune-1, Npe Cell Line 	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Western blot, RIP, Luciferase reporter assay etc.	26482776	The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma.	We found that MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity. Furthermore, we found that there was reciprocal repression between MALAT1 and miR-1, and slug was identified as a downstream target of miR-1. Taking these observations into consideration, we proposed that MALAT1 regulated CSC activity and radioresistance by modulating miR-1/slug axis, which indicated that MALAT1 could act as a therapeutic target for NPC patients	MI0000651	Tumour Biol 2016 Mar 37, 4025-33 doi:10.1007/s13277-015-4227-z PMID:26482776
2522	LncRNA	MALAT1	miR-205	c-Fos	A-498	Renal Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25600645	Long noncoding RNA MALAT1 promotes aggressive renal cell carcinoma through Ezh2 and interacts with miR-205.	We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	MI0000285	Cancer Res 2015 Apr 1 75, 1322-31 doi:10.1158/0008-5472.Can-14-2931 PMID:25600645
2523	LncRNA	MALAT1	miR-205	EZH2	A-498	Renal Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25600645	Long noncoding RNA MALAT1 promotes aggressive renal cell carcinoma through Ezh2 and interacts with miR-205.	We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. Reciprocal interaction between MALAT1 and miR-205 was also observed.	MI0000285	Cancer Res 2015 Apr 1 75, 1322-31 doi:10.1158/0008-5472.Can-14-2931 PMID:25600645
2524	LncRNA	MALAT1	miR-101	B-MYB	Kyse30, Kyse150, Kyse450	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25538231	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217inhibits proliferation, migration and invasion of esophageal squamous cell carcinoma cells.	In this study, we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated upregulation of P21 and P27 expression and the inhibition of B-MYB expression.	MI0000103	J Biol Chem 2015 Feb 13 290, 3925-35 doi:10.1074/jbc.M114.596866 PMID:25538231
2525	LncRNA	MALAT1	miR-217	B-MYB	Kyse30, Kyse150, Kyse450	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	25538231	Silencing of long noncoding RNA MALAT1 by miR-101 and miR-217inhibits proliferation, migration and invasion of esophageal squamous cell carcinoma cells.	In this study, we provide first evidences that a posttranscriptional regulation mechanism of MALAT1 by miR-101 and miR-217 exists in ESCC cells. This posttranscriptional silencing of MALAT1 could significantly suppress the proliferation of ESCC cells through the arrest of G2/M cell cycle, which may be due to MALAT1-mediated upregulation of P21 and P27 expression and the inhibition of B-MYB expression.	MI0000293	J Biol Chem 2015 Feb 13 290, 3925-35 doi:10.1074/jbc.M114.596866 PMID:25538231
2526	LncRNA	MALAT1	miR-125b	SIRT7	T24, 5737, Sv-Huc-1, Hek 293T	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, ChIP, Luciferase reporter assay, Cell proliferation assay etc.	24512851	Hsa-miR-125b suppresses bladder cancer development by down-regulating oncogene SIRT7 and oncogenic long noncoding RNA MALAT1.	Hsa-miR-125b was down-regulated in bladder cancer compared with matched normal urothelium. Both SIRT7 and MALAT1 were up-regulated in bladder cancer compared with matched normal urothelium. Upregulation of hsa-miR-125b or downregulation of SIRT7 inhibited proliferation, motility and increased apoptosis.	MI0000446	FEBS Lett 2013 Oct 25, 10.1016/j.febslet.2013.10.023 doi:10.1016/j.febslet.2013.10.023 PMID:24512851
2527	LncRNA	MEG3	miR-1297	PTEN	Nccit	Testicular Germ Cell Tumor	Homo sapiens (human)	qPCR, RNAi, Western blot, Luciferase reporter assay, ISH, MTT assay etc.	27158395	Crosstalk between Meg3 and miR-1297 regulates growth of testicular germ cell tumor through PTEN/PI3K/AKT pathway.	Compared to paired adjacent non-tumor tissue (NT), and found that Meg3 levels were significantly decreased and miR-1297 levels were unchanged in TGCT. Luciferase report assay showed that Meg3 overexpression abolished the effects of miR-1297 on 3'-UTR of PTEN mRNA, possibly through competitive binding, which was supported by double fluorescent in situ hybridization showing co-localization of intracellular Meg3 and miR-1297 signals in TGCT cells. Moreover, Meg3 overexpression abolished the inhibitory effects of miR-1297 on PTEN, resulting in deactivation of Akt and decreases in cell growth.	MI0006358	Am J Transl Res 2016  8, 1091-9,  PMID:27158395
2528	LncRNA	MEG3	miR-29a	DNMT1	Hepg2 And Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, MTT assay etc.	26321746	Dendrosomal curcumin increases expression of the long non-coding RNA gene MEG3 via up-regulation of epi-miRs in hepatocellular cancer.	In result we found that the DNC dependent overexpression of miR-29a and miR-185 can down-regulate the expression of DNMT1, 3A and 3B and subsequently overexpresses MEG3.	MI0000087	Phytomedicine 2015 Sep 15 22, 961-7 doi:10.1016/j.phymed.2015.05.071 PMID:26321746
2529	LncRNA	MEG3	miR-185	DNMT1	Hepg2 And Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, MTT assay etc.	26321746	Dendrosomal curcumin increases expression of the long non-coding RNA gene MEG3 via up-regulation of epi-miRs in hepatocellular cancer.	In result we found that the DNC dependent overexpression of miR-29a and miR-185 can down-regulate the expression of DNMT1, 3A and 3B and subsequently overexpresses MEG3.	MI0000482	Phytomedicine 2015 Sep 15 22, 961-7 doi:10.1016/j.phymed.2015.05.071 PMID:26321746
2530	LncRNA	MEG3	miR-21	p53	Hela, Caski	Cervical Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	26574780	Long noncoding RNA MEG3 is downregulated in cervical cancer and affects cell proliferation and apoptosis by regulating miR-21.	We observed that MEG3 was downregulated in cervical cancer tissues, compared to the adjacent normal tissues, and was negatively related with FIGO stages, tumor size, lymphatic metastasis, HR-HPV infection and the expression of homo sapiens microRNA-21 (miR-21). Furthermore, we focused on the function and molecular mechanism of MEG3, finding that overexpression of MEG3 reduced the level of miR-21-5p expression, causing inhibition of proliferation and increased apoptosis in cervical cancer cells. In summary, our findings indicate that MEG3 function as a tumor suppressor by regulating miR-21-5p, resulting in the inhibition of tumor growth in cervical cancer.	MI0000077	Cancer Biol Ther 2016  17, 104-13 doi:10.1080/15384047.2015.1108496 PMID:26574780
2531	LncRNA	MEG3	miR-141	E2F3	Ges-1	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot etc.	26233544	MiR-141 Inhibits Gastric Cancer Proliferation by Interacting with Long Noncoding RNA MEG3 and Down-Regulating E2F3 Expression.	We found that expression of both miR-141 and MEG3 was significantly reduced in GC compared with levels in matched nonmalignant tissues. Positive correlation between miR-141 and MEG3 was found in both tumor tissues and control tissues. Furthermore, the over-expression of either miR-141 or MEG3 in 7901 and MKN45 cells inhibited cell proliferation and cell cycle progression and promoted cell apoptosis. E2F3 was identified as a target of miR-141, and its inhibition significantly reduced MEG3 expression. E2F3 over-expression partly reversed the changes caused by transfection of miR-141 mimic, and inhibition of miR-141 or MEG3 overrides MEG3- or miR-141-induced modulation of cell growth in GC.	MI0000457	Dig Dis Sci 2015 Nov 60, 3271-82 doi:10.1007/s10620-015-3782-x PMID:26233544
2532	LncRNA	MEG3	miR-181	BCL-2	Mgc-803, Hgc-27, Mkn-45, Sgc-7901, Bgc-823, Ags	Gastric Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay, RNA pull-down assay etc.	26253106	Long non-coding RNA MEG3 functions as a competing endogenous RNA to regulate gastric cancer progression.	MEG3 is decreased in GC patients and cell lines, and its expression was associated with metastatic GC. Furthermore, ectopic expression of MEG3 in HGC-27 and MGC-803 cells inhibited cell proliferation, migration, invasion, and promoted cell apoptosis, which might be due to MEG3 sequestering oncogenic miR-181 s in GC cells. Furthermore, MEG3 could up-regulated Bcl-2 via its competing endogenous RNA (ceRNA) activity on miR-181a.	MI0000223	J Exp Clin Cancer Res 2015 Aug 8 34, 79 doi:10.1186/s13046-015-0197-7 PMID:26253106
2533	LncRNA	MEG3	miR-148a	DNMT1	Sgc-7901, Bgc-823, Ges-1 Etc.	Gastric Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot etc.	24515776	MiR-148a regulates MEG3 in gastric cancer by targeting DNA methyltransferase 1.	We examined the expression of MEG3 in 52 gastric cancer samples using quantitative qPCR and found the down-regulation of MEG3 in both gastric cancer tissues and cell lines. The positive correlation of MEG3 and miR-148a was further confirmed in SGC-7901 and BGC-823 gastric cancer cell lines. Hypermethylation of MEG3 differentially methylated regions was identified by methylation-specific PCR, and MEG3 expression was increased with the inhibition of methylation with siRNA to DNMT-1 in gastric cancer cells. In addition, transfection of MEG3 siRNA into gastric cancer cells diminished the suppression of proliferation induced by overexpression of miR-148a.	MI0000253	Med Oncol 2014 Mar 31, 879 doi:10.1007/s12032-014-0879-6 PMID:24515776
2534	LncRNA	MEG3	miR-26a	DNMT3B	Scc-15, Cal27	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	microarray, MSP-PCR, RNAi, Western blot etc.	24343426	Expression, regulation and roles of miR-26a and MEG3 in tongue squamous cell carcinoma.	We report here that miR-26a and lncRNA MEG3 gene expression were both strongly reduced in TSCC compared with levels in matched nonmalignant tissues, and combined low expression levels of both miR-26a and MEG3 emerged as an independent prognostic factor for poor clinical outcome in TSCC patients. 	MI0000083	Int J Cancer 2014 Nov 15 135, 2282-93 doi:10.1002/ijc.28667 PMID:24343426
2535	LncRNA	MEG3	miR-29	DNMT1	HCC cell lines and human HCC tissue	Hepatocellular Carcinoma	Homo sapiens (human)	microarray, qPCR etc.	21625215	microRNA-29 can regulate expression of the long non-coding RNA gene MEG3 in hepatocellular cancer.	RNA in situ hybridization showed intense cytoplasmic expression of MEG3 in non-neoplastic liver with absent or very weak expression in HCC tissues. Enforced expression of MEG3 in HCC cells significantly decreased both anchorage-dependent and -independent cell growth, and induced apoptosis. We confirmed a similar miR-29a-dependent modulation of DNMT protein expression in HCC cells.	MI0000087	Oncogene 2011 Nov 24 30, 4750-6 doi:10.1038/onc.2011.193 PMID:21625215
2536	LncRNA	GTL2	miR-29	DNMT1	HCC cell lines and human HCC tissue	Hepatocellular Carcinoma	Mus musculus (mouse)	microarray, qPCR etc.	21625215	microRNA-29 can regulate expression of the long non-coding RNA gene MEG3 in hepatocellular cancer.	The expression of miR-29a in several HCC cell lines and human HCC tissues correlated with expression of MEG3 with a P-value of 0.04. Over-expression of miR-29a in HCC cells increased MEG3 expression. The effects of miR-29a on MEG3 expression were further evaluated in vivo using genetically engineered mice with a hepatocyte-specific knockout of miR-29 a/b1. The murine analog of MEG3, named GTL2 is located on chromosome 12. Compared with the expression in liver tissues in wild-type mice, GTL2 expression was remarkably reduced in liver tissues from miR-29 KO mice under basal conditions. All together these studies suggest that miR-29 may indirectly modulate MEG3/GTL2 expression by acting on the methylation machinery.	MI0000087	Oncogene 2011 Nov 24 30, 4750-6 doi:10.1038/onc.2011.193 PMID:21625215
2537	LncRNA	MIF	miR-586	c-Myc	Hela	Cervical Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27317567	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw7-mediated c-Myc degradation	In this study, we demonstrate that lncRNA㎝IF (Myc inhibitory factor), which is transcribed by c㎝yc, is able to reduce c㎝yc expression. Mechanistically, lncRNA㎝IF competes with coding mRNA Fbxw7 for miR586 and relieves the inhibitory effect of miR586 on Fbxw7, thereby leading to increased Fbxw7 expression and decreased c㎝yc level.	MI0003594	EMBO Rep 2016 Aug 17, 1204-20 doi:10.15252/embr.201642067 PMID:27317567
2538	LncRNA	MIF	miR-586	c-Myc	A549	Lung Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27317567	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw8-mediated c-Myc degradation	In this study, we demonstrate that lncRNA㎝IF (Myc inhibitory factor), which is transcribed by c㎝yc, is able to reduce c㎝yc expression. Mechanistically, lncRNA㎝IF competes with coding mRNA Fbxw7 for miR586 and relieves the inhibitory effect of miR586 on Fbxw7, thereby leading to increased Fbxw8 expression and decreased c㎝yc level.	MI0003594	EMBO Rep 2016 Aug 17, 1204-20 doi:10.15252/embr.201642067 PMID:27317567
2539	LncRNA	MIF	miR-586	c-Myc	H1299	Lung Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27317567	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw9-mediated c-Myc degradation	In this study, we demonstrate that lncRNA㎝IF (Myc inhibitory factor), which is transcribed by c㎝yc, is able to reduce c㎝yc expression. Mechanistically, lncRNA㎝IF competes with coding mRNA Fbxw7 for miR586 and relieves the inhibitory effect of miR586 on Fbxw7, thereby leading to increased Fbxw9 expression and decreased c㎝yc level.	MI0003594	EMBO Rep 2016 Aug 17, 1204-20 doi:10.15252/embr.201642067 PMID:27317567
2540	LncRNA	MIF	miR-586	c-Myc	Hct116	Colon Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27317567	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw10-mediated c-Myc degradation	In this study, we demonstrate that lncRNA㎝IF (Myc inhibitory factor), which is transcribed by c㎝yc, is able to reduce c㎝yc expression. Mechanistically, lncRNA㎝IF competes with coding mRNA Fbxw7 for miR586 and relieves the inhibitory effect of miR586 on Fbxw7, thereby leading to increased Fbxw10 expression and decreased c㎝yc level.	MI0003594	EMBO Rep 2016 Aug 17, 1204-20 doi:10.15252/embr.201642067 PMID:27317567
2541	LncRNA	MIF	miR-586	c-Myc	Mcf7	Breast Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	27317567	LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw11-mediated c-Myc degradation	In this study, we demonstrate that lncRNA㎝IF (Myc inhibitory factor), which is transcribed by c㎝yc, is able to reduce c㎝yc expression. Mechanistically, lncRNA㎝IF competes with coding mRNA Fbxw7 for miR586 and relieves the inhibitory effect of miR586 on Fbxw7, thereby leading to increased Fbxw11 expression and decreased c㎝yc level.	MI0003594	EMBO Rep 2016 Aug 17, 1204-20 doi:10.15252/embr.201642067 PMID:27317567
2542	LncRNA	MINCR	miR-26a-5p	EZH2	Gallbladder Cancer tissues	Gallbladder Cancer	Homo sapiens (human)	qPCR, RIP, Dual-luciferase reporter assay etc.	27345740	Long non-coding RNA MINCR promotes gallbladder cancer progression through stimulating EZH2 expression.	High MINCR expression levels in GBC were positively associated with tumor volume and lymph node metastasis and were negatively correlated with overall survival (OS). Upregulation of MINCR and enhancer of zeste homolog 2 (EZH2) in GBC coincided with the downregulation of miR-26a-5p in GBC. Mechanistically, MINCR/miR-26a-5p/EZH2 axis was found to be involved in cell proliferation, cell invasive and apoptosis in GBC cells. Moreover, knockdown of MINCR suppressed cell proliferation, decreased S-phase cell numbers, increased cell apoptosis, and inhibited cell invasion by inhibiting the epithelial-mesenchymal transition (EMT) phenomenon in GBC cells.	MIMAT0000082	Cancer Lett 2016 Sep 28 380, 122-33 doi:10.1016/j.canlet.2016.06.019 PMID:27345740
2543	LncRNA	MIR155HG	miR-155	BIC	Ramos, Jy25, Cb33, U266, Jurkat, K562, Hl60 Etc.	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qPCR, Northern blot etc.	15738415	Accumulation of miR-155 and BIC RNA in human B cell lymphomas.	Relative to the control B cells, BIC RNA levels were elevated from 2- to 10-fold in DLBCL cells, with one sample showing an increase of >20-fold. 	MI0000681	Proc Natl Acad Sci U S A 2005 Mar 8 102, 3627-32 doi:10.1073/pnas.0500613102 PMID:15738415
2544	LncRNA	MIR31HG	miR-193b	CCND1	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2545	LncRNA	MIR31HG	miR-193b	NT5E	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2546	LncRNA	MIR31HG	miR-193b	PLAU	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2547	LncRNA	MIR31HG	miR-193b	STARD7	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2548	LncRNA	MIR31HG	miR-193b	STMN1	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2549	LncRNA	MIR31HG	miR-193b	YWHAZ	Aspc-1, Panc-1, Cfpac-1, Hs 766T, Sw 1990, Mia Paca-2, And Bxpc-3	Pancreatic Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RIP, Dual-luciferase reporter assay, ISH etc.	26549028	Long noncoding RNA MIR31HG exhibits oncogenic property in pancreatic ductal adenocarcinoma and is negatively regulated by miR-193b.	In this study, we discovered that lncRNA MIR31HG is markedly upregulated in PDAC. Knockdown of MIR31HG significantly suppressed PDAC cell growth, induced apoptosis and G1/S arrest, and inhibited invasion, whereas enhanced expression of MIR31HG had the opposite effects. Inhibition of miR-193b expression significantly upregulated the MIR31HG level, while overexpression of miR-193b suppressed MIR31HG's expression and function, suggesting that MIR31HG is negatively regulated by miR-193b.	MI0003137	Oncogene 2016 Jul 14 35, 3647-57 doi:10.1038/onc.2015.430 PMID:26549028
2550	LncRNA	NEAT1	miR-98-5p	CTR1	A549, H460, H1299	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Dual-luciferase reporter assay etc.	27270317	NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells.	In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it.	MIMAT0000096	Oncotarget 2016 Jul 12 7, 43337-43351 doi:10.18632/oncotarget.9712 PMID:27270317
2551	LncRNA	NEAT1	miR-214	NA	Cbms, Tams, Bmdms, Raw 264.7	Thyroid Cancer	Homo sapiens (human)	qPCR, RNAi, Western blot, RNA pull-down assay, Cell migration and invasion assay etc.	28000845	Long non-coding RNA NEAT1 promotes malignant progression of thyroid carcinoma by regulating miRNA-214.	NEAT1 was highly expressed in patients with thyroid cancer. NEAT1 knockout inhibited thyroid cancer cell survival, migration and invasion, along with reduced β-catenin (a direct target of miRNA-214) protein expression. Furthermore, NEAT1 significantly accelerated thyroid cancer cell growth and metastasis in vitro and increased tumor size in vivo. Upregulation of NEAT1 decreased the expression of miRNA-214, presenting a reciprocal repression correlation.	MI0000290	Int J Oncol 2017 Feb 50, 708-716 doi:10.3892/ijo.2016.3803 PMID:28000845
2552	LncRNA	NEAT1	miR-204	ZEB1	Cne-2, Hone-1, 5-8F, Sune-1 Etc.	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	27020592	The long non-coding RNA NEAT1 regulates epithelial to mesenchymal transition and radioresistance in through miR-204/ZEB1 axis in nasopharyngeal carcinoma	We found that lncRNA NEAT1 was significantly upregulated in NPC cell lines and tissues. Knockdown of NEAT1 could sensitize NPC cells to radiation in vitro. Further investigation found that NEAT1 regulated radioresistance by modulating EMT phenotype. Furthermore, we found that there was reciprocal repression between NEAT1 and miR-204. ZEB1 was identified as a downstream target of miR-204 and NEAT1 upregulated ZEB1 expression by negatively regulating miR-204 expression.	MI0000284	Tumour Biol 2016 Sep 37, 11733-11741 doi:10.1007/s13277-015-4773-4 PMID:27020592
2553	LncRNA	DSCR8	miR-485-5p	FZD7	MHCC-97 L, HepG2, Hep3B, Huh7, and SMMC-7721	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30154476	Long non-coding RNA DSCR8 acts as a molecular sponge for miR-485-5p to activate Wnt/β-catenin signal pathway in hepatocellular carcinoma	 Luciferase reporter gene assay, RIP assay, and rescue experiments demonstrated that DSCR8 functioned as a competing endogenous RNA (ceRNA) by sponging miR-485-5p in HCC cells. Furthermore, gain- and loss-of-function studies showed that miR-485-5p activated Wnt/β-catenin signal pathway by targeting Frizzled-7 (FZD7). Moreover, DSCR8 activated Wnt/β-catenin signal pathway to promote HCC progression by DSCR8/miR-485-5p/FZD7 axis. Statistical analysis revealed that DSCR8 and miR-485-5p were closely related to some malignant clinicopathological features and 5-year survival rates of HCC patients.	MIMAT0002175	Cell Death Dis 2018 Aug 28 9, 851 doi:10.1038/s41419-018-0937-7 PMID:30154476
2554	LncRNA	RP11-523G9.3	miR-19b-3p	RUNX2	hMSCs	Ossification Of The Ligamentum Flavum	Homo sapiens (human)	qPCR	30161026	A Transcriptome-Level Study Identifies Changing Expression Profiles for Ossification of the Ligamentum Flavum of the Spine	Given the evidence that the deregulated lncRNAs ENST00000608133 and ENST00000599584, which were actually targets of miR-19b-3p, are related to ossification by regulation, at least, of RUNX2, which is also regulated by miR-19b-3p and circ_0050139, we conclude that the deregulated miRNAs, lncRNAs, and circRNAs regulate ossification-associated genes. Furthermore, we confirmed the co-regulation with experiments showing that overexpression of miR-19b-3p downregulates the levels of ENST00000608133, ENST00000599584, and circ_0050139.	MIMAT0000074	Mol Ther Nucleic Acids 2018 Sep 7 12, 872-883 doi:10.1016/j.omtn.2018.07.018 PMID:30161026
2555	LncRNA	CTB-180A7.6	miR-19b-3p	RUNX2	hMSCs	Ossification Of The Ligamentum Flavum	Homo sapiens (human)	qPCR	30161026	A Transcriptome-Level Study Identifies Changing Expression Profiles for Ossification of the Ligamentum Flavum of the Spine	Given the evidence that the deregulated lncRNAs ENST00000608133 and ENST00000599584, which were actually targets of miR-19b-3p, are related to ossification by regulation, at least, of RUNX2, which is also regulated by miR-19b-3p and circ_0050139, we conclude that the deregulated miRNAs, lncRNAs, and circRNAs regulate ossification-associated genes. Furthermore, we confirmed the co-regulation with experiments showing that overexpression of miR-19b-3p downregulates the levels of ENST00000608133, ENST00000599584, and circ_0050139.	MIMAT0000074	Mol Ther Nucleic Acids 2018 Sep 7 12, 872-883 doi:10.1016/j.omtn.2018.07.018 PMID:30161026
2556	Circular RNA	hsa_circ_0050139	miR-19b-3p	RUNX2	hMSCs	Ossification Of The Ligamentum Flavum	Homo sapiens (human)	qPCR	30161026	A Transcriptome-Level Study Identifies Changing Expression Profiles for Ossification of the Ligamentum Flavum of the Spine	Given the evidence that the deregulated lncRNAs ENST00000608133 and ENST00000599584, which were actually targets of miR-19b-3p, are related to ossification by regulation, at least, of RUNX2, which is also regulated by miR-19b-3p and circ_0050139, we conclude that the deregulated miRNAs, lncRNAs, and circRNAs regulate ossification-associated genes. Furthermore, we confirmed the co-regulation with experiments showing that overexpression of miR-19b-3p downregulates the levels of ENST00000608133, ENST00000599584, and circ_0050139.	MIMAT0000074	Mol Ther Nucleic Acids 2018 Sep 7 12, 872-883 doi:10.1016/j.omtn.2018.07.018 PMID:30161026
2557	LncRNA	NEAT1	miR-506	ZEB1	OVCAR3, A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30154460	Long noncoding RNA NEAT1, regulated by LIN28B, promotes cell proliferation and migration through sponging miR-506 in high-grade serous ovarian cancer.	Gene expression profile data and dual luciferase reporter assay results demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for miR-506 to promote cell proliferation and migration. Western blotting was used to detect the levels of miR-506 target genes, including ZEB1, Vimentin, and Snail2, following miR-506 overexpression in A2780 cells. The levels of miR-506 target genes were detected by Western blotting when NEAT1 was downregulated in A2780 and OVCAR3 cells.	MI0003193	Cell Death Dis 2018 Aug 28 9, 861 doi:10.1038/s41419-018-0908-z PMID:30154460
2558	LncRNA	NEAT1	miR-506	Vimentin	OVCAR3, A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30154460	Long noncoding RNA NEAT1, regulated by LIN28B, promotes cell proliferation and migration through sponging miR-506 in high-grade serous ovarian cancer.	Gene expression profile data and dual luciferase reporter assay results demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for miR-506 to promote cell proliferation and migration. Western blotting was used to detect the levels of miR-506 target genes, including ZEB1, Vimentin, and Snail2, following miR-506 overexpression in A2780 cells. The levels of miR-506 target genes were detected by Western blotting when NEAT1 was downregulated in A2780 and OVCAR3 cells.	MI0003193	Cell Death Dis 2018 Aug 28 9, 861 doi:10.1038/s41419-018-0908-z PMID:30154460
2559	LncRNA	NEAT1	miR-506	Snail2	OVCAR3, A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30154460	Long noncoding RNA NEAT1, regulated by LIN28B, promotes cell proliferation and migration through sponging miR-506 in high-grade serous ovarian cancer.	Gene expression profile data and dual luciferase reporter assay results demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for miR-506 to promote cell proliferation and migration. Western blotting was used to detect the levels of miR-506 target genes, including ZEB1, Vimentin, and Snail2, following miR-506 overexpression in A2780 cells. The levels of miR-506 target genes were detected by Western blotting when NEAT1 was downregulated in A2780 and OVCAR3 cells.	MI0003193	Cell Death Dis 2018 Aug 28 9, 861 doi:10.1038/s41419-018-0908-z PMID:30154460
2560	LncRNA	RP11-79H23.3	miR-107	PTEN	EJ, T24, and BIU87	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30149689	LncRNA RP11-79H23.3 Functions as a Competing Endogenous RNA to Regulate PTEN Expression through Sponging hsa-miR-107 in the Development of Bladder Cancer.	we identified that RP11-79H23.3 could directly bind to miR-107 and abolish the suppressive effect on target gene PTEN, which leads to inactivation of the PI3K/Akt signaling pathway. Taken together, we first demonstrated that RP11-79H23.3 might suppress the pathogenesis and development of BC by acting as a sponge for miR-107 to increase PTEN expression.	MI0000114	Int J Mol Sci 2018 Aug 26 19 doi:10.3390/ijms19092531 PMID:30149689
2561	LncRNA	LINC01133	miR-106a-3p	APC	SUN-216, BGC-823, AGS, BGC-803, NUGC4, MKN74, MKN45, SGC-7901, and HGC-27	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30134915	LINC01133 as ceRNA inhibits gastric cancer progression by sponging miR-106a-3p to regulate APC expression and the Wnt/β-catenin pathway.	Our findings suggest that reduced expression of LINC01133 is associated with aggressive tumor phenotypes and poor patient outcomes in GC. LINC01133 inhibits GC progression and metastasis by acting as a ceRNA for miR-106a-3p to regulate APC expression and the Wnt/β-catenin pathway, suggesting that LINC01133 may serve as a potential prognostic biomarker and anti-metastatic therapeutic target for GC.	MIMAT0004517	Mol Cancer 2018 Aug 22 17, 126 doi:10.1186/s12943-018-0874-1 PMID:30134915
2562	LncRNA	NONhsaG007671	miR-199a-3p	Hopx	cardiac tissues	Myocardial Infarction	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30125571	Loss of long non-coding RNA CRRL promotes cardiomyocyte regeneration and improves cardiac repair by functioning as a competing endogenous RNA.	Through loss-of-function approaches, we found that CRRL knockdown promotes neonatal rat CM proliferation both in vivo and in vitro. Furthermore, we demonstrated that CRRL acts as a competing endogenous RNA (ceRNA) by directly binding to miR-199a-3p and thereby increasing the expression of Hopx, a target gene of miR-199a-3p and a critical negative regulatory factor of CM proliferation. Thus, CRRL suppresses cardiomyocyte regeneration by directly binding to miR-199a-3p, indicating that loss of CRRL facilitates myocardial regeneration and may be a new potential therapeutic strategy for heart failure.	MIMAT0000232	J Mol Cell Cardiol 2018 Sep 122, 152-164 doi:10.1016/j.yjmcc.2018.08.013 PMID:30125571
2563	LncRNA	KRAL	miR-141	Keap1	HepG2 and HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30119680	lncRNA KRAL reverses 5-fluorouracil resistance in hepatocellular carcinoma cells by acting as a ceRNA against miR-141.	The quantitative analysis indicated that KRAL and Keap1 were significantly decreased and that Nrf2 was increased in HepG2/5-FU and SMMC-7721/5-FU cells compared with the corresponding expression levels in the respective parental cells. Overexpression of KRAL increased Keap1 expression, and inactivating the Nrf2-dependent antioxidant pathway could reverse the resistance of HepG2/5-FU and SMMC-7721/5-FU cells to 5-FU. Moreover, KRAL functioned as a competitive endogenous RNA (ceRNA) by effectively binding to the common miR-141 and then restoring Keap1 expression. These findings demonstrated that KRAL is an important regulator of Keap1; furthermore, the ceRNA network involving KRAL may serve as a treatment strategy against 5-FU resistance in hepatocellular carcinoma cells.	MI0000457	Cell Commun Signal 2018 Aug 17 16, 47 doi:10.1186/s12964-018-0260-z PMID:30119680
2564	LncRNA	SNHG16	miR-15a	TLR4	RAW264.7	Neonatal Sepsis	Homo sapiens (human)	Rescue assays	30119242	LncRNA SNHG16 reverses the effects of miR-15a/16 on LPS-induced inflammatory pathway.	NHG16 was uncovered to significantly downregulated both miR-15a and miR-16. According to the result of subcellular fractionation assay, SNHG16 was mainly located in the cytoplasm of RAW264.7 cell, indicating the potential ceRNA role of SNHG16. Mechanism investigations revealed that SNHG16 could act as a ceRNA to upregulate TLR4 which is the target mRNA of miR-15a/16 cluster. At last, rescue assays demonstrated that SNHG16 reversed the effects of miR-15a/16 on LPS-induced inflammatory pathway.	MI0000069	Biomed Pharmacother 2018 Oct 106, 1661-1667 doi:10.1016/j.biopha.2018.07.105 PMID:30119242
2565	LncRNA	SNHG16	miR-16	TLR4	RAW264.7	Neonatal Sepsis	Homo sapiens (human)	rescue assays	30119242	LncRNA SNHG16 reverses the effects of miR-15a/16 on LPS-induced inflammatory pathway.	NHG16 was uncovered to significantly downregulated both miR-15a and miR-16. According to the result of subcellular fractionation assay, SNHG16 was mainly located in the cytoplasm of RAW264.7 cell, indicating the potential ceRNA role of SNHG16. Mechanism investigations revealed that SNHG16 could act as a ceRNA to upregulate TLR4 which is the target mRNA of miR-15a/16 cluster. At last, rescue assays demonstrated that SNHG16 reversed the effects of miR-15a/16 on LPS-induced inflammatory pathway.	MI0000070	Biomed Pharmacother 2018 Oct 106, 1661-1667 doi:10.1016/j.biopha.2018.07.105 PMID:30119242
2566	LncRNA	MEG3	miR-141	PDCD4	HT29/OXA and HCT116/OXA cells	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30119236	Overexpression of MEG3 sensitizes colorectal cancer cells to oxaliplatin through regulation of miR-141/PDCD4 axis.	MEG3 was down-regulated in oxaliplatin-resistant CRC tissues and cell lines. Low MEG3 expression was correlated with poor prognosis of CRC patients. Overexpression of MEG3 improved oxaliplatin sensitivity of HT29/OXA and HCT116/OXA cells. MEG3 suppressed miR-141 expression in HCT116/OXA cells. Moreover, MEG3 elevated PDCD4 expression through targeting miR-141, acting as a competing endogenous RNA (ceRNA). miR-141 inhibition or PDCD4 up-regulation could mimic the functional role in oxaliplatin resistance, which was counteracted by overexpression of MEG3.	MI0000457	Biomed Pharmacother 2018 Oct 106, 1607-1615 doi:10.1016/j.biopha.2018.07.131 PMID:30119236
2567	LncRNA	SBF2-AS1	miR-149-5p	TGFBR1	HepG2 and HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30115383	Long non-coding RNA SBF2-AS1 promotes hepatocellular carcinoma progression through regulation of miR-140-5p-TGFBR1 pathway.	We found that the expression levels of SBF2-AS1 were significantly up-regulated in HCC tissues and correlated with poor prognosis. SBF2-AS1 knockdown could inhibit the proliferation of HCC cells and attenuate the development of HCC tumor in vivo. Moreover, wound healing and Transwell assays revealed that down-regulation of SBF2-AS1 suppressed the migration and invasion of HCC cells by modulating epithelial-mesenchymal transition (EMT) ability. Mechanistically, we observed that SBF2-AS1 served as a competing endogenous RNA (ceRNA) of miR-140-5p. Subsequently, transforming growth factor beta receptor 1 (TGFBR1) was certified as a direct target of miR-140-5p and enforcing SBF2-AS1 expression elevated TGFBR1 expression in HCC.	MIMAT0000450	Biochem Biophys Res Commun 2018 Sep 18 503, 2826-2832 doi:10.1016/j.bbrc.2018.08.047 PMID:30115383
2568	LncRNA	SNHG5	miR-26a	ROCK1	Mg63	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30114643	Long non-coding RNA SNHG5 sponges miR-26a to promote the tumorigenesis of osteosarcoma by targeting ROCK1.	Elevated expression of SNHG5 was correlated with poor clinical outcome and prognosis in OS patients. SNHG5 functioned as a sponge for miR-26a and promoted proliferation, invasion and migration, and accelerated G1 to S phase transition in OS cells. SNHG5 functioned as a competing endogenous RNA (ceRNA) for miR-26a and activated the ROCK signaling pathway through the miR-26a-ROCK1 axis.	MI0000083	Biomed Pharmacother 2018 Nov 107, 598-605 doi:10.1016/j.biopha.2018.08.025 PMID:30114643
2569	LncRNA	HOXA11-AS	miR-454-3p	STAT3	A549 and H157	Lung Cancer	Homo sapiens (human)	Rescue assays	30099826	LncRNA HOXA11-AS drives cisplatin resistance of human LUAD cells via modulating miR-454-3p/Stat3.	 the HOXA11-AS/miR-454-3p/Stat3 (signal transducer and activator of transcription 3) pathway was found to influence the cisplatin resistance of LUAD cells. HOXA11-AS specifically acted as a competing endogenous RNA (ceRNA) in LUAD cells. The combinations among these three genes were demonstrated. Finally, rescue assays were applied to demonstrate the ceRNA pattern consisting of HOXA11-AS, miR-454-3p and Stat3.	MIMAT0003885	Cancer Sci 2018 Oct 109, 3068-3079 doi:10.1111/cas.13764 PMID:30099826
2570	LncRNA	AP000695.4	miR-101-3p	ZEB1	OvCa cell lines	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30098599	LncRNA PTAR promotes EMT and invasion-metastasis in serous ovarian cancer by competitively binding miR-101-3p to regulate ZEB1 expression.	our study showed that PTAR expression was positively correlated with the expression level of ZEB1 in the mesenchymal OvCa samples. Meanwhile, we found that silencing miR-101 promoted cell migration, whereas the overexpression of miR-101 suppressed EMT and cell migration in OvCa cell lines through the regulation of ZEB1. Further analysis showed that enhanced expression of PTAR promoted EMT and metastasis through the regulation of miR-101, whereas silencing PTAR led to the attenuation of TGF-β1-induced tumorigenicity in ovarian cancer cells. Mechanistically, we found that PTAR acted as a ceRNA of miR-101, as forced expression of PTAR reduced the expression and activity of miR-101. More importantly, the knockdown of PTAR reduced tumorigenicity and metastasis in vivo.	MIMAT0000099	Mol Cancer 2018 Aug 11 17, 119 doi:10.1186/s12943-018-0870-5 PMID:30098599
2571	LncRNA	NEAT1	miR-9-5p	PTEN?	Hela Cells	Cervical Cancer	Homo sapiens (human)	qPCR	30096244	Long noncoding RNA NEAT1 promoted the growth of cervical cancer cells via sponging miR-9-5p.	Overexpression of NEAT1 promoted the proliferation and migration of cervical cancer cells. Molecular study uncovered that NEAT1 functioned as competitive endogenous RNA (ceRNA) to bind miR-9-5p and suppress the expression of miR-9-5p. Consistently, highly expressed NEAT1 attenuated the inhibitory effect of miR-9-5p on the expression of PTEN and POU2F1, which were the targets of miR-9-5p. In agreement with the negative regulation of NEAT1 on miR-9-5p, restoration of miR-9-5p inhibited the promotion of NEAT1 on the growth of cervical cancer cells.	MIMAT0000441	Biochem Cell Biol 2019 Apr 97, 100-108 doi:10.1139/bcb-2018-0111 PMID:30096244
2572	LncRNA	NEAT1	miR-9-5p	POU2F1	Hela Cells	Cervical Cancer	Homo sapiens (human)	qPCR	30096244	Long noncoding RNA NEAT1 promoted the growth of cervical cancer cells via sponging miR-9-5p.	Overexpression of NEAT1 promoted the proliferation and migration of cervical cancer cells. Molecular study uncovered that NEAT1 functioned as competitive endogenous RNA (ceRNA) to bind miR-9-5p and suppress the expression of miR-9-5p. Consistently, highly expressed NEAT1 attenuated the inhibitory effect of miR-9-5p on the expression of PTEN and POU2F1, which were the targets of miR-9-5p. In agreement with the negative regulation of NEAT1 on miR-9-5p, restoration of miR-9-5p inhibited the promotion of NEAT1 on the growth of cervical cancer cells.	MIMAT0000441	Biochem Cell Biol 2019 Apr 97, 100-108 doi:10.1139/bcb-2018-0111 PMID:30096244
2573	LncRNA	MALAT1	miR-140-5p	HDAC4	hFOB 1.19	Osteosarcoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30094957	Long noncoding RNA MALAT1 regulates HDAC4-mediated proliferation and apoptosis via decoying of miR-140-5p in osteosarcoma cells.	Through an online prediction, a series of luciferase assays and RNA pull-down assays, we demonstrated that both MALAT1 and HDAC4 were the targets of microRNA-140-5p (miR-140-5p) via sharing a similar microRNA responding elements. Even further, we revealed that MALAT1 served as a ceRNA of HDAC4 via decoying of miR-140-5p. Finally, we proved that MALAT1 promoted OS tumor growth in an in vivo animal study. In summary, the outcomes of this study demonstrated the complex ceRNA network among MALAT, miR-140-5p, and HDAC4-mediated proliferation and apoptosis in OS.	MIMAT0000431	Cancer Med 2018 Sep 7, 4584-4597 doi:10.1002/cam4.1677 PMID:30094957
2574	LncRNA	HOXA-AS2	miR-520c-3p	POU2F1	U2OS, Saos-2, HOS and MG-63	Osteosarcoma	Homo sapiens (human)	qPCR,Luciferase reporter assay etc.	30081707	Long non-coding RNA HOXA-AS2 promotes migration and invasion by acting as a ceRNA of miR-520c-3p in osteosarcoma cells.	In vitro experiments revealed that HOXA-AS2 knockdown significantly inhibited OS cells proliferation by promoting apoptosis and causing G1 arrest, whereas HOXA-AS2 overexpression promoted cell proliferation. Further functional assays indicated that HOXA-AS2 significantly promoted OS cell migration and invasion by promoting epithelial-mesenchymal transition (EMT). Bioinformatics online programs predicted that HOXA-AS2 sponge miR-520c-3p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOXA-AS2 could negatively regulate the expression of miR-520c-3p in OS cells.	MIMAT0002846	Cell Cycle 2018  17, 1637-1648 doi:10.1080/15384101.2018.1489174 PMID:30081707
2575	LncRNA	PVT1	miR-128	VEGFC	Bladder Cancer tissues	Bladder Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Chromatin immunoprecipitation assays	30076714	LncRNA PVT1 regulates VEGFC through inhibiting miR-128 in bladder cancer cells.	we demonstrated that PVT1 expression levels affect the proliferation and migration ability of bladder cancer cells. Moreover, PVT1 knockdown significantly decreased the proliferation capacity of bladder cancer cells in nude mice. Luciferase assays and RNA-binding protein immunoprecipitation were performed to investigate the potential mechanism of ceRNAs in the regulation of PVT1 and VEGFC. The results showed that the increased number of PVT1 transcripts interacted directly with miR-128 to decrease miR-128 binding to the VEGFC 3'-untranslated region.	MI0000447	J Cell Physiol 2019 Feb 234, 1346-1353 doi:10.1002/jcp.26929 PMID:30076714
2576	Circular RNA	Circ_008913	miR-889	DAB2IP	HaCaT	Carcinogenesis	Homo sapiens (human)	qPCR	30167605	Circ008913, via miR-889 regulation of DAB2IP/ZEB1, is involved in the arsenite-induced acquisition of CSC-like properties by human keratinocytes in carcinogenesis.	MicroRNA (miR)-889 suppressed the expression of DAB2IP and was involved in regulation of cancer stem cells (CSCs). Moreover, overexpression of circ008913 with pLCDH-circ008913 or transfection with an miR-889 inhibitor reduced the capacity of T-HaCaT cells for colony formation, invasion, migration, and the sizes of tumors in nude mice, effects that were reversed by co-transfection with an miR-889 mimic. These results suggest that, in HaCaT cells, arsenite decreases circ008913 levels, which act as a sponge for miR-889 and down-regulate the miR-889 target, DAB2IP, which, in turn, up-regulates ZEB1, increases mRNA levels of the cell-surface markers of skin stem cells, and is involved in arsenite-induced acquisition of CSC-like properties that lead to malignant transformation.	MI0005540	Metallomics 2018 Sep 19 10, 1328-1338 doi:10.1039/c8mt00207j PMID:30167605
2577	Circular RNA	Circ_008913	miR-889	ZEB1	HaCaT	Carcinogenesis	Homo sapiens (human)	qPCR	30167605	Circ008913, via miR-889 regulation of DAB2IP/ZEB1, is involved in the arsenite-induced acquisition of CSC-like properties by human keratinocytes in carcinogenesis.	MicroRNA (miR)-889 suppressed the expression of DAB2IP and was involved in regulation of cancer stem cells (CSCs). Moreover, overexpression of circ008913 with pLCDH-circ008913 or transfection with an miR-889 inhibitor reduced the capacity of T-HaCaT cells for colony formation, invasion, migration, and the sizes of tumors in nude mice, effects that were reversed by co-transfection with an miR-889 mimic. These results suggest that, in HaCaT cells, arsenite decreases circ008913 levels, which act as a sponge for miR-889 and down-regulate the miR-889 target, DAB2IP, which, in turn, up-regulates ZEB1, increases mRNA levels of the cell-surface markers of skin stem cells, and is involved in arsenite-induced acquisition of CSC-like properties that lead to malignant transformation.	MI0005540	Metallomics 2018 Sep 19 10, 1328-1338 doi:10.1039/c8mt00207j PMID:30167605
2578	Circular RNA	CEP128	miR-145-5p	SOX11	Bladder Cancer tissues	Bladder Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30134837	Circular RNA CEP128 acts as a sponge of miR-145-5p in promoting the bladder cancer progression via regulating SOX11.	circCEP128 and SOX11 were observed significantly up-regulated in bladder cancer tissues, while the expression of miR-145-5p was decreased in cancer samples compared to normal samples. Cytoscape was used to visualize circCEP128-miRNA-target gene interactions based on the TargetScan and circular RNA interactome, which revealed that circCEP128 served as a sponge of miR-145-5p and indirectly regulated SOX11. Knockdown of circCEP128 induced the inhibition of cell proliferation and the increased bladder cancer cell apoptosis rate.	MIMAT0000437	Mol Med 2018 Jul 31 24, 40 doi:10.1186/s10020-018-0039-0 PMID:30134837
2579	Circular RNA	Circ_104670	miR-17-3p	MMP-2	Nucleus pulposus tissues	Intervertebral Disc Degeneration	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30089772	CircularRNA_104670 plays a critical role in intervertebral disc degeneration by functioning as a ceRNA	The present study uncovers and validates IDD-specific circRNA transcriptome profiles, in which circRNA_104670 is upregulated in human IDD tissues and regulates mRNA (MMP-2) by directly sponging miRNA-17-3p (ceRNA). These data may provide a novel potential therapeutic target for patients with IDD.	MIMAT0000071	Exp Mol Med 2018 Aug 6 50, 1-12 doi:10.1038/s12276-018-0125-y PMID:30089772
2580	Circular RNA	Circ_DOCK1	miR-196a-5p	BIRC3	RT-112, 5637, BIU-87 and TCCSUP	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR,Luciferase reporter assay,in vitro knockdown etc	29286141	CircDOCK1 suppresses cell apoptosis via inhibition of miR196a5p by targeting BIRC3 in OSCC.	The knockdown of the expression of circDOCK1 led to the increase of apoptosis. Utilizing multiple bioinformatics methods, we predicted the interactions among circRNAs, miRNAs and genes, and built the circDOCK1/miR196a5p/BIRC3 axis. Both the silencing of circDOCK1 with small interfering RNA and the upregulation of the expression of miR196a5p with mimics led OSCC cells to increase apoptosis and decrease BIRC3 formation. We further confirmed this outcome by comparing the expression of circDOCK1, miR196a5p and BIRC3 in oral squamous carcinoma tissue with those in paracarcinoma tissue, and examining the expression profile of circRNAs in oral squamous carcinoma tissue and paracarcinoma tissue with microarray. 	MIMAT0000226	Oncol Rep 2018 Mar 39, 951-966 doi:10.3892/or.2017.6174 PMID:29286141
2581	LncRNA	FAL1	miR-637	AKT1	HSCR aganglionic tissues	Hirschsprungs Disease	Homo sapiens (human)	qPCR, Western blot	30062828	Long non-coding RNA FAL1 functions as a ceRNA to antagonize the effect of miR-637 on the down-regulation of AKT1 in Hirschsprung's disease.	AL1 expression was markedly down-regulated in HSCR aganglionic tissues and decreased FAL1 expression was associated with the diagnosis of HSCR. Cell functional analyses indicated that FAL1 overexpressing notably promoted cell proliferation and migration, while down-regulation of FAL1 suppressed cell proliferation and migration. Additionally, Flow cytometry assay demonstrated that knockdown of FAL1 induced markedly cell cycle stalled in the G0/G1 phase. Furthermore, FAL1 could positively regulate AKT1 expression by competitively binding to miR-637.	MI0003652	Cell Prolif 2018 Oct 51, e12489 doi:10.1111/cpr.12489 PMID:30062828
2582	LncRNA	lnc015192	miR-34a	Adam12	Breast tissues	Breast Cancer	Homo sapiens (human)	qPCR	30042416	Adam12 and lnc015192 act as ceRNAs in breast cancer by regulating miR-34a.	We found that Adam12 and lnc015192 were significantly upregulated in miR-34a knockout breast tissues. Knockdown of Adam12 and lnc015192 inhibited breast cancer cell migration, invasion, and epithelial-mesenchymal transition (EMT). Further experiments revealed that lnc015192 regulated Adam12 expression by functioning as a competing endogenous RNA (ceRNA) for miR-34a.	MI0000268	Oncogene 2018 Dec 37, 6316-6326 doi:10.1038/s41388-018-0410-1 PMID:30042416
2583	LncRNA	lncARSR	miR-200a	ZEB1	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000737	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2584	LncRNA	lncARSR	miR-200b	ZEB2	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000342	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2585	LncRNA	lncARSR	miR-200c	ZEBc	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000650	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2586	LncRNA	lncARSR	miR-200a	ZEB2	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000737	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2587	LncRNA	lncARSR	miR-200b	ZEB1	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000342	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2588	LncRNA	lncARSR	miR-200c	ZEBc	SKOV3, HO8910, ES-2, and CAOV3	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30034936	Long noncoding RNA lncARSR promotes epithelial ovarian cancer cell proliferation and invasion by association with HuR and miR-200 family.	We speculated that lncARSR regulated invasion and EMT through modulating ZEB1 and ZEB2. Analysis of the epithelial markers E-cadherin and ZO-1 and the mesenchymal markers N-cadherin and vimentin revealed that overexpression of lncARSR, but not the mutant, reduced E-cadherin and ZO-1 and increased N-cadherin and vimentin. Consistently, ectopic expression of miR-200a abolished these effects. Conversely, lncARSR depletion upregulated E-cadherin and ZO-1 and downregulated N-cadherin and vimentin, which was abolished by miR-200a inhibition. Together, these data suggest that lncARSR induces EMT through competitive binding of miR-200s.	MI0000650	Am J Cancer Res 2018  8, 981-992,  PMID:30034936
2589	LncRNA	linc00152	miR-125b-1	MCL-1	HO-8910, SKOV3 and A2780	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	30030896	Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR-125b with MCL-1 by regulating mitochondrial apoptosis pathways in ovarian cancer.	Knockdown of LINC00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC00152 and Myeloid cell leukemia-1 (MCL-1) were targeted by miR-125b and had the same miR-125b combining site. The miR-125b level was negatively correlated with the expression of LINC00152, while MCL-1 was positively related to the LINC00152 level. MiR-125b could affect LINC00152 levels as evaluated by qRT-PCR. Finally, we affirmed that LINC00152 mediated cell proliferation by affecting MCL-1 expression and MCL-1-mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ceRNA) of miR-125b.	MI0000446	Cancer Med 2018 Sep 7, 4530-4541 doi:10.1002/cam4.1547 PMID:30030896
2590	LncRNA	NRAL	miR-340-5p	Nrf2	HepG2 and HepG2/CDDP	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	30030687	NRAL mediates cisplatin resistance in hepatocellular carcinoma via miR-340-5p/Nrf2 axis.	A novel lncRNA, termed NRAL (Nrf2 regulation-associated lncRNA), was identified, and the initial results indicated that it was highly expressed in HepG2 cisplatin resistant cell lines compared to their parental counterparts. Functionally, NRAL depletion significantly enhanced CDDP-mediated cytotoxicity and apoptosis in two cisplatin-resistant HCC cell lines. Mechanistically, the results indicated that NRAL regulates Nrf2 expression through miR-340-5p serving as a competing endogenous RNA (ceRNA), thus influencing the CDDP-induced phenotype in HCC.	MIMAT0004692	J Cell Commun Signal 2019 Mar 13, 99-112 doi:10.1007/s12079-018-0479-x PMID:30030687
2591	LncRNA	MT1DP	miR-365	NRrf2	HepG2	Cadmium-Induced Oxidative Stress	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30027041	LncRNA MT1DP Aggravates Cadmium-Induced Oxidative Stress by Repressing the Function of Nrf2 and is Dependent on Interaction with miR-365.	Mechanistically, MT1DP induction under Cd stress decreases the nuclear factor erythroid 2-related factor 2 (Nrf2) level to evoke oxidative stress through the elevation of miR-365, which acted to repress the Nrf2 level via direct binding to its 3'UTR. In contrast to the competing endogenous RNA (ceRNA) mechanism, a new mechanism is proposed: MT1DP elevated the miR-365 level though stabilizing its RNA via direct binding.	MI0000767	Adv Sci (Weinh) 2018 Jul 5, 1800087 doi:10.1002/advs.201800087 PMID:30027041
2592	LncRNA	NONMMUT065582	miR-138	YAP1	Lung tissues	Lung Fibroblast Activation And Fibrosis	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30025992	lncRNA PFAR Promotes Lung Fibroblast Activation and Fibrosis by Targeting miR-138 to Regulate the YAP1-Twist Axis.	Knockdown of miR-138 promoted fibrogenesis by targeting regulation of yes-associated protein 1 (YAP1), whereas enhanced expression of miR-138 attenuated fibrogenesis in lung fibroblasts. Mechanistically, PFAR acted as competing endogenous RNA (ceRNA) of miR-138: forced expression of PFAR reduced the expression and activity of miR-138 to activate YAP1 and promote fibrogenesis in lung fibroblasts, whereas loss of YAP1 abrogated the pro-fibrotic effect of PFAR.	MI0000455	Mol Ther 2018 Sep 5 26, 2206-2217 doi:10.1016/j.ymthe.2018.06.020 PMID:30025992
2593	LncRNA	NONMMUT065582	miR-138	YAP1	Lung tissues	Lung Fibroblast Activation And Fibrosis	Mus musculus (mouse)	qPCR, Western blot, Luciferase reporter assay etc.	30025992	lncRNA PFAR Promotes Lung Fibroblast Activation and Fibrosis by Targeting miR-138 to Regulate the YAP1-Twist Axis.	Overexpression of PFAR promoted fibrogenesis through modulation of miR-138, whereas knockdown of PFAR attenuated TGF-β1-induced fibrogenesis in lung fibroblasts.Mechanistically, PFAR acted as competing endogenous RNA (ceRNA) of miR-138: forced expression of PFAR reduced the expression and activity of miR-138 to activate YAP1 and promote fibrogenesis in lung fibroblasts, whereas loss of YAP1 abrogated the pro-fibrotic effect of PFAR. More importantly, PFAR silencing alleviated BLM-induced lung fibrosis in mice.	MI0000455	Mol Ther 2018 Sep 5 26, 2206-2217 doi:10.1016/j.ymthe.2018.06.020 PMID:30025992
2594	LncRNA	H19	miR-874	AQPq	Blood tissues	Lipopolysaccharide Sepsis	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30021355	LncRNA H19 functions as an Aquaporin 1 competitive endogenous RNA to regulate microRNA-874 expression in LPS sepsis.	H19 and AQP1 decreased and accompanied with elevated miR-874 expression in sepsis samples, in vivo mice model and in vitro cells. There was negative relationship between expression of H19 and miR-874, and a positive correlation between H19 and AQP1 expression. However, H19 overexpression transfection significantly reversed LPS induced dysregulation in expression of miR-874 and AQP1, secretion of anti-inflammatory cytokines, and myocardial dysfunction in vivo and in vitro.	MI0005532	Biomed Pharmacother 2018 Sep 105, 1183-1191 doi:10.1016/j.biopha.2018.06.007 PMID:30021355
2595	LncRNA	H19	miR-874	AQPq	Blood tissues	Lipopolysaccharide Sepsis	Mus musculus (mouse)	qPCR, Western blot, Luciferase reporter assay etc.	30021355	LncRNA H19 functions as an Aquaporin 1 competitive endogenous RNA to regulate microRNA-874 expression in LPS sepsis.	H19 and AQP1 decreased and accompanied with elevated miR-874 expression in sepsis samples, in vivo mice model and in vitro cells. There was negative relationship between expression of H19 and miR-874, and a positive correlation between H19 and AQP1 expression. However, H19 overexpression transfection significantly reversed LPS induced dysregulation in expression of miR-874 and AQP1, secretion of anti-inflammatory cytokines, and myocardial dysfunction in vivo and in vitro.	MI0005532	Biomed Pharmacother 2018 Sep 105, 1183-1191 doi:10.1016/j.biopha.2018.06.007 PMID:30021355
2596	LncRNA	TUG1	miR-29b	aSMA	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2597	LncRNA	TUG1	miR-29b	COL1a1	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2598	LncRNA	TUG1	miR-29b	Mmp2	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2599	LncRNA	TUG1	miR-29b	Mmp9	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2600	LncRNA	TUG1	miR-29b	Mmp10	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2601	LncRNA	TUG1	miR-29b	Timp1	LX=2, HEK293T	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	30017186	TUG1 is involved in liver fibrosis and activation of HSCs by regulating miR-29b.	We demonstrated that Tug1 is over-expressed in the fibrotic livers and activated HSCs, but not injured hepatocytes. In addition, we assessed the function of Tug1 in HSCs and found that Tug1 promotes the expression of α-SMA, Col1α1, Mmp2/9/10 and Timp1. Mechanically, Tug1 promotes the expression of these pro-fibrogenic genes by down-regulating miR-29b, thus accelerating the progression of liver fibrosis. Further study revealed that TUG1was up-regulated in liver tissues of patients with cirrhosis.	MI0000105	Biochem Biophys Res Commun 2018 Sep 10 503, 1394-1400 doi:10.1016/j.bbrc.2018.07.054 PMID:30017186
2602	LncRNA	XIST	miR-211	CXCR4	OA chondrocyte	Osteoarthritis	Homo sapiens (human)	qRT-PCR	30005876	The role of lncRNA XIST/miR-211 axis in modulating the proliferation and apoptosis of osteoarthritis chondrocytes through CXCR4 and MAPK signaling.	Through direct binding, XIST served as a ceRNA for miR-211 to counteract miR-211-mediated CXCR4 repression, thereby modulating chondrocyte proliferation and apoptosis through downstream MAPK signaling. In OA tissues, miR-211 expression was significantly downregulated while CXCR4 mRNA expression was upregulated. miR-211 was negatively correlated with XIST and CXCR4, respectively, while XIST and CXCR4 was positively correlated in tissue samples.	MI0000287	Biochem Biophys Res Commun 2018 Sep 18 503, 2555-2562 doi:10.1016/j.bbrc.2018.07.015 PMID:30005876
2603	LncRNA	Linc01287	miR-298	STAT3	HepG-2, Huh7, Bel7402 and Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30001751	LINC01287/miR-298/STAT3 feedback loop regulates growth and the epithelial-to-mesenchymal transition phenotype in hepatocellular carcinoma cells.	Knockdown of LINC01287 decreased HCC cell growth and invasion both in vitro and in vivo. LINC01287 can negatively regulate miR-298 expression by acting as a ceRNA. miR-298 directly targeted STAT3 and inhibited its expression. LINC01287 exerted its function via the miR-298/STAT3 axis in HCC. Interestingly, STAT3 elevated LINC01287 expression via c-jun, which bound to the LINC01287 promoter. A feedback loop was also discovered between LINC01287 and the miR-298/STAT3 axis.	MI0005523	J Exp Clin Cancer Res 2018 Jul 13 37, 149 doi:10.1186/s13046-018-0831-2 PMID:30001751
2604	LncRNA	BDNF-AS	miR-130b-5p	PRDM5	Rat model	Acute Spinal Cord Injury	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	29995562	Knockdown of lncRNA BDNF-AS suppresses neuronal cell apoptosis via downregulating miR-130b-5p target gene PRDM5 in acute spinal cord injury.	The association among BDNF-AS, miR-130b-5p and PRDM5 were disclosed by RNA immunoprecipitation (RIP) assay, RNA pull-down assay and dual-luciferase reporter assay. Results BDNF-AS, PRDM5 and c-caspase 3 expression were significantly upregulated, while miR-130b-5p was suppressed in the ASCI group and neuronal cells following hypoxia treatment. BDNF-AS knockdown inhibited neuronal cell apoptosis. Further studies indicated that BDNF-AS functioned as a competing endogenous RNA (ceRNA) by sponging miR-130b-5p in neuronal cells. Further investigations demonstrated that PRDM5 was a target of miR-130b-5p and BDNF-AS knockdown exerted anti-apoptotic effects via miR-130b-5p/PRDM5 axis. 	MIMAT0004680	RNA Biol 2018  15, 1071-1080 doi:10.1080/15476286.2018.1493333 PMID:29995562
2605	Circular RNA	Circ_FBLIM1	miR-346	FBLIM1	HepG2, 7402 and 97H	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30053867	circFBLIM1 act as a ceRNA to promote hepatocellular cancer progression by sponging miR-346.	Microarray analysis and qRT-PCR verified a circRNA termed circFBLIM1 that was upregulated in HCC tissues and cell lines. Knockdown of circFBLIM1 inhibited proliferation, invasion and promoted apoptosis in HCC. Via luciferase reporter assays, circFBLIM1 and FBLIM1 were observed to directly bind to miR-346. Subsequent experiments showed that circFBLIM1 and FBLIM1 regulated the expression of each other by sponging miR-346.	MI0000826	J Exp Clin Cancer Res 2018 Jul 27 37, 172 doi:10.1186/s13046-018-0838-8 PMID:30053867
2606	Circular RNA	Circ_036186	miR-193b-3p	YWHAZ	HNSCC and para-carcinoma tissues	Head And Neck Squamous Carcinoma	Homo sapiens (human)	qRT-PCR	30066847	Competing endogenous RNA analysis reveals the regulatory potency of circRNA_036186 in HNSCC.	ifferentially expressed circRNAs were screened using an Arraystar Human CircRNA Array and verified by reverse transcription-quantitative polymerase chain reaction. Multiple bioinformatics methods and a hypergeometric test were employed to predict the interactions between RNAs and the functional circRNA-microRNA (miRNA)-mRNA axes in HNSCC. As a result, 287 circRNAs and 1,053 mRNAs were determined to be differentially expressed in HNSCC compared with the adjacent tissue. In addition, the expression levels of circRNA_036186 and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, ζ polypeptide (14-3-3ζ) were identified to be significantly different. A competing endogenous RNA (ceRNA) network was constructed, consisting of 5 circRNAs, 385 miRNAs and 96 mRNAs. Furthermore, we predicted that miR-193b-3p exerts a significant effect on 14-3-3ζ, and was significantly associated with the Hippo signaling pathway in HNSCC. 	MIMAT0002819	Int J Oncol 2018 Oct 53, 1529-1543 doi:10.3892/ijo.2018.4499 PMID:30066847
2607	Circular RNA	ciRS-7	miR-1299	MMPs	MDA-MB-231, BT-549	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30072582	Circular RNA ciRS-7 Maintains Metastatic Phenotypes as a ceRNA of miR-1299 to Target MMPs.	Functionally, down-regulation of ciRS-7 inhibited cell migration and invasion of TNBC cells. Knockdown of ciRS-7 expression also inhibited the liver and lung metastasis of TNBC cells in vivo. Mechanistic studies revealed that ciRS-7 contains twenty miR-1299 binding sites and functions as a ceRNA of miR-1299 in TNBC cells. High expression of ciRS-7 maintains the high migration and invasion properties of TNBC cells by acting as a ceRNA of miR-1299 to enhance the expression of matrix metalloproteinases family members (MMPs).	MI0006359	Mol Cancer Res 2018 Nov 16, 1665-1675 doi:10.1158/1541-7786.Mcr-18-0284 PMID:30072582
2608	Circular RNA	Circ_GFRA1	miR-34a	GFRA1	SKBR3, T47D, BT474, MCF-7, BT-483, BT-20, BT549, MDA-MB-468 and MDA-MB-231	Breast Cancer	Homo sapiens (human)	qRT-PCR	29037220	circGFRA1 and GFRA1 act as ceRNAs in triple negative breast cancer by regulating miR-34a.	Microarray analysis and qRT-PCR verified a circRNA termed circGFRA1 that was upregulated in TNBC. Kaplan-Meier survival analysis showed that upregulated circGFRA1 was correlated with poorer survival. Knockdown of circGFRA1 inhibited proliferation and promoted apoptosis in TNBC. Via luciferase reporter assays, circGFRA1 and GFRA1 was observed to directly bind to miR-34a. Subsequent experiments showed that circGFRA1 and GFRA1 regulated the expression of each other by sponging miR-34a.	MI0000268	J Exp Clin Cancer Res 2017 Oct 16 36, 145 doi:10.1186/s13046-017-0614-1 PMID:29037220
2609	Circular RNA	Circ_100290	miR-516b	FZD4	HCT116, SW480, HT29 and SW620	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30173892	CircRNA_100290 promotes colorectal cancer progression through miR-516b-induced downregulation of FZD4 expression and Wnt/β-catenin signaling.	Silencing circRNA_100290 markedly reduced cell proliferation rate, inhibited migration and invasion abilities, but promoted apoptosis in vitro. Mechanistically, our data revealed circRNA_100290 was a competing endogenous RNA (ceRNA) of FZD4 by sponging miR-516b, leading to activation of Wnt/β-catenin pathway. Rescue assay indicated that FZD4-induced activation of β-catenin pathway is indispensable for the function of circRNA_100290 in CRC.	MIMAT0002860	Biochem Biophys Res Commun 2018 Sep 26 504, 184-189 doi:10.1016/j.bbrc.2018.08.152 PMID:30173892
2610	Circular RNA	Circ_0032462	miR-142-5p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000433	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2611	Circular RNA	Circ_0028173	miR-142-5p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000433	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2612	Circular RNA	Circ_0005909	miR-142-5p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000433	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2613	Circular RNA	Circ_0032462	miR-338-3p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000763	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2614	Circular RNA	Circ_0028173	miR-338-3p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000763	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2615	Circular RNA	Circ_0005909	miR-338-3p	CADM1	MG63, U2OS, 143B, HOS and hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR	30153287	Circular RNAs hsa_circ_0032462, hsa_circ_0028173, hsa_circ_0005909 are predicted to promote CADM1 expression by functioning as miRNAs sponge in human osteosarcoma.	Differentially expressed circRNAs between OS and control, including 8 up-regulated and 102 down-regulated circRNAs, were generated and ceRNA analysis for 5 most up-regulated or 5 most down-regulated circRNAs in OS were then performed. The pathway enrichment analysis of gene expression profiles indicated differentially expressed genes (DEGs) of three gene profiles significantly enriched in cell cycle pathway, cell adhesion molecules (CAMs) pathway, oxidative phosphorylation pathway, cytokine-cytokine receptor interaction pathway, p53 signaling pathway and proteoglycans in cancer pathway, which were critical important pathways in the pathogenesis of OS. The Venn analysis showed that 2 (one is a pseudogene) up-regulated and 39 down-regulated DEGs were co-expressed in all three gene profiles. Then PPI networks of 41 co-expressed DEGs (up- and down-regulated DEGs) were constructed to predict their functions using the GeneMANIA. The expression levels of these related RNAs also matched our predictions really well.	MIMAT0000763	PLoS One 2018  13, e0202896 doi:10.1371/journal.pone.0202896 PMID:30153287
2616	Circular RNA	CircRNA_000479	miR-4753	BCL11A	HCC38, HCC1806, BT549, MDA-MB-231, MDA-MB-468, MDA-MB-415, MCF-7, T47D, BT474 and Skbr-3	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay	30083277	circEPSTI1 as a Prognostic Marker and Mediator of Triple-Negative Breast Cancer Progression.	Knockdown of circEPSTI1 inhibits TNBC cell proliferation and induces apoptosis. In vitro and in vivo experiments indicated that circEPSTI1 binds to miR-4753 and miR-6809 as a miRNA sponge to regulate BCL11A expression and affect TNBC proliferation and apoptosis. High levels of circEPSTI1 correlate with reduced survival in TNBC patients. The circEPSTI1-miR-4753/6809-BCL11A axis affect the proliferation and apoptosis of triple-negative breast cancer through the mechanism of competing endogenous RNAs (ceRNA). In addition, our results identify circEPSTI1 as an independent prognostic marker for survival in patients with TNBC.	MI0017392	Theranostics 2018  8, 4003-4015 doi:10.7150/thno.24106 PMID:30083277
2617	Circular RNA	CircRNA_000479	miR-6809	BCL11A	HCC38, HCC1806, BT549, MDA-MB-231, MDA-MB-468, MDA-MB-415, MCF-7, T47D, BT474 and Skbr-3	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay	30083277	circEPSTI1 as a Prognostic Marker and Mediator of Triple-Negative Breast Cancer Progression.	Knockdown of circEPSTI1 inhibits TNBC cell proliferation and induces apoptosis. In vitro and in vivo experiments indicated that circEPSTI1 binds to miR-4753 and miR-6809 as a miRNA sponge to regulate BCL11A expression and affect TNBC proliferation and apoptosis. High levels of circEPSTI1 correlate with reduced survival in TNBC patients. The circEPSTI1-miR-4753/6809-BCL11A axis affect the proliferation and apoptosis of triple-negative breast cancer through the mechanism of competing endogenous RNAs (ceRNA). In addition, our results identify circEPSTI1 as an independent prognostic marker for survival in patients with TNBC.	MI0022654	Theranostics 2018  8, 4003-4015 doi:10.7150/thno.24106 PMID:30083277
2618	Circular RNA	CircRNA8924	miR-518d-5p	CBX8	SiHa and HeLa	Cervical Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30007986	CircRNA8924 Promotes Cervical Cancer Cell Proliferation, Migration and Invasion by Competitively Binding to MiR-518d-5p /519-5p Family and Modulating the Expression of CBX8.	The luciferase reporter assay was used to determine the direct regulation of miR-518d-5p/519-5p and circRNA8924 or CBX8. The study demonstrated that the expression level of circRNA8924 in CC was significantly higher than that in the adjacent normal tissues (P < 0.001), and that it was also associated with tumor size, FIGO staging and myometrial invasion. The knockdown of circRNA8924 significantly inhibited the proliferation, migration and invasion of CC cells SiHa and HeLa. The expression level of miR-518d-5p/519-5p was negatively correlated with circRNA8924, and circRNA8924 regulated CBX8 by competitively binding to miR-518d-5p/519-5p.	MIMAT0005456	Cell Physiol Biochem 2018  48, 173-184 doi:10.1159/000491716 PMID:30007986
2619	Circular RNA	CircRNA8924	miR-519-5p	CBX8	SiHa and HeLa	Cervical Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30007986	CircRNA8924 Promotes Cervical Cancer Cell Proliferation, Migration and Invasion by Competitively Binding to MiR-518d-5p /519-5p Family and Modulating the Expression of CBX8.	The luciferase reporter assay was used to determine the direct regulation of miR-518d-5p/519-5p and circRNA8924 or CBX8. The study demonstrated that the expression level of circRNA8924 in CC was significantly higher than that in the adjacent normal tissues (P < 0.001), and that it was also associated with tumor size, FIGO staging and myometrial invasion. The knockdown of circRNA8924 significantly inhibited the proliferation, migration and invasion of CC cells SiHa and HeLa. The expression level of miR-518d-5p/519-5p was negatively correlated with circRNA8924, and circRNA8924 regulated CBX8 by competitively binding to miR-518d-5p/519-5p.	MI0003178	Cell Physiol Biochem 2018  48, 173-184 doi:10.1159/000491716 PMID:30007986
2620	Circular RNA	CircZFR	miR-1261	C8orf4	K-1, TPC-1, SW579 and FTC133	Thyroid Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay and CCK-8 assay	29842886	Circular RNA circZFR contributes to papillary thyroid cancer cell proliferation and invasion by sponging miR-1261 and facilitating C8orf4 expression.	We identified a new circRNA circZFR that was significantly upregulated in PTC tissues compared to adjacent normal tissues. Furthermore, circZFR expression level was negatively correlated with clinical severity. We found that circZFR knockdown dramatically inhibited the proliferation, migration and invasion of PTC cells in vitro. Mechanistically, we found circZFR could promote C8orf4 expression via serving as a competing endogenous RNA (ceRNA) of miR-1261 in PTC cells. Rescue assays indicated that restoration of C8orf4 significantly attenuated the inhibitory effects of circZFR knockdown on PTC cell proliferation, migration and invasion.	MI0006396	Biochem Biophys Res Commun 2018 Sep 3 503, 56-61 doi:10.1016/j.bbrc.2018.05.174 PMID:29842886
2621	Circular RNA	Circ_0008039	miR-432-5p	E2F3	BT-20, BT-474, MCF-7, BT549, MDA-MB-231, and SKBR-3	Breast Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	29807010	Circular RNA hsa_circ_0008039 promotes breast cancer cell proliferation and migration by regulating miR-432-5p/E2F3 axis.	By functional experiments, we found that hsa_circ_0008039 depletion significantly suppressed the proliferation, arrested cell-cycle progression and reduced migration in breast cancer. Mechanistic investigations suggested that hsa_circ_0008039 served as a competing endogenous RNA (ceRNA) of miR-432-5p. Subsequently, E2F3 was identified as the functional target of miR-432-5p and overexpression of hsa_circ_0008039 elevated E2F3 expression in breast cancer.	MIMAT0002814	Biochem Biophys Res Commun 2018 Jul 20 502, 358-363 doi:10.1016/j.bbrc.2018.05.166 PMID:29807010
2622	Circular RNA	Circ_PDE8A	miR-338	MACC1	BxPC-3, Capan-1, Hs 766T, Hs 766T, Aspc-1 and HEK-293	Pancreatic Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	29709702	Tumor-released exosomal circular RNA PDE8A promotes invasive growth via the miR-338/MACC1/MET pathway in pancreatic cancer.	We identified a circular RNA (circ-PDE8A) from liver-metastatic PDAC cells by microarray analysis, detected its expression levels in clinical tissues and found that high circ-PDE8A expression was correlated with lymphatic invasion, TNM stage and a poor survival rate of PDAC patients. Further study revealed that circ-PDE8A promotes the invasive growth of PDAC cells via upregulating MET. Circ-PDE8A acts as a ceRNA for miR-338 to regulate MACC1 and stimulates invasive growth via the MACC/MET/ERK or AKT pathways. We further imaged the exosome communication between tumor cells and identified the tumor secreted exosomes in blood circulation. 	MI0000814	Cancer Lett 2018 Sep 28 432, 237-250 doi:10.1016/j.canlet.2018.04.035 PMID:29709702
2623	Circular RNA	Circ_0001564	miR-29c-3p	NA	U2OS, Saos-2, HOS and MG-63	Osteosarcoma	Homo sapiens (human)	qRT-PCR	29229385	Circular RNA hsa_circ_0001564 regulates osteosarcoma proliferation and apoptosis by acting miRNA sponge.	In functional experiments, hsa_circ_001564 knockdown significantly suppressed the proliferation activity, induced cell cycle arrest in G0/G1 phase, and promoted apoptosis in HOS and MG-63 cells. Subsequently, we explored the probable mechanism of hsa_circ_001564, and fortunately, bioinformatics analysis revealed that miR-29c-3p contained the complementary binding region with hsa_circ_0001564, which was confirmed by dual-luciferase reporter assay. Moreover, rescue experiments illustrated that miR-29c-3p could reverse the oncogenesis effect of hsa_circ_001564.	MIMAT0000681	Biochem Biophys Res Commun 2018 Jan 15 495, 2369-2375 doi:10.1016/j.bbrc.2017.12.050 PMID:29229385
2624	Circular RNA	Circ_000984	miR-106b	CDK6	SW480, SW620 and HT29 cells	Colon Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	29207676	Circular RNA hsa_circ_000984 promotes colon cancer growth and metastasis by sponging miR-106b.	We found circular RNA hsa_circ_000984 encoded by the CDK6 gene was remarkably upregulated in the tissues of colorectal cancer (CRC) patients and in the CRC cell lines. Moreover, high expression level of hsa_circ_000984 was significantly associated with advanced colorectal cancer. Further analysis revealed that hsa_circ_000984 knockdown could inhibit cell proliferation, migration, invasion in vitro and tumor formation in vivo in CRC cell lines. Mechanically, we found that hsa_circ_000984 may act as a competing endogenous RNA (ceRNA) by competitively binding miR-106b and effectively upregulate the expression of CDK6, thereby inducing a series of malignant phenotypes of tumor cells.	MI0000734	Oncotarget 2017 Oct 31 8, 91674-91683 doi:10.18632/oncotarget.21748 PMID:29207676
2625	Circular RNA	Circ_0001982	miR-143	NA	MDA-MB-231, MCF-7, MDAMB-468, MDA-MB-435s	Breast Cancer	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	28933584	Circular RNA hsa_circ_0001982 Promotes Breast Cancer Cell Carcinogenesis Through Decreasing miR-143.	We screened the circRNA expression profiles in breast cancer tissue using circRNA microarray analysis. Totally 1705 circRNAs were identified to be significantly aberrant. Among these dysregulated circRNAs, hsa_circ_0001982 was markedly overexpressed in breast cancer tissue and cell lines. Bioinformatics analysis predicted that miR-143 acted as target of hsa_circ_0001982, which was confirmed by Dual-luciferase reporter assay. Loss-of-function and rescue experiments revealed that hsa_circ_0001982 knockdown suppressed breast cancer cell proliferation and invasion and induced apoptosis by targeting miR-143. 	MI0000459	DNA Cell Biol 2017 Nov 36, 901-908 doi:10.1089/dna.2017.3862 PMID:28933584
2626	Circular RNA	Circ_MYLK	miR-29a	VEGFA	EJ, T24, 5673 and BIU-87	Bladder Cancer	Homo sapiens (human)	RNA immunoprecipitation, Luciferase reporter assay and FISH	28687357	Circular RNA MYLK as a competing endogenous RNA promotes bladder cancer progression through modulating VEGFA/VEGFR2 signaling pathway.	We demonstrated that circRNA-MYLK could directly bind to miR-29a and relieve suppression for target VEGFA, which activated VEGFA/VEGFR2 signaling pathway. Functionally, we found that ectopically expressing circRNA-MYLK accelerated cell proliferation, migration, tube formation of HUVEC and rearranged cytoskeleton. Moreover, up-regulating circRNA-MYLK promoted epithelial-mesenchymal transition (EMT). Whereas circRNA-MYLK knockdown decreased cell proliferation, motility, and induced apoptosis. Finally, up-regulating circRNA-MYLK promoted the growth, angiogenesis and metastasis of BC xenografts.	MI0000087	Cancer Lett 2017 Sep 10 403, 305-317 doi:10.1016/j.canlet.2017.06.027 PMID:28687357
2627	Circular RNA	Circ_MYLK	miR-29a	VEGFR2	EJ, T24, 5673 and BIU-87	Bladder Cancer	Homo sapiens (human)	RNA immunoprecipitation, Luciferase reporter assay and FISH	28687357	Circular RNA MYLK as a competing endogenous RNA promotes bladder cancer progression through modulating VEGFA/VEGFR2 signaling pathway.	We demonstrated that circRNA-MYLK could directly bind to miR-29a and relieve suppression for target VEGFA, which activated VEGFA/VEGFR2 signaling pathway. Functionally, we found that ectopically expressing circRNA-MYLK accelerated cell proliferation, migration, tube formation of HUVEC and rearranged cytoskeleton. Moreover, up-regulating circRNA-MYLK promoted epithelial-mesenchymal transition (EMT). Whereas circRNA-MYLK knockdown decreased cell proliferation, motility, and induced apoptosis. Finally, up-regulating circRNA-MYLK promoted the growth, angiogenesis and metastasis of BC xenografts.	MI0000087	Cancer Lett 2017 Sep 10 403, 305-317 doi:10.1016/j.canlet.2017.06.027 PMID:28687357
2628	Circular RNA	Circ_010567	miR-141	TGFB1	C57BL/6 mice	Myocardial Fibrosis	Homo sapiens (human)	qPCR, Luciferase reporter assay etc.	28412345	A novel identified circular RNA, circRNA_010567, promotes myocardial fibrosis via suppressing miR-141 by targeting TGF-β1.	circRNA_010567 was markedly up-regulated in diabetic mice myocardium and cardiac fibroblasts (CFs) treated with Ang II. Bioinformatics analysis predicted circRNA_010567, sponge miR-141 and miR-141 directly target TGF-β1, which was validated by dual-luciferase assay. Subsequently, functional experiments revealed circRNA_010567 silencing could up-regulate miR-141 and down-regulate TGF-β1 expression, and suppress fibrosis-associated protein resection in CFs, including Col I, Col III and α-SMA. Results demonstrate the circRNA_010567/miR-141/TGF-β1 axis plays an important regulatory role in the diabetic mice myocardial fibrosis model.	MI0000457	Biochem Biophys Res Commun 2017 Jun 10 487, 769-775 doi:10.1016/j.bbrc.2017.04.044 PMID:28412345
2629	Circular RNA	Circ_010567	miR-141	TGFB1	C57BL/6 mice	Myocardial Fibrosis	Mus musculus (mouse)	qPCR, Luciferase reporter assay etc.	28412345	A novel identified circular RNA, circRNA_010567, promotes myocardial fibrosis via suppressing miR-141 by targeting TGF-β1.	circRNA_010567 was markedly up-regulated in diabetic mice myocardium and cardiac fibroblasts (CFs) treated with Ang II. Bioinformatics analysis predicted circRNA_010567, sponge miR-141 and miR-141 directly target TGF-β1, which was validated by dual-luciferase assay. Subsequently, functional experiments revealed circRNA_010567 silencing could up-regulate miR-141 and down-regulate TGF-β1 expression, and suppress fibrosis-associated protein resection in CFs, including Col I, Col III and α-SMA. Results demonstrate the circRNA_010567/miR-141/TGF-β1 axis plays an important regulatory role in the diabetic mice myocardial fibrosis model.	MI0000457	Biochem Biophys Res Commun 2017 Jun 10 487, 769-775 doi:10.1016/j.bbrc.2017.04.044 PMID:28412345
2630	LncRNA	H19	miR-107	NF1	BEAS-2B, A549 and HCC823	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30280776	LncRNA H19 serves as a ceRNA and participates in non-small cell lung cancer development by regulating microRNA-107	H19 is highly expressed in NSCLC, which promotes NSCLC development by regulating NF1 via competitive binding to microRNA-107.	MIMAT0000104	Eur Rev Med Pharmacol Sci 2018 Sep 22, 5946-5953 doi:10.26355/eurrev_201809_15925 PMID:30280776
2631	LncRNA	TP73-AS1	miR-194-5p	SDAD1	MGC-803, SGC-7901, BGC-823, MKN-28, AGS and GES-1	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30279010	LncRNA TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis	TP73-AS1 accelerates tumor progression in gastric cancer through regulating miR-194-5p/SDAD1 axis.	MIMAT0000460	Pathol Res Pract 2018 Dec 214, 1993-1999 doi:10.1016/j.prp.2018.09.006 PMID:30279010
2632	LncRNA	ADAMTS9-AS2	miR-182-5p	FOXF2	SKOV3, HO8910, A2780, OVCAR, and HOSEpiC	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, RIP etc.	30268751	LncRNA ADAMTS9-AS2 regulates ovarian cancer progression by targeting miR-182-5p/FOXF2 signaling pathway	Taken together, our data suggested that lncRNA ADAMTS9-AS2 decreased OC progression by regulating miR-182-5p/FOXF2 axis, indicating ADAMTS9-AS2 could serve as a potential therapeutic target for OC treatment.	MIMAT0000259	Int J Biol Macromol 2018 Dec 120, 1705-1713 doi:10.1016/j.ijbiomac.2018.09.179 PMID:30268751
2633	LncRNA	MEG3	miR-302a-3p	CRTC2	C57BL/6J mice	Diabetes Mellitus	Mus musculus (mouse)	qPCR, Western blot etc.	30260029	CREB﹗pregulated lncRNA MEG3 promotes hepatic gluconeogenesis by regulating miR302a3p〤RTC2 axis	CREB﹗pregulated MEG3〆nhanced hepatic gluconeogenesis via mediating miR302a3p〤RTC2 axis, revealing that MEG3 might be a potential target and therapeutic strategy for diabetes.	MIMAT0000684	J Cell Biochem 2019 Mar 120, 4192-4202 doi:10.1002/jcb.27706 PMID:30260029
2634	LncRNA	SNHG6	miR-26a-5p	E2F7	A549, H1299, H460, HCC827, NCl-H358 and NCl-H1650	Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30257360	SNHG6 functions as a competing endogenous RNA to regulate E2F7 expression by sponging miR-26a-5p in lung adenocarcinoma	Moreover, mechanistic experiments identified that SNHG6 functions as a competing endogenous RNA (ceRNA) through competitively sponging miR-26a-5p to regulate E2F7 expression, cell motility and EMT in LUAD cells. In summary, our findings reveal that SNHG6 may act as an oncogenic lncRNA in LUAD carcinogenesis by regulating the miR-26a-5p/E2F7 axis.	MIMAT0000082	Biomed Pharmacother 2018 Nov 107, 1434-1446 doi:10.1016/j.biopha.2018.08.099 PMID:30257360
2635	LncRNA	SNHG6	miR-760	FOXC1	LOVO, RKO, Ls174t, DLD1, HCT116	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30254467	Long noncoding RNA SNHG6 promotes the progression of colorectal cancer through sponging miR-760 and activation of FOXC1	Our results indicate that long non-coding RNA SNHG6 promotes colorectal cancer progression by sequestering miR-760 and activating FOXC1, our findings suggest that SNHG6 may serve as a potential therapeutic target for CRC.	MIMAT0004957	Onco Targets Ther 2018  11, 5743-5752 doi:10.2147/ott.S170246 PMID:30254467
2636	LncRNA	SNHG14	miR-340	NA	A549, NCI-H1975, NCI-H1299, SK-MES-1 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	30254102	Long non-coding RNA SNHG14 exerts oncogenic functions in non-small cell lung cancer through acting as a miR-340 sponge	Taken together, our study demonstrated that SNHG14/miR-340 axis might play a novel role in regulating the malignant behaviors of NSCLC, which provided a new potential diagnostic and therapeutic strategy for this malignant disease.	MI0000802	Biosci Rep 2019 Jan 31 39 doi:10.1042/bsr20180941 PMID:30254102
2637	LncRNA	SNHG15	miR-200a-3p	YAP1	BHP5-16, BCPAP, K1, and BHP2-7	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30237435	LncRNA SNHG15 acts as a ceRNA to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma	In summary, our findings demonstrated that SNHG15 serves as a competitively endogenous RNA (ceRNA) to regulate YAP1-Hippo signaling pathway by sponging miR-200a-3p in papillary thyroid carcinoma.	MIMAT0000682	Cell Death Dis 2018 Sep 20 9, 947 doi:10.1038/s41419-018-0975-1 PMID:30237435
2638	LncRNA	XLOC_006390	miR-331-3p	NRP2	SiHa, HeLa, CaSki, c-41, and c-33A	Cervical Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30207103	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p	Taken together, our study demonstrated that XLOC_006390 may serve as a ceRNA and reversely regulates the expression of miR-331-3p and miR-338-3p, thus facilitating cervical cancer tumorigenesis and metastasis.	MIMAT0000760	J Gynecol Oncol 2018 Nov 29, e95 doi:10.3802/jgo.2018.29.e95 PMID:30207103
2639	LncRNA	XLOC_006390	miR-338-3p	PKM2	SiHa, HeLa, CaSki, c-41, and c-33A	Cervical Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30207103	LncRNA XLOC_006390 facilitates cervical cancer tumorigenesis and metastasis as a ceRNA against miR-331-3p and miR-338-3p	Taken together, our study demonstrated that XLOC_006390 may serve as a ceRNA and reversely regulates the expression of miR-331-3p and miR-338-3p, thus facilitating cervical cancer tumorigenesis and metastasis.	MIMAT0000763	J Gynecol Oncol 2018 Nov 29, e95 doi:10.3802/jgo.2018.29.e95 PMID:30207103
2640	LncRNA	AFAP1-AS1	miR-146b-5p	EGFR	ASPC-1, BxPC-3, HPAC, MiaPaCa-2	Pancreatic Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30206930	Cucurbitacin B suppresses proliferation of pancreatic cancer cells by ceRNA: Effect of miR-146b-5p and lncRNA-AFAP1-AS1	Thus, CuB suppresses the proliferation, in vitro and in vivo, of PC cells through the ceRNA effect of AFAP1-AS1 on miR-146b-5p	MIMAT0002809	J Cell Physiol 2019 Apr 234, 4655-4667 doi:10.1002/jcp.27264 PMID:30206930
2641	LncRNA	HOTAIR	miR-206	CCND1	COV362, SKOV3, OVCAR3 and A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30205383	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer	HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.	MIMAT0000462	Cell Physiol Biochem 2018  49, 1289-1303 doi:10.1159/000493408 PMID:30205383
2642	LncRNA	HOTAIR	miR-206	CCND2	COV362, SKOV3, OVCAR3 and A2780	Ovarian Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30205383	LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer	HOTAIR enhancedCCND1andCCND2expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.	MIMAT0000462	Cell Physiol Biochem 2018  49, 1289-1303 doi:10.1159/000493408 PMID:30205383
2643	LncRNA	D63785	miR-422a	MEF2D	GES-1, SGC7901, MGC803, BGC823, and NCI-N87	Gastric Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30195778	The Long Noncoding RNA D63785 Regulates Chemotherapy Sensitivity in Human Gastric Cancer by Targeting miR-422a	This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D. 	MIMAT0001339	Mol Ther Nucleic Acids 2018 Sep 7 12, 405-419 doi:10.1016/j.omtn.2018.05.024 PMID:30195778
2644	LncRNA	OIP5-AS1	miR-143-3p	ITGA6	C33A, SiHa, HeLa, CaSki, ME180	Pancreatic Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30188591	Long noncoding RNA opa-interacting protein 5 antisense transcript 1 promotes proliferation and invasion through elevating integrin α6 expression by sponging miR-143-3p in cervical cancer	In conclusion, we demonstrated that OIP5〢S1 promoted proliferation and invasion of CC cells via increasing the ITGA6 expression by sponging miR1433p, which might be an effective therapeutic target for the treatment of patients with CC	MIMAT0000435	J Cell Biochem 2019 Jan 120, 907-916 doi:10.1002/jcb.27454 PMID:30188591
2645	LncRNA	HNF1A-AS1	miR-661	CDK4	MKN-45 cells and BGC-823	Gastric Cancer	Homo sapiens (human)	qPCR etc.	30185552	EGR1-mediated transcription of lncRNA-HNF1A-AS1 promotes cell cycle progression in gastric cancer	HNF1A-AS1 functioned as competing endogenous RNA (ceRNA) by binding to miR-661, upregulating the expression of cell division cycle 34 (CDC34), which is a direct target of miR-661.	MIMAT0003324	Cancer Res 2018 Oct 15 78, 5877-5890 doi:10.1158/0008-5472.Can-18-1011 PMID:30185552
2646	LncRNA	LOC728196	miR-513c	TCF7	U87, U251, LN229 and A172	Glioma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30179681	LncRNA LOC728196/miR-513c axis facilitates glioma carcinogenesis by targeting TCF7	We observed a reciprocal inhibition between LOC728196 and miR-513c. Rescue assay showed that either inhibition of miR-513c or TCF7 overexpression restored the abilities of proliferation, migration and invasion in LOC728196-silenced glioma cells.	MI0006649	Gene 2018 Dec 30 679, 119-125 doi:10.1016/j.gene.2018.08.081 PMID:30179681
2647	LncRNA	TINCR	miR-31-5p	CEBPA	Primary human ADSCs	Differentiation Of Adipose Tissue-Derived Mesenchymal Stem Cells	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30172905	LncRNA TINCR/miR-31-5p/C/EBP-α feedback loop modulates the adipogenic differentiation process in human adipose tissue-derived mesenchymal stem cells	Taken together, in hADSCs, lncRNA TINCR, miR-31 and C/EBP-a formed a feedback loop to modulate the adipogenic differentiation process.	MIMAT0000089	Stem Cell Res 2018 Oct 32, 35-42 doi:10.1016/j.scr.2018.08.016 PMID:30172905
2648	LncRNA	lnc-mg	miR-351-5p	LACTB	C57B/L6 mice	Skeletal Myogenesis	Mus musculus (mouse)	qPCR, Luciferase reporter assay etc.	30216112	MicroRNA-351-5p mediates skeletal myogenesis by directly targeting lactamase-b and is regulated by lnc-mg	Further analyses showed that lnc-mg acted as a molecular sponge for miR-351-5p, demonstrating its involvement in the negative regulation of LACTB by miR-351-5p during skeletal myogenesis. 	MIMAT0000609	Faseb j 2019 Feb 33, 1911-1926 doi:10.1096/fj.201701394RRR PMID:30216112
2649	LncRNA	PRNCR1	miR-448	HEY2	A549, SK-MES-1, Calu-3 and H1299	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30257372	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	All mechanism experiments revealed that lncRNA PRNCR1 exerted ceRNA function in NSCLC by regulating miR-448 and HEY2. 	MIMAT0001532	Biomed Pharmacother 2018 Nov 107, 1540-1547 doi:10.1016/j.biopha.2018.08.105 PMID:30257372
2650	LncRNA	FAL1	miR-637	NUPR1	HCT116, HT29, SW620, SW480 and LoVo	Colorectal Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30267804	LncRNA FAL1 promotes carcinogenesis by regulation of miR-637/NUPR1 pathway in colorectal cancer	Additionally, we demonstrate that lncRNA FAL1 acts as a sponge of miR-637, which functions as a suppressor via targeting and downregulation of NUPR1 expression	MIMAT0003307	Int J Biochem Cell Biol 2019 Jan 106, 46-56 doi:10.1016/j.biocel.2018.09.015 PMID:30267804
2651	LncRNA	OGFRP1	miR-124-3p	LYPD3	H1299, SPC-A1, A549, H1975, and HCC827)	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR, Western blot etc.	30274775	Long non-coding RNA OGFRP1 regulates LYPD3 expression by sponging miR-124-3p and promotes non-small cell lung cancer progression	Mechanistically, OGFRP1 could directly bind to miR-124-3p and effectively act as a competing endogenous RNA (ceRNA) for miR-124-3p to promote the expression of the target gene LYPD3. 	MIMAT0000422	Biochem Biophys Res Commun 2018 Oct 28 505, 578-585 doi:10.1016/j.bbrc.2018.09.146 PMID:30274775
2652	Pseudogene	PGK1P2	miR-330-5p	PGK1	Decidual tissues	Preeclampsia	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30177069	Dysfunction of pseudogene PGK1P2 is involved in preeclampsia by acting as a competing endogenous RNA of PGK1	We also found PGK1P2 acted as a competing endogenous RNA (ceRNA) to regulate PGK1 expression through miR-330-5p.	MIMAT0004693	Pregnancy Hypertens 2018 Jul 13, 37-45 doi:10.1016/j.preghy.2018.05.003 PMID:30177069
2653	Pseudogene	BRAFP1	miR-134	BRAF	HCT116 and HeLa	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	25843629	The BRAF pseudogene functions as a competitive endogenous RNA and induces lymphoma in vivo	We show that Braf-rs1 and its human ortholog, BRAFP1, elicit their oncogenic activity, at least in part, as competitive endogenous RNAs (ceRNAs) that elevate BRAF expression and MAPK activation in vitro and in vivo.	MI0000474	Cell 2015 Apr 9 161, 319-32 doi:10.1016/j.cell.2015.02.043 PMID:25843629
2654	Pseudogene	BRAFP1	miR-543	BRAF	HCT116 and HeLa	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	25843629	The BRAF pseudogene functions as a competitive endogenous RNA and induces lymphoma in vivo	We show that Braf-rs1 and its human ortholog, BRAFP1, elicit their oncogenic activity, at least in part, as competitive endogenous RNAs (ceRNAs) that elevate BRAF expression and MAPK activation in vitro and in vivo.	MIMAT0004954	Cell 2015 Apr 9 161, 319-32 doi:10.1016/j.cell.2015.02.043 PMID:25843629
2655	Pseudogene	BRAFP1	miR-653	BRAF	HCT116 and HeLa	Lymphoma	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	25843629	The BRAF pseudogene functions as a competitive endogenous RNA and induces lymphoma in vivo	We show that Braf-rs1 and its human ortholog, BRAFP1, elicit their oncogenic activity, at least in part, as competitive endogenous RNAs (ceRNAs) that elevate BRAF expression and MAPK activation in vitro and in vivo.	MI0003674	Cell 2015 Apr 9 161, 319-32 doi:10.1016/j.cell.2015.02.043 PMID:25843629
2656	Pseudogene	CYP4Z2P	miR-211	CYP4Z1	MCF-7 and MDA-MB231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25701119	The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1	Increased CYP4Z2P- and CYP4Z1-30 UTR expression promotes tumor angiogenesis in breast cancer partly via miRNA-dependent activation of PI3K/Akt and ERK1/2. The CYP4Z2P- and CYP4Z1-30 UTRs could thus be used as combinatorial miRNA inhibitors.	MI0000287	Breast Cancer Res Treat 2015 Feb 150, 105-18 doi:10.1007/s10549-015-3298-2 PMID:25701119
2657	Pseudogene	CYP4Z2P	miR-125a-3p	CYP4Z1	MCF-7 and MDA-MB231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25701119	The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1	Increased CYP4Z2P- and CYP4Z1-30 UTR expression promotes tumor angiogenesis in breast cancer partly via miRNA-dependent activation of PI3K/Akt and ERK1/2. The CYP4Z2P- and CYP4Z1-30 UTRs could thus be used as combinatorial miRNA inhibitors.	MIMAT0004602	Breast Cancer Res Treat 2015 Feb 150, 105-18 doi:10.1007/s10549-015-3298-2 PMID:25701119
2658	Pseudogene	CYP4Z2P	miR-197	CYP4Z1	MCF-7 and MDA-MB231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25701119	The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1	Increased CYP4Z2P- and CYP4Z1-30 UTR expression promotes tumor angiogenesis in breast cancer partly via miRNA-dependent activation of PI3K/Akt and ERK1/2. The CYP4Z2P- and CYP4Z1-30 UTRs could thus be used as combinatorial miRNA inhibitors.	MI0000239	Breast Cancer Res Treat 2015 Feb 150, 105-18 doi:10.1007/s10549-015-3298-2 PMID:25701119
2659	Pseudogene	CYP4Z2P	miR-1226	CYP4Z1	MCF-7 and MDA-MB231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25701119	The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1	Increased CYP4Z2P- and CYP4Z1-30 UTR expression promotes tumor angiogenesis in breast cancer partly via miRNA-dependent activation of PI3K/Akt and ERK1/2. The CYP4Z2P- and CYP4Z1-30 UTRs could thus be used as combinatorial miRNA inhibitors.	MI0006313	Breast Cancer Res Treat 2015 Feb 150, 105-18 doi:10.1007/s10549-015-3298-2 PMID:25701119
2660	Pseudogene	CYP4Z2P	miR-204	CYP4Z1	MCF-7 and MDA-MB231	Breast Cancer	Homo sapiens (human)	qPCR, Western blot etc.	25701119	The 3'UTR of the pseudogene CYP4Z2P promotes tumor angiogenesis in breast cancer by acting as a ceRNA for CYP4Z1	Increased CYP4Z2P- and CYP4Z1-30 UTR expression promotes tumor angiogenesis in breast cancer partly via miRNA-dependent activation of PI3K/Akt and ERK1/2. The CYP4Z2P- and CYP4Z1-30 UTRs could thus be used as combinatorial miRNA inhibitors.	MI0000284	Breast Cancer Res Treat 2015 Feb 150, 105-18 doi:10.1007/s10549-015-3298-2 PMID:25701119
2661	Pseudogene	PTENP1	miR-499-5p	PTEN	db/db mice	Insulin Resistance	Mus musculus (mouse)	qPCR, Western blot, Luciferase reporter assay etc.	27449620	Pseudogene PTENP1 Functions as a Competing Endogenous RNA (ceRNA) to Regulate PTEN Expression by Sponging miR-499-5p	More importantly, PTENP1 could directly bind miR-499-5p, thereby becoming a sink for miR-499-5p. PTENP1 overexpression results in the impairment of the insulin-signaling pathway and may function as a competing endogenous RNA for miR-499-5p, thereby contributing to insulin resistance.	MIMAT0003482	Biochemistry (Mosc) 2016 Jul 81, 739-47 doi:10.1134/s0006297916070105 PMID:27449620
2662	Pseudogene	PTENP1	miR-21	PTEN	786-O, ACHN, and SN12PM6	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	25249556	Pseudogene PTENP1 functions as a competing endogenous RNA to suppress clear-cell renal cell carcinoma progression	These results suggest that PTENP1 functions as a competing endogenous RNA (ceRNA) in ccRCC to suppress cancer progression	MI0000077	Mol Cancer Ther 2014 Dec 13, 3086-97 doi:10.1158/1535-7163.Mct-14-0245 PMID:25249556
2663	Pseudogene	CYP4Z2P	miR-125a-3p	CYP4Z1	MCF-7	Breast Cancer	Homo sapiens (human)	qPCR, Western blot, MIT etc.	26980484	Competing endogenous RNA networks of CYP4Z1 and pseudogene CYP4Z2P confer tamoxifen resistance in breast cancer	Our data demonstrates that the ceRNET between CYP4Z1 and pseudogene CYP4Z2P acts as a sub-ceRNET to promote CDK3 expression in ER-positive breast cancer and is a potential therapeutic target for treatment of tamoxifen-resistant breast cancer.	MIMAT0004602	Mol Cell Endocrinol 2016 May 15 427, 133-42 doi:10.1016/j.mce.2016.03.012 PMID:26980484
2664	Pseudogene	GBAP1	miR-22-3p	GBA	HEK293, HepG2, and HeLa	Pluripotent Stem Cells 	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	28983119	The GBAP1 pseudogene acts as a ceRNA for the glucocerebrosidase gene GBA by sponging miR-22-3p	Our results describe the first microRNA controlling GBA and suggest that the GBAP1 non-coding RNA functions as a GBA ceRNA.	MIMAT0000077	Sci Rep 2017 Oct 5 7, 12702 doi:10.1038/s41598-017-12973-5 PMID:28983119
2665	Pseudogene	HMGA1P7	miR-483	Egr1	MEFs and NIH3T3	Neoplasias	Homo sapiens (human)	qPCR etc.	29149041	The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism	Here, we report that HMGA1P7 upregulates miR-483 and miR-675 through a competing endogenous RNA mechanism with Egr1, a transcriptional factor that positively regulates miR-483 and miR-675 expression.	MI0002467	Genes (Basel) 2017 Nov 17 8 doi:10.3390/genes8110330 PMID:29149041
2666	Pseudogene	HMGA1P7	miR-675	Egr1	MEFs and NIH3T3	Neoplasias	Homo sapiens (human)	qPCR etc.	29149041	The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism	Here, we report that HMGA1P7 upregulates miR-483 and miR-675 through a competing endogenous RNA mechanism with Egr1, a transcriptional factor that positively regulates miR-483 and miR-675 expression.	MI0005416	Genes (Basel) 2017 Nov 17 8 doi:10.3390/genes8110330 PMID:29149041
2667	Pseudogene	FTH1 pseudogenes	miR-638	FTH1	DU145 and PC3	Prostate Cancer	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	29240947	A FTH1 gene:pseudogene:microRNA network regulates tumorigenesis in prostate cancer	In this study, we characterize the tumor-suppressive FTH1 gene:pseudogene network. This network is targeted by miR-638 and other oncogenic miRNAs	MIMAT0003308	Nucleic Acids Res 2018 Feb 28 46, 1998-2011 doi:10.1093/nar/gkx1248 PMID:29240947
2668	Pseudogene	PGK1P2	miR-330-5p	PGK1	hESCs	Preeclampsia	Homo sapiens (human)	qPCR, Western blot etc.	30177069	Dysfunction of pseudogene PGK1P2 is involved in preeclampsia by acting as a competing endogenous RNA of PGK1	We proved that PGK1 and PGK1P2 are a pair of ceRNAs against miR-330-5p and they play a vital role in human decidualization by regulating angiogenesis and glycolysis metabolism.	MIMAT0004693	Pregnancy Hypertens 2018 Jul 13, 37-45 doi:10.1016/j.preghy.2018.05.003 PMID:30177069
2669	Circular RNA	CircEGFR	miR-125a-3p	Fyn	Mouse	Granulosa Cell	Mus musculus (mouse)	qPCR, Western blot, Luciferase reporter assay etc.	30261810	Circular RNA expression profile in mouse cortex after traumatic brain injury	RNA immunoprecipitation and luciferase reporter assays demonstrated that circEGFR may act as a sponge for miR-125a-3p, thus modulating Fyn expression. 	MIMAT0004602	J Neurotrauma 2019 Apr 1 36, 1018-1028 doi:10.1089/neu.2018.5647 PMID:30261810
2670	Circular RNA	Circ-ITCH	miR-145	RASA1	SK-OV-3 and Caov-3	Ovarian Cancer	Homo sapiens (human)	qPCR etc.	30243714	The circular RNA circ-ITCH suppresses ovarian carcinoma progression through targeting miR-145/RASA1 signaling	Mechanically, we demonstrated that circ-TCH acts as a ceRNA to sponge miR-145, increases the level of RASA1, and inhibits the malignant progression of OC cells via the circ-ITCH-miR-145-RASA1 axis in vitro and in vivo.	MI0000461	Biochem Biophys Res Commun 2018 Oct 20 505, 222-228 doi:10.1016/j.bbrc.2018.09.060 PMID:30243714
2671	Circular RNA	hsa_circ_0012919	miR-125a-3p	DNMT1	Tissues	Systemic Lupus Erythematous	Homo sapiens (human)	qPCR, Western blot, Luciferase reporter assay etc.	30237316	The downregulation of hsa_circ_0012919, sponge for miR-125a-3p, contributes to DNA methylation of CD11a and CD70 in CD4+T cells of SLE	Hsa_circ_0012919 could be regarded as a biomarker for SLE and hsa_circ_0012919 was the ceRNA for miR-125a-3p.	MIMAT0004602	Clin Sci (Lond) 2018 Nov 15 132, 2285-2298 doi:10.1042/cs20180403 PMID:30237316
2672	Circular RNA	hsa_circ_0020123	miR-144	ZEB1	PC9, H1573, A549, SK-MES-1, H1299, and Calu-3	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	30210911	A novel circular RNA hsa_circ_0020123 exerts oncogenic properties through suppression of miR-144 in non-small cell lung cancer	In addition, hsa_circ_0020123 could upregulate ZEB1 and EZH2 through competitively binding with miR-144.	MI0000460	Am J Cancer Res 2018  8, 1387-1402,  PMID:30210911
2673	Circular RNA	hsa_circ_0020123	miR-144	EZH2	PC9, H1573, A549, SK-MES-1, H1299, and Calu-3	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR etc.	30210911	A novel circular RNA hsa_circ_0020123 exerts oncogenic properties through suppression of miR-144 in non-small cell lung cancer	In addition, hsa_circ_0020123 could upregulate ZEB1 and EZH2 through competitively binding with miR-144.	MI0000460	Am J Cancer Res 2018  8, 1387-1402,  PMID:30210911
2674	Circular RNA	hsa_circ_0080145	miR-29b	NA	Cancer stem cells	Chronic Myeloid Leukemia	Homo sapiens (human)	qPCR etc.	30205959	Global identification of circular RNAs in chronic myeloid leukemia reveals hsa_circ_0080145 regulates cell proliferation by sponging miR29b	Furthermore, functional experiments demonstrated that hsa_circ_0080145 knockdown significantly suppressed CML cell proliferation and hsa_circ_0080145 regulated CML cell proliferation by acting as an miR-29b sponge.	MI0000105	Biochem Biophys Res Commun 2018 Oct 12 504, 660-665 doi:10.1016/j.bbrc.2018.08.154 PMID:30205959
2675	Circular RNA	CircRNA-9119	miR-26a	PTGS2	Tissues	Development Of Receptive Endometrium	Capra hircus (goat)	qPCR, Western blot, Luciferase reporter assay etc.	29983139	CircRNA-9119 regulates the expression of prostaglandin-endoperoxide synthase 2 (PTGS2) by sponging miR-26a in the endometrial epithelial cells of dairy goat	Thus, a circRNA-9119-miR-26a-PTGS2 pathway in the endometrium was identified, and modulation of circRNA-9119-miR-26a-PTGS2 expression in EECs may emerge as a potential target to regulate the development of RE.	MI0000083	Reprod Fertil Dev 2018 Nov 30, 1759-1769 doi:10.1071/rd18074 PMID:29983139
2676	Circular RNA	hsa_circ_0036877	miR-519d-3p	Furin	Blood tissues	Preeclampsia	Homo sapiens (human)	qPCR, RIP etc.	29643944	Competing endogenous RNA expression profiling in pre-eclampsia identifies hsa_circ_0036877 as a potential novel blood biomarker for early pre-eclampsia	RNA immunoprecipitation (RIP) of AGO2 in htra-8 cells and qRT-PCR analysis of hsa_circ_0036877 expression in maternal whole peripheral blood samples of participants were then conducted to confirm that hsa_circ_0036877 is a ceRNA and potential novel blood biomarker for early PE, respectively.	MIMAT0002853	Clin Epigenetics 2018  10, 48 doi:10.1186/s13148-018-0482-3 PMID:29643944
2677	Circular RNA	CircEGFR	miR-125a-3p	Fyn	C57BL/6 mice	Granulosa Cell	Mus musculus (mouse)	qPCR, Western blot, RIP etc.	29634953	Circular RNA expression profiles of mouse ovaries during postnatal development and the function of circular RNA epidermal growth factor receptor in granulosa cells	RNA immunoprecipitation and luciferase reporter assays demonstrated that circEGFR may act as a sponge for miR-125a-3p, thus modulating Fyn expression.	MIMAT0004602	Metabolism 2018 Aug 85, 192-204 doi:10.1016/j.metabol.2018.04.002 PMID:29634953
2678	Circular RNA	CircRNA-chr19	miR-30b-3p	CLDN18	pCAGGS-L, pCAGGS-NP, pCAGGS-VP30, pCAGGS-VP35, and pCAGGS-T7	Ebola Virus	Homo sapiens (human)	qPCR, Western blot etc.	29209594	Genome-Wide Search for Competing Endogenous RNAs Responsible for the Effects Induced by Ebola Virus Replication and Transcription Using a trVLP System	Our results demonstrated that circRNA-chr19 targeting miR-30b-3p regulated CLDN18 expression by functioning as a ceRNA.	MIMAT0004589	Front Cell Infect Microbiol 2017  7, 479 doi:10.3389/fcimb.2017.00479 PMID:29209594
2679	LncRNA	LINC01410	miR-506-3p	WEE1	SK-N-SH, IMR-32, Kelly, and SH-SY5Y	Neuroblastoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32886453	Long noncoding RNA LINC01410 promotes the tumorigenesis of neuroblastoma cells by sponging microRNA-506-3p and modulating WEE1	The expression of LINC01410 and WEE1 was enhanced and miR-506-3p was inhibited in NBL. LINC01410 knockdown attenuated the cell proliferation, colony formation ability, and inhibited tumor growth. Moreover, LINC01410 silencing facilitated the apoptosis and arrested the cell cycle. LINC01410 interacted with miR-506-3p to elevate the WEE1 expression in NBL. Additionally, miR-506-3p inhibition or WEE1 overexpression weakened the reduction effects of sh-LINC01410 on cell proliferation, colony formation ability, apoptosis, and cell cycle.	NA	Cancer Med 2020 Nov 9, 8133-8143 doi:10.1002/cam4.3398 PMID:32886453
2680	LncRNA	TTN-AS1	miR-411-3p	NFAT	human tongue squamous carcinoma cell lines, including SCC-4, SCC-9, CAL-27 and BICR-16 cell 	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR，Flow cytometry assay，FISH，RIP，Luciferase reporter assay，Western blot etc.	32863773	LncRNA TTN-AS1 promotes the progression of oral squamous cell carcinoma via miR-411-3p/NFAT5 axis.	TTN-AS1 expression was stronger in OSCC cells. Knockdown of TTN-AS1 effectively restrained cell proliferation and migration but had inductive role in apoptosis. Moreover, TTN-AS1 could function as the miR-411-3p sponge in OSCC and miR-411-3p exerted the inhibitory functions on OSCC cell growth. In addition, NFAT5 was proven as the target of miR-411-3p. Rescue assay indicated that overexpressing NFAT5 could reverse the inhibitory function of TTN-AS1 depletion on cell growth.	NA	Cancer Cell Int 2020  20, 415 doi:10.1186/s12935-020-01378-6 PMID:32863773
2681	LncRNA	LBX2-AS1	miR-491-5p	NA	Human glioma cell lines U87MG, U251MG and A172 	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32863770	Long non-coding RNA LBX2-AS1 enhances glioma proliferation through downregulating microRNA-491-5p	Following study of GTEx and TCGA data, LBX2-AS1 was significantly elevated in glioma compared with normal brain and in GBM compared with LGG. Higher expression of LBX2-AS1 was associated with poor prognosis of patients with glioma. Expression of LBX2-AS1 was positively correlated with pathology classification of glioma. Knockdown of LBX2-AS1 inhibited cell proliferation and induced cell apoptosis in glioma. LBX2-AS1 have complimentary binding site for tumor suppressor miR-491-5p and we showed that LBX2-AS1 sponged miR-491-5p to upregulate TRIM28 expression in glioma cells. TRIM28 overexpression attenuated the effect of LBX2-AS1 knockdown on glioma cells.	NA	Cancer Cell Int 2020  20, 411 doi:10.1186/s12935-020-01433-2 PMID:32863770
2682	LncRNA	TMPO-AS1	miR-329-3p	FOXK1	Human liver epithelial cell (THLE-3) and HCC cells (Huh7, Hep3B, and LM3) 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc	32462698	LncRNA TMPO-AS1 promotes hepatocellular carcinoma cell proliferation, migration and invasion through sponging miR-329-3p to stimulate FOXK1-mediated AKT/mTOR signaling pathway	TMPO-AS1was upregulated in HCC tissues and cells and its depletion inhibits HCC cell proliferation, invasion, migration, and EMT process as well as tumor growth. Furthermore, TMPO-AS1 could bind with miR-329-3p, which suppressed HCC cell proliferation. FOXK1 served as the target gene of miR-329-3p and TMPO-AS1 upregulated FOXK1 by sponging miR-329-3p in HCC cells. Additionally, FOXK1 overexpression or miR-329-3p inhibitor neutralized the repressing effects of TMPO-AS1 knockdown on HCC development. Finally, it verified that TMPO-AS1 could regulate AKT/mTOR pathway via FOXK1 to promote HCC.	NA	Cancer Med 2020 Jul 9, 5235-5246 doi:10.1002/cam4.3046 PMID:32462698
2683	LncRNA	ZNRD1-AS1	miR-194	ZEB1	The human bladder epithelium cell line (SVHUC-1) and BC cell lines (RT4, UMUC3, T24, SW780, 5637, and RT112)	Bladder Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc	32862492	Knockdown of lncRNA ZNRD1-AS1 inhibits progression of bladder cancer by regulating miR-194 and ZEB1.	Knockdown of ZNRD1-AS1 suppressed BC cell development in vitro and in vivo via targeting miR-194 to regulate ZEB1, indicating a novel avenue for treatment of BC.	NA	Cancer Med 2020 Oct 9, 7695-7705 doi:10.1002/cam4.3373 PMID:32862492
2684	LncRNA	SNHG3	miR-485	ATG7	Mouse neuroblastoma Neuro-2a (N2a) cells	Autophagy-Induced Neuronal Cell Apoptosis	Mus musculus (mouse)	qRT-PCR,Western blot,Luciferase reporter assay etc	32860611	LncRNA SNHG3 promotes autophagy-induced neuronal cell apoptosis by acting as a ceRNA for miR-485 to up-regulate ATG7 expression.	In summary, from our experimental data, it was found thatLncRNA SNHG3 was highly expressed in the mouse modelof the tMCAO and cell model of OGD/R, while miR-485 waslowly expressed, and our further studies had found that theinterference with LncRNA SNHG3 improved brain I/R injuryvia up-regulating miR-485 and down-regulating ATG7 to restrain autophagy and neuronal cell apoptosis. Therefore, thisresearchmight provide new strategies for the treatment ofbrain I/R injury, which was of great significance	NA	Metab Brain Dis 2020 Dec 35, 1361-1369 doi:10.1007/s11011-020-00607-1 PMID:32860611
2685	LncRNA	DANCR	miR-216a-5p	NA	Human OSCC cell lines (SCC9,SCC15,SCC25,CAL-27 and Tca8113) and normal human oral keratinocytes (NHOKs)	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT?PCR,Western blot,Luciferase reporter assay,Flow cytometry assay etc	32860589	LncRNA DANCR regulates the growth and metastasis of oral squamous cell carcinoma cells via altering miR-216a-5p expression.	To conclude, our study found the up-regulated DANCR expression and the down-regulated miR-216a-5p expression in OSCC. Thus, DANCR could promote the cell growth, migration and invasion and suppress the cell apoptosis of OSCC cells via targeting miR-216a-5p, which may offer an alternative treatment of OSCC.	NA	Hum Cell 2020 Oct 33, 1281-1293 doi:10.1007/s13577-020-00411-0 PMID:32860589
2686	LncRNA	MCF2L-AS1	miR-874-3p	FOXM1	The human CRC cell lines (HCT116, HT-29, SW620, SW480, LoVo, RKO and DLD1) and normal human colonic epithelial cell line NCM46	Colorectal Cancer	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay etc	32860508	LncRNA MCF2L-AS1 aggravates proliferation, invasion and glycolysis of colorectal cancer cells via the crosstalk with miR-874-3p/FOXM1 signaling axis.	To sum up, our findings disclosed for the first time that MCF2L-AS1 modulated FOXM1 expression by binding to miR-874-3p, ultimately promoting tumorigenesis, invasiveness and glycolytic metabolism in CRC. We established and characterized a non-canonical MCF2L-AS1/miR-874-3p/FOXM1  crosstalk  that  regulated  tumorigenesis  and  glycolysis,  and highlighted the novel tumor stimulative properties of MCF2L-AS1 in CRC. This sheds a new insight into the regulation mechanism of MCF2L-AS1, and it provides a possible application for the CRC treatment.	NA	Carcinogenesis 2021 Feb 25 42, 263-271 doi:10.1093/carcin/bgaa093 PMID:32860508
2687	LncRNA	CASC7	miR-30c	IL-11	H9C2 cells	Heart Failure	Homo sapiens (human)	RT-PCR,Luciferase reporter assay,Western blot etc	32860492	Long non-coding RNA CASC7 is associated with the pathogenesis of heart failure via modulating the expression of miR-30c.	In summary, the expression of CASC7 was high while the expres-sion of miR-30c was low in plasma and peripheral blood monocytes collected from HF patients. Furthermore, miR-30c can be used as a diagnostic biomarker of HF, while CASC7 is a competing endog-enous RNA of miR-30c. CASC7 can indirectly regulate IL-11 expres-sion via miR-30. The results of this study provided a new perspective for lncRNA-directed diagnosis and treatment of HF.	NA	J Cell Mol Med 2020 Oct 24, 11500-11511 doi:10.1111/jcmm.15764 PMID:32860492
2688	LncRNA	RP11-1094M14.8	miR-1269a	CXCL9	GC cell lines (AGS, MKN45, NCI-N87 and MGC803) and the human gastric epithelial cell line (GES-1) 	Gastric Cancer	Homo sapiens (human)	qRT-PCR,Western blot etc.	32860283	A ceRNA network and a potential regulatory axis in gastric cancer with different degrees of immune cell infiltration	In conclusion, we provided a comprehensive view of the un-derlying mechanism for the progression of different degrees of immune infiltration of gastric cancer by constructing a ceRNA regulatory  network  and  axis.	NA	Cancer Sci 2020 Nov 111, 4041-4050 doi:10.1111/cas.14634 PMID:32860283
2689	LncRNA	SNHG16	miR-124-3p	MCP-1	HEK293T, FHC cells, and human CRC cell lines SW480,HCT116, DLD-1, and LOVO cells	Colorectal Cancer	Homo sapiens (human)	Western blot,qRT-PCR,Luciferase reporter assay,RIP etc.	32859986	LncRNA SNHG16 promotes colorectal cancer cell proliferation, migration, and epithelial-mesenchymal transition through miR-124-3p/MCP-1.	In conclusion, we highlight the primary role of SNHG16in proliferation, migration, and EMT of CRC cells through miR-124-3p/MCP-1 axis. Ourfindings support the notionthat the development of SNHG16/miR-124-3p/MCP-1 axis-targeted drugs is an effective strategy for treating CRC.	NA	Gene Ther 2020 Aug 28, 10.1038/s41434-020-0176-2 doi:10.1038/s41434-020-0176-2 PMID:32859986
2690	LncRNA	SNHG1	miR-9-5p	FtMt	Human  glioma  cell lines(U251, A172,  U87  and  SHG44),human  normal  glia  HEB  cells and human umbilical vein endothelial cells (HUVEC)	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,Flow cytometry assay,Luciferase reporter assay,RIP etc.	32858123	FtMt promotes glioma tumorigenesis and angiogenesis via lncRNA SNHG1/miR-9-5p axis.	To sum up, Figure 7shows a schematic representation of the proposed mechanism of FtMtas a novel candidate target  for the treatment of glioma.Specifically, FtMtmay  serve  as a therapeutic agent  for  glioma  treatment  based  on  the  finding  that  FtMt  depletion  suppresses  tumorigenesis  and angiogenesis of glioma cell through SNHG1/miR-9-5p axis. Despite the function of FtMt in glioma tumorigenesis  and  angiogenesis  thatare  covered  in  the  present  study,  further  investigation  is necessary to expound the role and the precise mechanisms whereby FtMt promotethe development of  glioma.  Anyway,  our  ultimate  goal  is  to  deeply  investigate  the  underlying  mechanism  and explore thepotential novel strategy for the treatment of glioma.	NA	Cell Signal 2020 Nov 75, 109749 doi:10.1016/j.cellsig.2020.109749 PMID:32858123
2691	LncRNA	XIST	miR-375	L1CAM	Human neuroblastoma cell lines (SK-N-AS, IMR-32, and Kelly)  and  human  umbilical  vascular  endothelium  cells  HUVEC 	Neuroblastoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot etc.	32857295	Downregulation of lncRNA XIST Represses Tumor Growth and Boosts Radiosensitivity of Neuroblastoma via Modulation of the miR-375/L1CAM Axis.	In summary, our results proved that XIST silencing repressed tumor growth and enhanced radiosensitivity in NB through regulation of the miR-375/L1CAM axis (Fig. 8). The research highlighted the prospect of XIST as a new target for NB treatment.	NA	Neurochem Res 2020 Nov 45, 2679-2690 doi:10.1007/s11064-020-03117-9 PMID:32857295
2692	LncRNA	GAS5	miR-362-5p	SMG1	TC cell lines TPC-1 and B-CPAP	Thyroid Cancer	Homo sapiens (human)	Flow cytometry assay,Luciferase reporter assay,qRT-PCR,Western blot etc.	32856394	LncRNA GAS5 sponges miR-362-5p to promote sensitivity of thyroid cancer cells to (131) I by upregulating SMG1.	Collectively, we found that GAS5 overexpression coulddownregulate miR-362-5p to inhibit resistance of TC cellsto131I by  upregulating  SMG1 and  inactivating theAkt/mTOR signaling pathway. This study may providenovel targets for TC therapy, while further studies arestill needed to deepen the understanding on detailedmechanisms of TC.	NA	IUBMB Life 2020 Nov 72, 2420-2431 doi:10.1002/iub.2365 PMID:32856394
2693	LncRNA	MEG3	miR-195-5p	FGFR2	Human pancreatic duct epithelial cells (HPDE)	Caerulein-Induced Inflammatory Injury 	Homo sapiens (human)	qRT-PCR,Flow cytometry assay,Western blot etc.	32856219	LncRNA MEG3 Participates in Caerulein-Induced Inflammatory Injury in Human Pancreatic Cells via Regulating miR-195-5p/FGFR2 Axis and Inactivating NF-κB Pathway.	In summary, this study mainly introduced the anti-inflammatory role of MEG3 in AP cell models. Through-out this paper, the inhibited MEG3/miR-195-5p/FGFR2regulatory axis associated with the NF-κB signaling path-way was incorporated into the pathogenesis of AP. Thisnovel finding characterized several promising biomarkersin diagnosis and therapy of AP and supplied a wide horizoninto understanding the pathogenesis of AP.	NA	Inflammation 2021 Feb 44, 160-173 doi:10.1007/s10753-020-01318-6 PMID:32856219
2694	LncRNA	NEAT1	miR-590-3p	NA	Cardiomyocytes (H9c2 cells) 	Lps-Induced Sepsis	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,RIP etc.	32855700	LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p.	In summary, the present study suggested that NEAT1 plays a promotive role in sepsis progression by sponging miR-590-3p. This is a novel mechanism by which NEAT1 acts on the progression of sepsis. The inhibitory effects of NEAT1 knockdown and miR-590-3p overexpression on LPS-induced cardiomyocyte damage can provide new strategies for the clinical treatment of sepsis. Hence, the discovery of the NEAT1/miR-590-3p axis may contribute to the development of new treatments for sepsis.	NA	Exp Ther Med 2020 Oct 20, 3290-3300 doi:10.3892/etm.2020.9079 PMID:32855700
2695	LncRNA	LINC00324	miR-3200-5p	BCAT1	Three human GC cell lines, AGS, MGC803, and MKN-45, and the human normal gastric epithelial cell line GES-1	Gastric Cancer	Homo sapiens (human)	qRT-PCR,luciferase reporter assay etc.	32855634	Silencing of Long Noncoding RNA LINC00324 Interacts with MicroRNA-3200-5p to Attenuate the Tumorigenesis of Gastric Cancer via Regulating BCAT1.	In conclusion, the expression of LINC00324 was upregulated in GC tissues and cells. Silencing of LINC00324 inhibited the proliferation, migration, and invasion of GC cells through regulating the miR-3200-5p/BCAT1 axis. Our research indicated that LINC00324 might act as a potential therapeutic target for GC. However, the detailed action mechanisms of LINC00324 on GC remain limited, and further researches are still needed.	NA	Gastroenterol Res Pract 2020  2020, 4159298 doi:10.1155/2020/4159298 PMID:32855634
2696	LncRNA	IGF2-AS	miR-150	IGF2	NCM-460, CCC-HIE-2, SW620, LoVo, HT29, HCT116, HCT8, DLD1and 293 T cell	Colorectal Cancer	Homo sapiens (human)	qPCR,luciferase reporter assay,RNA-seq etc.	32853944	Comprehensive ceRNA network analysis and experimental studies identify an IGF2-AS/miR-150/IGF2 regulatory axis in colorectal cancer.	In summary, we successfully built ceRNA regulatory networks toprovide a comprehensive understanding of detailed molecular me-chanisms underlying the pathogenesis of CRC using two independentdatasets. Importantly, we confirmed a potential regulatory axis thatIGF2-AS could regulate the expression of IGF2 by sponging miR-150that was validated in both CRC cell lines and clinical samples. Wesuppose that the IGF2-AS/miR-150/IGF2 axis may exert a critical rolein the development and progression of CRC.	NA	Pathol Res Pract 2020 Oct 216, 153104 doi:10.1016/j.prp.2020.153104 PMID:32853944
2697	LncRNA	FTX	miR-186	c-Met	Normal BMSCs and malignantly transformed BMSCs 	Malignant Phenotype In Bone Marrow Mesenchymal Stem Cells	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc..	32853911	The long noncoding RNA FTX promotes a malignant phenotype in bone marrow mesenchymal stem cells via the miR-186/c-Met axis.	Our study showed that BMSCs were malignantly transformed by GSCs in a dual-colour fluorescent tumour model. Moreover, lncRNA-FTX was found to  promote the  proliferation, migration and invasion of tBMSCs by  sponging miR-186 and functionally upregulating c-Met expression. Our findings provide a new perspective in that lncRNA-FTX/ miR-186/c-Met is  involved in  glioma progression, and this axis may serve as a new target for the treatment of glioma	NA	Biomed Pharmacother 2020 Nov 131, 110666 doi:10.1016/j.biopha.2020.110666 PMID:32853911
2698	LncRNA	MEG3	miR-7b	NLRP3	Mouse alveolar macrophages  	Lps-Induced Acute Lung Injury	Mus musculus (mouse)	qRT-PCR,Western blot,luciferase reporter assay,RIP,FISH etc.	32852284	Silencing of long non-coding RNA MEG3 alleviates Lps-Induced Acute Lung Injury by acting as a molecular sponge of microRNA-7b to modulate NLRP3.	Taken together, our findings provided evidence that lncRNA MEG3 acts as the internal competitive RNA of miR-7b. When lncRNA MEG3 was downregulated, the binding of miR-7b to NLRP3 increased and the lncRNA NLRP3 expression was inhibited, thus resulting in improved LPS-induced ALI (Figure 6). Our study proposes novel biological markers for the treatment of ALI, which could potentially provide a new perspective regarding the theoretical basis of the NLRP3 mechanism. However, our study was performed based on the model of LPS-induced ALI in cells and mice, with the clinical effects of the lncRNA MEG3/miR-7b/NLRP3 axis in LPS-induced ALI treatment still largely unknown. 	NA	Aging (Albany NY) 2020 Aug 27 12, 20198-20211 doi:10.18632/aging.103752 PMID:32852284
2699	LncRNA	NEAT1	miR-195a	BAX	Human Nucleus Pulposus Cells (HNPC, Cat. No. 4800)	Intervertebral Disc Degeneration	Mus musculus (mouse)	RT-PCR,Western blot,Luciferase reporter assay etc.	32850952	Silencing of Long Non-coding RNA NEAT1 Upregulates miR-195a to Attenuate Intervertebral Disk Degeneration via the BAX/BAK Pathway.	NEAT1 played its role in IVDD progression via partly by mediating the miR-195 expression and might be used as a potential target for IVDD therapy.	NA	Front Mol Biosci 2020  7, 147 doi:10.3389/fmolb.2020.00147 PMID:32850952
2700	LncRNA	LINC01705	miR-186-5p	TPR	The human normal mammary epithelial cell line MCF 10A and the breast cancer cell lines CAL-51, MCF-7, BT-20, BT-549, and AU565	Breast Cancer	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay,Western blot etc.	32849791	The Long Non-coding RNA LINC01705 Regulates the Development of Breast Cancer by Sponging miR-186-5p to Mediate TPR Expression as a Competitive Endogenous RNA.	In summary, LINC01705 acts as a competitive endogenous RNA to regulate TPR expression via sponging miR-186-5p, thereby regulating the progression of breast cancer.	NA	Front Genet 2020  11, 779 doi:10.3389/fgene.2020.00779 PMID:32849791
2701	LncRNA	FGD5-AS1	miR-153-3p	CITED2	Five gastric cancer cell lines, AGS, NIC-N87, SNU-1, SNU-5, and SNU-16	Gastric Cancer	Homo sapiens (human)	qRT-PCR,luciferase reporter assay etc.	32849774	Long Non-coding RNA FGD5-AS1 Regulates Cancer Cell Proliferation and Chemoresistance in Gastric Cancer Through miR-153-3p/CITED2 Axis.	We demonstrated that FGD5-AS1 can regulate human gastric cancer cell functions, possibly through its downstream epigenetic axis of hsa-miR-153-3p/CITED2.	NA	Front Genet 2020  11, 715 doi:10.3389/fgene.2020.00715 PMID:32849774
2702	LncRNA	OIP5-AS1	miR-367-3p	SPARC	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2703	LncRNA	OIP5-AS1	miR-424-5p	SPARC	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2704	LncRNA	OIP5-AS1	miR-143-3p	SPARC	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2705	LncRNA	MCF2L-AS1	miR-105-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2706	LncRNA	TMPO-AS1	hsa-let-7c-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2707	LncRNA	TMPO-AS1	hsa-let-7b-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2708	LncRNA	TMPO-AS1	hsa-let-7a-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2709	LncRNA	TMPO-AS1	hsa-let-7f-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2710	LncRNA	TMPO-AS1	hsa-let-7d-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2711	LncRNA	TMPO-AS1	hsa-let-7i-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2712	LncRNA	TMPO-AS1	hsa-let-7e-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2713	LncRNA	TMPO-AS1	hsa-let-7g-5p	SLC12A7	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2714	LncRNA	HCP5	miR-106b-5p	KYNU	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2715	LncRNA	HCP5	miR-106a-5p	KYNU	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2716	LncRNA	DLEU1	miR-106b-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2717	LncRNA	DLEU1	miR-124-3p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2718	LncRNA	DLEU1	miR-1224-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2719	LncRNA	DLEU1	miR-3934-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2720	LncRNA	HCP5	miR-106b-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2721	LncRNA	HCP5	miR-1-3p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2722	LncRNA	HCP5	miR-101-3p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2723	LncRNA	HCP5	miR-106a-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2724	LncRNA	PPP1R26-AS1	miR-122-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2725	LncRNA	CCDC18-AS1	miR-124-3p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2726	LncRNA	CCDC18-AS1	miR-1-3p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2727	LncRNA	MCF2L-AS1	miR-105-5p	TTF2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2728	LncRNA	TMPO-AS1	hsa-let-7f-5p	KIF21B	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2729	LncRNA	TMPO-AS1	hsa-let-7i-5p	KIF21B	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2730	LncRNA	TRG-AS1	hsa-let-7f-5p	KIF21B	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2731	LncRNA	TRG-AS1	hsa-let-7i-5p	KIF21B	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2732	LncRNA	PPP1R26-AS1	miR-122-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2733	LncRNA	DLEU1	miR-124-3p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2734	LncRNA	DLEU1	miR-1224-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2735	LncRNA	DLEU1	miR-940	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2736	LncRNA	TMPO-AS1	hsa-let-7c-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2737	LncRNA	TMPO-AS1	hsa-let-7b-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2738	LncRNA	TMPO-AS1	hsa-let-7a-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2739	LncRNA	TMPO-AS1	hsa-let-7f-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2740	LncRNA	TMPO-AS1	hsa-let-7d-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2741	LncRNA	TMPO-AS1	hsa-let-7i-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2742	LncRNA	TMPO-AS1	hsa-let-7e-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2743	LncRNA	TMPO-AS1	hsa-let-7g-5p	ACLY	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2744	LncRNA	MCF2L-AS1	miR-105-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2745	LncRNA	CCDC18-AS1	miR-1-3p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2746	LncRNA	SH3BP5-AS1	miR-1193	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2747	LncRNA	OIP5-AS1	hsa-let-7a-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2748	LncRNA	OIP5-AS1	miR-105-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2749	LncRNA	OIP5-AS1	miR-1179	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2750	LncRNA	OIP5-AS1	miR-1197	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2751	LncRNA	OIP5-AS1	miR-143-3p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2752	LncRNA	TTC28-AS1	miR-103a-3p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2753	LncRNA	TTC28-AS1	miR-106a-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2754	LncRNA	TMPO-AS1	hsa-let-7c-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2755	LncRNA	TMPO-AS1	hsa-let-7b-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2756	LncRNA	TMPO-AS1	hsa-let-7a-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2757	LncRNA	TMPO-AS1	hsa-let-7f-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2758	LncRNA	TMPO-AS1	hsa-let-7d-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2759	LncRNA	TMPO-AS1	hsa-let-7i-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2760	LncRNA	TMPO-AS1	hsa-let-7e-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2761	LncRNA	TMPO-AS1	hsa-let-7g-5p	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2762	LncRNA	TMPO-AS1	miR-1179	MSI2	NA	Gastric Cancer	Homo sapiens (human)	RNA-seq,Microarray etc.	32848739	Construction and Analysis of the Tumor-Specific mRNA-miRNA-lncRNA Network in Gastric Cancer.	In summary, we identified a survival-related gene-based ceRNA network using the WGCNA algorithm, and the constructed lncRNA–miRNA–mRNA ceRNA interactive network will probably provide a basis for additional inspection of the regulatory mechanisms of gastric cancer. Gastric cancer has high heterogeneity among its different histological and molecular subtypes. Thus, while we have selected the expression profiles with the largest sample size that we could obtain currently, we must admit that further experimental works and large cohorts are needed to verify our results and elucidate the prognostic value of ceRNA networks in gastric cancer.	NA	Front Pharmacol 2020  11, 1112 doi:10.3389/fphar.2020.01112 PMID:32848739
2763	LncRNA	LINC00173	miR-765	NUTF2	The normal human astrocyte (NHA) and glioma cell lines	Glioma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot etc.	32848473	Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma.	LINC00173 expression was elevated in glioma tissues and cells. LINC00173 high expression predicted poor prognosis. Loss of LINC00173 inhibited proliferation, migration and invasion. LINC00173 interacted with miR-765 to enhance NUTF2 expression. MiR-765 expression was negatively correlated with LINC00173 and NUTF2 in glioma tissues. NUTF2 level was increased in glioma tissues. NUTF2 overexpression rescued the potential of proliferation, migration and invasion in LINC00173-silenced cells.	NA	Cancer Manag Res 2020  12, 7211-7217 doi:10.2147/cmar.S262279 PMID:32848473
2764	LncRNA	LINC00662	miR-15a-5p	Notch2	Four human OS cell lines, HOS, MG63, SJSA-1, and U2OS, and the human fetal osteoblastic cell line, hFOB	Osteosarcoma	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay etc.	32848412	LINC00662 Long Non-Coding RNA Knockdown Attenuates the Proliferation, Migration, and Invasion of Osteosarcoma Cells by Regulating the microRNA-15a-5p/Notch2 Axis.	The study demonstrated that LINC00662 could be a potential biomarker for OS therapy, and LINC00662 knockdown suppressed the proliferation, migration, and invasion of OS cells by regulating the miR-15a-5p/Notch2 axis.	NA	Onco Targets Ther 2020  13, 7517-7530 doi:10.2147/ott.S256464 PMID:32848412
2765	LncRNA	RAET1K	miR-100-5p	LDHA	The L02 cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay, etc.	32152275	HIF1A activates the transcription of lncRNA RAET1K to modulate hypoxia-induced glycolysis in hepatocellular carcinoma cells via miR-100-5p	The HIF1A/lncRNA RAET1K/miR-100-5p axis modulates hypoxia-induced glycolysis in HCC cells and then might affect HCC progression	NA	Cell Death Dis 2020 Mar 9 11, 176 doi:10.1038/s41419-020-2366-7 PMID:32152275
2766	LncRNA	TUG1	miR-455-3p	HK2	Hepatoma samples 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot etc.	28802060	Taurine up-regulated gene 1 functions as a master regulator to coordinate glycolysis and metastasis in hepatocellular carcinoma	In conclusion, we have made a conceptual progress supporting the theory that altered glycolytic metabolism contributes to metastatic phenotypes. TUG1 reduced p21 expression through upregulation of EED expression and led to decrease p21-E2F1  interaction  and  enhance  miR-455-3p  expression.  Consequently, miR-455-3p repressed AMPKβ2 expression and contribute to increase HK2 and Snail expression. We have identified a novel pathway interlinking TUG1, miR-455-3p, AMPKβ2, AMPKα/mTOR, Snail and HK2, which regulates glycolysis, motility, and invasion of hepatoma cells. Our study provides the potential therapeutic strategies of targeting TUG1 and HK2 for the treatment of HCC. 	NA	Hepatology 2018 Jan 67, 188-203 doi:10.1002/hep.29462 PMID:28802060
2767	LncRNA	HOTAIR	miR-130a-3p	HIF1	CC cell lines (HepG2 and Huh7), normal human hepatic cell lineLO2 and 293 T cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,RIP,etc..	32062551	LncRNA HOTAIR knockdown inhibits glycolysis by regulating miR-130a-3p/HIF1A in hepatocellular carcinoma under hypoxia	In conclusion, here we indicated a novel mechanism underlying theglycolysis progression under hypoxia in HCC. HOTAIR expression wasincreased in HCC cells after hypoxia treatment. Knockdown of HOTAIRinhibited glycolysis in HCC cells stimulated with hypoxia, possibly byacting as a ceRNA network of HOTAIR/miR-130a-3p/HIF1A. This studymay provide a new therapeutic target for treatment of HCC	NA	Biomed Pharmacother 2020 May 125, 109703 doi:10.1016/j.biopha.2019.109703 PMID:32062551
2768	LncRNA	HOTAIR	miR-218	Bmi-1	A panel of HCC cell lines including HepG2, Bel7404, PLC5, Huh7 and immortalized non-tumorigenic  MIHA  cells  	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc..	26024833	Hotair mediates hepatocarcinogenesis through suppressing miRNA-218 expression and activating P14 and P16 signaling.	Hotair silence activates P16Ink4a and P14ARF signaling by enhancing miR-218  expression  and  suppressing  Bmi-1  expression,  resulting  in  the  suppression of tumorigenesis in HCC. 	NA	J Hepatol 2015 Oct 63, 886-95 doi:10.1016/j.jhep.2015.05.016 PMID:26024833
2769	LncRNA	HOTAIR	miR-1	FOXC1	HCC HepG2 and LO2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP,qRT-PCR,luciferase reporter assay etc.	27895772	HOTAIR, a long non-coding RNA driver of malignancy whose expression is activated by FOXC1, negatively regulates miRNA-1 in hepatocellular carcinoma	Taken together, these results suggest that HOTAIR is a FOXC1-activated driver of malignancy, which acts in part through the repression of miR-1.	NA	Oncol Lett 2016 Nov 12, 4061-4067 doi:10.3892/ol.2016.5127 PMID:27895772
2770	LncRNA	HOTAIR	miR-214-3p	FLOT1	HCC cell lines (Hep3B and HepG2) and normal hepatic cell line (L-02) 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc..	31933720	HOTAIR/miR-214-3p/FLOT1 axis plays an essential role in the proliferation, migration, and invasion of hepatocellular carcinoma	HOTAIR expression indirectly regulated FLOT1 expression through endogenous competition with miR-214-3p. HOTAIR/miR-214-3p/FLOT1 axis affected the cell proliferation, migration, and invasion of HCC.	NA	Int J Clin Exp Pathol 2019  12, 50-63,  PMID:31933720
2771	LncRNA	HOTAIR	miR-23b-3p	ZEB1	HCC  cell  lines  Huh7,  Hep3B,  HepG2,  MHCC97H  and  normal  hepatic  cells  L-02 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc..	29778425	LncRNA HOTAIR contributes to the malignancy of hepatocellular carcinoma by enhancing epithelial-mesenchymal transition via sponging miR-23b-3p from ZEB1	In  conclusion,  our  present  study  found  that  HOTAIR  was  overexpressed  in  HCC  tissues and  cell  lines  and  promoted  invas ion  and  migration  of  HCC  cells  by  enhanc ing  EMT.  H igh leve l  of  HOTAIR  inhibited  the  expression  of  miR-23b-3p  but  benefit  to  the  production of ZEB1.  HOTAIR  promoted  metastasis  in  HCC  by  enhancing  EMT  via  sponging  miR-23b-3p from  ZEB1  both in  vitroand in  vivo. The  HOTAIR-miR-23b-3p-ZEB1  axis  may  provide a new perspective for treatment of HCC.	NA	Gene 2018 Sep 5 670, 114-122 doi:10.1016/j.gene.2018.05.061 PMID:29778425
2772	LncRNA	MEG3	miR-483-3p	ERp29	The  HCC  cell  lines  HepG2  and  Human  Embryonic  Kidney  (HEK)293T  cell	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc..	31251997	High glucose regulates ERp29 in hepatocellular carcinoma by LncRNA MEG3-miRNA 483-3p pathway.	Our study established a role for regulatory pathway of MEG3/miR-483-3p/ ERp29 in HCC under the conditions of high glucose. Overall, our findings suggest that HG negatively regulates the expression of ERp29 by inhibiting the miRNA sponge role of MEG3 on miR-483-3p in HCC cells.	NA	Life Sci 2019 Sep 1 232, 116602 doi:10.1016/j.lfs.2019.116602 PMID:31251997
2773	LncRNA	MEG3	miR-9-5p	SOX11	Human embryonic kidney cell line (293T) and Human HCC cell lines (SK-HEP-1 and Huh7)	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Flow cytometry etc.	31531526	lncRNA MEG3 inhibits the growth of hepatocellular carcinoma cells by sponging miR-9-5p to upregulate SOX11	In the present study, we determined the expression of MEG3, miR-9-5p, and SOX11 in HCC tissues, and explored their interactions in HCC. Furthermore, we detected the effect of these molecules on HCC cell growth and apoptosis.	NA	Braz J Med Biol Res 2019  52, e8631 doi:10.1590/1414-431x20198631 PMID:31531526
2774	LncRNA	MEG3	miR-10a-5p	PTEN	The HepG2 HCC cell line 	Hepatocellular Carcinoma	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay etc.	31396320	LncRNA meg3 suppresses hepatocellular carcinoma in vitro and vivo studies	The results of this study confirmed that overexpression of lncRNA MEG3 leads to the inhibition of miRNA-10a-5p expression and the PTEN/AKT/Bcl-2/Bax/p53 and PTEN/AKT/MMP-2/9 signaling pathways. Thus, the biology of lncRNA MEG3 in HCC merits further study to evaluate its potential to serve as a therapeutic target for HCC.	NA	Am J Transl Res 2019  11, 4089-4099,  PMID:31396320
2775	LncRNA	NEAT1	miR-155	Tim-3	CD8+T cells	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,qRT-PCR,Flow cytometry,RIP etc.	30710754	Repression of lncRNA NEAT1 enhances the antitumor activity of CD8+T cells against hepatocellular carcinoma via regulating miR-155/Tim-3.	Viamodulating the miR-155/Tim-3 pathway, repression of NEAT1 restrained CD8+Tcell  apoptosis  and enhanced  the  cytolysis  activityagainst  HCC, implyingan  effective  target  for improving the outcome of immunotherapy.	NA	Int J Biochem Cell Biol 2019 May 110, 1-8 doi:10.1016/j.biocel.2019.01.019 PMID:30710754
2776	LncRNA	PVT1	miR-365	ATG3	Bel-7402, Huh7, Hep3B, HepG2 and Chang liver 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	30794914	Long non-coding RNA PVT1 promotes autophagy as ceRNA to target ATG3 by sponging microRNA-365 in hepatocellular carcinoma	In  conclusion,  our  study demonstrated PVT1  might  be  a  key  regulator participating in autophagy in HCC cells	NA	Gene 2019 May 20 697, 94-102 doi:10.1016/j.gene.2019.02.036 PMID:30794914
2777	LncRNA	HNF1A-AS1	miR-30b-5p	ATG5	HCC cell lines HepG2, SMMC-7721, PLC/PRF/5, Huh7 and normal liver cell line HL-7702 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,RIP etc.	27084450	Long non-coding RNA HNF1A-AS1 functioned as an oncogene and autophagy promoter in hepatocellular carcinoma through sponging hsa-miR-30b-5p	In our research, wefirst explored the expressionlevels and clinicopathological significance of HNF1A-AS1 in HCC.Then in vitro experiments revealed its roles in various biologicalbehaviors. Furthermore, we deemed HNF1A-AS1 as a ceRNA anddeeply probed its regulating mechanisms.	NA	Biochem Biophys Res Commun 2016 May 13 473, 1268-1275 doi:10.1016/j.bbrc.2016.04.054 PMID:27084450
2778	LncRNA	CCAT1	miR-181a-5p	ATG7	The human HCC cell lines (HCCLM3, Huh7, Hep3B, andHepG2) and a hepatocyte cell line (L02)	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,RT-PCR,Luciferase reporter assay etc.	31218739	LncRNA CCAT1 promotes autophagy via regulating ATG7 by sponging miR-181 in hepatocellular carcinoma	Our findings indicate CCAT1 may play a role in regulatingautophagy by sponging miR-181a-5p in HCC.	NA	J Cell Biochem 2019 Oct 120, 17975-17983 doi:10.1002/jcb.29064 PMID:31218739
2779	LncRNA	CCAT1	miR-490-3p	CDK1	The liver normal cell lines LO2 and four human HCC cell lines  MHCC97H,  MHCC97L,  Hep3B,  and  SMCC-7721  	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,RNAi etc.	28381168	Long non-coding RNA colon cancer-associated transcript 1 functions as a competing endogenous RNA to regulate cyclin-dependent kinase 1 expression by sponging miR-490-3p in hepatocellular carcinoma progression	In  conclusion,  this  study  demonstrated  that  CCAT1  influenced  tumor  progression  through  directly  binding  to  the  miR-490-3p  and  regulated  the  CDK1.  Targeting  the  ceRNA regulatory network involving in CCAT1 may be a novel therapeutic strategy for HCC.	NA	Tumour Biol 2017 Apr 39, 1010428317697572 doi:10.1177/1010428317697572 PMID:28381168
2780	LncRNA	CCAT1	miR-30c-2-3p	CCNE1	Human Hep3B cell line 	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,Luciferase reporter assay etc.	30773676	Upregulated LncRNA-CCAT1 promotes hepatocellular carcinoma progression by functioning as miR-30c-2-3p sponge.	In the present study, the ectopic expression of lncRNA-CCAT1 inHCC compared with the normal tissue was firstly founded. In addition,our data indicated that CCAT1 may play important roles in the metas-tasis of human patients. 	NA	Cell Biochem Funct 2019 Mar 37, 84-92 doi:10.1002/cbf.3375 PMID:30773676
2781	LncRNA	HCG11	miR-26a-5p	ATG12	HCC cell lines MHCC97-H, Hep3B, and nor-mal  liver  cell  line  THLE-2	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	31858580	LncRNA HCG11 accelerates the progression of hepatocellular carcinoma via miR-26a-5p/ATG12 axis	 LncRNA HCG11 accelerated the proliferation, metastasis, and autophagy while impeded the apoptosis of HCC cells via HCG11/miR-26a-5p/ATG12 axis. HCG11 might be a potential therapeutic target for the treatment of HCC. 	NA	Eur Rev Med Pharmacol Sci 2019 Dec 23, 10708-10720 doi:10.26355/eurrev_201912_19771 PMID:31858580
2782	LncRNA	LINC00665	miR-186-5p	MAP4K3	HCC cell lines (Huh-7, HepG2, HCCLM6, MHCC-97H, and Hep3B) and the human liver cell line HL-7702	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RNAi etc.	31433582	LINC00665 was involved in cell viability, apoptosis, and autophagy in HCC via miR-186-5p/MAP4K3 axis, which may provide a new approach for HCC treatment.	 LINC00665 was involved in cell viability, apoptosis, and autophagy in HCC via miR-186-5p/MAP4K3 axis, which may provide a new approach for HCC treatment. 	NA	Yonsei Med J 2019 Sep 60, 842-853 doi:10.3349/ymj.2019.60.9.842 PMID:31433582
2783	LncRNA	HULC	miR-107	SPHK1	Hepatoma cell lines HepG2, Huh7 and HepG2.2.15	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,ChIP,Luciferase reporter assay etc.	26540633	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1)	Long non-coding RNA HULC promotes tumor angiogenesis in liver cancer by up-regulating sphingosine kinase 1 (SPHK1)	NA	Oncotarget 2016 Jan 5 7, 241-54 doi:10.18632/oncotarget.6280 PMID:26540633
2784	LncRNA	HULC	miR-200a-3p	ZEB1	Seven human liver cancer cell lines (Huh-6, Huh-7, HepG2, BEL-7402, MHCC-97H, Sk-Hep1 and SMMC-7721) and a normal liver cell line (L02) 	Hepatocellular Carcinoma	Homo sapiens (human)	RT-PCR,Western blot etc.	27285757	LncRNA HULC enhances epithelial-mesenchymal transition to promote tumorigenesis and metastasis of hepatocellular carcinoma via the miR-200a-3p/ZEB1 signaling pathway. 	In the present study, we found the expression of HULC to be significantly up-regulated in HCC tissues as compared with that in normal tissues. This enhanced expression of HULC was correlated with poor patient prognosis. 	NA	Oncotarget 2016 Jul 5 7, 42431-42446 doi:10.18632/oncotarget.9883 PMID:27285757
2785	LncRNA	HULC	miR-2052	MET	HCC cell lines 97H and LM3	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot etc.	31645479	Long noncoding RNA HULC promotes hepatocellular carcinoma progression	In conclusion, our study found that HULC promotes the progression of liver cancer via the HULC/miR-2052/MET axis, providing a potential diagnostic and therapeutic target for HCC.	NA	Aging (Albany NY) 2019 Oct 23 11, 9111-9127 doi:10.18632/aging.102378 PMID:31645479
2786	LncRNA	HULC	miR-6825-5p	USP22	Human HCC cell lines including HepG2, Hep3B, PLC, Huh7, smmc7721 andhepatic cell line L02 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,qRT-PCR,Western blot,microarray etc.	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 andattenuates the chemosensitivity of HCC cells	In summary, we revealed in this study that HULC decreases theexpression and activities of the three miRNAs (miR-6825-5p,miR-6845-5p and miR-6886-3p), elevates the level of USP22protein, enhances the deubiquitination of Sirt1 and stabilizes it,which ultimately triggers the autophagy of HCC cells. Furthermore,the HULC/Sirt1/autophagy pathway is activated in the presence ofchemotherapeutic reagents, and interference of the pathwayenhances the chemosensitivity of HCC cells. Altogether, thesefindings illustrate a new function of HULC and the‘HULC/USP22/Sirt1/protective autophagy’pathway may serves as a novel targetfor developing sensitizing strategy to HCC chemotherapy	NA	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
2787	LncRNA	HULC	miR-6845-5p	USP22	Human HCC cell lines including HepG2, Hep3B, PLC, Huh7, smmc7721 andhepatic cell line L02 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,qRT-PCR,Western blot,microarray etc.	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 andattenuates the chemosensitivity of HCC cells	In summary, we revealed in this study that HULC decreases theexpression and activities of the three miRNAs (miR-6825-5p,miR-6845-5p and miR-6886-3p), elevates the level of USP22protein, enhances the deubiquitination of Sirt1 and stabilizes it,which ultimately triggers the autophagy of HCC cells. Furthermore,the HULC/Sirt1/autophagy pathway is activated in the presence ofchemotherapeutic reagents, and interference of the pathwayenhances the chemosensitivity of HCC cells. Altogether, thesefindings illustrate a new function of HULC and the‘HULC/USP22/Sirt1/protective autophagy’pathway may serves as a novel targetfor developing sensitizing strategy to HCC chemotherapy	NA	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
2788	LncRNA	HULC	miR-6886-3p	USP22	Human HCC cell lines including HepG2, Hep3B, PLC, Huh7, smmc7721 andhepatic cell line L02 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,qRT-PCR,Western blot,microarray etc.	28166203	LncRNA HULC triggers autophagy via stabilizing Sirt1 andattenuates the chemosensitivity of HCC cells	In summary, we revealed in this study that HULC decreases theexpression and activities of the three miRNAs (miR-6825-5p,miR-6845-5p and miR-6886-3p), elevates the level of USP22protein, enhances the deubiquitination of Sirt1 and stabilizes it,which ultimately triggers the autophagy of HCC cells. Furthermore,the HULC/Sirt1/autophagy pathway is activated in the presence ofchemotherapeutic reagents, and interference of the pathwayenhances the chemosensitivity of HCC cells. Altogether, thesefindings illustrate a new function of HULC and the‘HULC/USP22/Sirt1/protective autophagy’pathway may serves as a novel targetfor developing sensitizing strategy to HCC chemotherapy	NA	Oncogene 2017 Jun 22 36, 3528-3540 doi:10.1038/onc.2016.521 PMID:28166203
2789	LncRNA	DANCR	miR-214	CTNNB1	HCCLM3 cells 	Hepatocellular Carcinoma	Homo sapiens (human)	etc.	25964079	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1	We speculate that there can be a novel regulatory transcript-mediated release of targeted transcripts (CTNNB1 here) from miRNA repression (by lncRNA and mRNA DANCRhere), which would add the known crosstalk between established pathways.  	NA	Hepatology 2016 Feb 63, 499-511 doi:10.1002/hep.27893 PMID:25964079
2790	LncRNA	DANCR	miR-320a	CTNNB1	HCCLM3 cells 	Hepatocellular Carcinoma	Homo sapiens (human)	etc.	25964079	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1	We speculate that there can be a novel regulatory transcript-mediated release of targeted transcripts (CTNNB1 here) from miRNA repression (by lncRNA and mRNA DANCRhere), which would add the known crosstalk between established pathways.  	NA	Hepatology 2016 Feb 63, 499-511 doi:10.1002/hep.27893 PMID:25964079
2791	LncRNA	DANCR	miR-199a	CTNNB1	HCCLM3 cells 	Hepatocellular Carcinoma	Homo sapiens (human)	etc.	25964079	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1	We speculate that there can be a novel regulatory transcript-mediated release of targeted transcripts (CTNNB1 here) from miRNA repression (by lncRNA and mRNA DANCRhere), which would add the known crosstalk between established pathways.  	NA	Hepatology 2016 Feb 63, 499-511 doi:10.1002/hep.27893 PMID:25964079
2792	LncRNA	ANRIL	miR-384	STAT3	SMCC7721, HepG2, MHCC-97H, SNU-449, HUH-7, LO2 and HEK-293T cells 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,RIP etc.	31679275	Evaluation of LncRNA ANRIL Potential in Hepatic Cancer  Progression	ANRIL is involved in HCC progression by direct targeting of miR-384 and STAT3. Also, ANRIL could act as a potential candidate for HCC diagnosis, prognosis, and therapy. 	NA	J Environ Pathol Toxicol Oncol 2019  38, 119-131 doi:10.1615/JEnvironPatholToxicolOncol.2019028282 PMID:31679275
2793	LncRNA	ANRIL	miR-144	PBX3	Human HCC cell lines MHCC97 and Li-7 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot etc.	31609763	LncRNA ANRIL promotes cell growth, migration and invasion of hepatocellular carcinoma cells via sponging miR-144. Anticancer Drugs. 	In  summary,  our  data  demonstrated  that  ANRIL  pro-moted HCC cells growth, migration and invasion. One of possible mechanisms responsible for the tumour-pro-moting  actions  is  that  ANRIL  sponging  miR-144  to  derepress PBX3. Furthermore, miR-144 blocked PI3K/AKT  and  JAK/STAT  signalling  pathways  by  targeting  PBX3.	NA	Anticancer Drugs 2019 Nov 30, 1013-1021 doi:10.1097/cad.0000000000000807 PMID:31609763
2794	LncRNA	GAS5	miR-21	PDCD4	Three HCC cell lines (Bel-7402, SMMC-7721, andHCCLM3) and a normal liver cell line (L-02) wer	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,qRT-PCR,RNAi etc.	26404135	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21. 	Thus, GAS5 acts as a tumor suppressor in HCCs throughnegative regulation of miR-21 and its targets and proteinsabout migration and invasion in cancer cells, which may bea target for treating HCC.	NA	Tumour Biol 2016 Feb 37, 2691-702 doi:10.1007/s13277-015-4111-x PMID:26404135
2795	LncRNA	GAS5	miR-21	PTEN	Three HCC cell lines (Bel-7402, SMMC-7721, andHCCLM3) and a normal liver cell line (L-02) wer	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,qRT-PCR,RNAi etc.	26404135	Long noncoding RNA GAS5 suppresses the migration and invasion of hepatocellular carcinoma cells via miR-21. 	Thus, GAS5 acts as a tumor suppressor in HCCs throughnegative regulation of miR-21 and its targets and proteinsabout migration and invasion in cancer cells, which may bea target for treating HCC.	NA	Tumour Biol 2016 Feb 37, 2691-702 doi:10.1007/s13277-015-4111-x PMID:26404135
2796	LncRNA	HOXD-AS1	miR-421	SOX4	Four BCa cell lines, including MCF-7, MDA-MB-435,MDA-MB-231, and MDA-MB-468, and normal breastepithelial cell line MCF-10A 	Breast Cancer	Homo sapiens (human)	qRT-PCR,Western blot, Luciferase reporter assay etc.	30730081	Long noncoding RNA HOXD-AS1 induces epithelial-mesenchymal transition in breast cancer by acting as a competing endogenous RNA of miR-421.	In conclusion, the present study for the first timeidentified that HOXD-AS1 serves as an oncogene throughinducing malignant traits of human BCa. Our findingsprovide the convincing evidence for a novel HOXD-AS1/miR-421/SOX4  regulatory  axis  in  BCa,  undoubtedlyshedding new light on the diagnosis and treatment forthis malignant disease.	NA	J Cell Biochem 2019 Jun 120, 10633-10642 doi:10.1002/jcb.28353 PMID:30730081
2797	LncRNA	TALNEC2	miR-21	PDCD4	The cardiomyocytes cell line H9c2	Myocardial Ischamia Reperfusion Injury Injury 	Homo sapiens (human)	qRT-PCR,Western blot etc.	30861181	Long noncoding RNA TALNEC2 regulates myocardial ischemic injury in H9c2 cells by regulating miR-21/PDCD4-medited activation of Wnt/β-catenin pathway.	In conclusion, our findings reveal that overexpressionof TALNEC2 may aggravate hypoxia injury in H9c2 cellsvia regulating miR-21/PDCD4-medited activation of theWnt/β-catenin  pathway.  TALNEC2  may  serve  as  apromising therapeutic target in myocardial ischemia.However, clinical and in vivo studies in myocardialischemia were not performed in this study. More studiesare still needed to confirm our findings.	NA	J Cell Biochem 2019 Aug 120, 12912-12923 doi:10.1002/jcb.28562 PMID:30861181
2798	LncRNA	Linc00261	miR-558	TIMP4	The human trophoblast cell line (HTR-8/SVneo cells)	Pre-Eclampsia	Homo sapiens (human)	qRT-PCR,Flow cytometry,Western blot, Luciferase reporter assay etc.	30891826	Upregulated long noncoding RNA Linc00261 in pre-eclampsia and its effect on trophoblast invasion and migration via regulating miR-558/TIMP4 signaling pathway.	In conclusion, our results for the first time showed theupregulation of Linc00261 in the placental tissues ofsevere PE patients. The mechanistic results indicated thatLinc00261 exerted the suppressive effects on the tropho-blast invasion and migration via targeting miR-558/TIMP4axis, which may involve in the pathogenesis of PE.	NA	J Cell Biochem 2019 Aug 120, 13243-13253 doi:10.1002/jcb.28598 PMID:30891826
2799	LncRNA	TUG1	miR-145-5p	ROCK1	Laryngocarcinoma cell lines SNU46, SNU899 and UM-SCC-10B 	Laryngocarcinoma	Homo sapiens (human)	qRT-PCR,Western blot etc.	30916820	Upregulation of long noncoding RNA TUG1 contributes to the development of laryngocarcinoma by targeting miR-145-5p/ROCK1 axis.	To sum up, our study firstly demonstrated that TUG1was upregulated in laryngocarcinoma, and TUG1 wasinvolved in the development oflaryngocarcinoma throughsuppressing  miR-145-5p  to  activate  the  RhoA/ROCK/MMPs signaling. Therefore, TUG1 may push a utility inclinical applications for the treatment of laryngocarcinoma	NA	J Cell Biochem 2019 Aug 120, 13392-13402 doi:10.1002/jcb.28614 PMID:30916820
2800	LncRNA	CASC11	miR-150	NA	HT-1197 and HT-1376 two urinary bladder cancer cell lines	Bladder Cancer	Homo sapiens (human)	qRT-PCR etc.	30916832	lncRNA CASC11 promotes cancer cell proliferation in bladder cancer through miRNA-150.	In conclusion, lncRNA CASC11 was upregulated, while miRNA-150 was downregulated in patients with early-stage bladder cancer. lncRNA CASC11 may promote bladder cancer cell proliferation through the inhibition of miRNA-150.	NA	J Cell Biochem 2019 Aug 120, 13487-13493 doi:10.1002/jcb.28622 PMID:30916832
2801	LncRNA	PAPAS	miR-188-5p	NA	Two human HCC cell lines SNU-398 and SNU-182	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR etc.	30920025	LncRNA PAPAS promotes hepatocellular carcinoma by interacting with miR-188-5p.	In conclusion, PAPAS is overexpressed in HCC andPAPAS may promote HCC cell proliferation by forming anegative feedback regulation circle with miR-188-5p.	NA	J Cell Biochem 2019 Aug 120, 13494-13500 doi:10.1002/jcb.28623 PMID:30920025
2802	LncRNA	LINC00963	miR-204-3p	FN1	MG63, U2OS, HOS, Saos-2, and hFOB cell lines	Osteosarcoma	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay etc.	30975024	The LncRNA LINC00963 facilitates osteosarcoma proliferation and invasion by suppressing miR-204-3p/FN1 axis.	Our findings implied that LINC00963/miR-204-3p/FN1 can play an important role in proliferation and progression in osteosarcoma. LINC00963 has the potential to be a therapeutic target for osteosarcoma treatment	NA	Cancer Biol Ther 2019  20, 1141-1148 doi:10.1080/15384047.2019.1598766 PMID:30975024
2803	LncRNA	LINC00473	miR-374a-5p	SPIN1	Human ESCC cell lines (TE-1, EC9706, Eca109, andKyse450) and human normal human esophageal epithe-lial cell line (HET-1A) 	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	31017716	LINC00473/miR-374a-5p regulates esophageal squamous cell carcinoma via targeting SPIN1 to weaken the effect of radiotherapy.	In conclusion, the present study revealed for the first timethat LINC00473 regulated ESCC cell proliferation andradioresistance  through  miR-374a-5p/SPIN1  axis,  whichprovides a novel prognostic biomarker and a potentialtherapeutic target for ESCC. However, more assays should beconducted for further consolidation of this mechanism.	NA	J Cell Biochem 2019 Sep 120, 14562-14572 doi:10.1002/jcb.28717 PMID:31017716
2804	LncRNA	LINC00339	miR-152	ROCK1	Human normal liver epithelial cells (L02) and HCC cells(HUH7, HepG2, HUH-6, and SK-Hep-1)	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	31081143	LINC00339 regulates ROCK1 by miR-152 to promote cell proliferation and migration in hepatocellular carcinoma.	LINC00339 was highly expressed in HCC tissues and cell lines. LINC00339 promoted the cell proliferation, migration, and invasion of HCC cells, while knockout of LINC00339 showed the opposite trends. The proliferation and migration of HCC cells induced by LINC00339 overexpression were mostly reversed after transfected with miR-152 mimics. LINC00339 exerted oncogenesis effect on HCC progression by targeting miR-152/ROCK1, and the expression of LINC00339 was negatively correlated with miR-152 expression and positively correlated with ROCK1 expression in clinical HCC samples. Moreover, we also proved that LINC00339 overexpression exacerbated the tumor formation and metastases in nude mice and LINC00339 silence showed the opposite results.	NA	J Cell Biochem 2019 Sep 120, 14431-14443 doi:10.1002/jcb.28701 PMID:31081143
2805	LncRNA	SOX2-OT	miR-146b-5p	HNRNPA2B1	The human NPC cell lines (5-8F, NPC-TW01, C666-1,SUNE1)	Nasopharyngeal Cancer 	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay etc.	31099048	LncRNA SOX2-OT regulates proliferation and metastasis of nasopharyngeal carcinoma cells through miR-146b-5p/HNRNPA2B1 pathway.	In conclusion, our study was the first to elucidate themolecular mechanism of SOX2-OT in NPC. Our findingsproofed  that  SOX2-OT  exerted  cancerogenic  effectthrough  miR-146b-5p/HNRNPA2B1  axis.  The  SOX2-OT/miR-146b-5p/HNRNPA2B1 network may be a novelpromising therapeutic strategy for patients with NPC.	NA	J Cell Biochem 2019 Oct 120, 16575-16588 doi:10.1002/jcb.28917 PMID:31099048
2806	LncRNA	HOXA11-AS	miR-15a-3p	STAT3	Liver  cancer  cell  lines  (hepatocellular  carcinoma,CSQT-2, and HCCLM3; hepatoblastoma, Huh-6) andnormal liver cell line L02 	Liver Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	31099097	HOXA11-AS regulates JAK-STAT pathway by miR-15a-3p/STAT3 axis to promote the growth and metastasis in liver cancer.	Our study suggested that HOAX11-AS could regulate the JAK-STATsignaling pathway by miR-15a-3p/STAT3 axis to promote the progression of livercancer. Thus, HOXA11-AS may be regarded as an effective biomarker withdiagnostic, prognostic, and therapeutic potentials for liver cancer.	NA	J Cell Biochem 2019 Sep 120, 15941-15951 doi:10.1002/jcb.28871 PMID:31099097
2807	LncRNA	ANRIL	let-7a	HMGA2	The normal human ovarian surface epithelial cells (HOSEPiCs) and human ovarian cancer cells (cisplatin-sensitivestrain SKOV3 and cisplatin-resistant strain SKOV3/DDP)	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	31189742	LncRNA ANRIL affects the sensitivity of ovarian cancer to cisplatin via regulation of let-7a/HMGA2 axis.	In summary, our study found the up-expression of ANRIL in ovarian cancer tissues and drug-resistant cells, andsilencing ANRIL could increase let-7a to further reduce HMGA2, which can promote the apoptosis and improvethe cisplatin sensitivity of ovarian cancer cells. Therefore, this strategy provides an alternative therapeutic target forconquering cisplatin-resistance in ovarian cancer.	NA	Biosci Rep 2019 Jul 31 39 doi:10.1042/bsr20182101 PMID:31189742
2808	LncRNA	XIST	miR-376c-5p	OPN	THP-1 monocytic cell line	Proinflammatory M1 Macrophages On Apoptosis.	Homo sapiens (human)	Luciferase reporter assay etc.	31215024	XIST/miR-376c-5p/OPN axis modulates the influence of proinflammatory M1 macrophages on osteoarthritis chondrocyte apoptosis.	In the present study, we reveal that the overexpression of osteopontin (OPN), a cytokine, and a matrix protein involved in arthritis and chondrocyte apoptosis in OA, could exacerbate the inflammatory microenvironment in OA via promoting the production of proinflammation cytokines and the levels of degradative enzymes in M1 macrophages, therefore, enhancing the cytotoxicity of M1 macrophage on chondrocytes. XIST expression significantly increases in OA tissue specimens. XIST serves as a competing endogenous RNA for miR-376c-5p to compete with OPN for miR-376c-5p binding, thus counteracting miR-376c-5p-mediated OPN suppression. XIST knockdown could improve the inflammatory microenvironment in OA via acting on M1 macrophages, subsequently affecting the apoptosis of cocultured chondrocytes. miR-376c-5p inhibition exerts an opposing effect on M1 macrophages and cocultured chondrocytes, as well as significantly reverses the effect of XIST knockdown. As a further confirmation, XIST and OPN mRNA expression significantly increased in OA tissues and was positively correlated in tissue samples. In summary, we provide a novel mechanism of macrophages and the inflammatory microenvironment affecting chondrocyte apoptosis. XIST and OPN might be potential targets for OA treatment, which needs further in vivo experimental 	NA	J Cell Physiol 2020 Jan 235, 281-293 doi:10.1002/jcp.28968 PMID:31215024
2809	LncRNA	NORAD	miR-155-5p	NA	An immortal normal human ovarian epithelial cell line, HS832.Tc, and seven human EOC cell lines, SK-OV-3, CAOV-3,  CAOV-4,  OVCAR-3,  HEY-T30,  ES-2,  and  SW/626 	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay etc.	31250987	Long noncoding RNA NORAD is upregulated in epithelial ovarian cancer and its downregulation suppressed cancer cell functions by competing with miR-155-5p.	NORAD is upregulated in EOC. Inhibition of NORAD, possibly through endogenously competing against hsa-miR-155-5p, can be a new tumor-sup-pressing strategy in EOC.	NA	Cancer Med 2019 Aug 8, 4782-4791 doi:10.1002/cam4.2350 PMID:31250987
2810	LncRNA	ADAMTS9-AS2	miR-27a-3p	FOXO1	Three ccRCC cell lines (786-O, caki-1 and 769-P) and normal renal proximal tubular epithelial cell lines (HKC, HK-2) 	Clear Cell Renal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,RIP,Luciferase reporter assay etc.	31400752	LncRNA ADAMTS9-AS2 inhibits cell proliferation and decreases chemoresistance in clear cell renal cell carcinoma via the miR-27a-3p/FOXO1 axis.	In summary, an inhibitory role of ADAMTS9-AS2 in the proliferation and its lessened role in the chemoresistance was revealed in ccRCC. In addition, the ADAMTS9-AS2 - miR-27a-3p - FOXO1 axis was identified as an aspect of the underlying mechanism. Future research should consider the functional role of FOXO1 in chemoresistance and the concrete mechanism of ADAMTS9-AS2 (such as the phosphoinositide 3-kinase/Akt pathway) in the pathogenesis of ccRCC.	NA	Aging (Albany NY) 2019 Aug 10 11, 5705-5725 doi:10.18632/aging.102154 PMID:31400752
2811	LncRNA	HOTAIR	miR-126	CXCR4	Human gastric mucosal epithelial cell line GES-1, gastric cancer cell lines SNU-216, AGS, SGC-7901 and BGC-823 cells	Gastric Cancer	Homo sapiens (human)	RT-PCR,Western blot,Luciferase reporter assay etc.	31517442	lncRNA HOTAIR promotes gastric cancer proliferation and metastasis via targeting miR-126 to active CXCR4 and RhoA signaling pathway.	In conclusion, our study identified the critical role of lncRNA HOTAIR/miR-126/CXCR4/RhoA axis as in gastric cancer, providing a new thought for the targeted therapy of gastric cancer.	NA	Cancer Med 2019 Nov 8, 6768-6779 doi:10.1002/cam4.1302 PMID:31517442
2812	LncRNA	LINC02582	miR-200c	CHK1	MDA-MB-231, MCF-7, BT549, SKBR3, T47D, and BT474cell	Breast Cancer	Homo sapiens (human)	Western blot,RNAi,Microarray,qRT-PCR,Luciferase reporter assay etc.	31601781	Long noncoding RNA LINC02582 acts downstream of miR-200c to promote radioresistance through CHK1 in breast cancer cells.	In summary, we demonstrated thatLINC02582is adownstream target of miR-200c.LINC02582is requiredfor radioresistance in breast cancer cells. Mechanistically,LINC02582interacts with USP7 to deubiquitinate andstabilize CHK1, thus promoting radioresistance. Ourresults suggested that the miR-200c/LINC02582/USP7/CHK1 signaling axis is a potential target to improve theresponse of breast cancer to radiation therapy	NA	Cell Death Dis 2019 Oct 10 10, 764 doi:10.1038/s41419-019-1996-0 PMID:31601781
2813	LncRNA	LINC00518	miR-204-5p	AP1S2	The human malignant melanoma cell lines A375, A2058and SK-MEL-28 	Melanoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,FISH etc.	31712557	Long noncoding RNA LINC00518 acts as a competing endogenous RNA to promote the metastasis of malignant melanoma via miR-204-5p/AP1S2 axis.	In conclusion, we demonstrated that LINC00518 plays akey role in the malignant progression of melanoma.LINC00518 facilitates melanoma metastasis by spongingmiR-204-5p to release AP1S2 mRNA transcripts targetedby miR-204-5p, thereby promoting the AP1S2 expression.Studying the molecular mechanism of LINC00518 inmelanoma is of great significance to improve the under-standing of the molecular biological basis of melanomadevelopment and identify new therapeutic targets formelanoma patients.	NA	Cell Death Dis 2019 Nov 11 10, 855 doi:10.1038/s41419-019-2090-3 PMID:31712557
2814	LncRNA	NNT-AS1	miR-1301-3p	PODXL	Four bladder cancer cell lines (RT-4, UM-UC-3, J82, andT24) and human urothelial cell line, SV-HUC-1	Bladder Cancer	Homo sapiens (human)	qRT-PCR,Flow cytometry,RNAi,Luciferase reporter assay etc.	31782983	NNT-AS1 enhances bladder cancer cell growth by targeting miR-1301-3p/PODXL axis and activating Wnt pathway.	In conclusion, NNT-AS1 played a carcinogenic role inBC cell growth and enhanced BC cell growth by targetingmiR-1301-3p/PODXL axis and activating the Wnt path-way, which provides a helpful revelation for investigatingthe potential therapeutic methods for patients with BC.	NA	Neurourol Urodyn 2020 Feb 39, 547-557 doi:10.1002/nau.24238 PMID:31782983
2815	LncRNA	MALAT1	miR-608	HOXC4	Uveal melanoma cell lines MUM-2B, C918 and M619 and a retinal pigment epithelial (RPE) cell line	Uveal Melanoma	Homo sapiens (human)	Western blot,Flow cytometry etc.	31913701	Suppression of long noncoding RNA MALAT1 inhibits the development of uveal melanoma via microRNA-608-mediated inhibition of HOXC4.	Taken together, MALAT1 down-regulation may inhibit the proliferation, migration and invasion of uveal melanoma cells via miR-608-dependent downregulation of HOXC4.	NA	Am J Physiol Cell Physiol 2020 May 1 318, C903-c912 doi:10.1152/ajpcell.00262.2019 PMID:31913701
2816	LncRNA	MALAT1	miR-145	AQP4	Primary astrocytes were prepared from a post-natal day (PND) 7 cerebellum from C57BL/6J mice	Cerebral Ischemia-Reperfusion Injury	Mus musculus (mouse)	qPCR,Western blot,Flow cytometry etc.	32138732	LncRNA MALAT1 silencing protects against cerebral ischemia-reperfusion injury through miR-145 to regulate AQP4.	Taken together, our study confirmed that MALAT1 promotes cerebral ischemia-reperfusion injury by affecting AQP4 expression through competitively binding miR-145, indicating that MALAT1 might be a new therapeutic target for treatment cerebral ischemic stroke.	NA	J Biomed Sci 2020 Mar 6 27, 40 doi:10.1186/s12929-020-00635-0 PMID:32138732
2817	LncRNA	H19	let-7b	Stat3	Male Sprague-Dawley rats (200-220 g body)	Temporal Lobe Epileps	Mus musculus (mouse)	etc.	32648622	The lncRNA H19 binding to let-7b promotes hippocampal glial cell activation and epileptic seizures by targeting Stat3 in a rat model of temporal lobe epilepsy.	LncRNA H19   could    competitively bind   to  let-7b    to  promote hippocam-pal  glial  cell  activation  and  epileptic  seizures  by  targeting  Stat3  in  a  rat  model  of  temporal lobe epilepsy.	NA	Cell Prolif 2020 Aug 53, e12856 doi:10.1111/cpr.12856 PMID:32648622
2818	LncRNA	SNHG1	miR-361-3p	ZNF217	Neuroblastoma cell line (SK-N-SH and CHP92212) 	Alzheimers Disease	Homo sapiens (human)	qRT-PCR,Western blot,Flow cytometry,Luciferase reporter assay,RIP etc.	32741808	lncRNA SNHG1 Knockdown Alleviates Amyloid-β-Induced Neuronal Injury by Regulating ZNF217 via Sponging miR-361-3p in Alzheimer's Disease.	Conclusion: SNHG1 promoted cell injury by regulating the miR-361-3p/ZNF217 axis, which might provide a theoretical basis for molecular therapy of AD.	NA	J Alzheimers Dis 2020  77, 85-98 doi:10.3233/jad-191303 PMID:32741808
2819	LncRNA	CTBP1-AS2	miR-3163	ZNF217	Human cervical cancer cell lines, including SiHa (HPV positive),  HeLa  (HPV  positive),  MS751  (HPV  positive)  and  C33A  (HPV  negative)  as  well  as  the  normal  cervi-cal  epithelial  cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Western blot,,Luciferase reporter assay,FISH etc.	32742190	Long non-coding RNA CTBP1-AS2 enhances cervical cancer progression via up-regulation of ZNF217 through sponging miR-3163.	CTBP1-AS2 regulates CC progression via sponging miR-3163 to up-regulate ZNF217.	NA	Cancer Cell Int 2020  20, 343 doi:10.1186/s12935-020-01430-5 PMID:32742190
2820	LncRNA	MIAT	miR-149-5p	FOXM1	The NSCLC cell lines (H1650, SPC-A1, Calu3, A549 and H1299) and immortal human lung cell line BEAS-2B 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742195	Long noncoding RNA MIAT promotes non-small cell lung cancer progression by sponging miR-149-5p and regulating FOXM1 expression.	Our study reveals that MIAT acts as an oncogene in NSCLC via a novel MIAT/miR-149/FOXM1 axis, thus providing potential biomarkers and therapeutic targets for the management of NSCLC.	NA	Cancer Cell Int 2020  20, 348 doi:10.1186/s12935-020-01432-3 PMID:32742195
2821	LncRNA	FOXD3-AS1	miR-127-3p	MDM2	Normal human lung bronchial epithelial cells (NHBE) and NSCLC cell lines (A549 and H1299) 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742197	LncRNA FOXD3-AS1 promoted chemo-resistance of NSCLC cells via directly acting on miR-127-3p/MDM2 axis.	In conclusion, our study demonstrated the pivotal roles of FOXD3-AS1/miR-127-3p/MDM2 regulatory signaling pathways in cisplatin resistance of NSCLC cells (Fig. 7). The present study may provide new insights into overcoming cisplatin resistance in NSCLC treatment.	NA	Cancer Cell Int 2020  20, 350 doi:10.1186/s12935-020-01402-9 PMID:32742197
2822	LncRNA	MIAT	miR-181a	CTGF	The human LEC line SRA01/04	Age-Related Cataract	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742346	lncRNA MIAT increases cell viability, migration, EMT and ECM production in age-related cataracts by regulating the miR-181a/CTGF/ERK signaling pathway.	To  conclude,  MIAT  and  CTGF  expression  were  increased, while miR-181a was decreased in ARC tissues and TGF-β2-treated SRA01/04 cells.	NA	Exp Ther Med 2020 Aug 20, 1053-1063 doi:10.3892/etm.2020.8749 PMID:32742346
2823	LncRNA	MIAT	miR-181a	ERK	The human LEC line SRA01/04	Age-Related Cataract	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742346	lncRNA MIAT increases cell viability, migration, EMT and ECM production in age-related cataracts by regulating the miR-181a/CTGF/ERK signaling pathway.	To  conclude,  MIAT  and  CTGF  expression  were  increased, while miR-181a was decreased in ARC tissues and TGF-β2-treated SRA01/04 cells.	NA	Exp Ther Med 2020 Aug 20, 1053-1063 doi:10.3892/etm.2020.8749 PMID:32742346
2824	LncRNA	H19	miR-29a-3p	COL3A1	The microarray datasets that compared gene expression between GC tissues and nontumorous/normal tissues were downloaded on the Gene Expression Omnibus database	Gastric Cancer	Homo sapiens (human)	qRT-PCR etc.	32742441	The prognostic value of COL3A1/FBN1/COL5A2/SPARC-mir-29a-3p-H19 associated ceRNA network in Gastric Cancer through bioinformatic exploration.	In conclusion, we have established a novel mRNA-miRNA-lncRNA ceRNA network through integrating bioinformatic analysis and experiments on clinical samples. This network is significantly associated with the prognosis of patients with GC. In addition, it may also provide some new directions for studying the molecular mechanism of GC. However, further researches are still needed to validate this network.	NA	J Cancer 2020  11, 4933-4946 doi:10.7150/jca.45378 PMID:32742441
2825	LncRNA	H19	miR-29a-3p	FBN1	The microarray datasets that compared gene expression between GC tissues and nontumorous/normal tissues were downloaded on the Gene Expression Omnibus database	Gastric Cancer	Homo sapiens (human)	qRT-PCR etc.	32742441	The prognostic value of COL3A1/FBN1/COL5A2/SPARC-mir-29a-3p-H19 associated ceRNA network in Gastric Cancer through bioinformatic exploration.	In conclusion, we have established a novel mRNA-miRNA-lncRNA ceRNA network through integrating bioinformatic analysis and experiments on clinical samples. This network is significantly associated with the prognosis of patients with GC. In addition, it may also provide some new directions for studying the molecular mechanism of GC. However, further researches are still needed to validate this network.	NA	J Cancer 2020  11, 4933-4946 doi:10.7150/jca.45378 PMID:32742441
2826	LncRNA	H19	miR-29a-3p	COL5A2	The microarray datasets that compared gene expression between GC tissues and nontumorous/normal tissues were downloaded on the Gene Expression Omnibus database	Gastric Cancer	Homo sapiens (human)	qRT-PCR etc.	32742441	The prognostic value of COL3A1/FBN1/COL5A2/SPARC-mir-29a-3p-H19 associated ceRNA network in Gastric Cancer through bioinformatic exploration.	In conclusion, we have established a novel mRNA-miRNA-lncRNA ceRNA network through integrating bioinformatic analysis and experiments on clinical samples. This network is significantly associated with the prognosis of patients with GC. In addition, it may also provide some new directions for studying the molecular mechanism of GC. However, further researches are still needed to validate this network.	NA	J Cancer 2020  11, 4933-4946 doi:10.7150/jca.45378 PMID:32742441
2827	LncRNA	H19	miR-29a-3p	SPARC	The microarray datasets that compared gene expression between GC tissues and nontumorous/normal tissues were downloaded on the Gene Expression Omnibus database	Gastric Cancer	Homo sapiens (human)	qRT-PCR etc.	32742441	The prognostic value of COL3A1/FBN1/COL5A2/SPARC-mir-29a-3p-H19 associated ceRNA network in Gastric Cancer through bioinformatic exploration.	In conclusion, we have established a novel mRNA-miRNA-lncRNA ceRNA network through integrating bioinformatic analysis and experiments on clinical samples. This network is significantly associated with the prognosis of patients with GC. In addition, it may also provide some new directions for studying the molecular mechanism of GC. However, further researches are still needed to validate this network.	NA	J Cancer 2020  11, 4933-4946 doi:10.7150/jca.45378 PMID:32742441
2828	LncRNA	LncZEB1-AS1	miR-302b	EGFR	Human HCC (PLC, MHCC-97H, Hep3B, and Huh7) and control (NCM-460) cell lines	Hepatocellular Carcinoma Bone Metastasis	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay,Western blot etc.	32742459	LncZEB1-AS1 regulates hepatocellular carcinoma bone metastasis via regulation of the miR-302b-EGFR-PI3K-AKT axis.	In summary, we have provided novel evidence suggesting that lncZEB1-AS1 is an important regulator of HCC BM. We have additionally highlighted a previously undescribed lncZEB1-AS1-miR-302b-EGFR-PI3K-AKT signaling axis that may govern this metastatic process. This axis may be a viable target for therapeutic intervention in HCC patients as a means of significantly improving quality of life and extending patient survival.	NA	J Cancer 2020  11, 5118-5128 doi:10.7150/jca.45995 PMID:32742459
2829	LncRNA	LncZEB1-AS1	miR-302b	PI3K	Human HCC (PLC, MHCC-97H, Hep3B, and Huh7) and control (NCM-460) cell lines	Hepatocellular Carcinoma Bone Metastasis	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay,Western blot etc.	32742459	LncZEB1-AS1 regulates hepatocellular carcinoma bone metastasis via regulation of the miR-302b-EGFR-PI3K-AKT axis.	In summary, we have provided novel evidence suggesting that lncZEB1-AS1 is an important regulator of HCC BM. We have additionally highlighted a previously undescribed lncZEB1-AS1-miR-302b-EGFR-PI3K-AKT signaling axis that may govern this metastatic process. This axis may be a viable target for therapeutic intervention in HCC patients as a means of significantly improving quality of life and extending patient survival.	NA	J Cancer 2020  11, 5118-5128 doi:10.7150/jca.45995 PMID:32742459
2830	LncRNA	LncZEB1-AS1	miR-302b	AKT	Human HCC (PLC, MHCC-97H, Hep3B, and Huh7) and control (NCM-460) cell lines	Hepatocellular Carcinoma Bone Metastasis	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay,Western blot etc.	32742459	LncZEB1-AS1 regulates hepatocellular carcinoma bone metastasis via regulation of the miR-302b-EGFR-PI3K-AKT axis.	In summary, we have provided novel evidence suggesting that lncZEB1-AS1 is an important regulator of HCC BM. We have additionally highlighted a previously undescribed lncZEB1-AS1-miR-302b-EGFR-PI3K-AKT signaling axis that may govern this metastatic process. This axis may be a viable target for therapeutic intervention in HCC patients as a means of significantly improving quality of life and extending patient survival.	NA	J Cancer 2020  11, 5118-5128 doi:10.7150/jca.45995 PMID:32742459
2831	LncRNA	DGCR5	miR-3619-5p	MEK	NOZ, SGC-996, GBC-SD, OCUG and 293T cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742494	DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways.	In summary, our study characterized the role of DGCR5 in GBC for the first time, demonstrating that DGCR5 promotes GBC cell proliferation, migration and invasion by sponging miR-3619-5p via activating the MEK/ ERK1/2 and JNK/p38 MAPK pathways. These results underscore the importance of DGCR5/ miR-3619-5p/ MEK/ ERK1/2 and JNK/p38 MAPK axis in GBC. Our study provides the first evidence that DGCR5/miR-3619-5p network may be a novel biomarker for early diagnosis and treatment of GBC.	NA	J Cancer 2020  11, 5466-5477 doi:10.7150/jca.46351 PMID:32742494
2832	LncRNA	DGCR5	miR-3619-5p	ERK1	NOZ, SGC-996, GBC-SD, OCUG and 293T cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742494	DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways.	In summary, our study characterized the role of DGCR5 in GBC for the first time, demonstrating that DGCR5 promotes GBC cell proliferation, migration and invasion by sponging miR-3619-5p via activating the MEK/ ERK1/2 and JNK/p38 MAPK pathways. These results underscore the importance of DGCR5/ miR-3619-5p/ MEK/ ERK1/2 and JNK/p38 MAPK axis in GBC. Our study provides the first evidence that DGCR5/miR-3619-5p network may be a novel biomarker for early diagnosis and treatment of GBC.	NA	J Cancer 2020  11, 5466-5477 doi:10.7150/jca.46351 PMID:32742494
2833	LncRNA	DGCR5	miR-3619-5p	ERK2	NOZ, SGC-996, GBC-SD, OCUG and 293T cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32742494	DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways.	In summary, our study characterized the role of DGCR5 in GBC for the first time, demonstrating that DGCR5 promotes GBC cell proliferation, migration and invasion by sponging miR-3619-5p via activating the MEK/ ERK1/2 and JNK/p38 MAPK pathways. These results underscore the importance of DGCR5/ miR-3619-5p/ MEK/ ERK1/2 and JNK/p38 MAPK axis in GBC. Our study provides the first evidence that DGCR5/miR-3619-5p network may be a novel biomarker for early diagnosis and treatment of GBC.	NA	J Cancer 2020  11, 5466-5477 doi:10.7150/jca.46351 PMID:32742494
2834	LncRNA	DLX6-AS1	miR-577	NA	Three human CRC cell lines (HT29, SW620, and SW480) and one normal human colonic ep-ithelial cell line (NCM460)	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,RIP,etc..	32744645	Long noncoding RNA DLX6-AS1 functions as a competing endogenous RNA for miR-577 to promote malignant development of colorectal cancer.	DLX6-AS1 could promote the proliferation, migration, and invasion of CRC by sponging miR-577, which might offer a potential therapeutic target for CRC. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7540 doi:10.26355/eurrev_202007_22173 PMID:32744645
2835	LncRNA	SNHG14	miR-193a-3p	NA	Human  BC  cell  lines  (MCF-7,  LCC9,  T-47D,  SKBR3) and MCF-10A (normal human breast cell line)	Breast Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,etc..	32744648	Long noncoding RNA SNHG14 promotes breast cancer cell proliferation and invasion via sponging miR-193a-3p.	Conclusions: Our study uncovers a new oncogene in BC and suggests that SNHG14 could enhance BC cell proliferation and invasion via sponging miR-193a-3p, which provided a novel therapeutic target for BC patients. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7543 doi:10.26355/eurrev_202007_22179 PMID:32744648
2836	LncRNA	UCA1	miR-497-3p	NA	K1,  TPC-1,  SW579  and  Nthy-ori  3–1  (normal  human thyroid cell line) cells	Thyroid Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,etc..	32744660	Long noncoding RNA UCA1 promotes proliferation and metastasis of thyroid cancer cells by sponging miR-497-3p.	Conclusions: Knockdown of UCA1 could inhibit TC cell proliferation and metastasis via sponging miR-497-3p. Our findings might offer a new therapeutic intervention for TC patients. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7555 doi:10.26355/eurrev_202007_22203 PMID:32744660
2837	LncRNA	SNHG16	miR-200a-3p	NA	fresh  Wilms’  tumor  tissues. 	Wilms Tumor	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,etc..	32744667	Long noncoding RNA SNHG16 acts as an oncogene in Wilms' tumor through sponging miR-200a-3p.	SNHG16 induced the metastasis of Wilms' tumor via sponging miR-200a-3p. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7562 doi:10.26355/eurrev_202007_22219 PMID:32744667
2838	LncRNA	ZFPM2-AS1	miR-1226-3p	ITGB1	HCC  cell  lines  (HepG2,  Huh7,  SMMC-7721,  and   HCCLM3)   and   normal   hepatic   cell   line   H7702 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,FISH etc.	32744687	Long noncoding RNA ZFPM2-AS1 regulates ITGB1 by miR-1226-3p to promote cell proliferation and invasion in hepatocellular carcinoma.	ZFPM2-AS1 was overexpressed in HCC tissues and cell lines. High levels of ZFPM2-AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. ZFPM2-AS1 knockdown inhibited cell proliferation and invasion. ZFPM2-AS1 could directly bind to and negatively regulate miR-1226-3p expression. Moreover, ITGB1 was identified as a target gene of miR-1226-3p. ITGB1 was found to be directly negatively regulated by miR-1226-3p and indirectly upregulated by ZFPM2-AS1. Rescue assays demonstrated that ZFPM2-AS1 promotes HCC cell proliferation and invasion through modulating miR-1226/ITGB1 axis. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7612-7620 doi:10.26355/eurrev_202007_22259 PMID:32744687
2839	LncRNA	ADIPOQ	miR-219c-3p	TP53	Human  colorectal  cancer  cells  Caco-2  cells  	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,etc..	32744690	Decreased long noncoding RNA ADIPOQ promoted cell proliferation and metastasis via miR-219c-3p/TP53 pathway in colorectal carcinoma.	CONCLUSIONS:  For  the  first  time,  we  found that lncRNA-ADIPOQ was downregulated in hu-man colorectal cancer cells, which could facili-tate tumor proliferation, migration and invasion as a ceRNA by sponging with miR-219c-3p	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7645-7654 doi:10.26355/eurrev_202007_22265 PMID:32744690
2840	LncRNA	DBH-AS1	miR-233-3p	IGF-1R	Human  melanoma  cell  line  A375  and  kerati-nocyte cell line HaCaT 	Melanoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RIP etc.	32744696	LncRNA DBH-AS1 facilitates the tumorigenesis of melanoma by targeting miR-233-3p via IGF-1R/Akt signaling.	 Herein, we observed significant reductions in DBH-AS1 expression in melanoma tumor tissues and cell lines. Knockdown DBH-AS1 in melanoma cells impaired their proliferative, migratory, and invasive potential. We determined that DBH-AS1 was able to modulate insulin growth factor receptor (IGF-1R) expression as a competing endogenous RNA for DBH-AS1. In line with this finding, the knockdown DBH-AS1 was associated with decreases in the expression of glucose transporter (GLUT)-1 and a consequent inhibition of glucose uptake, lactate production, and ATP generation by melanoma cells. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7698-7708 doi:10.26355/eurrev_202007_22272 PMID:32744696
2841	LncRNA	DSCAM-AS1	miR-101	NA	Human  osteoblast  cells  (hFOB)  and  OS  cell  lines  (U2OS,  SAOS2  and  HOS)  	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,etc..	32744697	LncRNA DSCAM-AS1 promoted cell proliferation and invasion in osteosarcoma by sponging miR-101.	In the present study, it was demonstrated that DSCAM-AS1 expression was significantly upregulated in OS tissues and cells and high expression of DSCAM-AS1 predicted poor prognosis in OS patients. In addition, the silencing of DSCAM-AS1 suppressed the viability and invasion of OS cells, while DSCAM-AS1 overexpression promoted cell viability and invasion. Furthermore, we found that DSCAM-AS1 inhibited miR-101 expression by direct interaction and DSCAM-AS1 promoted OS progression by sponging miR-101. In addition, miR-101 expression was negatively correlated with DSCAM-AS1 expression. Patients with low miR-101 expression had a shorter overall survival time compared with those with high miR-101 expression. 	NA	Eur Rev Med Pharmacol Sci 2020 Jul 24, 7709-7717 doi:10.26355/eurrev_202007_22274 PMID:32744697
2842	LncRNA	Lnc-OC1	miR-34a	NA	The EC cell lines (Ishikawa) 	Endometrial Cancer	Homo sapiens (human)	MicroRNA,qRT-PCR,Luciferase reporter assay,Western blot,etc..	32748220	Inhibition of Lnc-OC1 Induced Cell Apoptosis and Decreased Cell Viability by Releasing miR-34a and Inhibiting PD-L1 in Endometrial Carcinoma.	In conclusion, we proved that Lnc-OC1/miR-34a/PD-L1axis played a crucial role in inhibiting endometrial carcinomacell growth in this work. Treatments that target Lnc-OC1might benefit for remitting EC and fighting drug resistance.	NA	Reprod Sci 2020 Oct 27, 1848-1856 doi:10.1007/s43032-020-00202-w PMID:32748220
2843	LncRNA	SLC16A1-AS1	miR-301b-3p	CHD5	HCC cell lines (Huh7, SMCC-7721, HepG2 and MHCC-97H) and normal human liver LO2 cells wer	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RIP etc.	32748357	SLC16A1-AS1 enhances radiosensitivity and represses cell proliferation and invasion by regulating the miR-301b-3p/CHD5 axis in hepatocellular carcinoma.	This study probed into the association between SLC16A1-AS1 and HCC. Our data demonstrated that SLC16A1-AS1suppressed HCC cellular processes as well as enhanced radio-sensitivity by targeting the miR-301b-3p/CHD5 axis, whichmay offer a new perspective into for HCC therapy	NA	Environ Sci Pollut Res Int 2020 Dec 27, 42778-42790 doi:10.1007/s11356-020-09998-1 PMID:32748357
2844	LncRNA	UCA1	miR-138-5p	CCR7	TSCC  cell  lines  (SCC4,  SCC15,  SCC25  and  CAL-27)  	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay etc.	32749849	Long noncoding RNA UCA1 regulates CCR7 expression to promote tongue squamous cell carcinoma progression by sponging miR-138-5p.	In summary, we concluded that UCA1 played an oncogenic role  in  TSCC through regulating  the miR-138-5p/CCR7  axis,  which  provided  a reliable  biomarker  for the clinical  treatment  of TSCC. 	NA	Neoplasma 2020 Nov 67, 1256-1265 doi:10.4149/neo_2020_191119N1187 PMID:32749849
2845	LncRNA	KCNQ1OT1	miR-149	S1PR1	The normal human healthy hepatic cell line WRL68 and thehuman HCC cell lines Bel-7402, HepG2, SMMC-7721 and Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot etc.	32753631	LncRNA KCNQ1OT1 regulates the invasion and migration of hepatocellular carcinoma by acting on S1PR1 through miR-149.	The expression levels of KCNQ1OT1, miR-149 and S1PR1 were detected by qRT-PCR assay. A dual luciferase reporter assay was used to detect the interaction between KCNQ1OT1 and miR-149, as well as miR-149 and S1PR1. The interaction between KCNQ1OT1 and miR-149 was further investigated by RNA pull-down assay. Wound healing assays and Transwell assays were carried out to determine cell migration and invasion. A xenograft tumour assay was used to validate the role of KCNQ1OT1 in vivo. KCNQ1OT1 and S1PR1 were significantly increased, but miR-149 was decreased in HCC cells. Luciferase reporter assays and RNA pull-down assays revealed that KCNQ1OT1 directly targeted miR-149. In addition, miR-149 bound to the 3'-UTR of S1PR1. Knockdown of KCNQ1OT1 or overexpression of miR-149 inhibited the invasion and migration of HCC cells. However, suppression of miR-149 could abrogate the effect of KCNQ1OT1 knockdown on the invasion and migration abilities of HCC cells. In vivo assays showed that KCNQ1OT1 knockdown suppressed tumour growth. This work suggests that lncRNA KCNQ1OT1 might act as a potential therapeutic target in HCC.	NA	Cancer Gene Ther 2020 Aug 5, 10.1038/s41417-020-0203-x doi:10.1038/s41417-020-0203-x PMID:32753631
2846	LncRNA	TMPO-AS1	miR-320a	SERBP1	HCC cells (HepG2, SNU-387, HCCLM3, SMMC-7721, Huh7) and normal human hepatic cell line, LO2 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,RIP etc.	32753892	lncRNA TMPO-AS1 Exerts Oncogenic Roles in HCC Through Regulating miR-320a/SERBP1 Axis.	Collectively, our results suggested that TMPO-AS1 was a promoting factor for the aggressive behaviors of HCC cell. 	NA	Onco Targets Ther 2020  13, 6539-6551 doi:10.2147/ott.S250355 PMID:32753892
2847	LncRNA	LINC01535	miR-214-3p	KCNC4	Human OS cell lines (MG63, Saos2, HOS, U2OS) andhuman  osteoblasts  (hFOB1.19) 	Osteosarcoma	Homo sapiens (human)	Western blot,RIP,FISH,Luciferase reporter assay etc.	32753970	LINC01535 Promotes the Development of Osteosarcoma Through Modulating miR-214-3p/KCNC4 Axis.	LINC01535, miR-214-3p and KCNC4 constituted an effective axis thatexerted a pregnant regulation in OS development, which is a quite meaningful discoveryfor exploring potential therapeutic methods for OS patients.	NA	Cancer Manag Res 2020  12, 5575-5585 doi:10.2147/cmar.S232757 PMID:32753970
2848	LncRNA	MALAT1	miR-205	PTK7	The ALL cell lines Jurkat (T cells), Reh (non-T/non-Bcells),CEM (T cells), Molt4 (T cells)	Acute Lymphoblastic Leukemia	Homo sapiens (human)	Western blot,Flow cytometry,Luciferase reporter assay etc.	32754978	LncRNA-MALAT1 regulates proliferation and apoptosis of acute lymphoblastic leukemia cells via miR-205-PTK7 pathway.	This study aims to investigate the functional roles and underlying mechanisms of MALAT1 in ALL. MALAT1 and miR-205 expression were assessed by real-time quantitative polymerase chain reaction (RT-qPCR). MTT assay and flow cytometry were performed to evaluate cell proliferation and apoptosis, respectively. Protein level of protein tyrosine kinase-7 (PTK7) was detected by Western blot assay. Dual luciferase reporter assay was conducted to confirm the binding of MALAT1 and miR-205, as well as miR-205 and PTK7. The levels of MALAT1 and PTK7 were upregulated in ALL samples. In contrast, miR-205 level was downregulated in ALL in ALL samples. Moreover, MALAT1 silencing or miR-205 overexpression restrained proliferation and promoted apoptosis of ALL cells. Mechanistically, MALAT1 sponged miR-205 to regulate PTK7 expression. In summary, MALAT1 affected ALL cell proliferation and apoptosis via regulating miR-205-PTK7 axis. Our results suggest that MALAT1-miR-205-PTK7 axis participates in the proliferation and apoptosis of ALL, which may provide a potential treatment target for ALL.	NA	Pathol Int 2020 Oct 70, 724-732 doi:10.1111/pin.12993 PMID:32754978
2849	LncRNA	HOTAIR	miR-204-5p	HMGB1	Two CCA cells (HuH28 an dHuCCT1) 	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR,Western blot,RIP etc.	32755793	LncRNA HOTAIR suppresses cell apoptosis, autophagy and induces cell proliferation in cholangiocarcinoma by modulating the miR-204-5p/HMGB1 axis.	Conclusion: These data unraveled that lncRNA HOTAIR regulated HMGB1 to suppress cell apoptosis, autophagy and induce cell proliferation by sponging miR-204-5p in CCA. Thus, this new regulatory pathway may provide new therapeutic targets for CCA. 	NA	Biomed Pharmacother 2020 Oct 130, 110566 doi:10.1016/j.biopha.2020.110566 PMID:32755793
2850	LncRNA	DLX6-AS1	miR-195-5p	VEGFA	The human bladder epithelium immortalized cell line SV-HUC-1 and BC cell lines T24, RT4, 5637, J82, and SW780	Bladder Cancer	Homo sapiens (human)	FISH,qRT-PCR,Western blot,Luciferase reporter assay,RIP etc.	32756011	Long non-coding RNA DLX6-AS1 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA signaling pathway.	Our study demonstrated that DLX6-AS1 played an oncogenic role in BC through miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK pathway.	NA	Aging (Albany NY) 2020 Aug 3 12, 16021-16034 doi:10.18632/aging.103374 PMID:32756011
2851	LncRNA	LINC01123	miR-34a-5p	TUFT1	Three human HCC cell lines (HepG2, Huh7 and Hep3B) and a normal human liver cell line (LO2) 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,RIP etc.	32760198	Long noncoding RNA LINC01123 promotes the proliferation and invasion of hepatocellular carcinoma cells by modulating the miR-34a-5p/TUFT1 axis.	In conclusion, we found that LINC01123 is an oncogene in HCC. The upregulated expression of LINC01123 in HCC tissues may potentially predict poor prognosis. LINC01123 accelerated HCC cell proliferation, migration and invasion by sponging miR-34a-5p and enhancing TUFT1 expression. This study may provide new insight into the pathogenesis of HCC.	NA	Int J Biol Sci 2020  16, 2296-2305 doi:10.7150/ijbs.45457 PMID:32760198
2852	LncRNA	KCNQ1OT1	miR-329-3p	CTNND1	Normal human colon epithelial NCM460 cells and CRC cell lines (T84, LS1034, HCT116, and SW480) 	Colorectal Cancer 	Homo sapiens (human)	RT-PCR,Flow cytometry,luciferase reporter assay,Western blot etc.	32760218	Long non-coding RNA KCNQ1OT1 up-regulates CTNND1 by sponging miR-329-3p to induce the proliferation, migration, invasion, and inhibit apoptosis of colorectal cancer cells.	Our results indicated that KCNQ1OT1 could positively regulate CTNND1 expression by sponging miR-329-3p, thereby boosting the progression of CRC. Our findings provided the underlying therapy targets for CRC.	NA	Cancer Cell Int 2020  20, 340 doi:10.1186/s12935-020-01425-2 PMID:32760218
2853	LncRNA	H1FX-AS1	miR-324-3p	DACT1	Four CC (SiHa, C-4I, HeLa and C-33A) and a normal cervical epithelial (End1/E6E7) cell lines	Cervical Cancer	Homo sapiens (human)	luciferase reporter assay,qRT-PCR etc.	32760225	A newly identified lncRNA H1FX-AS1 targets DACT1 to inhibit cervical cancer via sponging miR-324-3p.	Conclusion: A novel lncRNA H1FX-AS1 was identified, which acted as a competing endogenous RNA (ceRNA) of miR-324-3p to inhibit DACT1 mediated CC progression. Therefore, H1FX-AS1 is a new prognostic predictor and targeting the factors in the H1FX-AS1/miR-324-3p/DACT1 axis is the novel potential therapeutic strategy for CC. 	NA	Cancer Cell Int 2020  20, 358 doi:10.1186/s12935-020-01385-7 PMID:32760225
2854	LncRNA	HOXA-AS2	miR-302c-3p	ZFX	The human endometrial carcinoma cell line Ishikaw	Type I Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32760226	HOXA-AS2 promotes type I endometrial carcinoma via miRNA-302c-3p-mediated regulation of ZFX.	Conclusions: These findings suggest that HOXA-AS2 can act as a new therapeutic target for type I endometrial cancer. 	NA	Cancer Cell Int 2020  20, 359 doi:10.1186/s12935-020-01443-0 PMID:32760226
2855	LncRNA	SLCO4A1-AS1	miR-4701-5p	NFE2L1	LUAD  cell  lines  (PC-9,  Calu3,  A549,  and  HCC827)  and  human normal lung epithelial cell (BEAS-2B)	Lung Cancer	Homo sapiens (human)	qRT-PCR,FISH,RIP,Western blot,luciferase reporter assay etc.	32762035	SLCO4A1-AS1 promotes cell growth and induces resistance in lung adenocarcinoma y modulating miR-4701-5p/NFE2L1 axis to activate WNT pathway.	In conclusion, this study revealed a novel highly expressed lncRNA  SLCO4A1-AS1  in  LUAD.  SLCO4A1-AS1  pro-moted  cell  growth  and  inhibited  chemosensitivity  in  LUAD  via  miR-4701-5p/NFE2L1  axis  to  stimulate  WNT  pathway,  which  might  be  helpful  for  deciphering  novel  therapeutic  methods for LUAD patients.	NA	Cancer Med 2020 Oct 9, 7205-7217 doi:10.1002/cam4.3270 PMID:32762035
2856	LncRNA	TUG1	miR-498	RORA	Human periodontal ligament cells (hPDLCs) 	Periodontitis 	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32762066	Long non-coding RNA TUG1 participates in LPS-induced periodontitis by regulating miR-498/RORA pathway.	Conclusion: Therefore, TUG1 could protect against periodontitis via regulating miR-498/RORA mediated Wnt/β-catenin signaling. 	NA	Oral Dis 2021 Apr 27, 600-610 doi:10.1111/odi.13590 PMID:32762066
2857	LncRNA	HOXC13-AS	miR-378g	HOXC13	Normal oral keratinocytes (NHOK) and OSCC cells (Fadu, TSCCA,HSU3, SCC15) 	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,RIP,FISH etc.	32763778	HOXC13-AS accelerates cell proliferation and migration in oral squamous cell carcinoma via miR-378g/HOXC13 axis.	In conclusion, our studyfirstly showed that HOXC13-AS functionedas a ceRNA to accelerate the malignancy in OSCC via miR-378g/HOXC13 axis, providing new thoughts for improving the lncRNA-tar-geted treatment of OSCC	NA	Oral Oncol 2020 Dec 111, 104946 doi:10.1016/j.oraloncology.2020.104946 PMID:32763778
2858	LncRNA	LINC00665	miR-214-3p	PSMD10	five MM cell lines (MM.1S, U266, RPMI-8226, KM3 and H929) and normal plasma cells (nPCs)	Multiple Myeloma	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32764956	LINC00665 Promotes the Progression of Multiple Myeloma by Adsorbing miR-214-3p and Positively Regulating the Expression of PSMD10 and ASF1B.	LINC00665 can promote the expression of PSMD10 and ASF1B by inhibiting the expression of miR-214-3p, thus facilitating the proliferation and inhibiting apoptosis of MM cells.	NA	Onco Targets Ther 2020  13, 6511-6522 doi:10.2147/ott.S241627 PMID:32764956
2859	LncRNA	LINC00665	miR-214-3p	ASF1B	five MM cell lines (MM.1S, U266, RPMI-8226, KM3 and H929) and normal plasma cells (nPCs)	Multiple Myeloma	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32764956	LINC00665 Promotes the Progression of Multiple Myeloma by Adsorbing miR-214-3p and Positively Regulating the Expression of PSMD10 and ASF1B.	LINC00665 can promote the expression of PSMD10 and ASF1B by inhibiting the expression of miR-214-3p, thus facilitating the proliferation and inhibiting apoptosis of MM cells.	NA	Onco Targets Ther 2020  13, 6511-6522 doi:10.2147/ott.S241627 PMID:32764956
2860	LncRNA	MFI2-AS1	miR-125a-5p	TRIAP1	Human thyroid cancer cell lines (SW579, K1 and TPC-1) and normal thyroid follicular epithelial cell line Nthy-ori 3–1	Thyroid Cancer	Homo sapiens (human)	qRT-PCR,RIP,luciferase reporter assay etc.	32764987	Upregulation of TRIAP1 by the lncRNA MFI2-AS1/miR-125a-5p Axis Promotes Thyroid Cancer Tumorigenesis.	Our results elucidated a novel mechanism that MFI2-AS1 promotes thyroid cancer progression via the miR-125a-5p/TRIAP1 pathway.	NA	Onco Targets Ther 2020  13, 6967-6974 doi:10.2147/ott.S236476 PMID:32764987
2861	LncRNA	TP73-AS1	miR-27b-3p	LAPTM4B	Normal human bronchial epithelial cell line 16HBE14o	Lung Cancer	Homo sapiens (human)	Western blot,luciferase reporter assay etc.	32764992	Long Non-Coding RNA TP73-AS1 Promotes the Development of Lung Cancer by Targeting the miR-27b-3p/LAPTM4B Axis.	TP73-AS1 promoted the progression of lung cancer through regulating miR-27b-3p/LAPTM4B axis and it might be a potential target for diagnosis and treatment of lung cancer.	NA	Onco Targets Ther 2020  13, 7019-7031 doi:10.2147/ott.S234443 PMID:32764992
2862	LncRNA	MCM3AP-AS1	miR-15a	EIF4E	Human lymphoma cell lines Daudi and Namalwa	Lymphoma	Homo sapiens (human)	Flow Cytometry,luciferase reporter assay,Western blot etc.	32765087	Knockdown of lncRNA MCM3AP-AS1 Attenuates Chemoresistance of Burkitt Lymphoma to Doxorubicin Treatment via Targeting the miR-15a/EIF4E Axis.	This study identified a novel lncRNA, MCM3AP-AS1, that was upregulated in Burkitt lymphoma tissues and indicated poor prognosis. Knockdown of MCM3AP-AS1 increased drug sensitivity, enhanced cell cycle progression and facilitated apoptosis by regulating EIF4E and its downstream anti-apoptotic proteins in vitro and in vivo. MiR-15a functioned as the link between MCM3AP-AS1 and EIF4E. Therefore, targeting the MCM3AP-AS1/miR-15a/EIF4E axis might become a promising target in the treatment of B-NHL.	NA	Cancer Manag Res 2020  12, 5845-5855 doi:10.2147/cmar.S248698 PMID:32765087
2863	LncRNA	H19	miR-520a-3p	LIMK1	Three  HCC  cell  lines,  including  conventional  hepatocellular  carcinoma  cell  line  (Huh7)  and  two  highly  metastatic  HCC  cell  lines  (MHCC97-H  and  HCCLM3)	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Western blot,Flow cytometry,luciferase reporter assay etc.	32767662	Exosomal lncRNA H19 promotes the progression of hepatocellular carcinoma treated with Propofol via miR-520a-3p/LIMK1 axis	Conclusion: Circulating  H19  promoted  the  proliferation,  migration  and  invasion  and inhibited the apoptosis of HCC cells treated with Propofol through upregulating LIMK1 via sponging miR-520a-3p.	NA	Cancer Med 2020 Oct 9, 7218-7230 doi:10.1002/cam4.3313 PMID:32767662
2864	LncRNA	LINC00514	miR-28-5p	Rap1b	The normal pancreatic epithelial cell line (HPDE) and PC cell lines (BxPC-3, SW1990, PANC-1, AsPC-1, Capan-2, and MIAPaCa-2) 	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,RNAi,Western blot etc.	32771045	Long noncoding RNA LINC00514 accelerates pancreatic cancer progression by acting as a ceRNA of miR-28-5p to upregulate Rap1b expression.	Conclusions: This study is the first to characterize the oncogenic function of the long noncoding RNA LINC00514 in pancreatic cancer progression by acting as a competing endogenous RNA (ceRNA) of miR-28-5p to upregulate Rap1b expression. Understanding this molecular mechanism might contribute to further discoveries of better diagnostic and therapeutic options for pancreatic cancer. 	NA	J Exp Clin Cancer Res 2020 Aug 8 39, 151 doi:10.1186/s13046-020-01660-5 PMID:32771045
2865	LncRNA	HOTAIR	miR-206	TBX3	The human ovarian cancer cell  lines SKOV3 (human ovarian adenocarcinoma cells), ES2 (human ovarian clear cell carcinoma cells), and OVCAR3 (human ovarian adenocarcinoma cells) 	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32771526	HOTAIR maintains the stemness of ovarian cancer stem cells via the miR-206/TBX3 axis.	Collectively, this study highlights a role of HOTAIR in the stemness maintenance of  OCSCs. HOTAIR could serve as  a  miR-206 sponge, causing the up-regulated expression of TBX3 to promote the stemness of OCSCs. Identification of the HOTAIR/miR-206/TBX3 axis provides new insight into the molecular mechanisms underlying the regulation and maintenance of OCSCs, which might help to improve lncRNA-targeted diagnosis and treatment strategies for ovarian cancer. 	NA	Exp Cell Res 2020 Oct 15 395, 112218 doi:10.1016/j.yexcr.2020.112218 PMID:32771526
2866	LncRNA	TRG-AS1	miR-4500	BACH1	Human liver immortalized cell line THLE-2 and human HCC cell line SK-HEP-1 	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,FISH,RIP,Western blot，luciferase reporter assay etc.	32774161	LncRNA TRG-AS1 stimulates hepatocellular carcinoma progression by sponging miR-4500 to modulate BACH1.	Results: TRG-AS1 was conspicuously overexpressed in HCC cells. TRG-AS1 silencing apparently suppressed HCC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT). Mechanism exploration revealed that TRG-AS1 acted as a molecular sponge of miR-4500 to regulate BACH1. MiR-4500 silencing or BACH1 overexpression in BACH1-downregulated cells fully rescued cell proliferation migration, invasion and EMT progress. 	NA	Cancer Cell Int 2020  20, 367 doi:10.1186/s12935-020-01440-3 PMID:32774161
2867	LncRNA	LINC00441	miR-450b-5p	RAB10	Normal cervical cell line (Ect1/E6E7) and CC cell lines (HeLa, CaSki, SiHa and C33A) 	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Flow cytometry,Western blot,RIP，luciferase reporter assay etc.	32774162	LINC00441 promotes cervical cancer progression by modulating miR-450b-5p/RAB10 axis.	LINC00441 was upregulated in CC tissues and cells. Further, LINC00441 depletion repressed cell proliferation and motility in vitro as well as tumor growth in vivo. LINC00441 could sponge miR-450b-5p to upregulate RAB10 expression. Finally, miR-450b-5p inhibitor or RAB10 upregulation counteracted LINC00441 knockdown-mediated function on the development of CC. 	NA	Cancer Cell Int 2020  20, 368 doi:10.1186/s12935-020-01400-x PMID:32774162
2868	LncRNA	DLX6-AS1	miR-195-5p	FHL2	OC cell lines (SKOV3 and A2780), normal ovarian epithelial cell line (IOSE80), and human embryonic kidney cell (293 T)	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Flow cytometry,Western blot,luciferase reporter assay,RIP etc.	32774164	LncRNA DLX6-AS1 aggravates the development of ovarian cancer via modulating FHL2 by sponging miR-195-5p.	DLX6-AS1, as an oncogene in OC, accelerated tumor progression by up-regulating FHL2 via mediating miR-195-5p, suggesting that DLX6-AS1 was a hopeful target for the lncRNA-targeted therapy in OC.	NA	Cancer Cell Int 2020  20, 370 doi:10.1186/s12935-020-01452-z PMID:32774164
2869	LncRNA	ACTA2-AS1	miR-143-3p	SMAD3	Human Cervical cancer cell lines (HeLa, SiHa and CaSki) and human normal cervical epithelial cell line (HcerEpic)	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32774166	A novel mechanism by which ACTA2-AS1 promotes cervical cancer progression: acting as a ceRNA of miR-143-3p to regulate SMAD3 expression.	In summary, our study revealed that ACTA2-AS1 upregulates SMAD3 by competitively binding miR-143-3p, thereby accelerating CC progression. The ACTA2-AS1/miR-143-3p/SMAD3 axis can play a crucial role in cervical carcinogenesis, providing new clues for the early diagnosis and treatment of CC.	NA	Cancer Cell Int 2020  20, 372 doi:10.1186/s12935-020-01471-w PMID:32774166
2870	LncRNA	CASC2	miR-9-5p	PPARr	Human podocytes CIHP-1 	Diabetes Mellitus	Homo sapiens (human)	RIP,luciferase reporter assay,Western blot，qRT-PCR etc	32774472	Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy.	Conclusion: CASC2 increased cell viability, autophagy and inhibited cell apoptosis by regulating miR-9-5p/PPARγ axis, thus reducing the HG-induced podocytes injury. 	NA	Diabetol Metab Syndr 2020  12, 68 doi:10.1186/s13098-020-00574-8 PMID:32774472
2871	LncRNA	OIP5-AS1	miR-140-5p	HDAC7	Human lung cancer cells (A549 and H1299) 	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32774481	OIP5-AS1 modulates epigenetic regulator HDAC7 to enhance non-small cell lung cancer metastasis via miR-140-5p.	In summary, the present study suggested the oncogenic role of lncRNA OIP5-AS1 in NSCLC metastasis via miR-140-5p at the cellular and clinical levels. HDAC7 and VEGFA are two downstream effectors for mediating OIP5-AS1/miR-140-5p-regulated NSCLC metastasis. The present findings may provide an improved understanding of NSCLC progression and accelerate the development of diagnostic and therapeutic strategies for the treatment of NSCLC.	NA	Oncol Lett 2020 Oct 20, 7 doi:10.3892/ol.2020.11868 PMID:32774481
2872	LncRNA	XIST	miR-125b-5p	NLRC5	Three breast cancer cell lines (MCF-7, MDA-MB-231 and SKBR3 cells) and normal breast epithelial cell line (MCF-10A cells)	Breast Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,Flow cytometry etc.	32774715	The lncRNA XIST promotes the progression of breast cancer by sponging miR-125b-5p to modulate NLRC5.	Both XIST (a lncRNA) and NLRC5 are overexpressed, and miR-125b-5p is downregulated, in breast cancer tissues and cells. XIST suppression decreased cell growth, cell metastasis, and anti-apoptosis activity. Both XIST and NLRC5 contain binding sites for miR-125b-5p, as initially predicted in our study. Decreasing XIST levels increased miR-125b-5p expression, and the upregulation of miR-125b-5p produced similar inhibitory effects on breast cancer cells as that mediated by the loss of XIST. 	NA	Am J Transl Res 2020  12, 3501-3511,  PMID:32774715
2873	LncRNA	TGFB2-AS1	miR-340-5p	EDNRB	LUAD cells (A549 and PC9) and human lung epithelial cell (BEAS-2B)	Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay etc.	32774737	LncRNA TGFB2-AS1 regulates lung adenocarcinoma progression via act as a sponge for miR-340-5p to target EDNRB expression.	Taken together, our work indicated TGFB2-AS1 functions as a sponge for miR-340-5p to regulate EDNRB expression in LUAD. These findings identified a novel ceRNA regulatory axis, TGFB2-AS1/miR-340-5p/EDNRB, in LUAD, which will help us to understand the mechanisms behind LUAD progression.	NA	Am J Transl Res 2020  12, 3813-3821,  PMID:32774737
2874	LncRNA	LINC00665	miR-9-5p	ATF1	Human CRC cell lines (DLD-1, SW480, KM12, SW116 and SW620 cells) and normal colonic epithelial cell line NCM460	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,Flow cytometry etc.	32776307	LINC00665/miR-9-5p/ATF1 is a novel axis involved in the progression of colorectal cancer.	In summary, we conclude that LINC00665 promotes CRC progression by regulating the miR-9-5p/ATF1 axis, which is expected to expand understanding of the mechanisms of CRC progression and provide potential therapeutic targets for CRC.	NA	Hum Cell 2020 Oct 33, 1142-1154 doi:10.1007/s13577-020-00393-z PMID:32776307
2875	LncRNA	NFIA-AS2	miR-655-3p	ZFX	The glioma cell lines included A172, LN229, SHG44, U373-MG, U87, and U251	Glioma	Homo sapiens (human)	qRT-PCR,Western blot,luciferase reporter assay,RIP etc.	32779154	LncRNA NFIA-AS2 promotes glioma progression through modulating the miR-655-3p/ZFX axis.	In conclusion, NFIA-AS2 might be a prognostic bio-marker in glioma, and a novel network of NFIA-AS2, miR-655-3p, and ZFX in glioma was clarified in this study. NFIA-AS2 promoted glioma cell progression by spong-ing miR-655-3p to augment ZFX expression. These data would serve the purpose to explore promising therapeutic target and pave a way for better diagnosis in glioma.	NA	Hum Cell 2020 Oct 33, 1273-1280 doi:10.1007/s13577-020-00408-9 PMID:32779154
2876	LncRNA	HNF1A-AS1	miR-363-3p	MAP2K4	Human glioma cells (U87-MG, A172, U251, and T98G) and humannormal astrocytes normal astrocytes (NHA) 	Glioma	Homo sapiens (human)	qRT-PCR,Flow cytometry,Luciferase reporter assay,Western blot,RIP,ChIP etc.	32779194	Long noncoding RNA HNF1A-AS1 regulates proliferation and apoptosis of glioma through activation of the JNK signaling pathway via miR-363-3p/MAP2K4.	In conclusion, the high expression level of HNF1A-AS1 in gliomatissues and cell lines was activated by transcription factor MYC.Besides this, HNF1A-AS1 worked as a sponge of miR-363-3p topromote cell proliferation and inhibit apoptosis in glioma cells. Inaddition, we proved that HNF1A-AS1 regulates glioma cell growththrough activation of the JNK signaling pathway via the miR-363-3p/MAP2K4 axis.	NA	J Cell Physiol 2021 Feb 236, 1068-1082 doi:10.1002/jcp.29916 PMID:32779194
2877	LncRNA	GAS5	miR-92a-3p	E4BP4	CD4+T cell/B cell	Lupus Erythematosus	Homo sapiens (human)	qRT-PCR,Flow cytometry,Western blot etc.	32781006	LncRNA GAS5 suppresses CD4(+) T cell activation by upregulating E4BP4 via inhibiting miR-92a-3p in systemic lupus erythematosus.	In this study, we showed that lncRNA GAS5 was decreased in CD4+T cells and plasma from SLE patients. Overepression of GAS5 inhibited the activation of normal CD4+T cells and attenuated the self-reactivity of SLE CD4+T cells. Additionally, E4BP4 was involved in lncRNA GAS- mediated inhibition of  CD4+T  cell  activation. We  also  found that GAS5 upregulated E4BP4 by inhibiting miR-92a-3p expression. Collec-tively, the GAS5/miR-92a-3p/E4BP4 pathway plays an important role in inhibiting CD4+T  cell  activation in  SLE, which may be  a  potential therapeutic target for SLE treatment.	NA	Immunol Lett 2020 Nov 227, 41-47 doi:10.1016/j.imlet.2020.08.001 PMID:32781006
2878	LncRNA	LINC01410	miR-506-3p	WEE1	SK㎞㏒H, IMR2, Kelly, and SH㏒Y5Y	Neuroblastoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay，western blot	32886453	Long noncoding RNA LINC01410 promotes the tumorigenesis of neuroblastoma cells by sponging microRNA-506-3p and modulating WEE1	The expression of LINC01410 and WEE1 was enhanced and miR-506-3p was inhibited in NBL. LINC01410 knockdown attenuated the cell proliferation, colony formation ability, and inhibited tumor growth. Moreover, LINC01410 silencing facilitated the apoptosis and arrested the cell cycle. LINC01410 interacted with miR-506-3p to elevate the WEE1 expression in NBL. Additionally, miR-506-3p inhibition or WEE1 overexpression weakened the reduction effects of sh-LINC01410 on cell proliferation, colony formation ability, apoptosis, and cell cycle.	NA	Cancer Med 2020 Nov 9, 8133-8143 doi:10.1002/cam4.3398 PMID:32886453
2879	LncRNA	SNHG1	miR-143-3p	EZH2	T24 and 5637SV〩UC	Bladder Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,western blot	32885590	The long non-coding RNA SNHG1 promotes bladder cancer progression by interacting with miR-143-3p and EZH2	The long nonヽoding RNA (lncRNA) SNHG1 has been shown to be implicated in the progression of multiple human carcinomas. Nevertheless, the biological functions and potential mechanism of SNHG1 in bladder cancer (BC) are uncharacterized. In the present study, SNHG1 was found to be substantially upegulated in BC tissues and cells and was intimately correlated with the TNM stage, lymphatic invasion, metastasis and recurrenceゝree survival in BC patients. Downegulation of SNHG1 dramatically attenuated the proliferation, migration and invasion of BC cells, whereas the ectopic overexpression of SNHG1 had the opposite effects in vitro.	NA	J Cell Mol Med 2020 Oct 24, 11858-11873 doi:10.1111/jcmm.15806 PMID:32885590
2880	LncRNA	SNHG6	miR-485-3p	STYX	HCerEpiC,C-33 A, SiHa, HeLa, CaSki, HT-3	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32884447	LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p.	SNHG6 was expressed at a high level in CC cells. Silenced SNHG6 suppressed cell proliferation but promoted cell apoptosis. Additionally, silenced SNHG6 could sensitize CC cells to radiation treatment. miR-485-3p could bind to both SNHG6 and STYX. Knockdown of miR-485-3p or overexpression of STYX could abolish the effects of SNHG6 silencing on CC cell growth.	NA	Cancer Cell Int 2020  20, 424 doi:10.1186/s12935-020-01448-9 PMID:32884447
2881	LncRNA	NEAT1	miR-770-5p	PARP1	A2780 and SKOV3,A2780/DDP and SKOV3/DDP	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	32884343	NEAT1 Knockdown Suppresses the Cisplatin Resistance in Ovarian Cancer by Regulating miR-770-5p/PARP1 Axis.	Knockdown of NEAT1 inhibited cisplatin resistance in ovarian cancer cells by up-regulating miR-770-5p and down-regulating PARP1, providing a new target for improving the efficacy of cisplatin-based therapy in ovarian cancer.	NA	Cancer Manag Res 2020  12, 7277-7289 doi:10.2147/cmar.S257311 PMID:32884343
2882	LncRNA	LINC01089	miR-27b-3p	HOXA10	SW480, HT29, SW620, HCT116, as well as LoVo cells,NCM460 cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western Blot	32884303	LINC01089 Blocks the Proliferation and Metastasis of Colorectal Cancer Cells via Regulating miR-27b-3p/HOXA10 Axis	LINC01089 was down-regulated in CRC tissues and cell lines. LINC01089 overexpression impeded the proliferation and invasion of SW620 and LoVo cells, whereas LINC01089 knockdown increased the malignancy of SW480 and HT29 cells. Moreover, LINC01089 directly interacted with miR-27b-3p to repressed its expression and indirectly promoted the expression of HOXA10.	NA	Onco Targets Ther 2020  13, 8251-8260 doi:10.2147/ott.S256148 PMID:32884303
2883	LncRNA	LSINCT5	miR-20a-5p	XIAP	SOSP-9607, MG-63, U2OS, SAOS-2,hFOB	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	32884299	lncRNA LSINCT5 Regulates miR-20a-5p/XIAP to Inhibit the Growth and Metastasis of Osteosarcoma Cells	In this study, elevated LSINCT5 was found in OS tissue samples and OS cell strains, and the increased LSINCT5 was strongly related to the adverse prognosis of clinical patients. Functional assays showed that inhibition of LSINCT5 could up-regulate miR-20a-5p-mediated OS cells proliferation and metastasis. WB analysis and qP analysis showed that LSINCT5 regulated XIAP by mediating miR-20a-5p. Further cell behavior experiments showed that LSINCT5 acted as a miR-20a-5p sponge to inhibit proliferation and metastasis caused by XIAP. Finally, the results of animal models in vivo showed that LSINCT5 could regulate the tumor growth of OS.	NA	Onco Targets Ther 2020  13, 8209-8221 doi:10.2147/ott.S251843 PMID:32884299
2884	LncRNA	LINC01116	miR-203	SMAD5	Kit-8	Keloid Formation	Homo sapiens (human)	qRT-PCR,western blot	32883538	Long non-coding RNA LINC01116 accelerates the progression of keloid formation by regulating miR-203/SMAD5 axis	LINC01116 and SMAD5 were upregulated while miR-203 was downregulated in keloid tissues and keloid fibroblasts. LINC01116 knockdown suppressed the proliferation, migration, invasion, and ECM production but induced apoptosis in keloid fibroblasts through enhancing miR-203 and inhibiting SMAD5. Moreover, SMAD5 was identified as a direct target of miR-203 and miR-203 could directly bind to LINC01116. Besides, LINC01116 regulated SMAD5 expression by targeting miR-203.	NA	Burns 2021 May 47, 665-675 doi:10.1016/j.burns.2020.07.027 PMID:32883538
2885	LncRNA	SNHG3	miR-154-3p	Notch2	MCF-7, MDA-MB-231, HCC1937, BT474, SKBr-3,MCF10A	Breast Cancer	Homo sapiens (human)	qRT-PCR,Western blot	32883233	Long non-coding RNA SNHG3 promotes breast cancer cell proliferation and metastasis by binding to microRNA-154-3p and activating the notch signaling pathway	Highly expressed SNHG3 was observed in BC tissues. The growth of BC cells in vivo and in vitro was evidently repressed after silencing SNHG3. BC cell invasion and migration were inhibited by silencing SNHG3 in vitro. SNHG3 could act as a competing endogenous RNA of miR-154-3p and upregulate the Notch signaling pathway to promote BC cell development. Activation of the Notch signaling pathway can partly reverse the inhibition of cell activity induced by silencing SNHG3.	NA	BMC Cancer 2020 Sep 3 20, 838 doi:10.1186/s12885-020-07275-5 PMID:32883233
2886	LncRNA	SNHG17	miR-876-5p	ERLIN2	LN-215, ADF, U138 and A-382,NHA	Astrocytoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	32883232	SNHG17 drives malignant behaviors in astrocytoma by targeting miR-876-5p/ERLIN2 axis	SNHG17 could induce the progression of astrocytoma by sponging miR-876-5p to elevate the expression of ERLIN2. This study indicated that SNHG17 has a high potential to be a therapeutic target for astrocytoma.	NA	BMC Cancer 2020 Sep 3 20, 839 doi:10.1186/s12885-020-07280-8 PMID:32883232
2887	LncRNA	SNHG1	miR-3127-5p	FZD4	HeLa and SiHa	Cervical Cancer	Homo sapiens (human)	qRT-PCR，Northern blot，Western blot	32883110	SNHG1 represses the anti-cancer roles of baicalein in cervical cancer through regulating miR-3127-5p/FZD4/Wnt/b-catenin signaling	Our findings revealed that SNHG1 represses the antitumorigenic roles of baicalein in CC. Further mechanistic studies revealed that SNHG1 binds miR-3127-5p and functions as a microRNA sponge. Via agglutinating miR-3127-5p, SNHG1 up-regulates FZD4, a target of miR-3127-5p. Through up-regulating FZD4, SNHG1 further activates Wnt/b-catenin signaling. Collectively, these data presented that SNHG1 represses the antitumorigenic roles of baicalein in CC through modulating miR-3127-5p/FZD4/Wnt/b-catenin axis.	NA	Exp Biol Med (Maywood) 2021 Jan 246, 20-30 doi:10.1177/1535370220955139 PMID:32883110
2888	LncRNA	NEAT1	miR-202-3p	TIMD4	RL95, AN3CA,NE	Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	32882142	Overexpression of Nuclear Enriched Autosomal Transcript 1 Facilitates Cell Proliferation, Migration Invasion, and Suppresses Apoptosis in Endometrial Cancer by Targeting MicroRNA-202-3p/T Cell Immunoglobulin and Mucin Domain 4 Axis	NEAT1 was upregulated, whereas miR-202-3p was downregulated in EC tumors and cells. Depletion of NEAT1 restrained EC cell proliferation, migration, invasion, and improved apoptosis. MiR-202-3p was targeted by NEAT1 and could bind to TIMD4. Subsequently, it is observed that miR-202-3p inhibitor neutralized NEAT1 silencing mediated suppression on EC cell progression. Meanwhile, TIMD4 rescued miR-202-3p induced inhibition on cell progression in EC. Furthermore, it was obvious that NEAT1 facilitated TIMD4 expression by absorbing miR-202-3p in EC. Conclusions: Upregulation of NEAT1 accelerated EC cell progression through sponging miR-202-3p to facilitate TIMD4 expression, providing potential novel treatment method for EC.	NA	Cancer Biother Radiopharm 2020 Sep 2, 10.1089/cbr.2020.3902 doi:10.1089/cbr.2020.3902 PMID:32882142
2889	LncRNA	LOXL1-AS1	miR-21	RHOB	SiHa	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Western blot	32881598	Up-regulation of long non-coding RNA LOXL1-AS1 functions as an oncogene in cervical squamous cell carcinoma by sponging miR-21	We observed that LOXL1-AS1 was downregulated in CSCC. LOXL1-AS1 was predicted to interact with miR-21, while overexpression experiments showed that LOXL1-AS1 and miR-21 had no significant effects on the expression of each other. However, LOXL1-AS1 overexpression led to the upregulation of RHOB, a direct target of miR-21. Cell invasion and migration analysis showed decreased invasion and migration rates of CSCC cells after LOXL1-AS1 and RHOB overexpression. MiR-21 played an opposite role at reduced the effects of LOXL1-AS1 and RHOB overexpression.	NA	Arch Physiol Biochem 2020 Sep 3, 10.1080/13813455.2020.1804406, 1-5 doi:10.1080/13813455.2020.1804406 PMID:32881598
2890	LncRNA	JPX	miR-944	CDH2	SCC-15, SCC-25, HSC-2, SCC-9,NOK	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32881231	LncRNA JPX overexpressed in oral squamous cell carcinoma drives malignancy via miR-944/CDH2 axis	LncRNA JPX was discovered as highly expressed in OSCC cells. Silencing lncRNA JPX restrained OSCC cell proliferation, migration and invasion. Interestingly, lncRNA JPX bound with miR-944, and then augmented CDH2 via a competing endogenous RNA (ceRNA) mechanism. Importantly, overexpressed CDH2 recovered the suppression of silenced lncRNA JPX on the oncogenic behaviors of OSCC cells.	NA	Oral Dis 2021 May 27, 924-933 doi:10.1111/odi.13626 PMID:32881231
2891	LncRNA	MALAT1	miR-143-D14733p	RALGAPA2	breast cancer cell lines,tumor-derived cell lines	Breast Cancer	Homo sapiens (human)	qPCR	32880825	The interaction between MALAT1 target, miR1433p, and RALGAPA2 is afected by functional SNP rs3827693 in breast cancer	MALAT1 has been shown to promote breast cancer development and progression via repressing diferent RNA molecules such as miR-1, CDC42 [16], CD133 [17] and miR-448 [18]. In this study, we aimed to fnd more down-stream target(s) of MALAT1 in breast cancer. Here, we use a computational approach to shortlist the potential targets of MALAT1 and show that MALAT1 negatively correlates with miR-143-3p in clinical breast cancer samples. We then, fnd RALGAPA2 as a potential and novel target of miR-143-3p.	NA	Hum Cell 2020 Oct 33, 1229-1239 doi:10.1007/s13577-020-00422-x PMID:32880825
2892	LncRNA	SNHG7	miR-449a	NA	Rat pituitary, GH1, RC-4B/C, GH3 and MMQ	Pituitary Adenoma	Homo sapiens (human)	qPCR,Luciferase reporter assay	32880813	LncRNA SNHG7 sponges miR-449a to promote pituitary adenomas progression	We demonstrated that SNHG7-silencing delayed xenograft tumor progression, which was accompanied with increased miR-449a and decreased Ki67 intensity. Our study highlighted the essential oncogenic properties of the SNHG7/miR-449a axis in pituitary adenoma.	NA	Metab Brain Dis 2021 Jan 36, 123-132 doi:10.1007/s11011-020-00611-5 PMID:32880813
2893	LncRNA	MALAT1	miR-143-3p	MAGEA9	meidakai	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR,Western blot	32879299	Long Non-Coding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Cell Proliferation and Migration by Regulating miR-143-3p and MAGE Family Member A9 (MAGEA9) in Oral Squamous Cell Carcinoma	our results suggest that MALAT1 functions as a competing endogenous RNA (ceRNA) in promoting OSCC cell proliferation and migration abilities through the miR-143-3p/MAGEA9 axis, thus providing new therapeutic targets for treatment of OSCC.	NA	Med Sci Monit 2020 Sep 3 26, e924187 doi:10.12659/msm.924187 PMID:32879299
2894	LncRNA	LINC00301	miR-1276	HIF1a	H1299,95D,SK-MES-1,H460,H520,SK-LU-1,H1975,A549,H157,SPC-A1,16HBE,BEAS-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,Western blot,qRT-PCR,	32878637	FOXC1-mediated LINC00301 facilitates tumor progression and triggers an immune-suppressing microenvironment in non-small cell lung cancer by regulating the HIF1α pathway	our present research revealed the oncogenic roles of LINC00301 in clinical specimens as well as cellular and animal experiments, illustrating the potential roles and mechanisms of the FOXC1/LINC00301/EZH2/EAF2/pVHL/HIF1α and FOXC1/LINC00301/miR-1276/HIF1α pathways, which provides novel insights and potential theraputic targets to NSCLC.	NA	Genome Med 2020 Sep 2 12, 77 doi:10.1186/s13073-020-00773-y PMID:32878637
2895	LncRNA	NEAT1	miR-142-3p	FOXO1	hiPSC	Cardiovascular Disease	Homo sapiens (human)	Western blot,Luciferase reporter assay	32878634	Correction to: LncRNA-NEAT1 from the competing endogenous RNA network promotes cardioprotective efficacy of mesenchymal stem cell-derived exosomes induced by macrophage migration inhibitory factor via the miR-142-3p/FOXO1 signaling pathway	Exosomes obtained from MIF-pretreated MSCs have a protective effect on cardiomyocytes. The lncRNA-NEAT1 functions as an anti-apoptotic molecule via competitive endogenous RNA activity towards miR-142-3p. LncRNA-NEAT1/miR-142-3p/FOXO1 at least partially mediates the cardioprotective roles of exosomeMIF in protecting cardiomyocytes from apoptosis.	NA	Stem Cell Res Ther 2020 Sep 3 11, 376 doi:10.1186/s13287-020-01898-y PMID:32878634
2896	LncRNA	LINC00858	miR-134-5p	RAD18	SKOV3,Caov3,A2780IOSE-29	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase assays	32875345	Long noncoding RNA LINC00858 aggravates theoncogenic phenotypes ofovarian cancer cells throughmiR1345p/RAD18 signaling	LINC00858 were up-regulated in ovarian cancer tissues and cells, and its expression was elevated in advanced samples compared to early ones. Knocking down LINC00858 inhibited cell proliferation, motility and EMT, but accelerated cell apoptosis in ovarian cancer. Moreover, could be sponged by LINC00858 sponged miR-134-5p to enhance RAD18 expression in ovarian cancer. Also, silenced RAD18 could also restrain oncogenic behaviors of ovarian cancer cells. Rescue experiments showed that overexpressing RAD18 reversed the efects caused by knocking down LINC00858 on cellular processes.	NA	Arch Gynecol Obstet 2020 Nov 302, 1243-1254 doi:10.1007/s00404-020-05722-z PMID:32875345
2897	LncRNA	SNHG7	miR-193b	FAIM2	H125, 95D, A549，Beas-2B	Lung Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	29131440	miR-193b availability is antagonized by LncRNA-SNHG7 for FAIM2-induced tumour progression in non-small cell lung cancer.	The results indicated that miR-193b is indispensible for the ceRNA role of SNHG7 in FAIM2-supported tumourigenesis of lung cancer.	NA	Cell Prolif 2018 Feb 51 doi:10.1111/cpr.12406 PMID:29131440
2898	LncRNA	SNHG7	miR-324-3p	WNT2B	RWPE,LNCaP, PC-3 , Du-145	Prostate Cancer	Homo sapiens (human)	qPCR,Western blot	31324390	Knockdown of LncRNA SNHG7 inhibited epithelial-mesenchymal transition in prostate cancer though miR-324-3p/WNT2B axis in vitro	our study suggested that lncRNA SNHG7 could promote PCa EMT via miR-324-3p and WNT2B in vitro. The lncRNA SNHG7/miR-324-3p /WNT2B axis regulatory network might provide a potential new therapeutic strategy for PCa treatment.	NA	Pathol Res Pract 2019 Oct 215, 152537 doi:10.1016/j.prp.2019.152537 PMID:31324390
2899	LncRNA	SNHG7	miR-342-3p	ID4	AsPC-1, BxPC-3, SW1990, PANC-1,PaCa-2,HPDE6-C7,HEK293T	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR,Luciferase activity assay,Western blot	30949340	LncRNA SNHG7 promotes pancreatic cancer proliferation throughID4 bysponging miR-342-3p	We found that SNHG7 was overexpressed in both PC tissues and cell lines. High expression level of SNHG7 was correlated with the poor prognosis. SNHG7 knockdown inhibited the proliferation, migration and invasion of PC cells. Moreover, SNHG7 was found to regulate the expression of ID4 via sponging miR-342-3p. Additionally, this fnding was supported by in vivo experiments	NA	Cell Biosci 2019  9, 28 doi:10.1186/s13578-019-0290-2 PMID:30949340
2900	LncRNA	SNHG7	miR-216b	GALNT1	SW620,SW480	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay	29915311	LncRNA SNHG7 sponges miR-216b to promote proliferation and liver metastasis of colorectal cancer through upregulating GALNT1	SNHG7 positively regulated GALNT1 level through sponging miR-216b, and played an oncogenic role in CRC progression. Together, our study elucidated the role of SNHG7 as an miRNA sponge in CRC, and shed new light on lncRNA-directed diagnostics and therapeutics in CRC.	NA	Cell Death Dis 2018 Jun 18 9, 722 doi:10.1038/s41419-018-0759-7 PMID:29915311
2901	LncRNA	SNHG7	miR-5095	CTNNB1	HEB,GBM	Glioblastoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	29360452	Long noncoding RNA SNHG7 promotes the progression and growth of glioblastoma via inhibition of miR-5095	we demonstrated that SNHG7 promoted the proliferation, migration and invasion of GBM cells through the inhibition of miR-5095 and concomitant activation of Wnt/β-catenin signaling pathway. Taken together, the SNHG7/miR-5095 axis might be a potential target for the development of effective GBM therapy	NA	Biochem Biophys Res Commun 2018 Feb 5 496, 712-718 doi:10.1016/j.bbrc.2018.01.109 PMID:29360452
2902	LncRNA	MIR99AHG	miR-577	FOXP1	SGC7901, BGC823, MGC803, AGS , MKN45,GES-1	Gastric Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	32874129	Long noncoding RNA MIR99AHG promotes gastric cancer progression by inducing EMT and inhibiting apoptosis via miR577/FOXP1 axis	MIR99AHG was strongly up-regulated in human GC and contributed to cancer progression. Kaplan-Meier analysis revealed that up-regulating MIR99AHG expression was positively correlated with unfavorable overall survival (P < 0.01) of patients from our hospital and TCGA database. Knockdown of MIR99AHG expression inhibited cell proliferation, invasion, migration and promoted cell apoptosis. Moreover, MIR99AHG worked as an oncogenic gene though competing for endogenous RNA (ceRNA) of miR-577.	NA	Cancer Cell Int 2020  20, 414 doi:10.1186/s12935-020-01510-6 PMID:32874129
2903	LncRNA	PWRN1	miR-214-5p	NA	Saos-2, KHOS/NP, KHOS/312, SJSA-1, HOS and 143B cells,hFOB	Osteosarcoma	Homo sapiens (human)	qPCR,luciferase assay	32870579	Long noncoding RNA PWRN1 is lowly expressed in osteosarcoma and modulates cancer proliferation and migration by targeting hsa-miR-214-5p	We found that PWRN1 was downregulated in both osteosarcoma cells and human tumors. PWRN1 downregulation was correlated with advanced stage, metastasis, and low survival rate in cancer patients. PWRN1 overexpression in osteosarcoma cells significantly inhibited their proliferation, cisplatin chemoresistance, and in vivo growth. In addition, we demonstrated that PWRN1 directly bound miR-214-5p and suppressed its expression in osteosarcoma cells. Furthermore, we showed that miR-214-5p overexpression reversed the anti-cancer effects of PWRN1 on osteosarcoma cell proliferation and cisplatin chemoresistance.	NA	IUBMB Life 2020 Nov 72, 2444-2453 doi:10.1002/iub.2370 PMID:32870579
2904	LncRNA	LINC00662	miR-497-5p	CDC25A	C33A, HeLa, SiHa, SW756 and Caski,End1/E6E7 cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay，Western blot	32869878	LINC00662 contributes to the progression and the radioresistance of cervical cancer by regulating miR-497-5p and CDC25A	We demonstrated for the first time that LINC00662 expression was remarkably raised in CC tissues and cells. Cellular experiments confirmed that LINC00662 facilitated cell proliferation, migration, invasion and radiation resistance through the miR-497-5p/CDC25A axis, which might be a promising target for CC treatments.	NA	Cell Biochem Funct 2020 Dec 38, 1139-1151 doi:10.1002/cbf.3580 PMID:32869878
2905	LncRNA	TTTY15	miR-337-3p	JAK2	EC109, EC9706, TE-1, TE-3,HET-1A	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	32868648	Long noncoding RNA TTTY15 promotes growth and metastasis of esophageal squamous cell carcinoma by sponging microRNA-337-3p to upregulate the expression of JAK2	We explored the potential role of TTTY15 and the related mechanism in ESCC. We found that TTTY15 was upregulated in tissues of male patients with ESCC, and in-vitro study proved that TTTY15 could regulate the proliferation and metastasis of ESCC cells. Additionally, we further demonstrated that TTTY15 could upregulate JAK2 expression as a ‘competing endogenous RNA (ceRNA)’ for miR-337-3p, thus playing an oncogenic role in the pathogenesis of ESCC.	NA	Anticancer Drugs 2020 Nov 31, 1038-1045 doi:10.1097/cad.0000000000000960 PMID:32868648
2906	LncRNA	GSEC	miR-588	EIF5A2	MG63,143B, U2OS, U2R	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32868080	LncRNA GSEC promotes the proliferation, migration and invasion by sponging miR-588/ EIF5A2 axis in osteosarcoma	We found that the expression of LncRNA GSEC was up-regulated in osteosarcoma cell lines. Overexpression of LncRNA GSEC promoted the proliferating and migratory capacity, and inhibited the apoptosis of osteosarcoma cells. Conversely, knockdown of LncRNA GSEC resulted in the opposite effect. Mechanistically, we identified LncRNA GSEC functioned as the sponge of miR-588, thus inhibiting the miR-588/EIF5A2 signal pathway. In addition, the expression of miR-588 was negatively correlated with LncRNA GSEC, and the effect by silencing or overexpressing LncRNA GSEC could be rescued by the introduction of miR-588 mimics or inhibitors, respectively.	NA	Biochem Biophys Res Commun 2020 Nov 5 532, 300-307 doi:10.1016/j.bbrc.2020.08.056 PMID:32868080
2907	LncRNA	CTBP1-AS2	miR-155-5p	FOXO1	HGMCs	Diabetic Nephropathy	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	32868076	LncRNA CTBP1-AS2 alleviates high glucose-induced oxidative stress, ECM accumulation, and inflammation in diabetic nephropathy via miR-155-5p/FOXO1 axis	The expression of CTBP1-AS2 was downregulated, and miR-155-5p was highly expressed in peripheral blood of DN patients and HG-treated HGMCs. Further investigation revealed that CTBP1-AS2 overexpression inhibited proliferation, oxidative stress, ECM accumulation and inflammatory response in HG-induced HGMCs. Mechanical analysis revealed that CTBP1-AS2 regulated FOXO1 expression via sponging miR-155-5p. Rescue experiments demonstrated that miR-155-5p overexpression or FOXO1 inhibition reversed the effects of CTBP1-AS2 in HG-stimulated HGMCs.	NA	Biochem Biophys Res Commun 2020 Nov 5 532, 308-314 doi:10.1016/j.bbrc.2020.08.073 PMID:32868076
2908	LncRNA	ZNF281	miR-144	ROCK1	U2OS	Osteosarcoma	Homo sapiens (human)	qRT-PCR,Western blot	32863912	LncRNA-zinc finger protein 281 downregulates rho-associated coiled-coil containing protein kinase 1 by upregulating miR-144 in osteosarcoma	In tissues from patients with OS, ZNF281 was negatively associated with rho-associated coiled-coil containing protein kinase 1 (ROCK1), but positively associated with miR-144. In the U2OS cell line, ZNF281 overexpression mediated the upregulation of miR-44 and downregulation of ROCK1. miR-144 overexpression led to the downregulation of ROCK1, but failed to affect ZNF281. Expression of ZNF281 and miR-144 resulted in decreased cell migration and invasion, while ROCK1 overexpression resulted in increased invasion and migration of OS cells. In addition, ROCK1 overexpression attenuated the effects of ZNF281 and miR-144 overexpression. Thus, ZNF281 may downregulate ROCK1 by upregulating miR-144 and inhibit cancer cell invasion and migration in OS	NA	Oncol Lett 2020 Oct 20, 79 doi:10.3892/ol.2020.11940 PMID:32863912
2909	LncRNA	DLEU1	miR-490	SP1	HHUA, KLE, Ishikawa, ECC-1	Endometrial Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	30001771	Long non-coding RNA DLEU1 contributes to the development of endometrial cancer by sponging miR-490 to regulate SP1 expression	DLEU1 could sponge miR-490 and miR-490 inhibition significantly reversed the effects of DLEU1 suppression on the malignant behaviors of Ishikawa cells. Furthermore, SP1 was verified as a target of miR-490, and SP1 knockdown could reverse the effects of miR-490 inhibition on the malignant behaviors of Ishikawa cells. Besides, suppression of DLEU1 inhibited PI3K/AKT/GSK-3β pathway, while miR-490 inhibition activated this pathway that could be neutralized by SP1 knockdown. Our findings indicate that DLEU1 contributes to EC development by sponging miR-490 to regulate SP1 expression. DLEU1/miR-490/SP1 axis may provide a new strategy for EC therapy	NA	Pharmazie 2018 Jul 1 73, 379-385 doi:10.1691/ph.2018.8352 PMID:30001771
2910	LncRNA	DLEU1	miR-381	CXCR4	Panc, Capan,Miapaca, SW1990, Bxpc, HPDE6	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	30382579	Long noncoding RNA DLEU1 aggravates pancreatic ductal adenocarcinoma carcinogenesis via the miR-381/CXCR4 axis	Our study demonstrated the oncogenic role of DLEU1 in clinical PDAC specimens and cellular experiments, showing the potential involvement of DLEU1/miR81/CXCR4 pathway. These results provide novel insight into PDAC tumorigenesis.	NA	J Cell Physiol 2019 May 234, 6746-6757 doi:10.1002/jcp.27421 PMID:30382579
2911	LncRNA	PSMG3-AS1	miR-143-3p	NA	SNU-182 ,SNU-398	Liver Cancer	Homo sapiens (human)	qRT-PCR	32801875	miR-143-3p Targets lncRNA PSMG3-AS1 to Inhibit the Proliferation of Hepatocellular Carcinoma Cells	Our preliminary bioinformatics analysis showed that miR-143-3p can target PSMG3-AS1. We, therefore, analyzed the interaction between PSMG3-AS1 and miR-143-3p in HCC. We found that PSMG3-AS1 was upregulated, while miR-143-3p was downregulated in HCC. The expression levels of PSMG3AS1 and miR-143-3p were closely and inversely correlated with each other. High expression levels of PSMG3AS1 predicted poor survival. In HCC cells, overexpression of PSMG3-AS1 led to increased proliferation rates. Overexpression of miR-143-3p played an opposite role and reversed the effect of overexpression of PSMG3AS1.	NA	Cancer Manag Res 2020  12, 6303-6309 doi:10.2147/cmar.S242179 PMID:32801875
2912	LncRNA	NEAT1	miR-146b-5p	NA	MCF10A ,BT474, MCF-7, MDA-MB-231, MDA-MB-453, SK-BR-3	Breast Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801860	Long Non-Coding RNA NEAT1 Promotes the Proliferation, Migration, and Metastasis of Human Breast-Cancer Cells by Inhibiting miR-146b-5p Expression	Expression of lncRNA NEAT1 was upregulated in BC tissues and cell lines. High expression of lncRNA NEAT1 predicted poor overall survival in BC patients. Silencing of expression of lncRNA NEAT1 inhibited epithelial-mesenchymal transition (EMT) and suppressed the proliferation, migration and invasion of BC cells. Ectopic expression of lncRNA NEAT1 induced EMT and promoted BC progression. Mechanistic investigations revealed that miR-146b-5p was a direct target of lncRNA NEAT1, and its expression was correlated negatively with expression of lncRNA NEAT1 in BC tissues.	NA	Cancer Manag Res 2020  12, 6091-6101 doi:10.2147/cmar.S252295 PMID:32801860
2913	LncRNA	AGAP2-AS1	miR-628-5p	PTN	U251, LN229,A172 ,SHG44	Glioma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801858	Long Non-Coding RNA AGAP2-AS1/miR-628-5p/PTN Axis Modulates Proliferation, Migration, Invasion, and Apoptosis of Glioma Cells	AGAP2-AS1 expression was upregulated in glioma tissues and cells. Knockdown of AGAP2-AS1 inhibited the proliferation, migration and invasion, but facilitated apoptosis in glioma cells. Moreover, AGAP2-AS1 could directly bind to miR-628-5p and its overexpression reversed the anti-tumor effect of miR-628-5p restoration on the progression of glioma cells. In addition, miR-628-5p directly targeted PTN and its inhibition abolished the inhibitory effect of PTN knockdown on the progression of glioma cells. Furthermore, AGAP2-AS1 functioned as a competing endogenous RNA (ceRNA) by sponging miR-628-5p to modulate PTN expression. Besides, AGAP2-AS1 depletion reduced tumor growth by upregulating miR-628-5p and downregulating PTN.	NA	Cancer Manag Res 2020  12, 6059-6068 doi:10.2147/cmar.S250890 PMID:32801858
2914	LncRNA	HCG18	miR-152-3p	DNAJB12	MKN45, AGS, SCH, SNU638,GES-1	Gastric Cancer	Homo sapiens (human)	qRT-PCR, Luciferase reporter assay ,Western Blot	32801777	HNF1A-Induced lncRNA HCG18 Facilitates Gastric Cancer Progression by Upregulating DNAJB12 via miR-152-3p	It was found that HCG18 was upregulated in GC tissues and cell lines, and knockdown of HCG18 inhibited the proliferation, migration, and invasion of GC cells. Patients with high HCG18 expression had a shorter overall survival time compared with those with low HCG18 expression. In addition, transcription factor HNF1A could bind to the HCG18 promoter to facilitate its transcription. The upregulation of HCG18 could abolish the inhibitory effect of miR-152-3p overexpression on GC cell progression. Furthermore, DNAJB12 was demonstrated to be a target gene of miR-152-3p in GC cells, and HCG18 enhanced DNAJB12 expression by competitively binding with miR-152-3p. Finally, rescue assays proved that overexpression of DNAJB12 partially restored HCG18 knockdown-attenuated progression of GC cells.	NA	Onco Targets Ther 2020  13, 7641-7652 doi:10.2147/ott.S253391 PMID:32801777
2915	LncRNA	UCA1	miR-23b-3p	ZNF281	SW480,SW620	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801774	lncRNA UCA1 Contributes to 5-Fluorouracil Resistance of Colorectal Cancer Cells Through miR-23b-3p/ZNF281 Axis	The 5-FU resistance of CRC was positively related to the level of UCA1 and autophagy. UCA1 accelerated the 5-FU resistance of CRC cells through facilitating autophagy and suppressing apoptosis. MiR-23b-3p was a target of UCA1 in 293T and CRC cells. The knockdown of miR-23b-3p reversed the inhibitory effects of UCA1 interference on the 5-FU resistance and autophagy and the promoting impact on the apoptosis of CRC cells. ZNF281 could bind to miR-23b-3p in 293T cells. MiR-23b-3p elevated the 5-FU sensitivity through down-regulating ZNF281 in CRC cells. UCA1 interference enhanced the 5-FU sensitivity of CRC through miR-23b-3p/ZNF281 axis in vivo.	NA	Onco Targets Ther 2020  13, 7571-7583 doi:10.2147/ott.S258727 PMID:32801774
2916	LncRNA	STAT3	miR-1299	EGFR	BEAS-2B,H1299, A549, H358,H1975	Lung Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot	32801771	MiR-1299 Impedes the Progression of Non-Small-Cell Lung Cancer Through EGFR/PI3K/AKT Signaling Pathway	We found that the miR-1299 expression negatively corresponded with the clinical stage and overall survival in NSCLC patients. Overexpression of miR-1299 inhibited the migration, invasion, and EMT of A549 and H1975 cells. Meanwhile, we proved that miR-1299 is the sponge of EGFR. Besides, our results suggested that miR-1299 inhibits the progression of NSCLC cells through the PI3K/Akt signal pathway.	NA	Onco Targets Ther 2020  13, 7493-7502 doi:10.2147/ott.S250396 PMID:32801771
2917	LncRNA	LEMD1-AS1	miR-183-5p	TP53	human ovarian cancer cell lines	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801762	LEMD1-AS1 Suppresses Ovarian Cancer Progression Through Regulating miR-183-5p/TP53 Axis	The expression of LEMD1-AS1 was decreased in OC tissues and cell lines. Forced overexpression of LEMD1-AS1 inhibited the proliferation, migration and invasion of ovarian cancer cells and transplanted tumor growth in nude mice. We found that LEMD1-AS1 was mainly located in the cytoplasm of OC cells and contained complementary sites of miR-183-5p. Mechanistically, our results showed that LEMD1-AS1 could directly interact with miR-183-5p and tumor protein p53 (TP53). The anti-tumor role of LEMD1-AS1 on OC progression depended on miR-183-5p-mediated TP53 expression.	NA	Onco Targets Ther 2020  13, 7387-7398 doi:10.2147/ott.S250850 PMID:32801762
2918	LncRNA	ST7-AS1	miR-543	TRPM7	Ect1/E6E7, C-33A, SiHa, CaSki, HeLa,	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801754	Long Noncoding RNA ST7-AS1 Upregulates TRPM7 Expression by Sponging microRNA-543 to Promote Cervical Cancer Progression	ST7-AS1 was upregulated in cervical cancer tissues and cell lines. ST7-AS1 overexpression was correlated with a high International Federation of Gynecology and Obstetrics stage, frequent lymph node metastasis, deep cervical invasion, and short overall survival in patients with cervical cancer. ST7-AS1 inhibition hindered cervical cancer cell proliferation, migration, and invasion; ST7-AS1 downregulation resulted in marked cell apoptosis. Additionally, ST7-AS1 deficiency restricted cervical tumor growth in vivo. Mechanistically, ST7-AS1 functioned as competing endogenous RNA to increase TRPM7 expression by sponging miR-543. Intriguingly, rescue experiments revealed that miR-543 downregulation or TRPM7 overexpression abrogated the inhibitory actions of ST7-AS1 knockdown in the aggressive phenotype of cervical cancer cells.	NA	Onco Targets Ther 2020  13, 7257-7269 doi:10.2147/ott.S253868 PMID:32801754
2919	LncRNA	LINC00501	miR-129-5p	HMGB1	H1299, H460, SPC-A1, A549,  HEK293T ,16HBE	Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,RIP	32801746	LINC00501 Inhibits the Growth and Metastasis of Lung Cancer by Mediating miR-129-5p/HMGB1	LINC00501 was highly expressed in LC according to the database, and it was found that LINC00501 was upregulated in NSCLC specimens and cells, and the up-regulation indicated an unfavorable prognosis. Besides, knockdown of LINC00501 hindered the proliferation and invasion of NSCLC cells and intensified their apoptosis, and LINC00501 could be adopted as competitive endogenous RNA to regulate HMGB1 and tumorigenesis through miR-129-5p.	NA	Onco Targets Ther 2020  13, 7137-7149 doi:10.2147/ott.S254735 PMID:32801746
2920	LncRNA	DUXAP8	miR-409-3p	HK2	H1299, A549, H460 and PC-9,BEAS-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,luciferase assays	32801745	Long Non-Coding RNA DUXAP8 Facilitates Cell Viability, Migration, and Glycolysis in Non-Small-Cell Lung Cancer via Regulating HK2 and LDHA by Inhibition of miR-409-3p	DUXAP8 was highly expressed in NSCLC, while miR-409-3p was downregulated. High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients. Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis. Besides, DUXAP8 sponged miR-409-3p to promote HK2 and LDHA expression. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. Moreover, DUXAP8 downregulation markedly inhibited tumor growth in vivo.	NA	Onco Targets Ther 2020  13, 7111-7123 doi:10.2147/ott.S243542 PMID:32801745
2921	LncRNA	DUXAP9	miR-409-4p	LDHA	H1299, A549, H460 and PC-9,BEAS-3B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPT-PCR,Western blot,luciferase assays	32801746	Long Non-Coding RNA DUXAP8 Facilitates Cell Viability, Migration, and Glycolysis in Non-Small-Cell Lung Cancer via Regulating HK2 and LDHA by Inhibition of miR-409-4p	DUXAP8 was highly expressed in NSCLC, while miR-409-3p was downregulated. High expression of DUXAP8 was positively related to the grade division and negatively associated with the 5-year survival rate of NSCLC patients. Downregulated DUXAP8 significantly suppressed cell growth, metastasis and glycolysis. Besides, DUXAP8 sponged miR-409-3p to promote HK2 and LDHA expression. DUXAP8 promoted cell viability, migration and glycolysis by regulating miR-409-3p/HK2/LDHA axis. Moreover, DUXAP9 downregulation markedly inhibited tumor growth in vivo.	NA	Onco Targets Ther 2020  13, 7137-7149 doi:10.2147/ott.S254735 PMID:32801746
2922	LncRNA	TTN-AS1	miR-320a	neuropilin-1	NRP-1,RBE, HCCC9810, QBC939, CC262,  FRH0201	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32801339	LncRNA TTN-AS1 promotes the progression of cholangiocarcinoma via the miR-320a/neuropilin-1 axis	The present results demonstrate that lncRNA TTA-AS1 is a sponging ceRNA for miR-320a, which in turn downregulates neuropilin-1 in cholangiocarcinoma cells, indicating these three molecules represent potential biomarkers and therapeutic targets in the management of cholangiocarcinoma.	NA	Cell Death Dis 2020 Aug 15 11, 637 doi:10.1038/s41419-020-02896-x PMID:32801339
2923	LncRNA	GAS6-AS2	miR-3619-5p	ARL2	HuH7,MHCC97,THLE-2)	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot,Luciferase reporter assay	32799553	GAS6-AS2 Promotes Hepatocellular Carcinoma via miR-3619-5p/ARL2 Axis Under Insufficient Radiofrequency Ablation Condition	GAS6-AS2 was upregulated in Huh7-H and MHCC97-H cells relative to Huh7 and MHCC97 cells. GAS6-AS2 deficiency hampered cell proliferation, migration, invasion, epithelial-mesenchymal transition, and stemness in Huh7-H and MHCC97-H cells. Moreover, microRNA-3619-5p (miR-3619-5p) combined with GAS6-AS2 and ARL2 (ADP ribosylation factor-like GTPase 2) was the target gene of miR-3619-5p. GAS6-AS2 served as the competing endogenous RNA (ceRNA) of ARL2 via absorbing miR-3619-5p	NA	Cancer Biother Radiopharm 2020 Aug 14, 10.1089/cbr.2019.3541 doi:10.1089/cbr.2019.3541 PMID:32799553
2924	LncRNA	lncARSR	miR-34a-6p	HK2	SW480, SW620, HCT, HT9, Caco2,  RKO,NCM 460	Colorectal Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32798250	lncARSR sponges miR-34a-5p to promote colorectal cancer invasion and metastasis via hexokinase-1-mediated glycolysis	We identified lncARSR as an onco-lncRNA in CRC and demonstrated that the combination of lncARSR/miR-34a-5p/HK1 may be a potential prognostic biomarker of CRC.	NA	Cancer Sci 2020 Oct 111, 3938-3952 doi:10.1111/cas.14617 PMID:32798250
2925	LncRNA	LOC146880	miR-539-5p	ENO1	A549 , PC9,BEAS-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	32795333	A SNP-mediated lncRNA (LOC146880) and microRNA (miR-539-5p) interaction and its potential impact on the NSCLC risk	Association analysis showed that A allele of SNP rs140618127 was associated with low risk of NSCLC in the Chinese population. Lab experiments indicated that SNP rs140618127 contained a binding site for miR-539-5p and the binding between miR-539-5p and LOC146880 resulted in declined phosphorylation of an oncogene, ENO1. The reduced phosphorylation of ENO1 led to decreased phosphorylation of PI3K and Akt, which is further linked to the decline in cell proliferation and tumor progression.	NA	J Exp Clin Cancer Res 2020 Aug 14 39, 157 doi:10.1186/s13046-020-01652-5 PMID:32795333
2926	LncRNA	ZFPM2-AS1	miR-139	GDF10	Huh7 and HCCLM3 liver cancer cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase activity assay,Western blot,RIP	32795316	Long noncoding RNA ZFPM2-AS1 acts as a miRNA sponge and promotes cell invasion through regulation of miR-139/GDF10 in hepatocellular carcinoma	The expression level of lncRNA ZFPM2-AS1 was significantly higher in HCC tissues than in adjacent normal tissues, and higher ZFPM2-AS1 was remarkably related to poor survival. Functionally, silencing of lncRNA ZFPM2-AS1 inhibited cell proliferation, migration, invasion and promoted cell apoptosis in vitro. Bioinformatics analysis based on the miRcode and TargetScan databases showed that lncRNA ZFPM2-AS1 regulated GDF10 expression by competitively binding to miR-139. miR-139 and downregulated GDF10 reversed cell phenotypes caused by lncRNA ZFPM2-AS1 by rescue analysis.	NA	J Exp Clin Cancer Res 2020 Aug 14 39, 159 doi:10.1186/s13046-020-01664-1 PMID:32795316
2927	LncRNA	LINC02418	miR-4677-3p	KNL1	A549, SPC-A1, H1299 and PC-9,BEAS-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR,Luciferase activity assay,Western blot,RIP	32795273	LINC02418 promotes malignant behaviors in lung adenocarcinoma cells by sponging miR-4677-3p to upregulate KNL1 expression	High expression of LINC02418 was observed in LAD specimens and cells. Downregulation of LINC02418 obstructed the proliferation and motility of LAD cells. Moreover, LINC02418 negatively modulated miR-4677-3p expression and miR-4677-3p overexpression could repress cell proliferation and migration. Moreover, kinetochore scaffold 1 (KNL1) expression was negatively modulated by miR-4677-3p but positively regulated by LINC02418. Furthermore, miR-4677-3p could bind with LINC02418 (or KNL1). Finally, KNL1 overexpression reversed the inhibitory function of LINC02418 deficiency in the malignant behaviors of LAD cells.	NA	BMC Pulm Med 2020 Aug 14 20, 217 doi:10.1186/s12890-020-01229-0 PMID:32795273
2928	LncRNA	HCG11	miR-942-5p	GFI1	HeLa, C33A, SiHa, and Caski,Ect1/E6E7	Cervical Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32794340	Long noncoding RNA HCG11 inhibited growth and invasion in cervical cancer by sponging miR-942-5p and targeting GFI1	Our study aimed to explore the underlying mechanism of lncRNA human leukocyte antigen complex group 11 (HCG11) in cervical cancer (CC) progression. Long noncoding RNA HCG11 was downregulated in CC. Functional assays demonstrated that lncRNA HCG11 inhibited CC cell proliferation and invasion. Then, we confirmed that lncRNA HCG11 could directly bind to miR-942-5p. Moreover, inhibition of miR-942-5p suppressed the growth and invasion of CC cells, and growth factor-independent transcription repressor 1 (GFI1) gene was the target gene of miR-942-5p. Long noncoding RNA HCG11 increased the expression of GFI1 and suppressed cell proliferation and invasion by acting as a miR-942-5p sponge. Finally, the overexpression of lncRNA HCG11 suppressed the proliferation and metastasis of CC cells in vivo.	NA	Cancer Med 2020 Oct 9, 7062-7071 doi:10.1002/cam4.3203 PMID:32794340
2929	LncRNA	MEG3	Let-7i	SOST	Peripheral blood of AS patients	Ankylosis Spondylitis	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32793634	lncRNA MEG3 Suppresses the Progression of Ankylosis Spondylitis by Regulating the Let-7i/SOST Axis	The expression levels of MEG3 and SOST were decreased and let-7i was increased in AS patients. MEG3 could interact with let-7i in AS fibroblasts, and let-7i overexpression reversed the suppressive effect of MEG3 upregulation on the inflammation and bone formation of AS. Additionally, let-7i could target SOST, and SOST silencing reversed the inhibitory effect of let-7i inhibitor or MEG3 overexpression on the inflammation and bone formation of AS. Furthermore, SOST expression was positively regulated by MEG3, while was negatively regulated by let-7i. Our results revealed that lncRNA MEG3 promoted SOST expression to restrain the progression of AS by sponging let-7i, which provided a treatment target for AS.	NA	Front Mol Biosci 2020  7, 173 doi:10.3389/fmolb.2020.00173 PMID:32793634
2930	LncRNA	LINC01133	miR-216a-5p	TPT1	SW1990, PANC1, Capan-2 and BxPC-3,HPDE6	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,FISH	32792860	MiR-216a-5p inhibits tumorigenesis in Pancreatic Cancer by targeting TPT1/mTORC1 and is mediated by LINC01133	Our study revealed an important role of LINC01133/miR-216a-5p/TPT1 axis in the genesis and progression of PCs, which provides potential biomarkers for clinical diagnosis and therapy of PCs	NA	Int J Biol Sci 2020  16, 2612-2627 doi:10.7150/ijbs.46822 PMID:32792860
2931	LncRNA	LINC01134	miR-216a-6p	mTORC1	SW1990, PANC1, Capan-2 and BxPC-3,HPDE7	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase reporter assay,FISH	32792861	MiR-216a-5p inhibits tumorigenesis in Pancreatic Cancer by targeting TPT1/mTORC1 and is mediated by LINC01134	Our study revealed an important role of LINC01133/miR-216a-5p/TPT2 axis in the genesis and progression of PCs, which provides potential biomarkers for clinical diagnosis and therapy of PCs	NA	Int J Biol Sci 2020  16, 2628-2647 doi:10.7150/ijbs.47203 PMID:32792861
2932	LncRNA	PADNA	miR-194	FBXW7	HEK293	NA	Mus musculus (mouse)	qPCR,Luciferase activity assay,Western blot etc.	32791990	Knockdown of lincRNA PADNA promotes bupivacaine-induced neurotoxicity by miR-194/FBXW7 axis	The expression of lincRNA PADNA was significantly increased with increasing concentrations of bupivacaine. Functional analysis revealed that knockdown of lincRNA PADNA increased caspase3 activity and inhibited cell viability. Western blot analysis showed that knockdown of lincRNA PADNA promoted cleaved caspase3 levels. We also revealed that lincRNA PADNA may bind with miR-194. Knockdown of miR-194 rescued the function of lincRNA PADNA, suggesting that lincRNA PADNA may sponge miR-194. In addition, we provided new evidence that the lincRNA PADNA/miR-194/FBXW7 axis plays an important role in the neurotoxicity process.	NA	Mol Med 2020 Aug 13 26, 79 doi:10.1186/s10020-020-00209-8 PMID:32791990
2933	LncRNA	PCGEM1	miR-433-3p	WTAP	BEAS-2B,A549, NCI-H1299, NCI-H1650	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR,luciferase assay	32787827	LncRNA PCGEM1 accelerates non-small cell lung cancer progression via sponging miR-433-3p to upregulate WTAP	PCGEM1 was highly expressed in NSCLC cells, while miR-433-3p was lowly expressed in NSCLC cells. PCGEM1 silencing or miR-433-3p overexpression inhibited cell proliferation, migration and invasion but accelerated cell apoptosis. MiR-433-3p was proven be sponged by PCGEM1. Besides, WTAP was the target of miR-433-3p and it accelerated the progression of NSCLC. In the end, rescue experiments indicated that overexpression of WTAP or knockdown of miR-433-3p reversed the inhibited roles of silencing PCGEM1 on cell behavior.	NA	BMC Pulm Med 2020 Aug 12 20, 213 doi:10.1186/s12890-020-01240-5 PMID:32787827
2934	LncRNA	CASC2	miR-31-5p	KANK1	NOK-SI,CAL-27 and SCC9	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32787433	Long non-coding RNA CASC2 enhances cisplatin sensitivity in oral squamous cell cancer cells by the miR-31-5p/KANK1 axis	CASC2 boosted the DDP sensitivity and apoptosis of DDP-resistant OSCC cells by upregulating KANK1 via sponging miR-31-5p, and CASC2 might be a potential target for DDP-resistant OSCC treatment.	NA	Neoplasma 2020 Nov 67, 1279-1292 doi:10.4149/neo_2020_191029N1102 PMID:32787433
2935	LncRNA	LEF1-AS1	miR-10a-5p	MSI1	Huh7, HepG2,  PLC,HL702	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32786108	Long noncoding RNA LEF1-AS1 acts as a microRNA-10a-5p regulator to enhance MSI1 expression and promote chemoresistance in hepatocellular carcinoma cells through activating AKT signaling pathway	Our results unraveled LEF1-AS1 acts as a miR-10a-5p modulator to promote chemoresistance of HCC cells by stimulating MSI1 and activating the AKT signaling pathway, which might provide a novel therapeutic target for HCC.	NA	J Cell Biochem 2021 Jan 122, 86-99 doi:10.1002/jcb.29833 PMID:32786108
2936	LncRNA	NR2F1-AS1	miR-493-5p	ITGB1	BEAS-2B,H522, H460, and H1299	Lung Cancer	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase assays,RIP	32784268	Long noncoding RNA NR2F1-AS1 promotes the malignancy of non-small cell lung cancer via sponging microRNA-493-5p and thereby increasing ITGB1 expression	the NR2F1-AS1/miR-493-5p/ITGB1 pathway initiates pro-oncogenic behavior in NSCLC tumor progression, and the NR2F1-AS1/miR-493-5p/ITGB1 axis may provide new molecular targets for anticancer therapy against NSCLC.	NA	Aging (Albany NY) 2020 Aug 7 13, 7660-7675 doi:10.18632/aging.103564 PMID:32784268
2937	LncRNA	LNC473	miR-574	APAF1	HCT116, SW480, RKO, Caco-2, LOVO, HT29	Colorectal Cancer	Homo sapiens (human)	RT-PCR,qPCR,Luciferase reporter assay,Western blot,RIP	32784109	LNC473 Regulating APAF1 IRES-Dependent Translation via Competitive Sponging miR574 and miR15b: Implications in Colorectal Cancer	Our results uncover a novel LNC473-miR574/miR15b-APAF1 signaling axis, which provides new targets and crosstalk regulation mechanism for CRC prevention and treatment.	NA	Mol Ther Nucleic Acids 2020 Sep 4 21, 764-779 doi:10.1016/j.omtn.2020.07.009 PMID:32784109
2938	LncRNA	LNC474	miR-15b	APAF2	HCT116, SW480, RKO, Caco-2, LOVO, HT30	Colorectal Cancer	Homo sapiens (human)	RT-PCR,qPCR,Luciferase reporter assay,Western blot,RIP	32784110	LNC473 Regulating APAF1 IRES-Dependent Translation via Competitive Sponging miR574 and miR16b: Implications in Colorectal Cancer	Our results uncover a novel LNC473-miR574/miR15b-APAF2 signaling axis, which provides new targets and crosstalk regulation mechanism for CRC prevention and treatment.	NA	Cardiovasc Pathol 2020 Nov-Dec 49, 107263 doi:10.1016/j.carpath.2020.107263 PMID:32784110
2939	LncRNA	TPT1-AS1	miR-23a-5p	ECM1	U87	Glioblastoma	Homo sapiens (human)	qRT-PCR,Western blot,Luciferase assays	32783743	LncRNA TPT1-AS1 Sponges miR-23a-5p in Glioblastoma to Promote Cancer Cell Proliferation	The authors found miR-23a-5p was downregulated in GBM and TPT1-AS1 was upregulated in GBM, whereas the expression of these two was not significantly correlated. In GBM cells, overexpression of TPT1-AS1 did not affect the expression of miR-23a-5p, but upregulated ECM1. In cell proliferation assay, overexpression of TPT1-AS1 and ECM1 resulted in increased proliferation rate of GBM cells. Overexpression of miR-23a-5p attenuated the effects of overexpressing TPT1-AS1.	NA	Cancer Biother Radiopharm 2020 Aug 12, 10.1089/cbr.2019.3484 doi:10.1089/cbr.2019.3484 PMID:32783743
2940	LncRNA	HOTTIP	miR-615-3p	SMARCE1	SOV3, OVCAR3, A2780,HcerEpic	Ovarian Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay	32783402	Long noncoding RNA HOTTIP promotes the metastatic potential of ovarian cancer through the regulation of the miR-615-3p/SMARCE1 pathway	HOTTIP and miR-615-3p expression levels in ovarian cancer cells were negatively correlated, whereas HOTTIP and SMARCE1 expression levels were positively correlated. In nude mice, downregulation of HOTTIP reduced cell growth in vivo. In summary, lncRNA HOTTIP promotes the growth and metastatic phenotypes of ovarian cancer via regulating miR-615-3p/SMARCE1 pathway.	NA	Kaohsiung J Med Sci 2020 Dec 36, 973-982 doi:10.1002/kjm2.12282 PMID:32783402
2941	LncRNA	SNHG6	miR-186	NA	PC-3 and DU145	Prostate Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP	32782439	Long non-coding RNA SNHG6 regulates the sensitivity of prostate cancer cells to paclitaxel by sponging miR-186	SNHG6 expression was increased and miR-186 expression was reduced in drug-resistant PCa tissues and cells. SNHG6 knockdown elevated PTX-resistant PCa cells sensitivity to PTX in vitro and in vivo, and repressed proliferation, migration, and invasion of PTX-resistant PCa cells in vitro. Importantly, SNHG6 acted as a sponge of miR-186. Furthermore, miR-186 downregulation reversed SNHG6 silencing-mediated cell sensitivity to PTX, proliferation, migration, and invasion in PTX-resistant PCa cells.	NA	Cancer Cell Int 2020  20, 381 doi:10.1186/s12935-020-01462-x PMID:32782439
2942	LncRNA	LINC00992	miR-3935	GOLM1	RWPE-1, CRL-11609 , PC3 (CRL-1435), LNCaP (CRL-1740), C4–2 (CRL-3314),  DU145 (HTB-81),	Prostate Cancer	Homo sapiens (human)	qRT-PCR,Luciferase reporter assay,Western blot,RIP,FISH	32781986	LINC00992 contributes to the oncogenic phenotypes in prostate cancer via targeting miR-3935 and augmenting GOLM1 expression	Elevated levels of LINC00992 and GOLM1 were detected in prostate cancer tissues and cells. LINC00992 exerted facilitating functions in prostate cancer cell proliferation and migration. Mechanically, LINC00992 interacted with and negatively regulated miR-3935 to elevate GOLM1 expression in prostate cancer cells. In addition, the in vitro suppressive effect of silenced LINC00992 on prostate cancer cell proliferation and migration was reversed by GOLM1 upregulation. Likewise, LINC00992 depletion restrained tumor growth in vivo was offset by enhanced GOLM1 expression.	NA	BMC Cancer 2020 Aug 11 20, 749 doi:10.1186/s12885-020-07141-4 PMID:32781986
2943	LncRNA	Hoxaas3	miR-450b-5p	Runx1	cultured mouse lung fibroblasts	Idiopathic Pulmonary Fibrosis	Homo sapiens (human)	Western blot;qRT-PCR	32848140	LncRNA Hoxaas3 promotes lung fibroblast activation and fibrosis by targeting miR-450b-5p to regulate Runx1.	Overexpression of Hoxaas3 promoted fibrogenesis, whereas Hoxaas3 inhibition attenuated lung fibrosis both in vitro and in vivo, through regulation of miR-450b-5p. Furthermore, miR-450b-5p inhibition stimulated fibrogenesis by regulating runt-related transcription factor 1 (Runx1), whereas up-regulation of miR-450b-5p alleviated fibrogenesis in LF.	MIMAT0004909	Cell Death Dis 2020 Aug 26 11, 706 doi:10.1038/s41419-020-02889-w PMID:32848140
2944	Circular RNA	hsa_circ_0002577	miR-625-5p	IGF1R	HEC-1-B, AN3-CA, KLE, HEC1-A, and Ishikawa	Endometrial Cancer	Homo sapiens (human)	Western blot;qRT-PCR	32847606	CircRNA hsa_circ_0002577 accelerates endometrial cancer progression through activating IGF1R/PI3K/Akt pathway.	EC patients with higher expression of hsa_circ_0002577 showed poorer overall survival and more advanced tumor stage. EC cells transfected with Lv-circRNA showed promoted proliferation, migration, and invasion, whereas the delivery of sh-circRNA exerted an opposite effect. Further analyses showed that hsa_circ_0002577 acted as a miR-625-5p sponge in EC cells. IGF1R was a potential downstream target of miR-625-5p. The expression of IGF1R in EC tissues was significantly higher than that in matched controls. Hsa_circ_0002577 accelerated EC development by inducing IGF1R expression and activating PI3K/Akt signaling pathway.	MIMAT0003294	J Exp Clin Cancer Res 2020 Aug 26 39, 169 doi:10.1186/s13046-020-01679-8 PMID:32847606
2945	LncRNA	NEAT1	miR-140-3p	MAPK1	Human coronary endothelial cells (HCAECs) and human umbilical vein endothelial cells (HUVECs)	Atherosclerosis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	32844995	NEAT1/miR-140-3p/MAPK1 mediates the viability and survival of coronary endothelial cells and affects coronary atherosclerotic heart disease.	Transfection of pcNEAT1 significantly inhibited the survival rate of HCAECs and induced apoptosis of HCAECs. MiR-140-3p was down-regulated in HCAECs. NEAT1 directly targeted miR-140-3p, and the expression of miR-140-3p was inversely correlated with the expression of NEAT1 in CAD patients. In addition, co-transfection of NEAT1 with miR-140-3p mimic reversed the effect of pcNEAT1 on cell viability and apoptosis. mitogen-activated protein kinase 1 (MAPK1) was proved to be a target gene of miR-140-3p, and the miR-140-3p mimic was shown to reduce the expression of MAPK1 in HCAECs.	MIMAT0000427	Acta Biochim Biophys Sin (Shanghai) 2020 Sep 8 52, 967-974 doi:10.1093/abbs/gmaa087 PMID:32844995
2946	LncRNA	lnc-NOS2P3	miR-939-5p	iNOS	HUVECs, ATCC CRL730	Chronic Heart Failure	Homo sapiens (human)	Western blot;qRT-PCR	32844595	Differentially expressed lnc-NOS2P3-miR-939-5p axis in chronic heart failure inhibits myocardial and endothelial cells apoptosis via iNOS/TNFα pathway.	This study found CHF patients had elevated serum miR-939-5p, with greater increase in New York Heart Association (NYHA) I-II patients than in NYHA III-IV. Moreover, miR-939-5p was positively correlated with B-type natriuretic peptide (BNP) in NYHA III-IV patients, while not in NYHA I-II. Further study showed miR-939-5p mimics promoted cell proliferation and inhibited inflammatory cytokine-induced apoptosis of HUVECs and H9C2, while inhibition of endogenous miR-939-5p produced the opposite effects. Induced nitric oxide synthase (iNOS) and tumour necrosis factor α (TNFα) were identified as target genes of miR-939-5p.	MIMAT0004982	J Cell Mol Med 2020 Oct 24, 11381-11396 doi:10.1111/jcmm.15740 PMID:32844595
2947	LncRNA	lnc-NOS2P3	miR-939-5p	TNFa	HUVECs, ATCC CRL730	Chronic Heart Failure	Homo sapiens (human)	Western blot;qRT-PCR	32844595	Differentially expressed lnc-NOS2P3-miR-939-5p axis in chronic heart failure inhibits myocardial and endothelial cells apoptosis via iNOS/TNFα pathway.	This study found CHF patients had elevated serum miR-939-5p, with greater increase in New York Heart Association (NYHA) I-II patients than in NYHA III-IV. Moreover, miR-939-5p was positively correlated with B-type natriuretic peptide (BNP) in NYHA III-IV patients, while not in NYHA I-II. Further study showed miR-939-5p mimics promoted cell proliferation and inhibited inflammatory cytokine-induced apoptosis of HUVECs and H9C2, while inhibition of endogenous miR-939-5p produced the opposite effects. Induced nitric oxide synthase (iNOS) and tumour necrosis factor α (TNFα) were identified as target genes of miR-939-6p.	MIMAT0004982	J Cell Mol Med 2020 Oct 24, 11381-11396 doi:10.1111/jcmm.15740 PMID:32844595
2948	LncRNA	HCG11	miR-522-3p	SOCS5	NSCLC	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	32844573	Long non-coding RNA HCG11 sponging miR-522-3p inhibits the tumorigenesis of non-small cell lung cancer by upregulating SOCS5.	Downregulation of lncRNA HCG11 and upregulation of miR-522-3p were found in NSCLC tissues and cells, and abnormal expressions of lncRNA HCG11 and miR-522-3p were related to adverse clinical outcomes of NSCLC patients. LncRNA HCG11 acted as a molecular sponge for miR-522-3p. Functionally, lncRNA HCG11 inhibited cell viability, migration and invasion in NSCLC by downregulating miR-522-3p. Further, miR-522-3p directly targeted SOCS5. lncRNA HCG11 could positively regulate SOCS5 expression in NSCLC. In addition, HCG11 downregulation or miR-522-3p overexpression abolished the inhibitory effect of SOCS5 on cell viability, migration and invasion in NSCLC.	MIMAT0002868	Thorac Cancer 2020 Oct 11, 2877-2886 doi:10.1111/1759-7714.13624 PMID:32844573
2949	LncRNA	GABPB1-AS1	miR-519e-5p	Notch2	C33A, SiHa, and CaSki	Cervical Cancer	Homo sapiens (human)	Western blot;qRT-PCR	32844486	HPV16 E6 oncoprotein-induced upregulation of lncRNA GABPB1-AS1 facilitates cervical cancer progression by regulating miR-519e-5p/Notch2 axis.	Mechanistically, GABPB1-AS1 acted as a competing endogenous RNA (ceRNA) by sponging miR-519e-5p, resulting in the de-repression of its target gene Notch2 which is well known as an oncogene. Therefore, GABPB1-AS1 functioned as a tumor activator in CC pathogenesis by binding to miR-519e-5p and destroying its tumor suppressive function.	MIMAT0002828	Faseb j 2020 Oct 34, 13211-13223 doi:10.1096/fj.202000762R PMID:32844486
2950	LncRNA	PICSAR	miR-125b	YAP1	SCL-1 and SCC13;HaCaT	Cutaneous Squamous Cell Carcinoma	Homo sapiens (human)	qPCR;luciferase reporter assays;Western blot	32841663	Long non-coding RNA PICSAR knockdown inhibits the progression of cutaneous squamous cell carcinoma by regulating miR-125b/YAP1 axis.	Moreover, miR-125b could directly bind to PICSAR and its inhibition reversed the effect of PICSAR knockdown on proliferation, invasion and apoptosis in CSCC cells. In addition, YAP1 was a direct target of PICSAR and its overexpression attenuated the anti-cancer role of miR-125b in CSCC cells.	MIMAT0004592	Life Sci 2021 Jun 1 274, 118303 doi:10.1016/j.lfs.2020.118303 PMID:32841663
2951	LncRNA	MEG3	miR-223	TP53INP1	SRA01/ 04	Age-Related Cataract	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32841649	Long non-coding RNA MEG3 promotes cataractogenesis by upregulating TP53INP1 expression in age-related cataract.	Knockdown of MEG3 increased the viability and inhibited the apoptosis of LECs upon the oxidative stress induced by H2O2. MEG3 was localized in both nucleus and cytoplasm in LECs. MEG3 facilitated TP53INP1 expression via acting as miR-223 sponge and promoting P53 expression. Additionally, TP53INP1 knockdown alleviated H2O2-induced lens turbidity. In summary, MEG3 promoted ARC progression by up-regulating TP53INP1 expression through suppressing miR-223 and promoting P53 expression, which would provide a novel insight into the pathogenesis of ARC.	MIMAT0000280	Exp Eye Res 2020 Oct 199, 108185 doi:10.1016/j.exer.2020.108185 PMID:32841649
2952	LncRNA	TP73-AS1	miR-216a-5p	CUL4B	A549, H1299, HCC827 and Calu	Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32841514	Long non-coding RNA TP73-AS1 facilitates progression and radioresistance in lung cancer cells by the miR-216a-5p/CUL4B axis with exosome involvement.	TP73-AS1 silence inhibits migration and invasion while elevates apoptosis and radiosensitivity in lung cancer cells TP73-AS1 targets miR-216a-5p and miR-216a-5p targets CUL4B WHAT THIS STUDY ADDS: Downregulation of TP73-AS1 reduces tumor growth and radioresistance in vivo via the miR-216a-5p/CUL4B axis Exosomes from si-TP73-AS1-transfected cells inhibits lung cancer progression and radioresistance.	MIMAT0000273	Thorac Cancer 2021 Feb 12, 409 doi:10.1111/1759-7714.13602 PMID:32841514
2953	LncRNA	LINC00210	miR-342-3p	GFRA1	SOSP607 and UOS	Osteosarcoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32841458	LncRNA LINC00210 regulated radiosensitivity of osteosarcoma cells via miR-342-3p/GFRA1 axis.	LINC00210 and GFRA1 were up-regulated, and miR-342-3p was down-regulated in osteosarcoma tissues and cells. The expression of LINC00210 in osteosarcoma was negatively related to miR-342-3p expression and positively associated with GFRA1. Besides, there was a negative correlation between LINC00210 and GFRA1 expression in osteosarcoma. Also, LINC00210 and GFRA1 were up-regulated, and miR-342-3p was down-regulated in osteosarcoma cells exposed to 4 Gy irradiation treatment. Furthermore, either LINC00210 knockdown or miR-342-3p overexpression enhanced the radiosensitivity of osteosarcoma cells.	MIMAT0000753	J Clin Lab Anal 2020 Dec 34, e23540 doi:10.1002/jcla.23540 PMID:32841458
2954	LncRNA	ZFAS1	miR-590-3p	Cdc42	A549 and HCC827	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32841053	Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p.	Rescue experiments showed that miR-590-3p inhibitor reversed the cell proliferation function of lncRNA ZFAS1 knockdown in vitro. Furthermore, we confirmed that lncRNA ZFAS1 inhibited cell division cycle 42 (Cdc42) expression by regulating of miR-590-3p in NSCLC cells. Therefore, our study indicates that lncRNA ZFAS1/miR-590-3p axis is involved in NSCLC cell proliferation.	MIMAT0004801	Cell Transplant 2020 Jan-Dec 29, 963689720919435 doi:10.1177/0963689720919435 PMID:32841053
2955	LncRNA	SNHG6	miR-181	JAK2	HT29, HCT8, SW480 and HCT116 as well as FHC cell line	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32840014	Long non-coding RNA SNHG6 increases JAK2 expression by targeting miR-181 family to promote colorectal cancer cell proliferation.	Moreover, over-expressed SNHG6 significantly counteracted the inhibitory effect of miR-181 mimics on CRC cell proliferation as well as the promoting effect on apoptosis. Furthermore, SNHG6 over-expression and knock-down can promote and inhibit JAK2 expression, respectively, and miR-181 family members' function is opposite to SNHG6 by repressing JAK2.	MI0000289	J Gene Med 2020 Dec 22, e3262 doi:10.1002/jgm.3262 PMID:32840014
2956	LncRNA	WEE2-AS1	miR-520f-3p	SP1	A normal human astrocyte (NHA) cell line;T98 and U138	Glioblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32838835	Long noncoding RNA WEE2-AS1 plays an oncogenic role in glioblastoma by functioning as a molecular sponge for microRNA-520f-3p.	Mechanistically, WEE2-AS1 functionedas a molecular sponge for microRNA-520f-3p (miR-520f-3p) and consequentlyincreased specificity protein 1 (SP1) expression in GBM cells. A series of recoveryexperiments revealed that the inhibition of miR-520f-3p and upregulation of SP1 couldpartially abrogate the influences of WEE2-AS1 downregulation on GBM cells. Inconclusion, WEE2-AS1 can adsorb miR-520f-3p to increase endogenous SP1expression, thereby facilitating the malignancy of GBM.	MIMAT0002830	Oncol Res 2021 Mar 16 28, 591-603 doi:10.3727/096504020x15982623243955 PMID:32838835
2957	LncRNA	UCA1	miR-204	KIF20A	SiHa, HeLa, ME180, C33a, CaSki, and Ect1/E6E7	Cervical Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32835591	Long non-coding RNA UCA1 upregulates KIF20A expression to promote cell proliferation and invasion via sponging miR-204 in cervical cancer.	In addition, we found that lncRNA UCA1 could sponge miR-204 and promote the proliferation and invasion of cervical cancer cells via the up-regulating of KIF20A expression. As a result, the inhibiting of UCA1 could lower cervical cancer (CC) cells growth rate in vivo.Our results identified that UCA1 could serve as an oncogene in cervical cancer cell progression through the modulating of miR-204/KIF20A axis.	MI0000284	Cell Cycle 2020 Oct 19, 2486-2495 doi:10.1080/15384101.2020.1807666 PMID:32835591
2958	LncRNA	LncUBE2R2-AS1	miR-302b	EGFR	THLE-3 and Huh7, HepG2, MHCC-97H, and Hep3B	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32835579	LncUBE2R2-AS1 acts as a microRNA sponge of miR-302b to promote HCC progression via activation EGFR-PI3K-AKT signaling pathway.	Functional experiments showed that knockdown UBE2R2-AS1 inhibited HCC growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, UBE2R2-AS1/miR-302b/EGFR established the ceRNA network involved in the modulation of cell progression of HCC cells via activation of PI3K-AKT signaling pathway. Overall, UBE2R2-AS1 may exhibit an oncogenic function in HCC via acting as a sponge for miR-302b to up-regulate EGFR, and may serve as a potential therapeutic target and a prognostic biomarker for HCC patients.	MI0000772	Cell Cycle 2020 Oct 19, 2426-2435 doi:10.1080/15384101.2020.1795991 PMID:32835579
2959	LncRNA	MIAT	miR-490-3p	ICAM1	HA-VSMCs and HUVECs	Atherosclerosis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32833904	MIAT knockdown inhibits cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced vascular smooth muscle cells.	MIAT acted as a sponge of miR-490-3p and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration and invasion. ICAM1 was a direct target of miR-490-3p and ICAM1 silencing repressed the proliferation, migration and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration and invasion. MIAT knockdown could depress cell proliferation, migration and invasion via miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.	MIMAT0002806	Journal of Cardiovascular Pharmacology 2020 08/19 Publish Ahead of Print doi:10.1097/FJC.0000000000000901
2960	LncRNA	ZFAS1	miR-761	CDIP1	HL-1 cells	Acute Myocardial Infarction	Homo sapiens (human)	Western blot;qRT-PCR	32833901	Silencing of lncRNA ZFAS1 protects against hypoxia/reoxygenation-induced injury in HL-1 cells through targeting the miR-761/CDIP1 axis.	Furthermore, ZFAS1 regulated CDIP1 expression through acting as a miR-761 sponge. Additionally, CDIP1 silencing protected HL-1 cell from H/R-induced injury. Our current work suggested that the knockdown of ZFAS1 protected against H/R-induced injury in HL-1 cells at least partly through the regulation of miR-761/CDIP1 axis, illuminating a novel therapeutic avenue for AMI management.	MIMAT0010364	J Cardiovasc Pharmacol 2020 Nov 76, 564-573 doi:10.1097/fjc.0000000000000896 PMID:32833901
2961	LncRNA	TUG1	miR-532-5p	Sox8	H9c2 cells	Cardiac Ischemia Reperfusion Injury	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32833900	LncRNA TUG1 knockdown protects cardiomyocytes against hypoxia/reoxygenation-induced injury via regulating miR-532-5p/Sox8 axis.	UG1 directly bound to miR-532-5p, and miR-532-5p inhibition reversed the action of TUG1 knockdown on H/R-induced cardiomyocyte injury. Sox8 was a target of miR-532-5p, and miR-532-5p blunted H/R-induced cardiomyocyte injury by targeting Sox8. Additionally, TUG1 knockdown inhibited H/R-induced Sox8 elevation via miR-532-5p in H9c2 cells. TUG1 silence ameliorated H/R-induced cardiomyocytes injury via regulating miR-532-5p/Sox8 axis, suggesting a potential therapeutic target for preventing myocardial ischaemia/reperfusion injury.	MIMAT0002888	J Cardiovasc Pharmacol 2020 Nov 76, 556-563 doi:10.1097/fjc.0000000000000895 PMID:32833900
2962	LncRNA	NEAT1	miR-138-5p	ZFX	SUM-185, MCF-7, and T47D;MCF-10A	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32833504	Long Noncoding RNA NEAT1 Promotes the Progression of Breast Cancer by Regulating miR-138-5p/ZFX Axis.	NEAT1 was highly expressed and miR-138-5p was lowly expressed in BC tissues and cells. NEAT1 interference or miR-138-5p restoration repressed cell proliferation, migration, and invasion but accelerated apoptosis in BC cells. Moreover, miR-138-5p directly interacted with NEAT1 and its knockdown reversed the suppressive impact of NEAT1 downregulation on the progression of BC cells. In addition, ZFX was a downstream target of miR-138-5p and its upregulation attenuated the antitumor role of miR-138-5p in BC cells.	MIMAT0000430	Cancer Biother Radiopharm 2020 Aug 21, 10.1089/cbr.2019.3515 doi:10.1089/cbr.2019.3515 PMID:32833504
2963	LncRNA	LINC01541	miR-506-5p	WIF1	ESCs	Endometriosis	Homo sapiens (human)	Western blot;qRT-PCR	32833189	LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis.	Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression.	MIMAT0022701	Reprod Sci 2021 Mar 28, 665-674 doi:10.1007/s43032-020-00295-3 PMID:32833189
2964	LncRNA	RPPH1	miR-326	WNT2B	BEAS-2B normal lung epithelial cell line, as well as H358, A549, H1299 and H1650 NSCLC cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32831924	lncRNA RPPH1 promotes non-small cell lung cancer progression through the miR-326/WNT2B axis.	Moreover, the potential interactions between RPPH1, microRNA (miR)-326 and Wnt family member 2B (WNT2B) were investigated using luciferase reporter assays and co-transfection experiments. MiR-326 expression was directly inhibited by RPPH1. In A549 cells co-transfected with shRPPH1 and miR-326 inhibitor, the invading cell number significantly increased compared with cells transfected with shRPPH1 alone. In addition, E-cadherin expression levels were reduced, and vimentin was upregulated. MiR-326 overexpression partially reduced the resistance of A549 cells to CDDP induced by RPPH1 overexpression.	MI0000808	Oncol Lett 2020 Oct 20, 105 doi:10.3892/ol.2020.11966 PMID:32831924
2965	LncRNA	CCAT2	miR-217	TCF7L2	PCa PC3 and DU145 cell lines	Prostate Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32831916	Long non-coding RNA CCAT2 promotes prostate cancer cell proliferation and invasion by regulating the Wnt/β-catenin signaling pathway.	In addition, the luciferase reporter assay, RT-qPCR and western blotting results indicated that CCAT2 regulated transcription factor 7 like 2 (TCF7L2) expression by binding to microRNA-217. Further western blotting and TOPFlash assays indicated that CCAT2-knockdown inhibited the Wnt/β-catenin signaling pathway in DU145 and PC3 cell lines by inhibiting the expression of TCF7L2. However, CCAT2-knockdown-mediated effects were reversed by the Wnt/β-catenin signaling pathway activator lithium chloride (LiCl).	MI0000293	Oncol Lett 2020 Oct 20, 97 doi:10.3892/ol.2020.11958 PMID:32831916
2966	LncRNA	XIST	miR-337	JAK2	GES-1, HGC-27, AGS and HEK-293 T cells	Gastric Cancer	Homo sapiens (human)	luciferase reporter assays;Western blot	32830093	The lncRNA XIST promotes proliferation, migration and invasion of gastric cancer cells by targeting miR-337.	Compared with that in GES-1 cells, XIST expression was significantly up-regulated in AGS and HGC-27 cells. miR-337 expression in GC cell lines was decreased. The proliferation, invasion and migration of GC cells were simultaneously inhibited by XIST knockdown, and the relationship between XIST and miR-337 was confirmed by bioinformatics analysis. JAK2 is expected to be the target gene of miR-337. MiR-337 can negatively regulate JAK2 expression in vitro. In addition, si-XIST decreased JAK2 expression by up-regulating miR-337 in vitro, thereby inhibiting GC cell proliferation and migration. Therefore, we speculated that XIST regulates JAK2 by competing with miR-337 as a competitive endogenous lncRNA in GC.	MIMAT0004695	Arab J Gastroenterol 2020 Sep 21, 199-206 doi:10.1016/j.ajg.2020.07.010 PMID:32830093
2967	LncRNA	Linc-PINT	miR-523-3p	DKK1	ARPE-19;RB cells	Retinoblastoma	Homo sapiens (human)	luciferase reporter assays	32828314	LncRNA Linc-PINT inhibits miR-523-3p to hamper retinoblastoma progression by upregulating Dickkopf-1 (DKK1).	In addition, the dual-luciferase reporter gene system and RNA pull-down assay validated that Linc-PINT positively regulated DKK1 expressions by sponging miR-523-3p, and Linc-PINT inhibited RB progression by regulating miR-523-3p/DKK1 axis. Functionally, we found that both miR-523-3p overexpression and DKK1 silence abrogated the anti-cancer effects of overexpressed Linc-PINT on RB cells. Finally, Linc-PINT inhibited tumorigenicity of RB cells in xenograft mice models.	MIMAT0002840	Biochem Biophys Res Commun 2020 Sep 10 530, 47-53 doi:10.1016/j.bbrc.2020.06.120 PMID:32828314
2968	Circular RNA	CircEPSTI1	miR-1248	TRIM24	A549, H1299 and H460, as well as a normal human bronchial epithelial cell (HBEC) line	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32828310	Downregulation of circEPSTI1 represses the proliferation and invasion of non-small cell lung cancer by inhibiting TRIM24 via miR-1248 upregulation.	Subsequent data revealed that the tumor-promoting gene tripartite motif-containing protein 24 (TRIM24) is a target gene of miR-1248. The upregulation of TRIM24 partially reversed circEPSTI1 knockdown- or miR-1248 overexpression-induced tumor suppressive effect in NSCLC cells.	MI0006383	Biochem Biophys Res Commun 2020 Sep 10 530, 348-354 doi:10.1016/j.bbrc.2020.06.106 PMID:32828310
2969	LncRNA	PVT1	miR-214	TFR1	OGD/R PC12	Acute Ischemic Stroke	Homo sapiens (human)	qPCR;luciferase reporter assays;Western blot	32827544	LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p53.	PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.	MI0000290	Life Sci 2020 Nov 1 260, 118305 doi:10.1016/j.lfs.2020.118305 PMID:32827544
2970	LncRNA	PVT2	miR-215	p53	OGD/R PC12	Acute Ischemic Stroke	Homo sapiens (human)	qPCR;luciferase reporter assays;Western blot	32827544	LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p54.	PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.	MI0000290	Life Sci 2020 Nov 1 260, 118305 doi:10.1016/j.lfs.2020.118305 PMID:32827544
2971	LncRNA	lncRNA-F630028O10Rik	miR-1231-5p	Col1a1	NA	Spinal Cord Injury	Homo sapiens (human)	Western blot;qRT-PCR	32826878	TLR4 promotes microglial pyroptosis via lncRNA-F630028O10Rik by activating PI3K/AKT pathway after spinal cord injury.	This lncRNA functioned as a ceRNA for miR-1231-5p/Col1a1 axis and enhanced microglial pyroptosis after SCI by activating the PI3K/AKT pathway. Furthermore, we determined STAT1 was the upstream transcriptional factor of IncRNA-F630028O10Rik and was induced by the damage-responsive TLR4/MyD88 signal. Our findings provide new insights and a novel therapeutic strategy for treating SCI.	NA	Cell Death Dis 2020 Aug 10 11, 693 doi:10.1038/s41419-020-02824-z PMID:32826878
2972	LncRNA	LEF1-AS1	miR-489-3p	HIGD1A	U251 (astrocytoma), T98MG (glioblastoma), SWO38 and U373MG (astrocytoma), and control cell line (HEB and NHA)	Glioma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32826866	LEF1-AS1 accelerates tumorigenesis in glioma by sponging miR-489-3p to enhance HIGD1A.	Further, HIGD1A identified as the target gene of miR-489-3p was upregulated in glioma cells. HIGD1A silence could restrict the process of glioma. In rescue assays, upregulation of HIGD1A remedied the inhibitory impacts of LEF1-AS1 silence on glioma cell growth.	MIMAT0002805	Cell Death Dis 2020 Aug 11 11, 690 doi:10.1038/s41419-020-02823-0 PMID:32826866
2973	LncRNA	AC104041.1	miR-6817-3p	Wnt2B	CAL27 and 293T;SCC4 cells	Head And Neck Squamous Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	32826863	Antisense oligonucleotides targeting lncRNA AC104041.1 induces antitumor activity through Wnt2B/β-catenin pathway in head and neck squamous cell carcinomas.	Mechanistically, AC104041.1 mainly located in the cytoplasm and could function as ceRNA (competing endogenous RNA) for miR-6817-3p, thereby stabilized Wnt2B, and consequently inducing β-catenin nuclear translocation and activation. Moreover, we demonstrate that salinomycin, which as a highly effective antibiotic in the elimination of cancer stem cells through the Wnt/β-catenin signaling, could enhance the inhibition of tumor growth by antisense oligonucleotides (ASO) targeting AC104041.1 in HNSCC cells and PDXs (patient-derived xenograft) model.	MIMAT0027535	Cell Death Dis 2020 Aug 13 11, 672 doi:10.1038/s41419-020-02820-3 PMID:32826863
2974	LncRNA	SNAI3-AS1	miR-27a-3p	PEG10	The human HCC cell lines and the immortalized hepatic cells (Human) LO2	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32826862	LncRNA SNAI3-AS1 promotes PEG10-mediated proliferation and metastasis via decoying of miR-27a-3p and miR-34a-5p in hepatocellular carcinoma.	Further bioinformatics analysis and mechanistic experiments showed that SNAI3-AS1 functions as a competing endogenous RNA (ceRNA) to activate PEG10 by acting as a sponge for miR-27-3p and miR-34a-5p.	MIMAT0000084	Cell Death Dis 2020 Aug 11 11, 685 doi:10.1038/s41419-020-02840-z PMID:32826862
2975	LncRNA	SNAI3-AS1	miR-34a-5p	PEG10	The human HCC cell lines and the immortalized hepatic cells (Human) LO2	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32826862	LncRNA SNAI3-AS1 promotes PEG10-mediated proliferation and metastasis via decoying of miR-27a-3p and miR-34a-5p in hepatocellular carcinoma.	Further bioinformatics analysis and mechanistic experiments showed that SNAI3-AS1 functions as a competing endogenous RNA (ceRNA) to activate PEG10 by acting as a sponge for miR-27-3p and miR-34a-5p.	MIMAT0000255	Cell Death Dis 2020 Aug 11 11, 685 doi:10.1038/s41419-020-02840-z PMID:32826862
2976	LncRNA	UCA1	miR-873-5p	XIAP	H9c2	Mesenchymal Stem Cells	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32826854	Long noncoding RNA UCA1 from hypoxia-conditioned hMSC-derived exosomes: a novel molecular target for cardioprotection through miR-873-5p/XIAP axis.	lncRNA-UCA1 targeted miR-873 via sponging, reducing the latter's suppressive effects on its target XIAP, and this translated into AMPK phosphorylation and increased level of the antiapoptotic protein BCL2; and plasma derived from patients with AMI contained exosomes enriched with the lncRNA-UCA1, unlike that from normal subjects. This study demonstrates that Hypo-Exo lncRNA-UCA1 plays a cardioprotective role via the miR-873-5p/XIAP axis and circulating exosomal lncRNA-UCA1 may be a promising novel biomarker for the diagnosis of AMI.	MIMAT0004953	Cell Death Dis 2020 Aug 10 11, 696 doi:10.1038/s41419-020-02783-5 PMID:32826854
2977	LncRNA	XIST	miR-338-3p	PAX5	Normal cell line (FHC) and colorectal cancer cell lines(SW480 and SW620)	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32826710	Long noncoding RNA XIST knockdown suppresses the growth of colorectal cancer cells via regulating microRNA-338-3p/PAX5 axis.	XIST and PAX5 expression were increased, and miR-338-3p expression was decreased in colorectal cancer tissues and cells. XIST knockdown significantly repressed cell proliferation, migration and invasion, and accelerated apoptosis in colorectal cancer cells. Interestingly, XIST directly downregulated miR-338-3p expression to increase PAX5 level. As expected, XIST knockdown inhibited colorectal cancer cell growth by modulating miR-338-3p expression. Furthermore, miR-338-3p suppressed cell growth via downregulation of PAX5 level in colorectal cancer cells.	MIMAT0000763	Eur J Cancer Prev 2021 Mar 1 30, 132-142 doi:10.1097/cej.0000000000000596 PMID:32826710
2978	LncRNA	PCAT6	miR-185-5p	CBX2	Capan-2, AsPC-1, PANC1 and BxPC-3 and the normal human pancreatic duct epithelial cells (HPDE)	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32825947	LncRNA PCAT6 promotes the proliferation, migration and invasion of pancreatic ductal adenocarcinoma via regulating miR-185-5p/CBX2 axis.	For the mechanism, miR-185-5p expression was decreased and chromobox 2 (CBX2) expression was increased in PDAC, and further PCAT6 could upregulated the expression of oncogene CBX2 by sponging miR-185-5p. The results above suggested that PCAT6/miR-185-5p/CBX2 exerted crucial functions in tumorigenesis and progression of PDAC.	MIMAT0000455	Pathol Res Pract 2020 Sep 216, 153074 doi:10.1016/j.prp.2020.153074 PMID:32825947
2979	Circular RNA	hsa_circ_0008934	miR-145-5p	E2F3	SaOS2 and MG63;hFOB1.19	Osteosarcoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32822848	Hsa_circ_0008934 promotes the proliferation and migration of osteosarcoma cells by targeting miR-145-5p to enhance E2F3 expression.	Hsa_circ_0008934 was mainly distributed in the cytosol and positively regulated E2F3 expression in osteosarcoma cells. In addition, it directly bound with miR-145-5p to repress E2F3 expression and enhanced the tumorigenesis of MG63 cells in nude mice. qRT-PCR revealed that the intracellular injection of hsa_circ_0008934 lentivirus resulted in hsa_circ_0008934 overexpression and miR-145-5p downregulation.	MIMAT0000437	Int J Biochem Cell Biol 2020 Oct 127, 105826 doi:10.1016/j.biocel.2020.105826 PMID:32822848
2980	LncRNA	KCNQ1OT1	miR-15a	PD-L1	DU145 and PC-3	Prostate Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32821247	LncRNA KCNQ1OT1 sponges miR-15a to promote immune evasion and malignant progression of prostate cancer via up-regulating PD-L1.	KCNQ1OT1, PD-L1 and CD8 were increased, while miR-15a was decreased in PC tissues. MiR-15a directly bound to the 3'-UTR of PD-L1 and inhibited the expression of PD-L1. Overexpressing miR-15a in PC cells was sufficient to promote cytotoxicity and proliferation, while inhibit apoptosis of CD8+ T cells, and also suppressed viability, migration, invasion and EMT while promoted apoptosis of PC cells.	MI0000069	Cancer Cell Int 2020  20, 394 doi:10.1186/s12935-020-01481-8 PMID:32821247
2981	LncRNA	TUG1	miR-29c-3p	COL1A1	L-02;SMMC-7721, HeP3B, HepG2 and sk-Hep-1	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;qRT-PCR	32821161	lncRNA TUG1 Promotes Cell Proliferation, Migration, and Invasion in Hepatocellular Carcinoma via Regulating miR-29c-3p/COL1A1 Axis.	Dramatically increased expression of TUG1 was noticed in HCC tissues and cell lines. TUG1 knockdown restrained the proliferation, migration, and invasion, and promoted the apoptosis of HCC cells. TUG1 targeted miR-29c-3p and inhibited miR-29c-3p expression. Overexpression of miR-29c-3p inhibited the proliferation, migration and invasion of HCC cells. MiR-29c-3p directly targeted COL1A1 and down-regulated COL1A1 expression. In addition, downregulation of miR-29c-3p and upregulation of COL1A1 both reversed the effects of TUG1 knockdown on the proliferation, apoptosis, migration, and invasion of HCC cells.	MIMAT0000681	Cancer Manag Res 2020  12, 6837-6847 doi:10.2147/cmar.S256624 PMID:32821161
2982	LncRNA	LINC00491	miR-324-5p	SP1	H522, H460, SK-MES-1, A549,BEAS-2B	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32821159	Long Non-Coding RNA LINC00491 Contributes to the Malignancy of Non-Small-Cell Lung Cancer via Competitively Binding to microRNA-324-5p and Thereby Increasing Specificity Protein 1 Expression.	Mechanistically, LINC00491 functioned as a competing endogenous RNA by sponging microRNA-324-5p (miR-324-5p) in NSCLC cells. miR-324-5p was weakly expressed in NSCLC and exerted tumor-suppressing actions during cancer progression. Furthermore, specificity protein 1 (SP1) was validated as the direct target of miR-324-5p in NSCLC and was under the regulation of LINC00491 via sponging miR-324-5p.	MIMAT0000761	Cancer Manag Res 2020  12, 6779-6793 doi:10.2147/cmar.S264681 PMID:32821159
2983	LncRNA	HEIH	miR-98-5p	PI3K	HCCLM3 and Huh7	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32821157	LncRNA HEIH Confers Cell Sorafenib Resistance in Hepatocellular Carcinoma by Regulating miR-98-5p/PI3K/AKT Pathway.	HEIH was a sponge of miR-98-5p, and miR-98-5p inhibition reversed the sorafenib sensitivity induced by HEIH deletion in sorafenib-resistant HCC cells. MiR-98-5p inhibition could activate PI3K/AKT pathway, and enhanced sorafenib resistance by regulating the activation of PI3K/AKT pathway in sorafenib-resistant HCC cells. Besides, HEIH also activated PI3K/AKT pathway through regulating miR-98-5p in sorafenib-resistant HCC cells.	MIMAT0000096	Cancer Manag Res 2020  12, 6585-6595 doi:10.2147/cmar.S241383 PMID:32821157
2984	LncRNA	LOXL1-AS1	miR-708-5p	CD44-EGFR	HCT8, LoVo, SW620, Caco2 ， SW1463， HIEC	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32821123	Long Non-Coding RNA LOXL1-AS1 Enhances Colorectal Cancer Proliferation, Migration and Invasion Through miR-708-5p/CD44-EGFR Axis.	LOXL1-AS1 knockdown along with miR-708-5p overpresentation in CRC cell lines inhibited cell multiplication, migration, and invasion. The inhibiting effect of LOXL1-AS1 knockdown on CRC was reversed by upregulating the CD44-EGFR signal pathway. From the perspective of mechanism, LOXL1-AS1 imposes sponging upon miR-708-5p and thereby promotes the CD44-EGFR signal pathway in CRC cells.	MIMAT0004926	Onco Targets Ther 2020  13, 7615-7627 doi:10.2147/ott.S258935 PMID:32821123
2985	LncRNA	LINC00460	miR-613	SphK1	HT29, HCT116, SW480, LOVO,NCM460	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	32821121	Long Noncoding RNA LINC00460 Facilitates Colorectal Cancer Progression by Negatively Regulating miR-613.	In vivo studies, LINC00460 knockdown attenuated tumour growth. MiR-613 downregulation and SphK1 upregulation in the CRC tissues, and LINC00460 expression levels were inversely correlated with miR-613 expression and positively correlated with the SphK1 mRNA expression. Overall, LINC00460 modulated cell proliferation, migration, invasion and sphingosine kinase 1 (SphK1) expression in HT29 and LOVO cells, at least in most part, by regulating miR-613.	MI0003626	Onco Targets Ther 2020  13, 7555-7569 doi:10.2147/ott.S254489 PMID:32821121
2986	LncRNA	FTX	miR-214-5p	SOX4	HFOB1.19 cells and KHOS, MG63, U2OS, HOS,Saos-2	Osteosarcoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32821116	Upregulation of FTX Promotes Osteosarcoma Tumorigenesis by Increasing SOX4 Expression via miR-214-5p.	FTX could modulate the expression of miR-214-5p in osteosarcoma cell lines. sh-FTX inhibited the growth and metastasis of osteosarcoma. FTX could regulate the growth of osteosarcoma through miR-214-5p. The knockdown of miR-214-5p reversed the inhibitory effect of sh-FTX on osteosarcoma cell proliferation and growth in mice. Furthermore, FTX regulated the expression of SOX4 by acting as a sponge of miR-214-5p in osteosarcoma.	MIMAT0004564	Onco Targets Ther 2020  13, 7125-7136 doi:10.2147/ott.S238070 PMID:32821116
2987	Circular RNA	CircTHBS1	miR-211	CCND2	primary cells from glandular cystitis and normal controls	Primary Cystitis Glandularis	Homo sapiens (human)	qPCR;luciferase reporter assays	32820798	CircTHBS1 targeting miR-211/CCND2 pathway to promote cell proliferation and migration potential in primary cystitis glandularis cells.	In addition, we demonstrated that CircTHBS1 played a role in the adsorption of miR-211 by "sponge" in pCG. In turn, miR-211 can directly target CYCLIN D2 (CCND2) 3'UTR to perform its function. Finally, we confirmed the role and mechanism of CircTHBS1/miR-211/CCND2 regulation axis in pCGs.	MIMAT0022694	Biosci Rep 2020 Aug 21, 10.1042/bsr20201164 doi:10.1042/bsr20201164 PMID:32820798
2988	LncRNA	KTN1-AS1	miR-130a-5p	PDPK1	BEAS-2B,A549, PC-9, H1299,H1975, SPCA-1	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32820252	LncRNA KTN1-AS1 promotes the progression of non-small cell lung cancer via sponging of miR-130a-5p and activation of PDPK1.	Notably, miR-130a-5p overexpression suppressed NSCLC cell proliferation and increased apoptosis in vitro and in vivo, and this effect was reversed by KTN1-AS1 overexpression. Finally, we showed that KTN1-AS1 modulated the expression of 3-phosphoinositide-dependent protein kinase 1 (PDPK1), a miR-130a-5p target and key regulator of autophagy in NSCLC cells.	MIMAT0004593	Oncogene 2020 Sep 39, 6157-6171 doi:10.1038/s41388-020-01427-4 PMID:32820252
2989	LncRNA	MIR31HG	miR-361-3p	EMP1	CasKi, SiHa ,C33A,HcerEpic	Cervical Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32819595	MIR31HG exhibits oncogenic property and acts as a sponge for miR-361-3p in cervical carcinoma.	Mechanistically, MIR31HG was identified as an endogenous 'sponge' through competing for miR-361-3p binding to modulate the miRNA target, epithelial membrane protein 1 (EMP1).	MIMAT0004682	Biochem Biophys Res Commun 2020 Sep 3 529, 890-897 doi:10.1016/j.bbrc.2020.06.028 PMID:32819595
2990	LncRNA	THRIL	miR-424	ROCK2	MPVECs	Sepsis-Induced Acute Lung Injury	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32818819	LncRNA THRIL aggravates sepsis-induced acute lung injury by regulating miR-424/ROCK2 axis.	MiR-424 and Rho-associated kinase 2 (ROCK2) were predicted and verified as direct targets of THRIL and miR-424, respectively, by using dual-luciferase reporter assay. ROCK2 overexpression vector and shTHRIL were co-transfected into mouse pulmonary microvascular endothelial cells for 24 h before LPS treatment. Our results showed that THRIL was highly expressed in the lung of sepsis mice.	MIMAT0004749	Mol Immunol 2020 Oct 126, 111-119 doi:10.1016/j.molimm.2020.07.021 PMID:32818819
2991	LncRNA	LncRNA-SNHG29	miR-200b-3p	RUNX2	HASMCs,HCASMCs	Vascular Calcification	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32818704	LncRNA-SNHG29 inhibits vascular smooth muscle cell calcification by downregulating miR-200b-3p to activate the α-Klotho/FGFR1/FGF23 axis.	In the in vitro calcification model, SNHG29 was downregulated, while miR-200b-3p was upregulated. SNHG29 overexpression and miR-200b-3p knockdown significantly suppressed osteoblast-related factors (RUNX2 and BMP2), accompanied by activation of the α-Klotho/FGFR1/FGF23 axis, further inhibiting the formation of calcified nodules. Moreover, miR-200b-3p overexpression and α-Klotho knockdown reversed the SNHG29 overexpression-induced inhibitory effects on calcified VSMCs.	MIMAT0000318	Cytokine 2020 Dec 136, 155243 doi:10.1016/j.cyto.2020.155243 PMID:32818704
2992	LncRNA	LncRNA-SNHG29	miR-200b-3p	BMP2	HASMCs,HCASMCs	Vascular Calcification	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32818704	LncRNA-SNHG29 inhibits vascular smooth muscle cell calcification by downregulating miR-200b-3p to activate the α-Klotho/FGFR1/FGF23 axis.	In the in vitro calcification model, SNHG29 was downregulated, while miR-200b-3p was upregulated. SNHG29 overexpression and miR-200b-3p knockdown significantly suppressed osteoblast-related factors (RUNX2 and BMP2), accompanied by activation of the α-Klotho/FGFR1/FGF23 axis, further inhibiting the formation of calcified nodules. Moreover, miR-200b-3p overexpression and α-Klotho knockdown reversed the SNHG29 overexpression-induced inhibitory effects on calcified VSMCs.	MIMAT0000318	Cytokine 2020 Dec 136, 155243 doi:10.1016/j.cyto.2020.155243 PMID:32818704
2993	LncRNA	TP73-AS1	miR-539	MMP-8	WRL68,HepG2, SNU-182, MHCC97H and Huh-7	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32818670	LncRNA TP73-AS1/miR-539/MMP-8 axis modulates M2 macrophage polarization in hepatocellular carcinoma via TGF-β1 signaling.	We found TP73-AS1 and MMP-8 upregulation, and miR-539 downregulation in HCC tissues and cell lines. Lower TP73-AS1 and MMP-8 expressions and higher miR-539 expression were associated with higher survival rate of patients. M2-macrophage markers CD206, Arg-1 and CD163 were significantly upregulated in the tumor tissues. TP73-AS1 negatively and directly regulated miR-539 and knockdown of TP73-AS1 inhibited MMP-8 expression and M2 macrophage polarization.	MI0003514	Cell Signal 2020 Nov 75, 109738 doi:10.1016/j.cellsig.2020.109738 PMID:32818670
2994	LncRNA	DANCR	miR-4319	VAPB	MCF-10A,MCF-7 and HCC38	Breast Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32818383	lncRNA DANCR Promotes Proliferation and Metastasis of Breast Cancer Cells Through Sponging miR-4319 and Upregulating VAPB.	DANCR and VAPB were upregulated, while miR-4319 was downregulated in breast cancer tissues and cells. Knockdown of DANCR hindered proliferation, migration, and invasion and promoted apoptosis of breast cancer cells. DANCR knockdown inhibited breast cancer development through regulating miR-4319. Inhibition of miR-4319 restrained breast cancer cell progression by targeting VAPB. Moreover, DANCR regulated VAPB expression by sponging miR-4319 in breast cancer cells.	MIMAT0016870	Cancer Biother Radiopharm 2020 Aug 18, 10.1089/cbr.2020.3675 doi:10.1089/cbr.2020.3675 PMID:32818383
2995	LncRNA	lnc_000231	miR-497-5p	CCNE1	HeLa, CaSki, SiHa, C-33A and SW756	Cervical Cancer	Homo sapiens (human)	Northern blot;Western blot;qRT-PCR;luciferase reporter assays	32818316	E6 hijacks KDM5C/lnc_000231/miR-497-5p/CCNE1 axis to promote cervical cancer progression.	Mechanically, we demonstrated that E6 up-regulates lnc_000231 expression through promoting its promoter region H3K4me3 modification by destabilizing KDM5C. In vitro and in vivo results showed that lnc_000231 promotes cervical cancer cell proliferation and tumour formation by acting as miR-497-5p sponge and maintaining cyclin E1 (CCNE1) expression.	MIMAT0002820	J Cell Mol Med 2020 Oct 24, 11422-11433 doi:10.1111/jcmm.15746 PMID:32818316
2996	Circular RNA	CircHIPK3	miR-876-5p	PIK3R1	GES-1 and HGC-27	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32817745	CircHIPK3/miR-876-5p/PIK3R1 axis regulates regulation proliferation, migration, invasion, and glutaminolysis in gastric cancer cells.	Moreover, we also found that miR-876-5p, interacted with PIK3R1, was a target gene of circHIPK3. CircHIPK3 silencing induced effects on GC cells were abolished by silencing of miR-876-5p. In addition, upregulation of PIK3R1 inversed miR-876-5p overexpression-induced effects on GC cells.	MIMAT0004924	Cancer Cell Int 2020  20, 391 doi:10.1186/s12935-020-01455-w PMID:32817745
2997	LncRNA	CDKN2B-AS1	miR-141	CCND1	CRL-4031 and CRL-1611 Caki1 ,HTB-46	Renal Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32814766	LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.	An overexpression of CDKN2B-AS1 was observed in RCC compared to normal samples in TCGA and our in-house SFVAMC tissue cohorts. Reciprocally, we observed reduced expression of miR-141 in RCC compared to normal in the same cohorts. CDKN2B-AS1 shares regulatory miR-141 binding sites with CCND1 and CCND2 genes. Direct interactions of CDKN2B-AS1/miR-141/Cyclin D1-D2 were confirmed by RNA immunoprecipitation and luciferase reporter assays indicating that CDKN2B-AS1/miR-141/Cyclin D1-D2 acts as a ceRNA network in RCC. Functionally, attenuation of CDKN2B-AS1 and/or overexpression of miR-141 inhibited proliferation, clonogenicity, migration/invasion, induced apoptosis in vitro and suppressed tumor growth in xenograft mouse model. Further, overexpression of CDKN2B-AS1 is positively correlated with poor overall survival of RCC patients. Expression of miR-141 also robustly discriminated malignant from non-malignant tissues and its inhibition in normal RPTEC cells induced pro-cancerous characteristics. CDKN2B-AS1 attenuation or miR-141 overexpression decreased CCND1/CCND2 expression, resulting in reduced RAC1/pPXN that are involved in migration, invasion and epithelial-mesenchymal transition. This study, for the first time, deciphered the role of CDKN2B-AS1/miR-141/Cyclin D axis in RCC and highlights this network as a promising therapeutic target for the regulation of EMT driven metastasis in RCC.	MI0000457	Cell Death Dis 2020 Aug 19 11, 660 doi:10.1038/s41419-020-02877-0 PMID:32814766
2998	LncRNA	CDKN2B-AS1	miR-141	CCND2	CRL-4031 and CRL-1611 Caki1 ,HTB-46	Renal Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32814766	LncRNA CDKN2B-AS1/miR-141/cyclin D network regulates tumor progression and metastasis of renal cell carcinoma.	An overexpression of CDKN2B-AS1 was observed in RCC compared to normal samples in TCGA and our in-house SFVAMC tissue cohorts. Reciprocally, we observed reduced expression of miR-141 in RCC compared to normal in the same cohorts. CDKN2B-AS1 shares regulatory miR-141 binding sites with CCND1 and CCND2 genes. Direct interactions of CDKN2B-AS1/miR-141/Cyclin D1-D2 were confirmed by RNA immunoprecipitation and luciferase reporter assays indicating that CDKN2B-AS1/miR-141/Cyclin D1-D2 acts as a ceRNA network in RCC. Functionally, attenuation of CDKN2B-AS1 and/or overexpression of miR-141 inhibited proliferation, clonogenicity, migration/invasion, induced apoptosis in vitro and suppressed tumor growth in xenograft mouse model. Further, overexpression of CDKN2B-AS1 is positively correlated with poor overall survival of RCC patients. Expression of miR-141 also robustly discriminated malignant from non-malignant tissues and its inhibition in normal RPTEC cells induced pro-cancerous characteristics. CDKN2B-AS1 attenuation or miR-141 overexpression decreased CCND1/CCND2 expression, resulting in reduced RAC1/pPXN that are involved in migration, invasion and epithelial-mesenchymal transition. This study, for the first time, deciphered the role of CDKN2B-AS1/miR-141/Cyclin D axis in RCC and highlights this network as a promising therapeutic target for the regulation of EMT driven metastasis in RCC.	MI0000457	Cell Death Dis 2020 Aug 19 11, 660 doi:10.1038/s41419-020-02877-0 PMID:32814766
2999	LncRNA	PVT1	miR-186	SEMA4D	ACC 344,KL-058,BNCC342270	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32812642	SOX2 knockdown slows cholangiocarcinoma progression through inhibition of transcriptional activation of lncRNA PVT1.	LncRNA PVT1 bound to miR-186 and miR-186 was found to target SEMA4D. The overexpression of lncRNA PVT1 and SEMA4D, as well as the inhibition of miR-186 led to elevated CCA cell proliferation, migration, and invasion. In vivo experiments confirmed the inhibitory role of lncRNA PVT1 knockdown or SEMA4D knockdown in CCA.	MI0000483	Biochem J 2020 Sep 30 477, 3527-3540 doi:10.1042/bcj20200219 PMID:32812642
3000	LncRNA	TUG1	miR-34c	BRD4	BEAS-2B	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32812639	LncRNA TUG1 knockdown mitigates inflammatory injury induced by cigarette smoke extract in chronic obstructive pulmonary disease via miR-34c/BRD4 axis.	TUG1 was verified to sponge to miR-34c, and BRD4 was validated as a target of miR-34c. TUG1 depletion or miR-34c overexpression promoted cell proliferation but restrained apoptosis, inflammatory response in CSE-treated BEAS-2B cells. MiR-34c inhibitor mitigated the inhibitory effect on cell proliferation and the promotion effects on cell apoptosis, inflammatory response in CSE-treated BEAS-2B cells induced by TUG1 silencing.	MI0000743	Biosci Rep 2020 Aug 19, 10.1042/bsr20193896 doi:10.1042/bsr20193896 PMID:32812639
3001	LncRNA	EIF3J-AS1	miR-373-3p	AKT1	EC9706, TE-1,TE-8 cells	Esophageal Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR	32811869	LncRNA EIF3J-AS1 enhanced esophageal cancer invasion via regulating AKT1 expression through sponging miR-373-3p.	Functional experiments showed that knockdown EIF3J-AS1 inhibited ECa growth and metastasis through in vitro and in vivo experiments. Regarding the mechanism, EIF3J-AS1/miR-373-3p/AKT1 established the ceRNA network involved in the modulation of cell progression of ECa cells.	MIMAT0000726	Sci Rep 2020 Aug 18 10, 13969 doi:10.1038/s41598-020-70886-2 PMID:32811869
3002	LncRNA	LRRC75A-AS1	miR-380-3p	BAALC	MDA-MB-468, MDA-MB-436, MDA-MB-231 ,HCC-1937, MCF-10A	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32811810	Long non-coding RNA LRRC75A-AS1 facilitates triple negative breast cancer cell proliferation and invasion via functioning as a ceRNA to modulate BAALC.	Moreover, LRRC75A-AS1 (also named small nucleolar RNA host gene 29: SNHG29) was verified to act as the sponge of miR-380-3p to elevate BAALC expression in TNBC. Besides, LRRC75A-AS1 could negatively regulate miR-380-3p but positively regulate BAALC expression. Finally, rescue assays elucidated that LRRC75A-AS1 facilitated cell proliferation, invasion, and EMT processes in TNBC by targeting miR-380-3p/BAALC pathway. Taken together, our study revealed a novel ceRNA network of LRRC75A-AS1/miR-380-3p/BAALC in accelerating TNBC development, indicating new promising targets for TNBC treatment.	MIMAT0000735	Cell Death Dis 2020 Aug 18 11, 643 doi:10.1038/s41419-020-02821-2 PMID:32811810
3003	LncRNA	RP11-480I12.5-004	miR-29c-3p	AKT3	HBL-100,MCF-7, T47D, BT474, HCC1937, BT549, and MDA-MB-231	Breast Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;luciferase reporter assays	32810693	RP11-480I12.5-004 Promotes Growth and Tumorigenesis of Breast Cancer by Relieving miR-29c-3p-Mediated AKT3 and CDK6 Degradation.	RP11-480I12.5-004 mainly located in cytoplasm and increased AKT3 and CDK6 mRNA expression, at least in part, by competitively binding to miR-29c-3p. Six parental genes of RP11-480I12.5 were found, among which TUBA1B and TUBA1C were statistically linked to RP11-480I12.5 expression, possessed prognostic values, and were upregulated in breast cancer. Our findings suggested that pseudogene-derived long non-coding RNA (lncRNA) RP11-480I12.5-004 promoted growth and tumorigenesis of breast cancer via increasing AKT3 and CDK6 expression by competitively binding to miR-29c-3p.	MIMAT0000681	Mol Ther Nucleic Acids 2020 Sep 4 21, 916-931 doi:10.1016/j.omtn.2020.07.022 PMID:32810693
3004	LncRNA	RP11-480I12.5-004	miR-29c-3p	CDK6	HBL-100,MCF-7, T47D, BT474, HCC1937, BT549, and MDA-MB-231	Breast Cancer	Homo sapiens (human)	siRNA transfection;qRT-PCR;Dual-luciferase reporter assay	32810693	RP11-480I12.5-004 Promotes Growth and Tumorigenesis of Breast Cancer by Relieving miR-29c-3p-Mediated AKT3 and CDK6 Degradation.	RP11-480I12.5-004 mainly located in cytoplasm and increased AKT3 and CDK6 mRNA expression, at least in part, by competitively binding to miR-29c-3p. Six parental genes of RP11-480I12.5 were found, among which TUBA1B and TUBA1C were statistically linked to RP11-480I12.5 expression, possessed prognostic values, and were upregulated in breast cancer. Our findings suggested that pseudogene-derived long non-coding RNA (lncRNA) RP11-480I12.5-004 promoted growth and tumorigenesis of breast cancer via increasing AKT3 and CDK6 expression by competitively binding to miR-29c-3p.	MIMAT0000681	Mol Ther Nucleic Acids 2020 Sep 4 21, 916-931 doi:10.1016/j.omtn.2020.07.022 PMID:32810693
3005	LncRNA	LncRNA-H19	miR-124a	CDK2	MH7A	Rheumatoid Arthritis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32810279	LncRNA-H19 silencing suppresses synoviocytes proliferation and attenuates collagen-induced arthritis progression by modulating miR-124a.	Notably, lncRNA-H19 competitively bound to miR-124a, which directly targets CDK2 and MCP-1. It was confirmed that lncRNA-H19 regulates the proliferation of synoviocytes by acting as a sponge of miR-124a to modulate CDK2 and MCP-1 expression. Furthermore, the agonists of LXR inhibited lncRNA-H19-mediated miR-124a-CDK2/MCP-1 signalling pathway in synoviocytes.	NA	Rheumatology (Oxford) 2021 Jan 5 60, 430-440 doi:10.1093/rheumatology/keaa395 PMID:32810279
3006	LncRNA	LncRNA-H19	miR-124a	MCP-1	MH7A	Rheumatoid Arthritis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32810289	LncRNA-H19 silencing suppresses synoviocytes proliferation and attenuates collagen-induced arthritis progression by modulating miR-124a.	Notably, lncRNA-H19 competitively bound to miR-124a, which directly targets CDK2 and MCP-1. It was confirmed that lncRNA-H19 regulates the proliferation of synoviocytes by acting as a sponge of miR-124a to modulate CDK2 and MCP-1 expression. Furthermore, the agonists of LXR inhibited lncRNA-H19-mediated miR-124a-CDK2/MCP-1 signalling pathway in synoviocytes.	NA	Int J Dermatol 2021 Jan 60, e7-e8 doi:10.1111/ijd.15160 PMID:32810289
3007	LncRNA	MALAT1	miR-126-5p	CREB1	Human endometrium	Endometrial Stromal	Homo sapiens (human)	siRNA transfection;qRT-PCR;Dual-luciferase reporter assay;Western blot	32809092	LncRNA MALAT1 inhibits apoptosis of endometrial stromal cells through miR-126-5p-CREB1 axis by activating PI3K-AKT pathway.	In addition, miR-126-5p directly regulated CREB1 expression via binding to its 3' non-coding region. Finally, miR-126-5p inhibitor-mediated apoptosis inhibition was restrained by CREB1 silencing via inactivation of PI3K-AKT pathway in HESCs. Taken together, our study firstly demonstrates that MALAT1 regulates apoptosis of HESCs through miR-126-5p/CREB1 axis mediated PI3K/AKT pathway. Our findings explained the pathogenesis of endometriosis and offered promising therapeutic option for endometriosis.	MIMAT0000444	Mol Cell Biochem 2020 Dec 475, 185-194 doi:10.1007/s11010-020-03871-y PMID:32809092
3008	LncRNA	LncRNA-599547	miR-15b-5p	ALP	DPCs	Dermal Papilla Cells	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay	32808845	LncRNA-599547 contributes the inductive property of dermal papilla cells in cashmere goat through miR-15b-5p/Wnt10b axis.	The overexpression of lncRNA-599547 led to a significant increase of ALP and LEF1 expression in DPCs (p < 0.05), whereas, the siLncRNA-1 mediated silencing of lncRNA-599547 significantly down-regulated the expression of ALP and LEF1 in DPCs (p < 0.05). Based on biotin-labeled RNA pull-down assay, we found that lncRNA-599547 directly interacted with chi-miR-15b-5p in DPCs. Based on both overexpression and silencing analysis of lncRNA-599547, our results indicate that lncRNA-599547 promotes the expression of Wnt10b in DPCs but without modulating its promoter methylation level. Using the mRNA-3'UTR fragments of goat Wnt10b containing the predicted binding sites of chi-miR-15b-5p in Dual-luciferase Reporter Assays, we show that lncRNA-599547 modulates the expression of Wnt10b at the chi-miR-15b-5p mediated post-transcriptional level.	MIMAT0000417	Anim Biotechnol 2020 Aug 18, 10.1080/10495398.2020.1806860, 1-15 doi:10.1080/10495398.2020.1806860 PMID:32808845
3009	LncRNA	LncRNA-599547	miR-15b-5p	LEF1	DPCs	Dermal Papilla Cells	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay	32808845	LncRNA-599547 contributes the inductive property of dermal papilla cells in cashmere goat through miR-15b-5p/Wnt10b axis.	The overexpression of lncRNA-599547 led to a significant increase of ALP and LEF1 expression in DPCs (p < 0.05), whereas, the siLncRNA-1 mediated silencing of lncRNA-599547 significantly down-regulated the expression of ALP and LEF1 in DPCs (p < 0.05). Based on biotin-labeled RNA pull-down assay, we found that lncRNA-599547 directly interacted with chi-miR-15b-5p in DPCs. Based on both overexpression and silencing analysis of lncRNA-599547, our results indicate that lncRNA-599547 promotes the expression of Wnt10b in DPCs but without modulating its promoter methylation level. Using the mRNA-3'UTR fragments of goat Wnt10b containing the predicted binding sites of chi-miR-15b-5p in Dual-luciferase Reporter Assays, we show that lncRNA-599547 modulates the expression of Wnt10b at the chi-miR-15b-5p mediated post-transcriptional level.	MIMAT0000417	Anim Biotechnol 2020 Aug 18, 10.1080/10495398.2020.1806860, 1-15 doi:10.1080/10495398.2020.1806860 PMID:32808845
3010	LncRNA	ACTA2-AS1	miR-378a-3p	SOX7	BEAS-2B,A549, 201T, A-427, PC-9,239T	Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32808728	ACTA2-AS1 suppresses lung adenocarcinoma progression via sequestering miR-378a-3p and miR-4428 to elevate SOX7 expression.	In addition, we determined the suppressive effect of ACTA2-AS1 on LUAD cell invasion, migration and EMT progress. Mechanistically, ACTA2-AS1 exert functions as a competing endogenous RNA (ceRNA) through serving as a sponge for miR-378a-3p and miR-4428 to elevate SOX7 expression. Importantly, SOX7 silencing could recover the ACTA2-AS1-mediated cell functions.	MIMAT0000732	Cell Biol Int 2020 Dec 44, 2438-2449 doi:10.1002/cbin.11451 PMID:32808728
3011	LncRNA	ACTA2-AS1	miR-4428	SOX7	BEAS-2B,A549, 201T, A-427, PC-9,239T	Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32808728	ACTA2-AS1 suppresses lung adenocarcinoma progression via sequestering miR-378a-3p and miR-4428 to elevate SOX7 expression.	In addition, we determined the suppressive effect of ACTA2-AS1 on LUAD cell invasion, migration and EMT progress. Mechanistically, ACTA2-AS1 exert functions as a competing endogenous RNA (ceRNA) through serving as a sponge for miR-378a-3p and miR-4428 to elevate SOX7 expression. Importantly, SOX7 silencing could recover the ACTA2-AS1-mediated cell functions.	MI0016767	Cell Biol Int 2020 Dec 44, 2438-2449 doi:10.1002/cbin.11451 PMID:32808728
3012	LncRNA	CERS6-AS1	miR-125a-5p	BAP1	MDA-MB-468 and MDA-MB-231	Breast Cancer	Homo sapiens (human)	siRNA transfection;Dual-luciferase reporter assay	32808708	lncRNA CERS6-AS1 as ceRNA promote cell proliferation of breast cancer by sponging miR-125a-5p to upregulate BAP1 expression.	Furthermore, CERS6-AS1 regulated BC susceptibility gene 1-associated protein 1 (BAP1) expression via sponging miR-125a-5p via Western blot analysis and quantitative polymerase chain reaction arrays. Finally, we showed that miR-125a-5p had opposing effects to those of CERS6-AS1 on BC cells, demonstrating that CERS6-AS1 may promote cell proliferation and inhibit cell apoptosis via sponging miR-125a-5p.	MIMAT0000443	Mol Carcinog 2020 Oct 59, 1199-1208 doi:10.1002/mc.23249 PMID:32808708
3013	LncRNA	VPS9D1-AS1	miR-491-5p	GPX1	Molt-4 and Molt-3,PBMC	Acute Lymphoblastic Leukemia	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32808668	LncRNA VPS9D1-AS1 promotes cell proliferation in acute lymphoblastic leukemia through modulating GPX1 expression by miR-491-5p and miR-214-3p evasion.	Then, both miR-491-5p and miR-214-3p that was downregulated in ALL cells were affirmed to target GPX1. Subsequently, VPS9D1 antisense RNA 1 (VPS9D1-AS1) was recognized as the upstream regulator of miR-491-5p-miR-214-3p/GPX1 axis in a competing endogenous RNA (ceRNA) model. Importantly, we proved that VPS9D1-AS1 served as a tumor-promoter in ALL through elevating GPX1.	MIMAT0002807	Biosci Rep 2020 Oct 30 40 doi:10.1042/bsr20193461 PMID:32808668
3014	LncRNA	VPS9D1-AS1	miR-214-3p	GPX1	Molt-4 and Molt-3,PBMC	Acute Lymphoblastic Leukemia	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32808668	LncRNA VPS9D1-AS1 promotes cell proliferation in acute lymphoblastic leukemia through modulating GPX1 expression by miR-491-5p and miR-214-3p evasion.	Then, both miR-491-5p and miR-214-3p that was downregulated in ALL cells were affirmed to target GPX1. Subsequently, VPS9D1 antisense RNA 1 (VPS9D1-AS1) was recognized as the upstream regulator of miR-491-5p-miR-214-3p/GPX1 axis in a competing endogenous RNA (ceRNA) model. Importantly, we proved that VPS9D1-AS1 served as a tumor-promoter in ALL through elevating GPX1.	MIMAT0000271	Biosci Rep 2020 Oct 30 40 doi:10.1042/bsr20193461 PMID:32808668
3015	LncRNA	TUG1	miR-152-3p	PTEN	CRL-2266	Parkinsons Disease	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32808542	Long Non-coding RNA TUG1 Promotes Parkinson's Disease via Modulating MiR-152-3p/PTEN Pathway.	Further research showed that TUG1 sponged and regulated miR-152-3p expression. Silencing of TUG1 not only protected SH-SY5Y cells against cell apoptosis, oxidative stress and neuroinflammation in vitro, pathological damage and neuroinflammation in vivo, but also suppressed the expressions of PTEN and cleaved caspase-3, increased the expressions of TH and Bcl-2 in MPP+-treated SH-SY5Y cells. However, the protective role of siTUG1 in SH-SY5Y cells was significantly inhibited by miR-152-3p inhibitor. Thus, knocking down TUG1 might have a protective effect on PD through miR-152-3p/PTEN pathway.	MIMAT0000438	Hum Gene Ther 2020 Dec 31, 1274-1287 doi:10.1089/hum.2020.106 PMID:32808542
3016	LncRNA	UCA1	miR-296-3p	CDH1	P69 and M12	Prostate Cancer	Homo sapiens (human)	luciferase reporter assays	32805084	LncRNA UCA1 maintains the low-tumorigenic and nonmetastatic status by stabilizing E-cadherin in primary prostate cancer cells.	In addition, we also found that UCA1 acted as a sponge of miR-296-3p, which targeted E-cadherin gene CDH1 messenger RNA at the posttranscription level. Taken together, these findings demonstrated that UCA1 had a new important role in effectively keeping E-cadherin at a high level through a dual mechanism, which maintained primary prostate cancer cells at the low-tumorigenic and nonmetastatic status.	MIMAT0004679	Mol Carcinog 2020 Oct 59, 1174-1187 doi:10.1002/mc.23247 PMID:32805084
3017	LncRNA	TUG1	miR-221-3p	KIT	HL-60, THP-1, MV-4-11,AML-193,CD34+	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32804119	Silencing of long noncoding RNA TUG1 inhibits viability and promotes apoptosis of acute myeloid leukemia cells by targeting microRNA-221-3p/KIT axis.	The expression of TUG1 and KIT was up-regulated in AML, but miR-221-3p was down-regulated. TUG1 expression had obviously correlation with World Health Organization (WHO) grade in AML patients. The functional experiment stated that TUG1 silencing suppressed the viability and accelerated the apoptosis of AML cells. Moreover, the mechanical experiment demonstrated that TUG1 and KIT were both targeted by miR-221-3p with the complementary binding sites at 3'UTR.	MIMAT0000278	Clin Hemorheol Microcirc 2020  76, 425-437 doi:10.3233/ch-200906 PMID:32804119
3018	LncRNA	NEAT1	miR-185-5p	DNMT1	U87 and U251,SVG-p12	Glioma	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32803763	Long noncoding RNA NEAT1 promotes progression of glioma as a ceRNA by sponging miR-185-5p to stimulate DNMT1/mTOR signaling.	More important, NEAT1 expression was negatively correlated with miR-185-5p expression in glioma tissues. In vitro and in vivo experiments verified that NEAT1 was a competing endogenous RNA for miR-185-5p for promoting DNA methyltransferase 1 (DNMT1) expression and activated mammalian target of rapamycin (mTOR) signaling, thus inhibiting apoptosis, and promoting glioma migration, proliferation, and epithelial-mesenchymal transition process.	MIMAT0000455	J Cell Physiol 2021 Jan 236, 121-130 doi:10.1002/jcp.29644 PMID:32803763
3019	LncRNA	LincRNA-Cox2	miR-let-7a	STAT3	PASMCs	Pulmonary Arterial Hypertension	Homo sapiens (human)	luciferase reporter assay;Western blot	32803651	LincRNA-Cox2 promotes pulmonary arterial hypertension by regulating the let-7a-mediated STAT3 signaling pathway.	Meanwhile, lincRNA-COX2 regulated STAT3 through miR-let-7a and its effects on hypoxic PASMCs worked through miR-let-7a/STAT3 axis. To conclude, silencing lincRNA-COX2 attenuated the development of hypoxic PASMCs. LincRNA-COX2/miR-let-7a/STAT3 axis might be considered as a novel target to treat PAH.	NA	Mol Cell Biochem 2020 Dec 475, 239-247 doi:10.1007/s11010-020-03877-6 PMID:32803651
3020	LncRNA	MAFG-AS1	miR-765	PDX1	EC9706, EC109,KYSE30,KYSE150,Het-1A	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assay;Western blot	32801913	LncRNA MAFG-AS1 Accelerates Cell Migration, Invasion and Aerobic Glycolysis of Esophageal Squamous Cell Carcinoma Cells via miR-765/PDX1 Axis.	MAFG-AS1 competitively adsorbed miR-765, while miR-765 negatively modulated the expression of PDX1. miR-765 and PDX1 participated in the promotive effects of MAFG-AS1 on cell migration, invasion and aerobic glycolysis in ESCC cells.	MI0005116	Cancer Manag Res 2020  12, 6895-6908 doi:10.2147/cmar.S262075 PMID:32801913
3021	Circular RNA	CircEPSTI1	miR-145	HMGB3	A549, H1299, Calu-3, Calu-6 ,HBE1	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32801908	CircEPSTI1 Promotes the Progression of Non-Small Cell Lung Cancer Through miR-145/HMGB3 Axis.	miR-145 was validated as a target of circEPSTI1 in NSCLC cells. HMGB3 was a direct downstream target of miR-145 in NSCLC cells. The decreased abilities of proliferation, colony formation and metastasis caused by the silencing of circEPSTI1 were reversed by the depletion of miR-145 or the accumulation of HMGB3 in NSCLC cells.	MI0000461	Cancer Manag Res 2020  12, 6827-6836 doi:10.2147/cmar.S252893 PMID:32801908
3022	LncRNA	OIP5-AS1	miR-137	ZNF217	IOSE,HEY, A2780, SKOV3, OVCAR3	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	32801903	OIP5-AS1/miR-137/ZNF217 Axis Promotes Malignant Behaviors in Epithelial Ovarian Cancer.	OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) to elevate ZNF217 expression through sponging miR-137. Furthermore, miR-137 inhibition and ZNF217 upregulation can reverse the effects of silencing OIP5-AS1 on the cellular activities of ovarian cancer cells. Also, depleted OIP5-AS1 hindered tumor growth and metastasis in vivo.	MI0000454	Cancer Manag Res 2020  12, 6707-6717 doi:10.2147/cmar.S237726 PMID:32801903
3023	LncRNA	BLACAT1	miR-149-5p	KIF2A	AGS, MNK-45, MGC803 and SNU-5,GES-1	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot	32801897	Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A.	The expression of BLACAT1 and KIF2A was up-regulated in GC, but miR-149-5p expression was down-regulated. Silencing of BLACAT1 retarded the proliferation, migration and invasion of GC cells in vitro and the growth of tumor xenograft in vivo. Moreover, BLACAT1 acted as the molecular sponge of miR-149-5p to up-regulate KIF2A expression. At last, feedback experiments suggested that BLACAT1 accelerated the proliferation, migration and invasion of GC cells by regulating miR-149-5p/KIF2A axis.	MIMAT0000450	Cancer Manag Res 2020  12, 6629-6640 doi:10.2147/cmar.S258178 PMID:32801897
3024	LncRNA	IGFL2-AS1	miR-1224-5p	SATB1	TSCC cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot	34085359	IGFL2-AS1 facilitates tongue squamous cell carcinoma progression via Wnt/β-catenin signaling pathway	IGFL2-AS1 was significantly up-regulated in TSCC cells and tissues, and IGFL2-AS1 knockdown inhibited cell proliferation, migration, invasion and EMT in TSCC. Moreover, IGFL2-AS1 functioned as a competing endogenous RNA (ceRNA) to sponge miR-1224-5p and thereby modulated SATB homeobox 1 (SATB1) expression. Additionally, SATB1 activated the Wnt/β-catenin signaling pathway in TSCC cells and IGFL2-AS1 regulated the Wnt/β-catenin signaling pathway and TSCC progression via elevating SATB1 expression.	NA	Oral Dis 2021 Jun 4, 10.1111/odi.13935 doi:10.1111/odi.13935 PMID:34085359
3025	LncRNA	CASC9	miR-590-3p	NA	MCF7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;MTT assay	34084220	Long non-coding RNA CASC9/microRNA-590-3p axis participates in lutein-mediated suppression of breast cancer cell proliferation	CASC9 knockdown or overexpression of miR-590-3p inhibited the proliferation of breast cancer cells. Notably, simultaneous transfection with miR-590-3p mimics and CASC9 small interfering RNA increased the potency of lutein in inhibiting the proliferation of breast cancer cells. Taken together, these results suggest that the CASC9/miR-590-3p axis participates in the antiproliferative effects of lutein on breast cancer.	NA	Oncol Lett 2021 Jul 22, 544 doi:10.3892/ol.2021.12805 PMID:34084220
3026	LncRNA	PART1	miR-503-5p	BIRC5	I/R hearts and H/R cardiomyocytes	Myocardial Ischamia Reperfusion Injury Injury 	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;MTT assay	34082009	LncRNA PART1 alleviated myocardial ischemia/reperfusion injury via suppressing miR-503-5p/BIRC5 mediated mitochondrial apoptosis	Forced expression of PART1 remitted cardiac I/RI and H/R cardiomyocyte injury. Silencing of PART1 aggravated apoptosis and mitochondrial damage in cardiomyocytes. We found that PART1 functioned as a competing endogenous RNA of miR-503-5p, which decreased the expression of miR-503-5p. We further established BIRC5 as a target of miR-503-5p. Furthermore, PART1 prevented apoptosis and improved mitochondrial function in myocardial I/RI by targeting miR-503-5p/BIRC5.	NA	Int J Cardiol 2021 Jun 1, 10.1016/j.ijcard.2021.05.044 doi:10.1016/j.ijcard.2021.05.044 PMID:34082009
3027	LncRNA	linc00174	miR-150-5p	VEGFA	retinal microvascular endothelial cells	Diabetic Retinopathy	Homo sapiens (human)	Dual-luciferase reporter assay	34081870	A novel regulatory network of linc00174/miR-150-5p/VEGFA modulates pathological angiogenesis in diabetic retinopathy	Linc00174 was significantly elevated in patients with DR, as well as HG-stimulated HRMECs, of which knockdown repressed HG-induced proliferation, migration and angiogenesis. miR-150-5p was identified as a downstream effector to be involved in linc00174-mediated protective effects. miR-150-5p directly bound to the 3'-UTR of VEGFA. The linc00174/miR-150-5p/VEGFA axis was confirmed in retinal vascular dysfunction.	NA	Can J Physiol Pharmacol 2021 Jun 3, 10.1139/cjpp-2021-0036 doi:10.1139/cjpp-2021-0036 PMID:34081870
3028	LncRNA	lncRNA-EMS	miR-758-3p	WTAP	ECA-109	Esophageal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay	34081626	Hypoxia induces chemoresistance of esophageal cancer cells to cisplatin through regulating the lncRNA-EMS/miR-758-3p/WTAP axis	The targeting relationships between EMS and miR-758-3p, as well as miR-758-3p and WTAP, were verified by luciferase-based reporter assays and multiple quantitative assays after gene overexpression/knockdown. Moreover, we found significant correlations between tumor expressions of these molecules. Notably, higher levels of EMS/WTAP, or lower levels of miR-758-3p in tumors predicted worse survivals of EC patients. Furthermore, in a xenograft mouse model, targeted knockdown of EMS and WTAP in ECA-109 cells markedly attenuated the resistance of tumors to cisplatin treatments. Our study uncovers a critical lncRNA-EMS/miR-758-3p/WTAP axis in regulating hypoxia-mediated drug resistance to cisplatin in EC.	NA	Aging (Albany NY) 2021 Jun 3 13 doi:10.18632/aging.203062 PMID:34081626
3029	LncRNA	lncRNA-EMS	miR-758-3p	WTAP	ECA-109	Esophageal Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay	34081626	Hypoxia induces chemoresistance of esophageal cancer cells to cisplatin through regulating the lncRNA-EMS/miR-758-3p/WTAP axis	The targeting relationships between EMS and miR-758-3p, as well as miR-758-3p and WTAP, were verified by luciferase-based reporter assays and multiple quantitative assays after gene overexpression/knockdown. Moreover, we found significant correlations between tumor expressions of these molecules. Notably, higher levels of EMS/WTAP, or lower levels of miR-758-3p in tumors predicted worse survivals of EC patients. Furthermore, in a xenograft mouse model, targeted knockdown of EMS and WTAP in ECA-109 cells markedly attenuated the resistance of tumors to cisplatin treatments. Our study uncovers a critical lncRNA-EMS/miR-758-3p/WTAP axis in regulating hypoxia-mediated drug resistance to cisplatin in EC.	NA	Aging (Albany NY) 2021 Jun 3 13 doi:10.18632/aging.203062 PMID:34081626
3030	LncRNA	NEAT1	miR-22-3p	Ltb4r1	C57BL/6 mice, HL-1 cell line	Myocardial Infarction	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34081624	Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction	We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was down-regulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.	NA	Aging (Albany NY) 2021 Jun 3 13, 15307-15319 doi:10.18632/aging.203089 PMID:34081624
3031	LncRNA	NEAT1	miR-22-3p	Ltb4r1	C57BL/6 mice, HL-1 cell line	Coronary Heart Disease	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34081624	Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction	We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was down-regulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.	NA	Aging (Albany NY) 2021 Jun 3 13, 15307-15319 doi:10.18632/aging.203089 PMID:34081624
3032	LncRNA	NEAT1	miR-22-3p	Ltb4r1	C57BL/6 mice, HL-1 cell line	Myocardial Infarction	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34081624	Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction	We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was down-regulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.	NA	Aging (Albany NY) 2021 Jun 3 13, 15307-15319 doi:10.18632/aging.203089 PMID:34081624
3033	LncRNA	NEAT1	miR-22-3p	Ltb4r1	C57BL/6 mice, HL-1 cell line	Coronary Heart Disease	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34081624	Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction	We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was down-regulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.	NA	Aging (Albany NY) 2021 Jun 3 13, 15307-15319 doi:10.18632/aging.203089 PMID:34081624
3034	LncRNA	LBX2-AS1	miR-491-5p	S100A11	colorectal cancer tissues and cells, 	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay	34080639	ELK1-mediated upregulation of lncRNA LBX2-AS1 facilitates cell proliferation and invasion via regulating miR-491-5p/S100A11 axis in colorectal cancer	Silencing LBX2-AS1 markedly inhibited proliferative, migratory and invasive abilities of colorectal cancer cells. miR-491-5p expression was downregulated, while S100A11 expression was upregulated in colorectal cancer tissues and cells. Dual-luciferase reporter assays confirmed that LBX2-AS1 could block S100A11 degradation via competitively binding to miR-491-5p. Furthermore, LBX2-AS1 overexpression could notably reverse the inhibitory effect of miR-491-5p on proliferation and invasion of colorectal cancer cells. Taken together, LBX2-AS1 induced by transcription factor ELK1 may facilitate colorectal cancer cell proliferation and invasion via regulation of the miR-491-5p/S100A11 axis. Thus, LBX2-AS1 could be an underlying prognostic and diagnostic marker for colorectal cancer.	NA	Int J Mol Med 2021 Jul 48 doi:10.3892/ijmm.2021.4971 PMID:34080639
3035	LncRNA	SNHG20	miR-335-5p	E2F3	RB tissues and cell lines	Retinoblastoma	Homo sapiens (human)	qRT-PCR	34080033	Long non-coding RNA SNHG20 promotes cell proliferation, migration and invasion in retinoblastoma via the miR-335-5p/E2F3 axis	The impact of SNHG20 status on cell proliferation, survival, migration and invasion was determined using small interfering RNA and a range of established experimental assays. The SNHG20/microRNA (miR)-335-5p/E2F transcription factor 3 (E2F3) signaling axis was further investigated using a dual-luciferase activity reporter system and an RNA pull-down assay combined with bioinformatics analyses. SNHG20 expression was significantly increased in RB tissues and cell lines. Silencing of SNHG20 in RB cells was shown to inhibit cell proliferation, clonogenic survival, migration and invasion. Moreover, mechanistic investigations demonstrated that SNHG20 could enhance the expression of E2F3 by sponging of miR-335-5p. These data suggested that the long non-coding RNA SNHG20 may promote cell proliferation, migration and invasion in RB via the miR-335-5p/E2F3 axis.	NA	Mol Med Rep 2021 Aug 24 doi:10.3892/mmr.2021.12182 PMID:34080033
3036	LncRNA	HCG11	miR-875	SATB2	A549, H1299, H466, H460 and H358	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34080031	Long non-coding RNA HCG11 suppresses the malignant phenotype of non-small cell lung cancer cells by targeting a miR-875/SATB2 axis	Patients with high HCG11 expression had an increased survival rate compared with patients with low HCG11 expression. Further studies have shown that overexpression of HCG11 inhibited NSCLC cell proliferation in vitro and in vivo. Interestingly, it was observed that HCG11 expression was negatively associated with the expression levels of oncogenic microRNA-875 (miR-875) in patient specimens. Specifically, HCG11 served as a sponge of miR-875. Notably, it was determined that special AT-rich sequence-binding protein 2 (SATB2) was a direct target gene of miR-875, and overexpression of miR-875 largely abrogated the effects of HCG11 in NSCLC cells. In conclusion, HCG11 was shown to suppress the malignant properties of NSCLC cells by targeting a miR-875/SATB2 axis, and may therefore be a promising target for the treatment of NSCLC.	NA	Mol Med Rep 2021 Aug 24 doi:10.3892/mmr.2021.12191 PMID:34080031
3037	LncRNA	ILF3-AS1	miR-454-3p	PTEN	human CC tissues and cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34080029	Mechanism underlying long non-coding RNA ILF3-AS1-mediated inhibition of cervical cancer cell proliferation, invasion and migration, and promotion of apoptosis	miR-454-3p expression was negatively correlated with ILF3-AS1, and highly expressed in CC tissues and cells compared with ANTs and NCEs, respectively. PTEN, which was predicted and verified as the target gene for miR-454-3p, was significantly downregulated in CC tissues and cells compared with ANTs and NCEs, respectively. ILF3-AS1 expression was positively correlated with PTEN expression, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression. In conclusion, the present study indicated that ILF3-AS1 inhibited CC cell proliferation and migration, and promoted CC cell apoptosis by inhibiting epithelial-mesenchymal transition, and ILF3-AS1 overexpression partially reversed the inhibitory effect of miR-454-3p on PTEN expression.	NA	Mol Med Rep 2021 Aug 24 doi:10.3892/mmr.2021.12193 PMID:34080029
3038	LncRNA	ANRIL	miR-181a	SIRT1	H9c2 cardiomyocytes	Myocardial Ischamia Reperfusion Injury Injury 	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34080028	Critical role of SIRT1 upregulation on the protective effect of lncRNA ANRIL against hypoxia/reoxygenation injury in H9c2 cardiomyocytes	It was demonstrated that ANRIL upregulated SIRT1 expression by sponging microRNA-181a (miR-181a). In addition, ANRIL overexpression reduced lactate dehydrogenase release and apoptosis of H9c2 cardiomyocytes exposed to H/R, indicating that ANRIL prevented H/R-induced cardiomyocyte injury. Moreover, both miR-181a overexpression and SIRT1 knockdown significantly decreased the protective effects of ANRIL on H/R-induced cardiomyocyte injury, thus demonstrating that SIRT1 upregulation via sponging miR-181a is a critical mechanism that mediates the function of ANRIL. These results provided a novel mechanistic insight into the role of ANRIL in H/R-injured cardiomyocytes and suggested that the ANRIL/miR-181a/SIRT1 axis may be a therapeutic target for reducing MI/R injury.	NA	Mol Med Rep 2021 Aug 24 doi:10.3892/mmr.2021.12186 PMID:34080028
3039	Circular RNA	CircHECTD1	miR-320-5p	SLC2A1	C6, U87 and HEK-293T cells lines	Glioblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079759	CircHECTD1 Regulates Cell Proliferation and Migration by the miR-320-5p/SLC2A1 Axis in Glioblastoma Multiform	CircHECTD1 expression led to the promotion of proliferation and migration of GBM cells. In addition, circHECTD1 acted as a ceRNA to interact with miR-320-5p, which targeted the solute carrier family 2 member 1 (SLC2A1). In vivo experiments also revealed that circHECTD1 promoted tumor growth. Collectively, our findings showed that the circHECTD1-miR-320-5p-SLC2A1 regulatory pathway promoted the progression of GBM, suggesting that circHECTD1 may be a therapeutic target for GBM.	NA	Front Oncol 2021  11, 666391 doi:10.3389/fonc.2021.666391 PMID:34079759
3040	Circular RNA	CircHECTD1	miR-320-5p	SLC2A1	C6, U87 and HEK-293T cells lines	Glioblastoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34079759	CircHECTD1 Regulates Cell Proliferation and Migration by the miR-320-5p/SLC2A1 Axis in Glioblastoma Multiform	CircHECTD1 expression led to the promotion of proliferation and migration of GBM cells. In addition, circHECTD1 acted as a ceRNA to interact with miR-320-5p, which targeted the solute carrier family 2 member 1 (SLC2A1). In vivo experiments also revealed that circHECTD1 promoted tumor growth. Collectively, our findings showed that the circHECTD1-miR-320-5p-SLC2A1 regulatory pathway promoted the progression of GBM, suggesting that circHECTD1 may be a therapeutic target for GBM.	NA	Front Oncol 2021  11, 666391 doi:10.3389/fonc.2021.666391 PMID:34079759
3041	LncRNA	LINC01018	miR-499a-5p	PDCD4	AML tissues and cells	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079594	Long non-coding RNA LINC01018 inhibits the progression of acute myeloid leukemia by targeting miR-499a-5p to regulate PDCD4	 The interaction between PDCD4 and LINC01018 or miR-499a-5p was verified by RNA pull-down, RIP and dual-luciferase reporter assays. LINC01018 and PDCD4 were downregulated in AML, while miR-499a-5p was upregulated. LINC01018-overexpression suppressed AML cell proliferation and induced AML cell apoptosis, while miR-499a-5p transfection reversed these effects. LINC01018 acted as a sponge of miR-499a-5p, and PDCD4 was demonstrated to be targeted by miR-499a-5p. Knockdown of miR-499a-5p suppressed AML cell proliferation and promoted AML cell apoptosis, but silencing PDCD4 abolished this effect. LINC01018 inhibited AML cell growth by modulating PDCD4 through suppression of miR-499a-5p, providing a feasible theoretical basis for the treatment of AML.	NA	Oncol Lett 2021 Jul 22, 541 doi:10.3892/ol.2021.12802 PMID:34079594
3042	LncRNA	HCG11	miR-214-5p	SOX4	colorectal carcinoma cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079592	HLA complex group 11 is involved in colorectal carcinoma cisplatin resistance via the miR-214-5p/SOX4 axis	 HCG11 level was high in colorectal carcinoma tissues, which was associated with poor patient prognosis; however, chemotherapy may prevent the upregulation of HCG11 in colorectal carcinoma. HCG11-knockdown suppressed the proliferation, migration and chemotherapeutic sensitivity of colorectal carcinoma cells, whereas HCG11-overexpression enhanced chemotherapeutic sensitivity. miR-214-5p was revealed to be a target gene, and upon direct interaction, a negative regulator of HCG11 in colorectal carcinoma cells. Inhibition of miR-214-5p reversed the restriction of HCG11 on the malignant activity of colorectal carcinoma cells, while miR-214-5p mediated the chemotherapy-related intracellular EMT pathway. In conclusion, HCG11 is a vital oncogene of colorectal carcinoma involved in mediating the chemotherapeutic resistance of tumors.	NA	Oncol Lett 2021 Jul 22, 535 doi:10.3892/ol.2021.12796 PMID:34079592
3043	LncRNA	LINC00894	miR-429	ZEB1	breast cancer tissues	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079285	LINC00894 Enhances the Progression of Breast Cancer by Sponging miR-429 to Regulate ZEB1 Expression	 High expression of LINC00894 was observed in breast cancer cells, and its overexpression significantly expedited cell proliferation and invasion. Moreover, LINC00894 positively regulated the expression of ZEB1 by competitively binding to miR-429. These results suggest that LINC00894 competitively binds to miR-429 to mediate ZEB1 expression; consequently, it is implicated to play a role in the progression of breast cancer.	NA	Onco Targets Ther 2021  14, 3395-3407 doi:10.2147/ott.S277284 PMID:34079285
3044	LncRNA	GAS5	miR-34b-3p	EPHA4	Brain Microvascular Endothelial Cells	Deprivation	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079264	LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4	OGD/R-induced apoptosis and dysregulation in vascular endocrine system were largely alleviated by the knockdown of GAS5. GAS5 interacted with microRNA-34b-3p (miR-34b-3p), and GAS5 silencing protected bEnd.3 cells from OGD/R-induced injury partly through up-regulating miR-34b-3p. EPH receptor A4 (EPHA4) was a target of miR-34b-3p. GAS5 acted as the molecular sponge of miR-34b-3p to up-regulate EPHA4 in bEnd.3 cells. GAS5 interference protected against OGD/R-induced damage in bEnd.3 cells partly through down-regulating EPHA4.	NA	Neuropsychiatr Dis Treat 2021  17, 1667-1678 doi:10.2147/ndt.S302314 PMID:34079264
3045	LncRNA	GAS5	miR-34b-3p	EPHA4	Brain Microvascular Endothelial Cells	Reperfusion Injury	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079264	LncRNA GAS5 Silencing Attenuates Oxygen-Glucose Deprivation/Reperfusion-Induced Injury in Brain Microvascular Endothelial Cells via miR-34b-3p-Dependent Regulation of EPHA4	OGD/R-induced apoptosis and dysregulation in vascular endocrine system were largely alleviated by the knockdown of GAS5. GAS5 interacted with microRNA-34b-3p (miR-34b-3p), and GAS5 silencing protected bEnd.3 cells from OGD/R-induced injury partly through up-regulating miR-34b-3p. EPH receptor A4 (EPHA4) was a target of miR-34b-3p. GAS5 acted as the molecular sponge of miR-34b-3p to up-regulate EPHA4 in bEnd.3 cells. GAS5 interference protected against OGD/R-induced damage in bEnd.3 cells partly through down-regulating EPHA4.	NA	Neuropsychiatr Dis Treat 2021  17, 1667-1678 doi:10.2147/ndt.S302314 PMID:34079264
3046	LncRNA	TUG1	miR-29a	PTEN	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079224	Total Glucosides of Paeony Inhibited Autophagy and Improved Acute Kidney Injury Induced by Ischemia-Reperfusion via the lncRNA TUG1/miR-29a/PTEN Axis	TGP decreased the contents of BUN, creatinine, NGAL, Kim-1 and IL-18, and reduced the levels of inflammatory factors. LncRNA TUG1 and PTEN were downregulated, and miR-29a was upregulated in kidney tissues. The binding relationships between lncRNA TUG1 and miR-29a, and miR-29a and PTEN were confirmed. TGP suppressed PTEN expression via the lncRNA TUG1/miR-29a axis. Overexpressing lncRNA TUG1 attenuated the protective effect of TGP on AKI and autophagy in HK-2 cells. TGP improved cell viability and inhibited the autophagy in HR model of HK-2 cells via lncRNA TUG1/miR-29a/PTEN axis.	NA	Drug Des Devel Ther 2021  15, 2229-2242 doi:10.2147/dddt.S286606 PMID:34079224
3047	LncRNA	TUG1	miR-29a	PTEN	HK-2 cells	Acute Kidney Injury	Rattus (rat)	qRT-PCR;luciferase reporter assays;Western blot	34079224	Total Glucosides of Paeony Inhibited Autophagy and Improved Acute Kidney Injury Induced by Ischemia-Reperfusion via the lncRNA TUG1/miR-29a/PTEN Axis	TGP decreased the contents of BUN, creatinine, NGAL, Kim-1 and IL-18, and reduced the levels of inflammatory factors. LncRNA TUG1 and PTEN were downregulated, and miR-29a was upregulated in kidney tissues. The binding relationships between lncRNA TUG1 and miR-29a, and miR-29a and PTEN were confirmed. TGP suppressed PTEN expression via the lncRNA TUG1/miR-29a axis. Overexpressing lncRNA TUG1 attenuated the protective effect of TGP on AKI and autophagy in HK-2 cells. TGP improved cell viability and inhibited the autophagy in HR model of HK-2 cells via lncRNA TUG1/miR-29a/PTEN axis.	NA	Drug Des Devel Ther 2021  15, 2229-2242 doi:10.2147/dddt.S286606 PMID:34079224
3048	LncRNA	Lnc-408	miR-654-5p	LIMK1	MCF-7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079084	Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1	Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.	NA	Oncogene 2021 Jun 40, 4198-4213 doi:10.1038/s41388-021-01845-y PMID:34079084
3049	LncRNA	Lnc-408	miR-654-5p	MMP2	MCF-7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079084	Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1	Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.	NA	Oncogene 2021 Jun 40, 4198-4213 doi:10.1038/s41388-021-01845-y PMID:34079084
3050	LncRNA	Lnc-408	miR-654-5p	ITGB1	MCF-7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079084	Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1	Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.	NA	Oncogene 2021 Jun 40, 4198-4213 doi:10.1038/s41388-021-01845-y PMID:34079084
3051	LncRNA	Lnc-408	miR-654-5p	COL1A1	MCF-7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34079084	Long non-coding RNA Lnc-408 promotes invasion and metastasis of breast cancer cell by regulating LIMK1	Lnc-408 can enhance BC invasion and metastasis by regulating the expression of LIMK1. Mechanistically, Lnc-408 serves as a sponge for miR-654-5p to relieve the suppression of miR-654-5p on its target LIMK1. Knockdown or knockout of Lnc-408 in invasive BC cells clearly decreased LIMK1 levels, and ectopic Lnc-408 in MCF-7 cells increased LIMK1 expression to promote cell invasion. Lnc-408-mediated enhancement of LIMK1 plays a key role in cytoskeletal stability and promotes invadopodium formation in BC cells via p-cofilin/F-actin. In addition, the increased LIMK1 also facilitates the expression of MMP2, ITGB1, and COL1A1 by phosphorylating CREB. In conclusion, our findings reveal that Lnc-408 promotes BC invasion and metastasis via the Lnc-408/miR-654-5p/LIMK1 axis, highlighting a novel promising target for the diagnosis and treatment of BC.	NA	Oncogene 2021 Jun 40, 4198-4213 doi:10.1038/s41388-021-01845-y PMID:34079084
3052	LncRNA	LINC_00355	miR-15a-5p	PHF19	GC tissues and cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34078310	LINC_00355 promotes gastric cancer progression by upregulating PHF19 expression through sponging miR-15a-5p	LINC_00355 downregulation markedly increased cleaved caspase 3 and cleaved poly (ADP-ribose) polymerase protein levels, whereas decreased cyclin D1, cyclin E, matrix metalloproteinase (MMP) 9, MMP2, and N-cadherin protein levels in GC cells. However, LINC_00355 overexpression had the opposite effects. It was verified that LINC_00355 upregulated the expression of PHF19 through sponging miR-15a-5p. Furthermore, PHF19 overexpression reversed the effect of LINC_00355 knockdown on GC cell properties, including cell viability, migration, invasion, and apoptosis.	NA	BMC Cancer 2021 Jun 2 21, 657 doi:10.1186/s12885-021-08227-3 PMID:34078310
3053	LncRNA	ZFPM2	miR-515-5p	SOD2	A172, LN229, U87, T98G	Glioma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34077295	SP1-induced lncRNA ZFPM2 antisense RNA 1 (ZFPM2-AS1) aggravates glioma progression via the miR-515-5p/Superoxide dismutase 2 (SOD2) axis	We found that SP1 interacted with ZFPM2-AS1 promoter to transcriptionally activate ZFPM2-AS1 expression. Moreover, ZFPM2-AS1 was identified as a competing endogenous RNA (ceRNA) for miR-515-5p to target SOD2. Rescue assays verified that SOD2 overexpression partially abolished the suppressive impact of ZFPM2-AS1 silencing on glioma cell growth. In conclusion, this study corroborated the regulatory mechanism of SP1/ZFPM2-AS1/miR-515-5p/SOD2 axis in glioma, indicating that targeting ZFPM2-AS1 might be an effective way to treat glioma.	NA	Bioengineered 2021 Dec 12, 2299-2310 doi:10.1080/21655979.2021.1934241 PMID:34077295
3054	LncRNA	NEAT1	miR-335	c-Met	A549 and PC9 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076978	Long noncoding RNA NEAT1 aggravates sorafenib-resistance in non-small cell lung cancer via regulating miRNA-335/c-Met	Sorafenib treatment in A549 cells and PC9 cells attenuated the proliferation and induced apoptosis, which were more pronounced after silencing of NEAT1. MiR-335 was the downstream target of NEAT1, and its level was negatively regulated by NEAT1. Moreover, c-Met was the target gene of MiR -335. Rescue experiments verified the role of NEAT1/ MiR-335/c-Met regulatory loop in reducing the proliferative ability and inducing apoptosis of sorafenib-treated lung cancer cells.	NA	J buon 2021 Mar-Apr 26, 345-352,  PMID:34076978
3055	LncRNA	Linc-KIAA1737-2	miR-27a-3p	TLR4	HK-2 cell	Lps-Induced Hk-2 Cell Apoptosis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076840	Linc-KIAA1737-2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis	We found that Linc-KIAA1737-2 could be upregulated in HK-2 human proximal tubular epithelial cells by LPS treatment, and knock-down of this lncRNA significantly attenuated LPS-induced apoptosis in HK-2 cells, while its overexpression showed opposite effect. MiR-27a-3p was confirmed to interact with Linc-KIAA1737-2 in HK-2 cells by RNA pull-down and dual-luciferase assay. MiR-27a-3p mimic transfection significantly attenuated LPS-induced HK-2 cell apoptosis by downregulating the protein levels of TLR4 and NF-κB, which was overturned by overexpression of Linc-KIAA1737-2. Our results suggested that Linc-KIAA1737-2 could promote LPS-induced apoptosis in HK-2 cells, and presumably sepsis-induced acute kidney injury, by regulating the miR-27a-3p/TLR4/NF-κB axis.	NA	J Bioenerg Biomembr 2021 Jun 2, 10.1007/s10863-021-09897-1 doi:10.1007/s10863-021-09897-1 PMID:34076840
3056	LncRNA	Linc-KIAA1737-2	miR-27a-3p	NFKB	HK-2 cell	Lps-Induced Hk-2 Cell Apoptosis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076840	Linc-KIAA1737-2 promoted LPS-induced HK-2 cell apoptosis by regulating miR-27a-3p/TLR4/NF-κB axis	We found that Linc-KIAA1737-2 could be upregulated in HK-2 human proximal tubular epithelial cells by LPS treatment, and knock-down of this lncRNA significantly attenuated LPS-induced apoptosis in HK-2 cells, while its overexpression showed opposite effect. MiR-27a-3p was confirmed to interact with Linc-KIAA1737-2 in HK-2 cells by RNA pull-down and dual-luciferase assay. MiR-27a-3p mimic transfection significantly attenuated LPS-induced HK-2 cell apoptosis by downregulating the protein levels of TLR4 and NF-κB, which was overturned by overexpression of Linc-KIAA1737-2. Our results suggested that Linc-KIAA1737-2 could promote LPS-induced apoptosis in HK-2 cells, and presumably sepsis-induced acute kidney injury, by regulating the miR-27a-3p/TLR4/NF-κB axis.	NA	J Bioenerg Biomembr 2021 Jun 2, 10.1007/s10863-021-09897-1 doi:10.1007/s10863-021-09897-1 PMID:34076840
3057	LncRNA	NEAT1	miR-224-5p	IL-33	mouse bone marrow mononuclear cells	Macrophage M2A Polarization	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076838	The Long Non-coding RNA NEAT1/miR-224-5p/IL-33 Axis Modulates Macrophage M2a Polarization and A1 Astrocyte Activation	Long non-coding RNA NEAT1 and IL-33 expression levels were significantly upregulated in M2a macrophages; NEAT1 knockdown in M2a macrophages markedly reduced the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages. NEAT1 acted as a competing endogenous RNA (ceRNA) to regulate IL-33 expression by sponging miR-224-5p in M2a macrophages; NEAT1 knockdown upregulated miR-224-5p expression, while miR-224-5p inhibition increased the protein content and concentration of IL-33. miR-224-5p inhibition exerted the opposite effects on the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages compared to NEAT1 knockdown; the effects of NEAT1 knockdown were significantly reversed by miR-224-5p inhibition. M2a macrophage conditioned medium (CM) significantly suppressed the activation of A1 astrocytes. NEAT1 knockdown M2a macrophage CM led to enhanced A1 astrocyte activation while miR-224-5p-silenced M2a macrophage CM led to a blockade of A1 astrocyte activation; the effects of NEAT1 knockdown M2a macrophage CM on A1 astrocyte activation were significantly reversed by miR-224-5p inhibition in M2a macrophages. The NEAT1/miR-224-5p/IL-33 axis modulates macrophage M2a polarization, therefore affecting A1 astrocyte activation.	NA	Mol Neurobiol 2021 Jun 2, 10.1007/s12035-021-02405-x doi:10.1007/s12035-021-02405-x PMID:34076838
3058	LncRNA	NEAT1	miR-224-5p	IL-33	mouse bone marrow mononuclear cells	A1 Astrocyte Activation	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076838	The Long Non-coding RNA NEAT1/miR-224-5p/IL-33 Axis Modulates Macrophage M2a Polarization and A1 Astrocyte Activation	Long non-coding RNA NEAT1 and IL-33 expression levels were significantly upregulated in M2a macrophages; NEAT1 knockdown in M2a macrophages markedly reduced the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages. NEAT1 acted as a competing endogenous RNA (ceRNA) to regulate IL-33 expression by sponging miR-224-5p in M2a macrophages; NEAT1 knockdown upregulated miR-224-5p expression, while miR-224-5p inhibition increased the protein content and concentration of IL-33. miR-224-5p inhibition exerted the opposite effects on the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages compared to NEAT1 knockdown; the effects of NEAT1 knockdown were significantly reversed by miR-224-5p inhibition. M2a macrophage conditioned medium (CM) significantly suppressed the activation of A1 astrocytes. NEAT1 knockdown M2a macrophage CM led to enhanced A1 astrocyte activation while miR-224-5p-silenced M2a macrophage CM led to a blockade of A1 astrocyte activation; the effects of NEAT1 knockdown M2a macrophage CM on A1 astrocyte activation were significantly reversed by miR-224-5p inhibition in M2a macrophages. The NEAT1/miR-224-5p/IL-33 axis modulates macrophage M2a polarization, therefore affecting A1 astrocyte activation.	NA	Mol Neurobiol 2021 Jun 2, 10.1007/s12035-021-02405-x doi:10.1007/s12035-021-02405-x PMID:34076838
3059	LncRNA	NEAT1	miR-224-5p	IL-33	mouse bone marrow mononuclear cells	Macrophage M2A Polarization	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076838	The Long Non-coding RNA NEAT1/miR-224-5p/IL-33 Axis Modulates Macrophage M2a Polarization and A1 Astrocyte Activation	Long non-coding RNA NEAT1 and IL-33 expression levels were significantly upregulated in M2a macrophages; NEAT1 knockdown in M2a macrophages markedly reduced the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages. NEAT1 acted as a competing endogenous RNA (ceRNA) to regulate IL-33 expression by sponging miR-224-5p in M2a macrophages; NEAT1 knockdown upregulated miR-224-5p expression, while miR-224-5p inhibition increased the protein content and concentration of IL-33. miR-224-5p inhibition exerted the opposite effects on the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages compared to NEAT1 knockdown; the effects of NEAT1 knockdown were significantly reversed by miR-224-5p inhibition. M2a macrophage conditioned medium (CM) significantly suppressed the activation of A1 astrocytes. NEAT1 knockdown M2a macrophage CM led to enhanced A1 astrocyte activation while miR-224-5p-silenced M2a macrophage CM led to a blockade of A1 astrocyte activation; the effects of NEAT1 knockdown M2a macrophage CM on A1 astrocyte activation were significantly reversed by miR-224-5p inhibition in M2a macrophages. The NEAT1/miR-224-5p/IL-33 axis modulates macrophage M2a polarization, therefore affecting A1 astrocyte activation.	NA	Mol Neurobiol 2021 Jun 2, 10.1007/s12035-021-02405-x doi:10.1007/s12035-021-02405-x PMID:34076838
3060	LncRNA	NEAT1	miR-224-5p	IL-33	mouse bone marrow mononuclear cells	A1 Astrocyte Activation	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34076838	The Long Non-coding RNA NEAT1/miR-224-5p/IL-33 Axis Modulates Macrophage M2a Polarization and A1 Astrocyte Activation	Long non-coding RNA NEAT1 and IL-33 expression levels were significantly upregulated in M2a macrophages; NEAT1 knockdown in M2a macrophages markedly reduced the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages. NEAT1 acted as a competing endogenous RNA (ceRNA) to regulate IL-33 expression by sponging miR-224-5p in M2a macrophages; NEAT1 knockdown upregulated miR-224-5p expression, while miR-224-5p inhibition increased the protein content and concentration of IL-33. miR-224-5p inhibition exerted the opposite effects on the protein levels of IL-33 and M2a markers, IL-4 and IL-13 concentrations, and the bacterial killing capacity of M2a macrophages compared to NEAT1 knockdown; the effects of NEAT1 knockdown were significantly reversed by miR-224-5p inhibition. M2a macrophage conditioned medium (CM) significantly suppressed the activation of A1 astrocytes. NEAT1 knockdown M2a macrophage CM led to enhanced A1 astrocyte activation while miR-224-5p-silenced M2a macrophage CM led to a blockade of A1 astrocyte activation; the effects of NEAT1 knockdown M2a macrophage CM on A1 astrocyte activation were significantly reversed by miR-224-5p inhibition in M2a macrophages. The NEAT1/miR-224-5p/IL-33 axis modulates macrophage M2a polarization, therefore affecting A1 astrocyte activation.	NA	Mol Neurobiol 2021 Jun 2, 10.1007/s12035-021-02405-x doi:10.1007/s12035-021-02405-x PMID:34076838
3061	LncRNA	HCG11	miR-942-5p	BRMS1	AGS and HGC-27	Gastric Cancer	Homo sapiens (human)	qPCR,RNAi,Luciferase reporter assay,MTT assay etc.	34054958	Long Noncoding RNA HCG11 Acts as a Tumor Suppressor in Gastric Cancer by Regulating miR-942-5p/BRMS1 Axis	The invasion and migration abilities of GC cells were evaluated by Transwell assays. The binding sites between miR-942-5p and HCG11/BRMS1 were confirmed by dual-luciferase reporter assays. Results showed that LncRNA HCG11 was downregulated in GC cells. Functionally, overexpression of HCG11 inhibited GC cell proliferation, migration, and invasion. In addition, lncRNA HCG11 was found to act as a molecular sponge of miR-942-5p. Furthermore, miR-942-5p promoted GC progression by suppressing lncRNA HCG11 expression. Besides that, BRMS1 was confirmed as a direct target of miR-942-5p. More importantly, breast cancer metastasis suppressor 1 (BRMS1) inhibited GC progression by upregulating lncRNA HCG11 and downregulating miR-942-5p. 	NA	J Oncol 2021  2021, 9961189 doi:10.1155/2021/9961189 PMID:34054958
3062	LncRNA	MSC-AS1	miR-325	TRIM14	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34054957	LncRNA MSC-AS1 Promotes Colorectal Cancer Progression by Regulating miR-325/TRIM14 Axis	We found that MSC-AS1 and TRIM14 were upregulated in CRC tissues, while miR-325 was downregulated in CRC tissues. Functional experiments demonstrated that MSC-AS1 knockdown inhibited cell proliferation, migration, and invasion abilities in CRC cells. Additionally, miR-325 was proved to be a target miRNA of MSC-AS1, and TRIM14 might be a downstream gene of miR-325. Besides that, MSC-AS1 counteracted the inhibitory effect of miR-325 on the cell progression and TRIM14 expression.	NA	J Oncol 2021  2021, 9954214 doi:10.1155/2021/9954214 PMID:34054957
3063	LncRNA	GAS5	miR-93	PTEN	spinal cord injury mice model	Spinal Cord Injury	Homo sapiens (human)	qRT-PCR;Western blot	34054430	Silencing of Long Noncoding RNA Growth Arrest-Specific 5 Alleviates Neuronal Cell Apoptosis and Inflammatory Responses Through Sponging microRNA-93 to Repress PTEN Expression in Spinal Cord Injury	QRT-PCR demonstrated that GAS5 was significantly upregulated in both the SCI mice and hypoxic cellular models. GAS5 knockdown suppressed neuron cell apoptosis and inflammatory response in the SCI mice model. Further studies have indicated that GAS5 functions as a competing endogenous RNA (ceRNA) by sponging miR-93 in neuronal cells. In addition, PTEN was a target of miR-93, and GAS5 knockdown exhibited its anti-apoptotic and anti-inflammatory effects through the miR-93/PTEN axis. These findings suggest that the GAS5/miR-93/PTEN axis may be a promising therapeutic target for SCI.	NA	Front Cell Neurosci 2021  15, 646788 doi:10.3389/fncel.2021.646788 PMID:34054430
3064	LncRNA	GAS5	miR-93	PTEN	spinal cord injury mice model	Spinal Cord Injury	Mus musculus (mouse)	qRT-PCR;Western blot	34054430	Silencing of Long Noncoding RNA Growth Arrest-Specific 5 Alleviates Neuronal Cell Apoptosis and Inflammatory Responses Through Sponging microRNA-93 to Repress PTEN Expression in Spinal Cord Injury	QRT-PCR demonstrated that GAS5 was significantly upregulated in both the SCI mice and hypoxic cellular models. GAS5 knockdown suppressed neuron cell apoptosis and inflammatory response in the SCI mice model. Further studies have indicated that GAS5 functions as a competing endogenous RNA (ceRNA) by sponging miR-93 in neuronal cells. In addition, PTEN was a target of miR-93, and GAS5 knockdown exhibited its anti-apoptotic and anti-inflammatory effects through the miR-93/PTEN axis. These findings suggest that the GAS5/miR-93/PTEN axis may be a promising therapeutic target for SCI.	NA	Front Cell Neurosci 2021  15, 646788 doi:10.3389/fncel.2021.646788 PMID:34054430
3065	LncRNA	ILF3-AS1	miR-628-5p	MEIS2	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot; RIP assays	34053876	LncRNA ILF3-AS1 promotes cell migration, invasion and EMT process in hepatocellular carcinoma via the miR-628-5p/MEIS2 axis to activate the Notch pathway	The levels of proteins associated with epithelial-mesenchymal transition (EMT) process and the Notch pathway were detected by western blot analysis. Luciferase reporter, RNA pull down and RIP assays were used to investigate the relationship between ILF3-AS1 and downstream target genes. ILF3-AS1 competed with meis homeobox 2 (MEIS2) for miR-628-5p in hepatocellular carcinoma cells. ILF3-AS1 elevated the levels of key proteins on the Notch pathway. Rescue assays demonstrated that MEIS2 reversed the antitumor effects of silenced ILF3-AS1 on hepatocellular carcinoma. In vivo assays demonstrated that ILF3-AS1 silencing inhibited the hepatocellular carcinoma tumor growth.	NA	Dig Liver Dis 2021 May 27, 10.1016/j.dld.2021.04.036 doi:10.1016/j.dld.2021.04.036 PMID:34053876
3066	LncRNA	UCA1	miR-122-5p	SOX2	Cervical cancer stem cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	34053467	Exosomal lncRNA UCA1 modulates cervical cancer stem cell self-renewal and differentiation through microRNA-122-5p/SOX2 axis	Up-regulated UCA1 and SOX2 and down-regulated miR-122-5p were found in CaSki-Exo. Exosomes promoted invasion, migration, proliferation and restrained apoptosis of CD133+CaSki cells. Silencing UCA1 or up-regulating miR-122-5p degraded SOX2 expression, and reduced invasion, migration and proliferation of CD133+CaSki cells while advanced apoptosis and suppressed the tumor volume and weight in nude mice.	NA	J Transl Med 2021 May 30 19, 229 doi:10.1186/s12967-021-02872-9 PMID:34053467
3067	LncRNA	PCA3	miR-132-3p	SREBP1	LNCaP cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	34052307	LncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling	PCA3 was substantially upregulated in LNCaP cells in response to long-term antimony exposure. Functional studies indicated that abnormal PCA3 expression modulated antimony-induced proliferation and cellular triglyceride and cholesterol levels. In addition, PCA3 levels were found to be inversely correlated with MIR-132-3 P levels by acting as a decoy for MIR-132-3P. Besides, SREBP1 directly interacted with MIR-132-3 P to increase cell growth and disrupt lipid metabolism by targeting its 3'UTR regions. Taken together, our results revealed that lncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.	NA	Toxicol Lett 2021 Sep 15 348, 50-58 doi:10.1016/j.toxlet.2021.05.006 PMID:34052307
3068	LncRNA	WDFY3-AS2	miR-139-5p	SDC4	A2780-DDP	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34051810	LncRNA WDFY3-AS2 promotes cisplatin resistance and the cancer stem cell in ovarian cancer by regulating hsa-miR-139-5p/SDC4 axis	WDFY3-AS2 was highly expressed in OC A2780-DDP cells, and silencing WDFY3-AS2 significantly inhibited proliferation, migration and invasion but increased apoptosis in OC A2780-DDP cells. Additionally, WDFY3-AS2 significantly promoted the A2780-DDP cells tumorspheres. WDFY3-AS2 was predicted to impact OC by sponging miR-139-5p and regulating SDC4. The xenografts inoculated with A2780-DDP cells additionally confirmed that tumor growth in vivo was reduced by si-WDFY3-AS2 transfection. MiR-139-5p inhibitor or SDC4 overexpression could restore the suppressive influence of silenced WDFY3-AS2 on tumor growth.	NA	Cancer Cell Int 2021 May 29 21, 284 doi:10.1186/s12935-021-01993-x PMID:34051810
3069	LncRNA	PART1	miR-937-5p	MYO5A	breast cancer stem cells	Breast Cancer	Homo sapiens (human)	RT-PCR;Dual-luciferase reporter assay;Western blot;	34072264	LncRNA PART1 Promotes Proliferation and Migration, Is Associated with Cancer Stem Cells, and Alters the miRNA Landscape in Triple-Negative Breast Cancer	The altered miRNA landscape induced by PART1 explains most of the protein-coding gene regulation changes (e.g., MYO5A) induced by PART1 in TNBC.	NA	Cancers (Basel) 2021 May 27 13 doi:10.3390/cancers13112644 PMID:34072264
3070	LncRNA	HLA-F-AS1	miR-17-5p	CCND1	cSCC	Cutaneous Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34068010	Identifying an lncRNA-Related ceRNA Network to Reveal Novel Targets for a Cutaneous Squamous Cell Carcinoma	lncRNA HLA-F-AS1 and three mRNAs named AGO4, E2F1 and CCND1 were validated with the same expression patterns. We speculate that lncRNA HLA-F-AS1 may sponge miR-17-5p or miR-20b-5p to regulate the expression of CCND1 and E2F1 in the cSCC. The present study may provide potential diagnostic and therapeutic targets for cSCC patients.	NA	Biology (Basel) 2021 May 13 10 doi:10.3390/biology10050432 PMID:34068010
3071	LncRNA	HLA-F-AS1	miR-20b-5p	E2F1	cSCC	Cutaneous Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34068010	Identifying an lncRNA-Related ceRNA Network to Reveal Novel Targets for a Cutaneous Squamous Cell Carcinoma	lncRNA HLA-F-AS1 and three mRNAs named AGO4, E2F1 and CCND1 were validated with the same expression patterns. We speculate that lncRNA HLA-F-AS1 may sponge miR-17-5p or miR-20b-5p to regulate the expression of CCND1 and E2F1 in the cSCC. The present study may provide potential diagnostic and therapeutic targets for cSCC patients.	NA	Biology (Basel) 2021 May 13 10 doi:10.3390/biology10050432 PMID:34068010
3072	LncRNA	LINC00152	miR-103a	NA	RAFLS	Rheumatoid Arthritis	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34061447	LncRNA linc00152/NF-κB feedback loop promotes fibroblast-like synovial cells inflammation in rheumatoid arthritis via regulating miR-103a/TAK1 axis and YY1 expression	Our data suggested that the linc00152/NF-κB feedback loop promotes RAFLS inflammation via regulating miR-103a/TAK1 axis and YY1 expression.	NA	Immun Inflamm Dis 2021 Jun 1, 10.1002/iid3.417 doi:10.1002/iid3.417 PMID:34061447
3073	LncRNA	HILAR	miR-613	CXCR4	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3074	LncRNA	HILAR	miR-206	CXCR4	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3075	LncRNA	HILAR	miR-1-1-3p	CXCR4	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3076	LncRNA	HILAR	miR-613	JAG1	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3077	LncRNA	HILAR	miR-206	JAG1	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3078	LncRNA	HILAR	miR-1-1-3p	JAG1	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3079	LncRNA	HILAR	miR-613	Notch	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3080	LncRNA	HILAR	miR-206	Notch	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3081	LncRNA	HILAR	miR-1-1-3p	Notch	renal cancer cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;Chromatin immunoprecipitation;Western blot	34058384	Hypoxia-induced lncHILAR promotes renal cancer cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 signaling pathway	Knockdown of lncHILAR inhibited cell invasion and migration while overexpression of lncHILAR conversely facilitated cell invasion and migration of RCC cells. Notably, hypoxic RCC cells secreted exosomes packaged with lncHILAR which were taken up by normoxic RCC cells and then drove normoxic cell invasion. Mechanistically, hypoxia-induced-lncHILAR elevated RCC invasion and metastasis by acting as a competing endogenous (ce)RNA for miR-613/206/1-1-3p, which led to the upregulation of Jagged-1 and C-X-C Motif Chemokine Receptor 4 (CXCR4). Activation of the of Jagged-1/Notch/CXCR4 axis induced RCC metastasis. Hypoxia-induced lncHILAR promotes RCC cell invasion and metastasis via ceRNA for the miR-613/206/1-1-3p/Jagged-1/Notch/CXCR4 axis. The novel lncHILAR may thus serve as a potential biomarker and therapeutic target in RCC.	NA	Mol Ther 2021 May 28, 10.1016/j.ymthe.2021.05.020 doi:10.1016/j.ymthe.2021.05.020 PMID:34058384
3082	LncRNA	PITPNA-AS1	miR-448	ROCK1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assay;Western blot;	34055841	LncRNA PITPNA-AS1 as a Potential Diagnostic Marker and Therapeutic Target Promotes Hepatocellular Carcinoma Progression via Modulating miR-448/ROCK1 Axis	The newly identified PITPNA-AS/miR-448/ROCK1 axis promoted the oncogenicity of HCC cells. This novel axis is likely to be a promising HCC therapeutic aim.	NA	Front Med (Lausanne) 2021  8, 668787 doi:10.3389/fmed.2021.668787 PMID:34055841
3083	Circular RNA	CircADD2	miR-149-5p	AKT2	bone marrow cells,Jurkat,6T-CEM,Nalm-6,293T	Childhood Acute Lymphoblastic Leukemia	Homo sapiens (human)	qRT-PCR;Dual-luciferase reporter assay;Western blot;	34055775	Mechanism of circADD2 as ceRNA in Childhood Acute Lymphoblastic Leukemia	circADD2, as a tumor suppressor in ALL, can sponge miR-149-5p, and may serve as a potential biomarker for the diagnosis or treatment of ALL.	NA	Front Cell Dev Biol 2021  9, 639910 doi:10.3389/fcell.2021.639910 PMID:34055775
3084	LncRNA	SNHG1	miR-493-5p	ATG14	bladder cancer cells and tumor tissues	Bladder Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;MTT assay;Cell Invasion Assay;Western blot	34055628	Long Noncoding RNA SNHG1 Activates Autophagy and Promotes Cell Invasion in Bladder Cancer	SNHG1 plays an oncogenic role by acting as a sponge of miR-493-5p or as its ceRNA. Upregulation of SNHG1 promotes proliferation, invasion, and autophagy of bladder cancer cells through the miR-493-5p/ATG14/autophagy pathway. 	NA	Front Oncol 2021  11, 660551 doi:10.3389/fonc.2021.660551 PMID:34055628
3085	LncRNA	SLC25A25-AS1	miR-195-5p	ITGA2	Tumour tissues and matched adjacent healthy tissues	Non-Small Cell Lung Cancer	Homo sapiens (human)	RT-qPCR;luciferase reporter assays;Western blot;RIP	34055094	Long non-coding RNA SLC25A25-AS1 exhibits oncogenic roles in non-small cell lung cancer by regulating the microRNA-195-5p/ITGA2 axis	 By controlling the miR-195-5p/ITGA2 axis, SLC25A25-AS1 served tumour-promoting roles in NSCLC cells. 	NA	Oncol Lett 2021 Jul 22, 529 doi:10.3892/ol.2021.12790 PMID:34055094
3086	LncRNA	Rian	miR-421	NA	MLE-12 cells	Bronchopulmonary Dysplasia	Homo sapiens (human)	RT-PCR;Dual-luciferase reporter assay;MTT assay;Western blot;	34055080	Long non-coding RNA Rian protects against experimental bronchopulmonary dysplasia by sponging miR-421	All of these effects of Rian were markedly reversed by miR-421 mimics. 	NA	Exp Ther Med 2021 Jul 22, 781 doi:10.3892/etm.2021.10213 PMID:34055080
3087	LncRNA	Rian	miR-421	NA	MLE-12 cells	Bronchopulmonary Dysplasia	Mus musculus (mouse)	RT-PCR;Dual-luciferase reporter assay;MTT assay;Western blot;	34055080	Long non-coding RNA Rian protects against experimental bronchopulmonary dysplasia by sponging miR-421	All of these effects of Rian were markedly reversed by miR-421 mimics. 	NA	Exp Ther Med 2021 Jul 22, 781 doi:10.3892/etm.2021.10213 PMID:34055080
3088	LncRNA	OIP5-AS1	miR-128-3p	SLC7A11	prostate cancer cell lines (PC3 and DU145)	Prostate Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34051661	LncRNA OIP5-AS1 inhibits ferroptosis in prostate cancer with long-term cadmium exposure through miR-128-3p/SLC7A11 signaling	Mechanistically, we demonstrated that OIP5-AS1 served as an endogenous sponge of miR-128-3p to regulate the expression of SLC7A11, a surrogate marker of ferroptosis. Moreover, miR-128-3p decreased cell viability by enhancing ferroptosis. Taken together, our data indicate that lncRNA OIP5-AS1 promotes PCa progression and ferroptosis resistance through miR-128-3p/SLC7A11 signaling.	NA	Ecotoxicol Environ Saf 2021 Sep 1 220, 112376 doi:10.1016/j.ecoenv.2021.112376 PMID:34051661
3089	LncRNA	HOXA11-AS	miR-3619-5p	SALL4	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot	34050851	Long noncoding HOXA11-AS knockdown suppresses the progression of non-small cell lung cancer by regulating miR-3619-5p/SALL4 axis	HOXA11-AS and SALL4 were upregulated while miR-3619-5p was downregulated in NSCLC tissues and cells. HOXA11-AS knockdown suppressed cell proliferation, migration, invasion, and glycolysis but promoted apoptosis in NSCLC cells. Moreover, miR-3619-5p could directly bind to HOXA11-AS and its inhibition attenuated the inhibitory effect of HOXA11-AS knockdown on progression of NSCLC cells. Furthermore, SALL4 was a direct target of miR-3619-5p and its overexpression reversed the anti-tumor role of miR-3619-5p in NSCLC cells. Besides, HOXA11-AS modulated SALL4 expression via sponging miR-3619-5p. Additionally, silencing HOXA11-AS inhibited tumor growth though upregulating miR-3619-5p and downregulating SALL4. Collectively, HOXA11-AS knockdown inhibited the progression of NSCLC by regulating miR-3619-5p/SALL4 axis, which might offer a novel avenue for interpreting the mechanism of NSCLC development.	NA	J Mol Histol 2021 May 29, 10.1007/s10735-021-09981-1 doi:10.1007/s10735-021-09981-1 PMID:34050851
3090	LncRNA	Linc00284	miR-27a	c-Met	CRC tissues and colorectal cancer cell lines HCT116 and SW480	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Western blot	34050266	Oncogenic long intervening noncoding RNA Linc00284 promotes c-Met expression by sponging miR-27a in colorectal cancer	Mechanistically, Linc00284 promotes c-Met expression by acting as miR-27a sponge, leading to the activation of downstream signaling pathways, thereby causing malignant phenotypes of CRC cells. Taken together, Linc00284 exhibits oncogenic function and the disturbance of Linc00284/miR-27a/c-Met regulatory axis contributes to CRC progression, providing new insight into the pathogenesis of colorectal cancer. 	NA	Oncogene 2021 Jun 40, 4151-4166 doi:10.1038/s41388-021-01839-w PMID:34050266
3091	LncRNA	Linc00284	miR-27a	c-Met	CRC tissues and colorectal cancer cell lines HCT116 and SW480	Colorectal Cancer	Mus musculus (mouse)	qRT-PCR;Western blot	34050266	Oncogenic long intervening noncoding RNA Linc00284 promotes c-Met expression by sponging miR-27a in colorectal cancer	Mechanistically, Linc00284 promotes c-Met expression by acting as miR-27a sponge, leading to the activation of downstream signaling pathways, thereby causing malignant phenotypes of CRC cells. Taken together, Linc00284 exhibits oncogenic function and the disturbance of Linc00284/miR-27a/c-Met regulatory axis contributes to CRC progression, providing new insight into the pathogenesis of colorectal cancer. 	NA	Oncogene 2021 Jun 40, 4151-4166 doi:10.1038/s41388-021-01839-w PMID:34050266
3092	Circular RNA	hsa_circ_0008234	miR-574-5p	RND3	LUAC cell lines(H1299 and PC9)	Lung Cancer	Homo sapiens (human)	qRT-PCR	34050132	hsa_circ_0008234 inhibits the progression of lung adenocarcinoma by sponging miR-574-5p	In terms of its possible mechanism, circ_0008234 mainly was present in the cytoplasm and competed with miR-574-5p to regulate RND3 (Rho family GTPase 3). Our results revealed that circ_0008234 inhibited the progression of LUAC through a competing endogenous RNA (ceRNA)-based mechanism and provided potential biomarkers and therapeutic targets for LUAC treatment.	NA	Cell Death Discov 2021 May 28 7, 123 doi:10.1038/s41420-021-00512-1 PMID:34050132
3093	LncRNA	DNM3OS	miR-127-5p	GREM2	mesenchymal stem cells	NA	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34049478	LncRNA DNM3OS regulates GREM2 via miR-127-5p to suppress early chondrogenic differentiation of rat mesenchymal stem cells under hypoxic conditions	MiR-127-5p levels were upregulated, while DNM3OS and GREM2 levels were downregulated in rMSCs induced to undergo chondrogenic differentiation, and those changes were attenuated by hypoxic conditions (1% O2). Further in vitro experiments revealed that downregulation of miR-127-5p reduced the production of proteoglycans and expression of chondrogenic differentiation markers (COL1A1, COL2A1, SOX9, and ACAN) and osteo/chondrogenic markers (BMP-2, p-SMAD1/2). MiR-127-5p overexpression produced the opposite results in rMSCs induced to undergo chondrogenic differentiation under hypoxic conditions. GREM2 was found to be a direct target of miR-127-5p, which was suppressed in rMSCs undergoing chondrogenic differentiation. Moreover, DNM3OS could directly bind to miR-127-5p and inhibit chondrogenic differentiation of rMSCs via regulating GREM2.	NA	Cell Mol Biol Lett 2021 May 28 26, 22 doi:10.1186/s11658-021-00269-6 PMID:34049478
3094	LncRNA	LINC01116	miR-3141	TGFB1	keloid tissues and fibroblasts	Keloid	Homo sapiens (human)	qRT-PCR;Western blot;luciferase reporter;RNA immunoprecipitation (RIP);RNA pull-down assays	34048784	LINC01116 regulates proliferation, migration, and apoptosis of keloid fibroblasts by the TGF-β1/SMAD3 signaling via targeting miR-3141	Our data showed that LINC01116 targeted miR-3141 by directly binding to miR-3141. LINC01116 was up-regulated and miR-3141 was down-regulated in human keloid tissues and fibroblasts. LINC01116 knockdown or miR-3141 overexpression suppressed keloid fibroblast proliferation, migration, and promoted cell apoptosis. Moreover, miR-3141 was a downstream mediator of LINC01116 function. MiR-3141 regulated the TGF-β1/SMAD3 signaling by directly targeting TGF-β1. Furthermore, TGF-β1 was identified as a direct and functional target of miR-3141. LINC01116 regulated the TGF-β1/SMAD3 signaling through miR-3141. Additionally, LINC01116 knockdown diminished the subcutaneous keloid growth in vivo.	NA	Anal Biochem 2021 Aug 15 627, 114249 doi:10.1016/j.ab.2021.114249 PMID:34048784
3095	LncRNA	LINC01116	miR-3141	SMAD3	keloid tissues and fibroblasts	Keloid	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34048784	LINC01116 regulates proliferation, migration, and apoptosis of keloid fibroblasts by the TGF-β1/SMAD3 signaling via targeting miR-3141	Our data showed that LINC01116 targeted miR-3141 by directly binding to miR-3141. LINC01116 was up-regulated and miR-3141 was down-regulated in human keloid tissues and fibroblasts. LINC01116 knockdown or miR-3141 overexpression suppressed keloid fibroblast proliferation, migration, and promoted cell apoptosis. Moreover, miR-3141 was a downstream mediator of LINC01116 function. MiR-3141 regulated the TGF-β1/SMAD3 signaling by directly targeting TGF-β1. Furthermore, TGF-β1 was identified as a direct and functional target of miR-3141. LINC01116 regulated the TGF-β1/SMAD3 signaling through miR-3141. Additionally, LINC01116 knockdown diminished the subcutaneous keloid growth in vivo.	NA	Anal Biochem 2021 Aug 15 627, 114249 doi:10.1016/j.ab.2021.114249 PMID:34048784
3096	LncRNA	LINC01133	miR-199a-5p	SNAI1	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34047479	LINC01133 promotes hepatocellular carcinoma progression by sponging miR-199a-5p and activating annexin A2	Genomic copy numbers of LINC01133 were increased in HCC, which were positively related with the elevated expression of LINC01133. Increased copy number of LINC01133 predicted the poor prognosis in HCC patients. LINC01133 overexpression in HCC cells promoted proliferation and aggressive phenotypes in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. LINC01133 sponged miR-199a-5p, resulting in enhanced expression of SNAI1, which induced epithelial-to-mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate the ANXA2/STAT3 signaling pathway.	NA	Clin Transl Med 2021 May 11, e409 doi:10.1002/ctm2.409 PMID:34047479
3097	LncRNA	LINC01133	miR-199a-5p	SNAI1	HCC cell lines	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34047479	LINC01133 promotes hepatocellular carcinoma progression by sponging miR-199a-5p and activating annexin A2	Genomic copy numbers of LINC01133 were increased in HCC, which were positively related with the elevated expression of LINC01133. Increased copy number of LINC01133 predicted the poor prognosis in HCC patients. LINC01133 overexpression in HCC cells promoted proliferation and aggressive phenotypes in vitro, and facilitated tumor growth and lung metastasis in vivo, whereas LINC01133 knockdown had the opposite effects. LINC01133 sponged miR-199a-5p, resulting in enhanced expression of SNAI1, which induced epithelial-to-mesenchymal transition (EMT) in HCC cells. In addition, LINC01133 interacted with Annexin A2 (ANXA2) to activate the ANXA2/STAT3 signaling pathway.	NA	Clin Transl Med 2021 May 11, e409 doi:10.1002/ctm2.409 PMID:34047479
3098	LncRNA	TMEM161B-AS1	miR-23a-3p	HIF1AN	ESCC tissues and ESCC cell lines	OEsophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34046994	TMEM161B-AS1 suppresses proliferation, invasion and glycolysis by targeting miR-23a-3p/HIF1AN signal axis in oesophageal squamous cell carcinoma	Mechanistically, TMEM161B-AS1 manipulated HIF1AN expression by competitively sponging miR-23a-3p in ESCC cells. MiR-23a-3p mimic and HIF1AN siRNA partly reversed cell phenotypes mediated by TMEM161B-AS1 in ESCC cells. Collectively, TMEM161B-AS1, miR-23a-3p and HIF1AN may be tightly involved in ESCC development and progression as well as patients' prognosis, and TMEM161B-AS1/miR-23a-3p/HIF1AN signal axis may be a promising target for the treatment of ESCC patients.	NA	J Cell Mol Med 2021 May 27, 10.1111/jcmm.16652 doi:10.1111/jcmm.16652 PMID:34046994
3099	LncRNA	NEAT1	miR-182-5p	WISP1	MH-S cells	Acute Lung Injury	Homo sapiens (human)	luciferase reporter assays;Western blot	34046810	LncRNA NEAT1 Knockdown Alleviates Lps-Induced Acute Lung Injury by Modulation of miR-182-5p/WISP1 Axis	For mechanism analysis, NEAT1 was identified as the sponge for miR-182-5p to positively regulate WISP1 expression. Moreover, NEAT1 knockdown could accelerate cell viability and inhibit cell apoptosis and inflammation in LPS-induced MH-S cells by elevating miR-182-5p and decreasing WISP1 in LPS-exposed MH-S cells. In addition, NEAT1 deficiency blocked the activation of NF-κB pathway caused by LPS in MH-S cells. NEAT1 overexpression restrained cell viability and facilitated cell apoptosis and inflammation in LPS-exposed MH-S cells through miR-182-5p/WISP1 axis.	NA	Biochem Genet 2021 May 27, 10.1007/s10528-021-10081-8 doi:10.1007/s10528-021-10081-8 PMID:34046810
3100	LncRNA	NEAT1	miR-182-5p	WISP1	MH-S cells	Acute Lung Injury	Mus musculus (mouse)	luciferase reporter assays;Western blot	34046810	LncRNA NEAT1 Knockdown Alleviates Lps-Induced Acute Lung Injury by Modulation of miR-182-5p/WISP1 Axis	For mechanism analysis, NEAT1 was identified as the sponge for miR-182-5p to positively regulate WISP1 expression. Moreover, NEAT1 knockdown could accelerate cell viability and inhibit cell apoptosis and inflammation in LPS-induced MH-S cells by elevating miR-182-5p and decreasing WISP1 in LPS-exposed MH-S cells. In addition, NEAT1 deficiency blocked the activation of NF-κB pathway caused by LPS in MH-S cells. NEAT1 overexpression restrained cell viability and facilitated cell apoptosis and inflammation in LPS-exposed MH-S cells through miR-182-5p/WISP1 axis.	NA	Biochem Genet 2021 May 27, 10.1007/s10528-021-10081-8 doi:10.1007/s10528-021-10081-8 PMID:34046810
3101	LncRNA	SNHG16	miR-520a-3p	MAPK1	NPC tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	RT-PCR;luciferase reporter assays;Western blot	34045897	LncRNA SNHG16 Facilitates Nasopharyngeal Carcinoma Progression by Acting as ceRNA to Sponge miR-520a-3p and Upregulate MAPK1 Expression	SNHG16 was overexpressed in NPC tissues and cells. High SNHG16 expression indicated a poor prognosis. SNHG16 knockdown could cause significant inhibition on cell proliferation and metastasis, induce cell apoptosis in NPC cells, and repressed tumor growth and metastasis in vivo. Additionally, SNHG16 could directly bind to miR-520a-3p, thus positively regulating MAPK1 expression. Moreover, functional analysis indicated that miR-520a-3p exerted a tumor-suppressing role in NPC progression. Rescue assays demonstrated that MAPK1 upregulation could abrogate the inhibitory effects on NPC cell proliferation and metastasis, as well as the promoting effects on NPC cell apoptosis caused by SNHG16 knockdown. In conclusion, SNHG16 contributed to the proliferation and metastasis of NPC cells by modulating the miR-520a-3p/MAPK1 axis.	NA	Cancer Manag Res 2021  13, 4103-4114 doi:10.2147/cmar.S305544 PMID:34045897
3102	LncRNA	SNHG16	miR-520a-3p	MAPK1	NPC tissues and cells	Nasopharyngeal Cancer	Mus musculus (mouse)	RT-PCR;luciferase reporter assays;Western blot	34045897	LncRNA SNHG16 Facilitates Nasopharyngeal Carcinoma Progression by Acting as ceRNA to Sponge miR-520a-3p and Upregulate MAPK1 Expression	SNHG16 was overexpressed in NPC tissues and cells. High SNHG16 expression indicated a poor prognosis. SNHG16 knockdown could cause significant inhibition on cell proliferation and metastasis, induce cell apoptosis in NPC cells, and repressed tumor growth and metastasis in vivo. Additionally, SNHG16 could directly bind to miR-520a-3p, thus positively regulating MAPK1 expression. Moreover, functional analysis indicated that miR-520a-3p exerted a tumor-suppressing role in NPC progression. Rescue assays demonstrated that MAPK1 upregulation could abrogate the inhibitory effects on NPC cell proliferation and metastasis, as well as the promoting effects on NPC cell apoptosis caused by SNHG16 knockdown. In conclusion, SNHG16 contributed to the proliferation and metastasis of NPC cells by modulating the miR-520a-3p/MAPK1 axis.	NA	Cancer Manag Res 2021  13, 4103-4114 doi:10.2147/cmar.S305544 PMID:34045897
3103	LncRNA	LINC01158	miR-6734-3p	CENPK	glioma cell lines (U87, SHG44, T98G and U251)	Glioma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34044826	LINC01158 works as an oncogene in glioma via sponging miR-6734-3p to boost CENPK expression	LINC01158 and CENPK were both overexpressed in glioma and a positive regulation of LINC01158 on CENPK was corroborated. LINC01158 served a pro-proliferative and anti-apoptotic part in glioma by sponging miR-6734-3p to augment CENPK.	NA	Cancer Cell Int 2021 May 27 21, 280 doi:10.1186/s12935-021-01931-x PMID:34044826
3104	LncRNA	HCG18	miR-188-5p	FOXC1	OS tissues and cell lines	Pediatric Osteosarcoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34041718	Knockdown of HCG18 Inhibits Cell Viability, Migration and Invasion in Pediatric Osteosarcoma by Targeting miR-188-5p/FOXC1 Axis	HCG18 expression was elevated in OS tissues, and enhanced HCG18 expression was related to metastasis. HCG18 silencing repressed the viability, migration and invasion of OS cells. Moreover, HCG18 interacted with miR-188-5p. MiR-188-5p up-regulation repressed cell viability, invasion and migration in OS cells. FOXC1, a known target of miR-188-5p, was negatively modulated by miR-188-5p. Furthermore, miR-188-5p inhibition or FOXC1 over-expression partially abolished the reduced of cell viability, invasion and migration mediated by HCG18 silencing in OS cell lines. This study revealed that HCG18 knockdown repressed the viability, invasion and migration of OS cells by targeting miR-188-5p and regulating FOXC1 expression. Thus, HCG18/ miR-188-5p/FOX may be a hopeful target for OS therapy.	NA	Mol Biotechnol 2021 May 26, 10.1007/s12033-021-00343-6 doi:10.1007/s12033-021-00343-6 PMID:34041718
3105	LncRNA	NEAT1	miR-320	NPAS2	Cardiac fibroblast	Atrial Fibrosis	Homo sapiens (human)	qRT-PCR;Luciferase Activity Assay;Western blot	34040522	LncRNA Nuclear-Enriched Abundant Transcript 1 Regulates Atrial Fibrosis via the miR-320/NPAS2 Axis in Atrial Fibrillation	We demonstrated that NEAT1 could negatively regulate miR-320 expression by acting as a competitive endogenous RNA (ceRNA). miR-320 directly targeted neuronal per arnt sim domain protein 2 (NPAS2) and suppressed its expression. We observed that NEAT1 exerted its function via the miR-320-NPAS2 axis in cardiac fibroblasts. These findings indicate that NEAT1 exerts a significant effect on atrialfibrosis and that this lncRNA is a new potential molecular target for AF treatment.	NA	Front Pharmacol 2021  12, 647124 doi:10.3389/fphar.2021.647124 PMID:34040522
3106	LncRNA	NEAT1	miR-320	NPAS2	Cardiac fibroblast	Atrial Fibrosis	Mus musculus (mouse)	qRT-PCR;Luciferase Activity Assay;Western blot	34040522	LncRNA Nuclear-Enriched Abundant Transcript 1 Regulates Atrial Fibrosis via the miR-320/NPAS2 Axis in Atrial Fibrillation	 We demonstrated that NEAT1 could negatively regulate miR-320 expression by acting as a competitive endogenous RNA (ceRNA). miR-320 directly targeted neuronal per arnt sim domain protein 2 (NPAS2) and suppressed its expression. We observed that NEAT1 exerted its function via the miR-320-NPAS2 axis in cardiac fibroblasts. These findings indicate that NEAT1 exerts a significant effect on atrialfibrosis and that this lncRNA is a new potential molecular target for AF treatment.	NA	Front Pharmacol 2021  12, 647124 doi:10.3389/fphar.2021.647124 PMID:34040522
3107	LncRNA	LINC01410	miR-545-3p	HK2	NB tissues and cells	Neuroblastoma	Homo sapiens (human)	qRT-PCR;Luciferase Activity Assay;Western blot	34040388	Long Noncoding RNA LINC01410 Suppresses Tumorigenesis and Enhances Radiosensitivity in Neuroblastoma Cells Through Regulating miR-545-3p/HK2 Axis	LINC01410 and HK2 were highly expressed while miR-545-3p was lowly expressed in NB tissues and cells. LINC01410 knockdown inhibited tumorigenesis by repressing cell proliferation and invasion, and increased the radiosensitivity via inhibiting colony formation rates and glycolysis. LINC01410 knockdown also suppressed tumor growth in vivo. Moreover, miR-545-3p could bind to LINC01410 and its downregulation reversed the effects of LINC01410 knockdown on tumorigenesis and radiosensitivity. Additionally, HK2 was a direct target of miR-545-3p and its overexpression attenuated the effects of miR-545-3p restoration on suppression of tumorigenesis and promotion of radiosensitivity. Besides, LINC01410 functioned as a molecular sponge of miR-545-3p to regulate HK2 expression.	NA	Onco Targets Ther 2021  14, 3225-3238 doi:10.2147/ott.S297969 PMID:34040388
3108	LncRNA	ST8SIA6-AS1	miR-145-5p	MAL2	CHOL tissues and cell lines	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR;Luciferase Activity Assay	34040387	LncRNA ST8SIA6-AS1 Promotes Cholangiocarcinoma Progression by Suppressing the miR-145-5p/MAL2 Axis	Findings revealed the enrichment of ST8SIA6-AS1 in CHOL tissues and cell lines. It was also found that ST8SIA6-AS1 facilitated cell growth and migration, but it reduced the apoptosis level of the CHOL cells. The results of experiments showed that ST8SIA6-AS1 sponged miR-145-5p, thereby allowing MAL2 to exert its biological function on CHOL cells.	NA	Onco Targets Ther 2021  14, 3209-3223 doi:10.2147/ott.S299634 PMID:34040387
3109	LncRNA	DLX6-AS1	miR-15a-5p	CXCL17	HCC tissues and cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	RT-PCR;Western blot	34039401	Exosomal DLX6-AS1 from hepatocellular carcinoma cells induces M2 macrophage polarization to promote migration and invasion in hepatocellular carcinoma through microRNA-15a-5p/CXCL17 axis	Promoted DLX6-AS1 and CXCL17 and reduced miR-15a-5p exhibited in HCC. HCC-exo induced M2 macrophage polarization to accelerate migration, invasion and epithelial mesenchymal transition in HCC, which was further enhanced by up-regulated DLX6-AS1 but impaired by silenced DLX6-AS1. Inhibition of miR-15a-5p promoted M2 macrophage polarization to stimulate the invasion and metastasis of HCC while that of CXCL17 had the opposite effects. DLX6-AS1 mediated miR-15a-5p to target CXCL17. DLX6-AS1 from HCC-exo promoted metastasis in the lung by inducing M2 macrophage polarization in vivo.	NA	J Exp Clin Cancer Res 2021 May 26 40, 177 doi:10.1186/s13046-021-01973-z PMID:34039401
3110	LncRNA	TUG1	miR-194	SIRT1	human hepatocytes (WRL-68	Liver Injury	Homo sapiens (human)	qRT-PCR;Western blot	34039367	Dexmedetomidine hydrochloride inhibits hepatocyte apoptosis and inflammation by activating the lncRNA TUG1/miR-194/SIRT1 signaling pathway	DEX notably reversed OGD-induced inflammation and apoptosis in WRL-68 cell. Meanwhile, the effect of OGD on TUG1, SIRT1 and miR-194 expression in WRL-68 cells was reversed by DEX treatment. However, TUG1 knockdown or miR-194 overexpression reversed the function of DEX in OGD-treated WRL-68 cells. Moreover, TUG1 could promote the expression of SIRT1 by sponging miR-194. Furthermore, knockdown of TUG1 promoted OGD-induced cell growth inhibition and inflammatory responses, while miR-194 inhibitor or SIRT1 overexpression partially reversed this phenomenon.	NA	J Inflamm (Lond) 2021 May 26 18, 20 doi:10.1186/s12950-021-00287-3 PMID:34039367
3111	LncRNA	RP11-51O6.1	miR-206	YAP1	CRC tissues	Colorectal Cancer	Homo sapiens (human)	luciferase reporter assays;Western blot	34038520	RP11-51O6.1 sponges miR-206 to accelerate colorectal cancer carcinogenesis and metastasis through upregulating YAP1	We reported that RP11-51O6.1 enhances cell migration and invasion in vitro. Mechanistic studies (Bioinformatics binding site analyses, the Luciferase reporter, Ago2 immunoprecipitation, the RNA pull-down, immunofluorescence colocalization, rescued assays and western blotting) implicated that RP11-51O6.1 could regulate YAP1 expression by competitively sponging miR-206 and blocking its activity in promoting CRC progression. Conclusively, our findings identify a novel RP11-51O6.1/miR-206/YAP1 regulatory axis that participates in CRC progression and development, suggesting RP11-51O6.1 is an exploitable biomarker and appealing therapeutic target in treating CRC.	NA	Carcinogenesis 2021 May 26, 10.1093/carcin/bgab044 doi:10.1093/carcin/bgab044 PMID:34038520
3112	LncRNA	XIST	miR-362	ROCK2	PC12 cells	Cerebral Ischemia	Homo sapiens (human)	RT-PCR;Western blot	34037903	Knockdown of XIST Attenuates Cerebral Ischemia/Reperfusion Injury Through Regulation of miR-362/ROCK2 Axis	In vitro, knockdown of XIST facilitated cell survival, inhibited apoptosis, and alleviated inflammation injury in OGDR PC12 cells. In vivo, inhibition of XIST remarkably reduced the neurological impairments, promoted neuron proliferation, and suppressed apoptosis in MCAO mice. Mechanistically, XIST acted as a competing endogenous RNA of miR-362 to regulate the downstream gene ROCK2. In conclusion, depletion of XIST attenuated I/R-induced neurological impairment and inflammatory response via the miR-362/ROCK2 axis. These findings offer a potential novel strategy for ischemic stroke therapy.	NA	Neurochem Res 2021 May 26, 10.1007/s11064-021-03354-6 doi:10.1007/s11064-021-03354-6 PMID:34037903
3113	LncRNA	XIST	miR-362	ROCK2	PC12 cells	Cerebral Ischemia	Mus musculus (mouse)	RT-PCR;Western blot	34037903	Knockdown of XIST Attenuates Cerebral Ischemia/Reperfusion Injury Through Regulation of miR-362/ROCK2 Axis	In vitro, knockdown of XIST facilitated cell survival, inhibited apoptosis, and alleviated inflammation injury in OGDR PC12 cells. In vivo, inhibition of XIST remarkably reduced the neurological impairments, promoted neuron proliferation, and suppressed apoptosis in MCAO mice. Mechanistically, XIST acted as a competing endogenous RNA of miR-362 to regulate the downstream gene ROCK2. In conclusion, depletion of XIST attenuated I/R-induced neurological impairment and inflammatory response via the miR-362/ROCK2 axis. These findings offer a potential novel strategy for ischemic stroke therapy.	NA	Neurochem Res 2021 May 26, 10.1007/s11064-021-03354-6 doi:10.1007/s11064-021-03354-6 PMID:34037903
3114	LncRNA	XIST	miR-362	ROCK2	PC12 cells	Reperfusion Injury	Homo sapiens (human)	RT-PCR;Western blot	34037903	Knockdown of XIST Attenuates Cerebral Ischemia/Reperfusion Injury Through Regulation of miR-362/ROCK2 Axis	In vitro, knockdown of XIST facilitated cell survival, inhibited apoptosis, and alleviated inflammation injury in OGDR PC12 cells. In vivo, inhibition of XIST remarkably reduced the neurological impairments, promoted neuron proliferation, and suppressed apoptosis in MCAO mice. Mechanistically, XIST acted as a competing endogenous RNA of miR-362 to regulate the downstream gene ROCK2. In conclusion, depletion of XIST attenuated I/R-induced neurological impairment and inflammatory response via the miR-362/ROCK2 axis. These findings offer a potential novel strategy for ischemic stroke therapy.	NA	Neurochem Res 2021 May 26, 10.1007/s11064-021-03354-6 doi:10.1007/s11064-021-03354-6 PMID:34037903
3115	LncRNA	XIST	miR-362	ROCK2	PC12 cells	Reperfusion Injury	Mus musculus (mouse)	RT-PCR;Western blot	34037903	Knockdown of XIST Attenuates Cerebral Ischemia/Reperfusion Injury Through Regulation of miR-362/ROCK2 Axis	In vitro, knockdown of XIST facilitated cell survival, inhibited apoptosis, and alleviated inflammation injury in OGDR PC12 cells. In vivo, inhibition of XIST remarkably reduced the neurological impairments, promoted neuron proliferation, and suppressed apoptosis in MCAO mice. Mechanistically, XIST acted as a competing endogenous RNA of miR-362 to regulate the downstream gene ROCK2. In conclusion, depletion of XIST attenuated I/R-induced neurological impairment and inflammatory response via the miR-362/ROCK2 axis. These findings offer a potential novel strategy for ischemic stroke therapy.	NA	Neurochem Res 2021 May 26, 10.1007/s11064-021-03354-6 doi:10.1007/s11064-021-03354-6 PMID:34037903
3116	LncRNA	PCED1B-AS1	miR-411-3p	HIF1A	PDAC tissues and cells	Pancreatic Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34036383	Long non-coding RNA PCED1B-AS1 promotes pancreatic ductal adenocarcinoma progression by regulating the miR-411-3p/HIF-1α axis	We demonstrated that PCED1B-AS1 was significantly upregulated in PDAC tumor tissues, and its expression was associated with advanced Tumor-Node-Metastasis stage and lymph node metastasis. PCED1B-AS1 knockdown inhibited PDAC cell proliferation, invasion as well as epithelial-mesenchymal transition (EMT) in vitro. Mechanistically, PCED1B-AS1 was shown to target miR-411-3p, resulting in the upregulation of HIF-1α. In conclusion, PCED1B-AS1 expression was upregulated in PDAC tissues and cells, and it participated in promoting the proliferation, invasion and EMT of cancer cells by modulating the miR-411-3p/HIF-1α axis.	NA	Oncol Rep 2021 Jul 46 doi:10.3892/or.2021.8085 PMID:34036383
3117	LncRNA	DUXAP8	miR-9-3p	IGF1R	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34035852	Long non-coding RNA DUXAP8 promotes tumorigenesis by regulating IGF1R via miR-9-3p in hepatocellular carcinoma	miR-9-3p overexpression decreased the protein expression level of IGF1R, and miR-9-3p knockdown enhanced the protein expression level of IGF1R in HCC cells compared with the corresponding control groups. Moreover, compared with the corresponding control groups, DUXAP8 knockdown and miR-9-3p overexpression increased E-cadherin protein expression levels, and decreased Snail, Slug, N-cadherin and vimentin protein expression levels. However, miR-9-3p inhibitor and IGF1R overexpression reversed DUXAP8 knockdown- and miR-9-3p overexpression-induced effects, respectively. In addition, compared with the corresponding control groups, DUXAP8 knockdown and miR-9-3p overexpression suppressed proliferation, migration and invasion, which was reversed by miR-9-3p inhibitor and IGF1R overexpression, respectively. Moreover, miR-9-3p as the target of DUXAP8 and IGF1R as the target of miR-9-3p were verified in HCC cells. lncRNA DUXAP8 contributed to HCC tumorigenesis via the miR-9-3p/IGF1R axis, providing a novel therapeutic approach for HCC diagnosis and treatment.	NA	Exp Ther Med 2021 Jul 22, 755 doi:10.3892/etm.2021.10187 PMID:34035852
3118	LncRNA	LUCAT1	miR-375	YAP1	ccRCC tissues and RCC cell lines	Clear Cell Renal Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34035851	Long non-coding RNA LUCAT1 promotes the progression of clear cell renal cell carcinoma via the microRNA-375/YAP1 axis	The results revealed that LUCAT1 and YAP1 were upregulated and miR-375 was downregulated in ccRCC tissues and cells. LUCAT1 knockdown suppressed cell proliferation, migration and invasion, which were reversed by the inhibition of miR-375. In addition, YAP1 overexpression attenuated the inhibitory effects of miR-375 overexpression on cell proliferation, migration and invasion. Subsequent experiments suggested that LUCAT1 regulated YAP1 expression by sponging miR-375. Therefore, LUCAT1 exerted its role by regulating the miR-375/YAP1 axis in vitro. Moreover, LUCAT1 knockdown suppressed the growth of ccRCC xenograft tumors in vivo. These results collectively revealed that LUCAT1 promoted the proliferation, migration and invasion of ccRCC by the upregulation of YAP1 via sponging miR-375, which may be used as a potential therapeutic target for ccRCC.	NA	Exp Ther Med 2021 Jul 22, 754 doi:10.3892/etm.2021.10186 PMID:34035851
3119	LncRNA	LUCAT1	miR-375	YAP1	ccRCC tissues and RCC cell lines	Clear Cell Renal Cancer	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34035851	Long non-coding RNA LUCAT1 promotes the progression of clear cell renal cell carcinoma via the microRNA-375/YAP1 axis	The results revealed that LUCAT1 and YAP1 were upregulated and miR-375 was downregulated in ccRCC tissues and cells. LUCAT1 knockdown suppressed cell proliferation, migration and invasion, which were reversed by the inhibition of miR-375. In addition, YAP1 overexpression attenuated the inhibitory effects of miR-375 overexpression on cell proliferation, migration and invasion. Subsequent experiments suggested that LUCAT1 regulated YAP1 expression by sponging miR-375. Therefore, LUCAT1 exerted its role by regulating the miR-375/YAP1 axis in vitro. Moreover, LUCAT1 knockdown suppressed the growth of ccRCC xenograft tumors in vivo. These results collectively revealed that LUCAT1 promoted the proliferation, migration and invasion of ccRCC by the upregulation of YAP1 via sponging miR-375, which may be used as a potential therapeutic target for ccRCC.	NA	Exp Ther Med 2021 Jul 22, 754 doi:10.3892/etm.2021.10186 PMID:34035851
3120	LncRNA	MAFG-AS1	miR-339-5p	NFKB1	OC tissues and cells	Ovarian Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34035482	LncRNA MAFG-AS1 promotes the malignant phenotype of ovarian cancer by upregulating NFKB1-dependent IGF1	Further mechanistic investigations revealed that MAFG-AS1 upregulated the IGF1 expression pattern through recruitment of NFKB1, whereas MAFG-AS1 upregulated the NFKB1 expression pattern through binding to miR-339-5p. Thus, MAFG-AS1 overexpression accelerated the EMT, invasion, and migration of OC cells, which could be annulled by silencing of IGF1 or NFKB1. Besides, our in vitro findings were successfully recapitulated in the xenograft mice. These results determined that MAFG-AS1 stimulated the OC malignant progression by upregulating the NFKB1-mediated IGF1 via miR-339-5p, thus highlighting a novel potential therapeutic target against OC.	NA	Cancer Gene Ther 2021 May 25, 10.1038/s41417-021-00306-8 doi:10.1038/s41417-021-00306-8 PMID:34035482
3121	LncRNA	Linc-SCRG1	miR26a	SKP2	SNU-387 and Hep3B cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot	34034770	Correction to: Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2	Correction to: Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2	NA	J Exp Clin Cancer Res 2021 May 25 40, 176 doi:10.1186/s13046-021-01975-x PMID:34034770
3122	LncRNA	SNHG3	miR-515-5p	SUMO2	lung cancer tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Luciferase Assay	34032148	LncRNA SNHG3 Promotes Proliferation and Metastasis of Non-Small-Cell Lung Cancer Cells Through miR-515-5p/SUMO2 Axis	SNHG3 could positively regulate SUMO2 expression by sponging miR-515-5p. In addition, the rescue experiment showed that simultaneous transfection of miR-515-5p or SUMO2 siRNA could reverse the effect of SNHG3 expression on cell proliferation and metastasis. Collectively, our study demonstrates that SNHG3 can act on miR-515-5p in the form of competitive endogenous RNA (ceRNA) to regulate SUMO2 positively and thus affect the proliferation and metastasis of NSCLC cells. Findings in our study support that SNHG3/miR-515-5p/SUMO2 regulatory axis may become a potential therapeutic target for lung cancer.	NA	Technol Cancer Res Treat 2021 Jan-Dec 20, 15330338211019376 doi:10.1177/15330338211019376 PMID:34032148
3123	Circular RNA	hsa_circRNA_102229	miR-152-3p	PFTK1	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34031947	Hsa_circRNA_102229 facilitates the progression of triple-negative breast cancer via regulating the miR-152-3p/PFTK1 pathway	In TNBC tissues and cells, hsa_circ_102229 was remarkably up-regulated. Patients with TNBC presenting high hsa_circ_102229 exhibited poor prognosis. Moreover, hsa_circ_102229 could promote the migration, proliferation and invasion, whereas it inhibited the apoptosis of TNBC cells. Furthermore, hsa_circ_102229 directly targeted miR-152-3p and could regulate the expression of PFTK1 by targeting miR-152-3p. Rescue assays suggested that hsa_circ_102229 may exert its function in TNBC cells by regulating PFTK1. Additionally, knockdown of hsa_circ_102229 slowed down TNBC tumorigenesis and lung metastasis in a tumor xenograft animal model.	NA	J Gene Med 2021 May 24, 10.1002/jgm.3365, e3365 doi:10.1002/jgm.3365 PMID:34031947
3124	LncRNA	LINC00997	miR-574-3p	CUL2	CC tissues and cells	Cervical Cancer	Homo sapiens (human)	RT-qPCR; dual luciferase reporter assays	34031216	LINC00997/miR-574-3p/CUL2 promotes cervical cancer development via the MAPK signaling	Mechanistically, LINC00997 upregulated the expression of cullin 2 (CUL2) by interacting with miR-574-3p. Moreover, western blot analysis was employed to detect the protein levels of MAPK pathway-associated factors in CC cells. LINC00997 activated the MAPK signaling by increasing CUL2 expression, thus promoting malignant phenotypes of CC cells. In conclusion, the LINC00997/miR-574-3p/CUL2 axis contributes to CC cell proliferation, migration, invasion and autophagy via the activation of MAPK signaling.	NA	Mol Cell Biol 2021 May 24, 10.1128/mcb.00059-21 doi:10.1128/mcb.00059-21 PMID:34031216
3125	LncRNA	TUG1	miR-542-3p	TRIB2	CRC tissues and cells (LoVo and HCT116)	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	34030715	Long noncoding RNA TUG1 regulates the progression of colorectal cancer through miR-542-3p/TRIB2 axis and Wnt/β-catenin pathway	TUG1 was increased in CRC tissues and cells (LoVo and HCT116) in contrast with adjacent normal tissues and normal intestinal mucous cells (CCC-HIE-2). Downregulation of TUG1 or TRIB2 suppressed the proliferation, migration, invasion, and induced apoptosis in CRC cells. And knockdown of TUG1 repressed tumor growth in vivo. Besides, overexpression of TRIB2 reversed the effects of TUG1 depletion on the progression of CRC. Meanwhile, TUG1 interacted with miR-542-3p and TRIB2 was a target of miR-542-3p. Furthermore, miR-542-3p knockdown or TRIB2 overexpression partly reversed the suppression effect of TUG1 depletion on the Wnt/β-catenin pathway.	NA	Diagn Pathol 2021 May 24 16, 47 doi:10.1186/s13000-021-01101-7 PMID:34030715
3126	LncRNA	TUG1	miR-542-3p	TRIB2	CRC tissues and cells (LoVo and HCT116)	Colorectal Cancer	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays	34030715	Long noncoding RNA TUG1 regulates the progression of colorectal cancer through miR-542-3p/TRIB2 axis and Wnt/β-catenin pathway	TUG1 was increased in CRC tissues and cells (LoVo and HCT116) in contrast with adjacent normal tissues and normal intestinal mucous cells (CCC-HIE-2). Downregulation of TUG1 or TRIB2 suppressed the proliferation, migration, invasion, and induced apoptosis in CRC cells. And knockdown of TUG1 repressed tumor growth in vivo. Besides, overexpression of TRIB2 reversed the effects of TUG1 depletion on the progression of CRC. Meanwhile, TUG1 interacted with miR-542-3p and TRIB2 was a target of miR-542-3p. Furthermore, miR-542-3p knockdown or TRIB2 overexpression partly reversed the suppression effect of TUG1 depletion on the Wnt/β-catenin pathway.	NA	Diagn Pathol 2021 May 24 16, 47 doi:10.1186/s13000-021-01101-7 PMID:34030715
3127	LncRNA	FOXD2-AS1	miR-331-3p	PIAS3	synovial tissues	Rheumatoid Arthritis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34030529	LncRNA FOXD2-AS1 promotes cell proliferation and invasion of fibroblast-like synoviocytes by regulation of miR-331-3p/PIAS3 pathway in rheumatoid arthritis	 In summary, this study demonstrated that FOXD2-AS1 promoted RA progression via regulating the miR-331-3p/PIAS3 pathway, suggesting that therapeutic strategies based on the FOXD2-AS1/miR-331-3p/PIAS3 axis may represent a promising treatment approach for RA patients.	NA	Autoimmunity 2021 May 25, 10.1080/08916934.2021.1919879, 1-10 doi:10.1080/08916934.2021.1919879 PMID:34030529
3128	LncRNA	MIR155HG	miR-194-5p	MEF2A	murine cardiac muscle cell line (HL-1) and macrophage cell line (RAW 264.7)	Sepsis	Homo sapiens (human)	RT-qPCR; dual luciferase reporter assays	34030477	lncRNA MIR155HG Accelerates the Progression of Sepsis via Upregulating MEF2A by Sponging miR-194-5p	 In this study, we demonstrated that MIR155HG expression was significantly increased in sepsis blood samples, RAW 264.7, and HL-1 cells treated with LPS. Silencing of MIR155HG promoted cell viability and obstructed cell apoptosis and inflammation of RAW 264.7 and HL-1 cells treated with LPS. MiR-194-5p depletion abrogated cell viability promotion and suppressive effect on cell apoptosis and inflammation caused by MIR155HG knockdown. In addition, MIR155HG upregulated MEF2A through interaction with miR-194-5p. Finally, rescue assays indicated that MEF2A overexpression abolished the inhibitory effect on sepsis progression induced by MIR155HG deletion. In conclusion, MIR155HG promotes sepsis progression in an in vitro sepsis model by modulating the miR-194-5p/MEF2A axis. This discovery provides a promising biomarker for sepsis therapy.	NA	DNA Cell Biol 2021 Jun 40, 811-820 doi:10.1089/dna.2021.0038 PMID:34030477
3129	Circular RNA	hsa_circ_0000520	miR-556-5p	NLRP3	human nasal epithelial cell line	Allergic Rhinitis	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34028600	Targeting a novel hsa_circ_0000520/miR-556-5p/NLRP3 pathway-mediated cell pyroptosis and inflammation attenuates ovalbumin (OVA)-induced allergic rhinitis (AR) in mice models	Mechanistically, miR-556-5p targeted both hsa_circ_0000520 and 3' untranslated region (3'UTR) of NLRP3, and knock-down of hsa_circ_0000520 inactivated NLRP3-mediated epithelium pyroptosis through miR-556-5p in a ceRNA-dependent manner. Furthermore, we proved that both hsa_circ_0000520 ablation and miR-556-5p overexpression suppressed NLRP3-mediated cell pyroptosis to attenuate AR in mice models.	NA	Inflamm Res 2021 Jun 70, 719-729 doi:10.1007/s00011-021-01472-z PMID:34028600
3130	Circular RNA	hsa_circ_0000520	miR-556-5p	NLRP3	human nasal epithelial cell line	Allergic Rhinitis	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34028600	Targeting a novel hsa_circ_0000520/miR-556-5p/NLRP3 pathway-mediated cell pyroptosis and inflammation attenuates ovalbumin (OVA)-induced allergic rhinitis (AR) in mice models	Mechanistically, miR-556-5p targeted both hsa_circ_0000520 and 3' untranslated region (3'UTR) of NLRP3, and knock-down of hsa_circ_0000520 inactivated NLRP3-mediated epithelium pyroptosis through miR-556-5p in a ceRNA-dependent manner. Furthermore, we proved that both hsa_circ_0000520 ablation and miR-556-5p overexpression suppressed NLRP3-mediated cell pyroptosis to attenuate AR in mice models.	NA	Inflamm Res 2021 Jun 70, 719-729 doi:10.1007/s00011-021-01472-z PMID:34028600
3131	LncRNA	SNHG6	miR-125b-5p	BMPR1B	breast cancer cell lines	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34026654	LncRNA SNHG6/miR-125b-5p/BMPR1B Axis: A New Therapeutic Target for Triple-Negative Breast Cancer	Decreasing lncRNA SNHG6 expression in TNBC cells upregulated miR-125b-5p expression. Another side, inhibiting miR-125b-5p upregulated BMPR1B expression in these cells. Moreover, knocking down lncRNA SNHG6 downregulated BMPR1B expression in TNBC cells, and the finding was rescued in cells which were exposed to miR-125b-5p inhibitor. Downregulating miR-125b-5p mitigated the effect of suppressing lncRNA SNHG6 on TNBC cell proliferation, migration, and apoptosis.	NA	Front Oncol 2021  11, 678474 doi:10.3389/fonc.2021.678474 PMID:34026654
3132	LncRNA	KCNMB2-AS1	miR-3194-3p	SMAD5	bladder cancer tissues and cell lines	Bladder Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays	34026626	Long Noncoding RNA KCNMB2-AS1 Promotes SMAD5 by Targeting miR-3194-3p to Induce Bladder Cancer Progression	Here, we revealed the increased level of KCNMB2-AS1 in bladder cancer for the first time. Knockdown of KCNMB2-AS1 in vitro prevented the ability of proliferation, metastasis, and stemness of cancer cells. In vivo, the silencing of KCNMB2-AS1 also prevented tumor growth in vivo. Next, we revealed that KCNMB2-AS1 could interact with miR-3194-3p and uncovered that SAMD5 was a downstream target of miR-3194-3p.	NA	Front Oncol 2021  11, 649778 doi:10.3389/fonc.2021.649778 PMID:34026626
3133	Circular RNA	hsa_circ_0006168	miR-628-5p	IGF1R	human GBM cell lines A172 (CRL-1620) and LN229 (CRL-2611)	Glioblastoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34024251	Blocking hsa_circ_0006168 suppresses cell proliferation and motility of human glioblastoma cells by regulating hsa_circ_0006168/miR-628-5p/IGF1R ceRNA axis	hsa_circ_0006168 and IGF1R were upregulated, and miR-628-5p was downregulated in human GBM tissues and cells. Functionally, blocking hsa_circ_0006168 and overexpressing miR-628-5p suppressed cell proliferation, migration, invasion, and expression of Vimentin and Snail (mesenchymal markers) in A172 and LN229 cells, accompanied with increased E-cadherin (epithelial marker), decreased colony formation, and promoted apoptosis rate. Silencing miR-628-5p counteracted the suppression of hsa_circ_0006168 deficiency on these behaviors, and restoring IGF1R blocked miR-628-5p-mediated inhibition as well.	NA	Cell Cycle 2021 May 24, 10.1080/15384101.2021.1930357, 1-14 doi:10.1080/15384101.2021.1930357 PMID:34024251
3134	LncRNA	SOX2OT	miR-135a-5p	NR3C2	PC12 cells	Cerebral Ischemia-Reperfusion Injury	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34022287	Long noncoding RNA SOX2OT silencing alleviates cerebral ischemia-reperfusion injury via miR-135a-5p-mediated NR3C2 inhibition	The expression of SOX2OT and NR3C2 was increased, while miR-135a-5p was decreased in OGD/R-treated PC12 cells. SOX2OT silencing repressed the levels of LDH, MDA, ROS, IL-1β, IL-6, reduced the numbers of TUNEL positive cells, and elevated viability and SOD level in OGD/R-treated PC12 cells. Besides, SOX2OT targeted miR-135a-5p, and miR-135a-5p targeted NR3C2. Both miR-135a-5p downregulation and NR3C2 upregulation reversed the suppressive effects of SOX2OT knockdown on oxidative stress, apoptosis, and inflammation of OGD/R-treated PC12 cells. Furthermore, injection of sh-SOX2OT reduced the NDS, cerebral infarct, and cerebral edema in MCAO/R-treated rats.	NA	Brain Res Bull 2021 Aug 173, 193-202 doi:10.1016/j.brainresbull.2021.05.018 PMID:34022287
3135	LncRNA	SOX2OT	miR-135a-5p	NR3C2	PC12 cells	Cerebral Ischemia-Reperfusion Injury	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34022287	Long noncoding RNA SOX2OT silencing alleviates cerebral ischemia-reperfusion injury via miR-135a-5p-mediated NR3C2 inhibition	The expression of SOX2OT and NR3C2 was increased, while miR-135a-5p was decreased in OGD/R-treated PC12 cells. SOX2OT silencing repressed the levels of LDH, MDA, ROS, IL-1β, IL-6, reduced the numbers of TUNEL positive cells, and elevated viability and SOD level in OGD/R-treated PC12 cells. Besides, SOX2OT targeted miR-135a-5p, and miR-135a-5p targeted NR3C2. Both miR-135a-5p downregulation and NR3C2 upregulation reversed the suppressive effects of SOX2OT knockdown on oxidative stress, apoptosis, and inflammation of OGD/R-treated PC12 cells. Furthermore, injection of sh-SOX2OT reduced the NDS, cerebral infarct, and cerebral edema in MCAO/R-treated rats.	NA	Brain Res Bull 2021 Aug 173, 193-202 doi:10.1016/j.brainresbull.2021.05.018 PMID:34022287
3136	LncRNA	TUG1	miR-187-3p	TESC	PA tissues and cell lines (HP75 and GH3)	Pituitary Adenoma	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34021124	Long non-coding RNA TUG1/microRNA-187-3p/TESC axis modulates progression of pituitary adenoma via regulating the NF-κB signaling pathway	TUG1 inhibition downregulated TESC, which was targeted by miR-187-3p. In conclusion, this study suggests that TUG1 sponges miR-187-3p to affect PA development by elevating TESC and regulating the NF-κB signaling pathway.	NA	Cell Death Dis 2021 May 21 12, 524 doi:10.1038/s41419-021-03812-7 PMID:34021124
3137	LncRNA	TUG1	miR-187-3p	TESC	PA tissues and cell lines (HP75 and GH3)	Pituitary Adenoma	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34021124	Long non-coding RNA TUG1/microRNA-187-3p/TESC axis modulates progression of pituitary adenoma via regulating the NF-κB signaling pathway	TUG1 inhibition downregulated TESC, which was targeted by miR-187-3p. In conclusion, this study suggests that TUG1 sponges miR-187-3p to affect PA development by elevating TESC and regulating the NF-κB signaling pathway.	NA	Cell Death Dis 2021 May 21 12, 524 doi:10.1038/s41419-021-03812-7 PMID:34021124
3138	LncRNA	XIST	miR-200b-3p	ZEB1	Liver cancer tissues and cell lines	Liver Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34018840	LncRNA XIST promotes liver cancer progression by acting as a molecular sponge of miR-200b-3p to regulate ZEB1/2 expression	The lncRNA XIST was significantly upregulated in liver cancer, and increased lncRNA XIST expression was associated with a poor prognosis. The lncRNA XIST promoted liver cancer cell proliferation, migration, and invasion in vitro, and acted as a molecular sponge for miR-200b-3p, and also regulated the expression of ZEB1/2 via miR-200b-3p.	NA	J Int Med Res 2021 May 49, 3000605211016211 doi:10.1177/03000605211016211 PMID:34018840
3139	LncRNA	XIST	miR-200b-3p	ZEB2	Liver cancer tissues and cell lines	Liver Cancer	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34018840	LncRNA XIST promotes liver cancer progression by acting as a molecular sponge of miR-200b-3p to regulate ZEB1/2 expression	The lncRNA XIST was significantly upregulated in liver cancer, and increased lncRNA XIST expression was associated with a poor prognosis. The lncRNA XIST promoted liver cancer cell proliferation, migration, and invasion in vitro, and acted as a molecular sponge for miR-200b-3p, and also regulated the expression of ZEB1/2 via miR-200b-3p.	NA	J Int Med Res 2021 May 49, 3000605211016211 doi:10.1177/03000605211016211 PMID:34018840
3140	LncRNA	SNHG12	miR-766-5p	EIF5A	human vascular smooth muscle cells	NA	Homo sapiens (human)	RT-qPCR;luciferase reporter assays	34018346	Silencing of lncRNA SNHG12 inhibits proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/EIF5A axis	SNHG12 was significantly upregulated in ox-LDL-insulted hVSMCs. SNHG12 silencing inhibited ox-LDL-induced proliferation and migration of hVSMCs. Moreover, SNHG12 acted as a sponge of miR-766-5p, and miR-766-5p also interacted with EIF5A. EIF5A plasmids promoted the capacities of proliferation and migration in ox-LDL-induced hVSMCs. However, shRNA-SNHG12 counteracted the facilitation of EIF5A plasmids on hVSMCs biological behaviors.	NA	Adv Clin Exp Med 2021 May 20, 10.17219/acem/133496 doi:10.17219/acem/133496 PMID:34018346
3141	LncRNA	MEG3	miR-7-5p	Pax6	retinal pigment epithelium (RPE) cells	NA	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34018078	lncRNA MEG3, Acting as a ceRNA, Modulates RPE Differentiation Through the miR-7-5p/Pax6 Axis	Mechanistically, MEG3 functioned as a sponge for miR-7-5p to restore the expression of Pax6. Our study demonstrated that MEG3 exerts a protective role against AMD by maintaining RPE differentiation via miR-7-5p/Pax6 axis, suggesting a protective therapeutic target in AMD treatment.	NA	Biochem Genet 2021 May 20, 10.1007/s10528-021-10072-9 doi:10.1007/s10528-021-10072-9 PMID:34018078
3142	LncRNA	HULC	miR-663b	TLR4	human skin fibroblasts	Pediatric Burns	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34017408	Long non-coding RNA HULC regulates TLR4 expression by acting as ceRNA to attract miR-663b in skin fibroblasts of pediatric burns	LncRNA HULC may function as a molecular sponge to regulate the expression of the miR-663b/TLR4, and thereby inhibit the proliferation, invasion, and ECM synthesis of thermal-injured HSF cells. HULC knockdown might significantly promote wound healing in children after burns.	NA	Am J Transl Res 2021  13, 2499-2510,  PMID:34017408
3143	LncRNA	MEG8	miR-454-3p	TNF	BIPA tissues and cell lines	Bone-Invasive Pituitary Adenomas	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34016788	LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas	Mechanistically, MEG8 promotes TNF-α expression by sponging miR-454-3p, which ultimately leads to the occurrence of bone destruction. The mechanism is confirmed in vivo and in vitro. 	NA	Aging (Albany NY) 2021 May 19 13, 14342-14354 doi:10.18632/aging.203048 PMID:34016788
3144	LncRNA	MEG8	miR-454-3p	TNF	BIPA tissues and cell lines	Bone-Invasive Pituitary Adenomas	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34016788	LncRNA MEG8 promotes TNF-α expression by sponging miR-454-3p in bone-invasive pituitary adenomas	Mechanistically, MEG8 promotes TNF-α expression by sponging miR-454-3p, which ultimately leads to the occurrence of bone destruction. The mechanism is confirmed in vivo and in vitro. 	NA	Aging (Albany NY) 2021 May 19 13, 14342-14354 doi:10.18632/aging.203048 PMID:34016788
3145	LncRNA	LOC146880	miR-328-5p	FSCN1	ESCC tissues and cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR; Western blot; dual luciferase reporter assays	34016787	LncRNA LOC146880 promotes esophageal squamous cell carcinoma progression via miR-328-5p/FSCN1/MAPK axis	Bioinformatics analysis, dual luciferase reporter assays, and RNA immunoprecipitation assays showed that LOC146880 regulates FSCN1 expression in ESCC cells by sponging miR-328-5p. Moreover, FSCN1 expression correlated with activation of the MAPK signaling pathway in ESCC cells and tissues. 	NA	Aging (Albany NY) 2021 May 18 13, 14198-14218 doi:10.18632/aging.203037 PMID:34016787
3146	LncRNA	LOC146880	miR-328-5p	FSCN1	ESCC tissues and cell lines	Esophageal Squamous Cancer	Mus musculus (mouse)	qPCR; Western blot; dual luciferase reporter assays	34016787	LncRNA LOC146880 promotes esophageal squamous cell carcinoma progression via miR-328-5p/FSCN1/MAPK axis	Bioinformatics analysis, dual luciferase reporter assays, and RNA immunoprecipitation assays showed that LOC146880 regulates FSCN1 expression in ESCC cells by sponging miR-328-5p. Moreover, FSCN1 expression correlated with activation of the MAPK signaling pathway in ESCC cells and tissues. 	NA	Aging (Albany NY) 2021 May 18 13, 14198-14218 doi:10.18632/aging.203037 PMID:34016787
3147	LncRNA	MIAT	miR-641	STIM1	human vascular smooth muscle cells	NA	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34016053	Long non-coding RNA MIAT regulates ox-LDL-induced cell proliferation, migration and invasion by miR-641/STIM1 axis in human vascular smooth muscle cells	MIAT silencing hindered ox-LDL-induced cell proliferation, migration and invasion by downregulating STIM1 expression through binding to miR-641 in VSMCs. The mechanism provided us with a new target for AS therapy.	NA	BMC Cardiovasc Disord 2021 May 20 21, 248 doi:10.1186/s12872-021-02048-9 PMID:34016053
3148	LncRNA	H19	miR-139	CXCR4	nucleus pulposus cells	NA	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34015968	LncRNA H19 aggravates intervertebral disc degeneration by promoting the autophagy and apoptosis of nucleus pulposus cells via the miR-139/CXCR4/NF-κB axis	Downregulation of H19 inhibited autophagy and apoptosis of DNPCs. LncRNA H19 sponged miR-139-3p to inhibit CXCR4 expression. si-H19 and miR-139-3p inhibitor co-treatment induced autophagy and apoptosis, and enhanced CXCR4 expression. si-H19 decreased p-p65 phosphorylation, while si-H19 and miR-139-3p inhibitor co-treatment partially elevated p-p65 phosphorylation. 	NA	Stem Cells Dev 2021 May 20, 10.1089/scd.2021.0009 doi:10.1089/scd.2021.0009 PMID:34015968
3149	Circular RNA	ABCB10	miR-588	CXCR4	AMC-HN-8 and Hep-2 cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34015764	Circular RNA ABCB10 contributes to laryngeal squamous cell carcinoma (LSCC) progression by modulating the miR-588/CXCR4 axis	Mechanically, circABCB10 served as a sponge for microRNAs-588 (miR-588) and miR-588 could target and down-regulated chemokine receptor 4 (CXCR4) expression in LSCC cells. The overexpression of CXCR4 or miR-588 inhibitor could reverse circABCB10 depletion-attenuated malignant phenotypes of LSCC cells.	NA	Aging (Albany NY) 2021 May 18 13, 14078-14087 doi:10.18632/aging.203025 PMID:34015764
3150	LncRNA	LOC100129620	miR-335-3p	CDK6	Osteosarcoma cell lines(U2OS, MG63, HOS, and Saos-2)	Osteosarcoma	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34015762	LncRNA LOC100129620 promotes osteosarcoma progression through regulating CDK6 expression, tumor angiogenesis, and macrophage polarization	LOC100129620 can bind to miR-335-3p and regulate its function. MiR-335-3p mediates the regulatory effects of LOC100129620 on CDK6. LOC100129620 promotes the formation of blood vessels and the polarization of macrophages. 	NA	Aging (Albany NY) 2021 May 18 13, 14258-14276 doi:10.18632/aging.203042 PMID:34015762
3151	Protein	MEG3	miR-141	SCARA5	Normal bladder cell line, SV-HUC-1 and BC cell lines	Bladder Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34015283	SCARA5 regulated by MEG3/miR-141 axis attenuates proliferation, migration and invasion of bladder cancer	MEG3 suppressed proliferation, decreased invasive and migrative cell number of BC cells at least partly via sponging miR-141. The tumor suppressive effects of SCARA5 were positive regulated by MEG3. Luciferase activity assay indicated that MEG3 targeted miR-141 and miR-141 targeted SCARA5.	NA	Life Sci 2021 May 17, 10.1016/j.lfs.2021.119619, 119619 doi:10.1016/j.lfs.2021.119619 PMID:34015283
3152	LncRNA	LOC100912373	miR-17-5p	PDK1	synovial tissue of the knee joint	Rheumatoid Arthritis	Mus musculus (mouse)	RT-qPCR; Western blot	34013364	Astragaloside regulates lncRNA LOC100912373 and the miR-17-5p/PDK1 axis to inhibit the proliferation of fibroblast-like synoviocytes in rats with rheumatoid arthritis	The results revealed that AST inhibited FLS proliferation, reduced lncRNA LOC100912373 expression levels, increased miR-17-5p expression levels, and decreased the PDK1 and p-AKT expression levels.	NA	Int J Mol Med 2021 Jul 48 doi:10.3892/ijmm.2021.4963 PMID:34013364
3153	Circular RNA	Circ_010567	miR-141	DAPK1	rat cardiomyocyte cell line H9c2	Myocardial Infarction	Mus musculus (mouse)	qRT-PCR;luciferase reporter assays;Western blot	34012592	CircRNA 010567 plays a significant role in myocardial infarction via the regulation of the miRNA-141/DAPK1 axis	circRNA 010567 sponges miR-141 and DAPK1 was a direct target of miR-141. Mechanistic investigations revealed that circRNA 010567-siRNA impaired the release of CK-MB and cTnI, and promoted the viability of mitochondria in hypoxia-induced H9c2 cells, while these findings were reversed by the miR-141 inhibitor.	NA	J Thorac Dis 2021 Apr 13, 2447-2459 doi:10.21037/jtd-21-212 PMID:34012592
3154	LncRNA	MEG3	miR-18a-3p	GSDMD	tubular epithelial cells	Acute Kidney Injury	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34012408	Long Non-coding RNA MEG3 Promotes Renal Tubular Epithelial Cell Pyroptosis by Regulating the miR-18a-3p/GSDMD Pathway in Lipopolysaccharide-Induced Acute Kidney Injury	Bioinformatics analysis screened out miR-18a-3P, and further experiments demonstrated that MEG3 controls GSDMD expression by acting as a ceRNA for miR-18a-3P to promote TECs pyroptosis. 	NA	Front Physiol 2021  12, 663216 doi:10.3389/fphys.2021.663216 PMID:34012408
3155	LncRNA	MEG3	miR-18a-3p	GSDMD	tubular epithelial cells	Acute Kidney Injury	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34012408	Long Non-coding RNA MEG3 Promotes Renal Tubular Epithelial Cell Pyroptosis by Regulating the miR-18a-3p/GSDMD Pathway in Lipopolysaccharide-Induced Acute Kidney Injury	Bioinformatics analysis screened out miR-18a-3P, and further experiments demonstrated that MEG3 controls GSDMD expression by acting as a ceRNA for miR-18a-3P to promote TECs pyroptosis. 	NA	Front Physiol 2021  12, 663216 doi:10.3389/fphys.2021.663216 PMID:34012408
3156	Circular RNA	HIPK2	miR-338-3p	CHTOP	human DDP-resistant OvCa tumors and cells	Ddp-Resistant Ovarian Cancer	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34012271	CircHIPK2 Contributes to DDP Resistance and Malignant Behaviors of DDP-Resistant Ovarian Cancer Cells Both in vitro and in vivo Through circHIPK2/miR-338-3p/CHTOP ceRNA Pathway	CircHIPK2 might be a tumor promoter in OvCa and was associated with DDP resistance. Silencing circHIPK2 might suppress DDP-resistant OvCa through regulating miR-338-3p/CHTOP axis.	NA	Onco Targets Ther 2021  14, 3151-3165 doi:10.2147/ott.S291823 PMID:34012271
3157	LncRNA	PAX8-AS1	miR-1252-5p	GNB1	osteoblasts	Osteoporosis	Homo sapiens (human)	RT-qPCR; Western blot; dual luciferase reporter assays	34012023	PAX8-AS1 knockdown facilitates cell growth and inactivates autophagy in osteoblasts via the miR-1252-5p/GNB1 axis in osteoporosis	 The results illustrated that PAX8-AS1 was upregulated in the proximal tibia of OP rats. PAX8-AS1 silencing promoted the viability and inhibited the apoptosis and autophagy of osteoblasts. PAX8-AS1 interacted with miR-1252-5p. GNB1 was negatively regulated by miR-1252-5p. In addition, the impacts of PAX8-AS1 knockdown on osteoblasts were counteracted by GNB1 overexpression.	NA	Exp Mol Med 2021 May 53, 894-906 doi:10.1038/s12276-021-00621-y PMID:34012023
3158	LncRNA	PAX8-AS1	miR-1252-5p	GNB1	osteoblasts	Osteoporosis	Mus musculus (mouse)	RT-qPCR; Western blot; dual luciferase reporter assays	34012023	PAX8-AS1 knockdown facilitates cell growth and inactivates autophagy in osteoblasts via the miR-1252-5p/GNB1 axis in osteoporosis	 The results illustrated that PAX8-AS1 was upregulated in the proximal tibia of OP rats. PAX8-AS1 silencing promoted the viability and inhibited the apoptosis and autophagy of osteoblasts. PAX8-AS1 interacted with miR-1252-5p. GNB1 was negatively regulated by miR-1252-5p. In addition, the impacts of PAX8-AS1 knockdown on osteoblasts were counteracted by GNB1 overexpression.	NA	Exp Mol Med 2021 May 53, 894-906 doi:10.1038/s12276-021-00621-y PMID:34012023
3159	LncRNA	GAS5	miR-579-3p	SIRT1	human-derived proximal tubule epithelial cells HK-2	Sepsis	Homo sapiens (human)	qRT-PCR;luciferase reporter assays;Western blot	34010066	LncRNA GAS5 inhibits miR-579-3p to activate SIRT1/PGC-1α/Nrf2 signaling pathway to reduce cell pyroptosis in sepsis-associated renal injury	GAS5 negatively and directly regulated miR-579-3p to reduce cell pyroptosis via activation of SIRT1/PGC-1a/Nrf2 pathway. In addition, miR-579-3p suppressed PGC-1a/Nrf2 pathway to induce cell pyroptosis by directly targeting SIRT1. What's more, overexpression of GAS5, or knockdown of miR-579-3p, enhanced SIRT1 expression that led to the improved survival rate, reduced the weight loss, and relieved renal injuries in septic mice.	NA	Am J Physiol Cell Physiol 2021 May 19, 10.1152/ajpcell.00394.2020 doi:10.1152/ajpcell.00394.2020 PMID:34010066
3160	LncRNA	LINC01013	miR-6795-5p	FMNL3	hepatocellular carcinoma stem cell	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;	33847733	Novel role of LINC01013/miR-6795-5p/FMNL3 axis in the regulation of hepatocellular carcinoma stem cell features.	Cancer stem cells (CSCs) are major contributors to tumor initiation, recurrence, and metastasis of hepatocellular carcinoma (HCC). Some long non-coding RNAs have been reported as modulators of stem-like properties in cancer cells. However, the role of LINC01013 in liver CSCs has not yet been clarified. In this study, we aimed to elucidate the expression pattern and functions of LINC01013 in HCC. HCC tissues and normal controls were collected, and the expression pattern of LINC01013 and miR-6795-5p was identified by quick real-time polymerase chain reaction. Cell counting kit-8 assay, colony formation, and spheroid formation were performed to measure cell viability, proliferation, and self-renewal of HCC cell lines. The expression of stem markers was detected by western blot analysis. The effect of LINC01013 on viability, proliferation, and stem-like properties was detected through gain-of-function and loss-of-function experiments. The direct interaction among LINC01013, miR-6795-5p, and FMNL3 was testified by dual-luciferase reporter gene assay. Tumor-bearing mice were constructed to ascertain the functions of LINC01013 in vivo. HCC tissues showed increased LINC01013 and FMNL3 expression, while it showed a decreased miR-6795-5p expression as compared to the relative controls. Moreover, the high level of LINC01013 was closely related to the poor prognosis of HCC patients. LINC01013 directly binds to miR-6795-5p and subsequently relieves FMNL3. Silencing LINC01013, FMNL3, or overexpression of miR-6795-5p could suppress spheroid and colony formation, proliferation, as well as expression of stemness markers in HepG2 and SNU-182 cells. LINC01013 knockdown suppressed growth and stem-like traits of HCC cells in vivo by reducing FMNL3 expression. LINC01013/miR-6795-5p/FMNL3 axis may be a novel therapeutic target for HCC.	NA	Acta Biochim Biophys Sin (Shanghai). 2021 May 21;53(6):652-662. doi: 10.1093/abbs/gmab040.
3161	Circular RNA	CircPIKfyve	miR-21-3p	MAVS	M. miiuyspleen cells (MspC),M. miiuykidney cells (MKC),M. miiuymus-cle cells (MMC),M. miiuybrain cells (MBrC), andM. miiuyintestine cells (MIC)	Antiviral Immunitymmunity	Teleost fish (fish)	FISH	33536171	Circular RNA circPIKfyve acts as a sponge of miR-21-3p to enhance antiviral immunity through regulating MAVS in teleost fish.	Circular RNAs (circRNAs) are a class of widespread and diverse covalently closed circular endogenous RNAs that exert crucial functions in regulating gene expression in mammals. However, the function and regulation mechanism of circRNAs in lower vertebrates are still unknown. Here, we discovered a novel circRNA derived from PIKfyve, named circPIKfyve, that is related to the antiviral responses in teleost fish. The results showed that circPIKfyve plays essential roles in host antiviral immunity and inhibition of SCRV replication. Moreover, we also found that the antiviral effect inhibited by miR-21-3p could be reversed with the addition of circPIKfyve. In mechanism, our data revealed that circPIKfyve is a competitive endogenous RNA (ceRNA) of MAVS by sponging miR-21-3p, leading to activation of NF-κB/IRF3 pathway, which then enhance the innate antiviral responses. In addition, we firstly found that RNA binding protein QKI is involved in the formation and regulation of circPIKfyve. Our results provided a strong basis that circRNAs to play a regulatory role in antiviral immune responses in teleost fish.Importance: Here, we identified a novel circRNA, namely, circPIKfyve, that can act as a key regulator of the innate immune response in teleost fish. circPIKfyve acts as a molecular sponge by competitive adsorbing of miR-21-3p, thereby increasing the abundance of MAVS and activating the downstream NF-κB/IRF3 pathway to enhance the antiviral response. In addition, this study was the first to find that QKI protein is involved in regulating the formation of circPIKfyve in fish. The overall results of this study suggest that circPIKfyve plays an active regulatory role in the antiviral immune response of teleost fish.	NA	J Virol. 2021 Feb 3;95(8):e02296-20. doi: 10.1128/JVI.02296-20.
3162	LncRNA	SNHG14	miR-124-3p	FSTL-1	OA tissues	Osteoarthritis	Rattus (rat)	qRT-PCR	33539913	Downregulation of lncRNA SNHG14 attenuates osteoarthritis by inhibiting FSTL-1 mediated NLRP3 and TLR4/NF-κB pathway through miR-124-3p.	Osteoarthritis (OA) is the joint pain and dysfunction syndrome caused by severe joint degeneration. The overproduced inflammatory mediators contribute greatly to OA development. It is reported that long non-coding RNA (lncRNA) takes part in many inflammatory diseases. Here, we mainly explored the function of lncRNA SNHG14 in OA process and its specific mechanisms. An OA rat model was induced by destabilizing the medial meniscus (DMM) and IL-1β (5 ng/mL) was used to mediate an OA cell model in particular chondrocytes (AC). Gain- or loss-of functional assays of SNHG14 and miR-124-3p were carried out to explore their roles in OA development. The experimental statistics illustrated that lncRNA SNHG14 and IL-1β mRNA expression were both increased in OA tissues, while miR-124-3p was lowly-expressed. Linear regression analysis showed that SNHG14 and miR-124-3p had negative relationship in the OA tissues. In the in vitro experiments, downregulation of lncRNA SNHG14 promoted the proliferation of IL-1β-treated AC and inhibited cell apoptosis and COX-2, iNOS, TNF-α, IL-6 expression. Moreover, lncRNA SNHG14 inhibited miR-124-3p expression as a miRNA sponge. MiR-124-3p targeted the 3'non-translated region (3'UTR) of FSTL-1 and TLR4 and inhibited their expressions. Also, the in vivo experiments confirmed that knocking down SNHG14 relieved the progression of OA in rats via inhibiting inflammatory responses. In conclusion, this study confirmed that downregulation of lncRNA SNHG14 inhibits FSTL-1-mediated activation of NLRP3 and TLR4/NF-κB signalling pathway activation by targeting miR-124-3p, thus attenuating inflammatory reactions in OA.	NA	Life Sci. 2021 Apr 1;270:119143. doi: 10.1016/j.lfs.2021.119143. Epub 2021 Feb 1.
3163	LncRNA	XIST	miR-29c-3p	NFAT5	LPS Stimulated Astrocyte Cell	Secretion Of Inflammatory Cytokines	Rattus (rat)	RIP assay;Western blot;Flow Cytometry assay;	33776905	Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression.	BACKGROUND: Astrocyte activation promotes glutamate accumulation and secretion of inflammatory factors, mainly responsible for epilepsy. Long noncoding RNA (lncRNA) X-inactive-specific transcript (XIST) regulates inflammation; however, the biological role and regulatory mechanism of XIST during astrocyte activation remain unclear. METHODS: In the present study, rat epilepsy model and lipopolysaccharide (LPS)-treated CTX-TNA2 were established. XIST and miR-29c-3p expression were evaluated using quantitative real-time polymerase chain reaction. Nuclear factor of activated T cells 5 (NFAT5) was measured using western blot analysis. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and L-glutamate levels in the culture supernatants were assessed using enzyme-linked immunosorbent assay. The binding between XIST and miR-29c-3p and between miR-29c-3p and the 3'-UTR of NFAT5 was analyzed using dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and Biotin pull-down assay. The proliferation and apoptosis were evaluated using CCK8 and flow cytometry, respectively. RESULTS: XIST expression and NFAT5 protein level was increased, whereas miR-29c-3p expression was decreased in the epilepsy rat model and LPS-treated CTX-TNA2 cells. Silenced XIST expression, miR-29c-3p overexpression, or silenced NFAT5 expression inhibited the secretion of IL-1β, IL-6, and TNF-α and promoted glutamate transport in LPS-treated CTX-TNA2 cells. miR-29c-3p was the potential miRNA sponged by XIST. NFAT5 acted as a direct binding target of miR-29c-3p. Silenced miR-29c-3p expression or NFAT5 overexpression reversed the effect of silenced XIST expression on LPS-treated CTX-TNA2.XIST and miR-29c-3p treatment does not affect NFAT5 mRNA expression, but affects NFAT5 protein level. Furthermore, underexpressed XIST or overexpressed miR-29c-3p in LPS-stimulated CTX-TNA2 can attenuate neuronal apoptosis induced by LPS-stimulated CTX-TNA2. CONCLUSION: LncRNA XIST promotes the secretion of inflammatory cytokines in LPS- treated CTX-TNA2 via sponging miR-29c-3p and regulating NFAT5 expression.	NA	Front Endocrinol (Lausanne). 2021 Mar 12;12:573143. doi: 10.3389/fendo.2021.573143. eCollection 2021.
3164	LncRNA	LINC02288	miR-374a-3p	RTN3	chondrocyte	Chondrocyte Apoptosis And Inflammation	Rattus (rat)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;luciferase assay;Luciferase reporter assay;RNA immunoprecipitation;	33491257	LINC02288 promotes chondrocyte apoptosis and inflammation through miR-374a-3p targeting RTN3.	BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) is related to the occurrence of osteoarthritis (OA). In the present study, we explored the role of LINC02288 and its regulatory mechanism in OA development. METHODS: GSE113825 was obtained from Gene Expression Omnibus (GEO) database and analyzed to identify the differentially expressed lncRNAs in OA. Gene enrichment analyses and Kyoto Encyclopedia of Genes and Genomes biological process analysis were performed through Metascape (http://metascape.org/gp). The interactions among LINC02288, miR-374a-3p and RTN3 were determined using RNA immunoprecipitation (RIP) assays and dual luciferase reporter assays. Chondrocyte apoptosis was examined using flow cytometry. Western blot assays were conducted to assess the pro-apoptotic and anti-apoptotic markers. RESULTS: We identified a total of 4,491 differentially expressed lncRNAs. We focused on LINC02288 as the top-ranked up-regulated lncRNA in OA as indicated by a significant p-value. LINC02288 was significantly up-regulated, which was further verified by a real-time polymerase chain reaction. Down-regulation of LINC02288 significantly reduced the apoptosis of OA chondrocytes induced by interleukin-1β and the production of pro-inflammatory cytokines. These effects were further verified in an OA rat model. An RIP assay and dual luciferase assay further confirmed that LINC02288 served as a sponge of miR-374a-3p. Moreover, the overexpression of RTN3 could partially reverse the effects of LINC02288 knockdown, mediating inhibitory effects on chondrocyte apoptosis and the inflammatory response. Down-regulation of LINC02288 alleviated OA development in an in vivo OA animal model. CONCLUSIONS: Our findings indicate that LINC02288 contributes to OA progression by targeting the miR-374a-3p/RTN3 axis, which might provide a promising molecular therapy strategy for OA.	NA	J Gene Med. 2021 May;23(5):e3314. doi: 10.1002/jgm.3314. Epub 2021 Mar 25.
3165	LncRNA	MALAT1	miR-302d-3p	LIF	ovarian tissues and ovarian granulosa cells	Polycystic Ovary Syndrome	Rattus (rat)	qRT-PCR	33465389	Down-regulation of MALAT1 aggravates polycystic ovary syndrome by regulating MiR-302d-3p-mediated leukemia inhibitory factor activity.	AIMS: Accumulating evidence have shown the important roles of long noncoding RNA (lncRNA) in controlling different diseases. In the present study, we tried to explore the role which lncRNA MALAT1 plays in polycystic ovary syndrome (PCOS) with the involvement of microRNA-302d-3p (miR-302d-3p) and leukemia inhibitory factor (LIF). METHODS: A PCOS rat model was established and characterized, followed by treatment with si-MALAT1, oe-MALAT1, miR-302d-3p mimic, or miR-302d-3p inhibitor constructs. Serum hormonal levels were detected to evaluate endocrine conditions. The effect of MALAT1 and miR-302d-3p on activities of ovarian granulosa cells was assessed, as well as the involvement of LIF. RESULTS: MALAT1 expression was shown to be downregulated in ovarian tissue of PCOS rats. Overexpression of MALAT1 in vitro promoted proliferation and inhibited apoptosis of ovarian granulosa cells. Overexpression of MALAT1 in vivo reduced the ovarian tissue injury and endocrine disorders accompanied with decreased level of FSH and elevated serum levels of E2, T, and LH in the PCOS rat. Overexpression of MALAT1 also promoted the expression of LIF, which could be reversed by overexpression of miR-302d-3p, indicating that MALAT1 up-regulated the expression of LIF via miR-302d-3p. Furthermore, overexpression of MALAT1 reduced endocrine disorders and ovarian tissue damage via the miR-302d-3p/LIF axis. CONCLUSION: Our study highlighted that MALAT1 plays a protective role in reducing ovarian tissue damage and endocrine disorder in PCOS by regulating the miR-302d-3p/LIF axis.	NA	Life Sci. 2021 Jul 15;277:119076. doi: 10.1016/j.lfs.2021.119076. Epub 2021 Jan 16.
3166	Circular RNA	CircAgtpbp1	miR-543-5p	GH	Rat Pituitary Cells	Secretion Of Growth Hormone	Rattus (rat)	ELISA;FISH;qRT-PCR;Western blot;FISH;	33672649	CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells.	CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT-PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT-PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT-PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.	NA	Animals (Basel). 2021 Feb 20;11(2):558. doi: 10.3390/ani11020558.
3167	LncRNA	HOTAIR	miR-17-5p	STAT3	H9c2 cells	Ischemia Reperfusion Injury	Rattus (rat)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33883889	HOTAIR/miR-17-5p Axis is Involved in the Propofol-Mediated Cardioprotection Against Ischemia/Reperfusion Injury.	BACKGROUND: Propofol (PPF) ameliorates ischemia/reperfusion (I/R) injury in multiple organs by reducing apoptosis and release of pro-inflammatory cytokines. This study aims to explore the mechanism of PPF in attenuating myocardial ischemia-reperfusion injury (MIRI). MATERIALS AND METHODS: Rat MIRI model was established, and PPF pre-treatment was performed 10 min before I/R. H9c2 cardiomyocytes treated with hypoxia/reoxygenation (H/R) were used to establish an in vitro model. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate HOTAIR and miR-17-5p expression levels. Flow cytometry was employed to detect the apoptosis of H9c2 cells. The interaction between HOTAIR and miR-17-5p was determined by bioinformatics analysis, luciferase reporter gene analysis, and RNA immunoprecipitation experiments. STAT3 and p-STAT3 expressions were detected by Western blot. RESULTS: PPF pre-treatment significantly reduced creatine kinase isoenzyme (CK-MB) and serum lactate dehydrogenase (LDH) levels in the serum of the rats with MIRI. PPF pre-treatment remarkably up-regulated HOTAIR expression and down-regulated miR-17-5p expression in both in vivo and in vitro models. HOTAIR adsorbed miR-17-5p to repress the expression of miR-17-5p. PPF pre-treatment markedly inhibited cardiomyocyte apoptosis induced by I/R or H/R. HOTAIR knockdown could partially reverse the protective effects of PPF on MIRI. HOTAIR could activate STAT3 signaling via repressing miR-17-5p expression. CONCLUSION: PPF protects the MIRI by modulating the HOTAIR/miR-17-5p/STAT3 axis.	NA	Clin Interv Aging. 2021 Apr 15;16:621-632. doi: 10.2147/CIA.S286429. eCollection 2021.
3168	LncRNA	CCDC144NL-AS1	miR-940	WDR5	HCC cell line MHCC97H,L02	Hepatocellular Carcinoma	Mus musculus (mouse)	ChIP;qPCR;RT-qPCR;Western blot;Immunohistochemistry;	33977095	LncRNA-CCDC144NL-AS1 Promotes the Development of Hepatocellular Carcinoma by Inducing WDR5 Expression via Sponging miR-940.	PURPOSE: This work was initiated to offer solid evidence regarding the expression and roles of long noncoding RNA (lncRNA) CCDC144NL-AS1 in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: Cell Counting Kit-8 assay, flow cytometric analysis, and invasion assays were used to explore the malignant biological characteristics of cells. Immunohistochemistry (IHC), Western blotting analysis, and real-time quantitative PCR (RT-qPCR) were used to analyze the expression level of related proteins and nucleic acids. Bl6/Rag2/GammaC double knockout mice were used for HCC modeling to address the therapeutic value of CCDC144NL-AS1. RESULTS: CCDC144NL-AS1 was significantly upregulated in HCC tissue and had a marked relationship with the 5-year prognosis. In vitro study revealed that CCDC144NL-AS1 was highly expressed in HCC cell line MHCC97H but lowly expressed in normal hepatic cell line L02. Overexpression of CCDC144NL-AS1 in L02 enhanced the invasion and proliferation abilities of cells but inhibited the apoptosis rate. Knockdown of CCDC144NL-AS1 in MHCC97H weakened the invasion and proliferation abilities of cells but increased the apoptosis rate. CCDC144NL-AS1 was found to sponge miR-940 to induce the expression of WD repeat domain 5 (WDR5). ChIP-seq analysis identified that matrix metalloproteinase (MMP) 2, MMP9, and cyclin-dependent kinase (CDK) 1, CDK2, and CDK4 were all targets of WDR5. The recruitment of WDR5 to the promoter of these target genes upregulated the histone H3 lysine 4 trimethylation (H3K4me3) level in these regions and further induced the transcription of MMP2, MMP9, CDK1, CDK2, and CDK4. In vivo study revealed that compared to the normal liver tissue, CCDC144NL-AS1, WDR5, MMP2, MMP9, CDK1, CDK2, and CDK4 were all significantly upregulated in HCC tissue from the same mouse, while miR-940 was decreased. Besides, knockdown of CCDC144NL-AS1 or WDR5 or overexpression of miR-940 could all inhibit tumor growth. CONCLUSION: CCDC144NL-AS1 drives HCC development by inducing MMP2/MMP9 and CDK1/CDK2/CDK4 expressions through miR-940/WDR5-regulated epigenetic pathway.	NA	J Hepatocell Carcinoma. 2021 May 3;8:333-348. doi: 10.2147/JHC.S306484. eCollection 2021.
3169	Circular RNA	CircSLC7A2	miR-4498	TIMP3	OA tissues	Osteoarthritis	Mus musculus (mouse)	qPCR;RT-qPCR;Western blot;	33960555	CircSLC7A2 protects against osteoarthritis through inhibition of the miR-4498/TIMP3 axis.	OBJECTIVES: Circular RNAs (circRNAs) are noncoding RNAs that compete against other endogenous RNA species, such as microRNAs, and have been implicated in many diseases. In this study, we investigated the role of a new circRNA (circSLC7A2) in osteoarthritis (OA). MATERIALS AND METHODS: The relative expression of circSLC7A2 was significantly lower in OA tissues than it was in matched controls, as shown by real-time quantitative polymerase chain reaction (RT-qPCR). Western blotting, RT-qPCR and immunofluorescence experiments were employed to evaluate the roles of circSLC7A2, miR-4498 and TIMP3. The in vivo role and mechanism of circSLC7A2 were also conformed in a mouse model. RESULTS: circSLC7A2 was decreased in OA model and the circularization of circSLC7A2 was regulated by FUS. Loss of circSLC7A2 reduced the sponge of miR-4498 and further inhibited the expression of TIMP3, subsequently leading to an inflammatory response. We further determined that miR-4498 inhibitor reversed circSLC7A2-knockdown-induced OA phenotypes. Intra-articular injection of circSLC7A2 alleviated in vivo OA progression in a mouse model of anterior cruciate ligament transection (ACLT). CONCLUSIONS: The circSLC7A2/miR-4498/TIMP3 axis of chondrocytes catabolism and anabolism plays a critical role in OA development. Our results suggest that circSLC7A2 may serve as a new therapeutic target for osteoarthritis.	NA	Cell Prolif. 2021 Jun;54(6):e13047. doi: 10.1111/cpr.13047. Epub 2021 May 7.
3170	LncRNA	GAS5	miR-217	Prox1	HG-induced lymphatic endothelial cells	Lymphangiogenesis 	Mus musculus (mouse)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	33865922	Long noncoding RNA GAS5 accelerates diabetic wound healing and promotes lymphangiogenesis via miR-217/Prox1 axis.	BACKGROUND: Diabetes is usually the leading cause of chronic non-healing wounds. LncRNA-GAS5 has been verified to be involved in the regulation of diabetes or high glucose (HG)-stimulated cells. However, its regulatory roles in diabetic wound healing need further investigation. METHOD: GAS5, miR-217 and Prox1 were identified by qRT-PCR. MTT, flow cytometry assay, wound-healing assay and tube formation were used to analyze cell viability, apoptosis, migration and tube formation capacity. Western blotting was carried out to detect the protein expression of c-Myc, CyclinD1, CDK4, Bcl-2, Prox1, VEGFR-3 and LYVE-1. Bioinformatics and luciferase assay were performed to predict and validate the binding sites of miR-217 on GAS5 and Prox1. Immunofluorescence staining detected the expression and distribution of Prox1. The wound healing rate was also assessed by setting up the diabetic mouse model. H&E staining assessed the distribution of inflammatory cells and fibroblasts in the wound tissues. RESULTS: GAS5 was significantly down-regulated whereas miR-217 was obviously up-regulated in diabetic skin, HG-induced lymphatic endothelial cells (LECs) and diabetic mouse model. GAS5 sponged miR-217 to up-regulate Prox1. GAS5 overexpression or miR-217 inhibition rescued the impairments of cell viability, migration and lymphatic vessel formation and the facilitation of apoptosis of LECs caused by HG. Similar impacts were observed on the protein level of VEGFR-3, LYVE-1, and Prox1. GAS5 promoted wound healing and lymphangiogenesis in the diabetic mouse model. CONCLUSION: GAS5 sponged miR-217 to up-regulate Prox1 and promote lymphangiogenesis and diabetic wound healing. This might provide novel therapeutic strategy to improve the efficacy of diabetic wound healing.	NA	Mol Cell Endocrinol. 2021 Jul 15;532:111283. doi: 10.1016/j.mce.2021.111283. Epub 2021 Apr 15.
3171	LncRNA	USP30-AS1	miR-299-3p	PTP	cervical cancer cells	Cervical Cancer	Mus musculus (mouse)	RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33986866	Long non-coding RNA USP30-AS1 aggravates the malignant progression of cervical cancer by sequestering microRNA-299-3p and thereby overexpressing PTP4A1.	USP30 antisense RNA 1 (USP30-AS1) has been studied in bladder urothelial carcinoma. However, the detailed role of USP30-AS1 in cervical cancer remains to be elucidated. Therefore, the present study determined whether USP30-AS1 is implicated in cervical cancer malignancy, and investigated relevant molecular mechanisms. USP30-AS1 expression was measured via reverse transcription-quantitative PCR. Functional experiments, including the Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and mouse tumour model, were performed in order to elucidate the roles of USP30-AS1. The target of USP30-AS1 was predicted using bioinformatics analysis, which was further verified via RNA immunoprecipitation and luciferase reporter assays. Herein, USP30-AS1 overexpression was detected in cervical cancer sample data from The Cancer Genome Atlas and our cohort. Patients with cervical cancer expressing high levels of USP30-AS1 exhibited shorter overall survival than those with low USP30-AS1 expression. In vitro and in vivo experiments revealed that USP30-AS1 interference promoted cell apoptosis; restrained cell proliferation, migration and invasion in vitro, and hindered tumour growth in vivo. Mechanistically, USP30-AS1 competed for microRNA-299-3p (miR-299-3p) in cervical cancer and lowered the regulatory actions of miR-299-3p on protein tyrosine phosphatase type IVA (PTP4A1), resulting in PTP4A1 overexpression. Furthermore, rescue experiments confirmed that miR-299-3p interventions or exogenous PTP4A1 could counteract the cancer-inhibiting actions of USP30-AS1 silencing on cervical cancer cells. In conclusion, the miR-299-3p/PTP4A1 axis is the downstream effector of USP30-AS1 in cervical cancer, forming the USP30-AS1/miR-299-3p/PTP4A1 pathway. This newly identified competing endogenous RNA pathway may offer a novel theoretical and experimental basis for developing promising new strategies for the targeted therapy of cervical cancer.	NA	Oncol Lett. 2021 Jul;22(1):505. doi: 10.3892/ol.2021.12766. Epub 2021 Apr 29.
3172	LncRNA	LNC00115	miR-7	ERK	ovarian cancer cells	Ovarian Cancer	Mus musculus (mouse)	qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	34007214	LNC00115 Mediates Cisplatin Resistance by Regulating the miR-7/ERK Signalling Pathway in Ovarian Cancer.	BACKGROUND: Ovarian cancer has one of the highest mortality rates among all gynaecological malignancies, and increasing evidence suggests that lncRNAs are widely involved in the development of ovarian tumours. This study aimed to investigate the mechanism of the LNC00115/miR-7/ERK axis in the cisplatin resistance of ovarian cancer cells. METHODS: The expression of miR-7 and LNC00115 in ovarian cancer cell lines and tissues was detected by qRT-PCR. The ovarian cancer cell lines were constructed by overexpressing or knocking down the expression of LNC00115 or miR-7. CCK-8, transwell invasion, Western blot, immunohistochemistry, and luciferase reporter assays were carried out to identify the targets of LNC00115 and explore its roles and mechanisms in ovarian cancer. A nude mouse model was established, and the expression of LNC00115, miR-7 and ERK was detected. The changes in the tumours and body weights of the nude mice were measured. RESULTS: LNC00115 was upregulated in ovarian cancer tissues and cisplatin-resistant ovarian cancer cells. Moreover, LNC00115 promoted the cisplatin resistance, invasion and migration of ovarian cancer cells. LNC00115 was shown to directly target miR-7, and miR-7 was downregulated in ovarian cancer tissues and cisplatin-resistant ovarian cancer cells. miR-7 inhibited the cisplatin resistance, invasion and migration of ovarian cancer cells and directly targeted ERK. ERK was overexpressed in cisplatin-resistant ovarian cancer cells and ovarian cancer tissues. In animal experiments, overexpression of LNC00115 enhanced the cisplatin resistance of ovarian cancer cells, while miR-7 had the opposite effect. Mechanistically, LNC00115 sponged miR-7 to increase the expression of ERK, which in turn enhanced the cisplatin resistance of ovarian cancer. CONCLUSION: Our data clarify the mechanism by which the LNC00115/miR-7/ERK axis promotes cisplatin resistance and provide a new clinical strategy for combating cisplatin resistance in ovarian cancer.	NA	Cancer Manag Res. 2021 May 11;13:3817-3826. doi: 10.2147/CMAR.S295097. eCollection 2021.
3173	LncRNA	LINC02308	miR-30e-3p	TM4SF1	glioma tissues and cells	Glioma 	Mus musculus (mouse)	microarray;Western blot;	33945031	LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis.	BACKGROUND: Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma. METHODS: The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308. RESULTS: LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1. CONCLUSIONS: LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway. Graphical Abstract Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.	NA	Cell Biol Toxicol. 2021 May 4. doi: 10.1007/s10565-021-09604-1.
3174	LncRNA	GSEC	miR-202-5p	AXL	NA	Triple Negative Breast Cancer	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA immunoprecipitation;Luciferase report assay;RNA immunoprecipitation;	33907418	lncRNA GSEC Promotes the Progression of Triple Negative Breast Cancer (TNBC) by Targeting the miR-202-5p/AXL Axis.	BACKGROUND: This study aimed to explore the biological functions of G-quadruplex-forming sequence containing lncRNA (GSEC) in triple negative breast cancer (TNBC). METHODS: The expression of GSEC in TNBC tissues was evaluated by qRT-PCR. Cell viability was evaluated by Cell Counting Kit-8 assay. Cell proliferation was evaluated by 5-ethynyl-20-deoxyuridine (EdU) staining assay. Cell invasion and migration were evaluated by Transwell assay. Gain- and loss-function assays were performed to assess the biological functions of GSEC in TNBC. The interactions between GSEC, miR-202-5p and AXL were determined by luciferase report assay and RNA immunoprecipitation (RIP) assay. In addition, a nude mouse xenograft model was used to confirm the oncogenic role of GSEC in TNBC. RESULTS: GSEC was significantly upregulated in TNBC tissues and cancer cell lines, and high level of GSEC was associated with advanced tumor stage, positive lymph-node metastasis and the poor prognosis of TNBC patients. Knockdown of GSEC effectively inhibited TNBC cell proliferation, invasion and migration in vitro. GSEC regulated the expression of AXL by directly sponging miR-202-5p. Downregulation of miR-202-5p attenuated GSEC knockdown-induced inhibition on TNBC cell proliferation, invasion and migration in vitro. Meanwhile, overexpression of AXL obviously reversed the inhibitory effects of miR-202-5p mimics in TNBC progression in vitro. CONCLUSION: GSEC functioned as a potential oncogene and promoted AXL-mediated TNBC progression by sponging miR-202-5p, which might be a novel diagnostic and therapeutic target for TNBC.	NA	Onco Targets Ther. 2021 Apr 20;14:2747-2759. doi: 10.2147/OTT.S293832. eCollection 2021.
3175	LncRNA	MALAT1	miR-200c	NRF2	MPC-5 cells	Podocyte Pyroptosis	Mus musculus (mouse)	qRT-PCR;Western blot;Flow Cytometry assay;	33880049	Atorvastatin Regulates MALAT1/miR-200c/NRF2 Activity to Protect Against Podocyte Pyroptosis Induced by High Glucose.	BACKGROUND: Diabetic nephropathy (DN) is one of the main complications of diabetes mellitus (DM), which leads to the long-term loss of kidney functions. Long noncoding RNAs (LncRNAs) can alleviate DN by interacting with microRNAs (miRNAs). In this work, we aimed to explore the effects of the MALAT1/miR-200c/NRF2 regulatory axis on the pyroptosis and oxidative stress (Oxidative stress, OS) of renal podocytes in high glucose (HG) environment and whether the lipid-lowering drug atorvastatin (AT) can relieve renal OS through this approach. METHODS: MPC-5, a mouse podocyte cell line, was induced by HG as a cell model. The protein expressions of caspase-1, GSDMD, NLRP3, NRF2, etc. were detected by Western blotting and immunofluorescence, and the mRNA level of caspase-1, GSDMD, NLRP3, NRF2, MALAT1, miR-200c was tested by qRT-PCR. The cell pyroptosis of podocytes treated with AT was verified by CCK-8 or flow cytometry. The levels of Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were measured by spectrophotometer, respectively. RESULTS: The caspase-1 was upregulated in time-dependent manner and got the peak at 48 h and 30 mmol/L respectively in MPC-5 cells treated with HG. Further, the expression of GSDMD, MALAT1 and miR-200c were increased, while the level of NRF2, HO-1, OS-related indicators, were decreased simultaneously. Knockdown the MALAT1 protected MPC-5 cells from pyroptosis and OS induced by HG. However, overexpressing miR-200c in control-group cells increased pyroptosis and upregulated the OS level with HG culture medium. Further, atorvastatin protected MPC-5 cells from cell pyroptosis and downregulated the level of renal OS via attenuating the expression of MALAT1 and miR-200c. CONCLUSION: Atorvastatin protects podocyte cells via MALAT1/miR-200c/NRF2 signal pathway from pyroptosis and OS induced by HG.	NA	Diabetes Metab Syndr Obes. 2021 Apr 13;14:1631-1645. doi: 10.2147/DMSO.S298950. eCollection 2021.
3176	LncRNA	HOTAIR	miR-130a	ATG2B	gastrointestinal stromal tumor cells	Gastrointestinal Stromal Tumor	Mus musculus (mouse)	qRT-PCR	33824300	LncRNA-HOTAIR activates autophagy and promotes the imatinib resistance of gastrointestinal stromal tumor cells through a mechanism involving the miR-130a/ATG2B pathway.	Gastrointestinal stromal tumors (GISTs) are common neoplasms of the gastrointestinal tract that can be treated successfully using C-kit target therapy and surgery; however, imatinib chemoresistance is a major barrier to success in therapy. The present study aimed to discover alternative pathways in imatinib-resistant GISTs. Long noncoding RNAs (lncRNAs) are newly discovered regulators of chemoresistance. Previously, we showed that the lncRNA HOTAIR was upregulated in recurrent GISTs. In this study, we analyzed differentially expressed lncRNAs after imatinib treatment and found that HOTAIR displayed the largest increase. The distribution of HOTAIR in GISTs was shifted from nucleus to cytoplasm after imatinib treatments. The expression of HOTAIR was validated as related to drug sensitivity through Cell Counting Kit-8 assays. Moreover, HOTAIR was associated strongly with cell autophagy and regulated drug sensitivity via autophagy. Mechanistically, HOTAIR correlated negatively with miRNA-130a in GISTs. The downregulation of miRNA-130a reversed HOTAIR-small interfering RNA-induced suppression of autophagy and imatinib sensitivity. We identified autophagy-related protein 2 homolog B (ATG2B) as a downstream target of miR-130a and HOTAIR. ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity. Finally, HOTAIR was shown to influence the autophagy and imatinib sensitivity of GIST cells in mouse tumor models. Our results suggested that HOTAIR targets the ATG2B inhibitor miR-130a to upregulate the level of cell autophagy so that promotes the imatinib resistance in GISTs.	NA	Cell Death Dis. 2021 Apr 6;12(4):367. doi: 10.1038/s41419-021-03650-7.
3177	LncRNA	ZFAS1	miR-200	ZEB1	colon cancer cell lines (HT29 and SW480)	Colon Adenocarcinoma	Mus musculus (mouse)	qRT-PCR	33771981	Long non-coding RNA ZFAS1 is a major regulator of epithelial-mesenchymal transition through miR-200/ZEB1/E-cadherin, vimentin signaling in colon adenocarcinoma.	Colon adenocarcinoma is a common cause of cancer-related deaths worldwide. Epithelial-mesenchymal transition is a major regulator of cancer metastasis, and increased understanding of this process is essential to improve patient outcomes. Long non-coding RNA (lncRNA) are important regulators of carcinogenesis. To identify lncRNAs associated with colon carcinogenesis, we performed an exploratory differential gene expression analysis comparing paired colon adenocarcinoma and normal colon epithelium using an RNA-sequencing data set. This analysis identified lncRNA ZFAS1 as significantly increased in colon cancer compared to normal colon epithelium. This finding was validated in an institutional cohort using laser capture microdissection. ZFAS1 was also found to be principally located in the cellular cytoplasm. ZFAS1 knockdown was associated with decreased cellular proliferation, migration, and invasion in two colon cancer cell lines (HT29 and SW480). MicroRNA-200b and microRNA-200c (miR-200b and miR-200c) are experimentally validated targets of ZFAS1, and this interaction was confirmed using reciprocal gene knockdown. ZFAS1 knockdown regulated ZEB1 gene expression and downstream targets E-cadherin and vimentin. Knockdown of miR-200b or miR-200c reversed the effect of ZFAS1 knockdown in the ZEB1/E-cadherin, vimentin signaling cascade, and the effects of cellular migration and invasion, but not cellular proliferation. ZFAS1 knockdown was also associated with decreased tumor growth in an in vivo mouse model. These results demonstrate the critical importance of ZFAS1 as a regulator of the miR-200/ZEB1/E-cadherin, vimentin signaling cascade.	NA	Cell Death Discov. 2021 Mar 26;7(1):61. doi: 10.1038/s41420-021-00427-x.
3178	LncRNA	Lnc-ORA	miR-532-3p	IGF2BP2	skeletal muscle cells	Skeletal Muscle Myogenesis	Mus musculus (mouse)	qRT-PCR	33548229	Lnc-ORA interacts with microRNA-532-3p and IGF2BP2 to inhibit skeletal muscle myogenesis.	Skeletal muscle is one of the most important organs of the animal body. Long noncoding RNAs (lncRNAs) play a crucial role in the regulation of skeletal muscle development via several mechanisms. We recently identified lnc-ORA in a search for lncRNAs that influence adipogenesis, finding it impacted adipocyte differentiation by regulating the PI3K/AKT/mTOR pathway. However, whether lnc-ORA has additional roles, specifically in skeletal muscle myogenesis, is not known. Here, we found that lnc-ORA was significantly differentially expressed with age in mouse skeletal muscle tissue and predominantly located in the cytoplasm. Overexpression of lnc-ORA promoted C2C12 myoblast proliferation and inhibited myoblast differentiation. In contrast, lnc-ORA knockdown repressed myoblast proliferation and facilitated myoblast differentiation. Interestingly, silencing of lnc-ORA rescued dexamethasone (Dex)-induced muscle atrophy in vitro. Furthermore, adeno-associated virus 9 (AAV9)-mediated overexpression of lnc-ORA decreased muscle mass and the cross-sectional area of muscle fiber by upregulating the levels of muscle atrophy-related genes and downregulating the levels of myogenic differentiation-related genes in vivo. Mechanistically, lnc-ORA inhibited skeletal muscle myogenesis by acting as a sponge of miR-532-3p, which targets the phosphatase and tensin homologue (PTEN) gene; the resultant changes in PTEN suppressed the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. Additionally, lnc-ORA interacted with insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and reduced the stability of myogenesis genes such as myogenic differentiation 1 (MyoD) and myosin heavy chain (MyHC). Collectively, these findings indicate that lnc-ORA could be a novel underlying regulator of skeletal muscle development.	NA	J Biol Chem. 2021 Feb 3:100376. doi: 10.1016/j.jbc.2021.100376.
3179	LncRNA	SNHG1	miR-376	FOXK1	HCC cells	Hepatocellular Carcinoma	Mus musculus (mouse)	RNA immunoprecipitation;RNA immunoprecipitation;	34095464	SNHG1 knockdown upregulates miR-376a and downregulates FOXK1/Snail axis to prevent tumor growth and metastasis in HCC.	Long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs), and genes are emerging players in cancer progression. In the present study, we explored the roles and interactions of oncogenic lncRNA small nucleolar RNA host gene 1 (SNHG1), miR-376, forkhead box protein K1 (FOXK1), and Snail in hepatocellular carcinoma (HCC). Expression of SNHG1, miR-376, and FOXK1 in HCC was characterized in clinical HCC tissues of 75 patients with HCC. The interactions between SNHG1 and miR-376 and between miR-376 and FOXK1 were predicted and confirmed by dual-luciferase reporter gene and RNA immunoprecipitation assays. Overexpression and knockdown experiments were performed in HCC cells to examine the effects of the SNHG1/miR-376/FOXK1/Snail axis on viability, apoptosis, invasiveness, and migrating abilities. Their effects on tumor growth and metastasis were validated in nude mouse models. SNHG1 and FOXK1 were upregulated, and miR-376a was downregulated in HCC. SNHG1 knockdown contributed to suppression of HCC cell viability, invasion, and migration properties and promotion of apoptosis. SNHG1 could competitively bind to miR-376a to upregulate its target gene FOXK1, which upregulated Snail. SNHG1 knockdown delayed cancer progression both in vitro and in vivo by upregulating miR-376a and downregulating FOXK1 and Snail. SNHG1 knockdown exerts anti-tumor activity in HCC, suggesting a therapeutic target.	NA	Mol Ther Oncolytics. 2021 Feb 4;21:264-277. doi: 10.1016/j.omto.2021.02.002. eCollection 2021 Jun 25.
3180	LncRNA	SNHG14	miR-199b	AQP4	BV2 cells	Ischemic Brain Injury	Mus musculus (mouse)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33609254	Long Noncoding RNA SNHG14 Promotes Ischemic Brain Injury via Regulating miR-199b/AQP4 Axis.	BACKGROUND: Ischemic stroke is the leading cause of disability worldwide. Long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of cerebral ischemia. This study aimed to investigate the role and mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) in ischemic brain injury. METHODS: Cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice. The expression of SNHG14 in MCAO mouse model was detected by quantitative real-time PCR (qRT-PCR). The levels of SNHG14, microRNA-199b (miR-199b) and aquaporin 4 (AQP4) in oxygen-glucose deprivation (OGD)-stimulated BV2 cells were determined by qRT-PCR or western blot assay. Cell proliferation and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. The levels of pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The levels of oxidative stress markers were examined using commercial kits. The relationships among SNHG14, miR-199b and AQP4 were confirmed by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. RESULTS: SNHG14 was up-regulated in MCAO mouse model. Depletion of SNHG14 lessened cerebral ischemia in MCAO mouse model. SNHG14 silencing inhibited inflammation and oxidative stress in OGD-exposed BV2 cells. MiR-199b level was decreased, while AQP4 level was increased in OGD-treated BV2 cells. Knockdown of miR-199b reversed the effect of SNHG14 knockdown on ischemic damage in OGD-stimulated BV2 cells. Moreover, AQP4 overexpression abolished the effect of miR-199b on ischemic injury in OGD-treated BV2 cells. Furthermore, SNHG14 indirectly regulate AQP4 expression by sponging miR-199b. CONCLUSIONS: Knockdown of SNHG14 attenuated ischemic brain injury by inhibiting inflammation and oxidative stress through the miR-199b/AQP4 axis.	NA	Neurochem Res. 2021 May;46(5):1280-1290. doi: 10.1007/s11064-021-03265-6. Epub 2021 Feb 20.
3181	LncRNA	MALAT1	miR-205	CREB1	mouse granulosa cell	Granulosa Cell Apoptosis	Mus musculus (mouse)	qRT-PCR	33681369	lncRNA MALAT1 Regulates Mouse Granulosa Cell Apoptosis and 17β-Estradiol Synthesis via Regulating miR-205/CREB1 Axis.	Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a known long noncoding RNA, was reported to play a crucial role in follicular growth and ovarian disease. However, the physiological function of MALAT1 in mouse granulosa cells (mGCs) remains largely unclear. The aims of this study were to determine the biological function and molecular mechanism of MALAT1 in mGCs. We knocked down MALAT1 in mGCs by using siRNA against MALAT1. We found that knockdown of MALAT1 promoted apoptosis and caspase-3/9 activities in mGCs. Enzyme-linked immunosorbent assay demonstrated that knockdown of MALAT1 significantly decreased the production of estradiol (E2) and progesterone (P4) in mGCs. Mechanistically, MALAT1 serves as a competing endogenous RNA (ceRNA) to sponge microRNA-205 (miR-205), thereby facilitating its downstream target of cyclic AMP response element- (CRE-) binding protein 1 (CREB1). Furthermore, CREB1 overexpression or miR-205 downregulation partially recovered the effect of MALAT1 depletion in mGCs. In summary, these findings suggested that MALAT1 regulated apoptosis and estradiol synthesis of mGCs through the miR-205/CREB1 axis.	NA	Biomed Res Int. 2021 Feb 17;2021:6671814. doi: 10.1155/2021/6671814. eCollection 2021.
3182	LncRNA	NONMMUT055714	miR-7684-5p	SORLA	POCD mouse model	Postoperative Cognitive Dysfunction	Mus musculus (mouse)	qRT-PCR	33902009	LncRNA NONMMUT055714 acts as the sponge of microRNA-7684-5p to protect against postoperative cognitive dysfunction.	Postoperative cognitive dysfunction (POCD) is a neurological complication of surgery especially common in elderly patients. In this study, we investigated the role of NONMMUT055714 in POCD via regulation of miR-7684-5p. In a POCD mouse model, we induced overexpression of NONMUTT055714 via transfection of lentivrus into the hippocampus, and used the Morris water maze for assessment of cognitive function. Silencing of NONMUTT055714 and miR-7684-5p was induced in primary hippocampal neurons to observe the effects of these regulatory RNAs on cellular processes. Bioinformatics analysis and a double luciferase reporter experiment were performed to further explore the relationship between NONMMUT055714, miR-7684-5p, and SORLA. Cell and animal rescue experiments were performed to verify the ability of miR-7684-5p to reverse the protective effects of NONMMUT055714 overexpression in POCD. We observed that NONMMUT055714 has decreased expression in the POCD mouse model. Overexpression of NONMMUT055714 protected against cognitive impairment of the POCD mouse model in vivo. We identified miR-7684-5p as a NONMMUT055714-related miRNA and in turn as an upstream regulator of SORLA. We found that NONMMUT055714 downregulation is associated with decreased SORLA, increased Aβ and p-tau expression, increased inflammatory biomarkers, increased markers of oxidative stress, and increased neuronal apoptosis in vitro. The effects of NONMMUT055714 downregulation were reversed by silencing miR-7684-5p in vitro and in vivo. Taken together, our findings suggest that NONMMUT055714 is protective against the development of POCD via its function as a ceRNA (or miRNA sponge) in the regulation of miR-7684-5p and SORLA. We therefore propose NONMMUT055714 as a novel target for the investigation and prevention of POCD.	NA	Aging (Albany NY). 2021 Apr 26;13(9):12552-12564. doi: 10.18632/aging.202932. Epub 2021 Apr 26.
3183	LncRNA	H19	miR-143	ATG7	HL-1 cells	6-Gingerol Relieves Myocardial Ischamia Reperfusion Injury	Mus musculus (mouse)	Flow cytometry assay;Western blot;Flow Cytometry assay;Immunohistochemistry;	33758383	6-Gingerol relieves myocardial ischaemia/reperfusion injury by regulating lncRNA H19/miR-143/ATG7 signaling axis-mediated autophagy.	Myocardial ischemia/reperfusion injury (MIRI) causes severe damage in cardiac tissue, thereby resulting in a high rate of mortality. 6-Gingerol (6-G) is reported to play an essential role in alleviating MIRI. However, the underlying mechanism remains obscure. This study was intended to explore the potential mechanism by which 6-G functions. Q-PCR was employed to quantify the relative RNA levels of long noncoding RNA (lncRNA) H19 (H19), miR-143, and ATG7, an enzyme essential for autophagy, in HL-1 cells. Western blotting, immunofluorescence, and immunohistochemistry were employed for protein evaluation in cultured cells or mouse tissues. Cell viability, cytotoxicity, and apoptosis were analysed by CCK-8, LDH, and flow cytometry assays, respectively. The binding sites for miR-143 were predicted using starBase software and experimentally validated through a dual-luciferase reporter system. Here, we found that 6-G elevated cellular H19 expression in hypoxia/reoxygenation (H/R)-treated HL-1 cells. Moreover, 6-G increased Bcl-2 expression but reduced cleaved caspase 3 and caspase 9 protein levels. Mechanistically, H19 directly interacted with miR-143 and lowered its cellular abundance by acting as a molecular sponge. Importantly, ATG7 was validated as a regulated gene of miR-143, and the depletion of miR-143 by H19 caused an increased in ATG7 expression, which in turn promoted the autophagy process. Last, mouse experiments highly supported our in vitro findings that 6-G relieves MIRI by enhancing autophagy. The H19/miR-143/ATG7 axis was shown to be critical for the function of 6-G in relieving MIRI.	NA	Lab Invest. 2021 Jul;101(7):865-877. doi: 10.1038/s41374-021-00575-9. Epub 2021 Mar 23.
3184	LncRNA	HOTAIR	miR-20b	NLRP3	synovial fluid mononuclear cells	Gouty Arthritis	Mus musculus (mouse)	ChIP;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;RNA immunoprecipitation;RNA pull-down;	33467979	Long non-coding RNA HOTAIR knockdown alleviates gouty arthritis through miR-20b upregulation and NLRP3 downregulation.	This study aimed to determine the mechanism underlying the regulation of gout by the HOX transcript antisense RNA (HOTAIR) long non-coding RNA (lncRNA). The expression levels of HOTAIR, miR-20b, and Nlrp3 were estimated by qRT-PCR and western blotting. The methylation level of HOTAIR was detected by methylation-specific PCR. The recruitment of DNA methyltransferase 1 (DNMT1) to the lncRNA HOTAIR promoter was confirmed by a ChIP assay. RNA immunoprecipitation and RNA pull-down assays were used to confirm the interaction between HOTAIR and miR-20b. LncRNA HOTAIR and Nlrp3 expression was upregulated, and that of miR-20b was downregulated in synovial fluid mononuclear cells (SFMCs) collected from patients with gouty arthritis and monosodium urate (MSU)-stimulated THP-1 cells. Interleukin (IL)-1β level increased substantially upon stimulation by MSU crystals. The methylation percentage of HOTAIR was reduced in SFMCs from patients with gouty arthritis and MSU-stimulated THP-1 cells. DNMT1 expression was downregulated in MSU-stimulated THP-1 cells, and DNMT1 knockdown increased lncRNA HOTAIR expression. In addition, the interaction of HOTAIR with miR-20b was confirmed. HOTAIR knockdown suppressed Nlrp3 expression and the secretion of inflammatory cytokines via miR-20b regulation. Finally, in vivo experiments showed that HOTAIR knockdown alleviated ankle swelling in a mouse model of gouty arthritis. These findings suggest that lncRNA HOTAIR knockdown suppresses inflammatory cytokine secretion by upregulating miR-20b and downregulating NLRP3, thereby alleviating ankle swelling in gouty arthritis.	NA	Cell Cycle. 2021 Feb;20(3):332-344. doi: 10.1080/15384101.2021.1874696. Epub 2021 Jan 20.
3185	LncRNA	LINC00680	miR-568	AKT3	HCC tissues and cells	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	33499874	LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3.	BACKGROUND: Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. METHODS: QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study. RESULTS: We found that LINC00680 was remarkably upregulated in HCC tissues. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K. CONCLUSION: LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.	NA	J Exp Clin Cancer Res. 2021 Jan 26;40(1):45. doi: 10.1186/s13046-021-01854-5.
3186	Circular RNA	CircST6GALNAC6	miR-200a-3p	STMN1	BCa tissues and cells	Bladder Cancer	Mus musculus (mouse)	ChIP;FISH;microarray;qRT-PCR;RIP assay;RNA immunoprecipitation;Chromatin immunoprecipitation;FISH;Luciferase activity assay;RNA immunoprecipitation;	33568625	circST6GALNAC6 suppresses bladder cancer metastasis by sponging miR-200a-3p to modulate the STMN1/EMT axis.	Bladder cancer (BCa) is an aggressive malignancy because of its distant metastasis and high recurrence rate. Circular RNAs (circRNAs) exert critical regulatory functions in cancer progression. However, the expression patterns and roles of circRNAs in BCa have not been well investigated. In this study, we first screened circRNA expression profiles using a circRNA microarray of paired BCa and normal tissues, and the expression of circST6GALNAC6 was confirmed by qRT-PCR and fluorescence in situ hybridization (FISH). MTT, colony formation and Transwell assays were performed to measure cell proliferation, migration and invasion. We investigated the regulatory effect of circST6GALNAC6 on miRNA and its target genes to explore the potential regulatory mechanisms of circST6GALNAC6 by chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), MS2-tagged RNA affinity purification (MS2-TRAP), immunofluorescence (IF) and dual luciferase activity assays. A nude mouse xenograft model was used to examine the functions of circST6GALNAC6/STMN1 in tumour metastasis in vivo. We found that 881 circRNAs were significantly dysregulated in BCa tissues compared to normal tissues. circST6GALNAC6(hsa_circ_0088708) was downregulated in BCa tissues and cells. Overexpression of circST6GALNAC6 effectively inhibited the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and suppressed BCa metastasis in vivo. Mechanistically, we showed that the SP1 transcription factor, which binds to the circST6GALNAC6 mRNA transcript, activates circST6GALNAC6 transcription. Next, we verified that circST6GALNAC6 serves as a sponge that directly binds miR-200a-3p to regulate stathmin (STMN1) expression. Furthermore, we found that STMN1 is involved in circST6GALNAC6/miR-200a-3p axis-regulated BCa EMT and metastasis. Thus, our findings indicate an important underlying mechanism in BCa metastasis by which SP1-induced circST6GALNAC6 sponges miR-200a-3p to promote STMN1/EMT signalling. This mechanism could provide pivotal potential prognostic biomarkers and therapeutic targets for BCa.	NA	Cell Death Dis. 2021 Feb 10;12(2):168. doi: 10.1038/s41419-021-03459-4.
3187	Circular RNA	CircST6GALNAC6	miR-200a-3p	EMT	BCa tissues and cells	Bladder Cancer	Mus musculus (mouse)	ChIP;FISH;microarray;qRT-PCR;RIP assay;RNA immunoprecipitation;Chromatin immunoprecipitation;FISH;Luciferase activity assay;RNA immunoprecipitation;	33568625	circST6GALNAC6 suppresses bladder cancer metastasis by sponging miR-200a-3p to modulate the STMN1/EMT axis.	Bladder cancer (BCa) is an aggressive malignancy because of its distant metastasis and high recurrence rate. Circular RNAs (circRNAs) exert critical regulatory functions in cancer progression. However, the expression patterns and roles of circRNAs in BCa have not been well investigated. In this study, we first screened circRNA expression profiles using a circRNA microarray of paired BCa and normal tissues, and the expression of circST6GALNAC6 was confirmed by qRT-PCR and fluorescence in situ hybridization (FISH). MTT, colony formation and Transwell assays were performed to measure cell proliferation, migration and invasion. We investigated the regulatory effect of circST6GALNAC6 on miRNA and its target genes to explore the potential regulatory mechanisms of circST6GALNAC6 by chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), MS2-tagged RNA affinity purification (MS2-TRAP), immunofluorescence (IF) and dual luciferase activity assays. A nude mouse xenograft model was used to examine the functions of circST6GALNAC6/STMN1 in tumour metastasis in vivo. We found that 881 circRNAs were significantly dysregulated in BCa tissues compared to normal tissues. circST6GALNAC6(hsa_circ_0088708) was downregulated in BCa tissues and cells. Overexpression of circST6GALNAC6 effectively inhibited the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and suppressed BCa metastasis in vivo. Mechanistically, we showed that the SP1 transcription factor, which binds to the circST6GALNAC6 mRNA transcript, activates circST6GALNAC6 transcription. Next, we verified that circST6GALNAC6 serves as a sponge that directly binds miR-200a-3p to regulate stathmin (STMN1) expression. Furthermore, we found that STMN1 is involved in circST6GALNAC6/miR-200a-3p axis-regulated BCa EMT and metastasis. Thus, our findings indicate an important underlying mechanism in BCa metastasis by which SP1-induced circST6GALNAC6 sponges miR-200a-3p to promote STMN1/EMT signalling. This mechanism could provide pivotal potential prognostic biomarkers and therapeutic targets for BCa.	NA	Cell Death Dis. 2021 Feb 10;12(2):168. doi: 10.1038/s41419-021-03459-4.
3188	LncRNA	HCP5	miR-3619-5p	HDAC9	RB tissues and cell lines	Retinoblastoma	Mus musculus (mouse)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33693951	Knockdown of long non-coding RNA HCP5 suppresses the malignant behavior of retinoblastoma by sponging miR-3619-5p to target HDAC9.	A number of studies have verified the vital effects of long non-coding RNAs on the malignant behaviour of retinoblastoma (RB). The objective of the present study was to examine the specific role and mechanisms of HLA complex P5 (HCP5) in RB. For this purpose, reverse transcription-quantitative polymerase chain reaction was used to determine the expression of HCP5, microRNA (miRNA/miR)-3619-5p and histone deacetylase 9 (HDAC9). A 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay was conducted to detect cell viability. Transwell assays were used to evaluate the abilities of cell migration and invasion. A mouse tumor model was established to explore the functions of HCP5 in RB in vivo. The interactions between HCP5, miR-3619-5p and HDAC9 were confirmed by a dual-luciferase reporter assay. The protein expression of HDAC9 was determined by western blot analysis. The results revealed that the expression levels of HCP5 and HDAC9 were upregulated, whereas those of miR-3619-5p were downregulated in RB tissues and cell lines. The downregulation of HCP5 or the overexpression of miR-3619-5p suppressed RB cell proliferation, migration and invasion in vitro. Simultaneously, the knockdown of HCP5 suppressed tumor growth in mice in vivo. In addition, HCP5 was directly bound to miR-3619-5p and inversely correlated with miR-3619-5p. HDAC9 was found to be a target gene of and negatively regulated by miR-3619-5p. HCP5 expression also positively correlated with HDAC9 expression. Rescue experiments revealed that the overexpression of HDAC9 or the inhibition of miR-3619-5p reversed the inhibition of RB cell viability, migration and invasion induced by the knockdown of HCP5. On the whole, the present study demonstrates that the silencing of HCP5 exerts an anti-tumor effect in RB by sponging miR-3619-5p to target HDAC9.	NA	Int J Mol Med. 2021 May;47(5):74. doi: 10.3892/ijmm.2021.4907. Epub 2021 Mar 11.
3189	LncRNA	LINC01116	miR-744-5p	MDM2	glioma tissues and cells	Glioma	Mus musculus (mouse)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33760190	LINC01116 promotes the proliferation and invasion of glioma by regulating the microRNA-744-5p-MDM2-p53 axis.	Long non-coding RNAs (lncRNAs) have been implicated in the development and progression of tumors. However, the roles and underlying mechanisms of long intergenic non-protein coding RNA 1116 (LINC01116), a member of the lncRNA family, in glioma progression are largely unclear. The expression of LINC01116 and microRNA (miR)-744-5p in glioma tissues and cells was detected by reverse transcription-quantitative PCR. The influences of LINC01116 or miR-744-5p on cell proliferation and invasion were evaluated by Cell Counting Kit-8, colony formation and Transwell assays, and western blotting was used to detect the expression of p53 pathway proteins. A dual-luciferase reporter system was used to locate common binding sites between miR-744-5p and LINC01116 or the 3' untranslated region of E3 ubiquitin-protein ligase Mdm2 (MDM2). RNA immunoprecipitation was used to determine the interactions between RNAs and proteins. Moreover, a xenograft mouse model was constructed to investigate the effects of LINC01116 in vivo, followed by a TdT-mediated dUTP nick end labeling assay to determine the degree of apoptosis in nude mouse tumors. LINC01116 was found to be highly expressed in glioma tissues, which was associated with a malignant phenotype. LINC01116 promoted the proliferation and invasiveness of glioma cells, and inhibited the p53 pathway by preserving the expression of MDM2 mRNA via miR-744-5p sponging. Furthermore, a low degree of miR-744-5p expression was observed in glioma tissues, which was negatively associated with the expression of LINC01116. Overexpression of miR-744-5p inhibited the proliferation and invasiveness of glioma cells, which was rescued by LINC01116. Finally, LINC01116 knockdown inhibited tumor growth in nude mice. In conclusion, LINC01116 is aberrantly expressed and promotes the progression of glioma by regulating the miR-744-5p-MDM2-p53 pathway. In future, targeting LINC01116 may therefore be a potential therapeutic approach for patients with glioma.	NA	Mol Med Rep. 2021 May;23(5):366. doi: 10.3892/mmr.2021.12005. Epub 2021 Mar 24.
3190	LncRNA	IRAK4	miR-19a	p53	SA-β-gal-positive cells	NA	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;	33664669	LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis.	Purpose: Cardiomyocyte senescence is associated with a progressive decline in cardiac physiological function and the risk of cardiovascular events. lncRNA H19 (H19), a well-known long noncoding RNA (lncRNA), is involved in the pathophysiological process of multiple cardiovascular disease such as heart failure, cardiac ischemia and fibrosis. However, the role of H19 in cardiomyocyte senescence remains to be further explored. Methods: Senescence-associated β-galactosidases (SA-β-gal) staining was used to detect cardiomyocyte senescence. Western blot, qRT-PCR and luciferase reporter assay were employed to evaluate the role of H19 in cardiomyocyte senescence and its underling molecular mechanism. Results: H19 level was significantly increased in high glucose-induced senescence cardiomyocytes and aged mouse hearts. Overexpression of H19 enhanced the number of SA-β-gal-positive cells, and the expression of senescence-related proteins p53 and p21, whereas H19 knockdown exerted the opposite effects. Mechanistically, H19 was demonstrated as a competing endogenous RNA (ceRNA) for microRNA-19a (miR-19a): H19 overexpression downregulated miR-19a level, while H19 knockdown upregulated miR-19a. The expression of SOSC1 was dramatically increased in senescence cardiomyocytes and aged mouse hearts. Further experiments identified SOCS1 as a downstream target of miR-19a. H19 upregulated SOCS1 expression and activated the p53/p21 pathway by targeting miR-19a, thus promoting the cardiomyocytes senescence. Conclusion: Our results show that H19 is a pro-senescence lncRNA in cardiomyocytes acting as a ceRNA to target the miR-19a/SOCS1/p53/p21 pathway. Our research reveals a molecular mechanism of cardiomyocyte senescence regulation and provides a novel target of the therapy for senescence-associated cardiac diseases.	NA	Front Pharmacol. 2021 Feb 16;12:631835. doi: 10.3389/fphar.2021.631835. eCollection 2021.
3191	LncRNA	IRAK4	miR-19a	p21	SA-β-gal-positive cells	NA	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;	33664669	LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis.	Purpose: Cardiomyocyte senescence is associated with a progressive decline in cardiac physiological function and the risk of cardiovascular events. lncRNA H19 (H19), a well-known long noncoding RNA (lncRNA), is involved in the pathophysiological process of multiple cardiovascular disease such as heart failure, cardiac ischemia and fibrosis. However, the role of H19 in cardiomyocyte senescence remains to be further explored. Methods: Senescence-associated β-galactosidases (SA-β-gal) staining was used to detect cardiomyocyte senescence. Western blot, qRT-PCR and luciferase reporter assay were employed to evaluate the role of H19 in cardiomyocyte senescence and its underling molecular mechanism. Results: H19 level was significantly increased in high glucose-induced senescence cardiomyocytes and aged mouse hearts. Overexpression of H19 enhanced the number of SA-β-gal-positive cells, and the expression of senescence-related proteins p53 and p21, whereas H19 knockdown exerted the opposite effects. Mechanistically, H19 was demonstrated as a competing endogenous RNA (ceRNA) for microRNA-19a (miR-19a): H19 overexpression downregulated miR-19a level, while H19 knockdown upregulated miR-19a. The expression of SOSC1 was dramatically increased in senescence cardiomyocytes and aged mouse hearts. Further experiments identified SOCS1 as a downstream target of miR-19a. H19 upregulated SOCS1 expression and activated the p53/p21 pathway by targeting miR-19a, thus promoting the cardiomyocytes senescence. Conclusion: Our results show that H19 is a pro-senescence lncRNA in cardiomyocytes acting as a ceRNA to target the miR-19a/SOCS1/p53/p21 pathway. Our research reveals a molecular mechanism of cardiomyocyte senescence regulation and provides a novel target of the therapy for senescence-associated cardiac diseases.	NA	Front Pharmacol. 2021 Feb 16;12:631835. doi: 10.3389/fphar.2021.631835. eCollection 2021.
3192	LncRNA	LBX1-AS1	miR-182-5p	FOXO3	OSCC cells	Oral Squamous Cell Cancer	Mus musculus (mouse)	microarray;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33816238	Exosomal LncRNA LBX1-AS1 Derived From RBPJ Overexpressed-Macrophages Inhibits Oral Squamous Cell Carcinoma Progress via miR-182-5p/FOXO3.	OBJECTIVES: Macrophage-derived exosomes (Mφ-Exos) are involved in tumor onset, progression, and metastasis, but their regulation in oral squamous cell carcinoma (OSCC) is not fully understood. RBPJ is implicated in macrophage activation and plasticity. In this study, we assessed the role of Mφ-Exos with RBPJ overexpression (RBPJ-OE Mφ-Exos) in OSCC. MATERIALS AND METHODS: The long non-coding RNA (lncRNA) profiles in RBPJ-OE Mφ-Exos and THP-1-like macrophages (WT Mφ)-Exos were evaluated using lncRNA microarray. Then the functions of Mφ-Exo-lncRNA in OSCC cells were assessed via CCK-8, EdU, and Transwell invasion assays. Besides, luciferase reporter assay, RNA immunoprecipitation, and Pearson's correlation analysis were adopted to confirm interactions. Ultimately, a nude mouse model of xenografts was used to further analyze the function of Mφ-Exo-lncRNAs in vivo. RESULTS: It was uncovered that lncRNA LBX1-AS1 was upregulated in RBPJ-OE Mφ-Exos relative to that in WT Mφ-Exos. RBPJ-OE Mφ-Exos and LBX1-AS1 overexpression inhibited OSCC cells to proliferate and invade. Meanwhile, LBX1-AS1 knockdown boosted the tumor to grow in vivo. The effects of RBPJ-OE Mφ-Exos on OSCC cells can be reversed by the LBX1-AS1 knockdown. Additionally, mechanistic investigations revealed that LBX1-AS1 acted as a competing endogenous RNA of miR-182-5p to regulate the expression of FOXO3. CONCLUSION: Exo-LBX1-AS1 secreted from RBPJ-OE Mφ inhibits tumor progression through the LBX1-AS1/miR-182-5p/FOXO3 pathway, and LBX1-AS1 is probably a diagnostic biomarker and potential target for OSCC therapy.	NA	Front Oncol. 2021 Mar 17;11:605884. doi: 10.3389/fonc.2021.605884. eCollection 2021.
3193	LncRNA	LINC00261	miR-654-5p	SOCS3	LPS-treated HK-2 cells	Acute Kidney Injury	Mus musculus (mouse)	qRT-PCR	33481135	LINC00261 relieves the progression of sepsis-induced acute kidney injury by inhibiting NF-κB activation through targeting the miR-654-5p/SOCS3 axis.	Sepsis is a life-threatening disease, which can cause the dysfunction of multiple organs, including kidney. Recently, a number of studies found that the long non-coding RNA (lncRNA) is closely associated with the development and progression of sepsis; however, the role of long intergenic non-protein coding RNA 261 (LINC00261) in sepsis-induced acute kidney injury is poorly understood. In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). In conclusion, our results demonstrate that LINC00261 may regulate the progression of sepsis-induced acute kidney injury via the miR-654-5p/SOCS3/NF-κB pathway and therefore provides a new insight into the treatment of this disease.	NA	J Bioenerg Biomembr. 2021 Apr;53(2):129-137. doi: 10.1007/s10863-021-09874-8. Epub 2021 Jan 22.
3194	LncRNA	NEAT1_2	miR-491	TGM2	PTC and non-cancerous tissues	Papillary Thyroid Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;Immunohistochemistry;Luciferase reporter assay;RNA sequencing;	33738254	The NEAT1_2/miR-491 Axis Modulates Papillary Thyroid Cancer Invasion and Metastasis Through TGM2/NFκb/FN1 Signaling.	NEAT1 (nuclear paraspeckle assembly transcript 1) is an oncogenic long non-coding RNA (lncRNA) that facilitates tumorigenesis in multiple cancers. In papillary thyroid cancer (PTC), the molecular mechanism by which NEAT1 affects invasion and metastasis remains elusive. RNA sequencing was used to discover differentially expressed NEAT1_2 downstream genes. Protein and RNA expression analyses and immunohistochemistry detected the expression of NEAT1_2, Transglutaminase 2 (TGM2), and microRNA-491 (miR-491) among PTC and non-cancerous tissues. Transwell and wound healing assays, and a mouse model of lung metastasis were used for further functional analyses. Bioinformatics was performed to predict miRNAs binding to both NEAT1_2 and TGM2. Rescue experiments and dual-luciferase reporter assays were performed. In PTC tissues, NEAT1_2 expression was markedly increased and regulated TGM2 expression. TGM2 was overexpressed in PTC, correlating positively with exthyroidal extension and lymph node metastasis. TGM2 knockdown significantly inhibited invasion and metastasis. NEAT1_2 sponged miR-491, acting as a competing endogenous RNA to regulate TGM2 expression. Fibronectin 1 (FN1) was predicted as a TGM2 target. TGM2 could transcriptionally activate FN1 by promoting nuclear factor kappa B (NFκb) p65 nuclear translocation, ultimately promoting PTC invasion/metastasis. These findings identify that NEAT1_2 sponges miR-491 to regulate TGM2 expression. TGM2 activates FN1 via NFκb to promote PTC invasion and metastasis.	NA	Front Oncol. 2021 Mar 2;11:610547. doi: 10.3389/fonc.2021.610547. eCollection 2021.
3195	LncRNA	SNHG14	miR-876-5p	SSR2	HCC tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33485374	Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis.	BACKGROUND: Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. RESULTS: In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. CONCLUSION: SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.	NA	J Exp Clin Cancer Res. 2021 Jan 23;40(1):36. doi: 10.1186/s13046-021-01838-5.
3196	LncRNA	DLGAP1-AS1	miR-149-5p	TGFB2	CRC cells	Colorectal Cancer	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33816780	The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway.	Colorectal carcinoma (CRC) ranks as the third most common malignancy. Long non-coding RNA DLGAP1-AS1 was reported to be dysregulated and to play a pivotal role in hepatocellular carcinoma (HCC). This work aims to analyze the functions and molecular basis of DLGAP1-AS1 in CRC progression and 5-fluorouracil resistance. Cell Counting Kit-8 (CCK-8) assay, Transwell assay, flow cytometry, and western blot were utilized to measure the CRC cell activity, invasiveness, and apoptosis. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene assay were adopted to verify the direct mutual action between DLGAP1-AS1 and miR-149-5p. The effect of DLGAP1-AS1 knockdown on tumor growth and chemosensitivity of 5-fluorouracil (5-FU) were investigated in the mouse CRC xenograft models. Functional assays showed that silencing DLGAP1-AS1 expression remarkably inhibited cell proliferation and aggressiveness ability and enhanced apoptosis rate and cell chemosensitivity to 5-FU. In addition, miR-149-5p was identified as a tumor suppressor and a direct downstream target of DLGAP1-AS1 in CRC. Furthermore, miR-149-5p was confirmed to directly bind to TGFB2 and DLGAP1-AS1 could regulate the expression of TGFB2 signaling pathway via miR-149-5p in CRC. These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC.	NA	Mol Ther Oncolytics. 2021 Jan 16;20:607-624. doi: 10.1016/j.omto.2021.01.003. eCollection 2021 Mar 26.
3197	LncRNA	GAS5	miR-449b	HMGB1	mouse tissues	Myocardial Injury	Mus musculus (mouse)	qRT-PCR	33645622	Long non-coding RNA GAS5 aggravates myocardial depression in mice with sepsis via the microRNA-449b/HMGB1 axis and the NF-κB signaling pathway.	Sepsis is a common cause of deaths of patients in intensive care unit. The study aims to figure out the role of long non-coding RNA (lncRNA) GAS5 in the myocardial depression in mice with sepsis. Cecal ligation and puncture (CLP) was applied to induce sepsis in mice, and then the heart function, myocardium structure, and the inflammatory response were evaluated. Differentially expressed lncRNAs in mice with sepsis were identified. Then gain- and loss-of-functions of GAS5 were performed in mice to evaluate its role in mouse myocardial depression. The lncRNA-associated microRNA (miRNA)-mRNA network was figured out via an integrative prediction and detection. Myocardial injury was observed by overexpression of high-mobility group box 1 (HMGB1) in septic mice with knockdown of GAS5 expression. Activity of NF-κB signaling was evaluated, and NF-κB inhibition was induced in mice with sepsis and overexpression of GAS5. Collectively, CLP resulted in myocardial depression and injury, and increased inflammation in mice. GAS5 was highly expressed in septic mice. GAS5 inhibition reduced myocardial depression, myocardial injury and inflammation responses in septic mice. GAS5 was identified to bind with miR-449b and to elevate HMGB1 expression, thus activating the NF-κB signaling. HMGB1 overexpression or NF-κB inactivation reduced the GAS5-induced myocardial depression and inflammation in septic mice. Our study suggested that GAS5 might promote sepsis-induced myocardial depression via the miR-449b/HMGB1 axis and the following NF-κB activation.	NA	Biosci Rep. 2021 Apr 30;41(4):BSR20201738. doi: 10.1042/BSR20201738.
3198	LncRNA	MALAT1	miR-515-3p	TRIM65	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33395541	Long Noncoding RNA MALAT1 Knockdown Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis in Non-Small-Cell Lung Cancer Cells Through Regulating miR-515-3p/TRIM65 Axis.	Background: Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and tripartite-motif protein family member 65 (TRIM65) in NSCLC. Materials and Methods: Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory and invasive abilities were detected by transwell assay. The interaction between miR-515-5p and MALAT1 or TRIM65 was predicted by starBase and then confirmed with the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or pull-down assay. Besides, mouse xenograft was conducted to analyze the effect of MALAT1 knockdown on tumor growth in vivo. Results: MALAT1 and TRIM65 expression was upregulated, and miR-515-5p expression was downregulated in NSCLC tissues and cells. Both MALAT1 knockdown and TRIM65 depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells. Interestingly, MALAT1 directly inhibited miR-515-5p expression and miR-515-5p decreased TRIM65 level through interaction. MALAT1 knockdown repressed NSCLC cell growth via modulation of miR-515-5p/TRIM65 axis. Furthermore, silencing MALAT1 inhibited tumor growth in vivo. Conclusions: Our findings demonstrated that MALAT1 depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/TRIM65 axis, providing the theoretical basis for the therapy of NSCLC.	NA	Cancer Biother Radiopharm. 2020 Dec 31. doi: 10.1089/cbr.2020.3730.
3199	Circular RNA	Circ_0003865	miR-3653-3p	GAS1	mouse model	Osteoporosis	Mus musculus (mouse)	Dual-luciferase reporter assay;qRT-PCR;RT-PCR;Western blot;Luciferase reporter assay;RNA pull-down;RNA sequencing;	33632317	Melatonin promotes bone marrow mesenchymal stem cell osteogenic differentiation and prevents osteoporosis development through modulating circ_0003865 that sponges miR-3653-3p.	BACKGROUND: Little is known about the implications of circRNAs in the effects of melatonin (MEL) on bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation and osteoporosis (OP) progression. The aim of our study was to investigate circRNAs in MEL-regulated BMSC differentiation and OP progression. METHODS: BMSC osteogenic differentiation was measured by qRT-PCR, western blot (WB), Alizarin Red, and alkaline phosphatase (ALP) staining. Differential circRNA and mRNA profiles of BMSCs treated by MEL were characterized by deep sequencing, followed by validation using RT-PCR, Sanger sequencing, and qRT-PCR. Silencing and overexpression of circ_0003865 were conducted for functional investigations. The sponged microRNAs and targeted mRNAs were predicted by bioinformatics and validated by qRT-PCR, RNA pull-down, and dual-luciferase reporter assay. The function of miR-3653-3p and circ_0003865/miR-3653-3p/growth arrest-specific gene 1 (GAS1) cascade was validated for the osteogenic differentiation of BMSCs by CCK-8, qRT-PCR, WB, Alizarin Red, and ALP staining. The effects of circ_0003865 on OP development were tested in murine OP model. RESULTS: MEL promoted osteogenic differentiation of BMSCs. RNA sequencing revealed significant alterations in circRNA and mRNA profiles associated with multiple biological processes and signaling pathways. Circ_0003865 expression in BMSCs was significantly decreased by MEL treatment. Silencing of circ_0003865 had no effect on proliferation while promoted osteogenic differentiation of BMSCs. Overexpression of circ_0003865 abrogated the promotion of BMSC osteogenic differentiation induced by MEL, but proliferation of BMSCs induced by MEL had no change whether circ_0003865 was overexpression or not. Furthermore, circ_0003865 sponged miR-3653-3p to promote GAS1 expression in BMSCs. BMSC osteogenic differentiation was enhanced by miR-3653-3p overexpression while BMSC proliferation was not affected. By contrast, miR-3653-3p silencing mitigated the promoted BMSC osteogenic differentiation caused by circ_0003865 silencing, but had no effect on proliferation. Finally, circ_0003865 silencing repressed OP development in mouse model. CONCLUSION: MEL promotes BMSC osteogenic differentiation and inhibits OP pathogenesis by suppressing the expression of circ_0003865, which regulates GAS1 gene expression via sponging miR-3653-3p.	NA	Stem Cell Res Ther. 2021 Feb 25;12(1):150. doi: 10.1186/s13287-021-02224-w.
3200	LncRNA	CircCDR1as	miR-432-5p	E2F3	PC tissues	Pancreatic Cancer	Mus musculus (mouse)	microarray;Western blot;	33593338	Circular RNA CDR1as promotes tumor progression by regulating miR-432-5p/E2F3 axis in pancreatic cancer.	BACKGROUND: Pancreatic cancer (PC), characterized with high growth rate and metastatic rate. It's urgently necessary to explore new mechanism of PC. Circular RNA/miRNA/mRNA network was widely reported to participate in the cancer progression. METHODS: In this research, circular RNA CDR1as (circCDR1as) was identified by microarray analysis and detected in pancreatic cancer (PC) tissues and cells. Transwell, colony-forming assay, nude mouse tumorigenicity assay were used to determine the function of circCDR1as in PC. Western blot, dual luciferase reporting test were applied to investigate the mechanism. RESULTS: We found that circCDR1as was highly expressed in PC tissues. The levels of circCDR1as in PC tissues and cells were higher than those in controls. CircCDR1as promoted the migration, invasion and proliferation of PC cells in vitro and tumor growth in vivo via mediating E2F3 expression by sponging miR-432-5p. CONCLUSIONS: In conclusion, circCDR1as could promote the development of PC and might be a novel diagnostic target for PC.	NA	Cancer Cell Int. 2021 Feb 16;21(1):112. doi: 10.1186/s12935-021-01812-3.
3201	LncRNA	GAS5	miR-194-3p	TXNIP	coronary vascular tissues and endothelial cells	Atherosclerosis	Mus musculus (mouse)	Immunohistochemistry;	33638792	Long Non-coding RNA GAS5 Worsens Coronary Atherosclerosis Through MicroRNA-194-3p/TXNIP Axis.	It is formerly conducted that long non-coding RNA growth arrest-specific 5 (GAS5) is involved in the process of coronary atherosclerosis (AS). The regulatory effects of GAS5 on the microRNA (miR)-194-3p/thioredoxin-interacting protein (TXNIP) axis in AS have been insufficiently explored yet. Thereafter, this work is started from GAS5/miR-194-3p/TXNIP axis in AS. AS rats were modeled to obtain their coronary vascular tissues and endothelial cells (ECs), in which GAS5, miR-194-3p, and TXNIP expression were tested. ECs were identified by immunohistochemistry. The mechanism among GAS5, miR-194-3p, and TXNIP was determined. ECs were transfected with inhibited GAS5 or overexpressed miR-194-3p to decipher their functions in proliferation and apoptosis of ECs in AS. Raised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. This work clearly manifests that inhibited GAS5 facilitates the growth of ECs through miR-194-3p-targeted TXNIP in AS, consolidating the basal reference to the curing for AS.	NA	Mol Neurobiol. 2021 Feb 27. doi: 10.1007/s12035-021-02332-x.
3202	LncRNA	LINC00470	miR-580-3p	WEE1	glioma cells	Glioma 	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33663509	Long non-coding RNA LINC00470 in serum derived exosome: a critical regulator for proliferation and autophagy in glioma cells.	BACKGROUND: To explore the mechanism of LINC00470 in serum exosomes from glioma patients regulating the autophagy and proliferation of glioma cells. METHODS: Exosomes were extracted from glioma patients (GBM-exo). Expression of LINC00470 in exosomes was analyzed with the clinicopathological characteristics of glioma patients. Glioma mouse model was established. The effects of LINC00470, miR-580-3p and WEE1 on cell autophagy and proliferation, as well as the activation of PI3K/AKT/mTOR pathway were measured. Dual luciferase reporter assay and RNA immunoprecipitation (RIP) were conducted to validate the binding of LINC00470 and miR-580-3p and of miR-580-3p and WEE1. RESULTS: LINC00470 overexpressed in GBM-exo and associated with disease severity and postoperative survival time of glioma patients. GBM-exo deteriorated tumor progression in nude mice. Cells incubated with GBM-exo or transfected with pcDNA3.1-LINC00470/miR-580-3p inhibitor/pcDNA3.1-WEE1 had less autophagosome, downregulated LC3-II/LC3-I and Beclin1 expression levels and increased expression of p62 as well as strengthened proliferation ability. The PI3K/AKT/mTOR pathway was activated. LINC00470 competitively bound to miR-580-3p with WEE1. CONCLUSION: LINC00470 in GBM-exo can bind to miR-580-3p in glioma cells to regulate WEE1 expression and activate the PI3K/AKT/mTOR pathway, thereby inhibiting autophagy and enhancing the proliferation of glioma cells.	NA	Cancer Cell Int. 2021 Mar 4;21(1):149. doi: 10.1186/s12935-021-01825-y.
3203	LncRNA	MALAT1	miR-26b-5p	Mfn1	cardiac microvascular endothelial cells	Myocardial Infarction	Mus musculus (mouse)	luciferase assay;	33667993	The lncRNA Malat1 regulates microvascular function after myocardial infarction in mice via miR-26b-5p/Mfn1 axis-mediated mitochondrial dynamics.	RATIONALE: Myocardial infarction (MI) is a leading cause of cardiovascular mortality globally. The improvement of microvascular function is critical for cardiac repair after MI. Evidence now points to long non-coding RNAs (lncRNAs) as key regulators of cardiac remodelling processes. The lncRNA Malat1 is involved in the development and progression of multiple cardiac diseases. Studies have shown that Malat1 is closely related to the regulation of endothelial cell regeneration. However, the potential molecular mechanisms of Malat1 in repairing cardiac microvascular dysfunction after MI remain unreported. METHODS AND RESULTS: The present study found that Malat1 is upregulated in the border zone of infarction in mouse hearts, as well as in isolated cardiac microvascular endothelial cells (CMECs). Targeted knockdown of Malat1 in endothelial cells exacerbated oxidative stress, attenuated angiogenesis and microvascular perfusion, and as a result decreased cardiac function in MI mice. Further studies showed that silencing Malat1 obviously inhibited CMEC proliferation, migration and tube formation, which was at least in part attributed to disturbed mitochondrial dynamics and activation of the mitochondrial apoptosis pathway. Moreover, bioinformatic analyses, luciferase assays and pull-down assays indicated that Malat1 acted as a competing endogenous RNA (ceRNA) for miR-26b-5p and formed a signalling axis with Mfn1 to regulate mitochondrial dynamics and endothelial functions. Overexpression of Mfn1 markedly reversed the microvascular dysfunction and CMEC injuries that were aggravated by silencing Malat1 via inhibition of excessive mitochondrial fragments and mitochondria-dependent apoptosis. CONCLUSIONS: The present study elucidated the functions and mechanisms of Malat1 in cardiac microcirculation repair after MI. The underlying mechanisms of the effects of Malat1 could be attributed to its blocking effects on miR-26b-5p/Mfn1 pathway-mediated mitochondrial dynamics and apoptosis.	NA	Redox Biol. 2021 May;41:101910. doi: 10.1016/j.redox.2021.101910. Epub 2021 Feb 22.
3204	LncRNA	MCM3AP-AS1	miR-193a-5p	SENP1	CRC tissues and matched noncancerous tissues (NCTs)	Colorectal Cancer	Mus musculus (mouse)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33686713	Long noncoding RNA MCM3AP-AS1 enhances cell proliferation and metastasis in colorectal cancer by regulating miR-193a-5p/SENP1.	BACKGROUND: Accumulating evidences have shown that long noncoding RNAs (lncRNAs) play key roles in many diseases, including cancer. Several studies reported that MCM3AP antisense RNA 1 (MCM3AP-AS1) was associated with the tumorigenesis and progression. However, the specific function and mechanism of MCM3AP-AS1 in colorectal cancer (CRC) have not been fully understood. METHODS: The expression of MCM3AP-AS1 was detected by quantitative reverse transcription PCR (RT-qPCR) in CRC tissues and matched noncancerous tissues (NCTs). CCK-8 assay, colony formation assay, transwell assay, xenograft and lung metastasis mouse models were used to examine the tumor-promoting function of MCM3AP-AS1 in vitro and in vivo. The binding relationship between MCM3AP-AS1, miR-193a-5p and sentrin-specific peptidase 1 (SENP1) were screened and identified by databases, RT-qPCR, dual luciferase reporter assay and western blot. RESULTS: In the present study, we got that the expression of MCM3AP-AS1 was higher in CRC tissues than in paired NCTs, and increased MCM3AP-AS1 expression was associated with adverse outcomes in CRC patients. Functional experiments in vitro revealed that silencing of MCM3AP-AS1 could inhibit the proliferation, colony formation, migratory, and invasive abilities of CRC cells. The mouse models of xenograft and lung metastasis further confirmed that in vivo silencing MCM3AP-AS1 could significantly inhibit the growth and metastasis of CRC. Further mechanism studies indicated that MCM3AP-AS1 could sponge miR-193a-5p and inhibit the activity of it. What is more, SENP1 was proved to be a novel target of miR-193a-5p and could be upregulated by MCM3AP-AS1. At last, we observed that SENP1 overexpression in CRC tissues was closely related to unfavorable prognosis. CONCLUSION: Taken together, we identified in CRC the MCM3AP-AS1/miR-193a-5p/SENP1 regulatory axis, which affords a therapeutic possibility for CRC.	NA	Cancer Med. 2021 Apr;10(7):2470-2481. doi: 10.1002/cam4.3830. Epub 2021 Mar 8.
3205	LncRNA	NEAT1	miR-126	TRAF7	primary endothelial cells	Subclinical Hypothyroidism	Mus musculus (mouse)	RT-PCR;Western blot;luciferase assay;	33677813	Long non-coding RNA NEAT1 regulates endothelial functions in subclinical hypothyroidism through miR-126/TRAF7 pathway.	Subclinical hypothyroidism (SCH) is associated with increased risks of endothelial dysfunction and atherosclerosis, but the mechanisms remain unclear. In our previous study, microRNA-126-3p was downregulated in SCH, but the role and regulatory mechanism of miR-126 in SCH has not been investigated. A SCH mouse model was established by feeding mice methimazole. Both primary endothelial cells (ECs) and HUVECs were cultured. The expression levels of key molecules were detected via quantitative RT-PCR, western blotting, and immunofluorescence. Wire myography was used to analyze the changes in vascular tones. A dual-luciferase assay was used to investigate the relationship between lncRNAs, microRNAs and target genes. In detail, it was shown that the expression levels of miR-126-3p were significantly decreased in both the SCH vasculature and HUVECs. MiR-126 supplementation suppressed HUVEC apoptosis and improved vascular function. Moreover, miR-126 could bind to the 3'-untranslated region of TRAF7, thus, regulating the C-FLIP pathway and endothelial apoptosis. Furthermore, lncRNA NEAT1 was upregulated upon TSH treatment and could function as a ceRNA and bind to miR-126, thus, modulating its expression level and vascular function. Finally, the NEAT1/miR-126/TRAF7 axis functions in response to TSH and regulates endothelial functions in SCH in vitro and in vivo. In conclusion, dysregulation of the NEAT1/miR-126/TRAF7 axis is responsible for impaired endothelial functions in SCH. Targeting this axis might become a promising treatment strategy or improving endothelial functions in SCH.	NA	Hum Cell. 2021 May;34(3):825-835. doi: 10.1007/s13577-021-00508-0. Epub 2021 Mar 7.
3206	LncRNA	NORAD	miR-495-3p	KLF5	mouse aorta tissues	Atherosclerosis	Mus musculus (mouse)	qRT-PCR	33636159	Silenced long non-coding RNA activated by DNA damage elevates microRNA-495-3p to suppress atherosclerotic plaque formation via reducing Krüppel-like factor 5.	OBJECTIVE: Atherosclerosis (AS) is an inflammatory disease and the formation of atherosclerotic plaque plays a critical role in AS progression. We aimed to investigate the effect of long non-coding RNA (lncRNA) activated by DNA damage (NORAD)/microRNA-495-3p (miR-495-3p)/Krüppel-like factor 5 (KLF5) axis on atherosclerotic plaque formation. METHODS: The ApoE(-/-) mice were fed a high-fat diet to construct AS mouse models and the modeled mice were treated with altered NORAD, miR-495-3p or KLF5. NORAD, miR-495-3p and KLF5 expression in mouse aorta tissues were evaluated, and the levels of inflammatory factors, oxidative stress factors, endothelial function indices and blood lipid in mice were all determined. The atherosclerotic plaque area, lipid deposition area, collagen fibers and CD68 expression in mouse aorta tissues were assessed. The regulatory relation between NORAD and miR-495-3p, and the target relation between miR-495-3p and KLF5 were confirmed. RESULTS: NORAD and KLF5 were increased whereas miR-495-3p was decreased in atherosclerotic mouse aortas. Inhibited NORAD or elevated miR-495-3p suppressed inflammation, oxidative stress, endothelial dysfunction, blood lipid level, atherosclerotic plaque area, collagen fibers and CD68 expression in atherosclerotic mouse aortas. Effects of elevated miR-495-3p on atherosclerotic mice could be reversed by up-regulation of KLF5. NORAD served as a sponge of miR-495-3p and miR-495-3p directly targeted KLF5. CONCLUSION: Silenced NORAD elevated miR-495-3p to suppress atherosclerotic plaque formation via reducing KLF5. Findings in our research may be helpful for exploring molecular mechanisms of AS.	NA	Exp Cell Res. 2021 Apr 15;401(2):112519. doi: 10.1016/j.yexcr.2021.112519. Epub 2021 Feb 23.
3207	LncRNA	PCA3	miR-140-5p	RFX7	atherosclerosis cells	Atherosclerosis 	Mus musculus (mouse)	qPCR;Western blot;Chromatin immunoprecipitation;	33578049	Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis.	OBJECTIVE: The purpose of this study was to explore the role of long noncoding RNA (lncRNA) prostate cancer antigen 3 (PCA3) in atherosclerosis and the underlying mechanism. METHODS: The Gene Expression Omnibus (GEO) datasets were used to divide differentially expressed lncRNAs, microRNAs (miRNAs), and mRNAs. The expression of PCA3, miR-140-5p, RFX7 and ABCA1 were determined by qPCR or Western blot in ox-LDL-treated macrophages. Macrophage lipid accumulation s was evaluated using the Oil Red O staining and high-performance liquid chromatography. Target relationships among PCA3, miR-140-5p, RFX7, and ABCA1 promoter area were validated via dual-luciferase reporter gene assay or chromatin immunoprecipitation assay. The apoE(-/-) mouse model in vivo was designed to evaluate the effect of PCA3 on the reverse cholesterol transport (RCT) and atherosclerosis. RESULTS: PCA3 was down-regulated in foam cells, whereas miR-140-5p was highly expressed. Overexpression of PCA3 promoted ABCA1-mediated cholesterol efflux and reduced lipid accumulation in macrophages. Besides, RFX7 bound to the ABCA1 promoter and increased ABCA1 expression. Targeted relationships and interactions on the expression between miR-140-5p and PCA3 or RFX7 were elucidated. PCA3 up-regulated ABCA1 expression by binding to miR-140-5p to up-regulate RFX7 and ABCA1 expression in macrophages. PCA3 promoted RCT and impeded the progression of atherosclerosis by sponging miR-140-5p in apoE(-/-) mice. Meanwhile, miR-140-5p also inhibit ABCA1 expression via downregulation of RFX7 to impede RCT and aggravate atherosclerosis. CONCLUSIONS: lncRNA PCA3 promotes ABCA1-mediated cholesterol efflux to inhibit atherosclerosis through sponging miR-140-5p and up-regulating RFX7.	NA	Biochim Biophys Acta Mol Cell Biol Lipids. 2021 May;1866(5):158904. doi: 10.1016/j.bbalip.2021.158904. Epub 2021 Feb 10.
3208	LncRNA	UCC	miR-143-3p	SOX5	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	qPCR;RIP assay;Western blot;	33824420	LncRNA UCC promotes epithelial-mesenchymal transition via the miR-143-3p/SOX5 axis in non-small-cell lung cancer.	Long non-coding RNAs (lncRNAs) have been found to play regulatory roles in cancers; for example, UCC was reported to promote colorectal cancer progression. However, the function of UCC in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, mRNA and protein levels were assessed using qPCR and western blots. Cell viability was assessed by colony-formation assays. The interaction between lncRNAs and miRNAs was detected by dual-luciferase reporter and RIP assays. The tumorigenesis of NSCLC cells in vivo was determined by xenograft assays. LncRNA UCC was highly expressed in both NSCLC tissues and cells. Knockdown of UCC expression suppressed the proliferation of NSCLC cells. In addition, a dual-luciferase reporter system and RIP assays showed that UCC specifically bound to miR-143-3p and acted as a sponge of miR-143-3p in NSCLC cells. The miR-143-3p inhibitor rescued the inhibitory effect of sh-UCC on the proliferation of NSCLC cells. Moreover, miR-143-3p and UCC showed opposite effects on the expression of SOX5, which promoted EMT in NSCLC cells. In addition, in a mouse model, knockdown of UCC expression alleviated EMT and NSCLC progression in vivo, which was consistent with the in vitro results. In the current study, we found that UCC induced the proliferation and migration of NSCLC cells both in vitro and in vivo by inducing the expression of SOX5 via miR-143-3p and subsequently promoted EMT in NSCLC.	NA	Lab Invest. 2021 Apr 6. doi: 10.1038/s41374-021-00586-6.
3209	LncRNA	ZNF561-AS1	miR-26a-3p	SRSF6	CRC tissues tissues and cell lines	Colorectal Cancer	Mus musculus (mouse)	RIP assay;Western blot;Luciferase reporter assay;	33622363	Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis.	BACKGROUND: Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. METHODS: ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. RESULTS: We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. CONCLUSION: In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.	NA	J Exp Clin Cancer Res. 2021 Feb 23;40(1):78. doi: 10.1186/s13046-021-01882-1.
3210	LncRNA	ZNF561-AS1	miR-128-5p	SRSF6	CRC tissues tissues and cell lines	Colorectal Cancer	Mus musculus (mouse)	RIP assay;Western blot;Luciferase reporter assay;	33622363	Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis.	BACKGROUND: Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. METHODS: ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. RESULTS: We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. CONCLUSION: In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.	NA	J Exp Clin Cancer Res. 2021 Feb 23;40(1):78. doi: 10.1186/s13046-021-01882-1.
3211	LncRNA	SNHG14	miR-124-3p	FSTL-1	OA tissues	Osteoarthritis	Mus musculus (mouse)	qRT-PCR	33539913	Downregulation of lncRNA SNHG14 attenuates osteoarthritis by inhibiting FSTL-1 mediated NLRP3 and TLR4/NF-κB pathway through miR-124-3p.	Osteoarthritis (OA) is the joint pain and dysfunction syndrome caused by severe joint degeneration. The overproduced inflammatory mediators contribute greatly to OA development. It is reported that long non-coding RNA (lncRNA) takes part in many inflammatory diseases. Here, we mainly explored the function of lncRNA SNHG14 in OA process and its specific mechanisms. An OA rat model was induced by destabilizing the medial meniscus (DMM) and IL-1β (5 ng/mL) was used to mediate an OA cell model in particular chondrocytes (AC). Gain- or loss-of functional assays of SNHG14 and miR-124-3p were carried out to explore their roles in OA development. The experimental statistics illustrated that lncRNA SNHG14 and IL-1β mRNA expression were both increased in OA tissues, while miR-124-3p was lowly-expressed. Linear regression analysis showed that SNHG14 and miR-124-3p had negative relationship in the OA tissues. In the in vitro experiments, downregulation of lncRNA SNHG14 promoted the proliferation of IL-1β-treated AC and inhibited cell apoptosis and COX-2, iNOS, TNF-α, IL-6 expression. Moreover, lncRNA SNHG14 inhibited miR-124-3p expression as a miRNA sponge. MiR-124-3p targeted the 3'non-translated region (3'UTR) of FSTL-1 and TLR4 and inhibited their expressions. Also, the in vivo experiments confirmed that knocking down SNHG14 relieved the progression of OA in rats via inhibiting inflammatory responses. In conclusion, this study confirmed that downregulation of lncRNA SNHG14 inhibits FSTL-1-mediated activation of NLRP3 and TLR4/NF-κB signalling pathway activation by targeting miR-124-3p, thus attenuating inflammatory reactions in OA.	NA	Life Sci. 2021 Apr 1;270:119143. doi: 10.1016/j.lfs.2021.119143. Epub 2021 Feb 1.
3212	LncRNA	XIST	miR-29c-3p	NFAT5	LPS Stimulated Astrocyte Cell	Secretion Of Inflammatory Cytokines	Mus musculus (mouse)	RIP assay;Western blot;Flow Cytometry assay;	33776905	Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression.	BACKGROUND: Astrocyte activation promotes glutamate accumulation and secretion of inflammatory factors, mainly responsible for epilepsy. Long noncoding RNA (lncRNA) X-inactive-specific transcript (XIST) regulates inflammation; however, the biological role and regulatory mechanism of XIST during astrocyte activation remain unclear. METHODS: In the present study, rat epilepsy model and lipopolysaccharide (LPS)-treated CTX-TNA2 were established. XIST and miR-29c-3p expression were evaluated using quantitative real-time polymerase chain reaction. Nuclear factor of activated T cells 5 (NFAT5) was measured using western blot analysis. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and L-glutamate levels in the culture supernatants were assessed using enzyme-linked immunosorbent assay. The binding between XIST and miR-29c-3p and between miR-29c-3p and the 3'-UTR of NFAT5 was analyzed using dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and Biotin pull-down assay. The proliferation and apoptosis were evaluated using CCK8 and flow cytometry, respectively. RESULTS: XIST expression and NFAT5 protein level was increased, whereas miR-29c-3p expression was decreased in the epilepsy rat model and LPS-treated CTX-TNA2 cells. Silenced XIST expression, miR-29c-3p overexpression, or silenced NFAT5 expression inhibited the secretion of IL-1β, IL-6, and TNF-α and promoted glutamate transport in LPS-treated CTX-TNA2 cells. miR-29c-3p was the potential miRNA sponged by XIST. NFAT5 acted as a direct binding target of miR-29c-3p. Silenced miR-29c-3p expression or NFAT5 overexpression reversed the effect of silenced XIST expression on LPS-treated CTX-TNA2.XIST and miR-29c-3p treatment does not affect NFAT5 mRNA expression, but affects NFAT5 protein level. Furthermore, underexpressed XIST or overexpressed miR-29c-3p in LPS-stimulated CTX-TNA2 can attenuate neuronal apoptosis induced by LPS-stimulated CTX-TNA2. CONCLUSION: LncRNA XIST promotes the secretion of inflammatory cytokines in LPS- treated CTX-TNA2 via sponging miR-29c-3p and regulating NFAT5 expression.	NA	Front Endocrinol (Lausanne). 2021 Mar 12;12:573143. doi: 10.3389/fendo.2021.573143. eCollection 2021.
3213	LncRNA	LINC02288	miR-374a-3p	RTN3	chondrocyte	Chondrocyte Apoptosis And Inflammation	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;luciferase assay;Luciferase reporter assay;RNA immunoprecipitation;	33491257	LINC02288 promotes chondrocyte apoptosis and inflammation through miR-374a-3p targeting RTN3.	BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) is related to the occurrence of osteoarthritis (OA). In the present study, we explored the role of LINC02288 and its regulatory mechanism in OA development. METHODS: GSE113825 was obtained from Gene Expression Omnibus (GEO) database and analyzed to identify the differentially expressed lncRNAs in OA. Gene enrichment analyses and Kyoto Encyclopedia of Genes and Genomes biological process analysis were performed through Metascape (http://metascape.org/gp). The interactions among LINC02288, miR-374a-3p and RTN3 were determined using RNA immunoprecipitation (RIP) assays and dual luciferase reporter assays. Chondrocyte apoptosis was examined using flow cytometry. Western blot assays were conducted to assess the pro-apoptotic and anti-apoptotic markers. RESULTS: We identified a total of 4,491 differentially expressed lncRNAs. We focused on LINC02288 as the top-ranked up-regulated lncRNA in OA as indicated by a significant p-value. LINC02288 was significantly up-regulated, which was further verified by a real-time polymerase chain reaction. Down-regulation of LINC02288 significantly reduced the apoptosis of OA chondrocytes induced by interleukin-1β and the production of pro-inflammatory cytokines. These effects were further verified in an OA rat model. An RIP assay and dual luciferase assay further confirmed that LINC02288 served as a sponge of miR-374a-3p. Moreover, the overexpression of RTN3 could partially reverse the effects of LINC02288 knockdown, mediating inhibitory effects on chondrocyte apoptosis and the inflammatory response. Down-regulation of LINC02288 alleviated OA development in an in vivo OA animal model. CONCLUSIONS: Our findings indicate that LINC02288 contributes to OA progression by targeting the miR-374a-3p/RTN3 axis, which might provide a promising molecular therapy strategy for OA.	NA	J Gene Med. 2021 May;23(5):e3314. doi: 10.1002/jgm.3314. Epub 2021 Mar 25.
3214	LncRNA	MALAT1	miR-302d-3p	LIF	ovarian tissues and ovarian granulosa cells	Polycystic Ovary Syndrome	Mus musculus (mouse)	qRT-PCR	33465389	Down-regulation of MALAT1 aggravates polycystic ovary syndrome by regulating MiR-302d-3p-mediated leukemia inhibitory factor activity.	AIMS: Accumulating evidence have shown the important roles of long noncoding RNA (lncRNA) in controlling different diseases. In the present study, we tried to explore the role which lncRNA MALAT1 plays in polycystic ovary syndrome (PCOS) with the involvement of microRNA-302d-3p (miR-302d-3p) and leukemia inhibitory factor (LIF). METHODS: A PCOS rat model was established and characterized, followed by treatment with si-MALAT1, oe-MALAT1, miR-302d-3p mimic, or miR-302d-3p inhibitor constructs. Serum hormonal levels were detected to evaluate endocrine conditions. The effect of MALAT1 and miR-302d-3p on activities of ovarian granulosa cells was assessed, as well as the involvement of LIF. RESULTS: MALAT1 expression was shown to be downregulated in ovarian tissue of PCOS rats. Overexpression of MALAT1 in vitro promoted proliferation and inhibited apoptosis of ovarian granulosa cells. Overexpression of MALAT1 in vivo reduced the ovarian tissue injury and endocrine disorders accompanied with decreased level of FSH and elevated serum levels of E2, T, and LH in the PCOS rat. Overexpression of MALAT1 also promoted the expression of LIF, which could be reversed by overexpression of miR-302d-3p, indicating that MALAT1 up-regulated the expression of LIF via miR-302d-3p. Furthermore, overexpression of MALAT1 reduced endocrine disorders and ovarian tissue damage via the miR-302d-3p/LIF axis. CONCLUSION: Our study highlighted that MALAT1 plays a protective role in reducing ovarian tissue damage and endocrine disorder in PCOS by regulating the miR-302d-3p/LIF axis.	NA	Life Sci. 2021 Jul 15;277:119076. doi: 10.1016/j.lfs.2021.119076. Epub 2021 Jan 16.
3215	Circular RNA	CircAgtpbp1	miR-543-5p	GH	Rat Pituitary Cells	Secretion Of Growth Hormone	Mus musculus (mouse)	ELISA;FISH;qRT-PCR;Western blot;FISH;	33672649	CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells.	CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT-PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT-PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT-PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.	NA	Animals (Basel). 2021 Feb 20;11(2):558. doi: 10.3390/ani11020558.
3216	LncRNA	HOTAIR	miR-17-5p	STAT3	H9c2 cells	Ischemia Reperfusion Injury	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33883889	HOTAIR/miR-17-5p Axis is Involved in the Propofol-Mediated Cardioprotection Against Ischemia/Reperfusion Injury.	BACKGROUND: Propofol (PPF) ameliorates ischemia/reperfusion (I/R) injury in multiple organs by reducing apoptosis and release of pro-inflammatory cytokines. This study aims to explore the mechanism of PPF in attenuating myocardial ischemia-reperfusion injury (MIRI). MATERIALS AND METHODS: Rat MIRI model was established, and PPF pre-treatment was performed 10 min before I/R. H9c2 cardiomyocytes treated with hypoxia/reoxygenation (H/R) were used to establish an in vitro model. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate HOTAIR and miR-17-5p expression levels. Flow cytometry was employed to detect the apoptosis of H9c2 cells. The interaction between HOTAIR and miR-17-5p was determined by bioinformatics analysis, luciferase reporter gene analysis, and RNA immunoprecipitation experiments. STAT3 and p-STAT3 expressions were detected by Western blot. RESULTS: PPF pre-treatment significantly reduced creatine kinase isoenzyme (CK-MB) and serum lactate dehydrogenase (LDH) levels in the serum of the rats with MIRI. PPF pre-treatment remarkably up-regulated HOTAIR expression and down-regulated miR-17-5p expression in both in vivo and in vitro models. HOTAIR adsorbed miR-17-5p to repress the expression of miR-17-5p. PPF pre-treatment markedly inhibited cardiomyocyte apoptosis induced by I/R or H/R. HOTAIR knockdown could partially reverse the protective effects of PPF on MIRI. HOTAIR could activate STAT3 signaling via repressing miR-17-5p expression. CONCLUSION: PPF protects the MIRI by modulating the HOTAIR/miR-17-5p/STAT3 axis.	NA	Clin Interv Aging. 2021 Apr 15;16:621-632. doi: 10.2147/CIA.S286429. eCollection 2021.
3217	LncRNA	SNHG14	miR-124-3p	FSTL-1	OA tissues	Osteoarthritis	Homo sapiens (human)	qRT-PCR	33539913	Downregulation of lncRNA SNHG14 attenuates osteoarthritis by inhibiting FSTL-1 mediated NLRP3 and TLR4/NF-κB pathway through miR-124-3p.	Osteoarthritis (OA) is the joint pain and dysfunction syndrome caused by severe joint degeneration. The overproduced inflammatory mediators contribute greatly to OA development. It is reported that long non-coding RNA (lncRNA) takes part in many inflammatory diseases. Here, we mainly explored the function of lncRNA SNHG14 in OA process and its specific mechanisms. An OA rat model was induced by destabilizing the medial meniscus (DMM) and IL-1β (5 ng/mL) was used to mediate an OA cell model in particular chondrocytes (AC). Gain- or loss-of functional assays of SNHG14 and miR-124-3p were carried out to explore their roles in OA development. The experimental statistics illustrated that lncRNA SNHG14 and IL-1β mRNA expression were both increased in OA tissues, while miR-124-3p was lowly-expressed. Linear regression analysis showed that SNHG14 and miR-124-3p had negative relationship in the OA tissues. In the in vitro experiments, downregulation of lncRNA SNHG14 promoted the proliferation of IL-1β-treated AC and inhibited cell apoptosis and COX-2, iNOS, TNF-α, IL-6 expression. Moreover, lncRNA SNHG14 inhibited miR-124-3p expression as a miRNA sponge. MiR-124-3p targeted the 3'non-translated region (3'UTR) of FSTL-1 and TLR4 and inhibited their expressions. Also, the in vivo experiments confirmed that knocking down SNHG14 relieved the progression of OA in rats via inhibiting inflammatory responses. In conclusion, this study confirmed that downregulation of lncRNA SNHG14 inhibits FSTL-1-mediated activation of NLRP3 and TLR4/NF-κB signalling pathway activation by targeting miR-124-3p, thus attenuating inflammatory reactions in OA.	NA	Life Sci. 2021 Apr 1;270:119143. doi: 10.1016/j.lfs.2021.119143. Epub 2021 Feb 1.
3218	LncRNA	XIST	miR-29c-3p	NFAT5	LPS Stimulated Astrocyte Cell	Secretion Of Inflammatory Cytokines	Homo sapiens (human)	RIP assay;Western blot;Flow Cytometry assay;	33776905	Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression.	BACKGROUND: Astrocyte activation promotes glutamate accumulation and secretion of inflammatory factors, mainly responsible for epilepsy. Long noncoding RNA (lncRNA) X-inactive-specific transcript (XIST) regulates inflammation; however, the biological role and regulatory mechanism of XIST during astrocyte activation remain unclear. METHODS: In the present study, rat epilepsy model and lipopolysaccharide (LPS)-treated CTX-TNA2 were established. XIST and miR-29c-3p expression were evaluated using quantitative real-time polymerase chain reaction. Nuclear factor of activated T cells 5 (NFAT5) was measured using western blot analysis. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and L-glutamate levels in the culture supernatants were assessed using enzyme-linked immunosorbent assay. The binding between XIST and miR-29c-3p and between miR-29c-3p and the 3'-UTR of NFAT5 was analyzed using dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and Biotin pull-down assay. The proliferation and apoptosis were evaluated using CCK8 and flow cytometry, respectively. RESULTS: XIST expression and NFAT5 protein level was increased, whereas miR-29c-3p expression was decreased in the epilepsy rat model and LPS-treated CTX-TNA2 cells. Silenced XIST expression, miR-29c-3p overexpression, or silenced NFAT5 expression inhibited the secretion of IL-1β, IL-6, and TNF-α and promoted glutamate transport in LPS-treated CTX-TNA2 cells. miR-29c-3p was the potential miRNA sponged by XIST. NFAT5 acted as a direct binding target of miR-29c-3p. Silenced miR-29c-3p expression or NFAT5 overexpression reversed the effect of silenced XIST expression on LPS-treated CTX-TNA2.XIST and miR-29c-3p treatment does not affect NFAT5 mRNA expression, but affects NFAT5 protein level. Furthermore, underexpressed XIST or overexpressed miR-29c-3p in LPS-stimulated CTX-TNA2 can attenuate neuronal apoptosis induced by LPS-stimulated CTX-TNA2. CONCLUSION: LncRNA XIST promotes the secretion of inflammatory cytokines in LPS- treated CTX-TNA2 via sponging miR-29c-3p and regulating NFAT5 expression.	NA	Front Endocrinol (Lausanne). 2021 Mar 12;12:573143. doi: 10.3389/fendo.2021.573143. eCollection 2021.
3219	LncRNA	LINC02288	miR-374a-3p	RTN3	chondrocyte	NA	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;luciferase assay;Luciferase reporter assay;RNA immunoprecipitation;	33491257	LINC02288 promotes chondrocyte apoptosis and inflammation through miR-374a-3p targeting RTN3.	BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) is related to the occurrence of osteoarthritis (OA). In the present study, we explored the role of LINC02288 and its regulatory mechanism in OA development. METHODS: GSE113825 was obtained from Gene Expression Omnibus (GEO) database and analyzed to identify the differentially expressed lncRNAs in OA. Gene enrichment analyses and Kyoto Encyclopedia of Genes and Genomes biological process analysis were performed through Metascape (http://metascape.org/gp). The interactions among LINC02288, miR-374a-3p and RTN3 were determined using RNA immunoprecipitation (RIP) assays and dual luciferase reporter assays. Chondrocyte apoptosis was examined using flow cytometry. Western blot assays were conducted to assess the pro-apoptotic and anti-apoptotic markers. RESULTS: We identified a total of 4,491 differentially expressed lncRNAs. We focused on LINC02288 as the top-ranked up-regulated lncRNA in OA as indicated by a significant p-value. LINC02288 was significantly up-regulated, which was further verified by a real-time polymerase chain reaction. Down-regulation of LINC02288 significantly reduced the apoptosis of OA chondrocytes induced by interleukin-1β and the production of pro-inflammatory cytokines. These effects were further verified in an OA rat model. An RIP assay and dual luciferase assay further confirmed that LINC02288 served as a sponge of miR-374a-3p. Moreover, the overexpression of RTN3 could partially reverse the effects of LINC02288 knockdown, mediating inhibitory effects on chondrocyte apoptosis and the inflammatory response. Down-regulation of LINC02288 alleviated OA development in an in vivo OA animal model. CONCLUSIONS: Our findings indicate that LINC02288 contributes to OA progression by targeting the miR-374a-3p/RTN3 axis, which might provide a promising molecular therapy strategy for OA.	NA	J Gene Med. 2021 May;23(5):e3314. doi: 10.1002/jgm.3314. Epub 2021 Mar 25.
3220	LncRNA	MALAT1	miR-302d-3p	LIF	ovarian tissues and ovarian granulosa cells	Polycystic Ovary Syndrome	Homo sapiens (human)	qRT-PCR	33465389	Down-regulation of MALAT1 aggravates polycystic ovary syndrome by regulating MiR-302d-3p-mediated leukemia inhibitory factor activity.	AIMS: Accumulating evidence have shown the important roles of long noncoding RNA (lncRNA) in controlling different diseases. In the present study, we tried to explore the role which lncRNA MALAT1 plays in polycystic ovary syndrome (PCOS) with the involvement of microRNA-302d-3p (miR-302d-3p) and leukemia inhibitory factor (LIF). METHODS: A PCOS rat model was established and characterized, followed by treatment with si-MALAT1, oe-MALAT1, miR-302d-3p mimic, or miR-302d-3p inhibitor constructs. Serum hormonal levels were detected to evaluate endocrine conditions. The effect of MALAT1 and miR-302d-3p on activities of ovarian granulosa cells was assessed, as well as the involvement of LIF. RESULTS: MALAT1 expression was shown to be downregulated in ovarian tissue of PCOS rats. Overexpression of MALAT1 in vitro promoted proliferation and inhibited apoptosis of ovarian granulosa cells. Overexpression of MALAT1 in vivo reduced the ovarian tissue injury and endocrine disorders accompanied with decreased level of FSH and elevated serum levels of E2, T, and LH in the PCOS rat. Overexpression of MALAT1 also promoted the expression of LIF, which could be reversed by overexpression of miR-302d-3p, indicating that MALAT1 up-regulated the expression of LIF via miR-302d-3p. Furthermore, overexpression of MALAT1 reduced endocrine disorders and ovarian tissue damage via the miR-302d-3p/LIF axis. CONCLUSION: Our study highlighted that MALAT1 plays a protective role in reducing ovarian tissue damage and endocrine disorder in PCOS by regulating the miR-302d-3p/LIF axis.	NA	Life Sci. 2021 Jul 15;277:119076. doi: 10.1016/j.lfs.2021.119076. Epub 2021 Jan 16.
3221	Circular RNA	CircAgtpbp1	miR-543-5p	GH	Rat Pituitary Cells	NA	Homo sapiens (human)	ELISA;FISH;qRT-PCR;Western blot;FISH;	33672649	CircAgtpbp1 Acts as a Molecular Sponge of miR-543-5p to Regulate the Secretion of GH in Rat Pituitary Cells.	CircRNAs have been identified to be expressed differently and stably in numerous species and tissues, but their functions in growth hormone (GH) secretion are still largely unknown. In summary, we have revealed a circRNA-miRNA-mRNA network that may play a biological role in the rat pituitary gland. First, we verified the chromosome location information of circAgtpbp1 according to sequencing analysis. The circAgtpbp1 characteristics were authenticated through PCR, qRT-PCR, treating with RNase and fluorescent in situ hybridization (FISH). Second, we detected the expression pattern of circAgtpbp1 in the rat anterior pituitary by qRT-PCR. We also designed circAgtpbp1 siRNA and constructed overexpression plasmid to evaluate the effect of circAgtpbp1 function on GH secretion by qRT-PCR, ELISA and Western blot. CircAgtpbp1 is a stable, truly circular molecule. We found that circAgtpbp1 interacted with miR-543-5p and can regulate GH secretion in pituitary cells through a circAgtpbp1-miR-543-5p-GH axis. Overall, the evidence generated by our study suggests that circAgtpbp1 can act as a sponge of miR-543-5p to reduce the inhibitory effect of miR-543-5p on Gh1 and further promote GH secretion. These findings expand our existing knowledge on the mechanisms of hormone regulation in the pituitary gland.	NA	Animals (Basel). 2021 Feb 20;11(2):558. doi: 10.3390/ani11020558.
3222	LncRNA	HOTAIR	miR-17-5p	STAT3	H9c2 cells	Ischemia Reperfusion Injury	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33883889	HOTAIR/miR-17-5p Axis is Involved in the Propofol-Mediated Cardioprotection Against Ischemia/Reperfusion Injury.	BACKGROUND: Propofol (PPF) ameliorates ischemia/reperfusion (I/R) injury in multiple organs by reducing apoptosis and release of pro-inflammatory cytokines. This study aims to explore the mechanism of PPF in attenuating myocardial ischemia-reperfusion injury (MIRI). MATERIALS AND METHODS: Rat MIRI model was established, and PPF pre-treatment was performed 10 min before I/R. H9c2 cardiomyocytes treated with hypoxia/reoxygenation (H/R) were used to establish an in vitro model. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to evaluate HOTAIR and miR-17-5p expression levels. Flow cytometry was employed to detect the apoptosis of H9c2 cells. The interaction between HOTAIR and miR-17-5p was determined by bioinformatics analysis, luciferase reporter gene analysis, and RNA immunoprecipitation experiments. STAT3 and p-STAT3 expressions were detected by Western blot. RESULTS: PPF pre-treatment significantly reduced creatine kinase isoenzyme (CK-MB) and serum lactate dehydrogenase (LDH) levels in the serum of the rats with MIRI. PPF pre-treatment remarkably up-regulated HOTAIR expression and down-regulated miR-17-5p expression in both in vivo and in vitro models. HOTAIR adsorbed miR-17-5p to repress the expression of miR-17-5p. PPF pre-treatment markedly inhibited cardiomyocyte apoptosis induced by I/R or H/R. HOTAIR knockdown could partially reverse the protective effects of PPF on MIRI. HOTAIR could activate STAT3 signaling via repressing miR-17-5p expression. CONCLUSION: PPF protects the MIRI by modulating the HOTAIR/miR-17-5p/STAT3 axis.	NA	Clin Interv Aging. 2021 Apr 15;16:621-632. doi: 10.2147/CIA.S286429. eCollection 2021.
3223	LncRNA	CCDC144NL-AS1	miR-940	WDR5	HCC cell line MHCC97H,L02	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;Western blot;Immunohistochemistry;	33977095	LncRNA-CCDC144NL-AS1 Promotes the Development of Hepatocellular Carcinoma by Inducing WDR5 Expression via Sponging miR-940.	PURPOSE: This work was initiated to offer solid evidence regarding the expression and roles of long noncoding RNA (lncRNA) CCDC144NL-AS1 in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: Cell Counting Kit-8 assay, flow cytometric analysis, and invasion assays were used to explore the malignant biological characteristics of cells. Immunohistochemistry (IHC), Western blotting analysis, and real-time quantitative PCR (RT-qPCR) were used to analyze the expression level of related proteins and nucleic acids. Bl6/Rag2/GammaC double knockout mice were used for HCC modeling to address the therapeutic value of CCDC144NL-AS1. RESULTS: CCDC144NL-AS1 was significantly upregulated in HCC tissue and had a marked relationship with the 5-year prognosis. In vitro study revealed that CCDC144NL-AS1 was highly expressed in HCC cell line MHCC97H but lowly expressed in normal hepatic cell line L02. Overexpression of CCDC144NL-AS1 in L02 enhanced the invasion and proliferation abilities of cells but inhibited the apoptosis rate. Knockdown of CCDC144NL-AS1 in MHCC97H weakened the invasion and proliferation abilities of cells but increased the apoptosis rate. CCDC144NL-AS1 was found to sponge miR-940 to induce the expression of WD repeat domain 5 (WDR5). ChIP-seq analysis identified that matrix metalloproteinase (MMP) 2, MMP9, and cyclin-dependent kinase (CDK) 1, CDK2, and CDK4 were all targets of WDR5. The recruitment of WDR5 to the promoter of these target genes upregulated the histone H3 lysine 4 trimethylation (H3K4me3) level in these regions and further induced the transcription of MMP2, MMP9, CDK1, CDK2, and CDK4. In vivo study revealed that compared to the normal liver tissue, CCDC144NL-AS1, WDR5, MMP2, MMP9, CDK1, CDK2, and CDK4 were all significantly upregulated in HCC tissue from the same mouse, while miR-940 was decreased. Besides, knockdown of CCDC144NL-AS1 or WDR5 or overexpression of miR-940 could all inhibit tumor growth. CONCLUSION: CCDC144NL-AS1 drives HCC development by inducing MMP2/MMP9 and CDK1/CDK2/CDK4 expressions through miR-940/WDR5-regulated epigenetic pathway.	NA	J Hepatocell Carcinoma. 2021 May 3;8:333-348. doi: 10.2147/JHC.S306484. eCollection 2021.
3224	Circular RNA	CircSLC7A2	miR-4498	TIMP3	OA tissues	Osteoarthritis	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33960555	CircSLC7A2 protects against osteoarthritis through inhibition of the miR-4498/TIMP3 axis.	OBJECTIVES: Circular RNAs (circRNAs) are noncoding RNAs that compete against other endogenous RNA species, such as microRNAs, and have been implicated in many diseases. In this study, we investigated the role of a new circRNA (circSLC7A2) in osteoarthritis (OA). MATERIALS AND METHODS: The relative expression of circSLC7A2 was significantly lower in OA tissues than it was in matched controls, as shown by real-time quantitative polymerase chain reaction (RT-qPCR). Western blotting, RT-qPCR and immunofluorescence experiments were employed to evaluate the roles of circSLC7A2, miR-4498 and TIMP3. The in vivo role and mechanism of circSLC7A2 were also conformed in a mouse model. RESULTS: circSLC7A2 was decreased in OA model and the circularization of circSLC7A2 was regulated by FUS. Loss of circSLC7A2 reduced the sponge of miR-4498 and further inhibited the expression of TIMP3, subsequently leading to an inflammatory response. We further determined that miR-4498 inhibitor reversed circSLC7A2-knockdown-induced OA phenotypes. Intra-articular injection of circSLC7A2 alleviated in vivo OA progression in a mouse model of anterior cruciate ligament transection (ACLT). CONCLUSIONS: The circSLC7A2/miR-4498/TIMP3 axis of chondrocytes catabolism and anabolism plays a critical role in OA development. Our results suggest that circSLC7A2 may serve as a new therapeutic target for osteoarthritis.	NA	Cell Prolif. 2021 Jun;54(6):e13047. doi: 10.1111/cpr.13047. Epub 2021 May 7.
3225	LncRNA	GAS5	miR-217	Prox1	HG-induced lymphatic endothelial cells	Lymphangiogenesis 	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	33865922	Long noncoding RNA GAS5 accelerates diabetic wound healing and promotes lymphangiogenesis via miR-217/Prox1 axis.	BACKGROUND: Diabetes is usually the leading cause of chronic non-healing wounds. LncRNA-GAS5 has been verified to be involved in the regulation of diabetes or high glucose (HG)-stimulated cells. However, its regulatory roles in diabetic wound healing need further investigation. METHOD: GAS5, miR-217 and Prox1 were identified by qRT-PCR. MTT, flow cytometry assay, wound-healing assay and tube formation were used to analyze cell viability, apoptosis, migration and tube formation capacity. Western blotting was carried out to detect the protein expression of c-Myc, CyclinD1, CDK4, Bcl-2, Prox1, VEGFR-3 and LYVE-1. Bioinformatics and luciferase assay were performed to predict and validate the binding sites of miR-217 on GAS5 and Prox1. Immunofluorescence staining detected the expression and distribution of Prox1. The wound healing rate was also assessed by setting up the diabetic mouse model. H&E staining assessed the distribution of inflammatory cells and fibroblasts in the wound tissues. RESULTS: GAS5 was significantly down-regulated whereas miR-217 was obviously up-regulated in diabetic skin, HG-induced lymphatic endothelial cells (LECs) and diabetic mouse model. GAS5 sponged miR-217 to up-regulate Prox1. GAS5 overexpression or miR-217 inhibition rescued the impairments of cell viability, migration and lymphatic vessel formation and the facilitation of apoptosis of LECs caused by HG. Similar impacts were observed on the protein level of VEGFR-3, LYVE-1, and Prox1. GAS5 promoted wound healing and lymphangiogenesis in the diabetic mouse model. CONCLUSION: GAS5 sponged miR-217 to up-regulate Prox1 and promote lymphangiogenesis and diabetic wound healing. This might provide novel therapeutic strategy to improve the efficacy of diabetic wound healing.	NA	Mol Cell Endocrinol. 2021 Jul 15;532:111283. doi: 10.1016/j.mce.2021.111283. Epub 2021 Apr 15.
3226	LncRNA	USP30-AS1	miR-299-3p	PTP	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33986866	Long non-coding RNA USP30-AS1 aggravates the malignant progression of cervical cancer by sequestering microRNA-299-3p and thereby overexpressing PTP4A1.	USP30 antisense RNA 1 (USP30-AS1) has been studied in bladder urothelial carcinoma. However, the detailed role of USP30-AS1 in cervical cancer remains to be elucidated. Therefore, the present study determined whether USP30-AS1 is implicated in cervical cancer malignancy, and investigated relevant molecular mechanisms. USP30-AS1 expression was measured via reverse transcription-quantitative PCR. Functional experiments, including the Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and mouse tumour model, were performed in order to elucidate the roles of USP30-AS1. The target of USP30-AS1 was predicted using bioinformatics analysis, which was further verified via RNA immunoprecipitation and luciferase reporter assays. Herein, USP30-AS1 overexpression was detected in cervical cancer sample data from The Cancer Genome Atlas and our cohort. Patients with cervical cancer expressing high levels of USP30-AS1 exhibited shorter overall survival than those with low USP30-AS1 expression. In vitro and in vivo experiments revealed that USP30-AS1 interference promoted cell apoptosis; restrained cell proliferation, migration and invasion in vitro, and hindered tumour growth in vivo. Mechanistically, USP30-AS1 competed for microRNA-299-3p (miR-299-3p) in cervical cancer and lowered the regulatory actions of miR-299-3p on protein tyrosine phosphatase type IVA (PTP4A1), resulting in PTP4A1 overexpression. Furthermore, rescue experiments confirmed that miR-299-3p interventions or exogenous PTP4A1 could counteract the cancer-inhibiting actions of USP30-AS1 silencing on cervical cancer cells. In conclusion, the miR-299-3p/PTP4A1 axis is the downstream effector of USP30-AS1 in cervical cancer, forming the USP30-AS1/miR-299-3p/PTP4A1 pathway. This newly identified competing endogenous RNA pathway may offer a novel theoretical and experimental basis for developing promising new strategies for the targeted therapy of cervical cancer.	NA	Oncol Lett. 2021 Jul;22(1):505. doi: 10.3892/ol.2021.12766. Epub 2021 Apr 29.
3227	LncRNA	LNC00115	miR-7	ERK	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	34007214	LNC00115 Mediates Cisplatin Resistance by Regulating the miR-7/ERK Signalling Pathway in Ovarian Cancer.	BACKGROUND: Ovarian cancer has one of the highest mortality rates among all gynaecological malignancies, and increasing evidence suggests that lncRNAs are widely involved in the development of ovarian tumours. This study aimed to investigate the mechanism of the LNC00115/miR-7/ERK axis in the cisplatin resistance of ovarian cancer cells. METHODS: The expression of miR-7 and LNC00115 in ovarian cancer cell lines and tissues was detected by qRT-PCR. The ovarian cancer cell lines were constructed by overexpressing or knocking down the expression of LNC00115 or miR-7. CCK-8, transwell invasion, Western blot, immunohistochemistry, and luciferase reporter assays were carried out to identify the targets of LNC00115 and explore its roles and mechanisms in ovarian cancer. A nude mouse model was established, and the expression of LNC00115, miR-7 and ERK was detected. The changes in the tumours and body weights of the nude mice were measured. RESULTS: LNC00115 was upregulated in ovarian cancer tissues and cisplatin-resistant ovarian cancer cells. Moreover, LNC00115 promoted the cisplatin resistance, invasion and migration of ovarian cancer cells. LNC00115 was shown to directly target miR-7, and miR-7 was downregulated in ovarian cancer tissues and cisplatin-resistant ovarian cancer cells. miR-7 inhibited the cisplatin resistance, invasion and migration of ovarian cancer cells and directly targeted ERK. ERK was overexpressed in cisplatin-resistant ovarian cancer cells and ovarian cancer tissues. In animal experiments, overexpression of LNC00115 enhanced the cisplatin resistance of ovarian cancer cells, while miR-7 had the opposite effect. Mechanistically, LNC00115 sponged miR-7 to increase the expression of ERK, which in turn enhanced the cisplatin resistance of ovarian cancer. CONCLUSION: Our data clarify the mechanism by which the LNC00115/miR-7/ERK axis promotes cisplatin resistance and provide a new clinical strategy for combating cisplatin resistance in ovarian cancer.	NA	Cancer Manag Res. 2021 May 11;13:3817-3826. doi: 10.2147/CMAR.S295097. eCollection 2021.
3228	LncRNA	LINC02308	miR-30e-3p	TM4SF1	glioma tissues and cells	Glioma 	Homo sapiens (human)	microarray;Western blot;	33945031	LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis.	BACKGROUND: Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma. METHODS: The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308. RESULTS: LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1. CONCLUSIONS: LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway. Graphical Abstract Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.	NA	Cell Biol Toxicol. 2021 May 4. doi: 10.1007/s10565-021-09604-1.
3229	LncRNA	GSEC	miR-202-5p	AXL	NA	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Luciferase report assay;RNA immunoprecipitation;	33907418	lncRNA GSEC Promotes the Progression of Triple Negative Breast Cancer (TNBC) by Targeting the miR-202-5p/AXL Axis.	BACKGROUND: This study aimed to explore the biological functions of G-quadruplex-forming sequence containing lncRNA (GSEC) in triple negative breast cancer (TNBC). METHODS: The expression of GSEC in TNBC tissues was evaluated by qRT-PCR. Cell viability was evaluated by Cell Counting Kit-8 assay. Cell proliferation was evaluated by 5-ethynyl-20-deoxyuridine (EdU) staining assay. Cell invasion and migration were evaluated by Transwell assay. Gain- and loss-function assays were performed to assess the biological functions of GSEC in TNBC. The interactions between GSEC, miR-202-5p and AXL were determined by luciferase report assay and RNA immunoprecipitation (RIP) assay. In addition, a nude mouse xenograft model was used to confirm the oncogenic role of GSEC in TNBC. RESULTS: GSEC was significantly upregulated in TNBC tissues and cancer cell lines, and high level of GSEC was associated with advanced tumor stage, positive lymph-node metastasis and the poor prognosis of TNBC patients. Knockdown of GSEC effectively inhibited TNBC cell proliferation, invasion and migration in vitro. GSEC regulated the expression of AXL by directly sponging miR-202-5p. Downregulation of miR-202-5p attenuated GSEC knockdown-induced inhibition on TNBC cell proliferation, invasion and migration in vitro. Meanwhile, overexpression of AXL obviously reversed the inhibitory effects of miR-202-5p mimics in TNBC progression in vitro. CONCLUSION: GSEC functioned as a potential oncogene and promoted AXL-mediated TNBC progression by sponging miR-202-5p, which might be a novel diagnostic and therapeutic target for TNBC.	NA	Onco Targets Ther. 2021 Apr 20;14:2747-2759. doi: 10.2147/OTT.S293832. eCollection 2021.
3230	LncRNA	MALAT1	miR-200c	NRF2	MPC-5 cells	Podocyte Pyroptosis	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33880049	Atorvastatin Regulates MALAT1/miR-200c/NRF2 Activity to Protect Against Podocyte Pyroptosis Induced by High Glucose.	BACKGROUND: Diabetic nephropathy (DN) is one of the main complications of diabetes mellitus (DM), which leads to the long-term loss of kidney functions. Long noncoding RNAs (LncRNAs) can alleviate DN by interacting with microRNAs (miRNAs). In this work, we aimed to explore the effects of the MALAT1/miR-200c/NRF2 regulatory axis on the pyroptosis and oxidative stress (Oxidative stress, OS) of renal podocytes in high glucose (HG) environment and whether the lipid-lowering drug atorvastatin (AT) can relieve renal OS through this approach. METHODS: MPC-5, a mouse podocyte cell line, was induced by HG as a cell model. The protein expressions of caspase-1, GSDMD, NLRP3, NRF2, etc. were detected by Western blotting and immunofluorescence, and the mRNA level of caspase-1, GSDMD, NLRP3, NRF2, MALAT1, miR-200c was tested by qRT-PCR. The cell pyroptosis of podocytes treated with AT was verified by CCK-8 or flow cytometry. The levels of Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were measured by spectrophotometer, respectively. RESULTS: The caspase-1 was upregulated in time-dependent manner and got the peak at 48 h and 30 mmol/L respectively in MPC-5 cells treated with HG. Further, the expression of GSDMD, MALAT1 and miR-200c were increased, while the level of NRF2, HO-1, OS-related indicators, were decreased simultaneously. Knockdown the MALAT1 protected MPC-5 cells from pyroptosis and OS induced by HG. However, overexpressing miR-200c in control-group cells increased pyroptosis and upregulated the OS level with HG culture medium. Further, atorvastatin protected MPC-5 cells from cell pyroptosis and downregulated the level of renal OS via attenuating the expression of MALAT1 and miR-200c. CONCLUSION: Atorvastatin protects podocyte cells via MALAT1/miR-200c/NRF2 signal pathway from pyroptosis and OS induced by HG.	NA	Diabetes Metab Syndr Obes. 2021 Apr 13;14:1631-1645. doi: 10.2147/DMSO.S298950. eCollection 2021.
3231	LncRNA	HOTAIR	miR-130a	ATG2B	gastrointestinal stromal tumor cells	Gastrointestinal Stromal Tumor	Homo sapiens (human)	qRT-PCR	33824300	LncRNA-HOTAIR activates autophagy and promotes the imatinib resistance of gastrointestinal stromal tumor cells through a mechanism involving the miR-130a/ATG2B pathway.	Gastrointestinal stromal tumors (GISTs) are common neoplasms of the gastrointestinal tract that can be treated successfully using C-kit target therapy and surgery; however, imatinib chemoresistance is a major barrier to success in therapy. The present study aimed to discover alternative pathways in imatinib-resistant GISTs. Long noncoding RNAs (lncRNAs) are newly discovered regulators of chemoresistance. Previously, we showed that the lncRNA HOTAIR was upregulated in recurrent GISTs. In this study, we analyzed differentially expressed lncRNAs after imatinib treatment and found that HOTAIR displayed the largest increase. The distribution of HOTAIR in GISTs was shifted from nucleus to cytoplasm after imatinib treatments. The expression of HOTAIR was validated as related to drug sensitivity through Cell Counting Kit-8 assays. Moreover, HOTAIR was associated strongly with cell autophagy and regulated drug sensitivity via autophagy. Mechanistically, HOTAIR correlated negatively with miRNA-130a in GISTs. The downregulation of miRNA-130a reversed HOTAIR-small interfering RNA-induced suppression of autophagy and imatinib sensitivity. We identified autophagy-related protein 2 homolog B (ATG2B) as a downstream target of miR-130a and HOTAIR. ATG2B downregulation reversed the effect of pEX-3-HOTAIR/miR-130a inhibitor on imatinib sensitivity. Finally, HOTAIR was shown to influence the autophagy and imatinib sensitivity of GIST cells in mouse tumor models. Our results suggested that HOTAIR targets the ATG2B inhibitor miR-130a to upregulate the level of cell autophagy so that promotes the imatinib resistance in GISTs.	NA	Cell Death Dis. 2021 Apr 6;12(4):367. doi: 10.1038/s41419-021-03650-7.
3232	LncRNA	ZFAS1	miR-200	ZEB1	colon cancer cell lines (HT29 and SW480)	Colon Adenocarcinoma	Homo sapiens (human)	qRT-PCR	33771981	Long non-coding RNA ZFAS1 is a major regulator of epithelial-mesenchymal transition through miR-200/ZEB1/E-cadherin, vimentin signaling in colon adenocarcinoma.	Colon adenocarcinoma is a common cause of cancer-related deaths worldwide. Epithelial-mesenchymal transition is a major regulator of cancer metastasis, and increased understanding of this process is essential to improve patient outcomes. Long non-coding RNA (lncRNA) are important regulators of carcinogenesis. To identify lncRNAs associated with colon carcinogenesis, we performed an exploratory differential gene expression analysis comparing paired colon adenocarcinoma and normal colon epithelium using an RNA-sequencing data set. This analysis identified lncRNA ZFAS1 as significantly increased in colon cancer compared to normal colon epithelium. This finding was validated in an institutional cohort using laser capture microdissection. ZFAS1 was also found to be principally located in the cellular cytoplasm. ZFAS1 knockdown was associated with decreased cellular proliferation, migration, and invasion in two colon cancer cell lines (HT29 and SW480). MicroRNA-200b and microRNA-200c (miR-200b and miR-200c) are experimentally validated targets of ZFAS1, and this interaction was confirmed using reciprocal gene knockdown. ZFAS1 knockdown regulated ZEB1 gene expression and downstream targets E-cadherin and vimentin. Knockdown of miR-200b or miR-200c reversed the effect of ZFAS1 knockdown in the ZEB1/E-cadherin, vimentin signaling cascade, and the effects of cellular migration and invasion, but not cellular proliferation. ZFAS1 knockdown was also associated with decreased tumor growth in an in vivo mouse model. These results demonstrate the critical importance of ZFAS1 as a regulator of the miR-200/ZEB1/E-cadherin, vimentin signaling cascade.	NA	Cell Death Discov. 2021 Mar 26;7(1):61. doi: 10.1038/s41420-021-00427-x.
3233	LncRNA	Lnc-ORA	miR-532-3p	IGF2BP2	skeletal muscle cells	NA	Homo sapiens (human)	qRT-PCR	33548229	Lnc-ORA interacts with microRNA-532-3p and IGF2BP2 to inhibit skeletal muscle myogenesis.	Skeletal muscle is one of the most important organs of the animal body. Long noncoding RNAs (lncRNAs) play a crucial role in the regulation of skeletal muscle development via several mechanisms. We recently identified lnc-ORA in a search for lncRNAs that influence adipogenesis, finding it impacted adipocyte differentiation by regulating the PI3K/AKT/mTOR pathway. However, whether lnc-ORA has additional roles, specifically in skeletal muscle myogenesis, is not known. Here, we found that lnc-ORA was significantly differentially expressed with age in mouse skeletal muscle tissue and predominantly located in the cytoplasm. Overexpression of lnc-ORA promoted C2C12 myoblast proliferation and inhibited myoblast differentiation. In contrast, lnc-ORA knockdown repressed myoblast proliferation and facilitated myoblast differentiation. Interestingly, silencing of lnc-ORA rescued dexamethasone (Dex)-induced muscle atrophy in vitro. Furthermore, adeno-associated virus 9 (AAV9)-mediated overexpression of lnc-ORA decreased muscle mass and the cross-sectional area of muscle fiber by upregulating the levels of muscle atrophy-related genes and downregulating the levels of myogenic differentiation-related genes in vivo. Mechanistically, lnc-ORA inhibited skeletal muscle myogenesis by acting as a sponge of miR-532-3p, which targets the phosphatase and tensin homologue (PTEN) gene; the resultant changes in PTEN suppressed the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. Additionally, lnc-ORA interacted with insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) and reduced the stability of myogenesis genes such as myogenic differentiation 1 (MyoD) and myosin heavy chain (MyHC). Collectively, these findings indicate that lnc-ORA could be a novel underlying regulator of skeletal muscle development.	NA	J Biol Chem. 2021 Feb 3:100376. doi: 10.1016/j.jbc.2021.100376.
3234	LncRNA	SNHG1	miR-376	FOXK1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	34095464	SNHG1 knockdown upregulates miR-376a and downregulates FOXK1/Snail axis to prevent tumor growth and metastasis in HCC.	Long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs), and genes are emerging players in cancer progression. In the present study, we explored the roles and interactions of oncogenic lncRNA small nucleolar RNA host gene 1 (SNHG1), miR-376, forkhead box protein K1 (FOXK1), and Snail in hepatocellular carcinoma (HCC). Expression of SNHG1, miR-376, and FOXK1 in HCC was characterized in clinical HCC tissues of 75 patients with HCC. The interactions between SNHG1 and miR-376 and between miR-376 and FOXK1 were predicted and confirmed by dual-luciferase reporter gene and RNA immunoprecipitation assays. Overexpression and knockdown experiments were performed in HCC cells to examine the effects of the SNHG1/miR-376/FOXK1/Snail axis on viability, apoptosis, invasiveness, and migrating abilities. Their effects on tumor growth and metastasis were validated in nude mouse models. SNHG1 and FOXK1 were upregulated, and miR-376a was downregulated in HCC. SNHG1 knockdown contributed to suppression of HCC cell viability, invasion, and migration properties and promotion of apoptosis. SNHG1 could competitively bind to miR-376a to upregulate its target gene FOXK1, which upregulated Snail. SNHG1 knockdown delayed cancer progression both in vitro and in vivo by upregulating miR-376a and downregulating FOXK1 and Snail. SNHG1 knockdown exerts anti-tumor activity in HCC, suggesting a therapeutic target.	NA	Mol Ther Oncolytics. 2021 Feb 4;21:264-277. doi: 10.1016/j.omto.2021.02.002. eCollection 2021 Jun 25.
3235	LncRNA	SNHG14	miR-199b	AQP4	BV2 cells	Ischemic Brain Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33609254	Long Noncoding RNA SNHG14 Promotes Ischemic Brain Injury via Regulating miR-199b/AQP4 Axis.	BACKGROUND: Ischemic stroke is the leading cause of disability worldwide. Long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of cerebral ischemia. This study aimed to investigate the role and mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) in ischemic brain injury. METHODS: Cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice. The expression of SNHG14 in MCAO mouse model was detected by quantitative real-time PCR (qRT-PCR). The levels of SNHG14, microRNA-199b (miR-199b) and aquaporin 4 (AQP4) in oxygen-glucose deprivation (OGD)-stimulated BV2 cells were determined by qRT-PCR or western blot assay. Cell proliferation and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. The levels of pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The levels of oxidative stress markers were examined using commercial kits. The relationships among SNHG14, miR-199b and AQP4 were confirmed by dual-luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. RESULTS: SNHG14 was up-regulated in MCAO mouse model. Depletion of SNHG14 lessened cerebral ischemia in MCAO mouse model. SNHG14 silencing inhibited inflammation and oxidative stress in OGD-exposed BV2 cells. MiR-199b level was decreased, while AQP4 level was increased in OGD-treated BV2 cells. Knockdown of miR-199b reversed the effect of SNHG14 knockdown on ischemic damage in OGD-stimulated BV2 cells. Moreover, AQP4 overexpression abolished the effect of miR-199b on ischemic injury in OGD-treated BV2 cells. Furthermore, SNHG14 indirectly regulate AQP4 expression by sponging miR-199b. CONCLUSIONS: Knockdown of SNHG14 attenuated ischemic brain injury by inhibiting inflammation and oxidative stress through the miR-199b/AQP4 axis.	NA	Neurochem Res. 2021 May;46(5):1280-1290. doi: 10.1007/s11064-021-03265-6. Epub 2021 Feb 20.
3236	LncRNA	MALAT1	miR-205	CREB1	mouse granulosa cell	NA	Homo sapiens (human)	qRT-PCR	33681369	lncRNA MALAT1 Regulates Mouse Granulosa Cell Apoptosis and 17β-Estradiol Synthesis via Regulating miR-205/CREB1 Axis.	Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a known long noncoding RNA, was reported to play a crucial role in follicular growth and ovarian disease. However, the physiological function of MALAT1 in mouse granulosa cells (mGCs) remains largely unclear. The aims of this study were to determine the biological function and molecular mechanism of MALAT1 in mGCs. We knocked down MALAT1 in mGCs by using siRNA against MALAT1. We found that knockdown of MALAT1 promoted apoptosis and caspase-3/9 activities in mGCs. Enzyme-linked immunosorbent assay demonstrated that knockdown of MALAT1 significantly decreased the production of estradiol (E2) and progesterone (P4) in mGCs. Mechanistically, MALAT1 serves as a competing endogenous RNA (ceRNA) to sponge microRNA-205 (miR-205), thereby facilitating its downstream target of cyclic AMP response element- (CRE-) binding protein 1 (CREB1). Furthermore, CREB1 overexpression or miR-205 downregulation partially recovered the effect of MALAT1 depletion in mGCs. In summary, these findings suggested that MALAT1 regulated apoptosis and estradiol synthesis of mGCs through the miR-205/CREB1 axis.	NA	Biomed Res Int. 2021 Feb 17;2021:6671814. doi: 10.1155/2021/6671814. eCollection 2021.
3237	LncRNA	NONMMUT055714	miR-7684-5p	SORLA	POCD mouse model	Postoperative Cognitive Dysfunction	Homo sapiens (human)	qRT-PCR	33902009	LncRNA NONMMUT055714 acts as the sponge of microRNA-7684-5p to protect against postoperative cognitive dysfunction.	Postoperative cognitive dysfunction (POCD) is a neurological complication of surgery especially common in elderly patients. In this study, we investigated the role of NONMMUT055714 in POCD via regulation of miR-7684-5p. In a POCD mouse model, we induced overexpression of NONMUTT055714 via transfection of lentivrus into the hippocampus, and used the Morris water maze for assessment of cognitive function. Silencing of NONMUTT055714 and miR-7684-5p was induced in primary hippocampal neurons to observe the effects of these regulatory RNAs on cellular processes. Bioinformatics analysis and a double luciferase reporter experiment were performed to further explore the relationship between NONMMUT055714, miR-7684-5p, and SORLA. Cell and animal rescue experiments were performed to verify the ability of miR-7684-5p to reverse the protective effects of NONMMUT055714 overexpression in POCD. We observed that NONMMUT055714 has decreased expression in the POCD mouse model. Overexpression of NONMMUT055714 protected against cognitive impairment of the POCD mouse model in vivo. We identified miR-7684-5p as a NONMMUT055714-related miRNA and in turn as an upstream regulator of SORLA. We found that NONMMUT055714 downregulation is associated with decreased SORLA, increased Aβ and p-tau expression, increased inflammatory biomarkers, increased markers of oxidative stress, and increased neuronal apoptosis in vitro. The effects of NONMMUT055714 downregulation were reversed by silencing miR-7684-5p in vitro and in vivo. Taken together, our findings suggest that NONMMUT055714 is protective against the development of POCD via its function as a ceRNA (or miRNA sponge) in the regulation of miR-7684-5p and SORLA. We therefore propose NONMMUT055714 as a novel target for the investigation and prevention of POCD.	NA	Aging (Albany NY). 2021 Apr 26;13(9):12552-12564. doi: 10.18632/aging.202932. Epub 2021 Apr 26.
3238	LncRNA	H19	miR-143	ATG7	HL-1 cells	6-Gingerol Relieves Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)	Flow cytometry assay;Western blot;Flow Cytometry assay;Immunohistochemistry;	33758383	6-Gingerol relieves myocardial ischaemia/reperfusion injury by regulating lncRNA H19/miR-143/ATG7 signaling axis-mediated autophagy.	Myocardial ischemia/reperfusion injury (MIRI) causes severe damage in cardiac tissue, thereby resulting in a high rate of mortality. 6-Gingerol (6-G) is reported to play an essential role in alleviating MIRI. However, the underlying mechanism remains obscure. This study was intended to explore the potential mechanism by which 6-G functions. Q-PCR was employed to quantify the relative RNA levels of long noncoding RNA (lncRNA) H19 (H19), miR-143, and ATG7, an enzyme essential for autophagy, in HL-1 cells. Western blotting, immunofluorescence, and immunohistochemistry were employed for protein evaluation in cultured cells or mouse tissues. Cell viability, cytotoxicity, and apoptosis were analysed by CCK-8, LDH, and flow cytometry assays, respectively. The binding sites for miR-143 were predicted using starBase software and experimentally validated through a dual-luciferase reporter system. Here, we found that 6-G elevated cellular H19 expression in hypoxia/reoxygenation (H/R)-treated HL-1 cells. Moreover, 6-G increased Bcl-2 expression but reduced cleaved caspase 3 and caspase 9 protein levels. Mechanistically, H19 directly interacted with miR-143 and lowered its cellular abundance by acting as a molecular sponge. Importantly, ATG7 was validated as a regulated gene of miR-143, and the depletion of miR-143 by H19 caused an increased in ATG7 expression, which in turn promoted the autophagy process. Last, mouse experiments highly supported our in vitro findings that 6-G relieves MIRI by enhancing autophagy. The H19/miR-143/ATG7 axis was shown to be critical for the function of 6-G in relieving MIRI.	NA	Lab Invest. 2021 Jul;101(7):865-877. doi: 10.1038/s41374-021-00575-9. Epub 2021 Mar 23.
3239	LncRNA	HOTAIR	miR-20b	NLRP3	synovial fluid mononuclear cells	Gouty Arthritis	Homo sapiens (human)	ChIP;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;RNA immunoprecipitation;RNA pull-down;	33467979	Long non-coding RNA HOTAIR knockdown alleviates gouty arthritis through miR-20b upregulation and NLRP3 downregulation.	This study aimed to determine the mechanism underlying the regulation of gout by the HOX transcript antisense RNA (HOTAIR) long non-coding RNA (lncRNA). The expression levels of HOTAIR, miR-20b, and Nlrp3 were estimated by qRT-PCR and western blotting. The methylation level of HOTAIR was detected by methylation-specific PCR. The recruitment of DNA methyltransferase 1 (DNMT1) to the lncRNA HOTAIR promoter was confirmed by a ChIP assay. RNA immunoprecipitation and RNA pull-down assays were used to confirm the interaction between HOTAIR and miR-20b. LncRNA HOTAIR and Nlrp3 expression was upregulated, and that of miR-20b was downregulated in synovial fluid mononuclear cells (SFMCs) collected from patients with gouty arthritis and monosodium urate (MSU)-stimulated THP-1 cells. Interleukin (IL)-1β level increased substantially upon stimulation by MSU crystals. The methylation percentage of HOTAIR was reduced in SFMCs from patients with gouty arthritis and MSU-stimulated THP-1 cells. DNMT1 expression was downregulated in MSU-stimulated THP-1 cells, and DNMT1 knockdown increased lncRNA HOTAIR expression. In addition, the interaction of HOTAIR with miR-20b was confirmed. HOTAIR knockdown suppressed Nlrp3 expression and the secretion of inflammatory cytokines via miR-20b regulation. Finally, in vivo experiments showed that HOTAIR knockdown alleviated ankle swelling in a mouse model of gouty arthritis. These findings suggest that lncRNA HOTAIR knockdown suppresses inflammatory cytokine secretion by upregulating miR-20b and downregulating NLRP3, thereby alleviating ankle swelling in gouty arthritis.	NA	Cell Cycle. 2021 Feb;20(3):332-344. doi: 10.1080/15384101.2021.1874696. Epub 2021 Jan 20.
3240	LncRNA	LINC00680	miR-568	AKT3	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	33499874	LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3.	BACKGROUND: Hepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity. METHODS: QRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study. RESULTS: We found that LINC00680 was remarkably upregulated in HCC tissues. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K. CONCLUSION: LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.	NA	J Exp Clin Cancer Res. 2021 Jan 26;40(1):45. doi: 10.1186/s13046-021-01854-5.
3241	Circular RNA	CircST6GALNAC6	miR-200a-3p	STMN1	BCa tissues and cells	Bladder Cancer	Homo sapiens (human)	ChIP;FISH;microarray;qRT-PCR;RIP assay;RNA immunoprecipitation;Chromatin immunoprecipitation;FISH;Luciferase activity assay;RNA immunoprecipitation;	33568625	circST6GALNAC6 suppresses bladder cancer metastasis by sponging miR-200a-3p to modulate the STMN1/EMT axis.	Bladder cancer (BCa) is an aggressive malignancy because of its distant metastasis and high recurrence rate. Circular RNAs (circRNAs) exert critical regulatory functions in cancer progression. However, the expression patterns and roles of circRNAs in BCa have not been well investigated. In this study, we first screened circRNA expression profiles using a circRNA microarray of paired BCa and normal tissues, and the expression of circST6GALNAC6 was confirmed by qRT-PCR and fluorescence in situ hybridization (FISH). MTT, colony formation and Transwell assays were performed to measure cell proliferation, migration and invasion. We investigated the regulatory effect of circST6GALNAC6 on miRNA and its target genes to explore the potential regulatory mechanisms of circST6GALNAC6 by chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), MS2-tagged RNA affinity purification (MS2-TRAP), immunofluorescence (IF) and dual luciferase activity assays. A nude mouse xenograft model was used to examine the functions of circST6GALNAC6/STMN1 in tumour metastasis in vivo. We found that 881 circRNAs were significantly dysregulated in BCa tissues compared to normal tissues. circST6GALNAC6(hsa_circ_0088708) was downregulated in BCa tissues and cells. Overexpression of circST6GALNAC6 effectively inhibited the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and suppressed BCa metastasis in vivo. Mechanistically, we showed that the SP1 transcription factor, which binds to the circST6GALNAC6 mRNA transcript, activates circST6GALNAC6 transcription. Next, we verified that circST6GALNAC6 serves as a sponge that directly binds miR-200a-3p to regulate stathmin (STMN1) expression. Furthermore, we found that STMN1 is involved in circST6GALNAC6/miR-200a-3p axis-regulated BCa EMT and metastasis. Thus, our findings indicate an important underlying mechanism in BCa metastasis by which SP1-induced circST6GALNAC6 sponges miR-200a-3p to promote STMN1/EMT signalling. This mechanism could provide pivotal potential prognostic biomarkers and therapeutic targets for BCa.	NA	Cell Death Dis. 2021 Feb 10;12(2):168. doi: 10.1038/s41419-021-03459-4.
3242	Circular RNA	CircST6GALNAC6	miR-200a-3p	EMT	BCa tissues and cells	Bladder Cancer	Homo sapiens (human)	ChIP;FISH;microarray;qRT-PCR;RIP assay;RNA immunoprecipitation;Chromatin immunoprecipitation;FISH;Luciferase activity assay;RNA immunoprecipitation;	33568625	circST6GALNAC6 suppresses bladder cancer metastasis by sponging miR-200a-3p to modulate the STMN1/EMT axis.	Bladder cancer (BCa) is an aggressive malignancy because of its distant metastasis and high recurrence rate. Circular RNAs (circRNAs) exert critical regulatory functions in cancer progression. However, the expression patterns and roles of circRNAs in BCa have not been well investigated. In this study, we first screened circRNA expression profiles using a circRNA microarray of paired BCa and normal tissues, and the expression of circST6GALNAC6 was confirmed by qRT-PCR and fluorescence in situ hybridization (FISH). MTT, colony formation and Transwell assays were performed to measure cell proliferation, migration and invasion. We investigated the regulatory effect of circST6GALNAC6 on miRNA and its target genes to explore the potential regulatory mechanisms of circST6GALNAC6 by chromatin immunoprecipitation (ChIP), RNA immunoprecipitation (RIP), MS2-tagged RNA affinity purification (MS2-TRAP), immunofluorescence (IF) and dual luciferase activity assays. A nude mouse xenograft model was used to examine the functions of circST6GALNAC6/STMN1 in tumour metastasis in vivo. We found that 881 circRNAs were significantly dysregulated in BCa tissues compared to normal tissues. circST6GALNAC6(hsa_circ_0088708) was downregulated in BCa tissues and cells. Overexpression of circST6GALNAC6 effectively inhibited the cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and suppressed BCa metastasis in vivo. Mechanistically, we showed that the SP1 transcription factor, which binds to the circST6GALNAC6 mRNA transcript, activates circST6GALNAC6 transcription. Next, we verified that circST6GALNAC6 serves as a sponge that directly binds miR-200a-3p to regulate stathmin (STMN1) expression. Furthermore, we found that STMN1 is involved in circST6GALNAC6/miR-200a-3p axis-regulated BCa EMT and metastasis. Thus, our findings indicate an important underlying mechanism in BCa metastasis by which SP1-induced circST6GALNAC6 sponges miR-200a-3p to promote STMN1/EMT signalling. This mechanism could provide pivotal potential prognostic biomarkers and therapeutic targets for BCa.	NA	Cell Death Dis. 2021 Feb 10;12(2):168. doi: 10.1038/s41419-021-03459-4.
3243	LncRNA	HCP5	miR-3619-5p	HDAC9	RB tissues and cell lines	Retinoblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33693951	Knockdown of long non-coding RNA HCP5 suppresses the malignant behavior of retinoblastoma by sponging miR-3619-5p to target HDAC9.	A number of studies have verified the vital effects of long non-coding RNAs on the malignant behaviour of retinoblastoma (RB). The objective of the present study was to examine the specific role and mechanisms of HLA complex P5 (HCP5) in RB. For this purpose, reverse transcription-quantitative polymerase chain reaction was used to determine the expression of HCP5, microRNA (miRNA/miR)-3619-5p and histone deacetylase 9 (HDAC9). A 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay was conducted to detect cell viability. Transwell assays were used to evaluate the abilities of cell migration and invasion. A mouse tumor model was established to explore the functions of HCP5 in RB in vivo. The interactions between HCP5, miR-3619-5p and HDAC9 were confirmed by a dual-luciferase reporter assay. The protein expression of HDAC9 was determined by western blot analysis. The results revealed that the expression levels of HCP5 and HDAC9 were upregulated, whereas those of miR-3619-5p were downregulated in RB tissues and cell lines. The downregulation of HCP5 or the overexpression of miR-3619-5p suppressed RB cell proliferation, migration and invasion in vitro. Simultaneously, the knockdown of HCP5 suppressed tumor growth in mice in vivo. In addition, HCP5 was directly bound to miR-3619-5p and inversely correlated with miR-3619-5p. HDAC9 was found to be a target gene of and negatively regulated by miR-3619-5p. HCP5 expression also positively correlated with HDAC9 expression. Rescue experiments revealed that the overexpression of HDAC9 or the inhibition of miR-3619-5p reversed the inhibition of RB cell viability, migration and invasion induced by the knockdown of HCP5. On the whole, the present study demonstrates that the silencing of HCP5 exerts an anti-tumor effect in RB by sponging miR-3619-5p to target HDAC9.	NA	Int J Mol Med. 2021 May;47(5):74. doi: 10.3892/ijmm.2021.4907. Epub 2021 Mar 11.
3244	LncRNA	LINC01116	miR-744-5p	MDM2	glioma tissues and cells	Glioma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33760190	LINC01116 promotes the proliferation and invasion of glioma by regulating the microRNA-744-5p-MDM2-p53 axis.	Long non-coding RNAs (lncRNAs) have been implicated in the development and progression of tumors. However, the roles and underlying mechanisms of long intergenic non-protein coding RNA 1116 (LINC01116), a member of the lncRNA family, in glioma progression are largely unclear. The expression of LINC01116 and microRNA (miR)-744-5p in glioma tissues and cells was detected by reverse transcription-quantitative PCR. The influences of LINC01116 or miR-744-5p on cell proliferation and invasion were evaluated by Cell Counting Kit-8, colony formation and Transwell assays, and western blotting was used to detect the expression of p53 pathway proteins. A dual-luciferase reporter system was used to locate common binding sites between miR-744-5p and LINC01116 or the 3' untranslated region of E3 ubiquitin-protein ligase Mdm2 (MDM2). RNA immunoprecipitation was used to determine the interactions between RNAs and proteins. Moreover, a xenograft mouse model was constructed to investigate the effects of LINC01116 in vivo, followed by a TdT-mediated dUTP nick end labeling assay to determine the degree of apoptosis in nude mouse tumors. LINC01116 was found to be highly expressed in glioma tissues, which was associated with a malignant phenotype. LINC01116 promoted the proliferation and invasiveness of glioma cells, and inhibited the p53 pathway by preserving the expression of MDM2 mRNA via miR-744-5p sponging. Furthermore, a low degree of miR-744-5p expression was observed in glioma tissues, which was negatively associated with the expression of LINC01116. Overexpression of miR-744-5p inhibited the proliferation and invasiveness of glioma cells, which was rescued by LINC01116. Finally, LINC01116 knockdown inhibited tumor growth in nude mice. In conclusion, LINC01116 is aberrantly expressed and promotes the progression of glioma by regulating the miR-744-5p-MDM2-p53 pathway. In future, targeting LINC01116 may therefore be a potential therapeutic approach for patients with glioma.	NA	Mol Med Rep. 2021 May;23(5):366. doi: 10.3892/mmr.2021.12005. Epub 2021 Mar 24.
3245	LncRNA	IRAK4	miR-19a	p53	SA-β-gal-positive cells	NA	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33664669	LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis.	Purpose: Cardiomyocyte senescence is associated with a progressive decline in cardiac physiological function and the risk of cardiovascular events. lncRNA H19 (H19), a well-known long noncoding RNA (lncRNA), is involved in the pathophysiological process of multiple cardiovascular disease such as heart failure, cardiac ischemia and fibrosis. However, the role of H19 in cardiomyocyte senescence remains to be further explored. Methods: Senescence-associated β-galactosidases (SA-β-gal) staining was used to detect cardiomyocyte senescence. Western blot, qRT-PCR and luciferase reporter assay were employed to evaluate the role of H19 in cardiomyocyte senescence and its underling molecular mechanism. Results: H19 level was significantly increased in high glucose-induced senescence cardiomyocytes and aged mouse hearts. Overexpression of H19 enhanced the number of SA-β-gal-positive cells, and the expression of senescence-related proteins p53 and p21, whereas H19 knockdown exerted the opposite effects. Mechanistically, H19 was demonstrated as a competing endogenous RNA (ceRNA) for microRNA-19a (miR-19a): H19 overexpression downregulated miR-19a level, while H19 knockdown upregulated miR-19a. The expression of SOSC1 was dramatically increased in senescence cardiomyocytes and aged mouse hearts. Further experiments identified SOCS1 as a downstream target of miR-19a. H19 upregulated SOCS1 expression and activated the p53/p21 pathway by targeting miR-19a, thus promoting the cardiomyocytes senescence. Conclusion: Our results show that H19 is a pro-senescence lncRNA in cardiomyocytes acting as a ceRNA to target the miR-19a/SOCS1/p53/p21 pathway. Our research reveals a molecular mechanism of cardiomyocyte senescence regulation and provides a novel target of the therapy for senescence-associated cardiac diseases.	NA	Front Pharmacol. 2021 Feb 16;12:631835. doi: 10.3389/fphar.2021.631835. eCollection 2021.
3246	LncRNA	IRAK4	miR-19a	p21	SA-β-gal-positive cells	NA	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33664669	LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis.	Purpose: Cardiomyocyte senescence is associated with a progressive decline in cardiac physiological function and the risk of cardiovascular events. lncRNA H19 (H19), a well-known long noncoding RNA (lncRNA), is involved in the pathophysiological process of multiple cardiovascular disease such as heart failure, cardiac ischemia and fibrosis. However, the role of H19 in cardiomyocyte senescence remains to be further explored. Methods: Senescence-associated β-galactosidases (SA-β-gal) staining was used to detect cardiomyocyte senescence. Western blot, qRT-PCR and luciferase reporter assay were employed to evaluate the role of H19 in cardiomyocyte senescence and its underling molecular mechanism. Results: H19 level was significantly increased in high glucose-induced senescence cardiomyocytes and aged mouse hearts. Overexpression of H19 enhanced the number of SA-β-gal-positive cells, and the expression of senescence-related proteins p53 and p21, whereas H19 knockdown exerted the opposite effects. Mechanistically, H19 was demonstrated as a competing endogenous RNA (ceRNA) for microRNA-19a (miR-19a): H19 overexpression downregulated miR-19a level, while H19 knockdown upregulated miR-19a. The expression of SOSC1 was dramatically increased in senescence cardiomyocytes and aged mouse hearts. Further experiments identified SOCS1 as a downstream target of miR-19a. H19 upregulated SOCS1 expression and activated the p53/p21 pathway by targeting miR-19a, thus promoting the cardiomyocytes senescence. Conclusion: Our results show that H19 is a pro-senescence lncRNA in cardiomyocytes acting as a ceRNA to target the miR-19a/SOCS1/p53/p21 pathway. Our research reveals a molecular mechanism of cardiomyocyte senescence regulation and provides a novel target of the therapy for senescence-associated cardiac diseases.	NA	Front Pharmacol. 2021 Feb 16;12:631835. doi: 10.3389/fphar.2021.631835. eCollection 2021.
3247	LncRNA	LBX1-AS1	miR-182-5p	FOXO3	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	microarray;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33816238	Exosomal LncRNA LBX1-AS1 Derived From RBPJ Overexpressed-Macrophages Inhibits Oral Squamous Cell Carcinoma Progress via miR-182-5p/FOXO3.	OBJECTIVES: Macrophage-derived exosomes (Mφ-Exos) are involved in tumor onset, progression, and metastasis, but their regulation in oral squamous cell carcinoma (OSCC) is not fully understood. RBPJ is implicated in macrophage activation and plasticity. In this study, we assessed the role of Mφ-Exos with RBPJ overexpression (RBPJ-OE Mφ-Exos) in OSCC. MATERIALS AND METHODS: The long non-coding RNA (lncRNA) profiles in RBPJ-OE Mφ-Exos and THP-1-like macrophages (WT Mφ)-Exos were evaluated using lncRNA microarray. Then the functions of Mφ-Exo-lncRNA in OSCC cells were assessed via CCK-8, EdU, and Transwell invasion assays. Besides, luciferase reporter assay, RNA immunoprecipitation, and Pearson's correlation analysis were adopted to confirm interactions. Ultimately, a nude mouse model of xenografts was used to further analyze the function of Mφ-Exo-lncRNAs in vivo. RESULTS: It was uncovered that lncRNA LBX1-AS1 was upregulated in RBPJ-OE Mφ-Exos relative to that in WT Mφ-Exos. RBPJ-OE Mφ-Exos and LBX1-AS1 overexpression inhibited OSCC cells to proliferate and invade. Meanwhile, LBX1-AS1 knockdown boosted the tumor to grow in vivo. The effects of RBPJ-OE Mφ-Exos on OSCC cells can be reversed by the LBX1-AS1 knockdown. Additionally, mechanistic investigations revealed that LBX1-AS1 acted as a competing endogenous RNA of miR-182-5p to regulate the expression of FOXO3. CONCLUSION: Exo-LBX1-AS1 secreted from RBPJ-OE Mφ inhibits tumor progression through the LBX1-AS1/miR-182-5p/FOXO3 pathway, and LBX1-AS1 is probably a diagnostic biomarker and potential target for OSCC therapy.	NA	Front Oncol. 2021 Mar 17;11:605884. doi: 10.3389/fonc.2021.605884. eCollection 2021.
3248	LncRNA	LINC00261	miR-654-5p	SOCS3	LPS-treated HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR	33481135	LINC00261 relieves the progression of sepsis-induced acute kidney injury by inhibiting NF-κB activation through targeting the miR-654-5p/SOCS3 axis.	Sepsis is a life-threatening disease, which can cause the dysfunction of multiple organs, including kidney. Recently, a number of studies found that the long non-coding RNA (lncRNA) is closely associated with the development and progression of sepsis; however, the role of long intergenic non-protein coding RNA 261 (LINC00261) in sepsis-induced acute kidney injury is poorly understood. In this study, we found the expression of LINC00261 was significantly decreased in the serum of patients with sepsis than healthy controls. A similar result was also observed in the mouse model of sepsis induced by lipopolysaccharide (LPS). Further investigations revealed that overexpression of LINC00261 improved the viability, suppressed the apoptosis and reduced the generation of inflammatory cytokines in LPS-treated HK-2 cells. Mechanistically, we confirmed that LINC00261 could function as a sponge to combine with microRNA-654-5p (miR-654-5p) which inhibits nuclear factor-κB (NF-κB) activity by targeting suppressor of cytokine signaling 3 (SOCS3). In conclusion, our results demonstrate that LINC00261 may regulate the progression of sepsis-induced acute kidney injury via the miR-654-5p/SOCS3/NF-κB pathway and therefore provides a new insight into the treatment of this disease.	NA	J Bioenerg Biomembr. 2021 Apr;53(2):129-137. doi: 10.1007/s10863-021-09874-8. Epub 2021 Jan 22.
3249	LncRNA	NEAT1_2	miR-491	TGM2	PTC and non-cancerous tissues	Papillary Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Immunohistochemistry;Luciferase reporter assay;RNA sequencing;	33738254	The NEAT1_2/miR-491 Axis Modulates Papillary Thyroid Cancer Invasion and Metastasis Through TGM2/NFκb/FN1 Signaling.	NEAT1 (nuclear paraspeckle assembly transcript 1) is an oncogenic long non-coding RNA (lncRNA) that facilitates tumorigenesis in multiple cancers. In papillary thyroid cancer (PTC), the molecular mechanism by which NEAT1 affects invasion and metastasis remains elusive. RNA sequencing was used to discover differentially expressed NEAT1_2 downstream genes. Protein and RNA expression analyses and immunohistochemistry detected the expression of NEAT1_2, Transglutaminase 2 (TGM2), and microRNA-491 (miR-491) among PTC and non-cancerous tissues. Transwell and wound healing assays, and a mouse model of lung metastasis were used for further functional analyses. Bioinformatics was performed to predict miRNAs binding to both NEAT1_2 and TGM2. Rescue experiments and dual-luciferase reporter assays were performed. In PTC tissues, NEAT1_2 expression was markedly increased and regulated TGM2 expression. TGM2 was overexpressed in PTC, correlating positively with exthyroidal extension and lymph node metastasis. TGM2 knockdown significantly inhibited invasion and metastasis. NEAT1_2 sponged miR-491, acting as a competing endogenous RNA to regulate TGM2 expression. Fibronectin 1 (FN1) was predicted as a TGM2 target. TGM2 could transcriptionally activate FN1 by promoting nuclear factor kappa B (NFκb) p65 nuclear translocation, ultimately promoting PTC invasion/metastasis. These findings identify that NEAT1_2 sponges miR-491 to regulate TGM2 expression. TGM2 activates FN1 via NFκb to promote PTC invasion and metastasis.	NA	Front Oncol. 2021 Mar 2;11:610547. doi: 10.3389/fonc.2021.610547. eCollection 2021.
3250	LncRNA	SNHG14	miR-876-5p	SSR2	HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33485374	Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis.	BACKGROUND: Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. RESULTS: In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. CONCLUSION: SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.	NA	J Exp Clin Cancer Res. 2021 Jan 23;40(1):36. doi: 10.1186/s13046-021-01838-5.
3251	LncRNA	DLGAP1-AS1	miR-149-5p	TGFB2	CRC cells	Colorectal Cancer	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33816780	The lncRNA DLGAP1-AS1/miR-149-5p/TGFB2 axis contributes to colorectal cancer progression and 5-FU resistance by regulating smad2 pathway.	Colorectal carcinoma (CRC) ranks as the third most common malignancy. Long non-coding RNA DLGAP1-AS1 was reported to be dysregulated and to play a pivotal role in hepatocellular carcinoma (HCC). This work aims to analyze the functions and molecular basis of DLGAP1-AS1 in CRC progression and 5-fluorouracil resistance. Cell Counting Kit-8 (CCK-8) assay, Transwell assay, flow cytometry, and western blot were utilized to measure the CRC cell activity, invasiveness, and apoptosis. RNA immunoprecipitation (RIP) and dual-luciferase reporter gene assay were adopted to verify the direct mutual action between DLGAP1-AS1 and miR-149-5p. The effect of DLGAP1-AS1 knockdown on tumor growth and chemosensitivity of 5-fluorouracil (5-FU) were investigated in the mouse CRC xenograft models. Functional assays showed that silencing DLGAP1-AS1 expression remarkably inhibited cell proliferation and aggressiveness ability and enhanced apoptosis rate and cell chemosensitivity to 5-FU. In addition, miR-149-5p was identified as a tumor suppressor and a direct downstream target of DLGAP1-AS1 in CRC. Furthermore, miR-149-5p was confirmed to directly bind to TGFB2 and DLGAP1-AS1 could regulate the expression of TGFB2 signaling pathway via miR-149-5p in CRC. These new findings indicate that DLGAP1-AS1 knockdown inhibited the progression of CRC and enhanced the 5-FU sensitivity of CRC cells through miR-149-5p/TGFB2 regulatory axis, suggesting that DLGAP1-AS1 may be a promising therapeutic target for CRC.	NA	Mol Ther Oncolytics. 2021 Jan 16;20:607-624. doi: 10.1016/j.omto.2021.01.003. eCollection 2021 Mar 26.
3252	LncRNA	GAS5	miR-449b	HMGB1	mouse tissues	Myocardial Injury	Homo sapiens (human)	qRT-PCR	33645622	Long non-coding RNA GAS5 aggravates myocardial depression in mice with sepsis via the microRNA-449b/HMGB1 axis and the NF-κB signaling pathway.	Sepsis is a common cause of deaths of patients in intensive care unit. The study aims to figure out the role of long non-coding RNA (lncRNA) GAS5 in the myocardial depression in mice with sepsis. Cecal ligation and puncture (CLP) was applied to induce sepsis in mice, and then the heart function, myocardium structure, and the inflammatory response were evaluated. Differentially expressed lncRNAs in mice with sepsis were identified. Then gain- and loss-of-functions of GAS5 were performed in mice to evaluate its role in mouse myocardial depression. The lncRNA-associated microRNA (miRNA)-mRNA network was figured out via an integrative prediction and detection. Myocardial injury was observed by overexpression of high-mobility group box 1 (HMGB1) in septic mice with knockdown of GAS5 expression. Activity of NF-κB signaling was evaluated, and NF-κB inhibition was induced in mice with sepsis and overexpression of GAS5. Collectively, CLP resulted in myocardial depression and injury, and increased inflammation in mice. GAS5 was highly expressed in septic mice. GAS5 inhibition reduced myocardial depression, myocardial injury and inflammation responses in septic mice. GAS5 was identified to bind with miR-449b and to elevate HMGB1 expression, thus activating the NF-κB signaling. HMGB1 overexpression or NF-κB inactivation reduced the GAS5-induced myocardial depression and inflammation in septic mice. Our study suggested that GAS5 might promote sepsis-induced myocardial depression via the miR-449b/HMGB1 axis and the following NF-κB activation.	NA	Biosci Rep. 2021 Apr 30;41(4):BSR20201738. doi: 10.1042/BSR20201738.
3253	LncRNA	MALAT1	miR-515-3p	TRIM65	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33395541	Long Noncoding RNA MALAT1 Knockdown Inhibits Proliferation, Migration, and Invasion and Promotes Apoptosis in Non-Small-Cell Lung Cancer Cells Through Regulating miR-515-3p/TRIM65 Axis.	Background: Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) and tripartite-motif protein family member 65 (TRIM65) in NSCLC. Materials and Methods: Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory and invasive abilities were detected by transwell assay. The interaction between miR-515-5p and MALAT1 or TRIM65 was predicted by starBase and then confirmed with the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or pull-down assay. Besides, mouse xenograft was conducted to analyze the effect of MALAT1 knockdown on tumor growth in vivo. Results: MALAT1 and TRIM65 expression was upregulated, and miR-515-5p expression was downregulated in NSCLC tissues and cells. Both MALAT1 knockdown and TRIM65 depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells. Interestingly, MALAT1 directly inhibited miR-515-5p expression and miR-515-5p decreased TRIM65 level through interaction. MALAT1 knockdown repressed NSCLC cell growth via modulation of miR-515-5p/TRIM65 axis. Furthermore, silencing MALAT1 inhibited tumor growth in vivo. Conclusions: Our findings demonstrated that MALAT1 depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/TRIM65 axis, providing the theoretical basis for the therapy of NSCLC.	NA	Cancer Biother Radiopharm. 2020 Dec 31. doi: 10.1089/cbr.2020.3730.
3254	Circular RNA	Circ_0003865	miR-3653-3p	GAS1	mouse model	Osteoporosis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RT-PCR;Western blot;Luciferase reporter assay;RNA pull-down;RNA sequencing;	33632317	Melatonin promotes bone marrow mesenchymal stem cell osteogenic differentiation and prevents osteoporosis development through modulating circ_0003865 that sponges miR-3653-3p.	BACKGROUND: Little is known about the implications of circRNAs in the effects of melatonin (MEL) on bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation and osteoporosis (OP) progression. The aim of our study was to investigate circRNAs in MEL-regulated BMSC differentiation and OP progression. METHODS: BMSC osteogenic differentiation was measured by qRT-PCR, western blot (WB), Alizarin Red, and alkaline phosphatase (ALP) staining. Differential circRNA and mRNA profiles of BMSCs treated by MEL were characterized by deep sequencing, followed by validation using RT-PCR, Sanger sequencing, and qRT-PCR. Silencing and overexpression of circ_0003865 were conducted for functional investigations. The sponged microRNAs and targeted mRNAs were predicted by bioinformatics and validated by qRT-PCR, RNA pull-down, and dual-luciferase reporter assay. The function of miR-3653-3p and circ_0003865/miR-3653-3p/growth arrest-specific gene 1 (GAS1) cascade was validated for the osteogenic differentiation of BMSCs by CCK-8, qRT-PCR, WB, Alizarin Red, and ALP staining. The effects of circ_0003865 on OP development were tested in murine OP model. RESULTS: MEL promoted osteogenic differentiation of BMSCs. RNA sequencing revealed significant alterations in circRNA and mRNA profiles associated with multiple biological processes and signaling pathways. Circ_0003865 expression in BMSCs was significantly decreased by MEL treatment. Silencing of circ_0003865 had no effect on proliferation while promoted osteogenic differentiation of BMSCs. Overexpression of circ_0003865 abrogated the promotion of BMSC osteogenic differentiation induced by MEL, but proliferation of BMSCs induced by MEL had no change whether circ_0003865 was overexpression or not. Furthermore, circ_0003865 sponged miR-3653-3p to promote GAS1 expression in BMSCs. BMSC osteogenic differentiation was enhanced by miR-3653-3p overexpression while BMSC proliferation was not affected. By contrast, miR-3653-3p silencing mitigated the promoted BMSC osteogenic differentiation caused by circ_0003865 silencing, but had no effect on proliferation. Finally, circ_0003865 silencing repressed OP development in mouse model. CONCLUSION: MEL promotes BMSC osteogenic differentiation and inhibits OP pathogenesis by suppressing the expression of circ_0003865, which regulates GAS1 gene expression via sponging miR-3653-3p.	NA	Stem Cell Res Ther. 2021 Feb 25;12(1):150. doi: 10.1186/s13287-021-02224-w.
3255	LncRNA	CircCDR1as	miR-432-5p	E2F3	PC tissues	Pancreatic Cancer	Homo sapiens (human)	microarray;Western blot;	33593338	Circular RNA CDR1as promotes tumor progression by regulating miR-432-5p/E2F3 axis in pancreatic cancer.	BACKGROUND: Pancreatic cancer (PC), characterized with high growth rate and metastatic rate. It's urgently necessary to explore new mechanism of PC. Circular RNA/miRNA/mRNA network was widely reported to participate in the cancer progression. METHODS: In this research, circular RNA CDR1as (circCDR1as) was identified by microarray analysis and detected in pancreatic cancer (PC) tissues and cells. Transwell, colony-forming assay, nude mouse tumorigenicity assay were used to determine the function of circCDR1as in PC. Western blot, dual luciferase reporting test were applied to investigate the mechanism. RESULTS: We found that circCDR1as was highly expressed in PC tissues. The levels of circCDR1as in PC tissues and cells were higher than those in controls. CircCDR1as promoted the migration, invasion and proliferation of PC cells in vitro and tumor growth in vivo via mediating E2F3 expression by sponging miR-432-5p. CONCLUSIONS: In conclusion, circCDR1as could promote the development of PC and might be a novel diagnostic target for PC.	NA	Cancer Cell Int. 2021 Feb 16;21(1):112. doi: 10.1186/s12935-021-01812-3.
3256	LncRNA	GAS5	miR-194-3p	TXNIP	coronary vascular tissues and endothelial cells	Atherosclerosis	Homo sapiens (human)	Immunohistochemistry;	33638792	Long Non-coding RNA GAS5 Worsens Coronary Atherosclerosis Through MicroRNA-194-3p/TXNIP Axis.	It is formerly conducted that long non-coding RNA growth arrest-specific 5 (GAS5) is involved in the process of coronary atherosclerosis (AS). The regulatory effects of GAS5 on the microRNA (miR)-194-3p/thioredoxin-interacting protein (TXNIP) axis in AS have been insufficiently explored yet. Thereafter, this work is started from GAS5/miR-194-3p/TXNIP axis in AS. AS rats were modeled to obtain their coronary vascular tissues and endothelial cells (ECs), in which GAS5, miR-194-3p, and TXNIP expression were tested. ECs were identified by immunohistochemistry. The mechanism among GAS5, miR-194-3p, and TXNIP was determined. ECs were transfected with inhibited GAS5 or overexpressed miR-194-3p to decipher their functions in proliferation and apoptosis of ECs in AS. Raised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. This work clearly manifests that inhibited GAS5 facilitates the growth of ECs through miR-194-3p-targeted TXNIP in AS, consolidating the basal reference to the curing for AS.	NA	Mol Neurobiol. 2021 Feb 27. doi: 10.1007/s12035-021-02332-x.
3257	LncRNA	LINC00470	miR-580-3p	WEE1	glioma cells	Glioma 	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33663509	Long non-coding RNA LINC00470 in serum derived exosome: a critical regulator for proliferation and autophagy in glioma cells.	BACKGROUND: To explore the mechanism of LINC00470 in serum exosomes from glioma patients regulating the autophagy and proliferation of glioma cells. METHODS: Exosomes were extracted from glioma patients (GBM-exo). Expression of LINC00470 in exosomes was analyzed with the clinicopathological characteristics of glioma patients. Glioma mouse model was established. The effects of LINC00470, miR-580-3p and WEE1 on cell autophagy and proliferation, as well as the activation of PI3K/AKT/mTOR pathway were measured. Dual luciferase reporter assay and RNA immunoprecipitation (RIP) were conducted to validate the binding of LINC00470 and miR-580-3p and of miR-580-3p and WEE1. RESULTS: LINC00470 overexpressed in GBM-exo and associated with disease severity and postoperative survival time of glioma patients. GBM-exo deteriorated tumor progression in nude mice. Cells incubated with GBM-exo or transfected with pcDNA3.1-LINC00470/miR-580-3p inhibitor/pcDNA3.1-WEE1 had less autophagosome, downregulated LC3-II/LC3-I and Beclin1 expression levels and increased expression of p62 as well as strengthened proliferation ability. The PI3K/AKT/mTOR pathway was activated. LINC00470 competitively bound to miR-580-3p with WEE1. CONCLUSION: LINC00470 in GBM-exo can bind to miR-580-3p in glioma cells to regulate WEE1 expression and activate the PI3K/AKT/mTOR pathway, thereby inhibiting autophagy and enhancing the proliferation of glioma cells.	NA	Cancer Cell Int. 2021 Mar 4;21(1):149. doi: 10.1186/s12935-021-01825-y.
3258	LncRNA	MALAT1	miR-26b-5p	Mfn1	cardiac microvascular endothelial cells	Myocardial Infarction	Homo sapiens (human)	luciferase assay;	33667993	The lncRNA Malat1 regulates microvascular function after myocardial infarction in mice via miR-26b-5p/Mfn1 axis-mediated mitochondrial dynamics.	RATIONALE: Myocardial infarction (MI) is a leading cause of cardiovascular mortality globally. The improvement of microvascular function is critical for cardiac repair after MI. Evidence now points to long non-coding RNAs (lncRNAs) as key regulators of cardiac remodelling processes. The lncRNA Malat1 is involved in the development and progression of multiple cardiac diseases. Studies have shown that Malat1 is closely related to the regulation of endothelial cell regeneration. However, the potential molecular mechanisms of Malat1 in repairing cardiac microvascular dysfunction after MI remain unreported. METHODS AND RESULTS: The present study found that Malat1 is upregulated in the border zone of infarction in mouse hearts, as well as in isolated cardiac microvascular endothelial cells (CMECs). Targeted knockdown of Malat1 in endothelial cells exacerbated oxidative stress, attenuated angiogenesis and microvascular perfusion, and as a result decreased cardiac function in MI mice. Further studies showed that silencing Malat1 obviously inhibited CMEC proliferation, migration and tube formation, which was at least in part attributed to disturbed mitochondrial dynamics and activation of the mitochondrial apoptosis pathway. Moreover, bioinformatic analyses, luciferase assays and pull-down assays indicated that Malat1 acted as a competing endogenous RNA (ceRNA) for miR-26b-5p and formed a signalling axis with Mfn1 to regulate mitochondrial dynamics and endothelial functions. Overexpression of Mfn1 markedly reversed the microvascular dysfunction and CMEC injuries that were aggravated by silencing Malat1 via inhibition of excessive mitochondrial fragments and mitochondria-dependent apoptosis. CONCLUSIONS: The present study elucidated the functions and mechanisms of Malat1 in cardiac microcirculation repair after MI. The underlying mechanisms of the effects of Malat1 could be attributed to its blocking effects on miR-26b-5p/Mfn1 pathway-mediated mitochondrial dynamics and apoptosis.	NA	Redox Biol. 2021 May;41:101910. doi: 10.1016/j.redox.2021.101910. Epub 2021 Feb 22.
3259	LncRNA	MCM3AP-AS1	miR-193a-5p	SENP1	CRC tissues and matched noncancerous tissues (NCTs)	Colorectal Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33686713	Long noncoding RNA MCM3AP-AS1 enhances cell proliferation and metastasis in colorectal cancer by regulating miR-193a-5p/SENP1.	BACKGROUND: Accumulating evidences have shown that long noncoding RNAs (lncRNAs) play key roles in many diseases, including cancer. Several studies reported that MCM3AP antisense RNA 1 (MCM3AP-AS1) was associated with the tumorigenesis and progression. However, the specific function and mechanism of MCM3AP-AS1 in colorectal cancer (CRC) have not been fully understood. METHODS: The expression of MCM3AP-AS1 was detected by quantitative reverse transcription PCR (RT-qPCR) in CRC tissues and matched noncancerous tissues (NCTs). CCK-8 assay, colony formation assay, transwell assay, xenograft and lung metastasis mouse models were used to examine the tumor-promoting function of MCM3AP-AS1 in vitro and in vivo. The binding relationship between MCM3AP-AS1, miR-193a-5p and sentrin-specific peptidase 1 (SENP1) were screened and identified by databases, RT-qPCR, dual luciferase reporter assay and western blot. RESULTS: In the present study, we got that the expression of MCM3AP-AS1 was higher in CRC tissues than in paired NCTs, and increased MCM3AP-AS1 expression was associated with adverse outcomes in CRC patients. Functional experiments in vitro revealed that silencing of MCM3AP-AS1 could inhibit the proliferation, colony formation, migratory, and invasive abilities of CRC cells. The mouse models of xenograft and lung metastasis further confirmed that in vivo silencing MCM3AP-AS1 could significantly inhibit the growth and metastasis of CRC. Further mechanism studies indicated that MCM3AP-AS1 could sponge miR-193a-5p and inhibit the activity of it. What is more, SENP1 was proved to be a novel target of miR-193a-5p and could be upregulated by MCM3AP-AS1. At last, we observed that SENP1 overexpression in CRC tissues was closely related to unfavorable prognosis. CONCLUSION: Taken together, we identified in CRC the MCM3AP-AS1/miR-193a-5p/SENP1 regulatory axis, which affords a therapeutic possibility for CRC.	NA	Cancer Med. 2021 Apr;10(7):2470-2481. doi: 10.1002/cam4.3830. Epub 2021 Mar 8.
3260	LncRNA	NEAT1	miR-126	TRAF7	primary endothelial cells	Subclinical Hypothyroidism	Homo sapiens (human)	RT-PCR;Western blot;luciferase assay;	33677813	Long non-coding RNA NEAT1 regulates endothelial functions in subclinical hypothyroidism through miR-126/TRAF7 pathway.	Subclinical hypothyroidism (SCH) is associated with increased risks of endothelial dysfunction and atherosclerosis, but the mechanisms remain unclear. In our previous study, microRNA-126-3p was downregulated in SCH, but the role and regulatory mechanism of miR-126 in SCH has not been investigated. A SCH mouse model was established by feeding mice methimazole. Both primary endothelial cells (ECs) and HUVECs were cultured. The expression levels of key molecules were detected via quantitative RT-PCR, western blotting, and immunofluorescence. Wire myography was used to analyze the changes in vascular tones. A dual-luciferase assay was used to investigate the relationship between lncRNAs, microRNAs and target genes. In detail, it was shown that the expression levels of miR-126-3p were significantly decreased in both the SCH vasculature and HUVECs. MiR-126 supplementation suppressed HUVEC apoptosis and improved vascular function. Moreover, miR-126 could bind to the 3'-untranslated region of TRAF7, thus, regulating the C-FLIP pathway and endothelial apoptosis. Furthermore, lncRNA NEAT1 was upregulated upon TSH treatment and could function as a ceRNA and bind to miR-126, thus, modulating its expression level and vascular function. Finally, the NEAT1/miR-126/TRAF7 axis functions in response to TSH and regulates endothelial functions in SCH in vitro and in vivo. In conclusion, dysregulation of the NEAT1/miR-126/TRAF7 axis is responsible for impaired endothelial functions in SCH. Targeting this axis might become a promising treatment strategy or improving endothelial functions in SCH.	NA	Hum Cell. 2021 May;34(3):825-835. doi: 10.1007/s13577-021-00508-0. Epub 2021 Mar 7.
3261	LncRNA	NORAD	miR-495-3p	KLF5	mouse aorta tissues	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33636159	Silenced long non-coding RNA activated by DNA damage elevates microRNA-495-3p to suppress atherosclerotic plaque formation via reducing Krüppel-like factor 5.	OBJECTIVE: Atherosclerosis (AS) is an inflammatory disease and the formation of atherosclerotic plaque plays a critical role in AS progression. We aimed to investigate the effect of long non-coding RNA (lncRNA) activated by DNA damage (NORAD)/microRNA-495-3p (miR-495-3p)/Krüppel-like factor 5 (KLF5) axis on atherosclerotic plaque formation. METHODS: The ApoE(-/-) mice were fed a high-fat diet to construct AS mouse models and the modeled mice were treated with altered NORAD, miR-495-3p or KLF5. NORAD, miR-495-3p and KLF5 expression in mouse aorta tissues were evaluated, and the levels of inflammatory factors, oxidative stress factors, endothelial function indices and blood lipid in mice were all determined. The atherosclerotic plaque area, lipid deposition area, collagen fibers and CD68 expression in mouse aorta tissues were assessed. The regulatory relation between NORAD and miR-495-3p, and the target relation between miR-495-3p and KLF5 were confirmed. RESULTS: NORAD and KLF5 were increased whereas miR-495-3p was decreased in atherosclerotic mouse aortas. Inhibited NORAD or elevated miR-495-3p suppressed inflammation, oxidative stress, endothelial dysfunction, blood lipid level, atherosclerotic plaque area, collagen fibers and CD68 expression in atherosclerotic mouse aortas. Effects of elevated miR-495-3p on atherosclerotic mice could be reversed by up-regulation of KLF5. NORAD served as a sponge of miR-495-3p and miR-495-3p directly targeted KLF5. CONCLUSION: Silenced NORAD elevated miR-495-3p to suppress atherosclerotic plaque formation via reducing KLF5. Findings in our research may be helpful for exploring molecular mechanisms of AS.	NA	Exp Cell Res. 2021 Apr 15;401(2):112519. doi: 10.1016/j.yexcr.2021.112519. Epub 2021 Feb 23.
3262	LncRNA	PCA3	miR-140-5p	RFX7	atherosclerosis cells	Atherosclerosis 	Homo sapiens (human)	qPCR;Western blot;Chromatin immunoprecipitation;	33578049	Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis.	OBJECTIVE: The purpose of this study was to explore the role of long noncoding RNA (lncRNA) prostate cancer antigen 3 (PCA3) in atherosclerosis and the underlying mechanism. METHODS: The Gene Expression Omnibus (GEO) datasets were used to divide differentially expressed lncRNAs, microRNAs (miRNAs), and mRNAs. The expression of PCA3, miR-140-5p, RFX7 and ABCA1 were determined by qPCR or Western blot in ox-LDL-treated macrophages. Macrophage lipid accumulation s was evaluated using the Oil Red O staining and high-performance liquid chromatography. Target relationships among PCA3, miR-140-5p, RFX7, and ABCA1 promoter area were validated via dual-luciferase reporter gene assay or chromatin immunoprecipitation assay. The apoE(-/-) mouse model in vivo was designed to evaluate the effect of PCA3 on the reverse cholesterol transport (RCT) and atherosclerosis. RESULTS: PCA3 was down-regulated in foam cells, whereas miR-140-5p was highly expressed. Overexpression of PCA3 promoted ABCA1-mediated cholesterol efflux and reduced lipid accumulation in macrophages. Besides, RFX7 bound to the ABCA1 promoter and increased ABCA1 expression. Targeted relationships and interactions on the expression between miR-140-5p and PCA3 or RFX7 were elucidated. PCA3 up-regulated ABCA1 expression by binding to miR-140-5p to up-regulate RFX7 and ABCA1 expression in macrophages. PCA3 promoted RCT and impeded the progression of atherosclerosis by sponging miR-140-5p in apoE(-/-) mice. Meanwhile, miR-140-5p also inhibit ABCA1 expression via downregulation of RFX7 to impede RCT and aggravate atherosclerosis. CONCLUSIONS: lncRNA PCA3 promotes ABCA1-mediated cholesterol efflux to inhibit atherosclerosis through sponging miR-140-5p and up-regulating RFX7.	NA	Biochim Biophys Acta Mol Cell Biol Lipids. 2021 May;1866(5):158904. doi: 10.1016/j.bbalip.2021.158904. Epub 2021 Feb 10.
3263	LncRNA	UCC	miR-143-3p	SOX5	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;RIP assay;Western blot;	33824420	LncRNA UCC promotes epithelial-mesenchymal transition via the miR-143-3p/SOX5 axis in non-small-cell lung cancer.	Long non-coding RNAs (lncRNAs) have been found to play regulatory roles in cancers; for example, UCC was reported to promote colorectal cancer progression. However, the function of UCC in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, mRNA and protein levels were assessed using qPCR and western blots. Cell viability was assessed by colony-formation assays. The interaction between lncRNAs and miRNAs was detected by dual-luciferase reporter and RIP assays. The tumorigenesis of NSCLC cells in vivo was determined by xenograft assays. LncRNA UCC was highly expressed in both NSCLC tissues and cells. Knockdown of UCC expression suppressed the proliferation of NSCLC cells. In addition, a dual-luciferase reporter system and RIP assays showed that UCC specifically bound to miR-143-3p and acted as a sponge of miR-143-3p in NSCLC cells. The miR-143-3p inhibitor rescued the inhibitory effect of sh-UCC on the proliferation of NSCLC cells. Moreover, miR-143-3p and UCC showed opposite effects on the expression of SOX5, which promoted EMT in NSCLC cells. In addition, in a mouse model, knockdown of UCC expression alleviated EMT and NSCLC progression in vivo, which was consistent with the in vitro results. In the current study, we found that UCC induced the proliferation and migration of NSCLC cells both in vitro and in vivo by inducing the expression of SOX5 via miR-143-3p and subsequently promoted EMT in NSCLC.	NA	Lab Invest. 2021 Apr 6. doi: 10.1038/s41374-021-00586-6.
3264	LncRNA	ZNF561-AS1	miR-26a-3p	SRSF6	CRC tissues tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	RIP assay;Western blot;Luciferase reporter assay;	33622363	Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis.	BACKGROUND: Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. METHODS: ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. RESULTS: We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. CONCLUSION: In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.	NA	J Exp Clin Cancer Res. 2021 Feb 23;40(1):78. doi: 10.1186/s13046-021-01882-1.
3265	LncRNA	ZNF561-AS1	miR-128-5p	SRSF6	CRC tissues tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	RIP assay;Western blot;Luciferase reporter assay;	33622363	Oncogenic lncRNA ZNF561-AS1 is essential for colorectal cancer proliferation and survival through regulation of miR-26a-3p/miR-128-5p-SRSF6 axis.	BACKGROUND: Long non-coding RNAs (lncRNA) are reported to influence colorectal cancer (CRC) progression. Currently, the functions of the lncRNA ZNF561 antisense RNA 1 (ZNF561-AS1) in CRC are unknown. METHODS: ZNF561-AS1 and SRSF6 expression in CRC patient samples and CRC cell lines was evaluated through TCGA database analysis, western blot along with real-time PCR. SRSF6 expression in CRC cells was also examined upon ZNF561-AS1 depletion or overexpression. Interaction between miR-26a-3p, miR-128-5p, ZNF561-AS1, and SRSF6 was examined by dual luciferase reporter assay, as well as RNA binding protein immunoprecipitation (RIP) assay. Small interfering RNA (siRNA) mediated knockdown experiments were performed to assess the role of ZNF561-AS1 and SRSF6 in the proliferative actives and apoptosis rate of CRC cells. A mouse xenograft model was employed to assess tumor growth upon ZNF561-AS1 knockdown and SRSF6 rescue. RESULTS: We find that ZNF561-AS1 and SRSF6 were upregulated in CRC patient tissues. ZNF561-AS1 expression was reduced in tissues from treated CRC patients but upregulated in CRC tissues from relapsed patients. SRSF6 expression was suppressed and enhanced by ZNF561-AS1 depletion and overexpression, respectively. Mechanistically, ZNF561-AS1 regulated SRSF6 expression by sponging miR-26a-3p and miR-128-5p. ZNF561-AS1-miR-26a-3p/miR-128-5p-SRSF6 axis was required for CRC proliferation and survival. ZNF561-AS1 knockdown suppressed CRC cell proliferation and triggered apoptosis. ZNF561-AS1 depletion suppressed the growth of tumors in a model of a nude mouse xenograft. Similar observations were made upon SRSF6 depletion. SRSF6 overexpression reversed the inhibitory activities of ZNF561-AS1 in vivo, as well as in vitro. CONCLUSION: In summary, we find that ZNF561-AS1 promotes CRC progression via the miR-26a-3p/miR-128-5p-SRSF6 axis. This study reveals new perspectives into the role of ZNF561-AS1 in CRC.	NA	J Exp Clin Cancer Res. 2021 Feb 23;40(1):78. doi: 10.1186/s13046-021-01882-1.
3266	LncRNA	OXCT1-AS1	miR-195	CDC25A	glioma cells	Glioblastoma	Homo sapiens (human)	Flow Cytometry assay;Luciferase activity assay;	33832517	Novel LncRNA OXCT1-AS1 indicates poor prognosis and contributes to tumorigenesis by regulating miR-195/CDC25A axis in glioblastoma.	BACKGROUND: Long noncoding RNAs (lncRNAs) contribute to multiple biological processes in human glioblastoma (GBM). However, identifying a specific lncRNA target remains a challenge. In this study, bioinformatics methods and competing endogenous RNA (ceRNA) network regulatory rules were used to identify GBM-related lncRNAs and revealed that OXCT1 antisense RNA 1 (OXCT1-AS1) is a potential therapeutic target for the treatment of glioma. METHODS: Based on the Gene Expression Omnibus (GEO) dataset, we identified differential lncRNAs, microRNAs and mRNAs and constructed an lncRNA-associated ceRNA network. The novel lncRNA OXCT1-AS1 was proposed to function as a ceRNA, and its potential target miRNAs were predicted through the database LncBase Predicted v.2. The expression patterns of OXCT1-AS1 in glioma and normal tissue samples were measured. The effect of OXCT1-AS1 on glioma cells was checked using the Cell Counting Kit 8 assay, cell colony formation assay, Transwell assay and flow cytometry in vitro. The dual-luciferase activity assay was performed to investigate the potential mechanism of the ceRNA network. Finally, orthotopic mouse models of glioma were created to evaluate the influence of OXCT1-AS1 on tumour growth in vivo. RESULTS: In this study, it was found that the expression of lncRNA OXCT1-AS1 was upregulated in both The Cancer Genome Atlas (TCGA) GBM patients and GBM tissue samples, and high expression of OXCT1-AS1 predicted a poor prognosis. Suppressing OXCT1-AS1 expression significantly decreased GBM cell proliferation and inhibited cell migration and invasion. We further investigated the potential mechanism and found that OXCT1-AS1 may act as a ceRNA of miR-195 to enhance CDC25A expression and promote glioma cell progression. Finally, knocking down OXCT1-AS1 notably attenuated the severity of glioma in vivo. CONCLUSION: OXCT1-AS1 inhibits glioma progression by regulating the miR-195-5p/CDC25A axis and is a specific tumour marker and a novel potential therapeutic target for glioma treatment.	NA	J Exp Clin Cancer Res. 2021 Apr 8;40(1):123. doi: 10.1186/s13046-021-01928-4.
3267	LncRNA	LINC01929	miR-137-3p	FOXC1	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;Luciferase activity assay;	33968763	Long Non-Coding RNA LINC01929 Accelerates Progression of Oral Squamous Cell Carcinoma by Targeting the miR-137-3p/FOXC1 Axis.	Recently, additional long noncoding RNAs (lncRNAs) have been identified and their possible roles were investigated in a variety of human tumors. One of these lncRNAs, LINC01929, promoted the progression of some cancers, whereas its expression and biological function in human oral squamous cell carcinoma (OSCC) remains still mostly uncertain. The LINC01929 expression in OSCC tissues or cell lines was identified via quantitative real-time polymerase chain reaction. The cell counting kit-8, transwell migration, wound-healing, and flow cytometry assays were utilized to characterize the functions of LINC01929 in OSCC cells. The interactive relationships between LINC01929 and miR-137-3p, miR-137-3p and Forkhead box C1 (FOXC1) were investigated by the dual-luciferase activity assay. Our findings demonstrated that LINC01929 was highly expressed in OSCC tissue samples and cell lines, whereas miR-137-3p expression was downregulated. LINC01929 acted as a carcinogenic lncRNA with accelerated OSCC cell proliferation, migration and invasion, and suppression of apoptosis. We further indicated that LINC01929 facilitated tumor growth in xenograft mouse models. Mechanistically, LINC01929 acted as a sponge for miR-137-3p to elevate FOXC1 expression, which is the target of miR-137-3p. In addition, downregulated miR-137-3p expression rescued the suppressive behaviors of LINC01929 knockdown on the biological behaviors of OSCC cells. Taken together, LINC01929 functioned as a tumor-promoting lncRNA via the miR-137-3p/FOXC1 axis in OSCC, suggesting novel targets for OSCC therapy.	NA	Front Oncol. 2021 Apr 21;11:657876. doi: 10.3389/fonc.2021.657876. eCollection 2021.
3268	LncRNA	NEAT1	miR-324-5p	KCT	glioma cell	Glioma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33982764	Long non-coding RNA NEAT1 regulates glioma cell proliferation and apoptosis by competitively binding to microRNA-324-5p and upregulating KCTD20 expression.	Previous studies have demonstrated that long non-coding RNAs (lncRNAs) serve a key role in the development and progression of several types of cancer, including glioma. The lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) contributes to cancer growth through its effects on cell proliferation, migration, invasion and drug resistance. However, the exact regulatory mechanisms via which NEAT1 acts in glioma are unclear. In the present study, the expression levels and function of NEAT1 in glioma tissues and cell lines were examined in vitro and in vivo. By reverse transcription-quantitative PCR and fluorescence in situ hybridization analysis, NEAT1 expression was upregulated in glioma tissues compared with in adjacent normal brain tissues, and elevated NEAT1 levels were associated with poor prognosis. Cell Counting Kit-8, colony formation, ethynyldeoxyuridine, flow cytometry and western blotting assays were performed to detect the effects of NEAT1 on cell biological behavior. Knockdown of NEAT1 in glioma cell lines was associated with cell cycle arrest at the G(0)/G(1) phase, decreased proliferation and elevated apoptosis in vitro, and resulted in reduced tumor growth and increased survival in a mouse xenograft model of glioma. Using bioinformatics analysis, RNA immunoprecipitation experiments and luciferase reporter assays, it was demonstrated that NEAT1 may competitively bind to microRNA (miR)-324-5p, thus blocking its interaction with target mRNAs. Potassium channel tetramerization protein domain containing 20 (KCTD20) was identified as a specific miR-324-5p target. Accordingly, the inhibition of NEAT1 resulted in the downregulation of KCTD20 through competitive binding with miR-324-5p, decreased cell proliferation and increased apoptosis. Concomitant NEAT1 knockdown and inhibition of miR-324-5p partially reversed the effects of NEAT1 knockdown on cell proliferation and apoptosis, and further regulated KCTD20 expression. Collectively, the present findings demonstrated that NEAT1 acted as a competing endogenous RNA for miR-324-5p, and identified the NEAT1/miR-324-5p/KCTD20 axis as a novel regulatory axis and a potential therapeutic target for human glioma.	NA	Oncol Rep. 2021 Jul;46(1):125. doi: 10.3892/or.2021.8076. Epub 2021 May 13.
3269	LncRNA	SNHG6	miR-543	LAMC1	BC cell lines	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	33782812	LncRNA SNHG6 promotes breast cancer progression and epithelial-mesenchymal transition via miR-543/LAMC1 axis.	PURPOSE: Breast cancer (BC) is the most prevalent cancer in women with an estimated incidence of 10% and the leading cause of mortality due to its heterogenous property and high metastasis rate. Development of novel therapy is very necessary and requires an understanding of molecular mechanisms. We investigated the function of SNHG6/miR-543/LAMC1 axis in BC. METHODS: Human BC tissues were obtained from diagnosed patients. BC cell lines and normal breast cells were used. QRT-PCR and Western blotting were employed to measure expression levels of SNHG6, miR-543, LAMC1, EMT-related proteins, and PI3K/AKT pathway. Dual-luciferase assay was performed to validate interactions of SNHG6/miR-543 and miR-543/LAMC1. Colony formation assay, flow cytometry, scratch wound healing assay, and transwell assay were utilized to assess the proliferation, apoptosis, migration, and invasion of BC cells. Nude mouse xenograft model was used the evaluate the function of SNHG6/miR-543 in tumor growth in vivo. RESULTS: SNHG6 and LAMC1 were elevated, but miR-543 was reduced in BC tissues and cells. SNHG6 interacted directly with miR-543, while miR-543 targeted LAMC1. Knockdown of SNHG6 suppressed BC cell proliferation, migration, invasion, EMT, and PI3K/AKT pathway, but promoted cell apoptosis, while miR-543 inhibitor or overexpression of LAMC1 reversed those effects. Overexpression of LAMC1 also blocked the effects of miR-543 on BC cell proliferation, migration, invasion, and EMT. Knockdown of SNHG6 restrained BC growth in vivo, while miR-543 inhibitor inhibited that suppression. CONCLUSION: SNHG6 promoted EMT and BC cell proliferation and migration by acting as a miR-543 sponge and disinhibiting LAMC1/PI3K/AKT pathway. SNHG6/miR-543/LAMC1 axis could serve as candidates for the development of therapeutic strategies for BC.	NA	Breast Cancer Res Treat. 2021 Mar 29. doi: 10.1007/s10549-021-06190-y.
3270	LncRNA	RMRP	miR-206	CCL2	pulmonary tissues	Pediatric Asthma	Homo sapiens (human)	ELISA;qPCR;	33511814	Pro-inflammatory and pro-fibrotic role of long non-coding RNA RMRP in pediatric asthma through targeting microRNA-206/CCL2 axis.	Asthma is an inflammatory pulmonary illness that plagues infants and young children. We carried out this investigation to examine the role of long noncoding RNA (lncRNA) RNA component of mitochondrial RNA processing endoribonuclease (RMRP) in an asthmatic mouse model induced by ovalbumin (OVA) and human airway smooth muscle cells (ASMCs). Eight-week-old mice were sensitized with OVA to simulate pediatric asthma. The expression patterns of RMRP, microRNA-206 (miR-206) and C-C motif ligand 2 (CCL2) in pulmonary tissues were evaluated by qPCR. In addition, the concentrations of interleukin (IL)-4, IL-5 and IL-13 cytokines in bronchoalveolar lavage fluid were detected by ELISA. The expression of RMRP and CCL2 was elevated, while miR-206 was reduced in OVA-induced mice. Our findings indicated that administration of RMRP overexpression in ASMCs increased the levels of biomarkers in asthma. RMRP functioned as a sponge for miR-206 to upregulate CCL2 expression. Blockade of the TGF-β/Smad2 signaling pathway in ASMCs overexpressing RMRP suppressed the inflammatory cytokines and cell viability, while enhancing apoptosis. The RMRP/miR-206/CCL2 regulatory axis is implicated in the occurrence of pediatric asthma.	NA	J Biol Regul Homeost Agents. 2021 Jan-Feb;35(1):71-83. doi: 10.23812/20-505-A.
3271	LncRNA	H19	miR-675	FADD	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33499244	The lncRNA H19-Derived MicroRNA-675 Promotes Liver Necroptosis by Targeting FADD.	The H19-derived microRNA-675 (miR-675) has been implicated as both tumor promoter and tumor suppressor and also plays a role in liver inflammation. We found that miR-675 promotes cell death in human hepatocellular carcinoma (HCC) cell lines. We show that Fas-associated protein with death domain (FADD), a mediator of apoptotic cell death signaling, is downregulated by miR-675 and a negative correlation exists between miR-675 and FADD expression in mouse models of HCC (p = 0.014) as well as in human samples (p = 0.017). We demonstrate in a mouse model of liver inflammation that overexpression of miR-675 promotes necroptosis, which can be inhibited by the necroptosis-specific inhibitor Nec-1/Nec-1s. miR-675 induces the level of both p-MLKL (Mixed Lineage Kinase Domain-Like Pseudokinase) and RIP3 (receptor-interacting protein 3), which are key signaling molecules in necroptosis, and enhances MLKL binding to RIP3. miR-675 also inhibits the levels of cleaved caspases 8 and 3, suggesting that miR-675 induces a shift from apoptosis to a necroptotic cellular pathway. In conclusion, downregulation of FADD by miR-675 promotes liver necroptosis in response to inflammatory signals. We propose that this regulation cascade can stimulate and enhance the inflammatory response in the liver, making miR-675 an important regulator in liver inflammation and potentially also in HCC.	NA	Cancers (Basel). 2021 Jan 22;13(3):411. doi: 10.3390/cancers13030411.
3272	LncRNA	Neat1	miR-148a-3p	Cyth3	hepatic stellate cells	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	33550894	LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate Cyth3.	Liver fibrosis is a common response to chronic liver injury, ultimately leading to cirrhosis. The activation of hepatic stellate cells (HSCs) plays a dominant role in liver fibrosis. The regulatory roles of long noncoding RNAs (lncRNAs) in multiple human diseases have been observed. This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. Upregulation of Neat1 and cytohesin 3 (Cyth3) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues. Knockdown of Neat1 or Cyth3 attenuated liver fibrosis and collagen deposition in vivo and the activation of HSCs in vitro. An miR-148a-3p and miR-22-3p inhibitor facilitated HSC activation and collagen fiber expression. Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate Cyth3 expression. Knockdown of Neat1 inhibited Cyth3 expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation. The ceRNA regulatory network may promote a better understanding of liver fibrogenesis, contribute to an original agreement of liver fibrosis etiopathogenesis and provide insights into the development of a novel domain of lncRNA-directed therapy against liver fibrosis.	NA	Cell Cycle. 2021 Mar-Mar;20(5-6):490-507. doi: 10.1080/15384101.2021.1875665. Epub 2021 Feb 8.
3273	LncRNA	Neat1	miR-22-3p	Cyth3	hepatic stellate cells	Liver Fibrosis	Homo sapiens (human)	qRT-PCR	33550894	LncRNA Neat1 expedites the progression of liver fibrosis in mice through targeting miR-148a-3p and miR-22-3p to upregulate Cyth3.	Liver fibrosis is a common response to chronic liver injury, ultimately leading to cirrhosis. The activation of hepatic stellate cells (HSCs) plays a dominant role in liver fibrosis. The regulatory roles of long noncoding RNAs (lncRNAs) in multiple human diseases have been observed. This study was dedicated to investigating the regulatory effects of the lncRNA nuclear paraspeckle assembly transcript 1 (Neat1) on liver fibrosis and HSC activation. Upregulation of Neat1 and cytohesin 3 (Cyth3) and downregulation of miR-148a-3p and miR-22-3p were observed in mouse fibrotic liver tissues. Knockdown of Neat1 or Cyth3 attenuated liver fibrosis and collagen deposition in vivo and the activation of HSCs in vitro. An miR-148a-3p and miR-22-3p inhibitor facilitated HSC activation and collagen fiber expression. Neat1 directly targeted miR-148a-3p and miR-22-3p to modulate Cyth3 expression. Knockdown of Neat1 inhibited Cyth3 expression via the competing endogenous RNA (ceRNA) mechanism of sponging miR-148a-3p and miR-22-3p to regulate liver fibrosis and HSC activation. The ceRNA regulatory network may promote a better understanding of liver fibrogenesis, contribute to an original agreement of liver fibrosis etiopathogenesis and provide insights into the development of a novel domain of lncRNA-directed therapy against liver fibrosis.	NA	Cell Cycle. 2021 Mar-Mar;20(5-6):490-507. doi: 10.1080/15384101.2021.1875665. Epub 2021 Feb 8.
3274	LncRNA	Neat1	miR-204-5p	Igf1	uterine tissues	Obesity 	Homo sapiens (human)	qRT-PCR	33588025	A synergy of estradiol with leptin modulates the long non-coding RNA NEAT1/ mmu-miR-204-5p/IGF1 axis in the uterus of high-fat-diet-induced obese ovariectomized mice.	Obesity increases the risk of developing cancers for both males and females. This study investigated potential crosstalk between estradiol and leptin signaling pathways within the endometrium of high-fat-diet-induced obese ovariectomized mice to gain insight into possible links between obesity and endometrial cancer. We administered 17-β estradiol (0.2 μg/mouse subcutaneously) and/or recombinant mouse leptin (1 μg/g Bwt intraperitoneally.,) for 20 h to high-fat-diet-induced obese ovariectomized mice. The uterine tissues of experimental animals after treatments were studied by histological, immunohistochemical, quantitative real-time PCR (gene/miRNAs), and methylation-specific PCR analyses. Quantitative real-time PCR analysis revealed significantly increased expression of Cyclin d1, Esr1, Igf1, Igfbp2, Vegf, Oct4, and Pgr after estradiol and leptin co-treatment. Methylation-specific PCR results indicated that the hormonal dependent transcriptional regulation of Vegf, Igf1, and Pgr is independent of promoter methylation. The decreased expression of mmu- miR-204-5p after estradiol and leptin treatments correlated with the increased expression of long non-coding RNA Neat1. Insilico analysis confirmed the interaction of Neat1 and mmu- miR-204-5p and gene targets of mmu-miR-204-5p, including Igf1 were analyzed in this study. Immunohistochemical analyses revealed subcellular localization and increased expression of ESR, VEGF, phospho-Estrogen Receptor-α (pTyr537), and LEPR proteins following estradiol and leptin exposure. Overall, the data from our in vivo studies suggest the regulation of Neat1-mmu-miR-204-5p- Igf1 axis and associated gene expression changes in uterine tissue after estradiol and leptin co-treatment. In humans, long-term exposure to estradiol and leptin can alter endometrial homeostasis through the NEAT1-miR-204-5p-Igf1 axis and favor carcinogenic pathways, which provide mechanistic insight into the obesity-associated endometrial cancer.	NA	J Steroid Biochem Mol Biol. 2021 May;209:105843. doi: 10.1016/j.jsbmb.2021.105843. Epub 2021 Feb 12.
3275	LncRNA	SNHG1	miR-125b-5p	MAPK1	SK-N-SH and MN9D cells	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33911864	Long Noncoding RNA SNHG1 Knockdown Ameliorates Apoptosis, Oxidative Stress and Inflammation in Models of Parkinson's Disease by Inhibiting the miR-125b-5p/MAPK1 Axis.	BACKGROUND: Parkinson's disease (PD) is a prevalent neurodegenerative disease. Long noncoding RNA small molecule RNA host gene 1 (SNHG1) has been reported to play critical roles in Parkinson's disease (PD) progression. The study aimed to further elucidate the mechanism of SNHG1 in PD pathogenesis. METHODS: The levels of SNHG1, miR-125b-5p and mitogen-activated protein kinase 1 (MAPK1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Cell viability and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The activity of Caspase-3 or Caspase-9 was measured using a Caspase-3 or Caspase-9 Assay Kit. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, lactic dehydrogenase (LDH) activity, reactive oxygen species (ROS) generation and superoxide dismutase (SOD) activity were gauged by enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter assay was performed to identify the relationship between miR-125b-5p and SNHG1 or MAPK1. The MPTP-induced PD mouse was used as an in vivo model of PD and MPP(+)-treated SK-N-SH and MN9D cells were used as in vitro models of PD. RESULTS: SNHG1 and MAPK1 were significantly up-regulated while miR-125b-5p was down-regulated in the MPTP-induced PD mouse model and MPP(+)-induced PD cell models. SNHG1 silence or miR-125b-5p overexpression protected against MPP(+)-evoked apoptosis, oxidative stress and inflammation in SK-N-SH and MN9D cells. Moreover, SNHG1 acted as a molecular sponge of miR-125b-5p, and the protective impact of SNHG1 silence on MPP(+)-evoked cell damage was reversed by miR-125b-5p inhibition. Furthermore, MAPK1 was a functional target of miR-125b-5p and its overexpression attenuated the effects of miR-125b-5p restoration in MPP(+)-triggered cell injury. In addition, the behavioral changes in MPTP-induced PD mouse in vivo model were relieved by SNHG1 silence. CONCLUSION: SNHG1 knockdown exerted neuroprotective effects in MPP(+)-evoked cytotoxicity through regulating the miR-125b-5p/MAPK1 axis both in human and mouse PD cell models, highlighting a possible target for PD therapy.	NA	Neuropsychiatr Dis Treat. 2021 Apr 22;17:1153-1163. doi: 10.2147/NDT.S286778. eCollection 2021.
3276	LncRNA	TRPM2-AS	miR-497	WEE1	RB tissues and cell lines	Retinoblastoma	Homo sapiens (human)	qRT-PCR	33986660	Long Noncoding RNA TRPM2-AS Promotes the Growth, Migration, and Invasion of Retinoblastoma via miR-497/WEE1 Axis.	Long noncoding RNAs (lncRNAs) exhibit vital roles in many types of cancer, including retinoblastoma (RB), the most common primary intraocular malignancy tumor of infancy. A novel lncRNA TRPM2-AS has been demonstrated to be related to multiple cancers; however, its role in RB remains unclear. Here, we aimed to investigate the function of TRPM2-AS in RB. In this study, TRPM2-AS expression in 35 human RB tissues and RB cell lines was detected by real-time PCR. And, the relationship between its expression and clinicopathological characteristics of RB patients was analyzed. RB cells' proliferation, migration, invasion, apoptosis, and cell cycle were explored after silencing TRPM2-AS. The mechanism of TRPM2-AS in RB was focused on miR-497/WEE1 axis. Additionally, the role and mechanism of TRPM2-AS were confirmed in a xenograft mouse model. We found TRPM2-AS expression was enhanced in RB tissues and cells. And, higher TRPM2-AS expression was related to advanced clinical stage and optic nerve invasion in patients. Downregulation of TRPM2-AS significantly inhibited proliferation, migration, and invasion, elevated apoptosis, attenuated G2/M phase arrest in RB cells, and suppressed tumor growth in vivo. TRPM2-AS acted as a ceRNA for miR-497 to positively regulate WEE1 expression. miR-497 inhibitor or WEE1 overexpression dramatically reversed the effects of TRPM2-AS downregulating on the malignant phenotypes of RB cells. Therefore, TRPM2-AS is an oncogenic lncRNA in RB, and it functions largely through the miR-497/WEE1 pathway. Despite the limited sample size, this study indicates that TRPM2-AS may be a candidate target in RB therapies.	NA	Front Pharmacol. 2021 Apr 12;12:592822. doi: 10.3389/fphar.2021.592822. eCollection 2021.
3277	Circular RNA	Circ-CNST	miR-578	LDHA	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33962616	Blocking circ-CNST suppresses malignant behaviors of osteosarcoma cells and inhibits glycolysis through circ-CNST-miR-578-LDHA/PDK1 ceRNA networks.	BACKGROUND: CircRNA CNST (circ-CNST) is a newly identified biomarker for prognosis of osteosarcoma (OS). However, its role in OS progression remains to be well documented. METHODS: Expression of circ-CNST, microRNA (miR)-578, lactate dehydrogenase A (LDHA), and pyruvate dehydrogenase kinase 1 (PDK1) was detected by quantitative real-time polymerase chain reaction and Western blotting. The physical interaction was confirmed by dual-luciferase reporter assay. Cell behaviors and glycolysis were measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide assay, colony formation assay, flow cytometry, transwell assays, xenograft experiment, and commercial kits. RESULTS: Circ-CNST was upregulated in human OS tissues and cells, accompanied with downregulation of miR-578 and upregulation of LDHA and PDK1. There were negative correlations between miR-578 expression and circ-CNST or LDHA/PDK1 in OS tissues. Moreover, high circ-CNST/LDHA/PDK1 or low miR-578 might predict shorter overall survival, advanced TNM stages, and lymph node metastasis. Physically, miR-578 was targeted by circ-CNST, and miR-578 could target LDHA/PDK1. Functionally, blocking circ-CNST and restoring miR-578 enhanced apoptosis rate and suppressed cell proliferation, colony formation, migration, and invasion in 143B and U2OS cells, accompanied with decreased glucose consumption, lactate production, and adenosine triphosphate (ATP)/adenosine diphosphate (ADP) ratio. Furthermore, in vivo growth of U2OS cells was retarded by silencing circ-CNST. Depletion of miR-578 could counteract the suppressive role of circ-CNST deficiency in 143B and U2OS cells, and restoring LDHA or PDK1 partially reversed the role of miR-578 inhibition as well. CONCLUSION: Circ-CNST knockdown could antagonize malignant behaviors and glycolysis of OS cells by regulating miR-578-LDHA/PDK1 axes.	NA	J Orthop Surg Res. 2021 May 7;16(1):300. doi: 10.1186/s13018-021-02427-0.
3278	Circular RNA	Circ-CNST	miR-578	LDHA	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33962616	Blocking circ-CNST suppresses malignant behaviors of osteosarcoma cells and inhibits glycolysis through circ-CNST-miR-578-LDHA/PDK1 ceRNA networks.	BACKGROUND: CircRNA CNST (circ-CNST) is a newly identified biomarker for prognosis of osteosarcoma (OS). However, its role in OS progression remains to be well documented. METHODS: Expression of circ-CNST, microRNA (miR)-578, lactate dehydrogenase A (LDHA), and pyruvate dehydrogenase kinase 1 (PDK1) was detected by quantitative real-time polymerase chain reaction and Western blotting. The physical interaction was confirmed by dual-luciferase reporter assay. Cell behaviors and glycolysis were measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide assay, colony formation assay, flow cytometry, transwell assays, xenograft experiment, and commercial kits. RESULTS: Circ-CNST was upregulated in human OS tissues and cells, accompanied with downregulation of miR-578 and upregulation of LDHA and PDK1. There were negative correlations between miR-578 expression and circ-CNST or LDHA/PDK1 in OS tissues. Moreover, high circ-CNST/LDHA/PDK1 or low miR-578 might predict shorter overall survival, advanced TNM stages, and lymph node metastasis. Physically, miR-578 was targeted by circ-CNST, and miR-578 could target LDHA/PDK1. Functionally, blocking circ-CNST and restoring miR-578 enhanced apoptosis rate and suppressed cell proliferation, colony formation, migration, and invasion in 143B and U2OS cells, accompanied with decreased glucose consumption, lactate production, and adenosine triphosphate (ATP)/adenosine diphosphate (ADP) ratio. Furthermore, in vivo growth of U2OS cells was retarded by silencing circ-CNST. Depletion of miR-578 could counteract the suppressive role of circ-CNST deficiency in 143B and U2OS cells, and restoring LDHA or PDK1 partially reversed the role of miR-578 inhibition as well. CONCLUSION: Circ-CNST knockdown could antagonize malignant behaviors and glycolysis of OS cells by regulating miR-578-LDHA/PDK1 axes.	NA	J Orthop Surg Res. 2021 May 7;16(1):300. doi: 10.1186/s13018-021-02427-0.
3279	Circular RNA	CircNFATC3	miR-23b-3p	RAI14	GC tissue cells,GC cell line	Gastric Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;	33840258	RAI14 Regulated by circNFATC3/miR-23b-3p axis Facilitates Cell Growth and Invasion in Gastric Cancer.	Circular RNAs (circRNAs) have been proved to act crucial roles in multiple malignancies including gastric cancer (GC). Retinoic acid induced 14 (RAI14) acts as an oncogene in human cancers, but the underlying mechanisms by which RAI14 is regulated by circRNA/miRNA axis remain elusive. The clinical value of RAI14, miR-23b-3p and circNFATC3 was estimated by The Cancer Genome Atlas and fluorescence in situ hybridization. The interplay between miR-23b-3p and RAI14 or circNFATC3 was determined by qRT-PCR, Western blot, luciferase gene report and RIP assays. Biological function assays and a subcutaneous xenograft model were executed to unveil the role of circNFATC3/miR-23b-3p/RAI14 axis in GC cells. As a consequence, upregulation of RAI14 and circNFATC3 or downregulation of miR-23b-3p was associated with poor prognosis in patients with GC. Restored miR-23b-3p depressed cell proliferation, colony formation, and cell invasion by targeting RAI14, whereas RAI14 facilitated cell progression and reversed the anti-tumor effects of miR-23b-3p in GC cells. Then, circNFATC3 had a co-localization with miR-23b-3p in the cytoplasm in GC tissue cells and could act as a sponge of miR-23b-3p in GC cell line. Silencing of circNFATC3 inhibited cell growth and in vivo tumorigenesis by upregulating miR-23b-3p and downregulating RAI14. In conclusion, our findings indicated that RAI14 facilitated cell growth and invasion and was regulated by circNFATC3/miR-23b-3p axis in GC.	NA	Cell Transplant. 2021 Jan-Dec;30:9636897211007055. doi: 10.1177/09636897211007055.
3280	LncRNA	NEAT1	miR-424-5p	MAPK14	Human pulmonary alveolar epithelial cells	Lps-Induced Acute Lung Injury	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Flow Cytometry assay;	33904112	Long non-coding RNA NEAT1 promotes Lps-Induced Acute Lung Injury by regulating miR-424-5p/MAPK14 axis.	BACKGROUND: Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in acute lung injury (ALI) pathogenesis, including lncRNA nuclear enriched abundant transcript 1 (NEAT1). OBJECTIVE: We aimed to further elucidate the functions and molecular mechanism of NEAT1 in ALI. METHODS: Human pulmonary alveolar epithelial cells (HPAEpiCs) stimulated by lipopolysaccharide (LPS) were served as a cellular model of ALI. Cell viability and cell apoptosis were determined by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. The expression of NEAT1, microRNA-424-5p (miR-424-5p), and mitogen-activated protein kinase 14 (MAPK14) was measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot analysis. Caspase activity was determined by caspase activity kit. The inflammatory responses were evaluated using enzyme-linked immunosorbent assay (ELISA). The oxidative stress factors were analyzed by corresponding kits. RESULTS: NEAT1 was upregulated in LPS-stimulated HPAEpiCs. NEAT1 knockdown weakened LPS-induced injury by inhibiting apoptosis, inflammation and oxidative stress in HPAEpiCs. Moreover, miR-424-5p was a direct target of NEAT1, and its knockdown reversed the effects caused by NEAT1 knockdown in LPS-induced HPAEpiCs. Furthermore, MAPK14 was a downstream target of miR-424-5p, and its overexpression attenuated the effects of miR-424-5p on reduction of LPS-induced injury in HPAEpiCs. Besides, NEAT1 acted as a sponge of miR-424-5p to regulate MAPK14 expression. CONCLUSION: NEAT1 knockdown alleviated LPS-induced injury of HPAEpiCs by regulating miR-424-5p/MAPK14 axis, which provided a potential therapeutic target for the treatment of ALI.	NA	Genes Genomics. 2021 Jul;43(7):815-827. doi: 10.1007/s13258-021-01103-1. Epub 2021 Apr 26.
3281	LncRNA	LUCAT1	miR-181-5p	Wnt	16HBE cells	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)	ELISA;qRT-PCR;RNA pull-down assay;Western blot;Rescue assay;RNA pull-down;	34125980	Expression of long non-coding RNA LUCAT1 in patients with chronic obstructive pulmonary disease and its potential functions in regulating cigarette smoke extract-induced 16HBE cell proliferation and apoptosis.	BACKGROUND: Chronic obstructive pulmonary disease (COPD), characterized by persistent airflow limitation, was a disease mediated by a combination of inflammatory factors, immune cells, and immune mediators. COPD was an inflammatory and autoimmune disease involving T-lymphocytes triggered by cigarette smoke and other factors that progressively affected the bronchi, lung parenchyma, and pulmonary blood vessels. LncRNAs were reported to be implicated in COPD pathogenesis and development. METHODS: Non-smokers, smokers (non-COPD), and COPD patients were randomly selected in an established COPD surveillance cohort. Demographic and clinical information of all subjects were collected. Pulmonary function was measured by post-bronchodilator testing. qRT-PCR and ELISA assays were performed to detect the expression levels of lncRNA LUCAT1, miR-181a-5p, and inflammatory cytokines. An in vitro exposure model was constructed using cigarette smoke extract (CSE)-induced human bronchial epithelial (16HBE) cells. The dual-luciferase reporter and RNA pull-down assays were used to detect the binding relationship between lncRNA LUCAT1 and miR-181a-5p; meanwhile, Spearman's correlation assay was used to verify the correlation between lncRNA LUCAT1 and miR-181a-5p. Afterward, the lncRNA LUCAT1 silencing plasmid was constructed and co-transfected with a miR-181a-5p inhibitor to evaluate the effects on CSE-induced 16HBE cell proliferation and apoptosis. Finally, a Western blot assay was utilized to determine the mechanism of lncRNA LUCAT1/miR-181a-5p/Wnt/β-catenin axis in COPD. RESULTS: LncRNA LUCAT1 was upregulated in the serums of COPD patients. Correlation analysis further confirmed the strong correlation between LUCAT1 expression and inflammatory cytokines IL-1β, IL-6, and TNF-α. Receiver operating characteristic (ROC) analysis verified the potential of LUCAT1 in COPD diagnosis. After treatment with CSE, LUCAT1 was significantly increased while its target miR-181a-5p was decreased in 16HBE cells. Cell proliferation and apoptosis assays showed that LUCAT1 silencing alleviated CSE's effects on 16HBE cell proliferation and apoptosis. Mechanically, rescue assays demonstrated that miR-181a-5p inhibition could partially counteract the impact of LUCAT1 on COPD progression through the Wnt/β-catenin pathway. CONCLUSIONS: LncRNA LUCAT1 may be a valuable indicator for differentiating COPD. Moreover, LncRNA LUCAT1/miR-181-5p/Wnt/β-catenin axis behaved as a critical role in COPD development, shedding new sights for clinical treatment.	NA	J Clin Lab Anal. 2021 Jun 14:e23823. doi: 10.1002/jcla.23823.
3282	LncRNA	SNHG12	miR-101-3p	CUL4B	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	34002487	LncRNA SNHG12 regulates the miR-101-3p/CUL4B axis to mediate the proliferation, migration and invasion of non-small cell lung cancer.	Mounting evidence has shown that long noncoding RNAs (lncRNAs) play critical roles in carcinogenesis and tumor progression. SNHG12 has been identified in multiple types of malignant tumors. However, the role of SNHG12 in human non-small cell lung cancer (NSCLC) is poorly characterized, and the relevant underlying mechanism remains unclear. The expression levels of SNHG12, miR-101-3p, and CUL4B in collected human NSCLC tumor tissues and NSCLC cell lines were tested via qRT-PCR. Then, NSCLC cellular proliferation, migration and invasion were determined, followed by MTT, scratch and Transwell assays. Dual-luciferase reporter assays and RNA pulldown assays were adopted to explore the target site. Moreover, western blotting was performed to detect the relevant protein expression concerning the CUL4B/PI3K/AKT pathway. This study clarified that SNHG12 knockdown significantly reduced proliferation, migration, invasion and EMT of NSCLC cells. Our data indicated that SNHG12 targeted and negatively regulated miR-101-3p, and this depletion reversed the inhibitory effect of si-SNHG12 on NSCLC cells. Furthermore, CUL4B was confirmed as a functional target of miR-101-3p, and its knockdown resulted in a strong alleviation of the NSLCL cell phenotype, which was enhanced by the silencing of miR-101-3p. Mechanistically, we found that SNHG12 regulated miR-101-3p to modulate the PI3K/AKT pathway mediated by CUL4B.These observations suggested that lncRNA SNHG12-mediated miR-101-3p downregulation regulated the malignant phenotype of NSCLC cells by targeting CUL4B through the PI3K/AKT pathway, which may present a path to novel therapeutic strategies for NSCLC therapy.	NA	Kaohsiung J Med Sci. 2021 May 17. doi: 10.1002/kjm2.12389.
3283	LncRNA	MSC-AS1	miR-33b-5p	GPAM	LUAD tissues and cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33821667	LncRNA MSC-AS1 facilitates lung adenocarcinoma through sponging miR-33b-5p to up-regulate GPAM.	Many reports have indicated that long non-coding RNAs (lncRNAs) are closely associated with the occurrence and development of various cancers. Musculin antisense RNA 1 (MSC-AS1) is a an lncRNA known to act as an oncogene in several types of human cancers; however, its specific function in lung adenocarcinoma (LUAD) is still unclear. For this study, we designed and conducted experiments to clarify the function of the lncRNA MSC-AS1 in LUAD and its underlying mechanisms. We found that the expression of MSC-AS1 was significantly higher in LUAD tissues and cells than that in normal ones. Through loss-of function assays, we confirmed that the proliferation of LUAD cells was significantly restrained by down-regulation of MSC-AS1 and the rate of cell apoptosis was accelerated. The results from our mechanistic experiments showed that MSC-AS1 interacts with microRNA-33b-5p (miR-33b-5p). Moreover, glycerol-3-phosphate acyltransferase, mitochondrial (GPAM) was found to be a direct target gene of miR-33b-5p, and it has similar functions to MSC-AS1. Further, inhibition of miR-33b-5p or overexpression GPAM reversed the inhibitory effects of MSC-AS1 silencing on LUAD cell growth. In short, MSC-AS1 facilitates LUAD progression through sponging miR-33b-5p to up-regulate GPAM.	NA	Biochem Cell Biol. 2021 Apr;99(2):241-248. doi: 10.1139/bcb-2020-0239. Epub 2020 Sep 21.
3284	LncRNA	CCAT1	miR-138-5p	HMGA1	PANC-1 cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33872661	Pancreatic cancer cells-derived exosomal long non-coding RNA CCAT1/microRNA-138-5p/HMGA1 axis promotes tumor angiogenesis.	OBJECTIVE: Pancreatic cancer (PC) cells-derived exosomes could mediate angiogenesis of human microvascular endothelial cells (HUVECs) in PC. Considering that, this research was implemented to figure out the concrete role of PC cells-derived exosomal long non-coding RNA colon cancer-associated transcript-1 (CCAT1) in PC with its regulation on microRNA-138-5p/high mobility group A1 (miR-138-5p/HMGA1) axis. METHODS: PC tissues and normal tissues were resected. PC cells (PANC-1) were interfered with plasmids to change CCAT1 and/or miR-138-5p expression. Exosomes were isolated from PANC-1 cells and co-cultured with HUVECs. The proliferation and apoptosis of PANC-1 and HUVECs were examined. The angiogenic ability of HUVECs was tested in vivo in xenografted tumors and in vitro. CCAT1, miR-138-5p and HMGA1 expression were determined, as well as their interactions. RESULTS: CCAT1 and HMGA1 expression were raised while miR-138-5p expression was reduced in PC. Silencing CCAT1 disrupted cell proliferation and stimulated apoptosis of PANC-1 cells. Knocked down CCAT1 from PANC-1 cells-derived exosomes promoted apoptosis and repressed proliferation of HUVECs. Down-regulated/up-regulated CCAT1 from PANC-1 cells-derived exosomes destroyed/enhanced the angiogenic ability of HUVECs in vivo and in vitro. CCAT1 mediated HMGA1 through competitively binding to miR-138-5p. Overexpression of miR-138-5p antagonized the effects of up-regulated CCAT1 on angiogenesis of HUVECs in vitro. CONCLUSION: It is informative that PANC-1 cells-derived exosomal CCAT1 strengthens angiogenesis of HUVECs through binding to miR-138-5p to elevate HMGA1 expression.	NA	Life Sci. 2021 Aug 1;278:119495. doi: 10.1016/j.lfs.2021.119495. Epub 2021 Apr 16.
3285	LncRNA	MNX1-AS1	miR-744-5p	bcl9	LSCC patients	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33821684	LncRNA MNX1-AS1 Contributes to Laryngeal Squamous Cell Carcinoma Growth and Migration by Regulating mir-744-5p/bcl9/β-Catenin Axis.	Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the progression of laryngeal squamous cell carcinoma (LSCC). Here, we aimed to disclose the role of MNX1-AS1 in LSCC progression, and explore whether MNX1-AS1 participates in LSCC progression via targeting miR-744-5p to active BCL9/β-catenin signaling. Sixty-five human LSCC tissues and the paracancerous normal tissues were recruited to determine the levels of MNX1-AS1, miR-744-5p and BCL9 using qRT-PCR. The interaction of miR-744-5p and MNX1-AS1/BCL9 was determined by using the RNA immunoprecipitation (RIP) assay and/or luciferase gene reporter assay. Cell viability, in vivo tumor formation, invasion and migration abilities were detected by MTT, Xenograft models and Transwell assays. MNX1-AS1 level was increased significantly in human LSCC tissues as compared with the normal tissues, which showed a positive correlation with BCL9 level while a negative correlation with miR-744-5p level. High level of MNX1-AS1 predicted a poor prognosis and an advanced clinical process in LSCC patients. miR-744-5p targeted upregulation weakened the luciferase activity of MNX1-AS1 and /BCL9, and downregulated their expression levels-wt, while showed no effect when the binding sites were mutated. Knockdown of MNX1-AS1 markedly weakened cell viability, migration, and invasion abilities, while BCL9 overexpression abolished these tendencies. In addition, MNX1-AS1 downregulation induced decreases in tumor volumes and weights in vivo, accompanied by reductions in BCL9, Ki-67 and β-catenin expression and an increase in miR-744-5p expression. Collectively, this study reveals that MNX1-AS1 contributes to cell growth and migration by regulating miR-744-5p/BCL9/β-catenin axis in LSCC.	NA	Cell Transplant. 2021 Jan-Dec;30:9636897211005682. doi: 10.1177/09636897211005682.
3286	LncRNA	MNX1-AS1	miR-744-5p	b-catenin	LSCC patients	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33821684	LncRNA MNX1-AS1 Contributes to Laryngeal Squamous Cell Carcinoma Growth and Migration by Regulating mir-744-5p/bcl9/β-Catenin Axis.	Increasing evidence has indicated that long noncoding RNAs (lncRNAs) are involved in the progression of laryngeal squamous cell carcinoma (LSCC). Here, we aimed to disclose the role of MNX1-AS1 in LSCC progression, and explore whether MNX1-AS1 participates in LSCC progression via targeting miR-744-5p to active BCL9/β-catenin signaling. Sixty-five human LSCC tissues and the paracancerous normal tissues were recruited to determine the levels of MNX1-AS1, miR-744-5p and BCL9 using qRT-PCR. The interaction of miR-744-5p and MNX1-AS1/BCL9 was determined by using the RNA immunoprecipitation (RIP) assay and/or luciferase gene reporter assay. Cell viability, in vivo tumor formation, invasion and migration abilities were detected by MTT, Xenograft models and Transwell assays. MNX1-AS1 level was increased significantly in human LSCC tissues as compared with the normal tissues, which showed a positive correlation with BCL9 level while a negative correlation with miR-744-5p level. High level of MNX1-AS1 predicted a poor prognosis and an advanced clinical process in LSCC patients. miR-744-5p targeted upregulation weakened the luciferase activity of MNX1-AS1 and /BCL9, and downregulated their expression levels-wt, while showed no effect when the binding sites were mutated. Knockdown of MNX1-AS1 markedly weakened cell viability, migration, and invasion abilities, while BCL9 overexpression abolished these tendencies. In addition, MNX1-AS1 downregulation induced decreases in tumor volumes and weights in vivo, accompanied by reductions in BCL9, Ki-67 and β-catenin expression and an increase in miR-744-5p expression. Collectively, this study reveals that MNX1-AS1 contributes to cell growth and migration by regulating miR-744-5p/BCL9/β-catenin axis in LSCC.	NA	Cell Transplant. 2021 Jan-Dec;30:9636897211005682. doi: 10.1177/09636897211005682.
3287	LncRNA	LINC01123	miR-516b-5p	Gli1	osteosarcoma cell	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33837611	LINC01123 enhances osteosarcoma cell growth by activating the Hedgehog pathway via the miR-516b-5p/Gli1 axis.	The lncRNA LINC01123 has been reported to act as an oncogene in many human cancers. Nevertheless, the function and underlying mechanism of LINC01123 in osteosarcoma (OS) remain unclear. This study aimed to explore the roles and mechanisms of LINC01123 in OS progression. In this study, the expression of LINC01123 was significantly upregulated in OS cell lines than in a human osteoblast cell line. Furthermore, in vitro and in vivo experiments confirmed that knockdown of LINC01123 suppressed cell progression. Mechanistically, LINC01123 acted as a competing endogenous RNA by sponging miR-516b-5p, thus, increasing Gli1 expression by directly targeting its 3'UTR. Taken together, LINC01123 enhances OS proliferation and metastasis via the miR-516b-5p/Gli1 axis. Therefore, LINC01123 may be a potential therapeutic target for OS treatment.	NA	Cancer Sci. 2021 Jun;112(6):2260-2271. doi: 10.1111/cas.14913. Epub 2021 May 7.
3288	LncRNA	UCA1	miR-331-3p	BRD4	colonic mucosa tissues	Ulcerative Colitis	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34140798	LncRNA UCA1 Accelerates the Progression of Ulcerative Colitis via Mediating the miR-331-3p/BRD4 Axis.	BACKGROUND: Ulcerative colitis (UC) has become one of the fastest-growing severe diseases worldwide with high morbidity. This research aimed to explore the function of lncRNA UCA1 in UC progression. METHODS: RT-qPCR analysis was used to examine the expression of UCA1 level in colonic mucosa tissues of UC patients. Then, fetal human cells (FHCs) were stimulated by LPS to induce inflammatory injury. CCK-8, flow cytometry and ELISA were adopted to determine the influence of UCA1 depletion on cell viability, apoptosis and pro-inflammatory factors levels in LPS-induced FHCs. The interaction between UCA1 and miR-331-3p or BRD4 was confirmed by luciferase reporter assay. The expressions of key factors involved in NF-κB pathway were assessed by Western blotting. RESULTS: LncRNA UCA1 level was elevated in colonic mucosa tissues of UC patients. LPS stimulation restrained cell viability and promoted the apoptosis and inflammatory factors levels, thus inducing FHCs inflammatory injury, while these effects were partially abolished by UCA1 knockdown. Moreover, it was found that UCA1 silence improved LPS-triggered cell injury via miR-331-3p. In addition, BRD4 was directly targeted by miR-331-3p, and BRD4 deficiency neutralized the effects of miR-331-3p repression on LPS-triggered injury in LPS-treated FHCs. CONCLUSION: Our data determined that UCA1 knockdown attenuated UC development via targeting the miR-331-3p/BRD4/NF-κB pathway.	NA	Int J Gen Med. 2021 Jun 10;14:2427-2435. doi: 10.2147/IJGM.S304837. eCollection 2021.
3289	LncRNA	PP7080	miR-670-3p	UHRF1BP1	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	33844396	PP7080 expedites the proliferation and migration of lung adenocarcinoma cells via sponging miR-670-3p and regulating UHRF1BP1.	BACKGROUND: An increasing body of evidence has revealed that long non-coding RNAs play a significant part in a variety of human cancers, including lung adenocarcinoma (LUAD). METHODS: The expression of PP7080, miR-670-3p and UHRF1BP1 in LUAD cells and tissues was detected using a quantitative real-time polymerase chain reaction. The role of PP7080 in LUAD cells was validated by CCK-8, flow cytometry, colony formation, transwell and wound healing assays. The binding capacity between PP7080/UHRF1BP1 and miR-670-3p was confirmed by luciferase reporter assays. Moreover, the interactional mechanism among PP7080, miR-670-3p and UHRF1BP1 was determined by means of RNA immunoprecipitation and western blot assays. RESULTS: The expression level of PP7080 is up-regulated in LUAD cells and tissues compared to their matched controls. Down-regulation of PP7080 restrained the proliferative and migratory abilities of LUAD cells, but induced cell apoptosis. PP7080 up-regulation led to the opposite results. Moreover, the binding ability between miR-670-3p and PP7080/UHRF1BP1 in LUAD cells was confirmed. A rescue assay revealed that PP7080 contributes to LUAD development by modulating the miR-670-3p/UHRF1BP1 signaling pathway. CONCLUSIONS: PP7080 expedites the proliferation and migration of LUAD cell via sponging miR-670-3p and modulating UHRF1BP1.	NA	J Gene Med. 2021 Apr 12:e3341. doi: 10.1002/jgm.3341.
3290	LncRNA	NEAT1	miR-93-5p	TXNI	human tubule epithelial (HK2) cells	Human Tubule Epithelial	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33885954	Long non-coding RNA NEAT1 promotes lipopolysaccharide-induced injury in human tubule epithelial cells by regulating miR-93-5p/TXNIP axis.	Many long non-coding RNAs (lncRNAs) have been found to play crucial roles in sepsis-induced acute kidney injury (AKI), including lncRNA nuclear-enriched abundant transcript 1 (NEAT1). We aimed to further elucidate the functions and molecular mechanism of NEAT1 in sepsis-induced AKI. Sepsis-induced AKI cell model was established by treatment with lipopolysaccharide (LPS) in human tubule epithelial (HK2) cells. Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Western blot assay was performed to measure all protein levels. The concentrations of inflammatory factors were evaluated using enzyme-linked immunosorbent assay (ELISA). The expression levels of inflammatory factors, NEAT1, microRNA-93-5p (miR-93-5p), and thioredoxin-interacting protein (TXNIP) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The oxidative stress factors were detected using corresponding kits. The interaction between miR-93-5p and NEAT1 or TXNIP was predicted by bioinformatics analysis and verified by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. NEAT1 was upregulated in serum of sepsis patients and LPS-induced HK2 cells. NEAT1 silence alleviated LPS-induced HK2 cell injury by inhibiting apoptosis, inflammation and oxidative stress. Moreover, miR-93-5p was a direct target of NEAT1, and suppression of NEAT1 weakened LPS-induced injury by upregulating miR-93-5p in HK2 cells. Furthermore, TXNIP was a downstream target of miR-93-5p, and miR-93-5p attenuated LPS-induced HK2 cell injury by downregulating TXNIP. In addition, NEAT1 regulated TXNIP expression by acting as a sponge of miR-93-5p. NEAT1 might aggravate LPS-induced injury in HK2 cells by regulating miR-93-5p/TXNIP axis, providing a potential therapeutic strategy for sepsis-associated AKI.	NA	Med Microbiol Immunol. 2021 Jun;210(2-3):121-132. doi: 10.1007/s00430-021-00705-6. Epub 2021 Apr 22.
3291	LncRNA	HOTAIR	miR-526b-3p	DHX33	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33843021	Long non-coding RNA HOTAIR promotes hepatocellular carcinoma progression by regulating miR-526b-3p/DHX33 axis.	BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common human cancers. Long non-coding RNAs (lncRNAs) play pivotal roles in progression of various cancers, including HCC. OBJECTIVE: We aimed to explore the exact role and underlying mechanism of lncRNA HOX transcript antisense intergenic RNA (HOTAIR) in HCC. METHODS: Quantitative real time polymerase chain reaction (qRT-PCR) was carried out to determine the levels of HOTAIR, DEAH-box helicase 33 (DHX33) and miR-526b-3p. Western blot assay was used to detect the protein level of DHX33. Besides, cell proliferation and apoptosis were assessed by methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Cell migration and invasion were detected by transwell assay. The interaction between miR-526b-3p and HOTAIR or DHX33 was predicted by starbase and confirmed by the dual-luciferase reporter assay. Murine xenograft model was established through injecting Huh7 cells transfected with sh-NC or sh-HOTAIR. RESULTS: The levels of HOTAIR and DHX33 were increased in HCC tissues and cells. Knockdown of either HOTAIR or DHX33 suppressed proliferation, migration and invasion but increased apoptosis in HCC cells. Moreover, DHX33 overexpression reversed the suppressive effect of HOTAIR knockdown on progression of HCC cells. Interestingly, miR-526b-3p could directly bind to HOTAIR, and DHX33 was a direct target of miR-526b-3p. Additionally, interference of HOTAIR restrained the tumor growth by upregulating miR-526b-3p and downregulating DHX33 in vivo. CONCLUSIONS: HOTAIR knockdown suppressed cell proliferation, migration and invasion, and promoted apoptosis via regulating miR-526b-3p/DHX33 axis in HCC cells, providing a potential avenue for treatment of HCC.	NA	Genes Genomics. 2021 Apr 12. doi: 10.1007/s13258-021-01098-9.
3292	LncRNA	THAP9-AS1	miR-133b	SOX4	ESCC tissues and cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	33854048	THAP9-AS1/miR-133b/SOX4 positive feedback loop facilitates the progression of esophageal squamous cell carcinoma.	Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors in the digestive system with a high incidence and poor prognosis. Long non-coding RNAs (LncRNA) have been reported to be closely associated with the occurrence and development of various human cancers. Data from GSE89102 shows an increase of THAP9-AS1 expression in ESCC. However, its functions and mechanisms underlying ESCC progression remain to be investigated. In this study, we found that THAP9-AS1 was overexpressed in ESCC tissues and cells. High THAP9-AS1 expression was positively correlated with tumor size, TNM stage, lymph node metastasis, and worse prognosis. Functionally, depletion of THAP9-AS1 suppressed cell proliferation, migration, and invasion, while enhanced apoptosis in vitro. Consistently, knockdown of THAP9-AS1 inhibited xenograft tumor growth in vivo. Mechanistically, THAP9-AS1 could serve as a competing endogenous RNA (ceRNA) for miR-133b, resulting in the upregulation of SOX4. Reciprocally, SOX4 bound to the promoter region of THAP9-AS1 to activate its transcription. Moreover, the anti-tumor property induced by THAP9-AS1 knockdown was significantly impaired due to miR-133b downregulation or SOX4 overexpression. Taken together, our study reveals a positive feedback loop of THAP9-AS1/miR-133b/SOX4 to facilitate ESCC progression, providing a potential molecular target to fight against ESCC.	NA	Cell Death Dis. 2021 Apr 14;12(4):401. doi: 10.1038/s41419-021-03690-z.
3293	LncRNA	MALAT1	miR-2355-3p	IL6ST	human renal tubular epithelial cells	Renal Fibrosis	Homo sapiens (human)	qRT-PCR	33995063	lncRNA MALAT1 Promotes Renal Fibrosis in Diabetic Nephropathy by Targeting the miR-2355-3p/IL6ST Axis.	Long noncoding RNA (lncRNAs) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been reported in diabetic nephropathy (DN) about its effect on podocyte function and cell heat shock induced by hyperglycemia. However, the biological mechanism of MALAT1 regulating DN fibrosis needs further study. In this study, SD rats were administrated with streptozotocin (STZ) to establish a diabetes model. In vitro, human renal tubular epithelial cells (HK-2 and 293T) were treated with high glucose (HG). Here, we found that MALAT1 was upregulated in renal tissues of diabetic rats and HG-treated cells, and HG treatment promoted cell proliferation and invasion. MALAT1 overexpression aggravated protein levels of collagen I (col I), collagen IV (col IV), fibronectin (FN), and laminin (LN) in HK-2 cells, while MALAT1 knockdown exerted the opposite effect. Moreover, the luciferase reporter gene and pull-down assays demonstrated that MALAT1 interacted with miR-2355-3p. The miR-2355-3p level was downregulated in diabetic rats and HG-treated cells, and MALAT1 overexpression inhibited the miR-2355-3p level. Bioinformatics prediction and luciferase reporter gene assay revealed that interleukin 6 signal transducer (IL6ST) was a target of miR-2355-3p. In addition, miR-2355-3p overexpression attenuated fibrosis-related gene levels in HG-treated cells by inhibiting IL6ST expression and inactivating the recombinant signal transducer and activator of the transcription 3 (STAT3) signaling pathway. Knockdown of miR-2355-3p reversed the inhibitory effect of MALAT1 knockdown on IL6ST, col I, col IV, FN, and LN protein levels in HG-induced cells. Overexpression of MALAT1 aggravated cell damage in HG-induced cells via the miR-2355-3p/IL6ST/STAT3 signaling pathway. Finally, enhanced renal fibrosis and kidney tissue damage were observed in diabetic rats. In conclusion, MALAT1 overexpression may enhance renal fibrosis in diabetic rats and cell damage in HG-induced HK-2 cells via the miR-2355-3p/IL6ST axis, which provides a new perspective of DN treatment.	NA	Front Pharmacol. 2021 Apr 29;12:647650. doi: 10.3389/fphar.2021.647650. eCollection 2021.
3294	LncRNA	DUXAP8	miR-635	TOP2A	OS cells	Osteosarcoma	Homo sapiens (human)	Luciferase reporter assay;	33982765	Long non-coding RNA-DUXAP8 regulates TOP2A in the growth and metastasis of osteosarcoma via microRNA-635.	Osteosarcoma (OS) is a malignant disease with high morbidity and mortality rates in children and adolescents. Evidence has indicated that long non-coding RNAs (lncRNAs) may serve important roles in human cancer progression, including OS. In the present study, the role of lnc-double homeobox A pseudogene 8 (DUXAP8) in the development of OS was identified. The expression of lncRNA-DUXAP8 was determined by reverse transcription-quantitative polymerase chain reaction in OS tissues. Cell proliferation was evaluated using Cell Counting kit-8 and colony formation assays, and Transwell assays were conducted to measure cell invasion. Cell migration was evaluated using a wound healing assay. The binding site between lnc-DUXAP8 and miR-635 RNAs was investigated using a luciferase reporter assay. The expression of lnc-DUXAP8 was significantly upregulated in OS samples and OS cell lines compared with normal tissues. High expression of lncRNA DUXAP8 was associated with shorter overall survival times. Knockdown of lncRNA DUXAP8 inhibited proliferation, migration and invasion in OS cells. Notably, mechanistic investigation revealed that lncRNA DUXAP8 predominantly acted as a competing endogenous RNA in OS by regulating the miR-635/topoisomerase alpha 2 (TOP2A) axis. lncRNA DUXAP8 is upregulated in OS, and lncRNA DUXAP8-knockdown serves a vital antitumor role in OS cell progression through the miR-635/TOP2A axis. The results of the present study suggested that lncRNA DUXAP8 may be a novel, promising biomarker for the diagnosis and prognosis of OS.	NA	Mol Med Rep. 2021 Jul;24(1):511. doi: 10.3892/mmr.2021.12150. Epub 2021 May 13.
3295	LncRNA	HOXA10	miR-29a	MCL-1	oral squamous cell carcinoma stem cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	33831733	Promotive effects of HOXA10 antisense RNA on the stemness of oral squamous cell carcinoma stem cells through a microRNA-29a/MCL-1/phosphatidyl inositol 3-kinase/protein kinase B axis.	OBJECTIVE: The aim of this study was to investigate the effects of long non-coding RNA (lncRNA) HOXA10 antisense RNA (HOXA10-AS) on the properties of oral squamous cell carcinoma (OSCC) stem cells and the molecular mechanism. DESIGN: Tumor and the paracancerous tissues were collected from 83 patients with OSCC. OSCC stem cells were extracted from a human OSCC cell line Tca8113. Silencing of HOXA10-AS was introduced in stem cells and then the malignant behaviors of cells were determined. The target transcripts of HOXA10-AS were predicted using integrated bioinformatics analyses. The interactions among HOXA10-AS, microRNA (miR)-29a and MCL-1 were validated, and their functions in stem cell behaviors in vivo and in vitro were explored. RESULTS: HOXA10-AS and MCL-1 were highly expressed while miR-29a was poorly expressed in the collected tumor tissues and the extracted OSCC stem cells. High expression of HOXA10-AS and MCL-1, while poor expression of miR-29a was relevant to poor prognosis in patients. Silencing of HOXA10-AS suppressed proliferation and tumor sphere formation ability of stem cells, and it reduced growth and metastasis of tumors in animals. HOXA10-AS served as a sponge for miR-29a and upregulated MCL-1 mRNA expression. Inhibition of miR-29a promoted, while silencing of MCL-1 suppressed the malignant behaviors of OSCC stem cells. In addition, HOXA-10-AS and MCL-1 were found to activate the phosphatidyl inositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. CONCLUSION: This study evidenced that HOXA10-AS enhances the stem cell property of OSCC stem cells through the miR-29a/MCL-1/PI3K/AKT axis.	NA	Arch Oral Biol. 2021 Jun;126:105114. doi: 10.1016/j.archoralbio.2021.105114. Epub 2021 Mar 31.
3296	LncRNA	MEG8	miR-497-5p	NOT	hemangioma endothelial cells	Hemangioma	Homo sapiens (human)	luciferase assay;	33839417	Silencing long non-coding RNA MEG8 inhibits the proliferation and induces the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis.	Even though long non-coding RNA (lncRNA) MEG8 plays vital roles in carcinogenesis of malignances, its roles and mechanisms in hemangioma remain unknown. Therefore, we evaluate the oncogenic roles of MEG8 in hemangioma. Small interfering RNA (siRNA)-mediated depletion of MEG8 inhibited the proliferation and increased MDA level in human hemangioma endothelial cells (HemECs). The inhibitors of ferroptosis (ferrostatin-1 and liproxstatin-1) abolished the MEG8 silence induced cell viability loss. Knockdown of MEG8 increased the miR-497-5p expression and reduced the mRNA and protein levels of NOTCH2. Using a dual-luciferase assay, we confirmed the binding between MEG8 and miR-497-5p, and between the miR-497-5p and 3'UTR of NOTCH2. We further found that silencing MEG8 significantly decreased the expressions of SLC7A11 and GPX4 both in mRNA and protein level and had no effect on the level of AIFM2. Importantly, blocking miR-497-5p abrogated the effects of MEG8 loss on cell viability, MDA level and expression levels of NOTCH2, SLC7A11 and GPX4 in HemECs. Taken together, our results suggested that knockdown of long non-coding RNA MEG8 inhibited the proliferation and induced the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis.	NA	Biochem Biophys Res Commun. 2021 Jun 4;556:72-78. doi: 10.1016/j.bbrc.2021.03.132. Epub 2021 Apr 8.
3297	LncRNA	LIFR-AS1	miR-29a	NFIA	osteosarcoma cell	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qPCR;qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33794884	Macrophages-derived exosomal lncRNA LIFR-AS1 promotes osteosarcoma cell progression via miR-29a/NFIA axis.	BACKGROUND: Osteosarcoma (OS) is the most common primary malignant bone tumor in young people. Tumor-associated macrophages (TAMs) have been reported to play an important role in the development of osteosarcoma. However, the detailed molecular mechanisms remain largely unknown and need to be elucidated. Recently, exosomes have been reported as the crucial mediator between tumor cells and the tumor microenvironment. And a lot of lncRNAs have been reported to act as either oncogenes or tumor suppressors in osteosarcoma. In this research, we aim to explore the role of macrophages-derived exosomal lncRNA in osteosarcoma development and further elucidated the potential molecular mechanisms involved. METHODS: TAMs were differentiated from human mononuclear cells THP-1, and a high-throughput microarray assay was used to analyze the dysregulated lncRNAs and miRNAs in osteosarcoma cells co-cultured with macrophages-derived exosomes. Western blot, qRT-PCR assays, and Dual-luciferase reporter assay were used to verify the interaction among LIFR-AS1, miR-29a, and NFIA. Cck-8, EdU, colony formation assay, wound-healing, and transwell assay were performed to explore the characterize the proliferation and metastasis ability of OS cells. And qPCR, Western blots, immunohistochemistry, and cell immunofluorescence were used to detect the expression of relative genes or proteins. RESULTS: In this study, we found that THP-1-induced macrophage-derived exosomes could facilitate osteosarcoma cell progression both in vitro and in vivo. Then, the results of the high-throughput microarray assay showed that LIFR-AS1 was highly expressed and miR-29a was lowly expressed. Furthermore, LIFR-AS1 was identified as a miR-29a sponge, and NFIA was validated as a direct target of miR-29a. Functional assays demonstrated that knockdown of exosomal LIFR-AS1 could attenuate the promotion effects of macrophages-derived exosomes on osteosarcoma cell progression and miR-29a inhibition could reserve the effect of LIFR-AS1-knockdown exosomes. Correspondingly, NFIA-knockdown could partially reverse the tumor inhibition effect of miR-29a on osteosarcoma cells. CONCLUSIONS: Taken together, macrophages-derived exosomal lncRNA LIFR-AS1 can promote osteosarcoma cell proliferation, invasion, and restrain cell apoptosis via miR-29a/NFIA axis, which can act as a potential novel therapeutic target for osteosarcoma therapy.	NA	Cancer Cell Int. 2021 Apr 1;21(1):192. doi: 10.1186/s12935-021-01893-0.
3298	LncRNA	DUXAP8	miR-3182	NUPR1	human epidermal melanocytes cells	Melanoma 	Homo sapiens (human)	qPCR;RT-qPCR;RNA pull-down;	33981357	DUXAP8 knockdown inhibits the development of melanoma by regulating the miR-3182/NUPR1 pathway.	Double homeobox A pseudogene 8 (DUXAP8) has been reported to regulate the growth of several types of cancers, such as breast cancer and ovarian cancer. However, its role in melanoma remains unclear. In the present study, the mechanism through which DUXAP8 regulates melanoma progression was explored. The expression levels of DUXAP8 were determined in 43 samples from patients with melanoma in different stages, as well as human epidermal melanocytes cells and malignant melanoma cell lines using reverse transcription-quantitative PCR (RT-qPCR). The prognosis of patients was analyzed using the Kaplan-Meier method. The relationship between lncRNA DUXAP8 expression and microRNA (miR)-3182 or nuclear protein 1 transcriptional regulator (NUPR1) levels was analyzed using Pearson's correlation. Luciferase reporter and RNA pull-down were used to examine the interactions between these molecules. Proliferation was assessed using Cell Counting-Kit-8. Transwell assays were used to examine cell migration and invasion. lncRNA DUXAP8 was upregulated in melanoma tissue and cells compared with normal tissues and cells. The levels of DUXAP8 inversely correlated with survival time of patients with melanoma. Knockdown of lncRNA DUXAP8 inhibited proliferation, migration and invasion of melanoma cells. lncRNA DUXAP8 targeted miR-3182, while miR-3182 targeted NUPR1. The overexpression of NUPR1 reversed the effects of DUXAP8 knockdown or miR-3182 mimic on melanoma progression. In conclusion, lncRNA DUXAP8 downregulation inhibits the development of melanoma by regulating the miR-3182/NUPR1 axis.	NA	Oncol Lett. 2021 Jul;22(1):495. doi: 10.3892/ol.2021.12756. Epub 2021 Apr 27.
3299	LncRNA	H19	miR-519d-3p	LD	gastric cancer cells 	Gastric Cancer	Homo sapiens (human)	ELISA;Western blot;Flow Cytometry assay;	33756038	H19 promotes aerobic glycolysis, proliferation, and immune escape of gastric cancer cells through the microRNA-519d-3p/lactate dehydrogenase A axis.	Long noncoding RNAs (lncRNAs) have been investigated in multiple human cancers including gastric cancer (GC). Our research aims to explore the role of H19 in aerobic glycolysis, proliferation, and immune escape of GC cells. The expression of H19 in GC samples was analyzed using Gene Expression Profiling Interactive Analysis, Gene Expression Omnibus data, and real-time quantitative PCR analysis. Relative quantification of glucose consumption and lactate production from cell supernatant were applied to assess the aerobic glycolysis of GC cells. Subcellular fractionation, luciferase reporter, and western blot assays certified the binding between genes. Cell Counting Kit-8 and colony formation assays were used to determine GC cell proliferation. Flow cytometry, ELISA, and real-time quantitative PCR assays were applied to analyze the immunosuppressive effect of H19. H19 was highly expressed in samples of patients with GC, and associated with tumor growth in vivo. H19 knockdown suppressed glucose consumption, lactate production, and proliferation of GC cells by regulating the microRNA (miR)-519d-3p/lactate dehydrogenase A (LDHA) axis. Both miR-519d-3p depletion and LDHA overexpression could reverse the H19 knockdown-induced decrease in aerobic glycolysis and proliferation. Moreover, conditioned medium from stable knockdown H19 GC cells modulated the activity of immune cells including γδT cells, Jurkat cells, and tumor-associated macrophages in a miR-519d-3p/LDHA/lactate axis-dependent manner. The H19/miR-519d-3p/LDHA axis mainly contributed to aerobic glycolysis, proliferation, and immune escape of GC cells.	NA	Cancer Sci. 2021 Jun;112(6):2245-2259. doi: 10.1111/cas.14896. Epub 2021 Apr 7.
3300	Circular RNA	Circ-PRKCI	miR-335	E2F3	PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33716239	Silencing circRNA protein kinase C iota (circ-PRKCI) suppresses cell progression and glycolysis of human papillary thyroid cancer through circ-PRKCI/miR-335/E2F3 ceRNA axis.	The circular RNA PRKCI (circ-PRKCI; ID: hsa_circ_0122683) is highly expressed in human papillary thyroid cancer (PTC) tumors according to GSE93522 dataset. However, its role in PTC tumorigenesis remains to be documented. Here, quantitative real-time PCR showed that expression of circ-PRKCI was abnormally upregulated in human PTC patients' tumors and cells, and higher circ-PRKCI might predict lymph node metastasis and recurrence. Functionally, cell behaviors were measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide assay, colony formation assay, fluorescence-activated cell sorting method, scratch wound assay, transwell assay, western blotting, and assay kits for glucose and lactate. As a result, circ-PRKCI knockdown could suppress cell cycle progression of PTC cells and restrain the abilities of cell proliferation, colony formation, wound closure, invasion, glucose consumption and lactate production, accompanied with decreased levels of matrix metalloproteinase-2 (MMP2), MMP9 and Snail. Moreover, above-mentioned inhibition could be imitated by overexpressing microRNA-335-5p (miR-335). Molecularly, circ-PRKCI functioned as a sponge for miR-335 and miR-335 could further targeted E2F transcription factor-3 (E2F3), according to dual-luciferase reporter assay and RNA immunoprecipitation. However, downregulating miR-335 diminished the effects of circ-PRKCI role on cell growth, metastasis and glycolysis in PTC cells; besides, there was a counteractive effect between miR-335 upregulation and E2F3 upregulation in PTC cells as well. Furthermore, xenograft experiment revealed that silencing circ-PRKCI could retard tumor growth of PTC cells in vivo. Collectively, circ-PRKCI exerted oncogenic role in PTC by antagonizing cell progression and glycolysis via regulating miR-335/E2F3 axis, suggesting circ-PRKCI was a potential biomarker and target for PTC.	NA	Endocr J. 2021 Mar 13. doi: 10.1507/endocrj.EJ20-0726.
3301	Circular RNA	Circ_0032822	miR-141	EF3	Head and Neck Squamous Cell Carcinoma Cells	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	qRT-PCR	33981611	The circ_0032822 Promotes the Proliferation of Head and Neck Squamous Cell Carcinoma Cells Through miR-141/EF3 Signaling Axis.	Head and neck squamous cell carcinoma (HNSCC) refers to an epithelial malignant tumor that originates in the head and neck, and over 600,000 new cases are reported every year, However, the overall prognosis is still poor due to local recurrence and distant metastasis after surgery. The circ_0032822 has been reported upregulated in human oral squamous cell carcinoma; however, the detailed function or mechanism remains unknown. In this study, we confirmed the upregulation of circ_0032822 in HNSCC tumor tissues. Functionally, the overexpression of circ_0032822 significantly promoted the proliferation of HNSCC cell lines along with the S phase arrest and reduced apoptosis, while downregulation of circ_0032822 has the opposite effect in vitro. Mechanistic analysis showed that circ_0032822 acted as a competing endogenous RNA of miR-141 to diminish the repressive effect of miR-141 on its target E2F3. In conclusion, we demonstrated that circ_0032822 functions as a tumor oncogene in HNSCC and that its function is regulated via the miR-141/E2F3 axis.	NA	Front Oncol. 2021 Apr 23;11:662496. doi: 10.3389/fonc.2021.662496. eCollection 2021.
3302	Circular RNA	hsa_circ_0058357	miR-24-3p	AVL9	NSCLC tissues and NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;Immunoblotting;luciferase assay;	33880595	hsa_circ_0058357 acts as a ceRNA to promote non-small cell lung cancer progression via the hsa-miR-24-3p/AVL9 axis.	Abnormal circular RNAs (circRNAs) are associated with biological processes in cancer; however, the function of circRNAs remains largely unknown in non-small cell lung cancer (NSCLC). The present study aimed to investigate the role of hsa_circ_0058357 on the progression of NSCLC. Cell proliferation, migration and apoptosis were determined using Cell Counting Kit-8, Transwell and flow cytometry assays, respectively. Gene [circRNA and microRNA (miR)] and protein expression levels were determined via reverse transcription-quantitative PCR and immunoblotting. A luciferase assay was employed to detect the binding of miR-24-3p with AVL9 cell migration associated (AVL9), while a cancer xenograft model was established to evaluate cancer growth in vivo. The results demonstrated that hsa_circ_0058357 was highly expressed in human NSCLC tissues and NSCLC cells compared with para-cancerous tissues and human bronchial epithelial (HBE) cells, respectively. Knockdown of hsa_circ_0058357 significantly suppressed cell viability, migration and tumor growth, while it promoted apoptosis in NSCLC cells. As a competing endogenous RNA, hsa_circ_0058357 knockdown contributed to the increase of miR-24-3p expression in NSCLC cells. Of note, overexpression of miR-24-3p markedly abolished the exogenous hsa_circ_0058357-induced excessive proliferation, migration and apoptosis resistance of NSCLC cells. Mechanistically, as a signaling molecule in late secretory pathway, AVL9 was also expressed at a high level in NSCLC tissues and cells, which could be directly suppressed by miR-24-3p. In the tumor tissues, along with growth inhibition, hsa_circ_0058357 knockdown also mediated the elevation of miR-24-3p and the reduction of AVL9. Thus, it was suggested that hsa_circ_0058357 may be a crucial regulation factor in NSCLC by sponging hsa-miR-24-3p, leading to a decrease in miR-24-3p expression, and subsequent increase in AVL9 expression. Therefore, hsa_circ_0058357 may serve as a potential target for diagnosis and gene therapy for NSCLC.	NA	Mol Med Rep. 2021 Jun;23(6):470. doi: 10.3892/mmr.2021.12109. Epub 2021 Apr 21.
3303	LncRNA	DUXAP8	miR-29a-3p	SAPCD2	triple negative breast cancer cells	Triple Negative Breast Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Flow Cytometry assay;Rescue assay;	33683171	YY1-inudced activation of lncRNA DUXAP8 promotes proliferation and suppresses apoptosis of triple negative breast cancer cells through upregulating SAPCD2.	Double homeobox A pseudogene 8 (DUXAP8) belongs to long non-coding RNAs (lncRNAs), which has been proven to promote the biological processes of multiple human cancers. Triple-negative breast cancer (TNBC) is the leading cause of cancer-related death in women worldwide. However, the specific role of lncRNA DUXAP8 and its underlying mechanism in TNBC remains to be unclear. We detected the expression of DUXAP8 in TNBC cells through qRT-PCR analysis. The effects of DUXAP8 silencing on TNBC cell proliferation and apoptosis were identified using CCK-8 assay, EdU assay, flow cytometry analysis and TUNEL assay. The downstream microRNA (miRNA) and messenger RNA (mRNA) of DUXAP8 were searched out through bioinformatics analysis and mechanism experiments. Rescue assays were conducted to verify the involvement of suppressor APC domain containing 2 (SAPCD2) in DUXAP8-mediated TNBC cell proliferation and apoptosis. DUXAP8 was highly expressed in TNBC cells compared to that in normal breast cells. Knockdown of DUXAP8 inhibited TNBC cell proliferation and accelerated cell apoptosis. DUXAP8 interacted with miR-29a-3p and thus enhanced the expression of SAPCD2. Moreover, YY1 transcription factor could bind to DUXAP8 promoter to activate the transcription of DUXAP8. YY1-induced transcriptional activation of DUXAP8 promotes TNBC cell growth through miR-29a-3p/SAPCD2 axis.	NA	Cancer Biol Ther. 2021 Mar 4;22(3):216-224. doi: 10.1080/15384047.2021.1881201. Epub 2021 Mar 8.
3304	LncRNA	NORAD	miR-363-3p	PEAK1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	CCK-8 assay;RNA pull-down assay;Western blot;RNA pull-down;	33742335	LncRNA NORAD, sponging miR-363-3p, promotes invasion and EMT by upregulating PEAK1 and activating the ERK signaling pathway in NSCLC cells.	Lung cancer is one of the most common malignant tumors in the world. Non-small cell lung cancer (NSCLC) accounts for about 80% of all lung cancers. About 75% of patients are in the middle and advanced stages at the time of discovery, and the 5-year survival rate is very low. The aim of this study was to investigate the role of long non-coding RNA (lncRNA) NORAD in the pathogenesis of NSCLC. We found that lncRNA NORAD was highly expressed in human NSCLC tissues and cell lines. The CCK-8 assay results showed that lncRNA NORAD had no effect on cell proliferation. The Transwell assay and Western blotting results showed that overexpression of lncRNA NORAD promoted the invasion and epithelial-mesenchymal transition (EMT) of NSCLC cells. Then bioinformatics analysis was used to screen for candidate miRNA bound with lncRNA NORAD and the target gene of miRNA in NSCLC. The luciferase reporter gene assay and RNA pull-down assay were used to verify the relationship. We found that miR-363-3p expression was down-regulated, whereas PEAK1 expression was upregulated in NSCLC cells. We performed gain and loss function test of lncRNA NORAD, miR-363-3p and PEAK1, the results showed that while miR-363-3p-mimic inhibited cell invasion and EMT by targeting PEAK1, lncRNA NORAD acted as a sponge of miR-363-3p and promoted cell invasion and EMT by increasing the expression of PEAK1. In addition, p-ERK expression was detected by Western blotting to observe the effects of lncRNA NORAD, miR-363-3p and PEAK1 on activation of the ERK signaling pathway. Taken together, lncRNA NORAD upregulated the expression of PEAK1 through sponging miR-363-3p, and then activated the ERK signaling pathway, thereby promoting the development of NSCLC.	NA	J Bioenerg Biomembr. 2021 Jun;53(3):321-332. doi: 10.1007/s10863-021-09892-6. Epub 2021 Mar 19.
3305	LncRNA	LINC00958	miR-211-5p	CENPK	TSCC cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	Flow cytometry assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33658048	LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway.	BACKGROUND: Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. METHODS: The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays. RESULTS: LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling. CONCLUSIONS: Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.	NA	Cancer Cell Int. 2021 Mar 3;21(1):147. doi: 10.1186/s12935-021-01808-z.
3306	LncRNA	XIST	miR-192	TRIM25	HCC tissues and HepG2.2.15 cells	Hepatitis B Virus-Related Hepatocellular Carcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;	33858324	LncRNA XIST upregulates TRIM25 via negatively regulating miR-192 in hepatitis B virus-related hepatocellular carcinoma.	BACKGROUND: Long non-coding RNA (lncRNA) XIST has been implicated in the progression of a variety of tumor diseases. The purpose of this study was to explore the molecular role of lncRNA XIST in human hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). METHODS: The expression levels of lncRNA XIST, miR-192 and TRIM25 in HBV-related HCC tissues and HepG2.2.15 cells were detected by qRT-PCR. Biological information and luciferin gene reporter assay were performed to detect the interaction among lncRNA XIST, miR-192 and TRIM25. CCk-8 assay, wound healing assay and colony formation assay were conducted to detect the proliferation and migration ability of HepG2.2.15 cells. RESULTS: qRT-PCR results showed that the expression levels of lncRNA XIST were remarkably increased in HBV-related HCC tissues and HepG2.2.15 cells. In addition, miR-192 was a direct target gene of lncRNA XIST, and the expression of miR-192 and lncRNA XIST were negatively correlated. Moreover, overexpression of miR-192 observably inhibited the proliferation and migration of HCC cells, while overexpression of lncRNA XIST showed an opposite effect. Furthermore, TRIM25 was a direct target of miR-192, and lncRNA XIST could up-regulate the expression of TRIM25 by targeting miR-192. CONCLUSION: LncRNA XIST could up-regulate the expression of TRIM25 by targeting and binding to miR-192, thus accelerating the occurrence and development of HCC.	NA	Mol Med. 2021 Apr 15;27(1):41. doi: 10.1186/s10020-021-00278-3.
3307	LncRNA	LINC01816	miR-34c-5p	CRABP2	THCA tissues and cells	Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33786631	LINC01816 promotes the migration, invasion and epithelial-mesenchymal transition of thyroid carcinoma cells by sponging miR-34c-5p and regulating CRABP2 expression levels.	Thyroid carcinoma (THCA) is a common type of endocrine system cancer and its current clinical treatment method is surgical resection. Long non-coding RNAs (lncRNAs) have been revealed to serve important roles in a variety of complex human diseases. Therefore, determining the association between lncRNAs and diseases may provide novel insight into disease-related lncRNAs, with the aim of improving disease treatments and diagnoses. Long intergenic non-protein coding RNA 1816 (LINC01816) was identified to be associated with the survival of patients with colorectal cancer using the IDHI-MIRW method. The present study aimed to investigate the role and molecular mechanism of LINC01816 in THCA. Analysis of datasets from The Cancer Genome Atlas database revealed that the upregulation of LINC01816 expression levels was associated with a variety of cancer types. Reverse transcription-quantitative PCR analysis demonstrated that compared with the normal thyroid tissues, the expression levels of LINC01816 were upregulated in THCA tissues. The results of wound healing and Transwell assays, and western blotting demonstrated that the overexpression of LINC01816 could strengthen the invasive and migratory abilities of THCA cells and enhance epithelial-mesenchymal transition progression. Analysis using the starBase website and dual-luciferase reporter assays identified that microRNA (miR)-34c-5p was a target of LINC01816. The overexpression of miR-34c-5p could inhibit the invasive and migratory abilities of THCA cells, in addition to inhibiting the cellular retinoic acid binding protein 2 (CRABP2) overexpression-induced effects on invasion, migration and EMT processes. In conclusion, the findings of the present study indicated that LINC01816 may be capable of sponging miR-34c-5p to upregulate CRABP2 expression levels, which subsequently promoted the invasion, migration and EMT of THCA cells. Therefore, targeting the LINC01816/miR-34c-5p/CRABP2 pathway may be an effective therapeutic approach for patients with THCA.	NA	Oncol Rep. 2021 May;45(5):81. doi: 10.3892/or.2021.8032. Epub 2021 Mar 31.
3308	Circular RNA	Circ_0114428	miR-495-3p	CRBN	HK2 cells	Sepsis-Induced Kidney Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;Flow cytometry assay;qRT-PCR;RIP assay; 	33830389	Circ_0114428 Regulates Sepsis-Induced Kidney Injury by Targeting the miR-495-3p/CRBN Axis.	Septic acute kidney injury (AKI) is considered as a severe and common complication of sepsis, with complex pathogenesis. Recently, Circular RNA (circRNA) is considered to be implicated in this disease. This study was intended to elucidate the role of circ_0114428 and the potential mechanism of action in sepsis-induced kidney injury. Sepsis-induced kidney injury cell model was established in human kidney 2 (HK2) cells by the treatment of lipopolysaccharide (LPS). The expression of circ_0114428, CRBN mRNA, and miR-495-3p was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was assessed by cell counting kit-8 (CCK-8) assay. The inflammatory response was monitored according to the release of proinflammatory factors by enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was evaluated by flow cytometry assay. The activities of oxidative indicators were examined using the corresponding kits. Endoplasmic reticulum (ER) stress-related proteins and CRBN protein were quantified by western blot. RNA immunoprecipitation (RIP) assay was performed to ensure whether circ_0114428 could interact with Argonaute 2 (Ago2) protein. The potential miRNAs targeted by circ_0114428 were predicted by the bioinformatics tool and screened by RNA pull-down assay. The interaction between miR-495-3p and circ_0114428 or CRBN was validated by dual-luciferase reporter assay. The results showed that circ_0114428 and CRBN were upregulated in septic AKI serum specimens and LPS-induced HK2 cells. Circ_0114428 knockdown attenuated LPS-induced apoptosis, inflammation, oxidative stress, and ER stress, which were rescued by CRBN overexpression. Further analysis revealed that miR-495-3p was targeted by circ_0114428 and directly bound to CRBN, and circ_0114428 regulated CRBN expression by sponging miR-495-3p. Besides, miR-495-3p inhibition also reversed the effects of circ_0114428 knockdown. In conclusion, circ_00114428 knockdown attenuated LPS-induced HK2 cell injury by regulating CRBN expression via targeting miR-495-3p.	NA	Inflammation. 2021 Apr 8. doi: 10.1007/s10753-021-01432-z.
3309	LncRNA	CCDC183-AS1	miR-589-5p	SKP1	HCC tissues and cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;	33541391	Long non-coding RNA CCDC183-AS1 acts AS a miR-589-5p sponge to promote the progression of hepatocellular carcinoma through regulating SKP1 expression.	BACKGROUND: Hepatocellular carcinoma (HCC) is a common type of malignant human cancer with high morbidity and poor prognosis, causing numerous deaths per year worldwide. Growing evidence has been demonstrated that long non-coding RNAs (lncRNAs) are closely associated with hepatocarcinogenesis and metastasis. However, the roles, functions, and working mechanisms of most lncRNAs in HCC remain poorly defined. METHODS: Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of CCDC183-AS1 in HCC tissues and cell lines. Cell proliferation, migration and invasion ability were evaluated by CCK-8 and transwell assay, respectively. Animal experiments were used to explore the role of CCDC183-AS1 and miR-589-5p in vivo. Bioinformatic analysis, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to confirm the regulatory relationship between CCDC183-AS1, miR-589-5p and SKP1. RESULTS: Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate. Functionally, overexpression of CCDC183-AS1 markedly promoted HCC cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo, whereas the downregulation of CCDC183-AS1 exerted opposite effects. MiR-589-5p inhibitor counteracted the proliferation, migration and invasion inhibitory effects induced by CCDC183-AS1 silencing. Mechanistically, CCDC183-AS1 acted as a ceRNA through sponging miR-589-5p to offset its inhibitory effect on the target gene SKP1, then promoted the tumorigenesis of HCC. CONCLUSIONS: CCDC183-AS1 functions as an oncogene to promote HCC progression through the CCDC183-AS1/miR-589-5p/SKP1 axis. Our study provided a novel potential therapeutic target for HCC patients.	NA	J Exp Clin Cancer Res. 2021 Feb 4;40(1):57. doi: 10.1186/s13046-021-01861-6.
3310	LncRNA	LINC00173	miR-641	RAB14	DDP-resistant HCC tissues and cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	Luciferase reporter assay;	33777195	Long non-coding RNA LINC00173 enhances cisplatin resistance in hepatocellular carcinoma via the microRNA-641/RAB14 axis.	A growing body of evidence indicates that long non-coding RNAs (lncRNAs) play crucial roles in the chemoresistance of human cancers. However, the molecular mechanisms underlying the functions of certain lncRNAs in the chemotherapeutic resistance of hepatocellular carcinoma (HCC) remain unclear. The aim of the present study was to investigate the function and potential mechanism of action of lncRNA LINC00173 in HCC cisplatin (DDP) resistance. Reverse transcription-quantitative PCR analysis indicated that LINC00173 was highly expressed in DDP-resistant HCC tissues and cell lines, and high expression levels of LINC00173 were found to be associated with poor prognosis in patients with HCC. Moreover, LINC00173-knockdown improved the DDP sensitivity of DDP-resistant HCC cells. A luciferase reporter assay also demonstrated that microRNA (miR)-641 was a direct target of LINC00173. miR-641 inhibition restored the promoting effect of LINC00173 knockdown on DDP sensitivity in HCC cells. Furthermore, RAB14 was identified as a target of miR-641, and RAB14 overexpression restrained the inducing effect of LINC00173 knockdown on HCC cell DDP sensitivity. The findings of the present study demonstrated that LINC00173 increased DDP resistance in HCC via the miR-641/RAB14 axis, which may represent a promising therapeutic strategy for HCC.	NA	Oncol Lett. 2021 May;21(5):371. doi: 10.3892/ol.2021.12632. Epub 2021 Mar 13.
3311	LncRNA	MALAT1	miR-181b-5p	MEF2A	peripheral blood of the CSF patients	Coronary Slow Flow Endothelial Dysfunction	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Chromatin immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;	33545365	The lncRNA MALAT1 participates in regulating coronary slow flow endothelial dysfunction through the miR-181b-5p-MEF2A-ET-1 axis.	BACKGROUND: Coronary slow flow (CSF) refers to coronary arteries with no obvious stenosis but have slow coronary flow without effective treatment. The main cause of CSF is endothelial dysfunction. The long non-coding RNA (lncRNA) MALAT1 is involved in regulating endothelial dysfunction, but its role in CSF endothelial dysfunction is still unclear. METHODS: We included 41 CSF patients and 37 controls in the study, who all underwent coronary angiography, echocardiography, and brachial artery flow-mediated dilatation (FMD) examination. Human umbilical vein endothelial cells (HUVECs) stimulated by oxygen-glucose deprivation were used as CSF-induced HUVECs. Plasma endothelin-1 (ET-1) concentrations were determined by enzyme-linked immunosorbent assay (ELISA). The expression levels of MALAT1, miR-181b-5p, myocyte enhancer factor 2A (MEF2A), and ET-1 were measured by qRT-PCR or western blotting. Cell proliferation was determined by 5-ethynyl-2'-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays. Apoptosis was examined by flow cytometry. The relationship between miR-181b-5p and MALAT1 or MEF2A was verified by dual-luciferase reporter assay. MEF2A binding directly to the ET-1 promoter region was verified via chromatin immunoprecipitation (ChIP) assay. RESULTS: MALAT1 and ET-1 were increased, and miR-181b-5p was decreased in the peripheral blood of the CSF patients, and could be used as predictors of CSF. In the CSF-induced HUVECs, MALAT1 was highly expressed, and MALAT1 knockdown improved endothelial function. In contrast, miR-181b-5p was downregulated in the CSF-induced HUVECs, and miR-181b-5p overexpression improved endothelial function. While MEF2A was highly enriched in CSF-induced HUVECs, MEF2A knockdown reduced ET-1 and increased the endothelial function of CSF-induced HUVECs as a transcriptional regulator of ET-1. MALAT1 modulated MEF2A expression positively by sponging miR-181b-5p. CONCLUSIONS: Endothelial function is reduced in CSF. MALAT1 participates in regulating CSF endothelial dysfunction through the miR-181b-5p-MEF2A-ET-1 axis, and could provide a new target for CSF treatment.	NA	Vascul Pharmacol. 2021 Jun;138:106841. doi: 10.1016/j.vph.2021.106841. Epub 2021 Feb 2.
3312	LncRNA	Circ-RNF13	miR-424-5p	TGIF2	HBV-infected human HCC tissues and HBV-expressing cells (Huh7-HBV and Hep3B-HBV)	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33714261	Circ-RNF13, as an oncogene, regulates malignant progression of HBV-associated hepatocellular carcinoma cells and HBV expression and replication through circ-RNF13/miR-424-5p/TGIF2 ceRNA pathway.	The circular RNA RNF13 (circ-RNF13; ID: hsa_circ_0067717) is a novel identified abnormally upregulated circRNA in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) patients. However, its role and mechanism remain to be further annotated. The expression of circ-RNF13, microRNA (miR)-424-5p, and TGFβ-induced factor homeobox 2 (TGIF2) were detected by real-time quantitative PCR and western blotting, and their interaction was confirmed by dual-luciferase reporter assay. Functional assays were performed using MTS assay, colony formation assay, flow cytometry, enzyme-linked immunosorbent assay, transwell assay, and xenograft tumor model, along with real-time quantitative PCR. Circ-RNF13 was upregulated in HBV-infected human HCC tissues and HBV-expressing cells (Huh7-HBV and Hep3B-HBV), accompanied with TGIF2 upregulation and miR-424-5p downregulation. Blocking circ-RNF13 enhanced the apoptosis rate of Huh7-HBV and Hep3B-HBV cells but inhibited cell viability, colony formation, migration, and invasion, along with suppressed tumor growth in vivo. Besides, HBV DNA copies and levels of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) were diminished by circ-RNF13 knockdown in Huh7-HBV and Hep3B-HBV cells. Mechanistically, circ-RNF13 and TGIF2 served as competing endogenous RNAs (ceRNAs) for miR-424-5p. Overexpressing miR-424-5p mimicked and silencing miR-424-5p counteracted the effects of circ-RNF13 depletion in HBV-expressing HCC cells in vitro. Consistently, TGIF2 restoration partially abrogated the role of miR-424-5p upregulation in Huh7-HBV and Hep3B-HBV cells. The circ-RNF13 sponged miR-424-5p to suppress HBV-associated HCC cells malignant progression and HBV infection by regulating TGIF2, providing a novel insight into the occurrence and treatment of HBV-associated HCC.	NA	Bosn J Basic Med Sci. 2021 Feb 18. doi: 10.17305/bjbms.2020.5266.
3313	Circular RNA	hsa_circ_0001666	miR-330-5p	ETV4	PTC tissues and cell lines	Papillary Thyroid Cancer	Homo sapiens (human)	microarray;Luciferase reporter assay;	33760216	Circular RNA hsa_circ_0001666 sponges miR-330-5p, miR-193a-5p and miR-326, and promotes papillary thyroid carcinoma progression via upregulation of ETV4.	Circular RNAs (circRNAs) are a group of regulators that affect the aggressive behaviors of several types of cancer. Hsa_circ_0001666 (also referred to as hsa_circ_000742) is a newly discovered circRNA that is upregulated in human papillary thyroid carcinoma (PTC) based on microarray analysis. However, the role of hsa_circ_0001666 in PTC progression remains unknown. Thus, the aim of the present study was to determine the potential function and underlying mechanism of hsa_circ_0001666 in PTC. The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Its expression was associated with lymph node metastasis of patients with PTC. Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G(1) phase and an increase in cell cycle-associated proteins. Apoptosis rates and expression levels of pro-apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)-330-5p, miR-193a-5p and miR-326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors. Thus, hsa_circ_0001666 may function as an oncogene, promoting PTC tumorigenesis via the miR-330-5p/miR-193a-5p/miR-326/ETV4 pathway. This provides a basis for identifying potential novel therapeutic targets for PTC.	NA	Oncol Rep. 2021 Apr;45(4):50. doi: 10.3892/or.2021.8001. Epub 2021 Mar 24.
3314	Circular RNA	hsa_circ_0001666	miR-193a-5p	ETV4	PTC tissues and cell lines	Papillary Thyroid Cancer	Homo sapiens (human)	microarray;Luciferase reporter assay;	33760216	Circular RNA hsa_circ_0001666 sponges miR-330-5p, miR-193a-5p and miR-326, and promotes papillary thyroid carcinoma progression via upregulation of ETV4.	Circular RNAs (circRNAs) are a group of regulators that affect the aggressive behaviors of several types of cancer. Hsa_circ_0001666 (also referred to as hsa_circ_000742) is a newly discovered circRNA that is upregulated in human papillary thyroid carcinoma (PTC) based on microarray analysis. However, the role of hsa_circ_0001666 in PTC progression remains unknown. Thus, the aim of the present study was to determine the potential function and underlying mechanism of hsa_circ_0001666 in PTC. The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Its expression was associated with lymph node metastasis of patients with PTC. Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G(1) phase and an increase in cell cycle-associated proteins. Apoptosis rates and expression levels of pro-apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)-330-5p, miR-193a-5p and miR-326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors. Thus, hsa_circ_0001666 may function as an oncogene, promoting PTC tumorigenesis via the miR-330-5p/miR-193a-5p/miR-326/ETV4 pathway. This provides a basis for identifying potential novel therapeutic targets for PTC.	NA	Oncol Rep. 2021 Apr;45(4):50. doi: 10.3892/or.2021.8001. Epub 2021 Mar 24.
3315	Circular RNA	hsa_circ_0001666	miR-326	ETV4	PTC tissues and cell lines	Papillary Thyroid Cancer	Homo sapiens (human)	microarray;Luciferase reporter assay;	33760216	Circular RNA hsa_circ_0001666 sponges miR-330-5p, miR-193a-5p and miR-326, and promotes papillary thyroid carcinoma progression via upregulation of ETV4.	Circular RNAs (circRNAs) are a group of regulators that affect the aggressive behaviors of several types of cancer. Hsa_circ_0001666 (also referred to as hsa_circ_000742) is a newly discovered circRNA that is upregulated in human papillary thyroid carcinoma (PTC) based on microarray analysis. However, the role of hsa_circ_0001666 in PTC progression remains unknown. Thus, the aim of the present study was to determine the potential function and underlying mechanism of hsa_circ_0001666 in PTC. The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Its expression was associated with lymph node metastasis of patients with PTC. Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G(1) phase and an increase in cell cycle-associated proteins. Apoptosis rates and expression levels of pro-apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)-330-5p, miR-193a-5p and miR-326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors. Thus, hsa_circ_0001666 may function as an oncogene, promoting PTC tumorigenesis via the miR-330-5p/miR-193a-5p/miR-326/ETV4 pathway. This provides a basis for identifying potential novel therapeutic targets for PTC.	NA	Oncol Rep. 2021 Apr;45(4):50. doi: 10.3892/or.2021.8001. Epub 2021 Mar 24.
3316	LncRNA	LINC00504	miR-876-3p	HMGB3	breast cancer tissues and cell lines	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33654429	LINC00504 Promotes the Malignant Biological Behavior of Breast Cancer Cells by Upregulating HMGB3 via Decoying MicroRNA-876-3p.	PURPOSE: Long intergenic non-protein coding RNA 504 (LINC00504) is a long non-coding RNA that has an important regulatory role in a variety of human cancers. In this study, LINC00504 expression in breast cancer tissues and cell lines was detected. Studies were also conducted to determine the impact of LINC00504 on the tumor behavior of breast cancer cells. The potential mechanisms underlying the oncogenic role of LINC00504 in breast cancer cells were elucidated in detail. METHODS: Expression of LINC00504 in breast cancer was analyzed by quantitative real-time polymerase chain reaction. The effects of LINC00504 on proliferation, apoptosis, in vitro migration and invasion, and in vivo tumor growth were elucidated using Cell Counting Kit-8 assay, flow cytometry, Transwell assays, and tumor xenograft models, respectively. Bioinformatics analyses in conjunction with RNA immunoprecipitation, luciferase reporter assays, and rescue experiments were conducted to investigate the underlying molecular mechanisms. RESULTS: LINC00504 was upregulated in breast cancer tissues and cell lines. Knocking down LINC00504 suppressed breast cancer cell proliferation, migration, and invasion and facilitated apoptosis in vitro. In addition, tumor growth in vivo was significantly inhibited by LINC00504 depletion. Regarding the underlying mechanism, LIN00504 could function as a competing endogenous RNA in breast cancer by sponging microRNA-876-3p (miR-876-3p), resulting in the upregulation of high mobility group box 3 (HMGB3). Rescue experiments further revealed that miR-876-3p downregulation or HMGB3 upregulation effectively reversed the inhibitory effects of LIN00504 deficiency on breast cancer cells. CONCLUSION: The LIN00504-miR-876-3p-HMGB3 axis shows carcinogenic effects in modulating the biological behavior of breast cancer cells. This pathway may represent an effective target for CRC diagnosis and anticancer therapy.	NA	Cancer Manag Res. 2021 Feb 22;13:1803-1815. doi: 10.2147/CMAR.S276290. eCollection 2021.
3317	Circular RNA	Circ_AFF2	miR-375	TAB2	RA blood samples and FLS-RA cells	Rheumatoid Arthritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33535081	Circ_AFF2 facilitates proliferation and inflammatory response of fibroblast-like synoviocytes in rheumatoid arthritis via the miR-375/TAB2 axis.	Circular RNAs (circRNAs) have been implicated in the pathological regulation of human diseases by acting as microRNA (miRNA) sponges to affect gene expression. CircRNA Fragile Mental Retardation 2 (circ_AFF2) was dysregulated in rheumatoid arthritis (RA), but little is known about its specific function and hidden molecular mechanism in RA. Circ_AFF2, miR-375 and TAK1-binding 2 (TAB2) expression levels were determined through the quantitative real-time polymerase chain reaction (qRT-PCR). Flow cytometry was performed to analyze cell cycle and apoptosis. Cell proliferation detection was conducted by 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) assay. The protein levels were measured using western blot. Inflammatory response was evaluated by enzyme-linked immunosorbent assay (ELISA). RNA pull-down assay was used to select the miRNA target of circ_AFF2. The interaction between miR-375 and circ_AFF2 or TAB2 was analyzed using the dual-luciferase reporter assay. Contrasted to normal samples and fibroblast-like synoviocytes (FLS), circ_AFF2 expression was upregulated in RA blood samples and FLS-RA cells. Cell cycle, proliferation and inflammatory response were blocked while apoptosis was promoted in FLS-RA after the downregulation of circ_AFF2. In addition, circ_AFF2 could interact with miR-375 and the function of circ_AFF2 was achieved by sponging miR-375 in FLS-RA cells. Moreover, TAB2 was a target of miR-375 and miR-375 repressed RA progression by decreasing TAB2 expression in FLS-RA cells. More importantly, circ_AFF2 promoted the expression of TAB2 by targeting miR-375. These findings clarified that circ_AFF2 induced cell progression, inflammatory response in FLS-RA cells via the miR-375/TAB2 axis. Circ_AFF2 could be used as a biomarker in the diagnosis and treatment of RA.	NA	Exp Mol Pathol. 2021 Apr;119:104617. doi: 10.1016/j.yexmp.2021.104617. Epub 2021 Jan 31.
3318	LncRNA	OIP5-AS1	miR-135a-5p	KLF5	human umbilical vein endothelial cells (HUVECs)	NA	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33778018	Silencing of OIP5-AS1 Protects Endothelial Cells From ox-LDL-Triggered Injury by Regulating KLF5 Expression via Sponging miR-135a-5p.	Background: Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of atherosclerosis. LncRNA OIP5 antisense RNA 1 (OIP5-AS1) has been found to be associated with the development of atherosclerosis. In this study, we further investigated the molecular basis of OIP5-AS1 in atherosclerosis pathogenesis. Methods: Oxidative low-density lipoprotein (ox-LDL) was used to treat human umbilical vein endothelial cells (HUVECs). The levels of OIP5-AS1, miR-135a-5p, and Krüppel-like factor 5 (KLF5) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell viability, migration, and apoptosis were evaluated using the Cell Counting Kit-8 (CCK-8), Transwell, and flow cytometry, respectively. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and malondialdehyde (MDA) were determined with enzyme-linked immunosorbent assay (ELISA). Targeted interactions among OIP5-AS1, miR-135a-5p, and KLF5 were confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Animal studies were performed to assess the role of OIP5-AS1 in atherosclerosis progression in vivo. Results: Our data showed the significant upregulation of OIP5-AS1 in atherosclerosis serum and ox-LDL-stimulated HUVECs. The silencing of OIP5-AS1 protected against ox-LDL-triggered cytotoxicity in HUVECs and diminished lipids secretion in ApoE(-/-) mice. Moreover, OIP5-AS1 functioned as a molecular sponge of miR-135a-5p, and miR-135a-5p was a functional mediator of OIP5-AS1 in regulating ox-LDL-induced HUVEC injury. KLF5 was a direct target of miR-135a-5p, and the increased expression of miR-135a-5p alleviated ox-LDL-induced cytotoxicity by downregulating KLF5. Furthermore, OIP5-AS1 influenced KLF5 expression through sponging miR-135a-5p. Conclusion: The current work identified that the silencing of OIP5-AS1 protected against ox-LDL-triggered cytotoxicity in HUVECs at least in part by influencing KLF5 expression via acting as a miR-135a-5p sponge.	NA	Front Cardiovasc Med. 2021 Mar 12;8:596506. doi: 10.3389/fcvm.2021.596506. eCollection 2021.
3319	LncRNA	SNHG16	miR-141-3p	SUSD2	WI-38 cells	NA	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;RNA pull-down assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33836533	LncRNA small nucleolar RNA host gene 16 (SNHG16) silencing protects lipopolysaccharide (LPS)-induced cell injury in human lung fibroblasts WI-38 through acting as miR-141-3p sponge.	Long noncoding RNA (LncRNA) small nucleolar RNA host gene 16 (SNHG16) is correlated with cell injuries, including pneumonia. However, its role and mechanism remain vague in pneumonia. The interplay among genes was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. SNHG16 and sushi domain containing 2 (SUSD2) were upregulated, and miRNA (miR)-141-3p was downregulated in the serum of acute pneumonia patients and lipopolysaccharide (LPS)-challenged human lung fibroblasts WI-38. LPS induced apoptosis, autophagy, and inflammatory response in WI-38 cells, which was significantly attenuated by SNHG16 knockdown and/or miR-141-3p overexpression. Notably, both SNHG16 and SUSD2 were identified as target genes of miR-141-3p. Besides, the suppressive role of SNHG16 knockdown in LPS-induced in WI-38 cells was partially abolished by miR-141-3p silencing, and the similar inhibition of miR-141-3p overexpression was further blocked by SUSD2 restoration. In conclusion, knockdown of SNHG16 could alleviate LPS-induced apoptosis, autophagy, and inflammation in WI-38 cells partially though the SNHG16/miR-141-3p/SUSD2 pathway.	NA	Biosci Biotechnol Biochem. 2021 Apr 24;85(5):1077-1087. doi: 10.1093/bbb/zbab016.
3320	LncRNA	SNHG15	miR-141	ICAM-1	Human glomerular mesangial cells (HGMCs)	Diabetic Nephropathy	Homo sapiens (human)	qRT-PCR	33506255	SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axis in vitro.	Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). The present study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.	NA	Biosci Rep. 2021 Feb 26;41(2):BSR20204099. doi: 10.1042/BSR20204099.
3321	LncRNA	linc01184	miR-331	HER2	CRC tissues and cells	Olorectal Cancer	Homo sapiens (human)	RACE;Western blot;RNA pull-down;	33564344	The Role, Function, and Mechanism of Long Intergenic Noncoding RNA1184 (linc01184) in Colorectal Cancer.	BACKGROUND: Long intergenic noncoding RNA1184 (linc01184) has been recently discovered; however, its role in human diseases is limited to date. The present study is aimed at investigating the expression pattern and mechanism of linc01184 in colorectal cancer (CRC) tumorigenesis. METHODS: The expression of linc01184 in CRC tissues and cell lines was compared with that in normal controls. The functions of linc01184 in CRC cells were identified by overexpression and small interfering RNA (siRNA) approaches in vitro. Meanwhile, the target gene prediction software, luciferase reporter, RNA pull-down, and western blotting assays were used to analyze the oncogenic mechanism. RESULTS: We found that linc01184 was obviously upregulated in CRC tissues and cells when compared to normal controls, and its upregulation had a positive association with the CRC progression. linc01184 knockdown significantly suppressed CRC cell proliferation and invasion and promoted apoptosis. Besides, linc01184 acted as a competitive endogenous RNA (ceRNA) by directly binding to microRNA-331 (miR-331), and its overexpression resulted in notable increases of human epidermal growth factor receptor 2 (HER2), phosphorylated Ser/Thr kinases (p-Akt), and extracellular regulated protein kinase 1/2 (p-ERK1/2) at posttranscriptional levels in CRC cells, which were antagonized by miR-331. CONCLUSIONS: The findings reveal for the first time that linc01184 is an enhancer for the proliferation and invasion of CRC by functioning as a ceRNA through the linc01184-miR-331-HER2-p-Akt/ERK1/2 pathway regulatory network.	NA	Dis Markers. 2021 Jan 29;2021:8897906. doi: 10.1155/2021/8897906. eCollection 2021.
3322	Circular RNA	Circ-TOP2A	miR-346	SUSD2	GM tissue specimens and cells(LN229)	Glioma	Homo sapiens (human)	Rescue assay;	33537815	Circ-TOP2A acts as a ceRNA for miR-346 and contributes to glioma progression via the modulation of sushi domain-containing 2.	Dysregulated circular RNAs (circRNAs) are involved in the carcinogenesis and progression of multiple human malignancies. Knowledge of circRNAs in glioma (GM) is limited and further study to uncover new therapeutic targets for GM is urgently required. The present study demonstrated that circ-TOP2A was elevated in GM tissue specimens and cells and that circ-TOP2A levels indicated an unfavorable clinical prognosis in GM. Functionally, circ-TOP2A knockdown reduced viability, migration and invasion and triggered apoptosis in LN229 cells. Ectopic expression of circ-TOP2A aggravated these malignant behaviors in U87MG cells. In terms of mechanism, RNA-seq was performed to discover the potential targets regulated by circ-TOP2A. Circ-TOP2A acted as a competing endogenous RNA to upregulate sushi domain-containing 2 (SUSD2) expression by sponging microRNA (miR) 346. Rescue assays revealed that the oncogenic function of circ-TOP2A was partially dependent on its regulation of the miR-346/SUSD2 axis. In conclusion, the present study identified that circ-TOP2A promoted GM proliferation and aggressiveness via miR-346/SUSD2 signaling, which is a potential prognostic biomarker and therapeutic target for GM.	NA	Mol Med Rep. 2021 Apr;23(4):255. doi: 10.3892/mmr.2021.11894. Epub 2021 Feb 4.
3323	LncRNA	HAND2-AS1	miR-143-3p	TNFAIP3	RA synovial tissues	Rheumatoid Arthritis	Homo sapiens (human)	RACE;RIP assay;Western blot;Flow Cytometry assay;	33549125	Mesenchymal stem cell-originated exosomal lncRNA HAND2-AS1 impairs rheumatoid arthritis fibroblast-like synoviocyte activation through miR-143-3p/TNFAIP3/NF-κB pathway.	BACKGROUND: Long non-coding RNA heart and neural crest derivatives expressed 2-antisense RNA 1 (HAND2-AS1) was found to be elevated in rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs). However, whether HAND2-AS1 functions as an exosomal lncRNA related to mesenchymal stem cells (MSCs) in RA progression is unknown. METHODS: The expression of HAND2-AS1, microRNA (miR)-143-3p, and tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) was detected using quantitative real-time polymerase chain reaction and Western blot. Cell proliferation, apoptosis, migration, and invasion were detected using cell counting kit-8, flow cytometry, and wound healing and transwell assays. The levels of tumor necrosis factor-α (TNF-α) and interleukins (IL)-6 were analyzed using enzyme-linked immunosorbent assay. The level of phosphorylated-p65 was examined by Western blot. The binding interaction between miR-143-3p and HAND2-AS1 or TNFAIP3 was confirmed by the dual-luciferase reporter and RIP assays. Exosomes were isolated by ultracentrifugation and qualified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. RESULTS: HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. Mechanistically, HAND2-AS1 directly sponged miR-143-3p and positively regulated TNFAIP3 expression, the target of miR-143-3p. Moreover, the effects of HAND2-AS1 on RA-FLSs were partially attenuated by miR-143-3p upregulation or TNFAIP3 knockdown. HAND2-AS1 could be packaged into hMSC-derived exosomes and absorbed by RA-FLSs, and human MSC-derived exosomal HAND2-AS1 also repressed above malignant biological behavior of RA-FLSs. CONCLUSION: MSC-derived exosomes participated in the intercellular transfer of HAND2-AS1 and suppressed the activation of RA-FLSs via miR-143-3p/TNFAIP3/NF-κB pathway, which provided a novel insight into the pathogenesis and treatment of RA.	NA	J Orthop Surg Res. 2021 Feb 6;16(1):116. doi: 10.1186/s13018-021-02248-1.
3324	LncRNA	XIST	miR-1264	WNT5A	vascular smooth muscle cells (VSMCs)	Aneurysm	Homo sapiens (human)	qRT-PCR	33501488	XIST knockdown suppresses vascular smooth muscle cell proliferation and induces apoptosis by regulating miR-1264/WNT5A/β-catenin signaling in aneurysm.	Long non-coding RNAs (lncRNAs) have been ascertained as vital modulators in abdominal aortic aneurysm (AAA) development. In this research, the function and molecular mechanisms of the lncRNA X-inactive specific transcript (XIST) in the evolution of vascular smooth muscle cells (VSMCs) were assessed. Results showed that XIST expression was increased but miR-1264 expression level was reduced in the serum of AAA patients. XIST depletion impeded human aorta VSMCs (HA-VSMCs') ability to proliferate and stimulate apoptosis, while repressing miR-1264 expression through an unmediated interaction. Additionally, the influence of XIST knockdown on apoptosis and proliferation could be rescued by an miR-1264 inhibitor. Subsequent molecular investigations indicated that WNT5A was miR-1264's target, and XIST functioned as a competing endogenous RNA (ceRNA) of miR-1264 to raise WNT5A expression. Further, an miR-1264 inhibitor stimulated the proliferation and suppressed the apoptosis of HA-VSMCs through the activation of WNT/β-catenin signaling. Taken together, XIST impeded the apoptosis and stimulated the proliferation of HA-VSMCs via the WNT/β-catenin signaling pathway through miR-1264, demonstrating XIST's underlying role in AAA.	NA	Biosci Rep. 2021 Mar 26;41(3):BSR20201810. doi: 10.1042/BSR20201810.
3325	LncRNA	LINC00473	miR-497-5p	ERK	lung cancer tissues and NSCLC cells (A549 and H1299)	Lung Cancer	Homo sapiens (human)	MTT assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33868467	lncRNA LINC00473 promotes proliferation, migration, invasion and inhibition of apoptosis of non-small cell lung cancer cells by acting as a sponge of miR-497-5p.	Lung cancer is the leading cause of cancer-associated death worldwide and exhibits a poor prognosis. The present study aimed to determine the effect of long non-coding (lnc)RNA-LINC00473 on the development of non-small cell lung cancer (NSCLC) cells by regulating the expression of microRNA (miR)-497-5p. Reverse transcription-quantitative PCR was conducted to detect the level of LINC00473 and miR-497-5p. An MTT assay, flow cytometry and Transwell tests were performed to evaluate the proliferation, apoptosis, migration and invasion of NSCLC cells. Western blotting was performed to detect the expression of apoptosis- and migration-related proteins. RNA immunoprecipitation and a luciferase reporter assay were performed to verify the regulatory relationship between lncRNA-LINC00473 and miR-497-5p. LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression. A negative correlation between LINC00473 and miR-497-5p was observed in lung cancer tissues. Proliferation, migration and invasion as well as the related protein levels were increased in A549 and H1299 transfected with pcDNA3.1-LINC00473, while the opposite results were obtained in A549 and H1299 transfected with small interfering (si)-LINC00473. Notably, it was demonstrated that LINC00473 could bind directly with miR-497-5p and inhibit its expression. miR-497-5p inhibitors reversed the effect of si-LINC00473. Furthermore, the present study demonstrated that LINC00473 promoted the malignant behaviour of NSCLC cells via regulating the ERK/p38 and MAPK signalling pathways and the expression of miR-497-5p.	NA	Oncol Lett. 2021 Jun;21(6):429. doi: 10.3892/ol.2021.12690. Epub 2021 Mar 30.
3326	LncRNA	LINC00473	miR-497-5p	p38	lung cancer tissues and NSCLC cells (A549 and H1299)	Lung Cancer	Homo sapiens (human)	MTT assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33868467	lncRNA LINC00473 promotes proliferation, migration, invasion and inhibition of apoptosis of non-small cell lung cancer cells by acting as a sponge of miR-497-5p.	Lung cancer is the leading cause of cancer-associated death worldwide and exhibits a poor prognosis. The present study aimed to determine the effect of long non-coding (lnc)RNA-LINC00473 on the development of non-small cell lung cancer (NSCLC) cells by regulating the expression of microRNA (miR)-497-5p. Reverse transcription-quantitative PCR was conducted to detect the level of LINC00473 and miR-497-5p. An MTT assay, flow cytometry and Transwell tests were performed to evaluate the proliferation, apoptosis, migration and invasion of NSCLC cells. Western blotting was performed to detect the expression of apoptosis- and migration-related proteins. RNA immunoprecipitation and a luciferase reporter assay were performed to verify the regulatory relationship between lncRNA-LINC00473 and miR-497-5p. LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression. A negative correlation between LINC00473 and miR-497-5p was observed in lung cancer tissues. Proliferation, migration and invasion as well as the related protein levels were increased in A549 and H1299 transfected with pcDNA3.1-LINC00473, while the opposite results were obtained in A549 and H1299 transfected with small interfering (si)-LINC00473. Notably, it was demonstrated that LINC00473 could bind directly with miR-497-5p and inhibit its expression. miR-497-5p inhibitors reversed the effect of si-LINC00473. Furthermore, the present study demonstrated that LINC00473 promoted the malignant behaviour of NSCLC cells via regulating the ERK/p38 and MAPK signalling pathways and the expression of miR-497-5p.	NA	Oncol Lett. 2021 Jun;21(6):429. doi: 10.3892/ol.2021.12690. Epub 2021 Mar 30.
3327	LncRNA	LINC00473	miR-497-5p	MAPK	lung cancer tissues and NSCLC cells (A549 and H1299)	Lung Cancer	Homo sapiens (human)	MTT assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33868467	lncRNA LINC00473 promotes proliferation, migration, invasion and inhibition of apoptosis of non-small cell lung cancer cells by acting as a sponge of miR-497-5p.	Lung cancer is the leading cause of cancer-associated death worldwide and exhibits a poor prognosis. The present study aimed to determine the effect of long non-coding (lnc)RNA-LINC00473 on the development of non-small cell lung cancer (NSCLC) cells by regulating the expression of microRNA (miR)-497-5p. Reverse transcription-quantitative PCR was conducted to detect the level of LINC00473 and miR-497-5p. An MTT assay, flow cytometry and Transwell tests were performed to evaluate the proliferation, apoptosis, migration and invasion of NSCLC cells. Western blotting was performed to detect the expression of apoptosis- and migration-related proteins. RNA immunoprecipitation and a luciferase reporter assay were performed to verify the regulatory relationship between lncRNA-LINC00473 and miR-497-5p. LINC00473 expression was upregulated in lung cancer tissues and NSCLC cells (A549 and H1299) when compared with adjacent tissues or human bronchial epithelial cell lines and the 5-year survival rate was lower in patients with high LINC00473 expression compared with in patients with low LINC00473 expression. A negative correlation between LINC00473 and miR-497-5p was observed in lung cancer tissues. Proliferation, migration and invasion as well as the related protein levels were increased in A549 and H1299 transfected with pcDNA3.1-LINC00473, while the opposite results were obtained in A549 and H1299 transfected with small interfering (si)-LINC00473. Notably, it was demonstrated that LINC00473 could bind directly with miR-497-5p and inhibit its expression. miR-497-5p inhibitors reversed the effect of si-LINC00473. Furthermore, the present study demonstrated that LINC00473 promoted the malignant behaviour of NSCLC cells via regulating the ERK/p38 and MAPK signalling pathways and the expression of miR-497-5p.	NA	Oncol Lett. 2021 Jun;21(6):429. doi: 10.3892/ol.2021.12690. Epub 2021 Mar 30.
3328	LncRNA	TUG1	miR-145-5p	NF-kB	bronchial epithelial cells	Airway Inflammatory	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Luciferase reporter assay;	33841139	The Influenza A Virus H3N2 Triggers the Hypersusceptibility of Airway Inflammatory Response via Activating the lncRNA TUG1/miR-145-5p/NF-κB Pathway in COPD.	Background: Patients with chronic obstructive pulmonary disease (COPD) are more susceptible to influenza A virus (IAV) with more severe symptoms, yet the underlying molecular mechanisms of the hypersusceptibility of airway inflammatory response remain unclear. Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-κBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-κBp65, NF-κBp65, TNF-α, and (Interleukin) IL-1β were examined with qRT-PCR, Western blotting, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-κB were verified with luciferase reporter assay. Results: The expressions of lncRNA TUG1, phospho-NF-κBp65, TNF-α, and IL-1β were increased significantly in pHBECs after being infected with IAV for 24 h (all p0.05). The detailed time analysis revealed that the NF-κBp65 in DHBE was activated earlier than that in NHBE by Western blotting and immunofluorescence. Knockdown of lncRNA TUG1 and miR-145-5p mimic attenuated the expressions of NF-κBp65, TNF-α, and IL-1β significantly. The miR-145-5p inhibitor and NF-κBp65 transfection reversed the attenuated expressions of NF-κBp65, TNF-α, and IL-1β. Conclusion: The IAV causes the hypersusceptibility of airway inflammatory response, which may be closely associated with more severe symptoms in AECOPD patients. The lncRNA TUG1 inhibitor may be a promising therapeutic strategy for AECOPD caused by IAV.	NA	Front Pharmacol. 2021 Feb 22;12:604590. doi: 10.3389/fphar.2021.604590. eCollection 2021.
3329	LncRNA	TUG1	miR-145-5p	p65	bronchial epithelial cells	Airway Inflammatory	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Luciferase reporter assay;	33841139	The Influenza A Virus H3N2 Triggers the Hypersusceptibility of Airway Inflammatory Response via Activating the lncRNA TUG1/miR-145-5p/NF-κB Pathway in COPD.	Background: Patients with chronic obstructive pulmonary disease (COPD) are more susceptible to influenza A virus (IAV) with more severe symptoms, yet the underlying molecular mechanisms of the hypersusceptibility of airway inflammatory response remain unclear. Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-κBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-κBp65, NF-κBp65, TNF-α, and (Interleukin) IL-1β were examined with qRT-PCR, Western blotting, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-κB were verified with luciferase reporter assay. Results: The expressions of lncRNA TUG1, phospho-NF-κBp65, TNF-α, and IL-1β were increased significantly in pHBECs after being infected with IAV for 24 h (all p0.05). The detailed time analysis revealed that the NF-κBp65 in DHBE was activated earlier than that in NHBE by Western blotting and immunofluorescence. Knockdown of lncRNA TUG1 and miR-145-5p mimic attenuated the expressions of NF-κBp65, TNF-α, and IL-1β significantly. The miR-145-5p inhibitor and NF-κBp65 transfection reversed the attenuated expressions of NF-κBp65, TNF-α, and IL-1β. Conclusion: The IAV causes the hypersusceptibility of airway inflammatory response, which may be closely associated with more severe symptoms in AECOPD patients. The lncRNA TUG1 inhibitor may be a promising therapeutic strategy for AECOPD caused by IAV.	NA	Front Pharmacol. 2021 Feb 22;12:604590. doi: 10.3389/fphar.2021.604590. eCollection 2021.
3330	LncRNA	TUG1	miR-145-5p	TNF-a	bronchial epithelial cells	Airway Inflammatory	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Luciferase reporter assay;	33841139	The Influenza A Virus H3N2 Triggers the Hypersusceptibility of Airway Inflammatory Response via Activating the lncRNA TUG1/miR-145-5p/NF-κB Pathway in COPD.	Background: Patients with chronic obstructive pulmonary disease (COPD) are more susceptible to influenza A virus (IAV) with more severe symptoms, yet the underlying molecular mechanisms of the hypersusceptibility of airway inflammatory response remain unclear. Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-κBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-κBp65, NF-κBp65, TNF-α, and (Interleukin) IL-1β were examined with qRT-PCR, Western blotting, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-κB were verified with luciferase reporter assay. Results: The expressions of lncRNA TUG1, phospho-NF-κBp65, TNF-α, and IL-1β were increased significantly in pHBECs after being infected with IAV for 24 h (all p0.05). The detailed time analysis revealed that the NF-κBp65 in DHBE was activated earlier than that in NHBE by Western blotting and immunofluorescence. Knockdown of lncRNA TUG1 and miR-145-5p mimic attenuated the expressions of NF-κBp65, TNF-α, and IL-1β significantly. The miR-145-5p inhibitor and NF-κBp65 transfection reversed the attenuated expressions of NF-κBp65, TNF-α, and IL-1β. Conclusion: The IAV causes the hypersusceptibility of airway inflammatory response, which may be closely associated with more severe symptoms in AECOPD patients. The lncRNA TUG1 inhibitor may be a promising therapeutic strategy for AECOPD caused by IAV.	NA	Front Pharmacol. 2021 Feb 22;12:604590. doi: 10.3389/fphar.2021.604590. eCollection 2021.
3331	LncRNA	TUG1	miR-145-5p	IL-1b	bronchial epithelial cells	Airway Inflammatory	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Luciferase reporter assay;	33841139	The Influenza A Virus H3N2 Triggers the Hypersusceptibility of Airway Inflammatory Response via Activating the lncRNA TUG1/miR-145-5p/NF-κB Pathway in COPD.	Background: Patients with chronic obstructive pulmonary disease (COPD) are more susceptible to influenza A virus (IAV) with more severe symptoms, yet the underlying molecular mechanisms of the hypersusceptibility of airway inflammatory response remain unclear. Methods: The primary human bronchial epithelial cells (pHBECs) were isolated from normal and COPD bronchial tissues (NHBE and DHBE) and cultured with/without IAV infection in vitro. DHBE cells were exposed to IAV for 24 h after knockdown of lncRNA TUG1 with short hairpin RNA (shRNA). Gain-of-function assays were performed with the miR-145-5p inhibitor and NF-κBp65 transfection. The expressions of lncRNA TUG1, miR-145-5p, phospho-NF-κBp65, NF-κBp65, TNF-α, and (Interleukin) IL-1β were examined with qRT-PCR, Western blotting, and ELISA. The interactions of lncRNA TUG1, miR-145-5p, and NF-κB were verified with luciferase reporter assay. Results: The expressions of lncRNA TUG1, phospho-NF-κBp65, TNF-α, and IL-1β were increased significantly in pHBECs after being infected with IAV for 24 h (all p0.05). The detailed time analysis revealed that the NF-κBp65 in DHBE was activated earlier than that in NHBE by Western blotting and immunofluorescence. Knockdown of lncRNA TUG1 and miR-145-5p mimic attenuated the expressions of NF-κBp65, TNF-α, and IL-1β significantly. The miR-145-5p inhibitor and NF-κBp65 transfection reversed the attenuated expressions of NF-κBp65, TNF-α, and IL-1β. Conclusion: The IAV causes the hypersusceptibility of airway inflammatory response, which may be closely associated with more severe symptoms in AECOPD patients. The lncRNA TUG1 inhibitor may be a promising therapeutic strategy for AECOPD caused by IAV.	NA	Front Pharmacol. 2021 Feb 22;12:604590. doi: 10.3389/fphar.2021.604590. eCollection 2021.
3332	LncRNA	ACTA2-AS1	miR-4428	BCL2L11	colon adenocarcinoma tissues and SW480 and HT29 cells	Colon Adenocarcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	33845844	LncRNA ACTA2-AS1 suppress colon adenocarcinoma progression by sponging miR-4428 upregulation BCL2L11.	BACKGROUND: Long non-coding RNA is considered to be essential to modulate the development and progression of human malignant cancers. And long non-coding RNA can act as crucial modulators by sponging the corresponding microRNA in tumorigenesis. We aimed to elucidate the function of ACTA2-AS1 and its molecular mechanism in colon adenocarcinoma. MATERIALS AND METHODS: The expression of ACTA2-AS1, miR-4428 and BCL2L11 in colon adenocarcinoma tissues were detected via qRT-PCR. SW480 and HT29 cells were transfected with shRNA ACTA2-AS1, OE ACTA2-AS1, miRNA mimics of miR-4428, miR-4428 inhibitor, si-BCL2L11 and over-expression of si-BCL2L11. Cell proliferation, colony formation and apoptosis were respectively assessed using CCK-8 assay, colony assay and flow cytometry. Luciferase reporter assay was performed to verify the targets of ACTA2-AS1 and miR-4428. Tumor subcutaneous xenograft mode was constructed to explore tumor growth in vivo. RESULTS: ACTA2-AS1 was obviously downregulated in human colon adenocarcinoma tissues and colon adenocarcinoma cell lines. Silence or over-expression of ACTA2-AS1 promoted or inhibited cell proliferation and colony formation abilities, and regulated apoptosis. The silence of ACTA2-AS1 resulted in the decrease of Bax and increase of Bal2, while restored in OE ACTA2-AS1 group when compared with the control transfected cells. In addition, luciferase reporter assay revealed that ACTA2-AS1 interacted with miR-4428 and suppressed its expression. miR-4428 could bind to 3' untranslated region of BCL2L11 and modulated the expression of BCL2L11 negatively. Knockdown of ACTA2-AS1 and over-expression of BCL2L11 reversed the biological function that ACTA2-AS1 mediated by knockdown ACTA2-AS1 alone. CONCLUSION: Our data demonstrated that ACTA2-AS1 could suppress colon adenocarcinoma progression via sponging miR-4428 to regulate BCL2L11 expression.	NA	Cancer Cell Int. 2021 Apr 12;21(1):203. doi: 10.1186/s12935-021-01769-3.
3333	Circular RNA	Circ_0010235	miR-433-3p	TIPRL	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33494763	Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis.	BACKGROUND: Non-small cell lung cancer (NSCLC) is a threat to human health. Circular RNAs (circRNAs) have been proved to function in NSCLC development. In this study, the role of circRNA hsa_circ_0010235 in NSCLC progression and the possible molecular mechanism were explored. METHODS: Expression of hsa_circ_0010235, miRNA (miR)-433-3p and TOR signaling pathway regulator-like (TIPRL) was examined by quantitative real-time PCR (qRT-PCR). Cell viability and clonogenicity were detected by cell counting kit-8 (CCK-8) assay and colony formation assay, respectively. Flow cytometry was performed to monitor cell apoptosis and cell cycle distribution. Western blot assay was employed to evaluate the protein levels of TIPRL, light chain 3 (LC3)-II/I and p62. Cell metastasis was assessed by Transwell and wound healing assays. The targeted relationship between miR-433-3p and hsa_circ_0010235 or TIPRL was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Furthermore, the role of hsa_circ_0010235 in vivo was investigated by xenograft assay. RESULTS: Hsa_circ_0010235 and TIPRL were highly expressed in NSCLC tissues and cells, while miR-433-3p was downregulated. Depletion of hsa_circ_0010235 or gain of miR-433-3p repressed proliferation and autophagy but promoted apoptosis in NSCLC cells. Hsa_circ_0010235 sponged miR-433-3p to upregulate TIPRL expression, so as to affect NSCLC development. Hsa_circ_0010235 knockdown also blocked tumor growth in vivo. CONCLUSION: Hsa_circ_0010235 knockdown suppressed NSCLC progression by regulating miR-433-3p/TIPRL axis, affording a novel mechanism of NSCLC progression.	NA	Cancer Cell Int. 2021 Jan 25;21(1):73. doi: 10.1186/s12935-021-01764-8.
3334	LncRNA	SNHG17	miR-384	ELF1	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	ChIP;RIP assay;Rescue assay;	33531646	SNHG17/miR-384/ELF1 axis promotes cell growth by transcriptional regulation of CTNNB1 to activate Wnt/β-catenin pathway in oral squamous cell carcinoma.	Increasing evidence proved the abnormal expression of long non-coding RNAs (lncRNAs) in various human malignancies, including oral squamous cell carcinoma (OSCC). Nevertheless, limited explorations concern the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) in OSCC. Herein, SNHG17 was disclosed to be remarkably upregulated in OSCC cell lines and promoted OSCC cell growth. Further mechanistic studies, including DNA/RNA pull down, RIP, ChIP, and luciferase reporter gene assays, were conducted. It was confirmed that Wnt/β-catenin signaling pathway was involved in the SNHG17-mediated OSCC cell growth. Moreover, E74 like ETS transcription factor 1 (ELF1) was identified as the transcription activator of CTNNB1 (β-catenin mRNA) in OSCC. Inspired by competing for endogenous RNAs (ceRNAs) network, we were pleasantly surprised to find that SNHG17 and ELF1 functioned as ceRNAs in OSCC via competitively binding to microRNA-384 (miR-384). By using rescue assays, we revealed that SNHG17 facilitated OSCC cell growth through modulating miR-384/ELF1 axis. Importantly, we certified that ELF1 was indispensable for SNHG17-affected OSCC progression. Collectively, it can be concluded that SNHG17/miR-384/ELF1 axis contributed to OSCC cell growth via promoting CTNNB1 expression, thus activating Wnt/β-catenin signaling pathway.	NA	Cancer Gene Ther. 2021 Feb 2. doi: 10.1038/s41417-021-00294-9.
3335	LncRNA	MIR181A2HG	miR-6832-5p	AKT2	vascular endothelial cell	NA	Homo sapiens (human)	qRT-PCR	33537821	Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.	Endothelial dysfunction and diabetic vascular disease induced by chronic hyperglycemia involve complex interactions among high glucose, long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs) and the Ser/Thr kinase AKT. However, the molecular mechanisms underlying the regulatory crosstalk between these have not yet been completely elucidated. Thus, the present study aimed to explore the molecular mechanisms whereby high glucose (HG)-induced lncRNA MIR181A2HG modulates human umbilical vein endothelial cell (HUVEC) proliferation and migration by regulating AKT2 expression. The persistent exposure of HUVECs to HG resulted in MIR181A2HG downregulation and thus reduced its ability to sponge miR-6832-5p, miR-6842-5p and miR-8056, subsequently leading to an increase in miR-6832-5p, miR-6842-5p and miR-8056 levels. Mechanistically, miR-6832-5p, miR-6842-5p and miR-8056 were found to target the 3'UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2. Thus, this also led to the suppression of HUVEC proliferation and migration, and the formation of capillary-like structures. Moreover, the suppression of HUVEC proliferation and migration induced by MIR181A2HG downregulation was accompanied by changes in glucose metabolism. On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis. The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG-induced endothelial dysfunction.	NA	Int J Mol Med. 2021 Apr;47(4):35. doi: 10.3892/ijmm.2021.4868. Epub 2021 Feb 4.
3336	LncRNA	MIR181A2HG	miR-6842-5p	AKT2	vascular endothelial cell	NA	Homo sapiens (human)	qRT-PCR	33537821	Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.	Endothelial dysfunction and diabetic vascular disease induced by chronic hyperglycemia involve complex interactions among high glucose, long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs) and the Ser/Thr kinase AKT. However, the molecular mechanisms underlying the regulatory crosstalk between these have not yet been completely elucidated. Thus, the present study aimed to explore the molecular mechanisms whereby high glucose (HG)-induced lncRNA MIR181A2HG modulates human umbilical vein endothelial cell (HUVEC) proliferation and migration by regulating AKT2 expression. The persistent exposure of HUVECs to HG resulted in MIR181A2HG downregulation and thus reduced its ability to sponge miR-6832-5p, miR-6842-5p and miR-8056, subsequently leading to an increase in miR-6832-5p, miR-6842-5p and miR-8056 levels. Mechanistically, miR-6832-5p, miR-6842-5p and miR-8056 were found to target the 3'UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2. Thus, this also led to the suppression of HUVEC proliferation and migration, and the formation of capillary-like structures. Moreover, the suppression of HUVEC proliferation and migration induced by MIR181A2HG downregulation was accompanied by changes in glucose metabolism. On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis. The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG-induced endothelial dysfunction.	NA	Int J Mol Med. 2021 Apr;47(4):35. doi: 10.3892/ijmm.2021.4868. Epub 2021 Feb 4.
3337	LncRNA	MIR181A2HG	miR-8056	AKT2	vascular endothelial cell	NA	Homo sapiens (human)	qRT-PCR	33537821	Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.	Endothelial dysfunction and diabetic vascular disease induced by chronic hyperglycemia involve complex interactions among high glucose, long non-coding RNAs (lncRNAs), microRNAs (miRNAs or miRs) and the Ser/Thr kinase AKT. However, the molecular mechanisms underlying the regulatory crosstalk between these have not yet been completely elucidated. Thus, the present study aimed to explore the molecular mechanisms whereby high glucose (HG)-induced lncRNA MIR181A2HG modulates human umbilical vein endothelial cell (HUVEC) proliferation and migration by regulating AKT2 expression. The persistent exposure of HUVECs to HG resulted in MIR181A2HG downregulation and thus reduced its ability to sponge miR-6832-5p, miR-6842-5p and miR-8056, subsequently leading to an increase in miR-6832-5p, miR-6842-5p and miR-8056 levels. Mechanistically, miR-6832-5p, miR-6842-5p and miR-8056 were found to target the 3'UTR of AKT2 mRNA in HUVECs, and the increase in their levels led to a decreased expression of AKT2. Thus, this also led to the suppression of HUVEC proliferation and migration, and the formation of capillary-like structures. Moreover, the suppression of HUVEC proliferation and migration induced by MIR181A2HG downregulation was accompanied by changes in glucose metabolism. On the whole, the present study demonstrates that the downregulation of lncRNA MIR181A2HG by HG impairs HUVEC proliferation and migration by dysregulating the miRNA/AKT2 axis. The MIR181A2HG/miRNA/AKT2 regulatory axis may thus be a potential therapeutic target for HG-induced endothelial dysfunction.	NA	Int J Mol Med. 2021 Apr;47(4):35. doi: 10.3892/ijmm.2021.4868. Epub 2021 Feb 4.
3338	Circular RNA	CircTP63	miR-155-5p	ZBTB18	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Flow Cytometry assay;luciferase assay;RNA pull-down;	33685441	CircTP63 promotes hepatocellular carcinoma progression by sponging miR-155-5p and upregulating ZBTB18.	BACKGROUND: Hepatocellular carcinoma (HCC) is the leading cause of tumor-related death worldwide due to high morbidity and mortality, yet lacking effective biomarkers and therapies. Circular RNAs (circRNAs) are a group of non-coding RNAs that regulate gene expression through interacting with miRNAs, implicating in the tumorigenesis and progression. A novel circRNA, circTP63, was reported to be an oncogene in HCC. However, its role in HCC remains unclear. METHODS: qRT-PCR was used to assess the mRNA levels of CircTP63 in 90 pairs of tumor and adjacent normal tissues from HCC patients, one human normal hepatic epithelial cell line and HCC cell lines. CCK-8, colony formation, transwell, and flow cytometry assays were performed to detect the cellular function of circTP63/miR-155-5p/ZBTB18 in HCC cells. HCC xenograft mice models were established to assess the in vivo effect of circTP63. Bioinformatic analysis, RNA pull-down and luciferase assays were used to determine the interaction among circTP63/miR-155-5p/ZBTB18. RESULTS: circTP63 was significantly upregulated in HCC tissues and cell lines. High circTP63 expression is closely associated with the tumor stages, lymph node metastasis, and poor prognosis of HCC patients. Functionally, knockdown of circTP63 inhibited cell proliferation, migration, invasion, and promoted cell apoptosis of HCC. Meanwhile, overexpression of circTP63 enhanced HCC progression. Mechanically, circTP63 was a sponge of miR-155-5p to facilitate the ZBTB18 expression, and the ZBTB18 expression in HCC tissues was negatively associated with the survival rate of HCC patients. Furthermore, rescued assays revealed that the reduced tumor-promoting effect on HCC cells induced by knockdown of circTP63 can be reversed by miR-155-5p inhibitor or ZBTB18 overexpression. CONCLUSION: Our data highlight a critical circTP63-miR-155-5p-ZBTB18 regulatory network involved in the HCC progression, gaining mechanistic insights into the function of circRNAs in HCC progression, and providing effective biomarkers and therapeutic targets for HCC treatment.	NA	Cancer Cell Int. 2021 Mar 8;21(1):156. doi: 10.1186/s12935-021-01753-x.
3339	Circular RNA	CircRNA_0007534	miR-206	GREM1	CC tissues and cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33446214	Knockdown of circRNA_0007534 suppresses the tumorigenesis of cervical cancer via miR-206/GREM1 axis.	BACKGROUND: Increasing evidence manifested that circular RNAs (circRNAs) acted as crucial regulators in human cancers by targeting the miRNA/mRNA axis, including cervical cancer (CC). Circ_0007534 was reported to promote CC cell proliferation and invasion by the miR-498/BMI-1 axis. The aim of this study was to explore a novel miRNA/mRNA network underlying circ_0007534 in CC regulation. METHODS: The quantitative real-time polymerase chain reaction (qRT-PCR) was implemented to examine the levels of circ_0007534, miR-206 and Gremlin1 (GREM1). Cell viability was determined using MTT assay. BrdU and colony formation assays were performed for analyzing cell proliferation. Cell apoptosis was assessed by flow cytometry. The protein levels of GREM1 and apoptotic markers (Bcl-2, Bax, C-Caspase3) were measured via western blot. Cell invasion was detected by transwell assay. The target relationship was analyzed by dual-luciferase reporter assay. The impact of circ_0007534 on CC growth in vivo was ascertained by xenograft assay. RESULTS: Circ_0007534 expression was aberrantly increased in CC tissues and cells. Functionally, knockdown of circ_0007534 reduced CC cell growth and invasion but motivated apoptosis. In the mechanism, circ_0007534 targeted miR-206 and its regulatory function was associated with sponging miR-206. Moreover, circ_0007534 was found to regulate GREM1 level by targeting miR-206. The inhibitory effect of si-circ_0007534 on the malignant progression of CC was reversed after GREM1 was overexpressed. Furthermore, circ_0007534 inhibition also reduced tumor growth of CC in vivo partially by regulating miR-206/GREM1 axis. CONCLUSION: These results suggested that knockdown of circ_0007534 promoted the level of miR-206 to induce the expression downregulation of GREM1, consequently inhibiting the progression of CC.	NA	Cancer Cell Int. 2021 Jan 14;21(1):54. doi: 10.1186/s12935-021-01749-7.
3340	LncRNA	AGAP2-AS1	miR-296	NOTCH2	lung cancer cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33972506	M2 macrophage-derived exosomal long non-coding RNA AGAP2-AS1 enhances radiotherapy immunity in lung cancer by reducing microRNA-296 and elevating NOTCH2.	Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) play vital roles in human diseases. We aimed to identify the effect of the lncRNA AGAP2 antisense RNA 1 (AGAP2-AS1)/miR-296/notch homolog protein 2 (NOTCH2) axis on the progression and radioresistance of lung cancer. Expression of AGAP2-AS1, miR-296, and NOTCH2 in lung cancer cells and tissues from radiosensitive and radioresistant patients was determined, and the predictive role of AGAP2-AS1 in the prognosis of patients was identified. THP-1 cells were induced and exosomes were extracted, and the lung cancer cells were respectively treated with silenced AGAP2-AS1, exosomes, and exosomes upregulating AGAP2-AS1 or downregulating miR-296. The cells were radiated under different doses, and the biological processes of cells were assessed. Moreover, the natural killing cell-mediated cytotoxicity on lung cancer cells was determined. The relationships between AGAP2-AS1 and miR-296, and between miR-296 and NOTCH2 were verified. AGAP2-AS1 and NOTCH2 increased while miR-296 decreased in radioresistant patients and lung cancer cells. The malignant behaviors of radioresistant cells were promoted compared with the parent cells. Inhibited AGAP2-AS1, macrophage-derived exosomes, and exosomes overexpressing AGAP2-AS1 or inhibiting miR-296 facilitated the malignant phenotypes of radioresistant lung cancer cells. Furthermore, AGAP2-AS1 negatively regulated miR-296, and NOTCH2 was targeted by miR-296. M2 macrophage-derived exosomal AGAP2-AS1 enhances radiotherapy immunity in lung cancer by reducing miR-296 and elevating NOTCH2. This study may be helpful for the investigation of radiotherapy of lung cancer.	NA	Cell Death Dis. 2021 May 10;12(5):467. doi: 10.1038/s41419-021-03700-0.
3341	LncRNA	BACE1-AS	miR-377-3p	CELF1	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33667514	LncRNA BACE1-AS enhances the invasive and metastatic capacity of hepatocellular carcinoma cells through mediating miR-377-3p/CELF1 axis.	AIMS: Hepatocellular carcinoma (HCC) is a malignant cancer that threatened human life seriously. Long non-coding RNA (lncRNA) BACE1-AS has been reported as a key regulator in tumorigenesis. Yet the specific correlation between BACE1-AS and HCC still needs further investigation. The primary purpose of our study is to reveal the exact correlation between BACE1-AS and HCC. MAIN METHODS: Bioinformatics via TCGA database revealed BACE1-AS closely related with HCC. qRT-PCR confirmed the abnormal BACE1-AS level in HCC tissues and cells. Databases prediction suggested that miR-377-3p might be a modulatory target of BACE1-AS and luciferase assay confirmed this hypothesis. Further study discovered that CELF1 also partook in the regulatory axis of BACE1-AS/miR-377-3p. Wound healing assays and transwell assays were utilized to investigate the impact of BACE1-AS, miR-377-3p and CELF1 in vitro. In vivo metastasis was examined by pulmonary metastasis model. KEY FINDINGS: This study found that BACE1-AS was overexpressed in HCC tissues and cell lines. Knockdown of BACE1-AS could restrain HCC progression in vitro, and inhibit pulmonary metastasis in vivo. MiR-377-3p was negatively modulated by BACE1-AS in HCC tumor tissues and cells. MiR-377-3p up-regulation inhibited HCC cells migration and invasion via inactivating EMT process. Moreover, CELF1 was identified as a downstream regulator of miR-377-3p and served as an oncogene in HCC cells. SIGNIFICANCE: Our findings supported that lncRNA BACE1-AS was up-regulated in HCC, promoting invasion and metastasis of hepatocellular carcinoma cells by modulating miR-377-3p/CELF1 axis via contributing to EMT pathway. BACE1-AS could be a potential biomarker in HCC for future treatment.	NA	Life Sci. 2021 Jun 15;275:119288. doi: 10.1016/j.lfs.2021.119288. Epub 2021 Mar 2.
3342	LncRNA	CASC7	miR-34a-5p	TP73	PTC tissues and cell lines (K1 and TPC-1)	Papillary Thyroid Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33706708	Long noncoding RNA CASC7 inhibits the proliferation and migration of papillary thyroid cancer cells by inhibiting miR-34a-5p.	Long noncoding RNAs (lncRNAs) play an essential role in the progression of papillary thyroid cancer (PTC). However, the expression and function of lncRNA cancer susceptibility candidate 7 (CASC7) in PTC remain unknown. The purpose of this study was to investigate the role and molecular mechanism of CASC7 in regulating PTC cell behavior. The expression of CASC7, miR-34a-5p, and tumor protein P73 (TP73) was determined by qRT-PCR and western blot. Cell proliferation was examined by MTT assay. Cell apoptosis was assessed by flow cytometry following Annexin V and PI staining. Cell migration was determined by Transwell migration assay. The interaction between miR-34a-5p and CASC7 or TP73 was examined by luciferase reporter assay. CASC7 and TP73 expression were significantly lower, whereas miR-34a-5p expression was higher in PTC tissues than the adjacent normal tissues. Furthermore, CASC7 overexpression inhibited cell proliferation and migration, whereas facilitated cell apoptosis in human PTC cell lines (K1 and TPC-1). Mechanistically, CASC7 acted as a sponge of miR-34a-5p to upregulate TP73 expression. Moreover, miR-34a-5p mimic transfection could abate the CASC7-regulated PTC cell proliferation, migration, and apoptosis. Collectively, CASC7 inhibited the proliferation and migration of PTC cells by sponging miR-34a-5p to upregulate TP73 expression.	NA	J Physiol Sci. 2021 Mar 11;71(1):9. doi: 10.1186/s12576-021-00793-2.
3343	Circular RNA	Circ_0007841	miR-151-3p	MEX3C	ovarian cancer tissues and cell lines	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33896797	Circ_0007841 accelerates ovarian cancer development through facilitating MEX3C expression by restraining miR-151-3p activity.	The critical importance of circular RNAs (circRNAs) in human cancers, including ovarian cancer, has been discovered in the recent years. However, the roles of circ_0007841 in ovarian cancer remain unknown. In the current study, it was found that circ_0007841 expression was upregulated in ovarian cancer tissues and cell lines. Upregulation of circ_0007841 in patients with ovarian cancer predicts poor prognosis. Loss-of-function experiments discovered that circ_0007841 knockdown suppressed the proliferation, migration and invasion of ovarian cancer cells in vitro and in vivo. In terms of mechanism, circ_0007841 worked as a competing endogenous RNA (ceRNA) for miR-151-3p to facilitate MEX3C expression. Restoration of MEX3C level recovered the proliferation, migration and invasion of ovarian cancer cells. In conclusion, this study demonstrated that circ_0007841/miR-151-3p/MEX3C axis exerted important oncogenic functions in ovarian cancer.	NA	Aging (Albany NY). 2021 Apr 25;13(8):12058-12066. doi: 10.18632/aging.202911. Epub 2021 Apr 25.
3344	Circular RNA	Circ_0134111	miR-515-5p	SOCS1	OA cartilage tissues and IL-1β-induced chondrocytes	Osteoarthritis 	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qPCR;RT-qPCR;RACE;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33684877	Circ_0134111 knockdown relieves IL-1β-induced apoptosis, inflammation and extracellular matrix degradation in human chondrocytes through the circ_0134111-miR-515-5p-SOCS1 network.	BACKGROUND: Osteoarthritis (OA) is characterized by chondrocyte injury and dysfunction, such as excessive apoptosis, inflammatory response and extracellular matrix (ECM) degradation. Circular RNA (circRNA) deregulation is reported to be involved in OA. Our study aimed to explore the role of circ_0134111 in OA. METHODS: Human chondrocytes were treated with interleukin-1β (IL-1β) to mimic OA cell model. The expression of circ_0134111, miR-515-5p and suppressor of cytokine signaling 1 (SOCS1) mRNA was measured by real-time quantitative polymerase chain reaction (RT-qPCR), and the protein levels of SOCS1 and apoptosis-/inflammation-/ECM-related markers were determined by western blot. Cell proliferation and cell apoptosis were assessed using cell counting kit-8 (CCK-8) and flow cytometry assay, respectively. For mechanism analysis, the predicted interaction between miR-515-5p and circ_0134111 or SOCS1 was verified by dual-luciferase reporter assay, pull-down assay and RNA immunoprecipitation (RIP) assay. Rescue experiments were performed to explore the interplay between miR-515-5p and circ_0134111 or SOCS1. RESULTS: Circ_0134111 was overexpressed in OA cartilage tissues and IL-1β-induced chondrocytes. IL-1β-induced chondrocyte apoptosis, inflammatory responses and ECM degradation were alleviated by circ_0134111 knockdown or miR-515-5p restoration. Circ_0134111 acted as miR-515-5p sponge to regulate miR-515-5p expression, and miR-515-5p deficiency reversed the effects of circ_0134111 knockdown in IL-1β-induced chondrocytes. MiR-515-5p directly bound to SOCS1, and circ_0134111 decoyed miR-515-5p to increase SOCS1 level. MiR-515-5p restoration alleviated IL-1β-induced chondrocyte apoptosis, inflammatory responses and ECM degradation, While SOCS1 overexpression partly abolished these effects. CONCLUSION: Circ_0134111 knockdown alleviated apoptosis, inflammatory responses and ECM degradation in OA cell model by mediating the miR-515-5p-SOCS1 network, hinting that circ_0134111 was involved in OA progression.	NA	Int Immunopharmacol. 2021 Jun;95:107495. doi: 10.1016/j.intimp.2021.107495. Epub 2021 Mar 5.
3345	Circular RNA	Circ_DOCK1	miR-132-3p	USP11	colorectal cancer cell lines (HCT116 and SW480)	Colorectal Cancer	Homo sapiens (human)	RIP assay;Western blot;Flow Cytometry assay;Immunohistochemistry;RNA pull-down;	33685455	Circ_DOCK1 regulates USP11 through miR-132-3p to control colorectal cancer progression.	BACKGROUND: Circular RNAs (circRNAs) take part in colorectal cancer malignancies. CircRNA dedicator of cytokinesis 1 (circ_DOCK1) is involved in colorectal cancer progression, but the mechanism underlying this circRNA that takes part in colorectal cancer development remains largely undetermined. METHODS: Tumor and normal para-cancerous tissues were collected from 42 colorectal cancer patients. Human colorectal cancer cell lines (HCT116 and SW480) were used for the experiments in vitro. Circ_DOCK1, microRNA (miR)-132-3p, and ubiquitin-specific protease 11 (USP11) levels were measured through quantitative real-time polymerase chain reaction and Western blotting. Cell growth, metastasis, and apoptosis were investigated via colony formation, 5-ethynyl-2'-deoxyuridine (EdU) staining, MTT, flow cytometry, Western blotting, and transwell analyses. The target association was evaluated via dual-luciferase reporter analysis, RNA pull-down, and immunoprecipitation (RIP). Xenograft assay was performed using HCT116 cells. USP11 and Ki67 levels in tumor tissues were detected via immunohistochemistry. RESULTS: Circ_DOCK1 expression was enhanced in colorectal cancer tissues and cells. Silencing circ_DOCK1 repressed cell growth, migration, and invasion, and facilitated apoptosis. Circ_DOCK1 sponged miR-132-3p, and miR-132-3p silence mitigated the effect of circ_DOCK1 interference on cell growth, metastasis, and apoptosis. MiR-132-3p targeted USP11, and circ_DOCK1 could regulate USP11 level by miR-132-3p. MiR-132-3p suppressed cell growth, metastasis, and apoptosis, and USP11 attenuated these effects. Knockdown of circ_DOCK1 decreased colorectal cancer cell xenograft tumor growth. CONCLUSION: Circ_DOCK1 interference suppressed cell growth and metastasis, and increased apoptosis of colorectal cancer via decreasing USP11 by increasing miR-132-3p.	NA	World J Surg Oncol. 2021 Mar 8;19(1):67. doi: 10.1186/s12957-021-02173-x.
3346	LncRNA	GAS5	miR-128-3p	HDAC4	RA synovial tissues and RAFLSs	Rheumatoid Arthritis	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;Rescue assay;RNA pull-down;	33611674	Long non-coding RNA GAS5 suppresses rheumatoid arthritis progression via miR-128-3p/HDAC4 axis.	Rheumatoid arthritis (RA) is a highly relevant public health problem. RA fibroblast-like synoviocytes (RAFLSs) play an important role in RA progression. Long non-coding RNA growth arrest-specific transcript 5 (GAS5) could improve RA by inducing RAFLSs apoptosis. However, the mechanism of GAS5 in RA remains unclear. RT-qPCR detected the expressions of GAS5, microRNA-128-3p (miR-128-3p), and histone deacetylase 4 (HDAC4) in RA synovial tissues and RAFLSs. Proliferation, apoptosis, migration, and invasion were measured by Cell Counting Kit-8 assay (CCK-8), flow cytometry, and transwell assays, severally. The protein levels of B-cell lymphoma-2 (Bcl-2), C-caspase 3, Bcl-2 related X protein (Bax), Tumor Necrosis factor-α (TNF-α), Interleukin 6 (IL-6), Interleukin 17 (IL-17), HDAC4, phosphorylation-protein kinase B (p-AKT), AKT, a phosphorylation-mechanistic target of rapamycin (p-mTOR), and mTOR were assessed by western blot assay. The interaction between miR-128-3p and GAS5 or HDAC4 was predicted by ENCORI or TargetScan Human and verified by the dual-luciferase reporter, RNA Immunoprecipitation (RIP), and RNA pull-down assays. GAS5 and HDAC4 were downregulated, and miR-128-3p was upregulated in RA synovial tissues and RAFLSs. Function analysis indicated that GAS5 curbed proliferation, migration, invasion, inflammation, and facilitated apoptosis of RAFLSs. Rescue assay confirmed that miR-128-3p overexpression or HDAC4 knockdown weakened the inhibitory effect of GAS5 or anti-miR-128-3p on RA development. GAS5 acted as a miR-128-3p sponge to upregulate HDAC4 expression. Besides, GAS5/miR-128-3p/HDAC4 axis regulated RA progression partially through the AKT/mTOR pathway. Our studies disclosed that GAS5 restrained inflammation in synovial tissue partly through regulating HDAC4 via miR-128-3p, suggesting a potential lncRNA-targeted therapy for RA treatment.	NA	Mol Cell Biochem. 2021 Jun;476(6):2491-2501. doi: 10.1007/s11010-021-04098-1. Epub 2021 Feb 20.
3347	LncRNA	HOXA-AS3	miR-675-3p	PDE5A	human pulmonary artery smooth muscle cells	Pulmonary Arterial Hypertension	Homo sapiens (human)	MTT assay;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33687636	LncRNA HOXA-AS3 Promotes the Progression of Pulmonary Arterial Hypertension through Mediation of miR-675-3p/PDE5A Axis.	Pulmonary arterial hypertension (PAH) seriously threatens the elder people. Long non-coding RNAs (lncRNAs) are involved in multiple diseases. However, the study of the lncRNAs in the occurrence of PAH is just beginning. For this, we sought to explore the biological function of lncRNA HOXA cluster antisense RNA 3 (HOXA-AS3) in PAH. Hypoxia (HYP) was used to mimic in vitro model of PAH. Gene and protein expressions in cells were detected by q-PCR and Western blotting, respectively. In addition, cell proliferation and viability were tested by CCK-8 and MTT assay. Cell apoptosis was measured by flow cytometry. Wound healing was used to detect cell migration. Furthermore, the connection of HOXA-AS3, miR-675-3p, and phosphodiesterase 5A (PDE5A) was verified by dual-luciferase report assay. HOXA-AS3 and PDE5A were upregulated in human pulmonary artery smooth muscle cells (HPASMCs) in the presence of HYP, while miR-675-3p was downregulated. Moreover, knockdown of HOXA-AS3 suppressed the growth and migration of HPASMCs, but induced the apoptosis. Overexpression of miR-675-3p achieved the same effect. MiR-675-3p inhibitor or overexpression of PDE5A notably reversed the inhibitory effect of HOXA-AS3 knockdown on PAH. Finally, HOXA-AS3 could sponge miR-675-3p, and PDE5A was directly targeted by miR-675-3p. HOXA-AS3 increased the development of PAH via regulation of miR-675-3p/PDE5 axis, which could be the potential biomarker for treatment of PAH.	NA	Biochem Genet. 2021 Mar 9. doi: 10.1007/s10528-021-10053-y.
3348	Circular RNA	hsa_circ_0006859	miR-431-5p	ROCK1	osteoporosis	Osteoporosis	Homo sapiens (human)	microarray;qRT-PCR;Western blot;Luciferase reporter assay;	33648601	Exosomal hsa_circ_0006859 is a potential biomarker for postmenopausal osteoporosis and enhances adipogenic versus osteogenic differentiation in human bone marrow mesenchymal stem cells by sponging miR-431-5p.	BACKGROUND: As one of the most common chronic diseases in the world, osteoporosis occurs especially in postmenopausal women. Circular RNAs (circRNAs) are emerging as major drivers in human disease. The aim of the present study was to analyse circRNA expression profiles in osteoporosis and to explore the clinical significance and the regulatory molecular mechanism of hsa_circ_0006859 during osteoporosis. METHODS: Exosomes were isolated from clinically collected serum samples. A circRNA microarray was performed to screen differentially expressed circRNAs. Quantitative real-time PCR (qRT-PCR) and western blot were performed to analyse target gene mRNA expression and protein expression. Alizarin red staining (ARS) was performed to evaluate the mineralization ability of human bone marrow mesenchymal stem cells (hBMSCs). Oil Red O staining was performed to evaluate the lipid droplet formation ability of hBMSCs. Bioinformatics analysis and the luciferase reporter assay were performed to investigate the interaction between two genes. RESULTS: Hsa_circ_0006859 was identified as one of the most upregulated circRNAs in the microarray analysis. Hsa_circ_0006859 in exosomes was upregulated in osteoporosis patients compared to healthy controls. Hsa_circ_0006859 differentiated osteopenia or osteoporosis patients from healthy controls with high sensitivity and specificity. Hsa_circ_0006859 suppressed osteoblastic differentiation and promoted adipogenic differentiation of hBMSCs. Hsa_circ_0006859 directly bound to miR-431-5p, and ROCK1 was identified as a novel target gene of miR-431-5p. Hsa_circ_0006859 is a competing endogenous RNA (ceRNA) of miR-431-5p that promotes ROCK1 expression. Hsa_circ_0006859 suppressed osteogenesis and promoted adipogenesis by sponging miR-431-5p to upregulate ROCK1. CONCLUSIONS: Exosomal hsa_circ_0006859 is a potential biomarker for postmenopausal osteoporosis and controls the balance between osteogenesis and adipogenesis in hBMSCs by sponging miR-431-5p.	NA	Stem Cell Res Ther. 2021 Mar 1;12(1):157. doi: 10.1186/s13287-021-02214-y.
3349	LncRNA	LINC00659	miR-143	UST-AS1	primary endothelial cells	Thrombosis	Homo sapiens (human)	qRT-PCR	33580494	Transcriptome Profiling Reveals the Endogenous Sponging Role of LINC00659 and UST-AS1 in High-Altitude Induced Thrombosis.	BACKGROUND: The pathophysiology of deep vein thrombosis (DVT) is considered as multifactorial, where thrombus formation is an interplay of genetic and acquired risk factors. Little is known about the expression profile and roles of long noncoding RNAs (lncRNAs) in human subjects developing DVT at high altitude. METHODS: Using RNAseQ, we compared peripheral blood mRNA and lncRNA expression profile in human high-altitude DVT (HA-DVT) patients with high-altitude control subjects. We used DESeq to identify differentially expressed (DE) genes. We annotated the lncRNAs using NONCODE 3.0 database. In silico putative lncRNA-miRNA association study unravels the endogenous miRNA sponge associated with our candidate lncRNAs. These findings were validated by small-interfering RNA (siRNA) knockdown assay of the candidate lncRNAs conducted in primary endothelial cells. RESULTS: We identified 1,524 DE mRNAs and 973 DE lncRNAs. Co-expressed protein-coding gene analysis resulted in a list of 722 co-expressed protein-coding genes with a Pearson correlation coefficients >0.7. The functional annotation of co-expressed genes and putative proteins revealed their involvement in the hypoxia, immune response, and coagulation cascade. Through its miRNA response elements to compete for miR-143 and miR-15, lncRNA-LINC00659 and UXT-AS1 regulate the expression of prothrombotic genes. Furthermore, in vitro RNA interference (siRNA) simultaneously suppressed lncRNAs and target gene mRNA level. CONCLUSION: This transcriptome profile describes novel potential mechanisms of interaction between lncRNAs, the coding genes, miRNAs, and regulatory transcription factors that define the thrombotic signature and may be used in establishing lncRNAs as a biomarker in HA-DVT.	NA	Thromb Haemost. 2021 Feb 12. doi: 10.1055/a-1390-1713.
3350	LncRNA	LINC00659	miR-15	UST-AS1	primary endothelial cells	Thrombosis	Homo sapiens (human)	qRT-PCR	33580494	Transcriptome Profiling Reveals the Endogenous Sponging Role of LINC00659 and UST-AS1 in High-Altitude Induced Thrombosis.	BACKGROUND: The pathophysiology of deep vein thrombosis (DVT) is considered as multifactorial, where thrombus formation is an interplay of genetic and acquired risk factors. Little is known about the expression profile and roles of long noncoding RNAs (lncRNAs) in human subjects developing DVT at high altitude. METHODS: Using RNAseQ, we compared peripheral blood mRNA and lncRNA expression profile in human high-altitude DVT (HA-DVT) patients with high-altitude control subjects. We used DESeq to identify differentially expressed (DE) genes. We annotated the lncRNAs using NONCODE 3.0 database. In silico putative lncRNA-miRNA association study unravels the endogenous miRNA sponge associated with our candidate lncRNAs. These findings were validated by small-interfering RNA (siRNA) knockdown assay of the candidate lncRNAs conducted in primary endothelial cells. RESULTS: We identified 1,524 DE mRNAs and 973 DE lncRNAs. Co-expressed protein-coding gene analysis resulted in a list of 722 co-expressed protein-coding genes with a Pearson correlation coefficients >0.7. The functional annotation of co-expressed genes and putative proteins revealed their involvement in the hypoxia, immune response, and coagulation cascade. Through its miRNA response elements to compete for miR-143 and miR-15, lncRNA-LINC00659 and UXT-AS1 regulate the expression of prothrombotic genes. Furthermore, in vitro RNA interference (siRNA) simultaneously suppressed lncRNAs and target gene mRNA level. CONCLUSION: This transcriptome profile describes novel potential mechanisms of interaction between lncRNAs, the coding genes, miRNAs, and regulatory transcription factors that define the thrombotic signature and may be used in establishing lncRNAs as a biomarker in HA-DVT.	NA	Thromb Haemost. 2021 Feb 12. doi: 10.1055/a-1390-1713.
3351	LncRNA	LINC00857	miR-370-3p	CBX3	DLBCL cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qRT-PCR	33657224	LINC00857 contributes to proliferation and lymphomagenesis by regulating miR-370-3p/CBX3 axis in diffuse large B-cell lymphoma.	Diffuse large B-cell lymphoma (DLBCL) remains to be a high aggressive and invasive malignancy with enigmatic etiology. Ectopic expression of long non-coding RNAs is widely involved in the progression of human cancers. We discovered that LINC00857 level was remarkably elevated in DLBCL tissues compared with non-tumor controls. High LINC00857 level predicts lower survival rate, more advanced tumor node metastasis and larger tumor size. LINC00857 overexpression promoted DLBCL cell proliferation and facilitated cell cycle as evidenced by elevated Cyclin D1 and proliferating cell nuclear antigen (PCNA) accompanying with reduced p21 level. LINC00857 overexpression also suppressed DLBCL cell apoptosis as evidenced by elevated Bcl-2 protein level, reduced Bax and cleaved caspase-3 protein levels. On the contrary, LINC00857 knockdown using short hairpin RNAs inhibited DLBCL cell proliferation yet induced cell apoptosis. LINC00857 knockdown also repressed tumor growth in vivo, concomitant with decreased Ki67 level. Besides, microRNA miR-370 was down-regulated in DLBCL tissues and served as a competitive endogenous RNA (ceRNA) target of LINC00857. We further validated that chromobox homolog 3 (CBX3) served as a downstream target gene of miR-370-3p. LINC00857 level was reversely correlated with miR-370-3p level yet positively correlated with CBX3 level. In addition, CBX3 overexpression alleviated the impact of LINC00857 knockdown on DLBCL cell survival. In conclusion, our findings indicated that LINC00857 contributes to DLBCL proliferation and lymphomagenesis through regulating miR-370-3p/CBX3 axis.	NA	Carcinogenesis. 2021 May 28;42(5):733-741. doi: 10.1093/carcin/bgab013.
3352	LncRNA	LINC00941	miR-877-3p	VEGFA	NSCLC cells and human umbilical vein endothelial cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	microarray;luciferase assay;	33869051	LINC00941 Promotes Progression of Non-Small Cell Lung Cancer by Sponging miR-877-3p to Regulate VEGFA Expression.	Long noncoding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. LINC00941 has been found to mediate the development of gastric cancer, and LINC00941 was negatively associated with the longer overall survival of lung adenocarcinoma patients. Herein, our aim was to investigate the effects and mechanisms of LINC00941 in NSCLC progression. Microarray was used to identify the change lncRNAs in NSCLC, LINC00941 was found to increase in tumor tissues and patients' plasma. Knockdown of LINC00941 didn't modulate the proliferation of NSCLC cells, but inhibition of LINC00941 in NSCLC cells suppressed the angiogenesis ability of human umbilical vein endothelial cells (HUVECs). Moreover, LINC00941 promoted tumorigenesis in vivo, while si-LINC00941 inhibited tumor development of NSCLC. VEGFA was should to be significantly modulated by LINC00941 in NSCLC cells, then luciferase assay proved that LINC00941 regulated VEGFA expression via interacting with miR-877-3p. Followed functional experiments indicated that overexpression of LINC00941 accelerated angiogenesis and NSCLC tumor progression via miR-877-3p/VEGFA axis both in vitro and in vivo. In conclusion, our results clarified the LINC00941 function for the first time, and LINC00941 promoted the progression of NSCLC, which was mediated by miR-877-3p/VEGFA axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment.	NA	Front Oncol. 2021 Mar 31;11:650037. doi: 10.3389/fonc.2021.650037. eCollection 2021.
3353	LncRNA	LINC01089	miR-152-3p	PTEN	NSCLC tissues and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33653358	LINC01089 functions as a ceRNA for miR-152-3p to inhibit non-small lung cancer progression through regulating PTEN.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to exert crucial functions in regulating the progression of human cancers. However, the function and mechanism of long intergenic non-protein coding RNA 01089 (LINC01089) in non-small cell lung cancer (NSCLC) have not been revealed. METHODS: The expression level of LINC01089, microRNA (miRNA, miR)-152-3p and phosphatase and tensin homolog deleted onc hromosome ten (PTEN) mRNA was detected by quantitative real-time PCR (qRT-PCR). After gain-of-function and loss-of-function models were established with NSCLC cell lines, the proliferation, migration and invasion of NSCLC cells were detected by cell counting kit-8 (CCK-8) assay, scratch healing assay, Transwell assay, respectively. Dual luciferase reporter assay was employed to validate the binding relationship between miR-152-3p and LINC01089 or the 3'UTR of PTEN. Western blot was used to detect PTEN expression in NSCLC cells after LINC01089 and miR-152-3p were selectively modulated. RESULTS: LINC01089 was down-regulated in NSCLC tissues and cells. Functional experiments showed that knockdown of LINC01089 could promote the proliferation, migration and invasion of NSCLC cells, while over-expression of LINC01089 had the opposite effects. miR-152-3p was identified as a functional target for LIN01089, and miR-152-3p could reverse the function of LINC01089. Additionally, LINC01089 could up-regulate the expression level of PTEN via repressing miR-152-3p. CONCLUSIONS: Down-regulation of LINC01089 promoted the progression of NSCLC through regulating miR-152-3p/PTEN axis.	NA	Cancer Cell Int. 2021 Mar 2;21(1):143. doi: 10.1186/s12935-021-01846-7.
3354	LncRNA	LINC02381	miR-503-5p	CDCA4	osteosarcoma tissues and cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33640603	ELK1-induced upregulation lncRNA LINC02381 accelerates the osteosarcoma tumorigenesis through targeting CDCA4 via sponging miR-503-5p.	Long noncoding RNAs (lncRNAs) have been identified as functional modulators in human tumors. The purpose of our study was to determine the expressing trend, clinical significance and functions of lncRNA LINC02381(LINC02381) in osteosarcoma. We observed that the expression of LINC02381 and cell division cycle-associated protein 4 (CDCA4) were distinctly increased in osteosarcoma specimens and cells, while miR-503-5p expression was decreased. Additionally, ETS transcription factor ELK1 (ELK1) could bind directly to the LINC02381 promoter region and activate its transcription. Clinical assays revealed that high LINC02381 was associated with advanced clinical progress and poor clinical outcome. Functionally, knockdown of LINC02381 suppressed the proliferation, migration and invasion of osteosarcoma cells. What's more, LINC02381 could down-regulate CDCA4 via sponging miR-503-5p, and there existed a negative correlation between LINC02381 expression and miR-503-5p expression in 92 osteosarcoma samples. Rescue experiments proved the carcinogenic role of LINC02381/miR-503-5p/CDCA4 axis in osteosarcoma progression. Overall, our data illustrated how LINC02381 played an oncogenic role in osteosarcoma and might offer a novel diagnostic and prognostic biomarker and potential therapeutic target for osteosarcoma.	NA	Biochem Biophys Res Commun. 2021 Apr 9;548:112-119. doi: 10.1016/j.bbrc.2021.02.072. Epub 2021 Feb 25.
3355	LncRNA	MALAT1	miR-200c	BMI1	human dental pulp cells	NA	Homo sapiens (human)	luciferase assay;	33772374	LncRNA MALAT1 Functions as a Competing Endogenous RNA to Regulate BMI1 Expression by Sponging miR-200c/miR-203 in the Control of the Differentiation of Pulp Cells.	BACKGROUND: Long non-coding RNAs (lncRNAs) and miRNAs (microRNAs) are considered as key regulators of several biological processes, including dental development. In this study, we explored the lncRNAs and miRNAs which are involved in dental development. METHOD: Real-time PCR was performed to identify the candidate lncRNAs and miRNAs involved in dental development. Bioinformatics analysis and luciferase assay were carried out to establish the regulatory relationships between MALAT1, miR-203 and miR-200c in dental development. RESULTS: Among all candidate lncRNAs, only MALAT1 was highly expressed in differentiated human dental pulp cells (hDPCs), and among all candidate miRNAs which are down-regulated in differentiated hDPCs, miR-203, and miR-200c are most decreased. Furthermore, MALAT1 was up-regulated while miR-203 and miR-200c were down-regulated in differentiated hDPCs in a time-dependent manner. MiR-203 and miR-200c were proved to bind to MALAT1. Moreover, BMI1 was identified as a target gene of miR-203 or miR-200c, and BMI1 was time-dependently decreased in hDPCs cultured with odontogenic medium. On the contrary, dentin sialophosphoprotein (DSPP), dentin matrix protein-1 (DMP-1), osteocalcin (OCN), and alkaline phosphatase (ALP), were time-dependently increased in hDPCs cultured with odontogenic medium. Finally, the overexpression of MALAT1 and the knockdown of miR-203/miR-200c both significantly increased the levels of BMI1, DSPP, DMP-1, OCN, and ALP, while the effect of knockdown of miR-203/miR-200c was much stronger than that of the overexpression of MALAT1. CONCLUSION: Our results demonstrated that MALAT1 functions as a competing endogenous RNA of miR-203 and miR-200c and accordingly promotes BMI1 expression. Therefore, MALAT1 may serve as a biomarker for dental development.	NA	Biochem Genet. 2021 Mar 26. doi: 10.1007/s10528-021-10054-x.
3356	LncRNA	MALAT1	miR-203	BMI1	human dental pulp cells	NA	Homo sapiens (human)	luciferase assay;	33772374	LncRNA MALAT1 Functions as a Competing Endogenous RNA to Regulate BMI1 Expression by Sponging miR-200c/miR-203 in the Control of the Differentiation of Pulp Cells.	BACKGROUND: Long non-coding RNAs (lncRNAs) and miRNAs (microRNAs) are considered as key regulators of several biological processes, including dental development. In this study, we explored the lncRNAs and miRNAs which are involved in dental development. METHOD: Real-time PCR was performed to identify the candidate lncRNAs and miRNAs involved in dental development. Bioinformatics analysis and luciferase assay were carried out to establish the regulatory relationships between MALAT1, miR-203 and miR-200c in dental development. RESULTS: Among all candidate lncRNAs, only MALAT1 was highly expressed in differentiated human dental pulp cells (hDPCs), and among all candidate miRNAs which are down-regulated in differentiated hDPCs, miR-203, and miR-200c are most decreased. Furthermore, MALAT1 was up-regulated while miR-203 and miR-200c were down-regulated in differentiated hDPCs in a time-dependent manner. MiR-203 and miR-200c were proved to bind to MALAT1. Moreover, BMI1 was identified as a target gene of miR-203 or miR-200c, and BMI1 was time-dependently decreased in hDPCs cultured with odontogenic medium. On the contrary, dentin sialophosphoprotein (DSPP), dentin matrix protein-1 (DMP-1), osteocalcin (OCN), and alkaline phosphatase (ALP), were time-dependently increased in hDPCs cultured with odontogenic medium. Finally, the overexpression of MALAT1 and the knockdown of miR-203/miR-200c both significantly increased the levels of BMI1, DSPP, DMP-1, OCN, and ALP, while the effect of knockdown of miR-203/miR-200c was much stronger than that of the overexpression of MALAT1. CONCLUSION: Our results demonstrated that MALAT1 functions as a competing endogenous RNA of miR-203 and miR-200c and accordingly promotes BMI1 expression. Therefore, MALAT1 may serve as a biomarker for dental development.	NA	Biochem Genet. 2021 Mar 26. doi: 10.1007/s10528-021-10054-x.
3357	LncRNA	MAPKAPK5-AS1	miR-154-5p	PLAGL2	HCC tissues and cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Chromatin immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33596983	Long non-coding RNA MAPKAPK5-AS1/PLAGL2/HIF-1α signaling loop promotes hepatocellular carcinoma progression.	BACKGROUND: Long non-coding RNAs (lncRNAs) are widely involved in human cancers' progression by regulating tumor cells' various malignant behaviors. MAPKAPK5-AS1 has been recognized as an oncogene in colorectal cancer. However, the biological role of MAPKAPK5-AS1 in hepatocellular carcinoma (HCC) has not been explored. METHODS: Quantitative real-time PCR was performed to detect the level of MAPKAPK5-AS1 in HCC tissues and cell lines. The effects of MAPKAPK5-AS1 on tumor growth and metastasis were assessed via in vitro experiments, including MTT, colony formation, EdU, flow cytometry, transwell assays, and nude mice models. The western blotting analysis was carried out to determine epithelial-mesenchymal transition (EMT) markers and AKT signaling. The interaction between MAPKAPK5-AS1, miR-154-5p, and PLAGL2 were explored by luciferase reporter assay and RNA immunoprecipitation. The regulatory effect of HIF-1α on MAPKAPK5-AS1 was evaluated by chromatin immunoprecipitation. RESULTS: MAPKAPK5-AS1 expression was significantly elevated in HCC, and its overexpression associated with malignant clinical features and reduced survival. Functionally, MAPKAPK5-AS1 knockdown repressed the proliferation, mobility, and EMT of HCC cells and induced apoptosis. Ectopic expression of MAPKAPK5-AS1 contributed to HCC cell proliferation and invasion in vitro. Furthermore, MAPKAPK5-AS1 silencing suppressed, while MAPKAPK5-AS1 overexpression enhanced HCC growth and lung metastasis in vivo. Mechanistically, MAPKAPK5-AS1 upregulated PLAG1 like zinc finger 2 (PLAGL2) expression by acting as an endogenous competing RNA (ceRNA) to sponge miR-154-5p, thereby activating EGFR/AKT signaling. Importantly, rescue experiments demonstrated that the miR-154-5p/PLAGL2 axis mediated the function of MAPKAPK5-AS1 in HCC cells. Interestingly, we found that hypoxia-inducible factor 1α (HIF-1α), a transcript factor, could directly bind to the promoter to activate MAPKAPK5-AS1 transcription. MAPKAPK5-AS1 regulated HIF-1α expression through PLAGL2 to form a hypoxia-mediated MAPKAPK5-AS1/PLAGL2/HIF-1α signaling loop in HCC. CONCLUSIONS: Our results reveal a MAPKAPK5-AS1/PLAGL2/HIF-1α signaling loop in HCC progression and suggest that MAPKAPK5-AS1 could be a potential novel therapeutic target of HCC.	NA	J Exp Clin Cancer Res. 2021 Feb 17;40(1):72. doi: 10.1186/s13046-021-01868-z.
3358	LncRNA	MBNL1-AS1	miR-181a-5p	PTEN	PCa cells	Prostate Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;luciferase assay;Rescue assay;	33648424	Muscleblind-like 1 antisense RNA 1 inhibits cell proliferation, invasion, and migration of prostate cancer by sponging miR-181a-5p and regulating PTEN/PI3K/AKT/mTOR signaling.	The present study aimed to investigate the role and underlying mechanisms of long non-coding RNA (lncRNA) muscleblind-like 1 antisense RNA 1 (MBNL1-AS1) in the progression of Prostate cancer (PCa). MBNL1-AS1 and microRNA (miR)-181a-5p expression in PCa tissues and several human PCa cell lines were analyzed, respectively, using StarBasev3.0 project and RT-qPCR assay. After MBNL1-AS1 overexpression, cell proliferation, invasion and migration were, respectively, evaluated using CCK-8, colony formation, transwell and wound healing assays. Dual luciferase assay were used for analysis of the interactions among MBNL1-AS1, miR-181a-5p, and phosphatase and tensin homolog (PTEN). Subsequently, the expression of PTEN and proteins in PI3K/AKT/mTOR signaling was examined using western blot analysis after transfection with miR-181a-5p mimic. The rescue assays were performed to investigate the effects of MBNL1-AS1 and miR-181a-5p on the functions of PCa cells and the expression of PTEN/PI3K/AKT/mTOR signaling by co-transfection with MBNL1-AS1 plasmid and miR-181a-5p mimic. Results indicated that MBNL1-AS1 was conspicuously downregulated while miR-181a-5p upregulating in PCa tissues and cell lines. MBNL1-AS1 overexpression decreased the abilities of cell proliferation, invasion, and migration. Further study revealed that MBNL1-AS1 acted as a sponge for miR-181a-5p and positively regulated PTEN by a sponge effect. Additionally, rescue assays proved that the effect of MBNL1-AS1-upregulation on the proliferation, invasion, and migration of PCa cells was dependent on miR-181a-5p. Furthermore, miR-181a-5p overexpression counteracted the expression of PTEN and proteins in PI3K/AKT/mTOR signaling exerted by MBNL1-AS1-upregulation in PCa cells. This study suggests that MBNL1-AS1 inhibits the progression of PCa via sponging miR-181a-5p and regulating PTEN/PI3K/AKT/mTOR pathway.	NA	Bioengineered. 2021 Dec;12(1):803-814. doi: 10.1080/21655979.2021.1890383.
3359	LncRNA	MEG3	miR-34a-3p	SIRT1	Caco-2 cells	Cardiac Arrest	Homo sapiens (human)	ELISA;qPCR;Western blot;	33569424	Maternally expressed 3 protects the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury via miR-34a-3p/sirtuin 1/nuclear factor kappa B signaling.	BACKGROUND: Cardiac arrest (CA), a common disease with a high mortality rate, is a leading cause of ischemia/reperfusion (I/R)-induced dysfunction of the intestinal barrier. Long non-coding RNAs (lncRNAs) play crucial roles in multiple pathological processes. However, the effect of the lncRNA maternally expressed 3 (MEG3) on intestinal I/R injury and the intestinal barrier has not been fully determined. Therefore, this study aimed to investigate the function of MEG3 in CA-induced intestinal barrier dysfunction. METHODS: The oxygen and glucose deprivation (OGD) model in the human colorectal adenocarcinoma Caco-2 cells and in vivo cardiac arrest-induced intestinal barrier dysfunction model in Sprague-Dawley (SD) rats were established. The effect and underlying mechanism of MEG3 on the intestinal barrier from cardiac arrest-induced ischemia/reperfusion injury were analyzed by methyl thiazolyl tetrazolium (MTT) assays, Annexin V-FITC/PI apoptosis detection kit, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) staining, quantitative polymerase chain reaction (qPCR) assays, Western blot analysis, luciferase reporter gene assays, transepithelial electrical resistance (TEER) measurements, immunofluorescence analysis, and enzyme-linked immunosorbent assay (ELISA) assays. RESULTS: Interestingly, we found that MEG3 could protect Caco-2 cells from oxygen-glucose deprivation (OGD)/reoxygenation-induced I/R injury by modulating cell proliferation and apoptosis. Moreover, MEG3 relieved OGD-induced intestinal barrier dysfunction in vitro, as demonstrated by its significant rescue effect on transepithelial electrical resistance and the expression of tight junction proteins such as occludin and claudin-1 (CLDN1), which were impaired in OGD-treated Caco-2 cells. Mechanistically, MEG3 inhibited the expression of inflammatory factors including interleukin (IL)-1β, tumor necrosis factor (TNF)-α, interferon-gamma (IFN)-γ, inflammatory factors including interleukin (IL)-10, and transforming growth factor beta (TGFb)-1, as well as nuclear factor-kappa B (NF-κB) signaling. In response to OGD treatment in vitro, MEG3 also activated the expression of sirtuin 1 (SIRT1) by Caco-2 cells via sponging miR-34a-3p. Furthermore, MEG3 relieved CA-induced intestinal barrier dysfunction through NF-κB signaling in vivo. CONCLUSIONS: LncRNA MEG3 can protect the intestinal barrier from cardiac arrest-induced I/R injury via miR-34a-3p/SIRT1/NF-κB signaling. This finding provides new insight into the mechanism by which MEG3 restores intestinal barrier function following I/R injury, presenting it as a potential therapeutic candidate or strategy in intestinal injury.	NA	Ann Transl Med. 2021 Jan;9(2):122. doi: 10.21037/atm-20-6438.
3360	Protein	MEG3	miR-93-5p	PTEN	Leydig cells	NA	Homo sapiens (human)	Cell transfection;Cell transfection;ELISA;qPCR;RIP assay;Western blot;	33639974	Silencing of MEG3 attenuated the role of lipopolysaccharides by modulating the miR-93-5p/PTEN pathway in Leydig cells.	BACKGROUND: Leydig cells reflect the activation of inflammation, decrease of androgen production, inhibition of cell growth and promotion of cell apoptosis under orchitis. Maternally expressed gene 3 (MEG3) exerts a crucial role in various human diseases, but under orchitis, the role and underlying molecular mechanism of MEG3 in Leydig cells remain unclear. METHODS: Lipofectamine 2000 was used for the cell transfections. qPCR and western blots assay were applied to assess the gene expression. ELISA assay was used to measure the TNFα, IL6 and testosterone secretion. CCK8 and EdU assay was employ to test the cell viability and proliferation respectively. Luciferase reporter and RIP assay were introduced to detect the binding of miR-93-5p with MEG3 and PTEN. RESULTS: Lipopolysaccharides (LPS) induced TNFα and IL6 secretion, lowered testosterone production, inhibited cell viability and proliferation, and induced cell apoptosis in Leydig cells. MEG3 was upregulated in Leydig cells treated with LPS and that knockdown of MEG3 inhibited the role of LPS in Leydig cells. MEG3 absorbed miR-93-5p and that suppression of miR-93-5p restored the role of silenced MEG3 in Leydig cells under LPS treatment. miR-93-5p inhibited PTEN expression and that over-expressed PTEN alleviated the effect of miR-93-5p in Leydig cells treated with LPS. LPS activated the MEG3/miR-93-5p/PTEN signalling pathway in Leydig cells. CONCLUSIONS: This study revealed that MEG3 serves as a molecular sponge to absorb miR-93-5p, thus leading to elevation of PTEN expression in Leydig cells under LPS treatment, offering a theoretical basis on which to establish potential new treatment strategies for orchitis.	NA	Reprod Biol Endocrinol. 2021 Feb 27;19(1):33. doi: 10.1186/s12958-021-00712-5.
3361	LncRNA	MIAT	miR-206	RAB22A	human umbilical vein endothelial cells	Injury Of Human Umbilical Vein Endothelial Cells	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33965771	LncRNA MIAT Mediates ox-LDL-Induced Endothelial Cell Injury Via miR-206/RAB22A Axis.	BACKGROUND: Long non-coding RNA myocardial infarction associated transcript (MIAT) has exerted significant effects on atherosclerosis (AS). The biological roles of MIAT in endothelial cell dysfunction are not thoroughly elucidated. METHODS: The expression of MIAT, microRNA (miR)-206 and Ras-related protein Rab-22A (RAB22A) was detected by quantitative real-time polymerase chain reaction and western blot. The injury of human umbilical vein endothelial cells (HUVECs) was evaluated by testing cell viability, invasion, migration, apoptosis, epithelial-mesenchymal transition capacities and inflammatory response using cell counting kit-8, transwell, wound healing assays, flow cytometry, western blot and enzyme-linked immunosorbent assay, respectively. The binding interaction between miR-206 and MIAT or RAB22A was confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. RESULTS: The expression of MIAT was up-regulated in ox-LDL-treated HUVECs, and knockdown of MIAT in ox-LDL-treated HUVECs remarkably promoted cell viability, invasion, migration, and epithelial-mesenchymal transition (EMT), as well as suppressed cell apoptosis and the levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α and endothelial nitric oxide synthase (eNOS). In a mechanical study, MIAT directly targeted miR-206, and miR-206 inhibition attenuated the protective effects of MIAT knockdown on ox-LDL-triggered HUVEC injury. Besides that, RAB22A was a target of miR-206, and RAB22A overexpression reversed the biological effects of miR-206 on ox-LDL-treated HUVECs. Additionally, we also proved MIAT could regulate RAB22A via miR-206 in HUVECs. CONCLUSION: MIAT knockdown impaired ox-LDL-induced HUVEC injury via regulating miR-206/RAB22A axis, suggesting the potential impacts of MIAT on AS occurrence, which revealed a potential therapeutic strategy for future clinic intervention in AS.	NA	J Surg Res. 2021 May 6;265:303-312. doi: 10.1016/j.jss.2021.02.029.
3362	LncRNA	MIR503HG	miR-143-3p	Smad3	HS tissues and human hypertrophic scar fibroblasts	Hypertrophic Scar	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33819360	LncRNA MIR503HG promotes hypertrophic scar progression via miR-143-3p-mediated Smad3 expression.	Hypertrophic scars (HSs) form due to unchecked proliferation of fibrous tissue after an injury to the skin. Recently, lncRNA MIR503HG was shown to be involved in HS. However, the mechanism by which MIR503HG affects the formation and progression of HS still needs further study. qRT-PCR was applied to examine the levels of MIR503HG and miR-143-3p in HS tissues and human hypertrophic scar fibroblasts (hHSFs). The relationships of MIR503HG, miR-143-3p and Smad3 were explored with a dual-luciferase reporter assay. Cell proliferation, apoptosis, and invasion were measured by CCK-8 assay, flow cytometry and transwell assay, respectively. The protein level of Smad3 was tested via Western blotting. MIR503HG was upregulated and miR-143-3p was downregulated in HS versus normal skin tissues. The knockdown of MIR503HG and the overexpression of miR-143-3p suppressed the proliferation and invasion of hHSF, and promoted cell apoptosis. MIR503HG bound to miR-143-3p while miR-143-3p directly targeted Smad3 to inhibit its expression. Suppression of miR-143-3p and overexpression of Smad3, respectively, reversed these effects of knockdown of MIR503HG and overexpression of miR-143-3p on hHSFs. Our research supports a model in which the MIR503HG/miR-143-3p/Smad3 axis serves as a critical regulator of HS, highlighting a promising therapeutic option for HS.	NA	Wound Repair Regen. 2021 Apr 5. doi: 10.1111/wrr.12913.
3363	LncRNA	MT1DP	miR-365	NRF-2	nucleus pulposus cells	Lumbar Disc Herniation	Homo sapiens (human)	qRT-PCR	33569453	Long non-coding RNA MT1DP interacts with miR-365 and induces apoptosis of nucleus pulposus cells by repressing NRF-2-induced anti-oxidation in lumbar disc herniation.	BACKGROUND: This study investigated the effects of the long non-coding (lnc) RNA MT1DP on the apoptosis of nucleus pulposus (NP) cells. The interactions between MT1DP and the microRNA miR-365, and its effects on the anti-oxidant activity of nuclear factor erythroid 2-related factor 2 (NRF-2) were investigated in lumbar disc herniation (LDH). METHODS: Human degenerative intervertebral disc NP tissues were obtained from 10 patients with LDH who underwent lumbar spine surgery. Normal intervertebral disc NP tissues were obtained from 10 patients with lumbar vertebrae fractures and used as negative controls (NCs). RESULTS: The gene expressions of MT1DP and miR-365 in human degenerative disc NP tissues and nucleus pulposus cells (NPCs) were significantly increased, while the level of NRF-2 was significantly decreased. Overexpression of MT1DP and miR-365 (MT1DP + miR-365) and inhibition of NRF-2 suppressed NP cell viability and induced apoptosis. MT1DP + miR-365 caused inflammation in NP cells by damaging the mitochondrial membrane. The combination of lnc-MT1DP and miR-365 reduced cell mitochondrial function and led to a decrease in the ability of cells to elimination reactive oxygen species (ROS). CONCLUSIONS: The combination of lnc-MT1DP and miR-365 damaged the cell mitochondrial membrane, reduced mitochondrial function and the ability to eliminate ROS, increased cell apoptosis, and caused LDH.	NA	Ann Transl Med. 2021 Jan;9(2):151. doi: 10.21037/atm-20-8123.
3364	LncRNA	OIP5-AS1	miR-320b	FOXM1	PC tumor tissues and PC cell lines	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;	33782807	OPA Interacting Protein 5 Antisense RNA 1 Expedites Cell Migration and Invasion Through FOXM1/ Wnt/β-Catenin Pathway in Pancreatic Cancer.	BACKGROUND: Pancreatic cancer (PC) is a digestive tract malignancy with poor prognosis. Long noncoding RNA (lncRNA) OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was regarded to be correlated with human malignancy, working as tumor suppressor or promoter on the basis of tumor types. However, the function of OIP5-AS1 in PC remained unclear. AIMS: The study focused on the function and regulatory mechanism of OIP5-AS1 in PC. METHODS: OIP5-AS1 expression was assessed by the quantitative reverse transcription PCR (RT-qPCR) in tumor tissues and PC cell lines. 5-ethynyl-2'-deoxyuridine (EdU) incorporation and cell counting kit-8 (CCK-8) assays were applied to detect cell proliferation ability. Through wound healing and transwell assays, cell migration and invasion capacities were estimated. Flow cytometry analysis was performed to examine apoptosis capability of PC cells. RESULTS: OIP5-AS1 downregulating inhibited cell proliferation, migration, and invasion capacities, while promoting cell apoptosis rates. As a competing endogenous RNA (ceRNA), OIP5-AS1 competed with Forkhead Box M1 (FOXM1) for the binding sites on microRNA-320b (miR-320b). OIP5-AS1 was able to upregulate FOXM1 expression via silencing miR-320b. Furthermore, FOXM1 served as an activator of Wnt/β-catenin pathway and mediated the effect of OIP5-AS1 on Wnt/β-catenin pathway. CONCLUSION: OIP5-AS1 expedites the proliferative, migrated, and invasive capability of PC cells, while repressing cell apoptosis through regulating miRNA-320b/FOXM1 axis and FOXM1/Wnt/β-catenin pathway in PC. OIP5-AS1 regulation on FOXM1/Wnt/β-catenin pathway may offer novel efficient markers for PC treatments.	NA	Dig Dis Sci. 2021 Mar 29. doi: 10.1007/s10620-021-06919-1.
3365	LncRNA	PCAT6	miR-326	hnRNPA2B1	liver cancer tissues and cells	Liver Cancer	Homo sapiens (human)	qRT-PCR	33907581	lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR-326/hnRNPA2B1 axis in liver cancer.	Liver cancer is one of the most common malignant human tumors with the highest morbidity and mortality rates of all cancer types in China. Evidence suggests that long non-coding RNA prostate cancer-associated transcript 6 (PCAT6) plays an essential role in tumor progression. However, the roles and mechanism of PCAT6 in liver cancer remain unclear. The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells in vitro and in vivo. A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. Mechanistically, silenced PCAT6 suppressed the malignant phenotype of liver cancer cells through upregulating the inhibitory effect of miR-326 on hnRNPA2B1 expression. Taken together, these data demonstrated that knockdown of PCAT6 inhibited liver cancer progression through regulation of the miR-326/hnRNPA2B1 axis, suggesting that PCAT6 functions as an oncogene and may be a useful biomarker for the future diagnosis and treatment of liver cancer.	NA	Oncol Lett. 2021 Jun;21(6):471. doi: 10.3892/ol.2021.12732. Epub 2021 Apr 13.
3366	LncRNA	RP11-301G19.1	miR-582-5p	HMGB2	MM cell lines	Multiple Myeloma	Homo sapiens (human)	microarray;Western blot;Luciferase reporter assay;	33707625	The LncRNA RP11-301G19.1/miR-582-5p/HMGB2 axis modulates the proliferation and apoptosis of multiple myeloma cancer cells via the PI3K/AKT signalling pathway.	Long non-coding RNAs (lncRNAs) have recently been reported to act as crucial regulators and prognostic biomarkers of human tumorigenesis. Based on microarray data, RP11-301G19.1 was previously identified as an upregulated lncRNA during B cell development. However, the effect of RP11-301G19.1 on multiple myeloma (MM) cells remains unclear. In the present study, the effects of RP11-301G19.1 on tumour progression were ascertained both in vitro and in vivo. Our results demonstrated that RP11-301G19.1 was upregulated in MM cell lines and that its downregulation inhibited the proliferation and cell cycle progression and promoted the apoptosis of MM cells. Bioinformatic analysis and luciferase reporter assay results revealed that RP11-301G19.1 can upregulate the miR-582-5p-targeted gene HMGB2 as a competing endogenous RNA (ceRNA). Furthermore, Western blot results indicated that RP11-301G19.1 knockdown decreased the levels of PI3K and AKT phosphorylation without affecting their total protein levels. Additionally, in a xenograft model of human MM, RP11-301G19.1 knockdown significantly inhibited tumour growth by downregulating HMGB2. Overall, our data demonstrated that RP11-301G19.1 is involved in MM cell proliferation by sponging miR-582-5p and may serve as a therapeutic target for MM.	NA	Cancer Gene Ther. 2021 Mar 11. doi: 10.1038/s41417-021-00309-5.
3367	LncRNA	SLC2A1-AS1	miR-508-5p	TFAP2A	LUAD cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33580997	TFAP2A-induced SLC2A1-AS1 promotes cancer cell proliferation.	Long non-coding RNAs (lncRNAs) are involved in the occurrence and development of human cancers including lung adenocarcinoma (LUAD). SLC2A1-AS1 is a novel lncRNA that has been reported to be exceptionally expressed in several cancer types. However, the expression and role of SLC2A1-AS1 in cancer remains largely unclear. In this study, it was revealed that lncRNA SLC2A1-AS1 was notably over-expressed in LUAD and was closely correlated with patients' overall survival (OS). Knockdown of SLC2A1-AS1 could significantly restrain cell proliferation of LUAD in vitro, while over-expression of SLC2A1-AS1 had the accelerative effect. SLC2A1-AS1 enriched in the cytoplasm of LUAD cells could directly bind to miR-508-5p and negatively regulate its level. The inhibitory effect of miR-508-5p on LUAD cell proliferation was in part abrogated by SLC2A1-AS1 manipulation. Moreover, the transcription factor activating enhancer binding protein 2 α (TFAP2A) was highly expressed in LUAD and predicted worse patients' OS. TFAP2A could directly bind to the promoter region of SLC2A1-AS1 encoding gene and positively regulate the transcription of SLC2A1-AS1 in LUAD cells. Furthermore, TFAP2A-induced SLC2A1-AS1 promoted cell proliferation of lung squamous cell carcinoma (LUSC) and pancreatic adenocarcinoma (PAAD). Collectively, these findings suggest that TFAP2A-mediated lncRNA SLC2A1-AS1 works as an oncogene to drive cancer cell proliferation.	NA	Biol Chem. 2021 Feb 19;402(6):717-727. doi: 10.1515/hsz-2020-0290. Print 2021 May 26.
3368	LncRNA	SLCO4A1-AS1	miR-150-3p	SLCO4A1	colon cancer stem cells	Colon Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33958701	LncRNA SLCO4A1-AS1 modulates colon cancer stem cell properties by binding to miR-150-3p and positively regulating SLCO4A1.	Long non-coding RNAs (lncRNAs) play important roles in a range of different human cancers. However, the role of lncRNA solute carrier organic anion transporter family member 4A1-AS1 (SLCO4A1-AS1) in colon cancer remains enigmatic. Hence, we aimed to explore the specific role of SLCO4A1-AS1 in colon cancer stem cells. Colon cancer-related differentially expressed lncRNA and mRNA were screened using microarray-based analysis, and the expression of SLCO4A1-AS1 and SLCO4A1 in colon cancer tissues was determined using reverse transcription quantitative polymerase chain reaction and western blot analysis. The interaction among SLCO4A1-AS1, microRNA-150-3p (miR-150-3p) and SLCO4A1 was verified using dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down. Moreover, SLCO4A1-AS1, miR-150-3p and/or SLCO4A1 were overexpressed or depleted in colon cancer cells to detect their effects on migration, invasion, sphere formation, apoptosis and tumorigenesis abilities of colon cancer stem CD133(+)CD44(+) cells using both in vitro and in vivo assays. SLCO4A1-AS1 and SLCO4A1 were screened as the differentially expressed lncRNA and mRNA in colon cancer tissues. SLCO4A1-AS1 was confirmed to competitively bind to miR-150-3p to elevate SLCO4A1 expression. Moreover, knockdown of SLCO4A1-AS1 decreased SLCO4A1 expression, thus inhibiting cell migration, invasion, sphere formation, and tumorigenesis abilities and enhancing the apoptosis of CD133(+)CD44(+) cells. Collectively, these findings provide evidence demonstrating that depleting SLCO4A1-AS1 competitively binds to miR-150-3p, which downregulates SLCO4A1 expression, thus hindering colon cancer progression.	NA	Lab Invest. 2021 Jul;101(7):908-920. doi: 10.1038/s41374-021-00577-7. Epub 2021 May 6.
3369	LncRNA	SNHG12	miR-30a-3p	RUNX2	RCC cells	Renal Cancer	Homo sapiens (human)	qRT-PCR	33787057	SNHG12 promotes carcinogenesis of human renal cell cancer via functioning as a competing endogenous RNA and sponging miR-30a-3p.	Small nucleolar RNA host gene 12 (SNHG12) has been indicated in the tumorigenesis of various human cancers, including clear cell renal cell carcinoma (ccRCC). However, the underlying mechanisms of SNHG12 driving progression of ccRCC remain incompletely understood. In the present study, we discovered that SNHG12 is up-regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients. SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. Furthermore, we discovered that miR-30a-3p, a putative ccRCC inhibitor, was competitively sponged by SNHG12. Via the crosstalk network, SNHG12 was capable of up-regulating multiple target genes of miR-30a-3p, namely, RUNX2, WNT2 and IGF-1R, which have been identified to facilitate tumorigenesis of ccRCC. Taken together, our present study suggested a novel ceRNA network, in which SNHG12 could promote the malignancy of ccRCC although competitively binding with miR-30a-3p and consequently release the expression of its downstream cancer-related genes.	NA	J Cell Mol Med. 2021 May;25(10):4696-4708. doi: 10.1111/jcmm.16417. Epub 2021 Mar 30.
3370	LncRNA	SNHG12	miR-30a-3p	WNT2	RCC cells	Renal Cancer	Homo sapiens (human)	qRT-PCR	33787057	SNHG12 promotes carcinogenesis of human renal cell cancer via functioning as a competing endogenous RNA and sponging miR-30a-3p.	Small nucleolar RNA host gene 12 (SNHG12) has been indicated in the tumorigenesis of various human cancers, including clear cell renal cell carcinoma (ccRCC). However, the underlying mechanisms of SNHG12 driving progression of ccRCC remain incompletely understood. In the present study, we discovered that SNHG12 is up-regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients. SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. Furthermore, we discovered that miR-30a-3p, a putative ccRCC inhibitor, was competitively sponged by SNHG12. Via the crosstalk network, SNHG12 was capable of up-regulating multiple target genes of miR-30a-3p, namely, RUNX2, WNT2 and IGF-1R, which have been identified to facilitate tumorigenesis of ccRCC. Taken together, our present study suggested a novel ceRNA network, in which SNHG12 could promote the malignancy of ccRCC although competitively binding with miR-30a-3p and consequently release the expression of its downstream cancer-related genes.	NA	J Cell Mol Med. 2021 May;25(10):4696-4708. doi: 10.1111/jcmm.16417. Epub 2021 Mar 30.
3371	LncRNA	SNHG12	miR-30a-3p	IGF-1R	RCC cells	Renal Cancer	Homo sapiens (human)	qRT-PCR	33787057	SNHG12 promotes carcinogenesis of human renal cell cancer via functioning as a competing endogenous RNA and sponging miR-30a-3p.	Small nucleolar RNA host gene 12 (SNHG12) has been indicated in the tumorigenesis of various human cancers, including clear cell renal cell carcinoma (ccRCC). However, the underlying mechanisms of SNHG12 driving progression of ccRCC remain incompletely understood. In the present study, we discovered that SNHG12 is up-regulated in ccRCC and that overexpression of SNHG12 predicted poor clinical outcome of ccRCC patients. SNHG12 knockdown notably inhibited proliferation and migration of RCC cells. Furthermore, we discovered that miR-30a-3p, a putative ccRCC inhibitor, was competitively sponged by SNHG12. Via the crosstalk network, SNHG12 was capable of up-regulating multiple target genes of miR-30a-3p, namely, RUNX2, WNT2 and IGF-1R, which have been identified to facilitate tumorigenesis of ccRCC. Taken together, our present study suggested a novel ceRNA network, in which SNHG12 could promote the malignancy of ccRCC although competitively binding with miR-30a-3p and consequently release the expression of its downstream cancer-related genes.	NA	J Cell Mol Med. 2021 May;25(10):4696-4708. doi: 10.1111/jcmm.16417. Epub 2021 Mar 30.
3372	LncRNA	SNHG7	miR-34a-5p	XBP1	human retinal microvascular endothelial cells	Diabetic Retinopathy	Homo sapiens (human)	qPCR;Western blot;Flow Cytometry assay;	33600866	MSC-derived exosomal lncRNA SNHG7 suppresses endothelial-mesenchymal transition and tube formation in diabetic retinopathy via miR-34a-5p/XBP1 axis.	AIMS: Diabetic retinopathy (DR) is the most common complication of type 2 diabetes mellitus, which could result in visual impairment. Accumulating studies have shown the implication of long non-coding RNAs (lncRNAs) in the pathogenesis of DR. Our aims are to investigate whether lncRNA SNHG7 plays a role during DR pathogenesis. MAIN METHODS: Human retinal microvascular endothelial cells (HRMECs) were treated with high glucose (HG) to build cell model. Relative expression of RNAs were examined using qPCR, and western blot or immunofluorescence analysis was adopted to detect the protein expression. Cell viability, migration and angiogenic capacity of HRMECs were estimated through CCK-8, transwell and tube formation experiments, respectively. Dual-luciferase reporter and RNA pull down assays were employed to verify the interplay between miR-34a-5p and SNHG7 or XBP1. Mesenchymal stem cells (MSCs) were identified by examining typical surface makers using flow cytometry and the differentiation abilities via Alizarin red, Oil red O and Alcian blue staining. MSC-derived exosomes were verified by transmission electron microscopy and western blot. KEY FINDINGS: LncRNA SNHG7 sponged to and negatively regulated miR-34a-5p. SNHG7 overexpression repressed HG induced endothelial-mesenchymal transition (EndMT) and tube formation of HRMECs, while miR-34a-5p overexpression could reverse this effect. miR-34a-5p targeted and negative regulated XBP1. Knockdown of miR-34a-5p repressed HG induced EndMT and tube formation, which were partially blocked by XBP1 inhibition. MSC-derived exosomes could transfer SNHG7 to HRMECs and modulated EndMT and tube formation. SIGNIFICANCE: The MSC-derived exosomal lncRNA SNHG7 suppresses EndMT and tube formation in HRMECs via miR-34a-5p/XBP1 axis.	NA	Life Sci. 2021 May 1;272:119232. doi: 10.1016/j.lfs.2021.119232. Epub 2021 Feb 16.
3373	LncRNA	TONSL-AS1	miR-197	BCL2	human primary coronary artery endothelial cells	Coronary Artery Disease	Homo sapiens (human)	Cell apoptosis assay;Cell migration assay;	33662410	LncRNA TONSL-AS1 participates in coronary artery disease by interacting with miR-197.	BACKGROUND: It has been reported that high expression levels of miR-197 can predict coronary artery disease (CAD). Our bioinformatics analysis showed that miR-197 may bind to long non-coding RNA (lncRNA) TONSL-AS1. This study aimed to investigate the role of TONSL-AS1 in CAD. METHODS: This study included 60 CAD patients and 60 healthy controls. Coronary angiography was performed to diagnose CAD. The interaction between TONSL-AS1 and miR-197 was predicted by IntaRNA2.0. Western-blot analysis was performed to illustrate the effect of MTONSL-AS1, miR-197 and BCL2 on human primary coronary artery endothelial cells (HCAECs). Cell migration assay was performed to explore the roles of MTONSL-AS1, miR-197 and BCL2 in regulating cell migration. Cell apoptosis assay was performed to investigate the role of MTONSL-AS1, miR-197 and BCL2 in regulating the apoptosis of HCAECs. RESULT: Significant differences in high-density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and gensini score were observed in patients with CAD. In addition, TONSL-AS1 was downregulated in CAD. Follow-up study revealed that low expression levels of TONSL-AS1 and high expression levels of miR-197 predicted poor survival of CAD patients. Overexpression experiments showed that TONSL-AS1 and miR-197 had no significant effect on the expression of each other. We speculated that MAFG-AS1 may sponge miR-145. Moreover, overexpression of TONSL-AS1 increased, while overexpression of miR-197 decreased the expression levels of BCL2. Furthermore, overexpression of TONSL-AS1 attenuated the effects of overexpression of miR-197 on migration and apoptosis of HCAECs. CONCLUSIONS: Therefore, the expression of TONSL-AS1 predicted the survival of CAD patients and it sponged miR-197 to inhibit the apoptosis of HCAECs.	NA	Microvasc Res. 2021 Jul;136:104152. doi: 10.1016/j.mvr.2021.104152. Epub 2021 Mar 1.
3374	LncRNA	TP73-AS1	miR-200a	MMP14	pancreatic cancer cell lines	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33683827	LncRNA TP73-AS1 enhances the malignant properties of pancreatic ductal adenocarcinoma by increasing MMP14 expression through miRNA -200a sponging.	Pancreatic ductal adenocarcinoma (PDAC) is an invasive and aggressive cancer that remains a major threat to human health across the globe. Despite advances in cancer treatments and diagnosis, the prognosis of PDAC patients remains poor. New and more effective PDAC therapies are therefore urgently required. In this study, we identified a novel host factor, namely the LncRNA TP73-AS1, as overexpressed in PDAC tissues compared to adjacent healthy tissue samples. The overexpression of TP-73-AS1 was found to correlate with both PDAC stage and lymph node metastasis. To reveal its role in PDCA, we targeted TP73-AS1 using LnRNA inhibitors in a range of pancreatic cancer (PC) cell lines. We found that the inhibition of TP73-AS1 led to a loss of MMP14 expression in PC cells and significantly inhibited their migratory and invasive capacity. No effects of TP73-AS1 on cell survival or proliferation were observed. Mechanistically, we found that TP73-AS1 suppressed the expression of the known oncogenic miR-200a. Taken together, these data highlight the prognostic potential of TP73-AS1 for PC patients and highlight it as a potential anti-PDAC therapeutic target.	NA	J Cell Mol Med. 2021 Apr;25(7):3654-3664. doi: 10.1111/jcmm.16425. Epub 2021 Mar 8.
3375	Circular RNA	ZNF609	miR-145	STMN1	NPC cells and HUVECs	Nasopharyngeal Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;ELISA;qRT-PCR;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	33943007	CircRNA ZNF609 promotes angiogenesis in nasopharyngeal carcinoma by regulating miR-145/STMN1 axis.	Nasopharyngeal carcinoma (NPC) is the most common type of human malignant tumor in the head and neck, and tumor angiogenesis is essential for its development. Here, we showed that the circRNA ZNF609/microRNA (miR)-145/Stathmin 1 (STMN1) axis regulated angiogenesis in NPC.Circ-ZNF609, miR-145, and STMN1 expression in NPC cells and NPC samples were examined using qRT-PCR. The protein levels of STMN1, VEGFR1, and VEGFR2 were evaluated using western blotting. VEGF level was determined by ELISA. The proliferation of NPC cells and HUVECs was examined using a CCK-8 assay. Transwell assays and wound-healing assays were applied to assess the migration of NPC cells and HUVECs, respectively. Angiogenesis of HUVECs was evaluated by an angiogenesis assay. In addition, a dual-luciferase reporter assay and RNA pull-down assays were employed to verify the binding relationship between circ-ZNF609 and miR-145 as well as between miR-145 and STMN1. Here, we showed that circ-ZNF609 and STMN1 expression was increased, while miR-145 expression was decreased in NPC cells and NPC samples. Circ-ZNF609 may negatively regulate miR-145 expression by acting as a ceRNA. Silencing circ-ZNF609 suppressed cell proliferation, migration, and angiogenesis in NPC, while knockdown of miR-145 reversed these effects. In addition, we found that STMN1 was the downstream target of miR-145. MiR-145 overexpression suppressed cell proliferation, migration, and angiogenesis in NPC, which was abolished by STMN1 overexpression. Our data suggested that circ-ZNF609 promotes cell proliferation, migration, and angiogenesis in NPC by upregulating the expression of STMN1 by sponging miR-145 in NPC.	NA	Kaohsiung J Med Sci. 2021 May 4. doi: 10.1002/kjm2.12381.
3376	LncRNA	AFAP1-AS1	miR-107	PDK4	ovarian cancer tissues	Ovarian Cancer	Homo sapiens (human)	Western blot;	33926489	Long non-coding RNA AFAP1-AS1 facilitates ovarian cancer progression by regulating the miR-107/PDK4 axis.	BACKGROUND: Abnormally expressed in various tumors, long non-coding RNAs (lncRNAs) feature prominently in tumor development, yet little is still known regarding the functional roles of lncRNA AFAP1 antisense RNA 1 (AFAP1-AS1) in ovarian cancer (OC). METHODS: The relative expression levels of lncRNA AFAP1-AS1, microRNA (miR)-107 and pyruvate dehydrogenase kinase isozyme 4 (PDK4) mRNA were assessed by quantitative real-time PCR. PDK4, PCNA and cyclin D1 expression levels were determined using Western blot analysis. Bioinformatics analysis and dual-luciferase gene reporter assay were conducted for identifying and validating the binding sequences between AFAP1-AS1 and miR-107, as well as between miR-107 and PDK4. Cell counting kit-8 assay was employed for detecting cell proliferation. Cell migration and invasion abilities were examined using Transwell assays. RESULTS: The present study revealed that AFAP1-AS1 expression was elevated in OC cells and tissues. AFAP1-AS1 expression and FIGO stage were positively correlated. AFAP1-AS1 knockdown repressed OC cell proliferation, migration and invasion. AFAP1-AS1 functioned as a sponge of miR-107, and miR-107 reversed the effects of AFAP1-AS1 on OC cells. It was validated that miR-107 was able to bind to PDK4, and AFAP1-AS1 regulated PDK4 expression by competitively binding with miR-107. Additionally, miR-107 modulated OC cell proliferation, migration and invasion via targeting PDK4. CONCLUSIONS: LncRNA AFAP1-AS1 serves as a tumor driver in the pathogenesis of OC via the miR-107/PDK4 axis.	NA	J Ovarian Res. 2021 Apr 29;14(1):60. doi: 10.1186/s13048-021-00808-x.
3377	LncRNA	SNHG1	miR-186	FUT8	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;ELISA;qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33872442	SNHG1/miR-186/FUT8 regulates cell migration and invasion in oral squamous cell carcinoma.	Recently, lncRNAs are associated with the progression and development of various cancers. We aimed to explore the effects of lncRNA SNHG1 on the proliferation, apoptosis, migration, and invasion of oral squamous cell carcinoma (OSCC) cells. Quantitative real-time PCR (RT-qPCR) was used for measurement of SNHG1 in OSCC cells. Cell proliferation, apoptosis, migration, and invasion were detected by CCK-8 assay, flow cytometry, Cell Death Detection ELISA PLUS kit, and transwell assays. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were used to clarify the relationship between SNHG1 and miR-186. SNHG1 was overexpressed in OSCC cells. SNHG1 silencing prevented cell proliferation and increased the incidence of apoptosis, DNA fragments, cleaved-caspase 3, and Bax protein levels. Cell migration and invasion were reduced after SNHG1 deletion, and MMP2 and MMP9 protein levels were decreased. SNHG1 overexpression promoted cell survival, migration, and invasion, reduced DNA fragments formation. Mechanistically, we demonstrated that SNHG1 could directly bind to miR-186 and positively regulated α1, 6-fucosyltransferase (FUT8) level. Functional investigation showed that miR-186 depletion reversed the roles of SNHG1 silencing in cell proliferation, apoptosis, and migration. Taken together, our findings illuminated that SNHG1 regulated cell proliferation, migration, and invasion by sponging miR-186 to depress FUT8 expression.	NA	Oral Dis. 2021 Apr 19. doi: 10.1111/odi.13878.
3378	LncRNA	EPB41L4A-AS2	miR-107	YBX1	NPC tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down;	34131399	LncRNA EPB41L4A-AS2 represses Nasopharyngeal Carcinoma Metastasis by binding to YBX1 in the Nucleus and Sponging MiR-107 in the Cytoplasm.	Nasopharyngeal carcinoma (NPC) is known for its potential to progress to the lymph nodes and distant metastases at an early stage. As an important regulator in tumorigenesis biological processes, the functions of lncRNA in NPC tumor development remain largely unclear. In this research, the expression of EPB41L4A-AS2 in NPC tissues and cells was analyzed via real-time quantitative polymerase chain reaction (qRT-PCR). CCK8, colony formation, and EDU experiments were used to determine the viability of NPC cells. Transwell and wound healing assays were performed to test NPC cell migration and invasion. RNA pull-down and mass spectrometry analysis were used to identify potential binding proteins. Then, a popliteal lymph node metastasis model was established to test NPC metastasis. EPB41L4A-AS2 is repressed by transforming growth factor-beta, which is downregulated in NPC cells and tissue. It is associated with the presence of distant metastasis and adverse outcomes. The univariate and multivariate survival assays confirmed that EPB41L4A-AS2 expression was an independent predictor of progression-free survival (PFS) in patients with NPC. Biological analyses showed that overexpression of EPB41L4A-AS2 reduced the metastasis and invasion of NPC in vitro and in vivo, but had no significant effect on cell proliferation. Mechanistically, in the nucleus we identified that EPB41L4A-AS2 relies on binding to YBX1 to reduce the stability of Snail mRNA to enhance the expression of E-cadherin and reverse the progression of epithelial-to-mesenchymal transition (EMT). In the cytoplasm, we found that EPB41L4A-AS2 blocked the invasion and migration of NPC cells by promoting LATS2 expression via sponging miR-107. In a whole, the findings of this study help to further understand the metastasis mechanism of NPC and could help in the prevention and treatment of NPC metastasis.	NA	Int J Biol Sci. 2021 May 11;17(8):1963-1978. doi: 10.7150/ijbs.55557. eCollection 2021.
3379	Circular RNA	Circ_0072083	miR-1252-5p	NANGO	glioma tissues and cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33975615	Warburg effect-promoted exosomal circ_0072083 releasing up-regulates NANGO expression through multiple pathways and enhances temozolomide resistance in glioma.	BACKGROUND: Temozolomide (TMZ) resistance limits its application in glioma. Exosome can carry circular RNAs (circRNAs) to regulate drug resistance via sponging microRNAs (miRNAs). miRNAs can control mRNA expression by regulate the interaction with 3'UTR and methylation. Nanog homeobox (NANOG) is an important biomarker for TMZ resistance. Hitherto, it is unknown about the role of exosomal hsa_circ_0072083 (circ_0072083) in TMZ resistance in glioma, and whether it is associated with NANOG via regulating miRNA sponge and methylation. METHODS: TMZ-resistant (n = 36) and sensitive (n = 33) patients were recruited. The sensitive cells and constructed resistant cells were cultured and exposed to TMZ. circ_0072083, miR-1252-5p, AlkB homolog H5 (ALKBH5) and NANOG levels were examined via quantitative reverse transcription polymerase chain reaction and western blot. The half maximal inhibitory concentration (IC50) of TMZ, cell proliferation, apoptosis, migration and invasion were analyzed via Cell Counting Kit-8, colony formation, flow cytometry, wound healing and transwell assays. The in vivo function was assessed using xenograft model. The N6-methyladenosine (m6A) level was analyzed via methylated RNA immunoprecipitation (MeRIP). Target relationship was investigated via dual-luciferase reporter assay and RNA immunoprecipitation. Warburg effect was investigated via lactate production, glucose uptake and key enzymes expression. Exosome was isolated and confirmed via transmission electron microscopy and specific protein expression. RESULTS: circ_0072083 expression was increased in TMZ-resistant glioma tissues and cells. circ_0072083 knockdown restrained the resistance of resistant cells via decreasing IC50 of TMZ, proliferation, migration, invasion and xenograft tumor growth and increasing apoptosis. circ_0072083 silence reduced NANOG expression via blocking ALKBH5-mediated demethylation. circ_0072083 could regulate NANOG and ALKBH5 via targeting miR-1252-5p to control TMZ resistance. Warburg effect promoted the release of exosomal circ_0072083 in resistant cells. Exosomal circ_0072083 from resistant cells increased the resistance of sensitive cells to TMZ in vitro and xenograft model. Exosomal circ_0072083 level was enhanced in resistant patients, and it had a diagnostic value and indicated a lower overall survival in glioma. CONCLUSION: Exosomal circ_0072083 promoted TMZ resistance via increasing NANOG via regulating miR-1252-5p-mediated degradation and demethylation in glioma.	NA	J Exp Clin Cancer Res. 2021 May 11;40(1):164. doi: 10.1186/s13046-021-01942-6.
3380	LncRNA	XIST	miR-98-5p	EDEM1	hippocampal neuronal cells	Inflammatory Injury	Homo sapiens (human)	qRT-PCR	34094712	lncRNA Xist regulates sevoflurane-induced social and emotional impairment by modulating miR-98-5p/EDEM1 signaling axis in neonatal mice.	Long non-coding RNA (lncRNA) X-inactive specific transcript (Xist) is involved in apoptosis and inflammatory injury. This study aimed to assess the role of lncRNA Xist in sevoflurane-induced social and emotional impairment and neuronal apoptosis in neonatal mice and hippocampal neuronal cells. The performance in social and emotional tests and the expression levels of lncRNA Xist and microRNA (miR)-98-5p after sevoflurane exposure were measured. Moreover, the effects of suppression of lncRNA Xist on neuronal apoptosis and endoplasmic reticulum (ER) stress were determined. Subsequently, the association among lncRNA Xist, miR-98-5p, and ER degradation-enhancing α-mannosidase-like 1 protein (EDEM1) was explored. Our results showed that lncRNA Xist increased, miR-98-5p decreased, and social and emotional impairment appeared after sevoflurane exposure. Furthermore, suppression of lncRNA Xist improved sevoflurane-induced social and emotional impairment and reduced sevoflurane-induced neuronal apoptosis and ER stress in vivo and in vitro. Moreover, lncRNA Xist negatively regulated miR-98-5p expression, and it contributed to sevoflurane-induced neuronal apoptosis and ER stress by sponging miR-98-5p. Additionally, EDEM1 was identified as a target of miR-98-5p. Our findings revealed that the knockdown of lncRNA Xist ameliorates sevoflurane-induced social and emotional impairment through inhibiting neuronal apoptosis and ER stress by targeting the miR-98-5p/EDEM1 axis.	NA	Mol Ther Nucleic Acids. 2021 Apr 16;24:939-950. doi: 10.1016/j.omtn.2021.04.010. eCollection 2021 Jun 4.
3381	LncRNA	LINC01194	miR-486-5p	GOLPH3	PCa cells	Prostate Cancer	Homo sapiens (human)	ChIP;RT-PCR;Western blot;Chromatin immunoprecipitation;luciferase assay;	33829439	PAX5-induced upregulation of LINC01194 exerts oncogenic properties by regulating GOLPH3 expression via miR-486-5p in prostate cancer.	OBJECTIVE: Several studies have demonstrated that long non-coding RNA can act as crucial roles during the progression of various tumors, including prostate cancer (PCa). We aimed to determine lncRNA LINC01194(LINC01194) expression in prostate cancer (PCa) and examine its influence on tumor behaviors of PCa cells. PATIENTS AND METHODS: RT-PCR was performed to examine LINC01194 and PAX5's expression levels in PCa tissues and cell lines. Luciferase reporter and chromatin immunoprecipitation (ChIP) assays were performed to explore whether PAX5 could activate the transcription of LINC01194. Cell viability, migration and invasion were assessed by CCK-8, colony formation, transwell assay and Wound-healing assays. Bioinformatics and Dual-Luciferase assays were used to investigate the interaction between LINC01194 and miR-486-5p, as well as between miR-486-5p and GOLPH3. Western blot was applied for detecting the expressions of the related proteins. RESULTS: LINC01194 was highly expressed in PCa specimens and cell lines. PAX5 could bind directly to LINC01194 promoter region and activate its transcription. Functionally, the proliferation and metastasis of PCa cells were substantially impeded by LINC01194 silencing in vitro and in vivo. Mechanistically, LINC01194 promoted PCa progression by serving as a sponge of miR-486-5p to increase GOLPH3 expression. CONCLUSIONS: Our study identifies LINC01194 as a tumor promotor in PCa and implicates the LINC01194/miR-486-5p/GOLPH3 axis in the PCa progression.	NA	Eur Rev Med Pharmacol Sci. 2021 Mar;25(6):2528-2541. doi: 10.26355/eurrev_202103_25416.
3382	LncRNA	PCAT1	miR-508-3p	NFIB	DLBCL cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33829443	LncRNA PCAT1 enhances cell proliferation, migration and invasion by miR-508-3p/NFIB axis in diffuse large B-cell lymphoma.	OBJECTIVE: In previous studies, PCAT1 has been proved to be a key carcinogenic driver in hepatocellular carcinoma. However, the regulatory mechanism of PCAT1 remains poorly understood in diffuse large B-cell lymphoma (DLBCL). PATIENTS AND METHODS: The expression of PCAT1, miR-508-3p and NFIB in DLBCL was detected by RT-qPCR assay. CCK-8 assay and transwell assay were used to measure cell proliferation, migration and invasion of DLBCL cells. Western blot assay was used to explore the protein expression of NFIB. Dual-Luciferase reporter assay was applied to measure the correlation between PCAT1, miR-508-3p and NFIB. RESULTS: PCAT1 was demonstrated to be upregulated in DLBCL tissues and cell lines. Besides, PCAT1 expression was associated with clinical stage and IPI score of DLBCL patients. Moreover, overexpression of PCAT1 promoted DLBCL cell proliferation, migration and invasion in vitro. Mechanistic investigation displayed that PCAT1 interplayed with miR-508-3p, while NFIB was a target gene of miR-508-3p. Further, miR-508-3p was in a downtrend while NFIB was increased in DLBCL tissues and cell lines. MiR-508-3p overexpression repressed DLBCL cell growth and metastasis, while PCAT1 overexpression reversed the inhibitory effect of miR-508-3p on the progression of DLBCL. Moreover, NFIB silencing suppressed DLBCL cell proliferation, migration and invasion, whereas PCAT1 vector or miR-508-3p knockdown destroyed the inhibitory of si-NFIB on the progression of DLBCL. CONCLUSIONS: Taken together, our findings validated that PCAT1 acted as completive endogenous RNA by sponging miR-508-3p and upregulating NFIB to facilitate DLBCL cell proliferation, migration and invasion.	NA	Eur Rev Med Pharmacol Sci. 2021 Mar;25(6):2567-2576. doi: 10.26355/eurrev_202103_25420.
3383	LncRNA	AFAP1-AS1	miR-15b	IGF1R	castration-resistant C4-2 cells	Prostate Cancer	Homo sapiens (human)	qPCR;	34126893	Long non-coding RNA AFAP1-AS1 facilitates prostate cancer progression by regulating miR-15b/IGF1R axis.	BACKGROUND: Prostate cancer (PCa) is a commonly diagnosed malignant cancer and is the second highest cause of cancer related death in men worldwide. Enzalutamide is the second-generation inhibitor of androgen receptor signaling and is the fundamental drug for the treatment of advanced PCa. However, the disease will eventually progress to metastatic castration-resistant prostate cancer (CRPC) and aggressive neuroendocrine prostate cancer (NEPC) because of androgen-deprivation therapy (ADT) resistance. The aim of the study was to investigate the role of long non-coding RNA (lncRNA) AFAP1-AS1 in ADT resistance. METHODS: Quantitative real-time PCR analysis (qPCR) was used to assess the expression of AFAP1-AS1 in PCa cell lines and tissues. Cell proliferation and invasion were assessed after AFAP1-AS1 knockdown using Cell Counting Kit (CCK)-8 and Transwell assay, respectively. A dual-luciferase reporter gene assay was carried out to validate the regulatory relationship among AFAP1-AS1, microRNA (miR)-15b, and insulin-like growth factor1 receptor (IGF1R). RESULTS: AFAP1-AS1 level was markedly increased in castration-resistant C4-2 cells and NE-like cells (PC3, DU145, and NCI-H660), compared with androgen-sensitive LNCaP cells. Enzalutamide treatment increased the expression of AFAP1-AS1 in vitro and in vivo. Functionally, AFAP1-AS1 knockdown repressed tumor cell proliferation and invasion. Mechanistically, AFAP1-AS1 functioned as an oncogene in PCa through binding to miR-15b and destroying its tumor suppressor function. Finally, we identified that AFAP1-AS1 up-regulated IGF1R expression by competitively binding to miR-15b to de-repress IGF1R. CONCLUSION: AFAP1-AS1 facilitates PCa progression by regulating miR-15b/IGF1R axis, indicating that AFAP1-AS1 may serve as a diagnostic biomarker and therapeutic target for PCa.	NA	Curr Pharm Des. 2021 Jun 11. doi: 10.2174/1381612827666210612052317.
3384	LncRNA	PVT1	miR-26a	KLF4	vascular smooth muscle cells	Abdominal Aortic Aneurysm Pyroptosis	Homo sapiens (human)	qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34141179	Curcumin nicotinate suppresses abdominal aortic aneurysm pyroptosis via lncRNA PVT1/miR-26a/KLF4 axis through regulating the PI3K/AKT signaling pathway.	Abdominal aortic aneurysm (AAA) is a chronic dilated disease of the aorta that is characterized by chronic inflammation. Curcumin (Cur) is previously showed to attenuate AAA by inhibiting inflammatory response in ApoE -/- mice. Since Cur has the limitations of aqueous solubility and instability. Here, we focus on the role of curcumin nicotinate (CurTn), a Cur derivative is derived from Cur and nicotinate. An in vitro model of AAA was established by treating vascular smooth muscle cells (VSMCs) with II (Ang-II). Gene and protein expressions were examined by quantitative real-time PCR (qPCR) or western blotting. Cell migration and pyroptosis were determined by transwell assay and flow cytometry. The interaction between plasmacytoma variant translocation 1 (PVT1), miR-26a and krüppel-like factor 4 (KLF4) was predicted by online prediction tool and confirmed by luciferase reporter assay. CurTn reduced Ang-II-induced AAA-associated proteins, inflammatory cytokine expressions, and attenuated pyroptosis in VSMCs. PVT1 overexpression suppressed the inhibitory effect of CurTn on AngII-induced pyroptosis and inflammatory in VSMCs by sponging miR-26a. miR-26a directly targeted KLF4 and suppressed its expression, which eventually led to the deactivation of the PI3K/AKT signaling pathway. Besides, the regulatory effect of CurTn on pyroptosis of VSMCs induced by Ang-II was reversed through the PVT1/miR-26a/KLF4 pathway. In short, CurTn suppressed VSMCs pyroptosis and inflammation though mediation PVT1/miR-26a/KLF4 axis by regulating the PI3K/AKT signaling pathway, CurTn might consider as a potential therapeutic target in the treatment of AAA.	NA	Toxicol Res (Camb). 2021 Jun 1;10(3):651-661. doi: 10.1093/toxres/tfab041. eCollection 2021 May.
3385	LncRNA	PVT1	miR-590-5p	FSTL1	airway smooth muscle cells	Asthma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Immunoblotting;Luciferase reporter assay;	33825599	The lncRNA PVT1/miR-590-5p/FSTL1 axis modulates the proliferation and migration of airway smooth muscle cells in asthma.	OBJECTIVE: Asthma is a prevalent chronic inflammatory airway disease that is characterised by airway remodelling and airway hyperresponsiveness. Abnormal proliferation and migration of airway smooth muscle cells (ASMCs) contribute to airway remodelling in asthma. However, the molecular mechanism underlying an increased ASMC mass in asthma remains elusive. Herein, we aimed at investigating the regulation of lncRNA PVT1 on ASMCs and focussing on the mechanism in the proliferation and migration. METHODS: Expression levels of lncRNA PVT1 and miR-590-5p in the serum collected from 24 children with asthma and 10 control children were determined by qRT-PCR. ASMCs proliferation and migration prior to and post platelet-derived growth factor subunit B (PDGF-BB) stimulation were examined by CCK-8 test and transwell assay. Dual-luciferase reporter assay was performed to determine miR-590-5p interaction with lncRNA PVT1 and follistatin-like 1 (FSTL1). Expression of lncRNA PVT1, miR-590-5p, FSTL1, C-Myc, cyclin D1, and cyclin-dependent kinase 1 (CDK1) was tested by quantitative real-time PCR (qRT-PCR) and immunoblotting analysis. RESULTS: The expression level of lncRNA PVT1 was higher but the expression level of miR-590-5p was lower in the serum of children with asthma than in control children. The expression level of lncRNA PVT1 was negatively correlated with the expression level of miR-590-5p in asthma. LncRNA PVT1 was upregulated upon PDGF-BB stimulation. LncRNA PVT1 knockdown by its specific shRNA repressed PDGF-BB-induced promotion of proliferation and migration in ASMCs and triggered an elevated miR-590-5p along with declined C-Myc, cyclin D1, and CDK1. The effects of lncRNA PVT1 knockdown on PDGF-BB-induced ASMCs were lost upon miR-590-5p inhibition. MiR-590-5p targeted FSTL1 gene and declined its expression, thus suppressing ASMC proliferation and migration following PDGF-BB stimulation and downregulating C-Myc, cyclin D1, and CDK1 expressions. The effects of miR-590-5p on PDGF-BB-induced ASMCs were lost upon FSTL1 overexpression. CONCLUSION: These results support the notion that the lncRNA PVT1/miR-590-5p/FSTL1 axis modulates ASMCs proliferation and migration following PDGF-BB stimulation, providing a potential therapeutic target to attenuate airway remodelling in asthma.	NA	Autoimmunity. 2021 May;54(3):138-147. doi: 10.1080/08916934.2021.1897977. Epub 2021 Apr 7.
3386	LncRNA	DLEU2L	miR-210-3p	BRCA2	Pancreatic Cancer Cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33968986	Long Non-coding RNA DLEU2L Targets miR-210-3p to Suppress Gemcitabine Resistance in Pancreatic Cancer Cells via BRCA2 Regulation.	Gemcitabine (GEM) resistance remains a challenging clinical issue to overcome in chemotherapy against pancreatic cancer. We previously demonstrated that miR-210 derived from pancreatic cancer stem cells enhanced the GEM-resistant properties of pancreatic cancer cells, thus identifying miR-210 as an oncogenic miRNA. Herein, we report the existence of an upstream effector that acts as a competing endogenous RNA (ceRNA) to miR-210. Bioinformatic screening was performed to identify lncRNAs with a binding relationship to miR-210. Overexpression and interference vectors were constructed to demonstrate the effect of ceRNA activity in pancreatic cell behavior, both in vitro and in vivo. DLEU2L (deleted in lymphocytic leukemia 2-like), which is expressed at low levels in pancreatic cancer tissues, was shown to exhibit a binding relationship with miR-210-3p. Overexpression of DLEU2L and silencing of miR-210-3p suppressed the proliferation, migration, and invasion of pancreatic cancer cells while promoting apoptosis. These effects occurred via the inhibition of the Warburg effect (aerobic glycolysis) and AKT/mTOR signaling. In addition, we showed that BRCA2 is a target gene of miR-210-3p, and the downregulation of miR-210-3p by DLEU2L effectively induced an upregulation of BRCA2 via the ceRNA mechanism. In vivo, DLEU2L overexpression and miR-210-3p interference suppressed pancreatic tumor progression, consistent with the results of in vitro studies. The findings of our study establish DLEU2L as a ceRNA to miR-210-3p and reveal the critical role of the DLEU2L/miR-210-3p crosstalk in targeting GEM resistance.	NA	Front Mol Biosci. 2021 Apr 22;8:645365. doi: 10.3389/fmolb.2021.645365. eCollection 2021.
3387	LncRNA	CCDC26	miR-422a	EZH2	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	CCK-8 assay;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34007185	Long Noncoding RNA CCDC26 Promotes Thyroid Cancer Malignant Progression via miR-422a/EZH2/Sirt6 Axis.	PURPOSE: Long noncoding RNAs are crucial regulators in thyroid cancer progression. However, the role of lncRNA CCDC26 in thyroid cancer remains unclear. Here, we aimed to explore the effect of CCDC26 on thyroid cancer progression and the underlying mechanism. MATERIALS AND METHODS: A total of 50 clinical thyroid cancer samples were studied in patients' samples, cultured cells, and nude mice before and after treatment using quantitative reverse transcription-PCR, CCK-8 assays, BrdU incorporation assays, Transwell assays, cell apoptosis analysis, luciferase reporter gene assay, RNA immunoprecipitation, Western blot analysis, and tumorigenicity analysis. RESULTS: CCDC26 expression was elevated in patients' thyroid cancer tissues and thyroid cancer cell lines. CCDC26 depletion remarkably reduced proliferation, invasion, and migration but induced apoptosis of thyroid cancer cells. Mechanically, miR-422a mimic remarkably reduced the luciferase activity of CCDC26 transfected cells but failed to affect cells transfected with CCDC26 containing the mutated miR-422a-binding site. RNA immunoprecipitation (RIP) assays showed that CCDC26 and miR-422a preferentially interacted with Ago2, but not IgG, in the micro-ribonucleoprotein complexes (miRNPs). CCDC26 depletion enhanced miR-422a expression and MiR-422a inhibitor reversed CCDC26 knockdown-induced inhibition of thyroid cancer progression in vitro. CCDC26 upregulated EZH2 and Sirt6 expression by sponging miR-422a in thyroid cancer cells. Tumorigenicity analysis in nude mice revealed that CCDC26 contributed to thyroid tumor growth via miR-422a/EZH2/Sirt6 axis in vivo. CONCLUSION: CCDC26 promotes thyroid cancer malignant progression via miR-422a/EZH2/Sirt6 axis. This finding provides new insights into the mechanism by which CCDC26 promotes malignant thyroid cancer development, advances our understanding of lncRNAs' association with thyroid cancer, and indicates that CCDC26 and miR-422a may serve as potential targets for thyroid cancer.	NA	Onco Targets Ther. 2021 May 11;14:3083-3094. doi: 10.2147/OTT.S282011. eCollection 2021.
3388	LncRNA	CCDC26	miR-422a	SIRT6	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	CCK-8 assay;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34007185	Long Noncoding RNA CCDC26 Promotes Thyroid Cancer Malignant Progression via miR-422a/EZH2/Sirt6 Axis.	PURPOSE: Long noncoding RNAs are crucial regulators in thyroid cancer progression. However, the role of lncRNA CCDC26 in thyroid cancer remains unclear. Here, we aimed to explore the effect of CCDC26 on thyroid cancer progression and the underlying mechanism. MATERIALS AND METHODS: A total of 50 clinical thyroid cancer samples were studied in patients' samples, cultured cells, and nude mice before and after treatment using quantitative reverse transcription-PCR, CCK-8 assays, BrdU incorporation assays, Transwell assays, cell apoptosis analysis, luciferase reporter gene assay, RNA immunoprecipitation, Western blot analysis, and tumorigenicity analysis. RESULTS: CCDC26 expression was elevated in patients' thyroid cancer tissues and thyroid cancer cell lines. CCDC26 depletion remarkably reduced proliferation, invasion, and migration but induced apoptosis of thyroid cancer cells. Mechanically, miR-422a mimic remarkably reduced the luciferase activity of CCDC26 transfected cells but failed to affect cells transfected with CCDC26 containing the mutated miR-422a-binding site. RNA immunoprecipitation (RIP) assays showed that CCDC26 and miR-422a preferentially interacted with Ago2, but not IgG, in the micro-ribonucleoprotein complexes (miRNPs). CCDC26 depletion enhanced miR-422a expression and MiR-422a inhibitor reversed CCDC26 knockdown-induced inhibition of thyroid cancer progression in vitro. CCDC26 upregulated EZH2 and Sirt6 expression by sponging miR-422a in thyroid cancer cells. Tumorigenicity analysis in nude mice revealed that CCDC26 contributed to thyroid tumor growth via miR-422a/EZH2/Sirt6 axis in vivo. CONCLUSION: CCDC26 promotes thyroid cancer malignant progression via miR-422a/EZH2/Sirt6 axis. This finding provides new insights into the mechanism by which CCDC26 promotes malignant thyroid cancer development, advances our understanding of lncRNAs' association with thyroid cancer, and indicates that CCDC26 and miR-422a may serve as potential targets for thyroid cancer.	NA	Onco Targets Ther. 2021 May 11;14:3083-3094. doi: 10.2147/OTT.S282011. eCollection 2021.
3389	LncRNA	TDRG1	miR-214-5p	CLIC4	BC cell 	Breast Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	33822672	Long non-coding RNA TDRG1 facilitates cell proliferation, migration and invasion in breast cancer via targeting miR-214-5p/CLIC4 axis.	Accumulated studies have revealed the critical role of long non-coding RNAs (lncRNAs) in the carcinogenesis and progression of various cancers. LncRNA TDRG1 has been reported to exhibit oncogenic potential in some cancers. However, its underlying mechanism regulating breast cancer (BC) remains obscure. QRT-PCR was used to measure the relative expression of mRNAs, and western blot was used to detect protein expression levels. CCK8 and CFSE assays were utilized to testify cell proliferation ability. Flow cytometry assay was used for cell apoptosis ability investigation. Transwell and tube formation assays were implemented to test cell migrating and invasive abilities. Relevant mechanism experiments were implemented to determine the molecular mechanism. TDRG1 was remarkably overexpressed in BC cell lines. TDRG1 knockdown suppressed cell proliferation, migration and invasion, but enhanced BC cell apoptosis. Mechanistically, TDRG1 acted as a miR-214-5p sponge to up-regulate CLIC4 expression. MiR-214-5p inhibition or CLIC4 overexpression could revive the tumor-suppressing effects induced by TDRG1 knockdown. TDRG1 promoted cell proliferation, migration, and invasion in BC, suggesting that TDRG1 could promisingly be a therapeutic target for BC.	NA	Cancer Biol Ther. 2021 Mar 4;22(3):248-256. doi: 10.1080/15384047.2020.1863120. Epub 2021 Apr 6.
3390	Circular RNA	Circ_NRIP1	miR-595	SEMA4D	ESCC tissues and cells	Esophageal Squamous Cancer (Escc)	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33957921	circ_NRIP1 is oncogenic in malignant development of esophageal squamous cell carcinoma (ESCC) via miR-595/SEMA4D axis and PI3K/AKT pathway.	BACKGROUND: The hsa_circ_0004771 derived from NRIP1 (called circ_NRIP1) is a recently identified oncogenic circRNA. Here, we intended to investigate the role and mechanism of circ_NRIP1 in esophageal squamous cell carcinoma (ESCC), a prevalent and aggressive type of esophageal cancer. METHODS: Expression of circ_NRIP1, miRNA-595-5p (miR-595) and semaphorin 4D (SEMA4D) was detected by RT-qPCR and western blotting. Cell growth was assessed by colony formation assay, MTS assay, flow cytometry, and xenograft experiment; migration and invasion were evaluated by transwell assay and western blotting. Dual-luciferase reporter assay identified the relationship among circ_NRIP1, miR-595 and SEMA4D. Western blotting measured phosphatidylinositol-3-hydroxykinase (PI3K)/AKT pathway-related proteins. RESULTS: Expression of circ_NRIP1 was upregulated in ESCC tissues and cells. Knockdown of circ_NRIP1 could enhance apoptosis rate and E-cadherin expression, but suppress colony formation, cell viability, migration, invasion, and snail expression in KYSE30 and KYSE450 cells, as well as retarded tumor growth in mice. The suppressive role of circ_NRIP1 knockdown in cell growth, migration and invasion in vitro was abated by blocking miR-595; meanwhile, miR-595 overexpression elicited similar anti-tumor role in KYSE30 and KYSE450 cells, which was abrogated by restoring SEMA4D. Notably, circ_NRIP1 was a sponge for miR-595, and SEMA4D was a target of miR-595. Besides, PI3K/AKT signal was inhibited by circ_NRIP1 knockdown and/or miR-595 overexpression via indirectly or directly regulating SEMA4D. CONCLUSION: circ_NRIP1 functioned as an oncogene in ESCC, and modulated ESCC cell growth, migration and invasion both in vitro and in vivo via targeting miR-595/SEMA4D axis and inhibiting PI3K/AKT signaling pathway.	NA	Cancer Cell Int. 2021 May 6;21(1):250. doi: 10.1186/s12935-021-01907-x.
3391	LncRNA	TRERNA1	miR-22-3p	NRAS	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA sequencing;	33839325	TRERNA1 upregulation mediated by HBx promotes sorafenib resistance and cell proliferation in HCC via targeting NRAS by sponging miR-22-3p.	Hepatocellular carcinoma (HCC) is among the most common malignancies and has an unfavorable prognosis. The hepatitis B virus-encoded X (HBx) protein is closely associated with hepatocarcinogenesis. Sorafenib is a unique targeted oral kinase inhibitor for advanced HCC. Long noncoding RNAs (lncRNAs) mediate HCC progression and therapeutic resistance by acting as competing endogenous RNAs (ceRNAs). However, the ceRNA regulatory mechanisms underlying sorafenib resistance in HBx-associated HCC remain largely unknown. In this study, we found that translation regulatory lncRNA 1 (TRERNA1) upregulation by HBx not only promoted HCC cell proliferation by regulating the cell cycle in vitro and in vivo but also correlated positively with poor prognosis in HCC. Importantly, TRERNA1 enhanced sorafenib resistance in HCC cells. RNA sequencing (RNA-seq) analysis indicated that NRAS proto-oncogene (NRAS) is a potential target of TRERNA1 that mediates aspects of hepatocellular carcinogenesis. TRERNA1 acts as a ceRNA to regulate NRAS expression by sponging microRNA (miR)-22-3p. In summary, we show that increased TRERNA1 expression induced by HBx reduces HCC cell sensitivity to sorafenib by activating the RAS/Raf/MEK/ERK signaling pathway. We reveal a novel regulatory mode by which the TRERNA1/miR-22-3p/NRAS axis mediates HCC progression and indicates that TRERNA1 might constitute a powerful tumor biomarker and therapeutic target in HCC.	NA	Mol Ther. 2021 Apr 9:S1525-0016(21)00198-2. doi: 10.1016/j.ymthe.2021.04.011.
3392	Circular RNA	Circ_0055625	miR-338-3p	MSI1	colon cancer tissues and cells	Colon Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33882945	Circ_0055625 knockdown inhibits tumorigenesis and improves radiosensitivity by regulating miR-338-3p/MSI1 axis in colon cancer.	BACKGROUND: Radiotherapy is a main therapeutic method for cancers, including colon cancer. In the current study, we aim to explore the effects of circular RNA (circRNA) circ_0055625 in the progression and radiosensitivity of colon cancer and the underlying mechanism. METHODS: The expression of circ_0055625 and musashi homolog 1 (MSI1) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). MSI1 protein expression was determined by Western blot. Cell proliferation was assessed by cell counting kit-8 (CCK-8) and colony formation assays. Cell survival fraction, apoptosis, and invasion were investigated by colony formation assay, flow cytometry analysis, and transwell invasion assay, respectively. Cell migration was detected by wound-healing and transwell migration assays. The binding relationship between microRNA-338-3p (miR-338-3p) and circ_0055625 or MSI1 was predicted by online databases and identified by Dual-Luciferase Reporter Assay. The effects of circ_0055625 silencing on the tumor formation and radiosensitivity of colon cancer in vivo were explored by in vivo tumor formation assay. RESULTS: Circ_0055625 and MSI1 were upregulated in colon cancer tissues and cells relative to control groups. Radiation treatment apparently increased the expression of circ_0055625 and MSI1 in colon cancer cells. Circ_0055625 knockdown or MSI1 silencing repressed cell proliferation, migration, and invasion and promoted cell apoptosis and radiosensitivity in colon cancer. Also, circ_0055625 silencing-mediated effects were attenuated by MSI1 overexpression. Additionally, circ_0055625 silencing reduced MSI1 expression, which could be attenuated by miR-338-3p inhibitor. Mechanically, circ_0055625 acted as a sponge for miR-338-3p to regulate MSI1. Furthermore, circ_0055625 knockdown hindered tumor growth and improved radiosensitivity in vivo. CONCLUSION: Circ_0055625 repression inhibited the progression and radioresistance of colon cancer by downregulating MSI1 through sponging miR-338-3p. This result might provide a theoretical basis for improving the therapy of colon cancer with radiation.	NA	World J Surg Oncol. 2021 Apr 21;19(1):131. doi: 10.1186/s12957-021-02234-1.
3393	LncRNA	cCSC1	miR-124-3p	CD44	CRC cell lines	Colorectal Cancer	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;	33887588	LncRNA-cCSC1 promotes cell proliferation of colorectal cancer through sponging miR-124-3p and upregulating CD44.	LncRNA-cCSC1 is highly expressed in colorectal cancer (CRC). The study was designed to evaluate the function and mechanism of lncRNA-cCSC1 in cell proliferation of CRC. RT-PCR was used to measure the expression levels of lncRNA-cCSC1 in CRC cell lines. CCK-8, colony formation, EdU staining, flow cytometry and Western blot were performed to examine the effect of interference with lncRNA-cCSC1 expression on cell proliferation. miR-124-3p and the target genes of miR-124-3p were investigated using bioinformatics analysis and verified by dual-luciferase reporter, RT-PCR and Western blot. Rescue experiments were carried out to confirm the role of miR-124-3p in cell proliferation of CRC. Our results showed that cell proliferation of CRC was promoted by lncRNA-cCSC1 upregulation and inhibited by lncRNA-cCSC1 downregulation. In addition, miR-124-3p is predicted to be the target of lncRNA-cCSC1 and is negatively correlated with lncRNA-cCSC1. Moreover, the addition of miR-124-3p mimics or inhibitor reversed the effects induced by lncRNA-cCSC1 overexpression or silencing on cell proliferation of CRC. Additionally, lncRNA-cCSC1 regulated the expression level of CD44, a target gene of miR-124-3p. Finally, we studied the effects of the lncRNA-cCSC1/miR-124-3p axis on CD44. These results indicate that lncRNA-cCSC1 promotes cell proliferation of CRC through sponging miR-124-3p and upregulating CD44.	NA	Biochem Biophys Res Commun. 2021 Jun 11;557:228-235. doi: 10.1016/j.bbrc.2021.04.018. Epub 2021 Apr 19.
3394	LncRNA	EWSAT1	miR-330-5p	ITGA5	NSCLC tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;	33928467	LncRNA EWSAT1 Regulates the Tumorigenesis of NSCLC as a ceRNA by Modulating miR-330-5p/ITGA5 Axis.	The aim of the study is to investigate how lncRNA EWSAT1 regulates the tumorigenesis of non-small cell lung cancer (NSCLC) as a ceRNA by modulating miR-330-5p/ITGA5 axis. qRT-PCR was conducted to evaluate the expression of EWSAT1 in NSCLC tissue. Then, A549 cells were selected and divided into Blank shScramble, shEWSAT1, miR-330-5p inhibitor, shEWSAT1 + miR-330-5p inhibitor, and siITGA5 and miR-330-5p inhibitor + siITGA5 groups. Besides, a series of in-vitro experiments were carried out to determine the changes in cell proliferation, apoptosis, invasion, and migration in each group. In addition, xenograft models were also constructed on nude mice to detect the tumor volume and weight, and the expression of Ki67 and apoptosis in xenograft tumor were evaluated. In NSCLC tissue and cell, EWSAT1 was upregulated significantly, demonstrating a correlation with tumor diameter, differentiation, lymph node metastasis, and TNM stage. Dual luciferase reporter gene assay confirmed targeting relationships among miR-330-5p, EWSAT1, and ITGA5. In comparison with the Blank group, the number of cell clones in the shEWSAT1 group and siITGA5 decreased, with declined invasion and migration but increased apoptotic rate. Meanwhile, ITGA5, MMP-2, and MMP-9 were downregulated with upregulated cleaved caspase-3. However, the changes above were totally reversed in the miR-330-5p inhibitor group, and miR-330-5p inhibitor transfection abolished the effect of shEWSAT1. In addition, subcutaneous xenotransplantation showed that the tumor growth in shEWSAT1 group retarded significantly, with downregulation of Ki67 and increase apoptotic rate. Silencing EWSAT1 could inhibit the expression of ITGA5 via upregulating miR-330-5p, thus, resulting in the inhibition of NSCLC cell growth.	NA	Biochem Genet. 2021 Apr 29. doi: 10.1007/s10528-021-10069-4.
3395	Circular RNA	Circ-E2F3	miR-204-5p	ROC	RB tissues and cells	Retinoblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33844975	Circ-E2F3 acts as a ceRNA for miR-204-5p to promote proliferation, metastasis and apoptosis inhibition in retinoblastoma by regulating ROCK1 expression.	BACKGROUND: Circular RNA (circRNA) plays an important role in the malignant progression of many tumors, including retinoblastoma (RB). However, the role and regulatory mechanism of circ-E2F3 in RB have not been fully elucidated. METHODS: Quantitative real-time PCR was used to measure circ-E2F3, miR-204-5p and Rho-associated protein kinase 1 (ROCK1) expression. Cell proliferation, apoptosis and metastasis were monitored by MTT, colony formation, flow cytometry, transwell and wound healing assays. Dual-luciferase reporter assay was employed to verify the relationship between miR-204-5p and circ-E2F3 or ROCK1. ROCK1 protein expression was detected by western blot assay. Mice xenograft models were built to assess the role of circ-E2F3 on RB tumor growth. RESULTS: Circ-E2F3 was upregulated in RB tissues and cells. Silencing of circ-E2F3 inhibited the proliferation, migration, invasion, and induced the apoptosis of RB cells in vitro, as well as reduced RB tumor growth in vivo. MiR-204-5p could be sponged by circ-E2F3, and its inhibitor reversed the suppressive effect of circ-E2F3 silencing on RB progression. In addition, ROCK1 was confirmed to interact with miR-204-5p. MiR-204-5p regulated RB progression by targeting ROCK1. Also, circ-E2F3 positively regulated ROCK1 expression by sponging miR-204-5p. CONCLUSION: Circ-E2F3 functioned as a tumor promoter in RB through the miR-204-5p/ROCK1 axis.	NA	Exp Mol Pathol. 2021 Jun;120:104637. doi: 10.1016/j.yexmp.2021.104637. Epub 2021 Apr 18.
3396	LncRNA	MYCNOS	miR-216b	FOXM1	glioblastoma cell	Glioblastoma	Homo sapiens (human)	CCK-8 assay;Cell proliferation assay;qPCR;RT-qPCR;Western blot;Luciferase activity assay;	33871770	LncRNA MYCNOS promotes glioblastoma cell proliferation by regulating miR-216b/FOXM1 axis.	MYCNOS is an oncogenic lncRNA in liver cancer, but its role in glioblastoma (GBM) is unknown. We predicted that MYCNOS might interact with miR-216b, which targets FOXM1 to perform tumor suppressive roles. This study was performed to analyze the role of MYCNOS in GBM and explore its potential interactions with miR-216b and FOXM1. MYCNOS expression in paired GBM and non-tumor tissues from 62 GBM patients was analyzed by RT-qPCR. The interaction between MYCNOS and miR-216b was predicted by IntaRNA 2.0 and confirmed by dual luciferase activity assay. Overexpression of MYCNOS, miR-216b, and FOXM1 was achieved in GBM cells, followed by performing RT-qPCR and Western blot to explore the relationship among them. CCK-8 assay was performed to explore the role of MYCNOS, miR-216b, and FOXM1 in regulating GBM cell proliferation. MYCNOS was upregulated in GBM tissues compared to the paired non-tumor tissues. MYCNOS is predicted to interact with miR-216b, but overexpression of MYCNOS and miR-216b failed to affect each other's expression significantly. Dual luciferase activity assay showed that MYCNOS and miR-216b could directly interact with each other. MYCNOS overexpression increased the expression of FOXM1, which is a direct target of miR-216b. Cell proliferation assay showed that MYCNOS and FOXM1 overexpression resulted in an increased proliferation rate of GBM cells, while miR-216b overexpression suppressed cell proliferation. Moreover, MYCNOS overexpression suppressed the role of miR-216b. MYCNOS may regulate FOXM1 expression of by serving as an endogenous sponge of miR-216b axis to promote the proliferation of GBM cells.	NA	Metab Brain Dis. 2021 Apr 19. doi: 10.1007/s11011-021-00729-0.
3397	LncRNA	MEG3	miR-141-3p	RBMS3	BC cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33845141	LncRNA MEG3 regulates breast cancer proliferation and apoptosis through miR-141-3p/RBMS3 axis.	Maternally expressed 3 (MEG3) and RNA binding motif single stranded interacting protein 3 (RBMS3) are abnormally expressed in breast cancer susceptibility genes (BRCA), but the mechanism of the two in breast cancer (BC) is unclear. By performing in vivo and in vitro experiments, we found that MEG3 and RBMS3 were low-expressed, negatively correlated with high-expressed miR-141-3p, were positively correlated with each other in BC. MEG3 targeted miR-141-3p, and miR-141-3p targeted RBMS3. MEG3, which was mainly distributed in BC cytoplasm, could down-regulate miR-141-3p and up-regulate RBMS3, and reverse effect of miR-141-3p on related gene expressions and on promoting cancer development. Overexpressed MEG3 inhibited growth of xenografts, promoted cell apoptosis via regulating apoptosis related factors, and up-regulated RBMS3 expression but down-regulated miR-141-3p. The findings of this study showed that MEG3 inhibited proliferation and promoted apoptosis of BC cells through the miR-141-3p/RBMS3 axis, and MEG3 inhibited growth of xenografts through miR-141-3p.	NA	Genomics. 2021 Apr 9;113(4):1689-1704. doi: 10.1016/j.ygeno.2021.04.015.
3398	LncRNA	FGD5-AS1	miR-520a-3p	KIAA1522	PC cells	Pancreatic Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;Rescue assay;	33794727	LncRNA FGD5-AS1 accelerates cell proliferation in pancreatic cancer by regulating miR-520a-3p/KIAA1522 axis.	In recent years, FGD5 antisense RNA 1 (FGD5-AS1) was confirmed to be the long non-coding RNAs (lncRNAs) that could accelerate the development of multiple cancers. Nevertheless, specific biological functions and latent mechanism of FGD5-AS1 were not yet clear in pancreatic cancer (PC). This research was aimed to search the functions of FGD5-AS1 on the PC progression. The expression of FGD5-AS1 in PC cells was tested by using RT-qPCR assay. Colony formation assay, EdU assay, flow cytometry assay and transwell assay as well as western blot were adopted to test the cell abilities of proliferation, apoptosis and migration, separately. Furthermore, RIP experiment and pull down assay were applied for validating the correlation FGD5-AS1, miR-520a-3p and KIAA1522. As a result, the abnormal high expression of FGD5-AS1 was observed in PC cells. And cell proliferative and migratory abilities could be restrained via FGD5-AS1 depletion. Moreover, FGD5-AS1 was proven to combine with miR-520a-3p directly. It was also confirmed that KIAA1522 could be targeted by miR-520a-3p. Rescue assay results indicated that overexpressed KIAA1522 could reverse the repressive function of silencing FGD5-AS1 on PC progression. Taken together, FGD5-AS1 accelerated cell proliferation and migration via sponging miR-520a-3p and upregulating KIAA1522.	NA	Cancer Biol Ther. 2021 Mar 4;22(3):257-266. doi: 10.1080/15384047.2021.1883184. Epub 2021 Apr 2.
3399	LncRNA	TINCR	miR-214-5p	ROCK1	hepatocellular carcinoma tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33797211	Retraction Note: lncRNA TINCR sponges miR-214-5p to upregulate ROCK1 in hepatocellular carcinoma.	unknown	NA	BMC Med Genet. 2021 Mar 12;21(1):1178. doi: 10.1186/s12881-020-01178-9.
3400	LncRNA	LINC00858	miR-3064-5p	CTGF	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;	34132366	Long non-coding RNA 00858 knockdown alleviates bladder cancer via regulation of the miR-3064-5p/CTGF axis.	The long non-coding RNA 00858 (LINC00858) has been reported to be an oncogene for various cancer diseases, including osteosarcoma and colorectal cancer. However, the expression pattern and function of LINC00858 in bladder cancer remain largely unknown. The expression level of LINC00858 was measured in tumor tissues and cell lines by RT-qPCR. The role of LINC00858 in bladder cancer cells were studied by gain- and loss-of-function strategies in vitro. Cell proliferation, migration and invasion were assessed by CCK-8, colony formation, wound healing and Transwell chamber assays. At the molecular level, dual luciferase reporter and RNA RIP assays were performed to identify the interaction among LINC00858, microRNA (miR)-3064-5p and cellular communication network factor 2 (CTGF). The results revealed that the expression level of LINC00858 was upregulated in bladder cancer tissues and cell lines including T24, J82 and 5637. Moreover, knockdown of LINC00858 suppressed cell proliferation, migration and invasion in vitro. Mechanistically, LINC00858 functioned as a competitive RNA to increase the expression level of oncogene CTGF by sequestering miR-3064-5p. In conclusion, LINC00858 knockdown inhibited the proliferation, migration and invasion of bladder cancer cells via regulation of the miR-3064-5p/CTGF axis.	NA	Oncol Rep. 2021 Aug;46(2):164. doi: 10.3892/or.2021.8115. Epub 2021 Jun 16.
3401	LncRNA	SH3PXD2A-AS1	miR-125b	STAT3	NA	Psoriasis 	Homo sapiens (human)	microarray;RIP assay;	33994260	STAT3/SH3PXD2A-AS1/miR-125b/STAT3 positive feedback loop affects psoriasis pathogenesis via regulating human keratinocyte proliferation.	Psoriasis is a chronic immune-mediated inflammatory dermatosis. STAT3 has been considered a critical regulator of psoriasis pathogenesis due to its role in inflammation and immune responses. Furthermore, alongside non-coding RNAs, including long non-coding RNAs (lncRNAs) and miRNAs, STAT3 also plays a critical role in psoriasis pathogenesis. Two sets of online microarray profiles (GSE50790 and GSE13355) were subsequently downloaded and analyzed to search for lncRNAs upregulated in psoriasis lesion tissues. The expression of lncRNA SH3PXD2A-AS1 could be remarkably upregulated in psoriasis specimens. SH3PXD2A-AS1 silence was found to suppress HaCaT cell proliferation and promote HaCaT cell apoptosis significantly. Meanwhile, SH3PXD2A-AS1 silence significantly increased cleaved-caspase-3 protein levels and inhibited S100A7, TNF-α, IL-6, p-STAT3, STAT3, CyclinD1, and survivin protein levels. Moreover, the expression of miR-125b could be substantially decreased within psoriasis lesion tissue samples, while miR-125b could negatively regulate the SH3PXD2A-AS1 and STAT3 expression. As predicted by an online tool and validated by luciferase reporter and RIP assays, miR-125b was found to bind to SH3PXD2A-AS1 and STAT3 3'UTR directly; SH3PXD2A-AS1 competed with 3'UTR of STAT3 for miR-125b binding to counteract miR-125b-mediated suppression of STAT3. STAT3 is known to activate the transcription of SH3PXD2A-AS1 through the targeting of its promoter region. It consequentially forms a regulatory feedback loop promoting SH3PXD2A-AS1 expression affecting HaCat cell proliferation and apoptosis. A novel STAT3 related mechanism whereby STAT 3/ SH3PXD2A-AS1/ miR-125b/STAT3 positive feedback loop which could potentially affect the pathogenesis of Psoriasis has been established.	NA	Cytokine. 2021 Aug;144:155535. doi: 10.1016/j.cyto.2021.155535. Epub 2021 May 13.
3402	LncRNA	NR2F1-AS1	miR-493-5p	GOLM1	melanoma tumors and cells	Melanoma	Homo sapiens (human)	RNA pull-down assay;Chromatin immunoprecipitation;RNA pull-down;	33822440	STAT3 activates the transcription of lncRNA NR2F1-AS1 to promote the progression of melanoma via regulating the miR-493-5p/GOLM1 axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) are vital regulators during the biological processes of melanoma. The present study aimed to uncover biological functions of lncRNA termed NR2F1 antisense RNA 1 (NR2F1-AS1) in melanoma and the potential mechanisms. METHODS: Relative levels of NR2F1-AS1 and miR-493-5p in a total of 137 paired primary melanoma tissues and corresponding non-tumor tissues, as well as three melanoma cell lines, were examined by a real-time polymerase chain reaction. The clinical significance of NR2F1-AS1 expression was analyzed statistically. The STAT3 binding motif in the promoter region of NR2F1-AS1 was identified by JASPAR (http://jaspar.genereg.net). The association between STAT3 and NR2F1-AS1 was determined by dual-luciferase reporter and chromatin immunoprecipitation assays. The effects of NR2F1-AS1 on cell proliferation, migration and were measured by cell counting kit-8 (CCK-8), Edu, transwell and wound healing assays. Dual-luciferase reporter and RNA pull-down assays were applied to validate the interaction among NR2F1-AS1, miR-493-5p and GOLM1. Furthermore, in vivo experiments were conducted to demonstrate the oncogenic role of NR2F1-AS1 in melanoma. RESULTS: Up-regulated NR2F1-AS1 and down-regulated miR-493-5p were detected in melanoma tumors and cells. The overexpression of NR2F1-AS1 was induced by STAT3. High NR2F1-AS1 expression was correlated to advanced tumor stage and poor prognosis of melanoma. Functional studies using CCK-8, Edu, transwell and wound healing assays revealed that the proliferative, migratory and invasive capacities of melanoma cells were attenuated by the by inhibition of NR2F1-AS1. Moreover, NR2F1-AS1 was able to up-regulate GOLM1 through recognizing and binding miR-493-5p. Furthermore, knockdown of miR-493-5p distinctly reversed these inhibitory effects of NR2F1-AS1 down-regulation on the tumorigenesis and progression of melanoma. CONCLUSIONS: Our findings demonstrate a key role for NR2F1-AS1 in melanoma progression via targeting miR-493-5p/GOLM1 axis.	NA	J Gene Med. 2021 Apr 6:e3338. doi: 10.1002/jgm.3338.
3403	LncRNA	AFAP1-AS1	miR-424-5p	STAT3	Endometrial stromal cells	Endometriosis 	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33949053	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-β/Smad signaling via miR-424-5p.	AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-β1 (TGF-β1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-β/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.	NA	J Obstet Gynaecol Res. 2021 May 4. doi: 10.1111/jog.14801.
3404	LncRNA	AFAP1-AS1	miR-424-5p	TGFb	Endometrial stromal cells	Endometriosis 	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33949053	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-β/Smad signaling via miR-424-5p.	AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-β1 (TGF-β1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-β/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.	NA	J Obstet Gynaecol Res. 2021 May 4. doi: 10.1111/jog.14801.
3405	LncRNA	HOTTIP	miR-101-3p	STC1	HXO-RB-44 cells	Retinoblastoma 	Homo sapiens (human)	qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	33784880	Knockdown of lncRNA HOTTIP Inhibits Retinoblastoma Progression by Modulating the miR-101-3p/STC1 Axis.	OBJECTIVE: Retinoblastoma (RB) is a frequent eye cancer in children. Long non-coding RNA (LncRNA) HOXA transcript at the distal tip (HOTTIP) is aberrantly expressed in cancer tissues. This study explores the underlying mechanism of lncRNA HOTTIP in RB. METHODS: HOTTIP expression in normal retinal cells and RB cell lines was detected using qRT-PCR. The proliferation of RB cells was measured using CCK-8 and EdU assays, and apoptosis was detected using flow cytometry and Western blotting after the transfection of si-HOTTIP into Y79 cells and pc-HOTTIP into HXO-RB-44 cells. The target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1 were predicted by bioinformatics website and verified using dual-luciferase reporter gene assay. The binding of HOTTIP and miR-101-3p was verified using RNA pull-down assay. STC1 mRNA and protein in RB cells were measured using qRT-PCR and Western blotting. Moreover, si-HOTTIP and in-miR-101-3p/in-NC, and si-HOTTIP and pc-STC1/pcDNA were co-transfected into Y79 cells respectively to evaluate cell proliferation and apoptosis. Xenograft study was conducted, and Ki67-positive expression was detected using immunohistochemical staining. RESULTS: HOTTIP expression was promoted in RB tissues and cells. Downregulation of HOTTIP inhibited proliferation and promoted apoptosis of Y79 cells, while upregulation of HOTTIP promoted proliferation and inhibited apoptosis of HXO-RB-44 cells. There were target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1. Inhibition of miR-101-3p or overexpression of STC1 reversed the effect of si-HOTTIP on the proliferation and apoptosis of RB cells. Xenograft study showed that knockdown of HOTTIP suppressed the growth of RB in vitro. CONCLUSION: It could be concluded that HOTTIP sponged miR-101-3p to upregulate STC1 expression, thereby promoting RB cell proliferation and inhibiting apoptosis.	NA	Technol Cancer Res Treat. 2021 Jan-Dec;20:1533033821997831. doi: 10.1177/1533033821997831.
3406	LncRNA	HAGLR	miR-93-5p	SRSF	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	34128362	HOXD Antisense Growth-Associated Long Noncoding RNA Promotes Triple-Negative Breast Cancer Progression by Activating Wnt Signaling Pathway.	PURPOSE: Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer owing to high heterogeneity, aggressive nature, and lack of treatment options, which has a substantial deleterious effect on patients' lives. HOXD antisense growth-associated long noncoding RNA (lncRNA) (HAGLR) plays tumor-promoting roles in many cancers. In this study, we aimed to explore the role of HAGLR in TNBC. METHODS: Quantitative real-time polymerase chain reaction assays were used to examine the expression of RNAs. Functional experiments were conducted to test the biological behavior of TNBC cells. Moreover, MS2-RNA immunoprecipitation, luciferase reporter, and RNA pull-down assays were conducted to verify the binding relationship between HAGLR, microRNA-143-5p (miR-143-5p), and serine- and arginine-rich splicing factor 1 (SRSF1). RESULTS: HAGLR was found to be highly expressed in TNBC tissues and cells, and inhibiting HAGLR suppressed cell proliferation, migration, and invasion and promoted cell apoptosis in TNBC. Meanwhile, miR-93-5p was shown to bind to HAGLR and SRSF1. In addition, SRSF1 plays an oncogenic role in TNBC. Importantly, HAGLR could activate the Wnt signaling pathway by sponging miR-93-5p to upregulate SRSF1; thus, accelerating TNBC progression. CONCLUSION: HAGLR could promote the progression of TNBC through the miR-93-5p/SRSF1 axis to activate the Wnt signaling pathway.	NA	J Breast Cancer. 2021 Apr 28. doi: 10.4048/jbc.2021.24.e24.
3407	LncRNA	XIST	miR-30d-5p	SIRT1	Schwann cells	Diabetic Peripheral Neuropathy 	Homo sapiens (human)	qRT-PCR	33996907	Long Non-coding RNA XIST Attenuates Diabetic Peripheral Neuropathy by Inducing Autophagy Through MicroRNA-30d-5p/sirtuin1 Axis.	Diabetic peripheral neuropathy (DPN) is a prevalent diabetes mellitus (Feldman et al., 2017) complication and the primary reason for amputation. Meanwhile, long non-coding RNAs (lncRNAs) are a type of regulatory non-coding RNAs (ncRNAs) that broadly participate in DPN development. However, the correlation of lncRNA X-inactive specific transcript (XIST) with DPN remains unclear. In this study, we were interested in the role of XIST in the modulation of DPN progression. Significantly, our data showed that the expression of XIST and sirtuin1 (SIRT1) was inhibited, and the expression of microRNA-30d-5p (miR-30d-5p) was enhanced in the trigeminal sensory neurons of the diabetic mice compared with the normal mice. The levels of LC3II and Beclin-1 were inhibited in the diabetic mice. The treatment of high glucose (HG) reduced the XIST expression in Schwann cells. The apoptosis of Schwann cells was enhanced in the HG-treated cells, but the overexpression of XIST could block the effect in the cells. Moreover, the levels of LC3II and Beclin-1 were reduced in the HG-treated Schwann cells, while the overexpression of XIST was able to reverse this effect. The HG treatment promoted the production of oxidative stress, while the XIST overexpression could attenuate this result in the Schwann cells. Mechanically, XIST was able to sponge miR-30d-5p and miR-30d-5p-targeted SIRT1 in the Schwann cells. MiR-30d-5p inhibited autophagy and promoted oxidative stress in the HG-treated Schwann cells, and SIRT1 presented a reversed effect. MiR-30d-5p mimic or SIRT1 depletion could reverse XIST overexpression-mediated apoptosis and autophagy of the Schwann cells. Thus, we concluded that XIST attenuated DPN by inducing autophagy through miR-30d-5p/SIRT1 axis. XIST and miR-30d-5p may be applied as the potential targets for DPN therapy.	NA	Front Mol Biosci. 2021 Apr 28;8:655157. doi: 10.3389/fmolb.2021.655157. eCollection 2021.
3408	LncRNA	SNHG9	miR-326	SOX9	glioma stem-like cells(GSC-87 and GSC-251 cells)	Glioma	Homo sapiens (human)	Luciferase reporter assay;	33789359	Long noncoding RNA SNHG9 facilitates growth of glioma stem-like cells via miR-326/SOX9 axis.	BACKGROUND: Glioma stem-like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. METHODS: GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC-87 and GSC-251, respectively. The interactions between miR-326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. RESULTS: SNHG9 expression was significantly higher in GSC-87 and GSC-251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR-326 to elevate the expression of SOX9, a direct target of miR-326. Moreover, transfection with miR-326 inhibitor counteracted SNHG9 knockdown-mediated inhibition of GSC cell growth. CONCLUSIONS: SNHG9 facilitates growth of GSCs via the miR-326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment.	NA	J Gene Med. 2021 Mar 31:e3334. doi: 10.1002/jgm.3334.
3409	LncRNA	KCNQ1OT1	miR-134	TRIM44	Weri-Rb1 and Y79 cells	Retinoblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	33818859	Long non-coding RNA KCNQ1OT1 promotes proliferation, migration and invasion via targeting miR-134 in retinoblastoma.	BACKGROUND: Long non-coding RNAs (lncRNAs) exert a significant role in carcinogenesis. lncRNA KCNQ1OT1 is detected in many tumors and is considered as an oncogene. The expression and mechanism of KCNQ1OT1 in retinoblastoma (Rb) are not clearly elucidated. METHODS: KCNQ1OT1, miR-134 and TRIM44 mRNA expression were examined by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Proliferation, migration and invasion of Weri-Rb1 and Y79 cells were tested by cell counting kit-8, colony formation, scratch and transwell assays. Meanwhile, the regulatory relationships among KCNQ1OT1, miR-134 and TRIM44 were clarified by several biological experiments, including dual-luciferase reporter assay, RNA immunoprecipitation, subcellular distribution, qRT-PCR and western blotting. RESULTS: lncRNA KCNQ1OT1 was up-regulated in Rb tissues and Rb cell lines. In addition, the expression of KCNQ1OT1 was negatively correlated with the disease-free survival rate of RB patients. Silencing KCNQ1OT1 could significantly inhibit the RB progression in vivo and in vitro. The analysis of the mechanism of KCNQ1OT1 showed that KCNQ1OT1 can sponge miR-134, and miR-134 may inhibit TRIM44 expression. Moreover, the rescue assays showed that KCNQ1OT1 promoted RB progression by regulating the miR-134/TRIM44 pathway. CONCLUSIONS: The present study indicates that a new KCNQ1OT1/miR-134/TRIM44 pathway regulates Rb progression. It may be used as a potential prognostic marker for Rb.	NA	J Gene Med. 2021 Jun;23(6):e3336. doi: 10.1002/jgm.3336. Epub 2021 May 3.
3410	LncRNA	DSCAM-AS1	miR-101-3p	USP47	NA	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33779298	Correction: Long non-coding RNA DSCAM-AS1 upregulates USP47 expression through sponging miR-101-3p to accelerate osteosarcoma progression.	unknown	NA	Biochem Cell Biol. 2021 Apr;99(2):272-273. doi: 10.1139/bcb-2021-0077. Epub 2021 Mar 29.
3411	LncRNA	LOC729178	miR-144-3p	PHLPP2	16HBE cells	Extract-Induced Inflammatory Injury 	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33847879	LncRNA LOC729178 acts as a sponge of miR-144-3p to mitigate cigarette smoke extract-induced inflammatory injury via regulating PHLPP2 in 16HBE cells.	Chronic obstructive pulmonary disease (COPD) is an inflammatory respiratory disease. Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of COPD. In the present study, we set to investigate the role and mechanism of LOC729178 on cigarette smoke extract (CSE)-induced inflammatory damage in 16HBE cells. The expression levels of LOC729178, miR-144-3p, and PH domain leucine-rich repeat protein phosphatase 2 (PHLPP2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell viability and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. Enzyme-linked immunosorbent assay (ELISA) assay was performed to evaluate the levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and IL-8. Targeted relationships among LOC729178, miR-144-3p, and PHLPP2 were verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Our data indicated that LOC729178 was underexpressed in COPD tissues and CSE-treated 16HBE cells. Exogenous expression of LOC729178 alleviated CSE-induced inflammatory injury in 16HBE cells. LOC729178 targeted miR-144-3p by directly binding to miR-144-3p. miR-144-3p was a downstream effector of LOC729178 function. PHLPP2 was identified as a direct and functional target of miR-144-3p. Furthermore, LOC729178 operated as a post-transcriptional regulator of PHLPP2 expression through miR-144-3p. Our current study suggested that LOC729178 overexpression alleviated CSE-induced inflammatory injury in 16HBE cells at least in part by up-regulating PHLPP2 via sponging miR-144-3p, providing a rationale for developing LOC729178 as a potential therapeutic agent against COPD.	NA	J Mol Histol. 2021 Jun;52(3):437-447. doi: 10.1007/s10735-021-09972-2. Epub 2021 Apr 13.
3412	LncRNA	GHRLOS	miR-346	APC	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Chromatin immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33968785	TP53-Activated lncRNA GHRLOS Regulates Cell Proliferation, Invasion, and Apoptosis of Non-Small Cell Lung Cancer by Modulating the miR-346/APC Axis.	Non-small cell lung cancer (NSCLC) is the main type of lung cancer with high mortality worldwide. To improve NSCLC therapy, the exploration of molecular mechanisms involved in NSCLC progression and identification of their potential therapy targeting is important. Long noncoding RNAs (lncRNAs) have shown important roles in regulating various tumors progression, including NSCLC. We found lncRNA GHRLOS was decreased in NSCLC cell lines and tissues which correlated with poor prognosis of NSCLC patients. However, the role and underlying mechanisms of lncRNA GHRLOS in NSCLC progression remains elusive. The expression of lncRNA GHRLOS was examined in NSCLC cell lines and biopsy specimens of patients with NSCLC by quantitative real time polymerase chain reaction (qRT-PCR). The effects of GHRLOS on proliferation, invasion and apoptosis of NSCLC cells were determined by both in vitro and in vivo experiments. The interaction between GHRLOS and TP53 was determined by dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) combined with qRT-PCR analysis. RNA immunoprecipitation (RIP) was conducted to validate the binding between GHRLOS and microRNA-346 (miR-346). Dual-luciferase reporter assays were also carried out to reveal the interaction between miR-346 and the 3' untranslated region (3'UTR) of adenomatous polyposis coli (APC) mRNA.Our data demonstrated that overexpression of lncRNA GHRLOS suppressed cancer cell proliferation and invasion as well as promoted cell apoptosis by regulating the expression of CDK2, PCNA, E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Moreover, lncRNA GHRLOS was upregulated by the binding of TP53 to the GHRLOS promoter. The binding target of lncRNA GHRLOS was identified to be miR-346. Impressively, overexpression of miR-346 promoted cell proliferation and invasion, as well as inhibited cell apoptosis, however, these effects can be blocked by overexpression of lncRNA GHRLOS both in vitro and in vivo. In summary, this study reveals lncRNA GHRLOS, upregulated by TP53, acts as a molecule sponge of miR-346 to cooperatively modulates expression of APC, a miR-346 target, and potentially inhibits NSCLC progression via TP53/lncRNA GHRLOS/miR-346/APC axis, which represents a novel pathway that could be useful in targeted therapy against NSCLC.	NA	Front Oncol. 2021 Apr 21;11:676202. doi: 10.3389/fonc.2021.676202. eCollection 2021.
3413	LncRNA	GAS5	miR-23a-3p	TLR4	THP-1 cells	Inflammatory Injury	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Flow Cytometry assay;Luciferase reporter assay;	33982771	lncRNA GAS5-mediated miR-23a-3p promotes inflammation and cell apoptosis by targeting TLR4 in a cell model of sepsis.	Sepsis is a syndrome characterized by organ dysfunction and an abnormal immune response to infection. A growing body of research has shown the importance of long non-coding RNAs (lncRNAs) in tumorigenesis, virus replication, inflammatory injury and other pathological processes. The aim of the present study was to explore the role and potential mechanism of the lncRNA growth arrest-specific 5 (GAS5) in the lipopolysaccharide (LPS)-induced inflammation and apoptosis of THP-1 cells. An in vitro sepsis model was established by treating THP-1 cells with LPS. Apoptosis was detected by flow cytometry. The expression levels of IL-6, IL-1β and TNF-α were detected using reverse transcription-quantitative PCR (RT-qPCR) and ELISA, and those of GAS5, microRNA (miR)-23a-3p and Toll-like receptor 4 (TLR4) were detected by RT-qPCR. The changes in the biological activity of THP-1 cells induced by the silencing of GAS5 and overexpression of miR-23a-3p and TLR4 were investigated. The relationships among GAS5, miR-23a-3p and TLR4 were analyzed using luciferase reporter assays. The results revealed that LPS increased the expression of GAS5 in THP-1 cells, and GAS5 knockdown effectively inhibited inflammation and cell apoptosis in the LPS-induced sepsis model. In addition, the results of the luciferase reporter assays indicated that both GAS5 and TLR4 directly target miR-23a-3p. The expression of miR-23a-3p was downregulated whereas that of TLR4 was upregulated in the septic cells. Further experiments showed that the overexpression of TLR4 attenuated the suppressive effects of miR-23a-3p overexpression and GAS5 knockdown on LPS-induced inflammation and apoptosis. In conclusion, the present study indicates that GAS5 strengthens LPS-induced inflammation and apoptosis via the miR-23a-3p/TLR4 pathway.	NA	Mol Med Rep. 2021 Jul;24(1):510. doi: 10.3892/mmr.2021.12149. Epub 2021 May 13.
3414	LncRNA	GAS5	miR-217	HDAC4	bronchial epithelial cells	Asthma 	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33864612	GAS5 regulates viability and apoptosis in TGF-β1-stimulated bronchial epithelial cells by regulating miR-217/HDAC4 axis.	BACKGROUND: Asthma is a serious respiratory disease that affects the physical and mental health of children. Airway epithelial apoptosis concomitantly mediated by transforming growth factor-β1 (TGF-β1) is a crucial component of asthma pathogenesis. LncRNA growth Arrest Specific 5 (GAS5), microRNA-217 (miR-217) and Histone deacetylase 4 (HDAC4) shown a close relationship with TGF-β1-induced injury of airway epithelial. However, the mechanism underlying TGF-β1-induced injury of airway epithelial in asthma still needs to be investigated. OBJECTIVE: We aimed to investigate the effect and underlying mechanism of GAS5/miR-217/HDAC4 axis in TGF-β1-stimulated bronchial epithelial cells. METHODS: The levels of were detected by quantitative real-time polymerase chain reaction (RT-qPCR). All protein levels were determined by western blot. Cell viability and apoptosis rate were assessed by Methyl thiazolyl tetrazolium (MTT) and Flow cytometry, respectively. The targeting relationship between miR-217 and GAS5 or HDAC4 was examined with dual-luciferase reporter assay. RESULTS: TGF-β1, GAS5, HDAC4 were up-regulated, while miR-217 was down-regulated in bronchial mucosal tissues of asthmatic children and TGF-β1-treated BEAS-2B cells. TGF-β1 could reduce cell viability and induce apoptosis, while these effects could be reversed by downregulation of GAS5 or HDAC4. Mechanically, GAS5 acted as a sponge for miR-217 to regulate the expression of HDAC4. Furthermore, overexpression of HDAC4 rescued the effects of GAS5 knockdown on viability and apoptosis of TGF-β1-induced BEAS-2B cells. GAS5 knockdown induced cell viability and hampered cell apoptosis in TGF-β1-stimulated BEAS-2B cells by regulating the miR-217/HDAC4 axis. CONCLUSIONS: The lncRNA GAS5/miR-217/HDAC4 axis played an important role in regulating TGF-β1-induced bronchial epithelial cells injury, thus contributing to asthma.	NA	Genes Genomics. 2021 Apr 17. doi: 10.1007/s13258-021-01092-1.
3415	Circular RNA	CircPSMA1	miR-637	Akt1-b	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR	33911067	Tumor-derived exosomal circPSMA1 facilitates the tumorigenesis, metastasis, and migration in triple-negative breast cancer (TNBC) through miR-637/Akt1/β-catenin (cyclin D1) axis.	Circular RNAs (circRNAs) are increasingly gaining importance and attention due to their diverse potential functions and their value as diagnostic biomarkers (disease specific). This study aims to explore the novel mechanisms by which exosome-contained circRNAs promote tumor development and metastasis in TNBC. We identified increased circRNA circPSMA1 in TNBC cells, their exosomes, and serum exosomes samples from TNBC patients. The overexpression of circPSMA1 promoted TNBC cell proliferation, migration, and metastasis both in vitro and in vivo. Moreover, we investigated the tumor-infiltrating immune cells (TICs) or stromal components in immune microenvironment (IME), and identified the significant differences in the immune cells between TNBC and non-TNBC samples. Mechanistically, circPSMA1 acted as a "miRNAs sponge" to absorb miR-637; miR-637 inhibited TNBC cell migration and metastasis by directly targeted Akt1, which recognized as a key immune-related gene and affected downstream genes β-catenin and cyclin D1. Subsequent co-culture experiments also demonstrated that exosomes from TNBC carrying large amounts of circPSMA1 could transmit migration and proliferation capacity to recipient cells. Kaplan-Meier plots showed that high expression of Akt1 and low expression of mir-637 are highly correlated with poor prognosis in patients with lymph node metastasis of TNBC. Collectively, all these results reveal that circPSMA1 functions as a tumor promoter through the circPSMA1/miR-637/Akt1-β-catenin (cyclin D1) regulatory axis, which can facilitate the tumorigenesis, metastasis, and immunosuppression of TNBC. Our research proposes a fresh perspective on novel potential biomarkers and immune treatment strategies for TNBC.	NA	Cell Death Dis. 2021 Apr 28;12(5):420. doi: 10.1038/s41419-021-03680-1.
3416	LncRNA	CASC11	miR-646	RAB11FIP2	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33937069	The LncRNA CASC11 Promotes Colorectal Cancer Cell Proliferation and Migration by Adsorbing miR-646 and miR-381-3p to Upregulate Their Target RAB11FIP2.	BACKGROUND: We previously reported that the long non-coding RNA (lncRNA) CASC11 promotes colorectal cancer (CRC) progression as an oncogene by binding to HNRNPK. However, it remains unknown whether CASC11 can act as a competitive endogenous RNA (ceRNA) in CRC. In this study, we focused on the role of CASC11 as a ceRNA in CRC by regulating miR-646 and miR-381-3p targeting of RAB11FIP2. METHODS: We identified the target microRNAs (miRNAs) of CASC11 and the target genes of miR-646 and miR-381-3p using bioinformatic methods. A dual-luciferase reporter assay was performed to validate the target relationship. Quantitative real-time PCR (qRT-PCR), western blotting (WB), and immunohistochemistry (IHC) were used to measure the RNA and protein expression levels. Rescue experiments in vitro and in vivo were performed to investigate the influence of the CASC11/miR-646 and miR-381-3p/RAB11FIP2 axis on CRC progression. RESULTS: We found that CASC11 binds to miR-646 and miR-381-3p in the cytoplasm of CRC cells. Moreover, miR-646 and miR-381-3p inhibitors reversed the suppressive effect of CASC11 silencing on CRC growth and metastasis in vitro and in vivo. We further confirmed that RAB11FIP2 is a mutual target of miR-646 and miR-381-3p. The expression levels of CASC11 and RAB11FIP2 in CRC were positively correlated and reciprocally regulated. Further study showed that CASC11 played an important role in regulating PI3K/AKT pathway by miR-646 and miR-381-3p/RAB11FIP2 axis. CONCLUSION: Our study showed that CASC11 promotes the progression of CRC as a ceRNA by sponging miR-646 and miR-381-3p. Thus, CASC11 is a potential biomarker and a therapeutic target of CRC.	NA	Front Oncol. 2021 Apr 15;11:657650. doi: 10.3389/fonc.2021.657650. eCollection 2021.
3417	LncRNA	CASC11	miR-381-3p	RAB11FIP2	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33937069	The LncRNA CASC11 Promotes Colorectal Cancer Cell Proliferation and Migration by Adsorbing miR-646 and miR-381-3p to Upregulate Their Target RAB11FIP2.	BACKGROUND: We previously reported that the long non-coding RNA (lncRNA) CASC11 promotes colorectal cancer (CRC) progression as an oncogene by binding to HNRNPK. However, it remains unknown whether CASC11 can act as a competitive endogenous RNA (ceRNA) in CRC. In this study, we focused on the role of CASC11 as a ceRNA in CRC by regulating miR-646 and miR-381-3p targeting of RAB11FIP2. METHODS: We identified the target microRNAs (miRNAs) of CASC11 and the target genes of miR-646 and miR-381-3p using bioinformatic methods. A dual-luciferase reporter assay was performed to validate the target relationship. Quantitative real-time PCR (qRT-PCR), western blotting (WB), and immunohistochemistry (IHC) were used to measure the RNA and protein expression levels. Rescue experiments in vitro and in vivo were performed to investigate the influence of the CASC11/miR-646 and miR-381-3p/RAB11FIP2 axis on CRC progression. RESULTS: We found that CASC11 binds to miR-646 and miR-381-3p in the cytoplasm of CRC cells. Moreover, miR-646 and miR-381-3p inhibitors reversed the suppressive effect of CASC11 silencing on CRC growth and metastasis in vitro and in vivo. We further confirmed that RAB11FIP2 is a mutual target of miR-646 and miR-381-3p. The expression levels of CASC11 and RAB11FIP2 in CRC were positively correlated and reciprocally regulated. Further study showed that CASC11 played an important role in regulating PI3K/AKT pathway by miR-646 and miR-381-3p/RAB11FIP2 axis. CONCLUSION: Our study showed that CASC11 promotes the progression of CRC as a ceRNA by sponging miR-646 and miR-381-3p. Thus, CASC11 is a potential biomarker and a therapeutic target of CRC.	NA	Front Oncol. 2021 Apr 15;11:657650. doi: 10.3389/fonc.2021.657650. eCollection 2021.
3418	LncRNA	LINC01006	miR-129-2-3p	CTNNB1	NA	Lung Cancer 	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	33753463	Long Noncoding RNA LINC01006 Facilitates Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition in Lung Adenocarcinoma via Targeting the MicroRNA 129-2-3p/CTNNB1 Axis and Activating Wnt/β-Catenin Signaling Pathway.	Lung adenocarcinoma (LUAD) is a common type of malignancy of lung cancers. Long intergenic noncoding RNAs (lincRNAs) have emerged as crucial regulators of various cancers, including LUAD. LINC01006 is a newly discovered long noncoding RNA (lncRNA) whose function in LUAD remains to be explored. This study is to explore the role of LINC01006 in LUAD. Quantitative real-time PCR (RT-qPCR) analysis and Western blotting were used to determine the expression levels and protein levels, respectively. Functional assays and animal experiments investigated the role of LINC01006 both in vivo and in vitro. Moreover, TOP/FOP assay was performed to detect the activation of the Wnt/β-catenin signaling pathway. The interaction between LINC01006 and microRNA 29-2-3-p (miR-29-2-3-p)/catenin beta 1 (CTNNB1) was explored by RNA binding protein immunoprecipitation (RIP), RNA pulldown, luciferase reporter assays, and rescue experiments. According to the results, LINC01006 was highly expressed in LUAD tissues and cell lines. LINC01006 knockdown significantly suppressed cell proliferative, migratory, and epithelial-mesenchymal transition (EMT) capacities and tumor development. Moreover, LINC01006 enhanced CTNNB1 via sequestering miR-129-2-3p and activated the Wnt/β-catenin pathway in LUAD. Overall, LINC01006 promotes LUAD development via activating the Wnt/β-catenin pathway, implying that LINC01006 might be a promising biomarker for LUAD treatment.	NA	Mol Cell Biol. 2021 May 21;41(6):e0038020. doi: 10.1128/MCB.00380-20. Epub 2021 May 21.
3419	LncRNA	TP73-AS1	miR-128-3p	GOLM1	PC tissues and cells	Pancreatic Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;luciferase assay;	34007135	Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis.	BACKGROUND: Previous studies have suggested that long non-coding RNAs (lncRNA) TP73-AS1 is significantly upregulated in several cancers. However, the biological role and clinical significance of TP73-AS1 in pancreatic cancer (PC) remain unclear. AIM: To investigate the role of TP73-AS1 in the growth and metastasis of PC. METHODS: The expression of lncRNA TP73-AS1, miR-128-3p, and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p. The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation, migration, and invasion abilities were verified by Cell Counting Kit-8, wound-healing, and transwell assays, as well as flow cytometry and Western blot analysis. The interactions among TP73-AS1, miR-128-3p, and GOLM1 were explored by bioinformatics prediction, luciferase assay, and Western blot. RESULTS: The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells. High TP73-AS1 expression was correlated with a poor prognosis. TP73-AS1 silencing inhibited PC cell proliferation, migration, and invasion in vitro as well as suppressed tumor growth in vivo. Mechanistically, TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p. CONCLUSION: Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis, which might provide a potential treatment strategy for patients with PC.	NA	World J Gastroenterol. 2021 May 7;27(17):1993-2014. doi: 10.3748/wjg.v27.i17.1993.
3420	LncRNA	DLEU2	miR-205-5p	TNF	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33764889	Long noncoding RNA DLEU2 drives the malignant behaviors of thyroid cancer through mediating the miR-205-5p/TNFAIP8 axis.	OBJECTIVE: Considering the plight in thyroid cancer therapy, we aimed to find novel therapeutic targets from a molecular perspective. METHODS: Quantitative real-time PCR (qRT-PCR) and Western blot assay were carried out to determine RNA and protein expression. Cell counting kit-8 (CCK8) assay, flow cytometry, transwell migration assay and aerobic glycolysis analysis were performed to analyze cell proliferation, apoptosis, migration and aerobic glycolysis of thyroid cancer cells. MiRcode and Starbase software were used to search the downstream genes of long noncoding RNA (lncRNA) deleted in lymphocytic leukemia 2 (DLEU2) and microRNA-205-5p (miR-205-5p), and the intermolecular combination was confirmed by dual-luciferase reporter assay. The in vivo role of DLEU2 in tumor growth was verified using the murine xenograft model. RESULTS: DLEU2 and tumor necrosis factor-α-induced protein 8 (TNFAIP8) were highly expressed in thyroid cancer tissues and cell lines. DLEU2 and TNRAIP8 promoted the proliferation, migration and aerobic glycolysis and restrained the apoptosis of thyroid cancer cells. DLEU2/miR-205-5p/TNFAIP8 signaling axis was identified in thyroid cancer cells. TNFAIP8 overexpression largely rescued the malignant phenotypes in DLEU2-silenced thyroid cancer cells. DLEU2 positively regulated TNFAIP8 expression by acting as miR-205-5p sponge in thyroid cancer cells. DLEU2 silencing blocked the growth of xenograft tumors in vivo. CONCLUSION: lncRNA DLEU2 exerted a pro-tumor role to promote proliferation, migration and aerobic glycolysis while repressing the apoptosis of thyroid cancer cells via miR-205-5p/TNFAIP8 axis.	NA	Endocr Connect. 2021 Apr 26;10(4):471-483. doi: 10.1530/EC-21-0046.
3421	LncRNA	CHRF	miR-146a	L1CAM	alveolar epithelial cells	Lung Fibrosis Disease	Homo sapiens (human)	qPCR;Western blot;	33754922	LncRNA CHRF promotes TGF-β1 induced EMT in alveolar epithelial cells by inhibiting miR-146a up-regulating L1CAM expression.	PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a type of progressive lung fibrosis disease. The survival time of diagnosed IPF patients is often only 2 years. Currently much evidence showed that the epithelial-mesenchymal transition (EMT) process is the main cause of the occurrence and development of IPF. LncRNA cardiac hypertrophy related factor (CHRF) was reported to be related with IPF development. Here we explored the functions and regulatory mechanisms of CHRF on EMT in IPF. MATERIALS AND METHODS: A549 cells were treated with transforming growth factor-β1 (TGF-β1) for 48 h to construct IPF cell model. CHRF and miR-146a expression were quantified using qPCR. The expression of L1 cell adhesion molecule (L1CAM) and EMT related indicators (E-cadherin, Vimentin, Slug and N-cadherin) were detected by qPCR and western blot. Dual luciferase reporter experiment was conducted to prove the molecular interaction of miR-146a and L1CAM, as well as CHRF and miR-146a. RESULTS: CHRF and L1CAM expression were significantly upregulated and promoted the EMT process in A549 after treatment of TGF-β1. MiR-146a was obviously down-regulated, and knockdown of CHRF inhibited the EMT process by up-regulating miR-146a, in A549 after treatment of TGF-β1. Meanwhile, overexpression of miR-146a inhibited EMT process via targeting L1CAM. In addition, L1CAM overexpression eliminated the inhibitory effect of sh-CHRF on the EMT process. CONCLUSIONS: These results provided evidence that CHRF promoted EMT process in A549 after treatment of TGF-β1, which proposed a new insight for depth understanding the pathological mechanisms of IPF.	NA	Exp Lung Res. 2021 Apr-May;47(4):198-209. doi: 10.1080/01902148.2021.1891354. Epub 2021 Mar 23.
3422	LncRNA	CRNDE	miR-451a	CDKN2D	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;RNA immunoprecipitation;RNA immunoprecipitation;	33882369	LncRNA CRNDE promotes the progression and angiogenesis of pancreatic cancer via miR-451a/CDKN2D axis.	BACKGROUND: The lncRNA colorectal neoplasia differentially expressed (lncRNA CRNDE) has been reported to play a pivotal role in various cancers. However, the expression and function of CRNDE in pancreatic cancer remain unclear. The objective of this study was to investigate the effects of CRNDE on pancreatic cancer and the underlying mechanisms. METHODS: The expression of CRNDE in pancreatic cancer tissues and cell lines was determined by RT-qPCR. Proliferation and angiogenesis were detected by MTT, colony formation, transwell and tube formation assays in vitro and in vivo. ELISA assay was used to detect the secretion of VEGFA. IHC was performed to test the expression levels of Ki67 and CD31. The binding sites between CRNDE, CDKN2D and miR-451a were predicted by bioinformatics analysis. Dual luciferase reporter and RNA immunoprecipitation assays were conducted to confirm the interaction with each other. RESULTS: The results showed that CRNDE was significantly up-regulated in pancreatic cancer tissues as well as cell lines. CRNDE overexpression promoted the progression and angiogenesis of pancreatic cancer cells in vitro and in vivo. Moreover, we identified that CRNDE functioned as a sponge for miR-451a and CRNDE overexpression inhibited the expression of miR-451a. Furthermore, we confirmed that miR-451a directly interacted with CDKN2D and negatively regulated CDKN2D expression. In addition, CRNDE was found to positively regulate CDKN2D expression and mediate pancreatic cancer cell proliferation and angiogenesis through miR-451a/CDKN2D axis. CONCLUSION: CRNDE modulates cell proliferation and angiogenesis via miR-451a/CDKN2D axis in pancreatic cancer, which provides a potential therapeutic target for pancreatic cancer treatment.	NA	Transl Oncol. 2021 Jul;14(7):101088. doi: 10.1016/j.tranon.2021.101088. Epub 2021 Apr 18.
3423	Circular RNA	CircRNA_2646	miR-124	PLP2	ESCC Eca109 and TE-1 cells	Esophageal Squamous Cancer	Homo sapiens (human)	Luciferase reporter assay;	33976115	CircRNA_2646 functions as a ceRNA to promote progression of esophageal squamous cell carcinoma via inhibiting miR-124/PLP2 signaling pathway.	MicroRNA-124 (miR-124) has been predicted as a tumor suppressor in esophageal squamous cell carcinoma (ESCC). However, factors contributing to miR-124 reduction remain unclear. Circular RNAs (circRNAs) are a new family of non-coding RNAs with gene regulatory potential via interacting with miRNAs. We predicted three circRNAs, including CircRNA_14359, CircRNA_2646, and CircRNA_129, that could interact with miR-124 by bioinformatics analysis and determined their expressions in ESCC tissues and adjacent normal tissues. We found that CircRNA_2646 was up-regulated in ESCC, negatively correlated with the expression of miR-124 and positively associated with TNM stage and lymph node metastasis of ESCC. Luciferase reporter assay showed that CircRNA_2646 interacted with miR-124 in ESCC Eca109 and TE-1 cells. Moreover, ectopical overexpression of CircRNA_2646 accelerated cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT), but restoration of miR-124 abrogated these functions and promoted Bcl-2-dependent cell apoptosis. Furthermore, it was found that the oncogene Proteolipid Protein 2 (PLP2) was the target gene of miR-124. In Eca109 and TE-1 cells, restoration of miR-124 decreased the level of PLP2 and inhibited PLP2-induced cell proliferation, migration, invasion, and EMT, but enhanced cell apoptosis. The in vivo study confirmed that CircRNA_2646 promoted ESCC development by repressing miR-124 and activating PLP2. Taken together, we identified that CircRNA_2646 functioned as an inhibitor in miR-124 signaling pathway in ESCC for carcinogenesis and could be a promising target for ESCC therapy.	NA	Cell Death Discov. 2021 May 11;7(1):99. doi: 10.1038/s41420-021-00461-9.
3424	LncRNA	MALAT1	miR-20b-5p	TXNIP	NA	Liver Inflammation	Homo sapiens (human)	ChIP;	33775752	The identify role and molecular mechanism of the MALAT1/hsa-mir-20b-5p/TXNIP axis in liver inflammation caused by CHB in patients with chronic HBV infection complicated with NAFLD.	BACKGROUND/AIMS: To identify the inflammatory damage caused by chronic hepatitis B (CHB) in patients of chronic hepatitis B virus (HBV) infection complicated with non-alcoholic fatty liver disease (NAFLD), then guiding clinicians to carry out antiviral treatment. METHODS: According to the pathological features of liver biopsy, treatment-naïve obese patients of chronic HBV infection complicated with NAFLD who had elevated alanine transaminase (ALT) were divided into CHB group and NASH group. Transcriptome chips were used to analyze the expression profiles of long non-coding RNA (lncRNA) and mRNA in liver puncture tissues from the two groups. The chip data of CHB and NASH groups were analyzed for differential expression analysis, gene function analysis, signal pathway analysis, target gene prediction and competing endogenous RNAs (ceRNA) network analysis. RESULTS: By comparing CHB group with NASH group, a total of 44 differentially expressed lncRNAs and 567 differentially expressed mRNAs were screened. GO analysis predicted that the differentially expressed mRNAs may affect monooxygenase activity and oxidoreductase activity. KEGG analysis predicted that the differentially expressed mRNAs may be related to signaling pathways involved in oxidative phosphorylation, phagosomes, and NAFLD. Differential analysis of lncRNA shown that the expression of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) in CHB group was significantly upregulated. Subsequently, through target gene prediction and ceRNA network analysis, we found thioredoxin interacting protein (TXNIP), which was significantly upregulated in the CHB group and had a ceRNA relationship with MALAT1. It is predicted that there may be a ceRNA regulation relationship of MALAT1/hsa-miR- 20b-5p/TXNIP. CONCLUSION: The MALAT1/hsa-miR-20b-5p/TXNIP axis may mediate CHB-induced inflammatory damage in chronic HBV infection complicated with NAFLD, and the mechanism may be related to the activation of NLRP3 inflammatory bodies and downstream inflammatory responses.	NA	Virus Res. 2021 Jun;298:198405. doi: 10.1016/j.virusres.2021.198405. Epub 2021 Mar 26.
3425	LncRNA	MT1JP	miR-24-3p	BCL2L2	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Rescue assay;RNA sequencing;	33974236	MT1JP-mediated miR-24-3p/BCL2L2 axis promotes Lenvatinib resistance in hepatocellular carcinoma cells by inhibiting apoptosis.	PURPOSE: Lenvatinib is a long-awaited alternative to Sorafenib for first-line targeted therapy of patients with advanced hepatocellular carcinoma (HCC). However, resistance to Lenvatinib results in tumor progression and has become a major obstacle to improving the prognosis of HCC patients. Exploring the mechanisms underlying Lenvatinib resistance is considered essential for the treatment of advanced HCC. METHODS: Lenvatinib resistant HCC (LR-HCC) cells were generated and potential long non-coding RNAs (Lnc-RNAs) upregulated in LR-HCC cells were identified by RNA sequencing. The effects of upregulated Lnc-RNAs were evaluated in vitro in cell models and in vivo in experimental animals using quantitative cell viability and apoptosis assays. RESULTS: We found that Lnc-RNA MT1JP (MT1JP) was upregulated in LR-HCC cells and inhibited the apoptosis signaling pathway. In addition, we found that sponging of microRNA-24-3p by MT1JP released Bcl-2 like 2 (BCL2L2), an anti-apoptotic protein, thereby forming a positive-feedback loop. The role of this feedback loop was validated using rescue assays. Additionally, we found that upregulation of MT1JP and BCL2L2 impaired the sensitivity of HCC cells to Lenvatinib both vitro and vivo. CONCLUSIONS: Our results suggest a novel molecular feedback loop between MT1JP and apoptosis signaling in Lenvatinib sensitive HCC cells.	NA	Cell Oncol (Dordr). 2021 May 11. doi: 10.1007/s13402-021-00605-0.
3426	LncRNA	GAS5	miR-217	STAT5	Th17 cells	Pneumonia 	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33862314	Long non-coding RNA GAS5 regulates Th17/Treg imbalance in childhood pneumonia by targeting miR-217/STAT5.	The imbalance of helper T (Th) 17 and regulatory T (Treg) cells plays an important role in the pathogenesis of pneumonia. This study aims to investigate the role and mechanism of long non-coding RNA growth arrest-specific 5 (GAS5) in the differentiation of Th17 cells and Tregs in childhood pneumonia. Expression of GAS5, miR-217, signal transducer and activator of transcription-5 (STAT5), receptor-related orphan receptor γt (RORγt), and transcription factor Forkhead box P3 (Foxp3) were examined by qRT-PCR and western blot. The percentage of Th17 cells and Tregs in CD4(+) T cells were measured by flow cytometry. The interaction between miR-217 and GAS5 or STAT5 was analyzed by luciferase reporter assay. Downregulated GAS5 expression and Treg cell percentage, and upregulated Th17 cell percentage were observed in pneumonia patients when compared with the healthy controls. Furthermore, GAS5 overexpression corrected the imbalanced Th17/Treg in peripheral blood CD4(+) T cells derived from pneumonia patients, and this effect was reversed by miR-217 mimic and STAT5 silencing. Mechanistically, GAS5 acted as a sponge of miR-217 to reduce binding of miR-217 to its target STAT5, leading to upregulation of STAT5 expression. Taken together, GAS5 corrects the Treg/Th17 imbalance by targeting the miR-217/STAT5 axis in childhood pneumonia.	NA	Cell Immunol. 2021 Jun;364:104357. doi: 10.1016/j.cellimm.2021.104357. Epub 2021 Apr 1.
3427	LncRNA	SNHG12	miR-516a-5p	HEG1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RIP assay;Western blot;Flow Cytometry assay;luciferase assay;	33774129	LncRNA SNHG12 promotes proliferation and epithelial mesenchymal transition in hepatocellular carcinoma through targeting HEG1 via miR-516a-5p.	Hepatocellular carcinoma (HCC) is the most common cancer and its prognosis is poor due to metastasis and recurrence. EMT is associated with metastasis. A deep understanding of regulatory mechanism of EMT is critical. LncRNA is involved in regulation of various biological processes including EMT. This study aimed to investigate the regulatory signal axis among lncRNA SNHG12, miR-516a-5p and the target gene HEG1 during EMT. Cell cycle and apoptosis were analyzed by flow cytometry. Tumorigenesis was analyzed by clone formation assay. Wound healing assay and transwell assay was performed to detect migration and invasion, respectively. Interaction among SNHG12, miR-516a-5p and HEG1 were analyzed by dual luciferase assay and RIP assay. We also detected expression of RNA and protein by QPCR and western blotting. Finally, tumor growth was analyzed by tumorigenesis assay in vivo. Ki-67 and HEG1 level in tumor tissues was analyzed by IHC. SNHG12 and HEG1 were upregulated, miR-516a-5p was downregulated in HCC cell lines. SNHG12 could interact with and inhibit miR-516a-5p. MiR-516a-5p could interact with HEG1 and inhibit HEG1 expression. Knock down SNHG12 inhibited proliferation, migration, invasion, EMT and promoted apoptosis of HCC cells. Such effects were antagonized by inhibiting miR-516a-5p. SNHG12 overexpression lead to opposite results. Similar results were observed in mice. SNHG12 could promote EMT in HCC through targeting and inhibiting miR-516a-5p, which eventually upregulated HEG1 expression, in both cell and mice.	NA	Cell Signal. 2021 Aug;84:109992. doi: 10.1016/j.cellsig.2021.109992. Epub 2021 Mar 24.
3428	Circular RNA	CircHIPK3	miR-29b	AKT3	NA	Ischemia Reperfusion Injury	Homo sapiens (human)	ChIP;qPCR;Immunohistochemistry;luciferase assay;	33951290	High glucose protects cardiomyocytes against ischaemia/reperfusion injury by suppressing myocardiocyte apoptosis via circHIPK3/miR-29b/AKT3 signalling.	High glucose promoted expression of AKT3, a direct target gene of miR-29b, by regulating circHIPK3 that functioned as ceRNA to sponge and down-regulate miR-29b. As a potential target gene of miR-29b, AKT3 plays a crucial role in the pathogenesis of myocardial ischaemia/reperfusion (I/R) injury, and this study aimed to investigate the potential role of high glucose in the outcome of I/R injury. qPCR and luciferase assay were carried out to investigate the relationship between the expression of circHIPK3, miR-29b and ATK3 mRNA. Immunohistochemistry and TUNEL were performed to analyse the relationship between AKT3 expression and apoptosis of myocardiocytes in vivo. No obvious difference in myocardial functions was observed between I/R and control rats under hyperglycaemia (HG) and normal glucose (NG) conditions, except that the infarct size/area at risk (IS/AR) ratio and the amount of h-FABP expression were different under HG and NG conditions. The expression of circHIPK3 and ATK3 was significantly elevated in the rats preconditioned by NG, whereas the expression of miR-29a was remarkably decreased. Meanwhile, the apoptosis of myocardial tissue was reduced in the rats preconditioned by NG. Luciferase assay confirmed that miR-29a played a repressive role in the expression of circHIPK3 and ATK3. And subsequent study indicated that the over-expressed AKT3 could rescue the increased cell apoptosis rate induced by the knockdown of circHIPK3. In this study, we demonstrated that high glucose protects cardiomyocytes against I/R associated injury by suppressing apoptosis and high glucose promoted the expression of AKT3 by regulating the expression of circHIPK3/miR-29b.	NA	J Cell Mol Med. 2021 May 5. doi: 10.1111/jcmm.16527.
3429	LncRNA	TUG1	miR-27b-3p	TAK1	NA	Hypertrophic Scar	Homo sapiens (human)	MTT assay;RACE;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33791919	LncRNA TUG1 exhibits pro-fibrosis activity in hypertrophic scar through TAK1/YAP/TAZ pathway via miR-27b-3p.	Hypertrophic Scar (HS) is a complicated fibrotic disease. In addition, its pathogenesis is still to be further explored. Long non-coding RNAs (lncRNAs) have been proved to be participated in multiple diseases, including HS. However, the role of lncRNA TUG1 in HS remains unclear. The expression level of RNA and protein in cells were detected by q-PCR and western blot, respectively. MTT assay was performed to test the cell proliferation. Cell migration was detected by transwell assay. Cell apoptosis was measured by flow cytometry. Dual luciferase report assay and RNA pull down were used to verify the relationship between TUG1, miR-27b-3p and TAK1.TUG1 and TAK1 were upregulated in HS, while miR-27b-3p was downregulated. Knockdown of TUG1 significantly suppressed the proliferation and migration and induced the apoptosis of HS fibroblasts (HSF). In addition, silencing of TUG1 notably inhibited the extracellular matrix (ECM) biosynthesis in HSF. Overexpression of miR-27b-3p has the same effect on HS as that of TUG1 knockdown. Meanwhile, TUG1 could sponge miR-27b-3p, and TAK1 was the direct target of miR-27b-3p. Furthermore, knockdown of TUG1 significantly suppressed the fibrosis in HS via miR-27b-3p/TAK1/YAP/TAZ axis mediation. LncRNA TUG1 promotes the fibrosis in HS via sponging miR-27b-3p and then activates TAK1/YAP/TAZ pathway, which may serve as a potential target for treatment of HS.	NA	Mol Cell Biochem. 2021 Mar 31. doi: 10.1007/s11010-021-04142-0.
3430	Circular RNA	CircCCND1	miR-187-3p	FGF9	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33733860	circCCND1 Regulates Oxidative Stress and FGF9 to Enhance Chemoresistance of Non-Small Cell Lung Cancer via Sponging miR-187-3p.	Circular RNAs have been shown to regulate cancer tumorigenesis and drug resistance. Recently, circCCND1 is reported to promote laryngeal squamous cell carcinoma; however, whether circCCND1 is implicated in non-small cell lung cancer (NSCLC) remains unclear. In this research, The Cancer Genome Atlas data of lung adenocarcinoma were analyzed to show gene expression and overall survival. 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide assay and cell colony formation assay were utilized to measure cell viability and proliferation of A549 and HCC827. Apoptosis was detected by TdT-mediated dUTP Nick-End Labeling assay. Besides, reverse transcription-quantitative PCR was used to examine gene expression. We observed that circCCND1 was significantly upregulated in lung cancer cells and patients. circCCND1 knockdown attenuated cell proliferation and induced apoptosis under cisplatin treatment. Mechanistically, circCCND1 interacted with miR-187-3p to regulate reactive oxygen species and FGF9 in NSCLC cells. Finally, miR-187-3p was demonstrated to rescue circCCND1 knockdown-modulated chemoresistance of NSCLC cells. In this study, our conclusions facilitate the understanding of NSCLC drug resistance to cisplatin.	NA	DNA Cell Biol. 2021 May;40(5):675-682. doi: 10.1089/dna.2020.6412. Epub 2021 Mar 17.
3431	LncRNA	PVT1	miR-325-3p	Snail1	Mesangial cells	Diabetic Nephropathy	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	33907435	LncRNA PVT1 Regulates High Glucose-Induced Viability, Oxidative Stress, Fibrosis, and Inflammation in Diabetic Nephropathy via miR-325-3p/Snail1 Axis.	BACKGROUND: Diabetic nephropathy (DN), as a complication of diabetes, is a leading cause of mortality in diabetic patients. It has been reported that lncRNA PVT1 (PVT1) could accelerate the progression of DN by promoting ECM accumulation and increasing the expression of fibronectin 1 (FN1). However, the underlying mechanism of PVT1 on DN remains unknown. METHODS: To study the effect of PVT1 on DN, mice were injected 50 mg/kg STZ to build the DN models. Mesangial cells (MCs) were induced by high glucose as in vitro model of DN. The expression level of PVT1, miR-325-3 and Snail1 was assessed by qRT-PCR and Western blot. Luciferase reporter assay, RNA pull-down and RIP were used to explore the interaction among PVT1, miR-325-3 and Snail1. RESULTS: In in vivo and in vitro DN models, the expression of PVT1 was upregulated. High glucose (HG) induced cell viability, oxidative stress, fibrosis and inflammation in MCs, which were reversed in the PVT1-KD MCs. The level of miR-325-3p was also increased in in vivo and in vitro experiments. Additionally, PVT1 can directly bind to miR-325-3p. Finally, Snail1 was a direct target of miR-325-3p. CONCLUSION: PVT1 inhibits viability, oxidative stress, fibrosis, and inflammation in DN via miR-325-3p/Snail1 axis.	NA	Diabetes Metab Syndr Obes. 2021 Apr 19;14:1741-1750. doi: 10.2147/DMSO.S303151. eCollection 2021.
3432	LncRNA	PVT1	miR-29a	HMGB1	NA	Sepsis-Induced Myocardial Injury	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;luciferase assay;	33840587	Knockdown of lncRNA PVT1 attenuated macrophage M1 polarization and relieved sepsis induced myocardial injury via miR-29a/HMGB1 axis.	BACKGROUND: LncRNA PVT1 was reported to be elevated in septic myocardial tissue. The underlying mechanism by which PVT1 aggravated sepsis induced myocardial injury needs further investigation. METHODS: Mice was subjected to LPS injection to mimic in vivo sepsis model. HE staining was applied to observe tissue injury. Cardiac function of mice was determined by echocardiography. Bone marrow derived macrophage (BMDM) was used to confirm the regulatory effect of PVT1 in macrophage polarization. Western blotting or qRT-PCR were performed to evaluate protein or mRNA levels, respectively. ELISA was conducted to determine cytokine levels. Interaction between PVT1 and miR-29a, miR-29a and HMGB1 were accessed by dual luciferase assay. RESULTS: Expression of PVT1 was elevated in myocardial tissue and heart infiltrating macrophages of sepsis mice. PVT1 knockdown alleviated LPS induced myocardial injury and attenuated M1 macrophage polarization. The mechanic study suggested that PVT1 targeted miR-29a, thus elevated expression of HMGB1, which was repressed by miR-29a targeting. The effect of PVT1 on M1 macrophage polarization was dependent on targeting miR-29a. CONCLUSION: PVT1 promoted M1 polarization and aggravated LPS induced myocardial injury via miR-29a/HMGB1 axis.	NA	Cytokine. 2021 Jul;143:155509. doi: 10.1016/j.cyto.2021.155509. Epub 2021 Apr 9.
3433	LncRNA	LINC00665	miR-379-5p	GRP78	GC cells	Gastric Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34149174	LINC00665/miR-379-5p/GRP78 regulates cisplatin sensitivity in gastric cancer by modulating endoplasmic reticulum stress.	Acquired resistance to cisplatin (DDP)-based chemotherapy greatly hinders the treatment of gastric cancer (GC). LINC00665 serves as an oncogene in GC. Hence, the current study was designed to investigate the regulatory effects of LINC00665 on DDP-resistance of GC. LINC00665 and miR-379-5p expression levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and Glucose regulated protein 78 (GRP78) protein level was measured by western blot assay. Interactions between LINC00665 and miR-379-5p or between miR-379-5p and GRP78 were verified by dual luciferase reporter assay. Cell counting kit 8 (CCK-8) assay and flow cytometry assay respectively determine the proliferative ability and apoptosis of GC cells. Western blot analysis was also performed to detect the protein levels of C/EBP-homologous protein (CHOP), X box binding protein (XBP1) and apoptosis-related proteins. In addition, GRP78 expression was evaluated by immunofluorescence. It was observed that the expression levels of LINC00665 and GRP78 were upregulated, and the expression level of miR-379-5p was downregulated in DDP-sensitive and DDP-resistant GC cell lines. What's more, GRP78 expression and the cell growth inhibition rates of DDP-sensitive and DDP-resistant GC cells had a negative correlation. Additionally, miR-379-5p was a target miRNA of LINC00665, and GRP78 was a target mRNA of miR-379-5p. Functional studies revealed that knockdown of LINC00665 inhibited DDP-resistant GC cell proliferation, induced apoptosis as well as suppressed Endoplasmic reticulum (ER) stress. Mechanistically, knockdown of LINC00665 downregulated GRP78 expression by strengthening miR-379-5p. LINC00665 silencing could overcome DPP-resistance of GC cells by downregulating GRP78 via sponging miR-379-5p, indicating that LINC00665 might be a potential therapeutic target for DDP- resistant GC patients.	NA	Cytotechnology. 2021 Jun;73(3):413-422. doi: 10.1007/s10616-021-00466-3. Epub 2021 Apr 26.
3434	LncRNA	MFAT1	miR-135a-5p-Tgfbr2	Smad4	NA	Skeletal Muscle Fibrosis	Homo sapiens (human)	qRT-PCR	33837645	Long non-coding RNA MFAT1 promotes skeletal muscle fibrosis by modulating the miR-135a-5p-Tgfbr2/Smad4 axis as a ceRNA.	Fibrosis after skeletal muscle injury is common in sports and can cause irreversible damage to the biomechanical properties of skeletal muscle. Long non-coding RNAs (lncRNAs) have been validated to act as important modulators in the fibrosis of various organs. Here, we reported a novel lncRNA (the skeletal muscle fibrosis-associated transcript 1, lnc-MFAT1), which was highly expressed in skeletal muscle fibrosis. We demonstrate that lnc-MFAT1 knockdown can reduce TGFβ-induced fibrosis in vitro and attenuate skeletal muscle fibrosis after acute contusion in mice. Further study showed that lnc-MFAT1 acted as a competitive endogenous RNA of miR-135a-5p. Besides, the miR-135a-5p inhibition obviously promoted TGFβ-induced fibrosis in vitro via enhancing its target genes Tgfbr2/Smad4. Moreover, we discovered that lnc-MFAT1 regulates Tgfbr2/Smad4 expression by sponging miR-135a-5p to exert competing endogenous RNA function, resulting in TGFβ pathway activation. In conclusion, our study identified a crucial role of lnc-MFAT1-miR-135a-Tgfbr2/Smad4 axis in skeletal muscle fibrosis, providing a promising treatment option against skeletal muscle fibrosis.	NA	J Cell Mol Med. 2021 May;25(9):4420-4433. doi: 10.1111/jcmm.16508. Epub 2021 Apr 9.
3435	LncRNA	ARAP1-AS1	miR-4735-3p	PLAGL2	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	34149172	LncRNA ARAP1-AS1 aggravates the malignant phenotypes of ovarian cancer cells through sponging miR-4735-3p to enhance PLAGL2 expression.	Ovarian cancer is one of the leading lethal gynecological cancers, causing serious harm to the health of female populations. Growing studies emphasize that lncRNAs serve as significant regulators in the tumorigenesis and evolution of numerous malignancies, including ovarian cancer. Recently, the oncogenic activity of lncRNA ARAP1-AS1 has been justified in a variety of cancers. However, the potential function of ARAP1-AS1 in ovarian cancer development is still unclear. Herein, we firstly revealed the expression profile of ARAP1-AS1 in ovarian cancer. Compared to normal samples and cells, upregulation of ARAP1-AS1 was observed in tissues and cells of ovarian cancer. Therewith, it was disclosed that knockdown of ARAP1-AS1 alleviated the carcinogenicity of ovarian cancer cells. Besides, our findings delineated that ARAP1-AS1 silence inhibited the expression of oncogene PLAGL2. Considering that ARAP1-AS1 was principally expressed in the the cytoplasm of ovarian cancer cells, we speculated that ARAP1-AS1 facilitated ovarian cancer progression via functioning as a ceRNA. Further investigations indicated that ARAP1-AS1 promoted PLAGL2 expression by competitively binding with miR-4735-3p. Of note, ARAP1-AS1 contributed to the malignant phenotypes of ovarian cancer cells through modulation of miR-4735-3p/PLAGL2 axis, revealing ARAP1-AS1 as a promising therapeutic target for ovarian cancer patients.	NA	Cytotechnology. 2021 Jun;73(3):363-372. doi: 10.1007/s10616-021-00463-6. Epub 2021 Apr 3.
3436	LncRNA	LINC01614	miR-520a-3p	SNX3	OS cells	Osteosarcoma 	Homo sapiens (human)	qRT-PCR	33753211	LINC01614 promotes osteosarcoma progression via miR-520a-3p/SNX3 axis.	Long noncoding RNAs (lncRNAs) have been reported as essential regulators in osteosarcoma (OS), the most malignant bone tumor usually observed in children and adolescents. In the present study, we detected differentially expressed lncRNAs among OS tissues through RNA-sequencing. Then through bioinformatics analysis, we constructed the aberrant lncRNAs regulatory networks, and detected the key-lncRNAs. We identified LINC01614 was most significantly up-regulated among OS tissues, which was positively correlated with the worse prognosis. Through related in vitro experiments, we confirmed that knockdown of LINC01614 could inhibit the proliferation, invasion, and metastasis activities of OS cells. Furthermore, we identified LINC01614 may promote the proliferation and invasion activities of OS cells, via binding miR-520a-3p and increase the expression of SNX3. In conclusion, we identified lncRNAs participate in various malignant behaviors in OS. We also proved that LINC01614 could function as competing endogenous RNAs and promote the proliferation, and invasion of OS cells through miR-520a-3p/SNX3 axis, and thus acts as a novel prognostic marker for OS in clinic.	NA	Cell Signal. 2021 Jul;83:109985. doi: 10.1016/j.cellsig.2021.109985. Epub 2021 Mar 20.
3437	LncRNA	SNHG1	miR-330-5p	DCLK1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33753110	LncRNA SNHG1 contributes to the cisplatin resistance and progression of NSCLC via miR-330-5p/DCLK1 axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) are involved in the occurrence and progression of multiple cancers, including non-small cell lung cancer (NSCLC). Herein, we explored the exact role and underlying mechanism of lncRNA small nucleolar RNA host gene 1 (SNHG1) in NSCLC. METHODS: The levels of SNHG1, microRNA-330-5p (miR-330-5p) and doublecortin-like kinase 1 (DCLK1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was carried out to measure the chemoresistance and proliferation of NSCLC cells. The metastasis and apoptosis of NSCLC cells were examined by transwell migration and invasion assays and flow cytometry. Western blot assay was conducted to detect the levels of proliferation-associated proteins and DCLK1. The interaction between miR-330-5p and SNHG1 or DCLK1 was predicted by StarBase and microT_CDS databases. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to validate these interactions. In vivo chemosensitivity experiment was conducted to assess the function of SNHG1 in the chemoresistance of NSCLC in vivo. RESULTS: SNHG1 was dramatically up-regulated in cisplatin (DDP)-resistant NSCLC tissues and cells. SNHG1 promoted the DDP resistance and malignant behaviors of NSCLC cells. SNHG1 functioned through targeting miR-330-5p, and si-SNHG1-mediated effects in NSCLC cells were attenuated by the addition of in-miR-330-5p. DCLK1 messenger RNA (mRNA) could directly bind to miR-330-5p, and miR-330-5p acted as a tumor suppressor in NSCLC through down-regulating DCLK1. SNHG1 silencing elevated the DDP sensitivity of NSCLC cells in vivo. CONCLUSION: SNHG1 elevated DDP resistance and malignant potential of NSCLC cells through elevating the level of DCLK1 via sponging miR-330-5p.	NA	Exp Mol Pathol. 2021 Jun;120:104633. doi: 10.1016/j.yexmp.2021.104633. Epub 2021 Mar 19.
3438	LncRNA	NORAD	miR-541-3p	PKM2	prostate cancer cell	Prostate Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RACE;luciferase assay;	33722248	Long non-coding RNA NORAD promotes the prostate cancer cell extracellular vesicle release via microRNA-541-3p-regulated PKM2 to induce bone metastasis of prostate cancer.	BACKGROUND: Bone metastasis is the leading cause of mortality and reduced quality of life in patients with metastatic prostate cancer (PCa). Long non-coding RNA activated by DNA damage (NORAD) has been observed to have an abnormal expression in various cancers. This article aimed to explore the molecular mechanism underlying the regulatory role of NORAD in bone metastasis of PCa. METHODS: NORAD expression in clinical PCa tissues and cell lines was detected with the application of qRT-PCR. Cancer cells were then transfected with plasmids expressing NORAD, after which Transwell assay and CCK-8 assay were carried out to detect proliferation, migration, and bone metastasis of PCa. NORAD downstream target molecules were screened through bioinformatics analysis, followed by further verification using dual luciferase assay. Extracellular vesicles (EVs) were labeled with PKH67 and interacted with bone marrow stromal cells. The gain- and loss-function method was applied to determine the internalization and secretion of PCa cells-derived EVs under the intervention of downstream target molecules or NORAD. RESULTS: PCa tissues and cell lines were observed to have a high expression of NORAD, particularly in tissues with bone metastasis. NORAD knockdown resulted in reduced secretion and internalization of EVs, and suppressed proliferation, migration, and bone metastasis of PCa cells. It was indicated that NORAD interacted with miR-541-3p, leading to the upregulation of PKM2. Forced expression of PKM2 promoted the transfer of PKH67-labeled EVs to bone marrow stromal cells. CONCLUSIONS: NORAD might serve as a ceRNA of miR-541-3p to promote PKM2 expression, thereby enhancing the development of bone metastasis in PCa by promoting internalization and transfer of EVs of cancer cells, providing an insight into a novel treatment for the disorder.	NA	J Exp Clin Cancer Res. 2021 Mar 16;40(1):98. doi: 10.1186/s13046-021-01891-0.
3439	LncRNA	NEAT1	miR-155-5p	MyD88	BEAS-2B cells	Bronchopneumonia 	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;	33719773	LncRNA NEAT1 activates MyD88/NF-κB pathway in bronchopneumonia through targeting miR-155-5p.	BACKGROUND: Bronchopneumonia is a disease of the respiratory tract. It leads to other complications and endangers life and health. Long non-coding RNA (lncRNA) participates in the occurrence and development of bronchopneumonia. Nuclear paraspeckle assembly transcript 1 (NEAT1) plays a key role in inflammatory diseases, but the function of NEAT1 in bronchopneumonia remains unclear. METHODS: RT-qPCR and Western blotting were performed to determine genes and proteins expressions. MTT was applied to test cell viability. Cell apoptosis was detected by flow cytometry. RIP was used to investigate the correlation between NEAT1 and miR-155-5p. The interaction between miR-155-5p and NEAT1 or MyD88 was evaluated by the dual-luciferase reporter gene. RESULTS: NEAT1 and MyD88 were upregulated in BEAS-2B cells by LPS, while miR-155-5p was downregulated. Knockdown of NEAT1 inhibited LPS-induced BEAS-2B cells growth inhibition by inhibiting the apoptosis. In addition, NEAT1 silencing suppressed LPS-induced inflammatory responses in BEAS-2B cells via suppression of TNF-α, IL-1β, IL-6, and IL-18. Meanwhile, NEAT1 is directly bound to miR-155-5p to regulate MyD88/NF-κB axis, and overexpression of miR-155-5p increased cell proliferation and suppressed inflammatory factors expression levels and cell apoptosis. Furthermore, sh-NEAT1-induced inhibition of BEAS-2B cells injury was partially reversed by miR-155-5p inhibitor or MyD88 overexpression. CONCLUSION: NEAT1 silencing suppressed LPS-induced BEAS-2B cells injury and inflammation by the mediation of miR-155-5p/MyD88/NF-κB axis. Thus, our study might shed new light on exploring the new strategies for the treatment of bronchopneumonia.	NA	Autoimmunity. 2021 Mar;54(2):104-113. doi: 10.1080/08916934.2021.1891534. Epub 2021 Mar 9.
3440	LncRNA	SNHG15	miR-451	c-Myc	BC cells	Breast Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;Western blot;Immunohistochemistry;	33952250	Targeting a novel LncRNA SNHG15/miR-451/c-Myc signaling cascade is effective to hamper the pathogenesis of breast cancer (BC) in vitro and in vivo.	BACKGROUND: To our knowledge, LncRNA SNHG15 exerted its tumor-promoting effects to facilitate the development of breast cancer (BC), but there still needed more data to elucidate the potential underlying mechanisms. METHODS: We examined genes expression status by performing Real-Time qPCR and Western Blot analysis, and cellular functions, including cell proliferation, viability, apoptosis, mobility, were measured by using the CCK-8 assay, colony formation assay, trypan blue staining assay, flow cytometer (FCM), transwell assay and wound scratch assay, respectively. The predicted targeting sites in LncRNA SNHG15, miR-451 and c-Myc 3'UTR were validated by dual-luciferase reporter gene system assay. Finally, we established the tumor-bearing mice models, and the expression status, including its enrichment and cellular localization were examined by immunohistochemistry (IHC) assay. RESULTS: Our data indicated LncRNA SNHG15 upregulated c-Myc to facilitate BC progression by sponging miR-451 in a competing endogenous RNA (ceRNA)-dependent manner in vitro and in vivo. Specifically, LncRNA SNHG15 and c-Myc were upregulated, while miR-451 was downregulated in BC cells and clinical tissues, compared to their normal counterparts. In addition, miR-451 negatively correlated with LncRNA SNHG15 and c-Myc, and LncRNA SNHG15 was positively relevant to c-Myc in BC tissues. Next, we validated that LncRNA SNHG15 sponged miR-451 to upregulate c-Myc in BC cells. Further gain- and loss-of-function experiments evidenced that LncRNA SNHG15 promoted, while miR-451 inhibited malignant phenotypes, including cell proliferation, viability, migration, invasion and epithelial-mesenchymal transition (EMT) in BC cells. Interestingly, the inhibiting effects of LncRNA SNHG15 ablation on BC progression were abrogated by both silencing miR-451 and overexpressing c-Myc. CONCLUSIONS: We concluded that targeting the LncRNA SNHG15/miR-451/c-Myc signaling cascade was novel to hamper BC progression, which broadened our knowledge in this field, and provided potential biomarkers for BC diagnosis and treatment.	NA	Cancer Cell Int. 2021 Mar 31;21(1):186. doi: 10.1186/s12935-021-01885-0.
3441	LncRNA	LSINCT5	miR-185-5p	ZNF703	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33721442	LncRNA LSINCT5 drives proliferation and migration of oral squamous cell carcinoma through the miRNA-185-5p/ZNF703 axis.	PURPOSE: To analyze the role of lncRNA LSINCT5 in oral squamous cell carcinoma (OSCC) progression and the molecular mechanism. METHODS: QRT-PCR was conducted to detect LSINCT5 levels in OSCC tissues and cell lines. Survival analysis in OSCC patients based on LSINCT5 levels was performed using Kaplan-Meier method. Influence of LSINCT5 on functions of OSCC cells were assessed by CCK-8, EdU and Transwell assay. Bioinformatic analysis and dual-luciferase reporter assay were carried out to identify the interaction between LSINCT5 and the miRNA (miR)-185-5p/zNF703 axis. Rescue experiments were conducted to uncover the molecular mechanism of LSINCT5 in regulating OSCC cell functions. RESULTS: LSINCT5 was upregulated in OSCC specimens and correlated to poor prognosis of OSCC. Knockdown of LSINCT5 inhibited proliferative and migratory capacities of OSCC. LSINCT5 could target and negatively regulate miR-185-5p. Moreover, miR-185-5p was the key downstream gene that was responsible for the carcinogenic role of LSINCT5 in regulating OSCC cell functions. The oncogenic gene ZNF703 was proven to be the target binding miR-185-5p. CONCLUSIONS: LSINCT5 is abnormally upregulated in OSCC specimens and drives its malignant progression through the miR-185-5p/ZNF703 axis.	NA	J BUON. 2021 Jan-Feb;26(1):124-131.
3442	LncRNA	LINC01977	miR-212-3p	GOLM1	NA	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	33869063	LINC01977 Promotes Breast Cancer Progression and Chemoresistance to Doxorubicin by Targeting miR-212-3p/GOLM1 Axis.	Long non-coding RNAs(lncRNAs) play an important role in cancer initiation and progression. However, hub lncRNAs involved in breast cancer still remain underexplored. In this study, integrated bioinformatics analysis was used to define LINC01977 as a key oncogenic driver in breast cancer. Subsequently, in vitro assays showed that LINC01977 could significantly promote breast cancer progression and chemoresistance to doxorubicin. To further investigate its biological mechanism, we performed dual-luciferase reporter assay, real-time PCR, RNA immunoprecipitation (RIP), and rescue assay. Our results indicated that LINC01977 may function as ceRNA to prevent GOLM1 gene from miRNA-mediated repression by sponging miR-212-3p. Overall, LINC01977 can serve as a novel prognostic indicator, and help develop more effective therapeutic approaches for breast cancer patients.	NA	Front Oncol. 2021 Mar 31;11:657094. doi: 10.3389/fonc.2021.657094. eCollection 2021.
3443	LncRNA	OGRU	miR-320	USP14	Müller cells	Diabetic Retinopathy	Homo sapiens (human)	qRT-PCR	33762162	Suppressing long noncoding RNA OGRU ameliorates diabetic retinopathy by inhibition of oxidative stress and inflammation via miR-320/USP14 axis.	Long noncoding RNAs (lncRNAs) are important regulators in various diseases including diabetic retinopathy (DR). In this study, DR patients exhibited significantly increased expression of serum LncRNA-OGRU compared with normal individuals. Streptozotocin (STZ)-challenged rats with DR also had higher OGRU expression in retinas than that of the control group, which was confirmed in Müller cells upon high glucose (HG) stimulation. OGRU knockdown remarkably decreased vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1) expression in HG-incubated Müller cells. HG-induced inflammatory response and oxidative stress in vitro were markedly mitigated by OGRU knockdown through restraining IκBɑ/nuclear factor kappa beta (NF-κB) and improving nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, respectively. Further studies indicated that OGRU suppression greatly restored miR-320 expression, and a negative correlation between them was detected in DR patients. We also found that miR-320 over-expression considerably restrained TGF-β1 signaling, and hindered inflammation and reactive oxygen species (ROS) production in HG-stimulated Müller cells. Additionally, OGRU knockdown or miR-320 over-expression could dramatically down-regulate ubiquitin-specific peptidase 14 (USP14) expression levels in HG-incubated Müller cells, and miR-320 could directly target USP14. Notably, OGRU/miR-320 axis-mediated TGF-β1 signaling, inflammation and ROS were largely dependent on USP14. Intriguingly, our results showed that USP14 directly interacted with transforming growth factor-beta type 1 receptor (TβR1), and impeded TβR1 ubiquitination and degradation. Furthermore, USP14 could also facilitate IκBɑ deubiquitination and degradation, exacerbating IκBɑ phosphorylation and NF-κB activation. Finally, our in vivo studies confirmed that OGRU knockdown considerably ameliorated DR progression in STZ-challenged rats through mediating the mechanisms observed in vitro. Collectively, these findings implicated that LncRNA-OGRU mediated DR progression through competing for miR-320 to regulate USP14 expression, and thus LncRNA-OGRU/miR-320/USP14 axis may be considered as a therapeutic target for DR treatment.	NA	Free Radic Biol Med. 2021 Jun;169:361-381. doi: 10.1016/j.freeradbiomed.2021.03.016. Epub 2021 Mar 21.
3444	LncRNA	LINC00943	miR-7-5p	CXCL12	SK-N-SH cells	Parkinsons Disease	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33886117	LINC00943 knockdown exerts neuroprotective effects in Parkinson's disease through regulates CXCL12 expression by sponging miR-7-5p.	BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative movement disorder, but the pathogenesis is still unclear. Long non-coding RNAs (lncRNAs) have been reported to play a prominent role in PD. OBJECTIVE: This study is designed to explore the role and mechanism of long intergenic non-coding RNA 00943 (LINC00943) in the N-methyl-4-phenylpyridine (MPP(+))-inducted PD model. METHODS: LINC00943, microRNA-7-5p (miR-7-5p), and the chemokine (C-X-C motif) ligand 12 (CXCL12, also referred to as SDF-1) level were examined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and apoptosis were analyzed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), and flow cytometry assays, severally. Protein levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and CXCL12 were assessed by western blot assay. The ROS generation and SOD activity were detected by the corresponding kits. The binding relationship between miR-7-5p and LINC00943 or CXCL12 was predicted by Starbase and then verified by a dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. RESULTS: LINC00943 and CXCL12 were increased, and miR-7-5p was decreased in MPP(+)-inducted SK-N-SH cells. LINC00943 silencing promoted cell viability, and repressed apoptosis and the inflammatory response in MPP(+)-treated SK-N-SH cells. The mechanical analysis discovered that LINC00943 acted as a sponge of miR-7-5p to regulate CXCL12 expression. CONCLUSIONS: LINC00943 knockdown could attenuate MPP(+)-triggered neuron injury by regulating the miR-7-5p/CXCL12 axis, hinting at a promising therapeutic target for PD treatment.	NA	Genes Genomics. 2021 Jul;43(7):797-805. doi: 10.1007/s13258-021-01084-1. Epub 2021 Apr 22.
3445	LncRNA	FGD5-AS1	miR-195-5p	NUAK2	breast cancer cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;RNA pull-down;	33880593	lncRNA FGD5-AS1 promotes breast cancer progression by regulating the hsa-miR-195-5p/NUAK2 axis.	Breast cancer is the second most prevalent cancer in women worldwide. Long non-coding RNAs (lncRNAs) have been identified as important regulators of tumorigenesis and tumor metastasis. lncRNA FGD5-AS1 has been previously reported as a carcinogenic gene, however its role in breast cancer has yet to be investigated. The present study aimed to understand the function of lncRNA FGD5-AS1 in breast cancer and examine the underlying molecular mechanisms. Sample tissues for downstream gene expression profiling were collected from patients with breast cancer (n=23). The effect of FGD5-AS1 overexpression on cell viability, invasion and migration has been studied in breast cancer cells (MDA-MB-231). Changes in glycolysis were monitored by comparing glucose consumption, lactate production and ATP levels. Using StarBase and TargetScan databases a putative interaction between FGD5-AS1, miR-195-5p and SNF1-like kinase 2 (NUAK2) was predicted in silico. Expression levels of FGD5-AS1, has-miR-195-5p and NUAK2 were validated by reverse transcription-quantitative PCR and interactions were validated using dual-luciferase reporter assays and RNA pull-down. High expression of lncRNA FGD5-AS1 was detected in breast cancer tissue samples and disease model cell lines. Silencing of FGD5-AS1 led to decreased cell proliferation, migration and invasion. It was identified that at a molecular level FGD5-AS1 serves as a sponge of miR-195-5p and alters the expression of its downstream target gene NUAK2. In breast cancer lncRNA FGD5-AS1 serve a key role in glycolysis and tumor progression via the miR-195-5p/NUAK2 axis. The findings of the present study indicated FGD5-AS1 as a candidate target for intervention in patients with breast cancer.	NA	Mol Med Rep. 2021 Jun;23(6):460. doi: 10.3892/mmr.2021.12099. Epub 2021 Apr 21.
3446	Circular RNA	Circ_03955	miR-3662	HIF1A	PC cells	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33864618	Circ_03955 promotes pancreatic cancer tumorigenesis and Warburg effect by targeting the miR-3662/HIF-1α axis.	OBJECTIVES: Former studies found that circRNAs play an important part in the occurrence of a variety of malignant biological characteristics that are critical for cancer progression. It has been shown that circ_03955 is highly expressed and implicated with quantities of biological processes in solid tumor. However, whether circ_03955 regulates the tumorigenesis and Warburg effect of pancreatic cancer (PC) remains largely unknown. MATERIALS AND METHODS: The level of circ_03955 in PC tissues and cell lines was determined by real-time qPCR (RT-qPCR). Loss-of-function and gain-of-function assays were employed to investigate the biological role of circ_03955 in cell proliferation, apoptosis, and glycolysis. RT-qPCR, western blotting, bioinformatics analysis, luciferase reporter assay, and in vivo tumorigenicity assay were employed to determine the underlying mechanisms. RESULTS: In this study, it was investigated that circ_03955 was up-regulated in PC clinical samples as well as PC cell lines and associated with poor clinical outcomes of PC patients. Functional assays revealed that circ_03955 exerts a certain stimulative effect on the growth of PC cells in vitro and in vivo. Circ_03955 also inhibited apoptosis and promotes Warburg effect in PC cells. Mechanistically, bioinformatics analysis indicated that circ_03955 acts as a sponge for microRNA (miR)-3662, and hypoxia-inducible factor 1ɑ (HIF-1ɑ) was one of the transcriptional targets of miR-3662. Importantly, genetic promoting of HIF-1ɑ or downregulation of miR-3662 largely compromised circ_03955 depletion mediated tumor-inhibiting effects. CONCLUSIONS: Taken together, circ_03955 functions as a tumor promoter through miR-3662/HIF-1α axis, which might provide a novel sight for PC treatment.	NA	Clin Transl Oncol. 2021 Apr 17. doi: 10.1007/s12094-021-02599-5.
3447	LncRNA	MIR503HG	miR-224-5p	HOXA9	TNBC cells	Tnbc 	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33869743	lncRNA MIR503HG inhibits cell proliferation and promotes apoptosis in TNBC cells via the miR-224-5p/HOXA9 axis.	Triple-negative breast cancer (TNBC) is a highly invasive subtype of breast cancer. This study investigated the molecular mechanism and influences of MIR503HG, miR-224-5p, and homeobox A9 (HOXA9) on TNBC cell growth and migration. Dual-luciferase reporter gene and RNA immunoprecipitation were performed to examine the regulation of MIR503HG, miR-224-5p, and HOXA9. Cell proliferation, apoptosis, migration, and invasion were evaluated by colony formation, flow cytometry, and Transwell assays. Finally, nude mice were employed to investigate the influence of MIR503HG on TNBC tumor growth. HOXA9 protein levels were detected by immunohistochemical staining. MIR503HG and HOXA9 expression were reduced in TNBC, while miR-224-5p was increased. Overexpression of MIR503HG or HOXA9 reduced the cell migration ability and proliferation and promoted apoptosis, and knockdown of MIR503HG or overexpression of miR-224-5p exhibited the opposite effects. Furthermore, MIR503HG promoted HOXA9 expression by inhibiting miR-224-5p. Overexpression of miR-224-5p reversed the effects of MIR503HG overexpression on TNBC cells, while overexpression of HOXA9 reversed the effect of MIR503HG knockdown. Additionally, an in vivo study proved that MIR503HG inhibited TNBC tumor growth via the miR-224-5p/HOXA9 axis. MIR503HG inhibited cell proliferation and promoted the apoptosis of TNBC cells via the miR-224-5p/HOXA9 axis, which may function as a novel target for the treatment of TNBC.	NA	Mol Ther Oncolytics. 2021 Mar 17;21:62-73. doi: 10.1016/j.omto.2021.03.009. eCollection 2021 Jun 25.
3448	LncRNA	DLGAP1-AS1	miR-1297	EZH2	NA	Glioma 	Homo sapiens (human)	RNA pull-down assay;Luciferase reporter assay;RNA pull-down;	33901010	Long noncoding RNA DLGAP1-AS1 promotes the progression of glioma by regulating the miR-1297/EZH2 axis.	Dysregulated lncRNAs have been implicated in a plethora of tumors, including glioma. One such oncogenic lncRNAs that has been reported in several cancers is the lncRNA DLGAP1 antisense RNA 1 (DLGAP1-AS1). This study seeks to characterize the expression of DLGAP1-AS1 in glioma tissues, which we found to be raised in both glioma samples and cell lines. Functional experiments revealed that DLGAP1-AS1 promoted in vitro glioma cell invasion, migration and proliferation. DLGAP1-AS1 was found to function as a miR-1297 sponge, based on information from luciferase reporter assays, RNA pull-down assays and publicly available online databases. miR-1297 was in turn found to functionally target EZH2. DLGAP1-AS1 modulated EZH2 expressions through miR-1297 sponging. Glioma progression appears to be supported DLGAP1-AS1 -promoted activation of the miR-1297/EZH2 axis. The components of this axis may function as therapeutic targets for glioma.	NA	Aging (Albany NY). 2021 Apr 26;13(8):12129-12142. doi: 10.18632/aging.202923. Epub 2021 Apr 26.
3449	LncRNA	PITPNA-AS1	miR-129-5p	UNC5B	papillary thyroid cancer cells	Papillary Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33706585	Long non-coding RNA PITPNA-AS1 regulates UNC5B expression in papillary thyroid cancer via sponging miR-129-5p.	BACKGROUND: Long non-coding RNA (lncRNA) PITPNA antisense RNA 1 (PITPNA-AS1) expression characteristics, function, and mechanism in papillary thyroid cancer are unclear. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was applied for detecting PITPNA-AS1, UNC-5 netrin receptor B (UNC5B) mRNA, and miR-129-5p expressions in papillary thyroid cancer tissues and cell lines. EdU assay, cell counting kit-8 (CCK-8) assay, wound healing assay, and flow cytometry analysis were performed to investigate the biological functions of PITPNA-AS1 in papillary thyroid cancer. Dual-luciferase reporter assay was utilized for determining whether PITPNA-AS1 and miR-129-5p, as well as UNC5B and miR-129-5p could directly bind to each other. Western blot assay was employed for measuring UNC5B protein expression level in papillary thyroid cancer cell lines. RESULTS: PITPNA-AS1 and UNC5B expressions were markedly increased in papillary thyroid cancer tissues and cell lines while miR-129-5p expression was down-regulated. Knockdown of PITPNA-AS1 could significantly inhibit papillary thyroid cancer cell growth and migration and promote cell apoptosis while UNC5B overexpression plasmids or miR-129-5p inhibitors counteracted the knockdown effect of PITPNA-AS1 on papillary thyroid cancer cells. PITPNA-AS1 targeted miR-129-5p to repress its expression and miR-129-5p targeted UNC5B to repress its expression. Silencing PITPNA-AS1 reduced the expression of UNC5B via regulating miR-129-5p expression. CONCLUSIONS: PITPNA-AS1 facilitated papillary thyroid cancer cell proliferation and migration, and suppressed apoptosis through miR-129-5p/UNC5B axis.	NA	Int J Biol Markers. 2021 Mar;36(1):10-19. doi: 10.1177/1724600820985528. Epub 2021 Mar 11.
3450	LncRNA	HIF1A-AS2	miR-30a-5p	SOX4	renal carcinoma cells	Renal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33710813	LncRNA HIF1A-AS2 accelerates malignant phenotypes of renal carcinoma by modulating miR-30a-5p/SOX4 axis as a ceRNA.	OBJECTIVE: Several reports have proposed that lncRNAs, as potential biomarkers, participate in the progression and growth of malignant tumors. HIF1A-AS2 is a novel lncRNA and potential biomarker, involved in the genesis and development of carcinomas. However, the molecular mechanism of HIF1A-AS2 in renal carcinoma is unclear. METHODS: The relative expression levels of HIF1A-AS2 and miR-30a-5p were detected using RT-qPCR in renal carcinoma tissues and cell lines. Using loss-of-function and overexpression, the biological effects of HIF1A-AS2 and miR-30a-5p in kidney carcinoma progression were characterized. Dual luciferase reporter gene analysis and Western blot were used to detect the potential mechanism of HIF1A-AS2 in renal carcinomas. RESULTS: HIF1A-AS2 was upregulated in kidney carcinoma tissues when compared with para-carcinoma tissues (P < 0.05). In addition, tumor size, tumor node mestastasis stage and differentiation were identified as being closely associated with HIF1A-AS2 expression (P < 0.05). Knockdown or overexpression of HIF1A-AS2 either restrained or promoted the malignant phenotype and WNT/β-catenin signaling in renal carcinoma cells (P < 0.05). MiR-30a-5p was downregulated in renal cancers and partially reversed HIF1A-AS2 functions in malignant renal tumor cells. HIF1A-AS2 acted as a microRNA sponge that actively regulated the relative expression of SOX4 in sponging miR-30a-5p and subsequently increased the malignant phenotypes of renal carcinomas. HIF1A-AS2 showed a carcinogenic effect and miR-30a-5p acted as an antagonist of the anti-oncogene effects in the pathogenesis of renal carcinomas. CONCLUSIONS: The HIF1A-AS2-miR-30a-5p-SOX4 axis was associated with the malignant progression and development of renal carcinoma. The relative expression of HIF1A-AS2 was negatively correlated with the expression of miR-30a-5p, and was closely correlated with SOX4 mRNA levels in renal cancers.	NA	Cancer Biol Med. 2021 Mar 12:j.issn.2095-3941.2020.0209. doi: 10.20892/j.issn.2095-3941.2020.0209.
3451	LncRNA	LINC01003	miR-33a-5p	PIM1	MM cells	Myeloma 	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Luciferase reporter assay;MTT assay;	33865032	Long non-coding RNA LINC01003 suppresses the development of multiple myeloma by targeting miR-33a-5p/PIM1 axis.	BACKGROUND: Numerous long non-coding RNAs (lncRNAs) are reported to affect the progression of multiple myeloma (MM). This study is aimed to explore the role and downstream mechanism of lncRNA LINC01003 in MM. MATERIALS AND METHODS: Xenograft tumor assay was used to assess the function of LINC01003 in MM in vivo. The mRNA expression levels of LINC01003, miR-33a-5p, and PIM1 were determined by quantitative real-time polymerase chain reaction. Cell viability was examined by MTT assay. Relative protein levels of apoptosis-related factors (Bcl-2 and Bax) and proviral integration site of the Moloney leukemia virus kinase 1 (PIM1) were detected via western blot. Adhesion-related proteins were measured by Enzyme-linked immunosorbent assay was used to determine the levels of adhesion-related proteins. Besides, the target relation among LINC01003, miR-33a-5p and PIM1 was tested via dual-luciferase reporter assay. RESULTS: Low expression of LINC01003 was observed in MM cell lines and peripheral blood samples of MM patients. Both LINC01003 up-regulation and miR-33a-5p down-regulation repressed cell viability and adhesion, and promoted apoptosis of MM cells. Moreover, LINC01003 suppressed the growth of xenograft tumor in mice. We then identified miR-33a-5p as a downstream target of LINC01003, and confirmed that PIM1 was a direct target gene of miR-33a-5p. Both high expression of miR-33a-5p and low expression of PIM1 reversed the suppressive effects of LINC01003 overexpression on cell adhesion and viability, and the promoting effect on apoptosis in MM cells. CONCLUSION: LINC01003 functioned as a sponge of miR-33a-5p to inhibit the development MM by regulating PIM1 expression.	NA	Leuk Res. 2021 Jul;106:106565. doi: 10.1016/j.leukres.2021.106565. Epub 2021 Mar 31.
3452	LncRNA	CRNDE	miR-28	NDRG2	MEC-1 and HG3 cells	Chronic Lymphocytic Leukemia	Homo sapiens (human)	Luciferase reporter assay;	33857783	Long non-coding RNA CRNDE suppressing cell proliferation is regulated by DNA methylation in chronic lymphocytic leukemia.	Long non-coding RNA CRNDE and DNA methylation play a vital role in the occurrence and development of chronic lymphocytic leukemia (CLL). This study attempted to investigate the biological role of CRNDE methylation in CLL. The expression and methylation levels of CRNDE in CLL cell lines (MEC-1 and HG3) before or after methylation inhibitor (5-Aza-2'-deoxycytidine, 5-Aza-CdR) treatment was detected by quantitative real-time PCR or methylation-Specific PCR. The relationship among CRNDE, miR-28 and NDRG2 was verified by luciferase reporter assay. The effect of CRNDE overexpression and 5-Aza-CdR treatment on cell proliferation and apoptosis of MEC-1 and HG3 cells were assessed by CCK8 and flow cytomery. Compared with normal B lymphocytes, CRNDE was down-regulated and the methylation level of CRNDE was increased in MEC-1 and HG3 cells. Then, 5-Aza-CdR treatment caused an increase of CRNDE expression in MEC-1 and HG3 cells by demethylation. The overexpression or demethylation of CRNDE inhibited cell proliferation and promoted apoptosis in MEC-1 and HG3 cells by up-regulating CRNDE expression. Moreover, CRNDE functioned as a competing endogenous RNA to repress miR-28, which controlled its down-stream target NDRG2. CRNDE overexpression inhibited cell proliferation and promoted apoptosis via miR-28/NDRG2 axis in CLL. In conclusion, our data elaborated that CRNDE expression was regulated by DNA methylation, and the protective effect of CRNDE on CLL was attributed to the inhibition of proliferation in CLL via miR-28/NDRG2 axis. Thus, this work highlights a novel competing endogenous RNA circuitry involving key regulators of CLL.	NA	Leuk Res. 2021 Jun;105:106564. doi: 10.1016/j.leukres.2021.106564. Epub 2021 Mar 29.
3453	LncRNA	FENDRR	miR-18a-5p	PGC-1a	Aortic Endothelial Cells	Mitochondrial Energy Metabolism Disorder	Homo sapiens (human)	qRT-PCR	33912133	LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway.	Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.	NA	Front Endocrinol (Lausanne). 2021 Apr 12;12:622665. doi: 10.3389/fendo.2021.622665. eCollection 2021.
3454	LncRNA	LINC01515	miR-325	CDCA5	NA	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR	33770322	LINC01515 promotes nasopharyngeal carcinoma progression by serving as a sponge for miR-325 to up-regulate CDCA5.	Long non-coding RNAs (LncRNAs) have gained widespread interest and attention as vital regulators in cancer occurrence and development. Nonetheless, the functions and mechanisms of lncRNAs involved in nasopharyngeal carcinoma (NPC) are largely unknown. By analysing the data from GSE61218, we identified a novel lncRNA LINC01515 which is altered in NPC. A series of experiments were performed to examine the exact roles of LINC01515 as well as the molecular mechanisms by which LINC01515 acted in NPC. LINC01515 expression was increased in NPC and that high LINC01515 expression was associated with a worse prognosis. Functionally, depletion of LINC01515 resulted in an inhibition of cell proliferation, migration and invasion, while apoptosis was promoted. Mechanistically, LINC01515 facilitated cell division cycle associated 5 (CDCA5) expression via serving as a sponge for miR-325. And more notably, miR-325 suppressed NPC progression in vitro by targeting CDCA5. Furthermore, the anti-tumor property induced by LINC01515 knockdown was partially reversed due to the overexpression of CDCA5. Taken together, LINC01515 exerted the carcinogenic effect in NPC through regulating miR-325/CDCA5 pathway. Our findings shed light on the possibility of exploiting LINC01515 as a prognostic biomarker or therapeutic target in NPC.	NA	J Mol Histol. 2021 Jun;52(3):577-587. doi: 10.1007/s10735-021-09969-x. Epub 2021 Mar 26.
3455	LncRNA	Ttc3-209	miR-484	Wnt8a	Retinal Ganglion Cells	Retinal Ischemia Reperfusion Injury	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;FISH;Western blot;FISH;Flow Cytometry assay;Luciferase reporter assay;	33687475	lncRNA Ttc3-209 Promotes the Apoptosis of Retinal Ganglion Cells in Retinal Ischemia Reperfusion Injury by Targeting the miR-484/Wnt8a Axis.	PURPOSE: Apoptosis of the retinal ganglion cells (RGCs) can cause irreversible damage to visual function after retinal ischemia reperfusion injury (RIR). Using a lncRNA chip assay, we selected lncRNA Ttc-209 and characterized its role in RGCs during ischemia reperfusion (I/R)-induced apoptosis. METHODS: We created an ischemic model of RGCs by applying Hank's balanced salt solution containing 10 μM antimycin A and 2 μM calcium ionophore for 2 hours. RIR was induced in mice by elevating the intraocular pressure to 120 mm Hg for 1 hour by cannulation of the cornea; this was followed by reperfusion. Real-time quantitative PCR was used to detect the expression levels of long noncoding RNA (lncRNA), microRNA (miRNA), and target gene mRNA. Western blotting, flow cytometry, immunofluorescent staining, and TUNEL assays were performed to detect cell apoptosis. Dual-luciferase reporter assays and FISH were used to identify endogenous competitive RNA (ceRNA) mechanisms that link lncRNAs, miRNAs, and target genes. We also used scotopic electroretinography examinations to evaluate visual function in treated mice. RESULTS: lncRNA Ttc3-209 was significantly upregulated after I/R injury and played a proapoptotic role in RGCs during I/R-induced apoptosis. Mechanistically, lncRNA Ttc3-209 is a ceRNA that competitively binds to miR-484 and upregulates the translation of its target (Wnt8a mRNA), thus promoting apoptosis in RGCs. CONCLUSIONS: Reducing the expression of lncRNA Ttc3-209 had a protective effect against apoptosis in RGCs. This may provide a new therapeutic option for the prevention of RGC apoptosis in response to RIR injury.	NA	Invest Ophthalmol Vis Sci. 2021 Mar 1;62(3):13. doi: 10.1167/iovs.62.3.13.
3456	LncRNA	OTUD6B-AS1	miR-21-5p	PNRC2	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;RNA pull-down;	33686892	LncRNA OTUD6B-AS1 inhibits many cellular processes in colorectal cancer by sponging miR-21-5p and regulating PNRC2.	Accumulating evidence has revealed that long noncoding RNAs (lncRNAs) play essential roles in regulating cellular process of various cancers. There have been many studies on the biological functions of lncRNAs in colorectal cancer (CRC). In this research, we explored the role and mechanism of lncRNA ovarian tumor domain containing 6B antisense RNA1 (OTUD6B-AS1) in CRC. Here, we detected OTUD6B-AS1 expression in CRC tissues and cells by RT-qPCR. Functional experiments were performed to test alterations in different cellular processes. Moreover, to verify the binding ability among the indicated RNA molecules, we carried out RIP, RNA pull-down and luciferase reporter assays. According to our data, OTUD6B-AS1 expression was low in CRC tissues and cells. Functionally, overexpression of OTUD6B-AS1 inhibited cell proliferation, migration, invasion and EMT, and promoted cell apoptosis. Bioinformatic analysis and mechanistical experiments confirmed that OTUD6B-AS1 could act as a competitive endogenous RNA (ceRNA) to upregulate Proline-Rich Nuclear Receptor Coactivator 2 (PNRC2) expression by sequestering miR-21-5p. Further rescue experiments validated the inhibitory function of the OTUD6B-AS1/miR-21-5p/PNRC2 axis in cellular process of CRC. Overall, OTUD6B-AS1 inhibits cellular development in CRC by sponging miR-21-5p and upregulating PNRC2, providing a novel insight into the exploration on CRC treatment.	NA	Hum Exp Toxicol. 2021 Mar 9:960327121997976. doi: 10.1177/0960327121997976.
3457	LncRNA	KCNQ1OT1	miR-223-3p	BCL2L2	lens epithelial cells	Lens Epithelial Cell Apoptosis 	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33744257	Long non-coding RNA KCNQ1OT1 promotes hydrogen peroxide-induced lens epithelial cell apoptosis and oxidative stress by regulating miR-223-3p/BCL2L2 axis.	Many long non-coding RNAs (lncRNAs) can exert crucial roles in the pathogenesis of cataract, including lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1). We aimed to further elucidate the biological role and regulatory molecular mechanism of KCNQ1OT1 in cataract. The expression of KCNQ1OT1 and miR-223-3p and BCL2 like 2 (BCL2L2) was examined by qRT-PCR. Cataract cell model was constructed by treatment with hydrogen peroxide (H(2)O(2)) in lens epithelial cells (SRA01/04). SRA01/04 cell viability and cell apoptosis were tested using CCK-8 assay and flow cytometry, respectively. Western blot (WB) was performed to measure the levels of apoptosis-related proteins and BCL2L2 protein. The oxidative stress factors were analyzed by corresponding kits. The interaction between miR-223-3p and KCNQ1OT1 or BCL2L2 was validated by dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. We found that KCNQ1OT1 was upregulated in cataract anterior lens capsule samples and H(2)O(2)-induced SRA01/04 cells. Knockdown of KCNQ1OT1 suppressed H(2)O(2)-induced SRA01/04 cell apoptosis and oxidative stress. KCNQ1OT1 acted as a sponge of miR-223-3p. Inhibition of miR-223-3p could abate the function of KCNQ1OT1 silence in H(2)O(2)-treated SRA01/04 cells. Additionally, BCL2L2 was a direct target of miR-223-3p, and miR-223-3p weakened H(2)O(2)-induced SRA01/04 cell apoptosis and oxidative stress by targeting BCL2L2. Collectively, the data suggest a role for the KCNQ1OT1/miR-223-3p/BCL2L2 axis in cataract formation but the data was generated using an epithelial cell line.	NA	Exp Eye Res. 2021 May;206:108543. doi: 10.1016/j.exer.2021.108543. Epub 2021 Mar 17.
3458	LncRNA	LINC00514	miR-6504-5p	CCDC71L	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;Luciferase reporter assay;Rescue assay;	33757509	LINC00514 upregulates CCDC71L to promote cell proliferation, migration and invasion in triple-negative breast cancer by sponging miR-6504-5p and miR-3139.	BACKGROUND: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain unclear in triple-negative breast cancer (TNBC). METHODS: Herein, we detected LINC00514 expression level in TNBC tissues and cells using RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed by colony formation, EdU, wound healing, transwell assays and flow cytometry analysis. RESULTS: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The results indicated that LINC00514 expression was upregulated in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and promoted cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was identified in TNBC tissues and cells. Overexpression of miR-6504-5p or miR-3139 inhibited cell growth and migration in TNBC. CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the anti-tumor influence of LINC00514 knockdown on TNBC cell proliferation, migration, invasion and apoptosis. CONCLUSIONS: LINC00514 promote cell proliferation, migration and invasion in triple-negative breast cancer by targeting the miR-6504-5p/miR-3139/CCDC71L axis in TNBC.	NA	Cancer Cell Int. 2021 Mar 23;21(1):180. doi: 10.1186/s12935-021-01875-2.
3459	LncRNA	LINC00514	miR-3139	CCDC71L	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;Luciferase reporter assay;Rescue assay;	33757509	LINC00514 upregulates CCDC71L to promote cell proliferation, migration and invasion in triple-negative breast cancer by sponging miR-6504-5p and miR-3139.	BACKGROUND: Long noncoding RNAs (lncRNAs) have recently identified as essential gene modulators in numerous cancers. Previous studies have confirmed the oncogenic role of long intergenic nonprotein-coding RNA 00514 (LINC00514) in some cancers. Nevertheless, its biological function and mechanism remain unclear in triple-negative breast cancer (TNBC). METHODS: Herein, we detected LINC00514 expression level in TNBC tissues and cells using RT-qPCR. The function of LINC00514 in TNBC cellular activities was assessed by colony formation, EdU, wound healing, transwell assays and flow cytometry analysis. RESULTS: The binding between miR-6504-5p/miR-3139 and LINC00514/CCDC71L was validated by luciferase reporter assay. The results indicated that LINC00514 expression was upregulated in TNBC tissues and cells. Furthermore, it was manifested that silenced LINC00514 restrained cell proliferative, migratory and invasive abilities and promoted cell apoptosis. In mechanism, LINC00514 was revealed to sequester miR-6504-5p and miR-3139 in TNBC cells. Furthermore, the low level of miR-6504-5p and miR-3139 was identified in TNBC tissues and cells. Overexpression of miR-6504-5p or miR-3139 inhibited cell growth and migration in TNBC. CCDC71L was recognized as a common downstream gene of miR-6504-5p and miR-3139. Rescue assay verified that overexpressed CCDC71L countervailed the anti-tumor influence of LINC00514 knockdown on TNBC cell proliferation, migration, invasion and apoptosis. CONCLUSIONS: LINC00514 promote cell proliferation, migration and invasion in triple-negative breast cancer by targeting the miR-6504-5p/miR-3139/CCDC71L axis in TNBC.	NA	Cancer Cell Int. 2021 Mar 23;21(1):180. doi: 10.1186/s12935-021-01875-2.
3460	LncRNA	LOC102176306	miR-1197-3p	PPARGC1A	Leydig cells	NA	Homo sapiens (human)	qRT-PCR	33730690	LncRNA LOC102176306 plays important roles in goat testicular development.	Long ncRNAs regulate a complex array of fundamental biological processes, while its molecular regulatory mechanism in Leydig cells (LCs) remains unclear. In the present study, we established the lncRNA LOC102176306/miR-1197-3p/peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) regulatory network by bioinformatic prediction, and investigated its roles in goat LCs. We found that lncRNA LOC102176306 could efficiently bind to miR-1197-3p and regulate PPARGC1A expression in goat LCs. Downregulation of lncRNA LOC102176306 significantly supressed testosterone (T) synthesis and ATP production, decreased the activities of antioxidant enzymes and mitochondrial complex I and complex III, caused the loss of mitochondrial membrane potential, and inhibited the proliferation of goat LCs by decreasing PPARGC1A expression, while these effects could be restored by miR-1197-3p inhibitor treatment. In addition, miR-1197-3p mimics treatment significantly alleviated the positive effects of lncRNA LOC102176306 overexpression on T and ATP production, antioxidant capacity and proliferation of goat LCs. Taken together, lncRNA LOC102176306 functioned as a sponge for miR-1197-3p to maintain PPARGC1A expression, thereby affecting the steroidogenesis, cell proliferation and oxidative stress of goat LCs. These findings extend our understanding of the molecular mechanisms of T synthesis, cell proliferation and oxidative stress of LCs.	NA	Reproduction. 2021 May;161(5):523-537. doi: 10.1530/REP-20-0568.
3461	LncRNA	LHFPL3-AS1	miR-362-5p	CHSY1	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;	33833527	LncRNA LHFPL3-AS1 Promotes Oral Squamous Cell Carcinoma Growth and Cisplatin Resistance Through Targeting miR-362-5p/CHSY1 Pathway.	BACKGROUND: Oral squamous cell carcinoma (OSCC) is a common oral cancer. The current study aims to elucidate the potential roles of long noncoding RNA (lncRNA) LHFPL3-AS1 in OSCC development. METHODS: Gene expression was measured by qRT-PCR in tumor tissues and cell lines. Loss-of-function assays were performed to analyze the effects of LHFPL3-AS1 on malignant behaviors. Bioinformatics analysis was conducted to explore the downstream signaling pathway of LHFPL3-AS1 in OSCC. RESULTS: LHFPL3-AS1 was highly expressed in OSCC tissues and cell lines. LHFPL3-AS1 was upregulated in cisplatin-resistant tumor cell lines. LHFPL3-AS1 level was correlated with survival rate. LHFPL3-AS1 knockdown suppressed OSCC proliferation, migration and invasion. LHFPL3-AS1 downregulation reduced cisplatin resistance of OSCC cells. LHFPL3-AS1 was the competing endogenous RNA (ceRNA) for miR-194-5p to enhance CHSY1 expression. CONCLUSION: LHFPL3-AS1/miR-362-5p/CHSY1 signaling pathway plays essential roles in regulating OSCC development and cisplatin resistance.	NA	Onco Targets Ther. 2021 Mar 31;14:2293-2300. doi: 10.2147/OTT.S298679. eCollection 2021.
3462	LncRNA	SNHG1	miR-298	SIK1	bEnd3 cells	Ogd/R-Induced Injury	Homo sapiens (human)	qRT-PCR	33677804	Long noncoding RNA SNHG1 protects brain microvascular endothelial cells against oxygen-glucose deprivation/reoxygenation-induced injury by sponging miR-298 and upregulating SIK1 expression.	OBJECTIVES: Growing evidence shows that long non-coding RNAs (lncRNAs) are widely involved in the progression of multiple diseases, including ischemic stroke. The aim of this study was to explore the function and underlying mechanism of lncRNAs small nucleolar RNA host gene 1 (SNHG1) in ischemic stroke. RESULTS: SNHG1 and salt-induced kinase 1 (SIK1) were upregulated in oxygen-glucose deprivation/reperfusion (OGD/R)-induced bEnd3 cells. SNHG1 downregulation promoted OGD/R-induced injury through decreasing cell proliferation and increasing apoptosis, which was reversed by upregulating SIK1 or downregulating miR-298. Moreover, SIK1 interference had similar functions with SNHG1 knockdown in OGD/R-treated bEnd3 cells. In addition, miR-298 was a direct target of SNHG1 and could specifically bind to SIK1. Furthermore, SNHG1 functioned as a molecular sponge of miR-298 to regulate SIK1 expression. CONCLUSION: SNHG1 knockdown enhanced OGD/R-induced injury in bEnd3 cells by regulating miR-298/SIK1 axis, which might provide promising therapeutic target for treatment of ischemic stroke.	NA	Biotechnol Lett. 2021 Jun;43(6):1163-1174. doi: 10.1007/s10529-021-03096-z. Epub 2021 Mar 6.
3463	LncRNA	DLEU1	miR-149-5p	CDK6	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33880596	Knockdown of lncRNA DLEU1 inhibits the tumorigenesis of oral squamous cell carcinoma via regulation of miR-149-5p/CDK6 axis.	Oral squamous cell carcinoma (OSCC) is a frequent malignant tumor worldwide. Long non-coding RNAs (lncRNAs) are known to play key roles in different types of cancer, including OSCC. It was previously reported that lncRNA deleted in lymphocytic leukemia 1 (DLEU1) is notably upregulated in OSCC; however, the role of DLEU1 in OSCC remains unclear. Gene and protein expression levels in OSCC cells were detected by reverse transcription-quantitative PCR and western blotting, respectively, in the present study. A Transwell assay was performed to measure cell migration and invasion. Flow cytometry was used to detect cell apoptosis, and the dual-luciferase reporter assay was applied to confirm the interaction between DLEU1, microRNA (miR)-149-5p and CDK6 in OSCC cells. DLEU1 expression was negatively associated with the survival rate of patients with OSCC. In addition, silencing of DLEU1 notably inhibited the proliferation of OSCC cells by inducing apoptosis. Meanwhile, DLEU1 directly bound to miR-149-5p, and CDK6 was found to be the direct target of miR-149-5p. Furthermore, DLEU1 knockdown-induced inhibition of OSCC cell proliferation was significantly reversed by the miR-149-5p antagomir. Knockdown of lncRNA DLEU1 reversed the proliferation of OSCC cells via regulation of the miR-149-5p/CDK6 axis. Thus, DLEU1 may serve as a novel target for treating OSCC.	NA	Mol Med Rep. 2021 Jun;23(6):447. doi: 10.3892/mmr.2021.12086. Epub 2021 Apr 21.
3464	LncRNA	ILF3-AS1	miR-4429	RAB14	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33525948	ILF3-AS1 promotes cell proliferation and inhibits cell apoptosis of breast cancer by binding with miR-4429 to upregulate RAB14.	As one of the leading causes of cancer-related deaths among women, breast cancer accounts for a 30% increase of incidence worldwide since 1970s. Recently, increasing studies have revealed that the long non-coding RNA ILF3-AS1 is involved in the progression of various cancers. Nevertheless, the role of ILF3-AS1 in breast cancer remains largely unknown. In the present study, we found that ILF3-AS1 was highly expressed in breast cancer tissues and cells. ILF3-AS1 silencing inhibited breast cancer cell proliferation, migration and invasion, and promoted cell apoptosis. ILF3-AS1 bound with miR-4429 in breast cancer cells. Moreover, RAB14 was a downstream target of miR-4429, and miR-4429 expression was negatively correlated with RAB14 or ILF3-AS1 expression in breast cancer tissues. The result of rescue experiments demonstrated that overexpression of RAB14 can reverse the inhibitory effect of ILF3-AS1 knockdown on breast cancer cell proliferation, migration and invasion. Overall, ILF3-AS1 promotes the malignant phenotypes of breast cancer cells by interacting with miR-4429 to regulate RAB14, which might offer a new insight into the underlying mechanism of breast cancer.	NA	Hum Exp Toxicol. 2021 Jul;40(7):1183-1193. doi: 10.1177/0960327121989422. Epub 2021 Feb 2.
3465	Circular RNA	CircPKNOX1	miR-370-3p	KIAA0355	nucleus pulposus (NP) cells	Intervertebral Disc Disease	Homo sapiens (human)	microarray;qPCR;RT-qPCR;RACE;Western blot;	33637685	Inhibition of intervertebral disc disease progression via the circPKNOX1-miR-370-3p-KIAA0355 axis.	The molecular mechanism underlying the development of intervertebral disc disease (IVDD) is not completely understood. Circular RNAs (circRNAs) play a significant role in the occurrence and development of various diseases, and studies have shown that circPKNOX1 is involved in the compensatory response of extracellular matrix synthesis and secretion of the nucleus pulposus (NP) cells. However, the mechanism through which circRNAs regulate IVDD progression remains unclear; therefore, in this study, we explored the significance of circPKNOX1 in IVDD. The expression of circRNAs in NP cells of normal and degenerative patients was detected using microarray analysis, and the role of circPKNOX1 in IVDD was confirmed using RT-qPCR. The interaction networks of circRNAs, miRNAs, and miRNA target genes were detected using bioinformatics analysis, RNA fluorescence in situ hybridization, and immunofluorescence analysis. We found that the expression of circPKNOX1 decreased in IVDD cells. The expression of circPKNOX1 in NP cells, observed using RT-qPCR and western blotting, was consistent with that observed using array screening. Overexpression of circPKNOX1 increased the expression of collagen II, aggrecan, and SOX9 and decreased that of ADAMTS4, ADAMTS-5, MMP3, and MMP13. We further demonstrated that circPKNOX1 played the role of a sponge by competitively binding miR-370-3p to reverse the inhibition of KIAA0355 expression. Our findings indicated that circPKNOX1 affected the progression of IVDD by regulating the expression of KIAA0355 via miR-370-3p. Therefore, circPKNOX1-based therapy may serve as an effective IVDD treatment strategy.	NA	Cell Death Discov. 2021 Feb 26;7(1):39. doi: 10.1038/s41420-021-00420-4.
3466	LncRNA	OIP5-AS1	miR-143-3p	TUB	treated with angiotensin II (AngII) and AD tissues	Aorta Wall Injury	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;RNA immunoprecipitation;RNA pull-down assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33577845	Lnc-OIP5-AS1 exacerbates aorta wall injury during the development of aortic dissection through upregulating TUB via sponging miR-143-3p.	AIMS: Dysfunction of major cells constituting the aortic wall is the pathological basis for AD development. Determining whether non-coding RNAs can influence AD progression by regulating these cellular functions and identifying some specific non-coding RNAs is of great significance in uncovering molecular mechanisms of the development of AD. MAIN METHODS: Microarray analyses and hierarchical clustering analysis were used to select candidate lncRNAs and miRNAs associated with AD. Dual-luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay were performed to verify the direct bonding relationship between genes. The regulatory effects of genes on cell function were examined in a series of experiments. KEY FINDINGS: We found that lnc-OIP5-AS1 was upregulated, whereas miR-143-3p was downregulated in cells treated with angiotensin II (AngII) and AD tissues. Lnc-OIP5-AS1 functioned as a competing endogenous RNA (ceRNA) of miR-143-3p to suppress the proliferation and mobility, but promote apoptosis of HAECs and HASMCs, and simultaneously result in the imbalances between MMP-2/9 and TIMP-2/1 in HASMCs and the excessive secretion of IL-6, IL-1β, and IL-17A of HAAFs. Moreover, overexpression or silence of TUB, a target gene of miR-143-3p, counteracted the influence of miR-143-3p or lnc-OIP5-AS1 on cells, respectively. SIGNIFICANCE: Our findings revealed that lncRNA OIP5-AS1 exacerbates aorta intima, media, and adventitia injury in the development of AD through upregulating TUB via sponging miR-143-3p and also support more detailed future studies by providing a novel molecular basis underlying AD formation.	NA	Life Sci. 2021 Apr 15;271:119199. doi: 10.1016/j.lfs.2021.119199. Epub 2021 Feb 10.
3467	LncRNA	DUXAP8	miR-223-3p	CXCR4	PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	Luciferase reporter assay;	33522355	Long non-coding RNA DUXAP8 promotes the cell proliferation, migration, and invasion of papillary thyroid carcinoma via miR-223-3p mediated regulation of CXCR4.	Papillary thyroid carcinoma (PTC) is a differentiated type of thyroid malignancy with a high incidence. Long non-coding RNA (lncRNA) DUXAP8 has been reported to participate in the proliferation, migration, and invasion of several cancer types. However, its association with PTC has not yet been reported. The current study aimed to investigate the role of DUXAP8 in PTC and revealed the underlying mechanisms. The expression of DUXAP8 was knocked down in two PTC cell lines and the effects of DUXAP8 on the PTC biological behavior were examined by cell counting kit-8 (CCK-8), wound healing, and transwell invasion assays. Luciferase reporter assay was used to detect the binding activity between miR-223-3p and DUXAP8. We found that knockdown of DUXAP8 inhibited the proliferation, migration, and invasion of PTC cells. DUXAP8 could sponge miR-223-3p through the specific binding site. CXCR4 was a target of miR-223-3p. The malignant phenotypes of the PTC cells were suppressed by the over-expression of miR-223-3p. Moreover, miR-223-3p inhibition or CXCR4 over-expression partly restored the proliferation, migration, and invasion activities of DUXAP8-downregulated PTC cells. The results evidenced that DUXAP8 acted as an oncogene in PTC, these effects seemed to partly dependent on the miR-223-3p/CXCR4 axis.	NA	Bioengineered. 2021 Dec;12(1):496-506. doi: 10.1080/21655979.2021.1882134.
3468	LncRNA	GAS6	miR-370-3p	TSPAN3	bone marrow (BM) tissues and cells,AML cells	Acute Myeloid Leukemia	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33523043	Long noncoding RNA GAS6 antisense RNA1 silencing attenuates the tumorigenesis of acute myeloid leukemia cells through targeting microRNA-370-3p/Tetraspanin3 axis.	PURPOSE: Acute myeloid leukemia (AML) is a type of hematologic malignancy. This study was attempt to explore the effect of long noncoding RNA GAS6 antisense RNA1 (GAS6-AS1) on pediatric AML and the regulation mechanisms. METHODS: GAS6-AS1, microRNA-370-3p (miR-370-3p), and Tetraspanin3 (TSPAN3) expression in bone marrow (BM) tissues and cells was determined by qRT-PCR. The correlation between GAS6-AS1 and clinicopathological features of pediatric patients with AML was assessed. In vitro, viability and migration and invasion of AML cells were evaluated via MTT and transwell assays, respectively. Interactions among GAS6-AS1, miR-370-3p, and TSPAN3 were revealed by dual-luciferase reporter assays. Western blot was applied to confirm the protein expression of TSPAN3. RESULTS: GAS6-AS1 and TSPAN3 expression was elevated in BM tissues of pediatric patients with AML and AML cells, but miR-370-3p expression was reduced. GAS6-AS1 expression was positively related to French-American-British (FAB) classification in pediatric patients with AML. In vitro, GAS6-AS1 deficiency restrained the viability, migration, and invasion of AML cells. Additionally, GAS6-AS1 mediated miR-370-3p expression indeed and TSPAN3 was identified as a target of miR-370-3p. Furthermore, miR-370-3p overexpression repressed the protein expression of TSPAN3. The feedback experiments demonstrated that miR-370-3p inhibition or TSPAN3 overexpression mitigated the suppressive effect of sh-GAS6-AS1 on the tumorigenesis of AML cells. CONCLUSION: GAS6-AS1 silencing restrained AML cell viability, migration, and invasion by targeting miR-370-3p/TSPAN3 axis, affording a novel therapeutic target for pediatric AML.	NA	Clin Hemorheol Microcirc. 2021;78(1):69-81. doi: 10.3233/CH-201039.
3469	LncRNA	NEAT1	miR-124-3p	PDE4B	SH-SY5Y cells	Parkinsons Disease	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	33522352	Long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) sponges microRNA-124-3p to up-regulate phosphodiesterase 4B (PDE4B) to accelerate the progression of Parkinson's disease.	Reportedly, long non-coding RNA (lncRNA) are crucial modulators in neurodegenerative diseases. Herein, we investigated the role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in Parkinson's disease (PD). In-vitro PD model was established based on SH-SY5Y cells treated with 1-methyl-4-phenylpyridinium (MPP+). NEAT1, microRNA (miR) -124-3p and phosphodiesterase 4B (PDE4B) expression levels were examined by qRT-PCR. CCK-8 assay and LDH release assay were adopted to delve into the cell viability and cytotoxicity, respectively. Besides, western blot was utilized to determine mTOR, p-mTOR and PDE4B expression levels. ELISA was executed to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6). Dual-luciferase reporter assay and RIP assay were used to probe the relationship between miR-124-3p and NEAT1 or PDE4B. We demonstrated that, in SH-SY5Y cells treated with MPP+, NEAT1 and PDE4B expression levels were raised, while miR-124-3p expression was repressed; NEAT1 depletion or miR-124-3p overexpression increased the cell viability and suppressed cell injury. Besides, miR-124-3p was confirmed as the direct target of NEAT1, and its down-regulation counteracted the impact of NEAT1 depletion on SH-SY5Y cells. PDE4B was as the downstream target of miR-124-3p, and its overexpression weakens the impact of miR-124-3p on SH-SY5Y cells. Additionally, NEAT1 decoyed miR-124-3p to modulate PDE4B expression. Collectively, in MPP+-induced SH-SY5Y cells, NEAT1 depletion increases cell viability, represses cytotoxicity and reduces inflammatory response by regulating miR-124-3p and PDE4B expression levels, suggesting that NEAT1 may be a promising target for treating PD.	NA	Bioengineered. 2021 Dec;12(1):708-719. doi: 10.1080/21655979.2021.1883279.
3470	LncRNA	HLA-F-AS1	miR-541-3p	TRABD	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33618253	STAT3-induced HLA-F-AS1 promotes cell proliferation and stemness characteristics in triple negative breast cancer cells by upregulating TRABD.	Breast cancer (BC) is one of the most common malignances and is a leading cause of cancer-related deaths in women globally. Triple negative breast cancer (TNBC) is a common subtype of BC. Emerging evidence has indicated the crucial roles of long noncoding RNAs (lncRNAs) in the tumorigenesis of TNBC. Our aim was to explore the role and regulatory mechanism of lncRNA HLA-F antisense RNA 1 (HLA-F-AS1) in TNBC cells. Cell counting kit-8 (CCK-8) assay, colony formation assay, flow cytometry analysis and western blot analysis were used to measure HLA-F-AS1-mediated cellular behaviors in TNBC. Xenograft tumor assay was applied to assess biological function of HLA-F-AS1 in vivo. Luciferase reporter assay and RNA pull down assay were used to verify the binding ability between molecules. Our findings demonstrated that HLA-F-AS1 expression was significantly upregulated in TNBC tissues and cells, and high level of HLA-F-AS1 indicated the poor prognosis of patients with TNBC. HLA-F-AS1 promoted TNBC progression by facilitating cell proliferation and stemness maintenance and inhibiting cell cycle arrest at G0/G1 stage and apoptosis in vitro as well as inducing tumor growth in vivo. HLA-F-AS1. In addition, signal transducer and activator of transcription 3 (STAT3) transcriptionally induced HLA-F-AS1 upregulation in TNBC cells via interacting with HLA-F-AS1 promoter. Moreover, HLA-F-AS1 acted as the molecular sponge of microRNA 541-3p (miR-541-3p) to elevate TRABD (TraB domain containing) expression in TNBC cells. Rescue experiments confirmed that the decrease of cell proliferation and stemness characteristics under silenced HLA-F-AS1 was rescued by TRABD overexpression in TNBC cells. In conclusion, STAT3-induced HLA-F-AS1 facilitates cell proliferation and stemness characteristics in TNBC by miR-541-3p-dependent upregulation of TRABD, which might provide a potential novel direction for the treatment of TNBC.	NA	Bioorg Chem. 2021 Apr;109:104722. doi: 10.1016/j.bioorg.2021.104722. Epub 2021 Feb 10.
3471	LncRNA	TTN-AS1	miR-139-5p	SPOCK1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33517826	Long non-coding RNA TTN antisense RNA 1 facilitates hepatocellular carcinoma progression via regulating miR-139-5p/SPOCK1 axis.	Reportedly, long non-coding RNAs (lncRNAs) are implicated in hepatocellular carcinoma (HCC) progression, yet little is known concerning the biological functions of TTN antisense RNA 1 (TTN-AS1) in HCC. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was performed for detecting TTN-AS1, SPOCK1 mRNA, and miR-139-5p expressions in HCC cells and tissues. After TTN-AS1 was overexpressed or knocked down in HCC cells, CCK-8 and 5-Ethynyl-2'-deoxyuridine (EdU) assays were carried out for examining cell multiplication. Transwell assays were conducted for evaluating HCC cell migration and invasion. Dual-luciferase reporter assay was employed for verifying the binding relationships between miR-139-5p and TTN-AS1, and between SPOCK1 3'UTR and miR-139-5p. Western blot was employed to measure SPOCK1, E-cadherin, N-cadherin, and Vimentin protein expressions. We demonstrated that, TTN-AS1 and SPOCK1 expression levels were remarkably enhanced in HCC cells and tissues, whereas miR-139-5p expression was observably reduced. Functional experiments suggested that TTN-AS1 knockdown markedly repressed HCC cell multiplication, migration, epithelial-mesenchymal transition (EMT), and invasion. In addition, TTN-AS1 interacted with miR-139-5p and decreased its expression. Moreover, SPOCK1 was a miR-139-5p target, and miR-139-5p inhibitors were able to reverse TTN-AS1 knockdown-induced inhibitory effect on SPOCK1 expression. SPOCK1 overexpression plasmid could counteract TTN-AS1 knockdown-induced inhibiting impact on HCC cell multiplication, migration, invasion, and EMT. In conclusion, TTN-AS1 expression level is remarkably enhanced in HCC, and TTN-AS1 can promote the multiplication, migration, invasion, and EMT of HCC cells via regulating miR-139-5p/SPOCK1 axis.	NA	Bioengineered. 2021 Dec;12(1):578-588. doi: 10.1080/21655979.2021.1882133.
3472	LncRNA	MEG3	miR-9-5p	KLF4	CHON-001 and ATDC5 cells	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33776787	LncRNA MEG3 Protects Chondrocytes From IL-1β-Induced Inflammation via Regulating miR-9-5p/KLF4 Axis.	BACKGROUND: Osteoarthritis (OA) is a chronic degenerative disease of the joints characterized by articular cartilage damage, subchondral bone remodeling, osteophyte formation, and inflammatory changes. This work aims to investigate the protective role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) against the apoptosis of chondrocytes. METHODS: Chondrocyte cell lines, CHON-001, and ATDC5 were treated with different doses of interleukin-1β (IL-1β) to mimic the inflammatory response during OA pathogenesis. Quantitative real-time polymerase chain reaction was performed to measure MEG3, miR-9-5p, and Krüppel-like factor 4 (KLF4) mRNA expression levels. MEG3 and KLF4 overexpression plasmids, MEG3 shRNA, miR-9-5p mimics, and miR-9-5p inhibitors were transfected into the cells. Cell counting kit-8, wound healing assay, and flow cytometry were conducted to determine cell viability, migration, and apoptotic rate. Dual-luciferase reporter assay was adopted to verify the targeting relationships among MEG3, miR-9-5p, and KLF4. Western blot was used to detect KLF4 protein expression. Enzyme-linked immunosorbent assay was employed to measure the levels of inflammatory factors. RESULTS: MEG3 expression in chondrocytes was down-regulated by the stimulation of IL-1β, and MEG3 negatively regulated miR-9-5p expression but positively regulated KLF4 expression. MEG3 overexpression strengthened the viability and migration of CHON-001 and ATDC5 cells but restrained the apoptosis and inflammatory response, while MEG3 knockdown had opposite effects. miR-9-5p inhibition or KLF4 overexpression could counteract the effects of MEG3 knockdown on chondrocytes. Besides that, MEG3 was proved to be a molecular sponge for miR-9-5p, and KLF4 was verified as the target of miR-9-5p. CONCLUSION: MEG3 can promote chondrocyte proliferation and migration and inhibit apoptosis and inflammation by sponging miR-9-5p to induce KLF4 expression, which provides a promising therapy target for OA treatment.	NA	Front Physiol. 2021 Mar 11;12:617654. doi: 10.3389/fphys.2021.617654. eCollection 2021.
3473	LncRNA	RNCR2	miR-495-3p	HK2	mmelanoma tissue specimens and cell lines	Melanoma	Homo sapiens (human)	qPCR;Western blot;Luciferase reporter assay;	33724862	lncRNA RNCR2 facilitates cell proliferation and epithelial-mesenchymal transition in melanoma through HK2-mediated Warburg effect via targeting miR-495-3p.	Melanoma is a potentially lethal skin cancer with a high death rate. LncRNAs were reported to be implicated in melanoma progression. However, the function and mechanisms of lncRNA RNCR2 in melanoma are little known. In this study, RNCR2, miR-495-3p, and HK2 expression levels were measured in melanoma tissue specimens and cell lines by qPCR. EdU and CCK8 assays were performed to assess cell proliferation. Enolase activity, ATP level, lactate production, and glucose consumption measurement kits were used to evaluate the glycolysis of tumor cells. Immunofluorescence and western blot were used to detect the expression of epithelial-mesenchymal transition (EMT) and glycolysis-related proteins. Luciferase reporter assay was applied to confirm the target relationships. The role of RNCR2 in tumorigenesis was examined using murine xenograft models. LncRNA RNCR2 was upregulated in melanoma tissues and cell lines. Cell function detection showed that RNCR2 knockdown remarkably inhibited cell proliferation and EMT via glycolysis, as well as reduced the growth of a tumor. Mechanically, RNCR2 was confirmed to bind to miR-495-3p and positively regulated HK2 expression level, and the miR-495-3p level was negatively correlated with RNCR2 or HK2 in melanoma tissues. Further, miR-495-3p downregulation or HK2 upregulation partially reversed RNCR2 knockdown-induced inhibition of melanoma cell growth, EMT, and glycolysis. Collectively, RNCR2 might be an oncogenic lncRNA to promote tumor cell glycolysis and accelerate tumor growth via the miR-495-3p/HK2 axis, providing a promising treatment target for melanoma.	NA	Neoplasma. 2021 Mar 17:201120N1255. doi: 10.4149/neo_2021_201120N1255.
3474	Circular RNA	CircCTNNA1	miR-363-3p	CXCL5	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33640021	CircCTNNA1 acts as a ceRNA for miR-363-3p to facilitate the progression of colorectal cancer by promoting CXCL5 expression.	BACKGROUND: Circular RNAs (circRNA) have been shown to be involved in the pathogenesis of colorectal cancer (CRC). CircCTNNA1 was found to be one of the upregulated circRNAs in CRC. However, there are few studies on circCTNNA1, so it is necessary to carry out further studies. METHODS: The expression of circCTNNA1, microRNA (miR)-363-3p, and chemokine C-X-C motif ligand 5 (CXCL5) was detected by quantitative real-time PCR (qRT-PCR). The protein levels of CXCL5 and metastasis markers were measured using western blot (WB) analysis. Cell proliferation, apoptosis, cell cycle, migration, and invasion were determined by cell counting kit 8 (CCK8) assay, colony formation assay, flow cytometry, and transwell assay. The relationship between miR-363-3p and circCTNNA1 or CXCL5 was evaluated via dual-luciferase reporter assay and RNA immunoprecipitation assay. Animal study was performed to explore the function of circCTNNA1 on CRC tumorigenesis. RESULTS: CircCTNNA1 and CXCL5 were highly expressed in CRC. Knockdown of circCTNNA1 could inhibit the proliferation, cell cycle, metastasis, and promote the apoptosis of CRC cells. MiR-363-3p could be sponged by circCTNNA1, and the inhibition effect of circCTNNA1 silencing on CRC progression could be reversed by miR-363-3p inhibitor. Moreover, miR-363-3p could interact with CXCL5, and CXCL5 overexpression also could reverse the suppressive effect of miR-363-3p on CRC progression. Downregulation of circCTNNA1 also could hinder the tumor growth of CRC in vivo. CONCLUSION: CircCTNNA1 enhanced CRC progression via regulating the miR-363-3p/CXCL5 axis.	NA	J Biol Res (Thessalon). 2021 Feb 27;28(1):7. doi: 10.1186/s40709-021-00135-8.
3475	LncRNA	GATA3-AS1	miR-30b-5p	Tex10	PC tissues and cell lines	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33760161	LncRNA GATA3-AS1-miR-30b-5p-Tex10 axis modulates tumorigenesis in pancreatic cancer.	Long noncoding RNAs (lncRNAs) have been widely recognized to play an important role in a variety of diseases. Abnormal regulation of lncRNA GATA3-antisense RNA 1 (AS1) occurs in several cancers, but whether it is involved in the progression of pancreatic cancer (PC) remains unknown. The present study aimed to investigate the biological effects of GATA3-AS1 in PC and to explore the underlying molecular mechanisms. Upregulation of GATA3-AS1 was revealed in PC tissues and cell lines. Knockdown of GATA3-AS1 in PANC-1 or AsPC-1 cells markedly reduced cell viability, cell proliferation, and cell invasion abilities, while cell apoptosis was increased. In addition, GATA3-AS1 knockdown suppressed the stemness of PANC-1 and AsPC-1 cells by decreasing the spheroid formation ability. A tumor xenograft in vivo assay demonstrated that GATA3-AS1 knockdown inhibited tumorigenicity of AsPC-1 cells. Furthermore, the microRNA (miR)-30b-5p downregulation and GATA3-AS1 upregulation were revealed in PC tissues and cell lines. Negative correlations were present between GATA3-AS1 and miR-30b-5p and between miR-30b-5p and testis-expressed protein 10 (Tex10) in the PC tissues, while GATA3-AS1 and Tex10 were positively correlated. GATA3-AS1 was then revealed to act as a competing endogenous RNA (ceRNA) for miR-30b-5p in regulating Tex10 expression. Moreover, the miR-30b-5p-Tex10 axis was confirmed to be involved in the regulation of biological effects of GATA3-AS1, including cell viability, cell proliferation, cell invasion, cell apoptosis, and cell stemness, as well as Wnt1/β-catenin signaling. Collectively, these data indicated that the GATA3-AS1-miR-30b-5p-Tex10 axis modulates tumorigenesis in PC, which may be associated with the Wnt/β-catenin signaling pathway.	NA	Oncol Rep. 2021 May;45(5):59. doi: 10.3892/or.2021.8010. Epub 2021 Mar 24.
3476	Circular RNA	Circ-0000212	miR-491	FOXP4	CRC cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33649850	circ-0000212 promotes cell proliferation of colorectal cancer by sponging miR-491 and modulating FOXP4 expression.	Colorectal cancer (CRC) is a lethal and common malignancy worldwide. Non-coding (nc)RNAs have been shown to modulate tumor progression in several types of cancer. The present study aimed to investigate the role of hsa_circ_0000212 in CRC, as a sponge of microRNA (miR)-491. The expression levels of miR-491 and forkhead box P4 (FOXP4) were analyzed using data from The Cancer Genome Atlas. The association between miR-491 and FOXP4 and the clinicopathological characteristics were also analyzed. A novel circular (circ)RNA, hsa_circ_0000212, was found to sponge miR-491 based on bioinformatics analysis. The potential binding site between miR-491 and FOXP4 or circ-0000212 was validated using luciferase and RNA immunoprecipitation assays. The expression levels and distribution of circ-0000212 was also determined. Cell Counting Kit-8 and colony formation assays were performed to determine the role of miR-491 or circ-0000212 on the proliferation of the CRC cells. Decreased miR-491 or increased FOXP4 expression levels were associated with the pathological stage in patients with CRC. In addition, miR-491 inhibited cell proliferation by targeting FOXP4. circ-0000212 was increased in CRC tissues and was predominantly localized in the cytoplasm. Furthermore, circ-0000212 augmented viability of the CRC cells by sponging miR-491 and modulating FOXP4. In conclusion, circ-0000212 may serve as a novel tumor-promoter and drug target in CRC.	NA	Mol Med Rep. 2021 Apr;23(4):300. doi: 10.3892/mmr.2021.11939. Epub 2021 Mar 2.
3477	LncRNA	ZNF674-AS1	miR-423-3p	p21	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33618674	ZNF674-AS1 antagonizes miR-423-3p to induce G0/G1 cell cycle arrest in non-small cell lung cancer cells.	BACKGROUND: ZNF674-AS1, a recently characterized long noncoding RNA, shows prognostic significance in hepatocellular carcinoma and glioma. However, the expression and function of ZNF674-AS1 in non-small cell lung cancer (NSCLC) are unclear. METHODS: In this work, we investigated the expression of ZNF674-AS1 in 83 pairs of NSCLC specimens and adjacent noncancerous lung tissues. The clinical significance of ZNF674-AS1 in NSCLC was analyzed. The role of ZNF674-AS1 in NSCLC growth and cell cycle progression was explored. RESULTS: Our data show that ZNF674-AS1 expression is decreased in NSCLC compared to normal tissues. ZNF674-AS1 downregulation is significantly correlated with advanced TNM stage and decreased overall survival of NSCLC patients. Overexpression of ZNF674-AS1 inhibits NSCLC cell proliferation, colony formation, and tumorigenesis, which is accompanied by a G0/G1 cell cycle arrest. Conversely, knockdown of ZNF674-AS1 enhances the proliferation and colony formation of NSCLC cells. Biochemically, ZNF674-AS1 overexpression increases the expression of p21 through downregulation of miR-423-3p. Knockdown of p21 or overexpression of miR-423-3p blocks ZNF674-AS1-mediated growth suppression and G0/G1 cell cycle arrest. In addition, ZNF674-AS1 expression is negatively correlated with miR-423-3p in NSCLC specimens. CONCLUSIONS: ZNF674-AS1 suppresses NSCLC growth by downregulating miR-423-3p and inducing p21. This work suggests the therapeutic potential of ZNF674-AS1 in the treatment of NSCLC.	NA	Cell Mol Biol Lett. 2021 Feb 22;26(1):6. doi: 10.1186/s11658-021-00247-y.
3478	Circular RNA	CircAGAP1	miR-15-5p	E2F3	ccRCC cells	Clear Cell Renal Cancer	Homo sapiens (human)	RNA immunoprecipitation;luciferase assay;Luciferase reporter assay;RNA immunoprecipitation;	33618745	CircAGAP1 promotes tumor progression by sponging miR-15-5p in clear cell renal cell carcinoma.	BACKGROUND: Accumulating evidence has revealed that circular RNAs (circRNAs), as novel noncoding RNAs, play critical roles in carcinogenesis and tumor progression. However, the functions and molecular mechanisms of circRNAs in clear cell renal cell carcinoma (ccRCC) are largely unknown. METHODS: The expression and functions of circAGAP1 were identified in clinical samples, ccRCC cells and in vivo animal models. The molecular mechanism of circAGAP1 was investigated by fluorescence in situ hybridization, RNA immunoprecipitation and luciferase assays. RESULTS: circAGAP1 (circ0058792) expression was significantly upregulated in ccRCC tissues compared to adjacent nontumor tissues. Moreover, the expression of circAGAP1 was closely related to the tumor size, nuclear grade and clinical stage of ccRCC in patients. Mechanistic studies demonstrated that cytoplasmic circAGAP1 targeted miR-15-5p in an RNA-induced silencing complex. Additionally, miR-15-5p expression was downregulated in ccRCC. Luciferase reporter assays showed that E2F transcription factor 3 (E2F3) was a target of miR-15-5p, and upregulated E2F3 expression was positively correlated with circAGAP1 in ccRCC. Furthermore, the tumor-promoting functions of circAGAP1 could be alleviated by miR-15-5p mimics in vitro and in vivo. CONCLUSION: Our results clarify that circAGAP1 exerts its oncogenic functions as a competitive endogenous RNA (ceRNA) by sponging miR-15-5p, which promotes E2F3 expression. Targeting circAGAP1 might be a new attractive therapeutic strategy in ccRCC.	NA	J Exp Clin Cancer Res. 2021 Feb 22;40(1):76. doi: 10.1186/s13046-021-01864-3.
3479	LncRNA	HCG18	miR-152-3p	RAB14	ccRCC tissues and cells	Clear Cell Renal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;	33732021	LncRNA HCG18 Promotes Clear Cell Renal Cell Carcinoma Progression by Targeting miR-152-3p to Upregulate RAB14.	BACKGROUND: Long noncoding RNAs (lncRNAs) have been regarded as crucial regulators in many cancers, including clear cell renal cell carcinoma (ccRCC). This research aimed to explore the biological role and molecular mechanism of lncRNA HCG18 in ccRCC. MATERIALS AND METHODS: The expression levels of HCG18, miR-152-3p and RAB14 were examined by RT-qPCR. Cell viability, migration and invasion were examined by CCK-8 and transwell assays. Luciferase reporter and RIP assays were adopted to verify the interaction between miR-152-3p and HCG18 or RAB14. RESULTS: It was found that HCG18 expression was highly expressed in ccRCC tissues and cells, and patients with high expression of HCG18 had a short overall survival time. Moreover, HCG18 depletion attenuated ccRCC cell viability, migration and invasion. In addition, miR-152-3p was confirmed as a downstream target of HCG18 and was inversely regulated by HCG18, and RAB14 was a target of miR-152-3p. Functional assays demonstrated that miR-152-3p silencing or RAB14 addition abolished the inhibitory effects of HCG18 knockdown on ccRCC progression. CONCLUSION: The results of the present study indicated that HCG18 accelerated the development and progression of ccRCC by upregulating RAB14 via sponging miR-152-3p, suggesting a potential therapeutic target for patients with ccRCC.	NA	Cancer Manag Res. 2021 Mar 11;13:2287-2294. doi: 10.2147/CMAR.S298649. eCollection 2021.
3480	LncRNA	FAM230B	miR-378a-3p	WNT5A	PTC tissues and PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	qRT-PCR	33578293	LncRNA FAM230B promotes the metastasis of papillary thyroid cancer by sponging the miR-378a-3p/WNT5A axis.	Emerging evidence indicates that the dysregulation of long non-coding RNAs (lncRNAs) plays critical roles in the progression of papillary thyroid cancer (PTC). In this study, we found consistently elevated expression levels of the lncRNA FAM230B in PTC tissues, both in newly generated RNA-seq data and in datasets from the GEO and TCGA databases. We demonstrated that the expression of FAM230B can be used for the diagnosis of PTC and is also strongly associated with lymph node metastasis. The potential biological functions of FAM230B and molecular mechanisms by which it regulates PTC progression were investigated. Functionally, FAM230B promoted the migration and invasion of PTC cells in vitro and in vivo. Mechanistically, FAM230B sponged miR-378a-3p and showed competitive binding to the 3'-UTR of WNT5A. FAM230B overexpression resulted in elevated WNT5A expression and thereby regulated the epithelial-mesenchymal transition in PTC cells. Finally, we verified that both miR-378a-3p overexpression and WNT5A silencing effectively offset the impacts of FAM230B on PTC cell migration and invasion. In conclusion, our study demonstrated the oncogenic function of the lncRNA FAM230B in PTC cells, providing a novel target for PTC diagnosis and therapy.	NA	Biochem Biophys Res Commun. 2021 Mar 26;546:83-89. doi: 10.1016/j.bbrc.2021.01.109. Epub 2021 Feb 9.
3481	LncRNA	RP11-379k17.4	miR-200c-3p	Noxa	primary endometrial cancer tissues (EC)	Endometrial Cancer	Homo sapiens (human)	qRT-PCR	33758604	Long non-coding RNA RP11-379k17.4 derived microRNA-200c-3p modulates human endometrial cancer by targeting Noxa.	Objective: The research paid close attention to the function of lncRNA-related endogenous competitive RNAs (ceRNAs) network in endometrial cancer (EC). Methods: 45 primary endometrial cancer tissues (EC) and 45 normal endometrium (NE) were included in the research. The online software StarbaseV2.0 was made use of forecasting the lncRNA which most likely contained microRNA-200c-3p combining sites and could interact with microRNA-200c-3p. Subsequently, we chose lncRNAs which were consistent with the characteristics of polyadenylation of lncRNAs and lower expression in EC than that of NE. After that, lncRNAs, which were related with the microRNA-200c-3p-noxa network, were identified. Results: Rp11-379k17.4, a new gene related to endometrial cancer, was identified as noncoding RNA. It was a more effective ceRNA associated with the microRNA-200c-3p-noxa network. Conclusion: LncRNAs possess microRNA response elements (MREs) and give scope to significant roles in the post-transcriptional mechanism in EC.	NA	J Cancer. 2021 Feb 22;12(8):2268-2274. doi: 10.7150/jca.51023. eCollection 2021.
3482	LncRNA	LINC01559	miR-511	SLC38A1	HCC HepG2 and Huh7 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33588099	Long non-coding RNA 01559 mediates the malignant phenotypes of hepatocellular carcinoma cells through targeting miR-511.	BACKGROUND: Long non-coding RNA 01559 (LINC01559) has been found to be associated with the tumorigenesis of malignant tumors. However, the expression pattern and the potential molecular mechanism of LINC01559 in hepatocellular carcinoma (HCC) progression remain unclear. METHODS: Expression profile and clinical data of patients with HCC were retrieved from The Cancer Genome Atlas database. The quantitative real-time PCR (qRT-PCR) and western blot assays were used to detect the mRNA and protein levels of indicated molecules. Loss-of-function of LINC01559 and microRNA-511 (miR-511) assays were implemented to validate their roles in regulating proliferation, invasion and migration of HCC HepG2 and Huh7 cells. Bioinformatics and luciferase reporter assays were used to determine the possible interactions between LINC01559, miR-511 and solute carrier family 38 member 1 (SLC38A1). RESULTS: LINC01559 was highly expressed, and related to poor prognosis in HCC patients. LINC01559-knockdown restrained the proliferation and growth of HepG2 and Huh7 cells. Furthermore, LINC01559 can function as a sponge for miR-511, which was downregulated in HCC patients. Downregulation of miR-511 significantly increased the cell viability, invasive and migratory capacities, and could abolish the suppressive effect of LINC01559-knockdown on these HCC cells. Moreover, SLC38A1 was a target of miR-511 and upregulated in HCC. Knockdown of LINC01559 significantly reduced while miR-511 inhibitor notably elevated the mRNA and protein levels of SLC38A1, which were abrogated by downregulation of LINC01559 and miR-511 simultaneously. CONCLUSIONS: LINC01559 functioned as a competitive endogenous RNA mediating the malignant phenotypes of HCC cells via sponging miR-511, and may be a considerable therapeutic bio-target in HCC.	NA	Clin Res Hepatol Gastroenterol. 2021 Mar;45(2):101648. doi: 10.1016/j.clinre.2021.101648. Epub 2021 Feb 12.
3483	LncRNA	EGOT	miR-211-5p	ErbB4	rectal cancer tissues and cells	Rectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33953571	LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4.	BACKGROUND/AIMS: Long non-coding ribonucleic acids (lncRNAs) are involved in the progression of cancers and affect the response to radiation therapy. This study was to investigate the mechanism of lncRNA EGOT in the radiosensitivity of rectal cancer. METHODS: The mRNA expression of EGOT, miR-211-5p and ErbB4 in rectal cancer tissues and cells was detected by qRT-PCR. The protein expression of ErbB4 was detected by Western blot. Dual-luciferase reporter assay and ribonucleic acid immunoprecipitation (RIP) were used to confirm the interaction between EGOT and miR-211-5p or miR-211-5p and ErbB4. Transfection technology was used to down-regulate and up-regulate the expression of EGOT and miR-211-5p in rectal cancer cells, respectively. MTT, colony formation and flow cytometry were used to detect the effect of EGOT and miR-211-5p on proliferation, invasion, migration and apoptosis of rectal cancer cells. RESULTS: The expression of EGOT was up-regulated in rectal cancer tissues and cells, and the expression of EGOT was related to the late stage of pathology. EGOT knockdown inhibited the proliferation and colony formation of rectal cancer cells and induced the apoptosis of rectal cancer cells. Moreover, EGOT knockdown was significantly enhanced the effects of radiotherapy on rectal cancer in vivo and in vitro. Furthermore, EGOT was found to serve as a sponge of miR-211-5p, and ErbB4 was a downstream target of miR-211-5p. EGOT enhanced the expression of ErbB4 by regulating miR-211-5p. MiR-211-5p inhibitor restored the effect of EGOT knockdown on the radiosensitivity of rectal cancer. CONCLUSION: Down-regulation of EGOT could inhibit the growth of rectal cancer cells by regulating the miR-211-5p/ErbB4 axis and improve the radiosensitivity of rectal cancer cells. EGOT may be a new therapeutic target for rectal cancer.	NA	Onco Targets Ther. 2021 Apr 28;14:2867-2878. doi: 10.2147/OTT.S256989. eCollection 2021.
3484	LncRNA	LncDBH-AS1	miR-155	AXIN1	NSCLC cell lines and tissue samples	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;	33506901	LncDBH-AS1 knockdown enhances proliferation of non-small cell lung cancer cells by activating the Wnt signaling pathway via the miR-155/AXIN1 axis.	OBJECTIVE: Dys-regulated long noncoding RNAs (lncRNAs) are involved in the cell growth of several malignancies and their aggressive phenotypes. LncRNA DBH-AS1 plays an important role in the advancement of various malignant tumors, but its contribution to non-small cell lung cancer (NSCLC) is still unexplored. This study intends to elucidate the role of the regulatory network of lncRNA DBH-AS1 in NSCLC progression. PATIENTS AND METHODS: The LncDBH-AS1 expression in 32 paired NSCLC patients' tissue samples and NSCLC cell lines were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The role of LncDBH-AS1 in NSCLC was investigated through cell counting kit-8 (CCK-8) assay and colony formation assay in vitro. Besides, the interaction between LncDBH-AS1 and miR-155 was also analyzed. RESULTS: The DBH-AS1 expression was significantly down-regulated in NSCLC cell lines and tissue samples. Decreased DBH-AS1 levels promoted the in vitro proliferation of the NSCLC cells. The mechanism was that DBH-AS1 regulated AXIN1 expression by sponging miR-155 in NSCLC cell lines. Importantly, LncDBH-AS1 might inhibit WNT/β-CATENIN activation in NSCLC cells. CONCLUSIONS: The progression of NSCLC is facilitated by DBH-AS1 via miR-155 interaction and up-regulation of AXIN1 expression.	NA	Eur Rev Med Pharmacol Sci. 2021 Jan;25(1):139-144. doi: 10.26355/eurrev_202101_24377.
3485	LncRNA	MIR4435-2HG	miR-383-5p	RBM3	HNSCC tissues and cell lines	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	Western blot;	33846802	Long non-coding RNA MIR4435-2HG promotes the progression of head and neck squamous cell carcinoma by regulating the miR-383-5p/RBM3 axis.	Recent studies have shown that long non-coding RNAs (lncRNAs) are strongly related to the progression of various types of cancer. The lncRNA MIR4435-2 host gene (MIR4435-2HG) has been recently recognized as a tumor-related lncRNA that is upregulated in several tumors. However, its possible functions in head and neck squamous cell carcinoma (HNSCC) remain unclear. In tShe present study, we observed that MIR4435-2HG expression was markedly upregulated in HNSCC tissues based on a Gene Expression Profiling Interactive Analysis dataset. This result was further confirmed in HNSCC tissues and cell lines using quantitative real-time polymerase chain reaction. In addition, the high expression level of MIR4435-2HG was significantly associated with poor disease-free survival and overall survival in all HNSCC cases and was associated with advanced tumor-metastasis-node stage and poor prognosis. In vitro and in vivo assays demonstrated that MIR4435-2HG knockdown suppressed HNSCC cell proliferation and invasion, epithelial-mesenchymal transition (EMT), and tumor growth as determined by Cell Counting Kit-8, Transwell assays and western blotting. Furthermore, MIR4435-2HG affected HNSCC cell proliferation and migration and EMT by modulating the microRNA miR-383-5p to positively regulate the protein expression level of RNA-binding motif protein 3 (RBM3). In conclusion, we provide a detailed analysis of the roles of MIR4435-2HG in HNSCC and identified the MIR4435-2HG/miR-383-5p/RBM3 axis as a potential therapeutic target for HNSCC treatment.	NA	Oncol Rep. 2021 Jun;45(6):99. doi: 10.3892/or.2021.8050. Epub 2021 Apr 13.
3486	LncRNA	WT1-AS	miR-206	NAMPT	NSCLC tissues	Lung Cancer	Homo sapiens (human)	qRT-PCR	33540574	Unravelling the Role of LncRNA WT1-AS/miR-206/NAMPT Axis as Prognostic Biomarkers in Lung Adenocarcinoma.	Lung cancer is the world's highest morbidity and mortality of malignant tumors, with lung adenocarcinoma (LUAD) as a major subtype. The competitive endogenous RNA (ceRNA) regulative network provides opportunities to understand the relationships among different molecules, as well as the regulative mechanisms among them in order to investigate the whole transcriptome landscape in cancer pathology. We designed this work to explore the role of a key oncogene, MYC, in the pathogenesis of LUAD, and this study aims to identify important long noncoding RNA (lncRNA)-microRNA (miRNA)- transcription factor (TF) interactions in non-small cell lung cancer (NSCLC) using a bioinformatics analysis. The Cancer Genome Atlas (TCGA) database, containing mRNA expression data of NSCLC, was used to determine the deferentially expressed genes (DEGs), and the ceRNA network was composed of WT1-AS, miR-206, and nicotinamide phosphoribosyltransferase (NAMPT) bashing on the MYC expression level. The Kaplan-Meier univariate survival analysis showed that these components may be closely related prognostic biomarkers and will become new ideas for NSCLC treatment. Moreover, the high expression of WT1-AS and NAMPT and low expression of miR-206 were associated with a shortened survival in NSCLC patients, which provided a survival advantage. In summary, the current study constructing a ceRNA-based WT1-AS/miR-206/NAMPT axis might be a novel important prognostic factor associated with the diagnosis and prognosis of LUAD.	NA	Biomolecules. 2021 Feb 2;11(2):203. doi: 10.3390/biom11020203.
3487	LncRNA	KCNQ1OT1	miR-211-5p	CHI3L1	PCa tissues and cells	Prostate Cancer	Homo sapiens (human)	RT-PCR;Western blot;Luciferase reporter assay;	33688211	LncRNA KCNQ1OT1 Promotes Proliferation, Invasion and Metastasis of Prostate Cancer by Regulating miR-211-5p/CHI3L1 Pathway.	BACKGROUND: Bone metastasis after failure of castration therapy is the main reason of death in patients with prostate cancer (PCa). Therefore, full awareness of the metastasis mechanism of PCa and discovery of new therapeutic targets are necessary. Studies showed that lncRNA was involved in the development of cancer. However, its potential role and molecular mechanism in PCa metastasis are still unclear. YKL-40 is an 18 glycosyl hydrolase family protein encoded by CHI3L1, which is involved in the invasion and metastasis of various tumors. A previous study of the authors found that YKL-40 was related to the invasion and metastasis of PCa cells. However, the cause of its abnormal expression in PCa remains unclear. The present study explored the role of lncRNA KCNQ1OT1/miR-211-5p/CHI3L1 regulatory axis in the proliferation, invasion, and metastasis of PCa. METHODS: RT-PCR and Western blot were used to measure the expression profiles of KCNQ1OT1 and YKL. CCK-8 and Transwell assays were used to examine their effects on cell proliferation and migration. Double luciferase reporter assay was used to verify the interactions between miR-211-5p and CHI3L1 3'-UTR. RESULTS: KCNQ1OT1 expression was upregulated in PCa tissues and cells. Downregulating this expression inhibited PCa cell invasion, proliferation, and metastasis. KCNQ1OT1 bound miR-211-5p competitively, and miR-211-5p targeted CHI3L1 3'-UTR. miR-211-5p expression was downregulated, whereas CHI3L1 (YKL-40) expression was upregulated. miR-211-5p levels were negatively correlated with KCNQ1OT1 expression and CHI3L1 mRNA. The decrease in YKL-40 expression in PCa cells induced by the downregulation of KCNQ1OT1 expression could be offset by miR-211-5p inhibitor transfection. CONCLUSION: This study showed that lncRNA KCNQ1OT1, as a ceRNA, upregulated CHI3L1 and promoted PCa progression through competitive binding to miR-211-5p.	NA	Onco Targets Ther. 2021 Mar 3;14:1659-1671. doi: 10.2147/OTT.S288785. eCollection 2021.
3488	LncRNA	MIR155HG	miR-129-5p	C1S	glioblastoma cell lines	Glioblastoma	Homo sapiens (human)	qRT-PCR	33579282	Construction of a competitive endogenous RNA network and analysis of potential regulatory axis targets in glioblastoma.	BACKGROUND: Glioblastoma is the most common primary malignant brain tumor. Because of the limited understanding of its pathogenesis, the prognosis of glioblastoma remains poor. This study was conducted to explore potential competing endogenous RNA (ceRNA) network chains and biomarkers in glioblastoma by performing integrated bioinformatics analysis. METHODS: Transcriptome expression data from The Cancer Genome Atlas database and Gene Expression Omnibus were analyzed to identify differentially expressed genes between glioblastoma and normal tissues. Biological pathways potentially associated with the differentially expressed genes were explored by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis, and a protein-protein interaction network was established using the STRING database and Cytoscape. Survival analysis using Gene Expression Profiling Interactive Analysis was based on the Kaplan-Meier curve method. A ceRNA network chain was established using the intersection method to align data from four databases (miRTarBase, miRcode, TargetScan, and lncBace2.0), and expression differences and correlations were verified by quantitative reverse-transcription polymerase chain reaction analysis and by determining the Pearson correlation coefficient. Additionally, an MTS assay and the wound-healing and transwell assays were performed to evaluate the effects of complement C1s (C1S) on the viability and migration and invasion abilities of glioblastoma cells, respectively. RESULTS: We detected 2842 differentially expressed (DE) mRNAs, 2577 DE long non-coding RNAs (lncRNAs), and 309 DE microRNAs (miRNAs) that were dysregulated in glioblastoma. The final ceRNA network consisted of six specific lncRNAs, four miRNAs, and four mRNAs. Among them, four DE mRNAs and one DE lncRNA were correlated with overall survival (p < 0.05). C1S was significantly correlated with overall survival (p= 0.015). In functional assays, knockdown of C1S inhibited the proliferation and invasion of glioblastoma cell lines. CONCLUSIONS: We established four ceRNA networks that may influence the occurrence and development of glioblastoma. Among them, the MIR155HG/has-miR-129-5p/C1S axis is a potential marker and therapeutic target for glioblastoma. Knockdown of C1S inhibited the proliferation, migration, and invasion of glioblastoma cells. These findings clarify the role of the ceRNA regulatory network in glioblastoma and provide a foundation for further research.	NA	Cancer Cell Int. 2021 Feb 12;21(1):102. doi: 10.1186/s12935-021-01789-z.
3489	LncRNA	TUG1	miR-320c	MMP-13	IL-1β-stimulated C28/I2 cells	Osteoarthritis	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RACE;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33981845	Long noncoding RNA TUG1 regulates degradation of chondrocyte extracellular matrix via miR-320c/MMP-13 axis in osteoarthritis.	Osteoarthritis (OA) is a common chronic joint disease. This study aimed to explore the function of long noncoding RNA taurine-upregulated gene 1 (TUG1) in the progression and initiation of OA. Levels of TUG1, microRNA-320c (miR-320c) and fucosyltransferase 4 (FUT4) were examined via quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and flow cytometry assays were used to detect cell viability and apoptosis, respectively. The expression of relative proteins was measured using Western blot. The interaction between miR-320c and TUG1 or FUT4 was confirmed utilizing dual-luciferase reporter and RNA immunoprecipitation assays. In this study, levels of TUG1 and FUT4 were distinctly upregulated, but miR-320c level significantly decreased in OA tissues and chondrocytes derived from OA tissues as well as in IL-1β-stimulated C28/I2 cells. Mechanically, TUG1 sponged miR-320c and miR-320c targeted FUT4. In addition, TUG1 knockdown accelerated cell proliferation and repressed apoptosis and extracellular matrix (ECM) degradation in IL-1β-induced C28/I2 cells, whereas these effects of TUG1 deletion were rescued by either miR-320c inhibitor or FUT4 upregulation. Meanwhile, TUG1 sponged miR-320c to regulate FUT4 expression in IL-1β-induced C28/I2 cells. Collectively, TUG1 modulated cell proliferation, apoptosis and ECM degradation in IL-1β-induced C28/I2 cells via the miR-320c/FUT4 axis, providing a new insight into the OA treatment.	NA	Open Life Sci. 2021 Apr 21;16(1):384-394. doi: 10.1515/biol-2021-0037. eCollection 2021.
3490	LncRNA	NEAT1	miR-491-5p	SOX3	OC cell lines and tissues	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33995475	NEAT1 Overexpression Indicates a Poor Prognosis and Induces Chemotherapy Resistance via the miR-491-5p/SOX3 Signaling Pathway in Ovarian Cancer.	BACKGROUND: Accumulated studies have reported that dysregulated long non-coding RNAs (lncRNAs) are crucial in ovarian cancer (OC) initiation and development. However, detailed biological functions of lncRNA NEAT1 during the progression of OC remains to be uncovered. PURPOSE: Our aim was to identify the role of NEAT1 in cisplatin resistance of ovarian cancer and the underlying mechanisms. METHODS: The expression patterns of NEAT1 in OC cell lines and tissue samples were identified by qRT-PCR. The cisplatin (DDP) sensitivity of OC cells was detected by MTT and CCK8 assay, while OC cell apoptosis and cell cycle were detected using flow cytometer assays. In addition, effects of NEAT1 on tumor growth were determined by xenograft tumor model. Luciferase reporter assay was conducted to prove the regulatory relation of miR-491-5p, NEAT1, and SOX3. Importantly, the expression of NEAT1 in exosomes from cisplatin-resistant patients was also determined by using qRT-PCR. RESULTS: In this study, upregulated NEAT1 was detected in OC cell lines and tissues. Meanwhile, NEAT1 was also increased in cisplatin-resistant OC cell lines and tissues. Upregulation of NEAT1 inhibited cisplatin-induced OC cell apoptosis and promoted cell proliferation, while knockdown of NEAT1 played the opposite role. These effects were also observed in vivo. Furthermore, direct interaction was observed between NEAT1 and miR-491-5p. NEAT1 led to the upregulation of miR-491-5p-targeted SOX3 mRNA. Importantly, this study also showed upregulated NEAT1 expression in serum exosomes derived from cisplatin-resistant patients. CONCLUSION: NEAT1 is vital in the chemoresistance of ovarian cancer through regulating miR-491-5p/SOX3 pathway, showing that NEAT1 might be a potential target for OC resistance treatment.	NA	Front Genet. 2021 Apr 29;12:616220. doi: 10.3389/fgene.2021.616220. eCollection 2021.
3491	LncRNA	SNHG16	miR-17-5p	CCND1	OSCC tissues and cell lines	Oral Squamous Cell Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;Western blot;	33654431	Silencing of LncRNA SNHG16 Downregulates Cyclin D1 (CCND1) to Abrogate Malignant Phenotypes in Oral Squamous Cell Carcinoma (OSCC) Through Upregulating miR-17-5p.	BACKGROUND: Targeting the long non-coding RNAs (LncRNAs)-microRNAs (miRNAs)-mRNA competing endogenous RNA (ceRNA) networks has been proved as an effective strategy to treat multiple cancers, including oral squamous cell carcinoma (OSCC). Based on this, the present study identified a novel LncRNA SNHG16/miR-17-5p/CCND1 signaling pathway that played an important role in regulating the pathogenesis of OSCC. METHODS: The expression levels of cancer-associated genes were examined by Real-Time qPCR and Western Blot at transcriptional and translated levels, respectively. CCK-8 assay was performed to determine cell proliferation, and cell apoptosis ratio was measured by the Annexin V-FITC/PI double staining assay. Transwell assay was performed to examine cell migration, and dual-luciferase reporter gene system assay was used to validate the ceRNA networks. RESULTS: LncRNA SNHG16 and CCND1 were upregulated, while miR-17-5p was downregulated in OSCC tissues and cell lines, compared to their normal counterparts. Also, miR-17-5p negatively correlated with both LncRNA SNHG16 and CCND1 mRNA, but LncRNA SNHG16 was positively relevant to CCND1 mRNA in OSCC tissues. By performing the gain- and loss-of-function experiments, we noticed that LncRNA SNHG16 overexpression aggravated the malignant phenotypes, such as cell proliferation, viability, migration and epithelial-mesenchymal transition (EMT) in OSCC cells, while LncRNA SNHG16 knock-down had opposite effects. Furthermore, our dual-luciferase reporter gene system evidenced that LncRNA SNHG16 sponged miR-17-5p to upregulate CCND1 in OSCC cells, and the inhibiting effects of LncRNA SNHG16 ablation on OSCC progression were abrogated by both downregulating miR-17-5p and overexpressing CCND1. Finally, the xenograft tumor-bearing mice models were established, and our data validated that LncRNA SNHG16 served as an oncogene to promote tumorigenicity of OSCC cells in vivo. CONCLUSION: Taken together, targeting the LncRNA SNHG16/miR-17-5p/CCND1 axis hindered the development of OSCC, and this study provided potential diagnostic and therapeutic biomarkers for OSCC in clinic.	NA	Cancer Manag Res. 2021 Feb 22;13:1831-1841. doi: 10.2147/CMAR.S298236. eCollection 2021.
3492	LncRNA	LINC00460	miR-320a	BGN	HNSCC cell lines	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	33833526	LINC00460 Promotes Cell Proliferation, Migration, Invasion, and Epithelial-Mesenchymal Transition of Head and Neck Squamous Cell Carcinoma via miR-320a/BGN Axis.	PURPOSE: Long non-coding RNAs (lncRNAs) play critical roles in cancer onset and development, including head and neck squamous cell carcinoma (HNSCC). This study aimed to investigate the biological role of LINC00460 and the mechanisms underlying epithelial-mesenchymal transition (EMT) in HNSCC. METHODS: Aberrantly LINC00460 expression in HNSCC and overall survival outcomes were constructed using the TCGA database. Quantitative real-time polymerase chain reaction (RT-qPCR) was applied to examine the LINC00460 expression level in HNSCC cell lines. The role of LINC00460 knockdown on HNSCC cell growth, migration, invasion, and EMT was investigated in vitro using cell counting kit-8 (CCK-8), colony formation, transwell assay, and Western blot assay. Besides, bioinformatics prediction, dual-luciferase reporter assay, and RNA immunoprecipitation (RIP) were performed to reveal the interaction among LINC00460 and its target genes. The function of the LINC00460/miR-320a/BGN axis in HNSCC cells was clarified by rescue assays. Furthermore, the in vivo effects of LINC00460 on tumor growth were investigated using mice xenograft models. RESULTS: In this study, LINC00460 was upregulated in HNSCC tissues and cells and was associated with poor clinical prognosis. Further functional analysis showed that LINC00460 knockdown decreased HNSCC cell proliferation, migration, invasion, as well as EMT in vitro. Mechanistic investigation indicated that LINC00460 sponged miR-320a to upregulate Biglycan (BGN) expression, thereby facilitating HNSCC progression and induced EMT. Moreover, knockdown of LINC00460 significantly suppressed the progression of HNSCC cells in vivo. CONCLUSION: Taken together, LINC00460 mediates miR-320a/BGN signaling axis to promote cell proliferation, migration, invasion, and induce the EMT process in HNSCC cells. Our findings elucidated a novel mechanism underlying the progression of HNSCC. LINC00460 could serve as a potential therapeutic target for the treatment of HNSCC.	NA	Onco Targets Ther. 2021 Mar 30;14:2279-2291. doi: 10.2147/OTT.S282947. eCollection 2021.
3493	LncRNA	ABHD11-AS1	miR-133a-3p	EZH2	ovarian cancer tissues	Ovarian Cancer	Homo sapiens (human)	ChIP;Flow Cytometry assay;luciferase assay;	33491971	EZH2-mediated lncRNA ABHD11-AS1 promoter regulates the progression of ovarian cancer by targeting miR-133a-3p.	Long-chain noncoding RNAs (lncRNAs) are involved in a wide range of biological and pathological processes in ovarian cancer. The purpose of this study was to investigate the effects of EZH2-mediated ABHD11-AS1 promoter on the pathogenesis of ovarian cancer. The expression levels of EZH2, ABHD11-AS1 and miR-133a-3p were examined in ovarian cancer tissues using reverse transcription-quantitative PCR. Cell proliferation was evaluated using cell counting kit 8 assay, and cell invasion/migration was determined using a Transwell assay. Cell apoptosis was evaluated using flow cytometry. Dual luciferase assay was performed to confirm the interaction between ABHD11-AS1 and miR-133a-3p. The binding site of H3K27me3 on ABHD11-AS1 promoter was confirmed by ChIP. The expression of ABHD11-AS1 was significantly upregulated in ovarian cancer samples, and its levels were closely associated with lymph node metastasis, tumor stage and 3-year survival rate. Furthermore, interference of ABHD11-AS1 suppressed the proliferation, migration and invasion of ovarian cancer cells, while cell apoptosis was promoted. Additionally, miR-133a-3p could be a novel target of ABHD11-AS1, and EZH2-mediated H3K27me3 protein might bind to ABHD11-AS1 promoter directly. Moreover, rescue experiments indicated that the effects caused by ABHD11-AS1 knockdown on the malignant characteristics of ovarian cancer cells were notably enhanced by miR-133a-3p mimics, whereas the influences on cell growth and metastasis induced by overexpressed ABHD11-AS1 were abrogated by the restoration of miR-133a-3p expression. In summary, EZH2-mediated enrichment of H3K27me3 on ABHD11-AS1 promoter could regulate the progression of ovarian cancer via miR-133a-3p. Therefore, EZH2/ABHD11-AS1/miR-133a-3p axis might be a putative candidate for targeted treatment of ovarian cancer.	NA	Anticancer Drugs. 2021 Mar 1;32(3):269-277. doi: 10.1097/CAD.0000000000001039.
3494	Circular RNA	Circ_0057558	miR-206	USP33	prostate cancer tissues and cell lines	Prostate Cancer	Homo sapiens (human)	luciferase assay;	33718387	Circular RNA circ_0057558 Controls Prostate Cancer Cell Proliferation Through Regulating miR-206/USP33/c-Myc Axis.	We previously reported the elevated expression of circ_0057558 in prostate cancer tissues and cell lines. Here, we aimed to determine the biological function of circ_0057558 in prostate cancer. In the current study, circ_0057558 knockdown in prostate cancer cells significantly repressed cell proliferation and colony formation, but promoted cell arrest and enhanced the sensitivity to docetaxel. Bioinformatics analysis prediction and RNA-pull down assay identified miR-206 as the potential binding miRNA of circ_0057558. A negative correlation was observed between the expression of miR-206 and circ_0057558 in prostate cancer tissues. miR-206 mimics rescued the function of circ_0057558 overexpression on prostate cancer cells. Further, the bioinformatics analysis and luciferase assay suggested that miR-206 may target ubiquitin-specific peptidase 33 (USP33). USP33 mRNA expression has negative correlation with miR-206 expression and positive correlation with circ_0057558 expression in prostate cancer tissues. USP33 overexpression partially blocked the effects of miR-206 mimics on prostate cell proliferation. USP33 could bind and deubiquitinate c-Myc. Increased c-Myc protein by circ_0057558 overexpression was partially reversed by miR-206 mimics. The proliferation inhibition activity of MYC inhibitor 361 (MYCi361) was more prominent in primary prostate cancer cells and patient-derived xenograft (PDX) model with higher level of circ_0057558. Collectively, circ_0057558 gives an impetus to cell proliferation and cell cycle control in prostate cancer cell lines by sponging miR-206 and positively regulating the transcription of the miR-206 target gene USP33.	NA	Front Cell Dev Biol. 2021 Feb 26;9:644397. doi: 10.3389/fcell.2021.644397. eCollection 2021.
3495	Circular RNA	CircRAB11FIP1	miR-129	ATG7	epithelial ovarian cancer (EOC) tissues	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129.	At present, no systematic and in-depth study is available on the function and potential mechanisms of circular RNA in autophagy. This study aimed to screen the expression profiles of circRNA, miRNA, and mRNA of ovarian cancer cells induced by Torin 1 (10 μM). The expression profiles of circRNA, miRNA, and mRNA were analyzed with next-generation sequencing technology. CircRAB11FIP1 expression was elevated in epithelial ovarian cancer (EOC) tissues than in normal ovarian tissues. Silencing circRAB11FIP1 inhibited the autophagic flux of ovarian cancer SKOV3 cells. However, circRAB11FIP1 overexpression activated the autophagic flux of ovarian cancer A2780 cells. CircRAB11FIP1-induced autophagy accelerated EOC proliferation and invasion. Also, circRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. Also, circRAB11FIP1 directly bound to the mRNA of fat mass and obesity-associated protein and promoted its expression. Then, circRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A. In general, this study demonstrated that circRAB11FIP1 regulated ATG7 and ATG14 by sponging miR-129. The data suggested that circRAB11FIP1 might serve as a candidate biomarker for EOC diagnosis and treatment.	NA	Cell Death Dis. 2021 Feb 26;12(2):219. doi: 10.1038/s41419-021-03486-1.
3496	Circular RNA	CircRAB11FIP1	miR-129	ATG14	epithelial ovarian cancer (EOC) tissues	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33637694	CircRAB11FIP1 promoted autophagy flux of ovarian cancer through DSC1 and miR-129.	At present, no systematic and in-depth study is available on the function and potential mechanisms of circular RNA in autophagy. This study aimed to screen the expression profiles of circRNA, miRNA, and mRNA of ovarian cancer cells induced by Torin 1 (10 μM). The expression profiles of circRNA, miRNA, and mRNA were analyzed with next-generation sequencing technology. CircRAB11FIP1 expression was elevated in epithelial ovarian cancer (EOC) tissues than in normal ovarian tissues. Silencing circRAB11FIP1 inhibited the autophagic flux of ovarian cancer SKOV3 cells. However, circRAB11FIP1 overexpression activated the autophagic flux of ovarian cancer A2780 cells. CircRAB11FIP1-induced autophagy accelerated EOC proliferation and invasion. Also, circRAB11FIP1 directly bound to miR-129 and regulated its targets ATG7 and ATG14. CircRAB11FIP1 bound to desmocollin 1to facilitate its interaction with ATG101. Also, circRAB11FIP1 directly bound to the mRNA of fat mass and obesity-associated protein and promoted its expression. Then, circRAB11FIP1 mediated mRNA expression levels of ATG5 and ATG7 depending on m6A. In general, this study demonstrated that circRAB11FIP1 regulated ATG7 and ATG14 by sponging miR-129. The data suggested that circRAB11FIP1 might serve as a candidate biomarker for EOC diagnosis and treatment.	NA	Cell Death Dis. 2021 Feb 26;12(2):219. doi: 10.1038/s41419-021-03486-1.
3497	LncRNA	ZEB1-AS1	miR-186-5p	ABCC1	TNBC cells(DOX-resistant MDA-MB-468 and MDA-MB-436 cells)	Triple Negative Breast Cancer	Homo sapiens (human)	MTT assay;RIP assay;Flow Cytometry assay;Luciferase reporter assay;MTT assay;RNA pull-down;	33493421	Ursolic Acid Enhances Cytotoxicity of Doxorubicin-Resistant Triple-Negative Breast Cancer Cells via ZEB1-AS1/miR-186-5p/ABCC1 Axis.	Background: Triple-negative breast cancer (TNBC) is the most serious subtype of breast cancer (BC) and has been a great health threat to females. Although chemotherapeutic agent contributes a lot to TNBC treatment, drug resistance has been a great obstacle for chemotherapies. Ursolic acid (UA), a pentacyclic triterpenoid compound, was reported to reverse paclitaxel resistance in BC. However, whether UA could affect the resistance of TNBC cells to other drugs such as doxorubicin (DOX) remains to be discovered. Materials and Methods: MTT assay, EdU assay, colony formation assay, and flow cytometry analysis were implemented to detect the viability, proliferation, and apoptosis of DOX-resistant MDA-MB-468 and MDA-MB-436 cells with or without UA treatment. Mechanism assays including RIP, RNA pull-down, and luciferase reporter assays verified the interaction between RNAs. Results: UA treatment hindered the growth and mitigated the DOX resistance of DOX-resistant MDA-MB-468 and MDA-MB-436 cells. Mechanistically, multidrug resistance-associated protein 1 (ABCC1) expression was downregulated by UA treatment. MiR-186-5p was verified to target ABCC1. Further, UA-inhibited ZEB1-AS1 (zinc finger E-box binding homeobox 1 antisense RNA 1) was verified as a competitive endogenous RNA (ceRNA) to upregulate ABCC1 through sponging miR-186-5p. Importantly, UA treatment impaired the malignant phenotypes of DOX-resistant MDA-MB-468 and MDA-MB-436 cells through ZEB1-AS1/ABCC1 axis. Conclusion: UA promotes TNBC cell sensitivity to DOX through inactivating ZEB1-AS1/miR-186-5p/ABCC1 signaling.	NA	Cancer Biother Radiopharm. 2021 Jan 25. doi: 10.1089/cbr.2020.4147.
3498	Circular RNA	Circ_0089153	miR-608	EGFR	ameloblastoma tissues	Ameloblastoma	Homo sapiens (human)	microarray;Luciferase reporter assay;	33523578	Identification of circ_0089153/miR-608/EGFR p53 axis in ameloblastoma via MAPK signaling pathway.	OBJECTIVES: This study investigated the role of circular RNAs (circRNAs) in the pathogenesis of ameloblastoma (AB), identifying potential novel targets for future targeted therapy. MATERIALS AND METHODS: CircRNA and microRNA (miRNA) profiling in AB were built with microarrays. Six novel circRNAs were validated, circ-miRNA networks were delineated. Hsa-miR-608 was filtered over cross-comparison between database screening, miRNA microarray and validated. Circ-miRNA binding sponge was validated via luciferase reporter assay. Downstream mRNAs were screened. Regulation between miRNAs and mRNAs was confirmed in vitro. Gene interaction networks and circRNA-miRNA-mRNA interaction pathway enrichment analyses were established. RESULTS: Six differentially expressed circRNAs were selected and validated. According to miRNAs and pathways predicted, six correlated miRNAs were selected, hsa-miR-608 was filtered and validated. The hsa_circ_0089153/hsa-miR-608 binding sponge was validated. Downstream gene interaction networks showed that EGFR and p53 had the strongest co-expression. In vitro transfection results confirmed the suppressive function of miR-608 and EGFR p53. Hsa_circ_0089153/hsa-miR-608/EGFR p53 interaction pathway enrichment analysis confirmed functions mainly enriched in MAPK and related signaling pathways regulating AB progression. CONCLUSIONS: Six novel circRNAs were identified. Hsa_circ_0089153/hsa-miR-608 sponging was validated, hsa-miR-608 downregulated EGFR and p53, which might further regulate cell proliferation, differentiation, apoptosis, and cell cycle processes via the MAPK signaling pathway.	NA	Oral Dis. 2021 Feb 1. doi: 10.1111/odi.13788.
3499	Circular RNA	Circ_0089153	miR-608	p53	ameloblastoma tissues	Ameloblastoma	Homo sapiens (human)	microarray;Luciferase reporter assay;	33523578	Identification of circ_0089153/miR-608/EGFR p53 axis in ameloblastoma via MAPK signaling pathway.	OBJECTIVES: This study investigated the role of circular RNAs (circRNAs) in the pathogenesis of ameloblastoma (AB), identifying potential novel targets for future targeted therapy. MATERIALS AND METHODS: CircRNA and microRNA (miRNA) profiling in AB were built with microarrays. Six novel circRNAs were validated, circ-miRNA networks were delineated. Hsa-miR-608 was filtered over cross-comparison between database screening, miRNA microarray and validated. Circ-miRNA binding sponge was validated via luciferase reporter assay. Downstream mRNAs were screened. Regulation between miRNAs and mRNAs was confirmed in vitro. Gene interaction networks and circRNA-miRNA-mRNA interaction pathway enrichment analyses were established. RESULTS: Six differentially expressed circRNAs were selected and validated. According to miRNAs and pathways predicted, six correlated miRNAs were selected, hsa-miR-608 was filtered and validated. The hsa_circ_0089153/hsa-miR-608 binding sponge was validated. Downstream gene interaction networks showed that EGFR and p53 had the strongest co-expression. In vitro transfection results confirmed the suppressive function of miR-608 and EGFR p53. Hsa_circ_0089153/hsa-miR-608/EGFR p53 interaction pathway enrichment analysis confirmed functions mainly enriched in MAPK and related signaling pathways regulating AB progression. CONCLUSIONS: Six novel circRNAs were identified. Hsa_circ_0089153/hsa-miR-608 sponging was validated, hsa-miR-608 downregulated EGFR and p53, which might further regulate cell proliferation, differentiation, apoptosis, and cell cycle processes via the MAPK signaling pathway.	NA	Oral Dis. 2021 Feb 1. doi: 10.1111/odi.13788.
3500	LncRNA	SNHG6	miR-429	FRS2	Wilms' tumor tissues and cells	Wilms Tumor	Homo sapiens (human)	Dual-luciferase reporter assay;RNA pull-down assay;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33481659	LncRNA SNHG6 Promotes Wilms' Tumor Progression Through Regulating miR-429/FRS2 Axis.	Background: Long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) has been reported to be an oncogene in a variety of cancers. However, the role of SNHG6 and its associated mechanisms in Wilms' tumor progression remain largely unknown. Methods: The expression of SNHG6, microRNA-429 (miR-429), and FGF receptor substrates 2 (FRS2) messenger RNA (mRNA) was detected by quantitative real-time polymerase chain reaction. Cell proliferation was analyzed through 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and plate colony assay. The apoptosis was assessed by flow cytometry. Cell glycolytic metabolism was analyzed through detecting the lactate dehydrogenase activity, glucose uptake, lactate production, and ATP level. The target relationship between miR-429 and SNHG6 or FRS2 was predicted by miRcode or Starbase and then validated by dual-luciferase reporter assay and RNA pull-down assay. Murine xenograft model was established to validate the function of SNHG6 in vivo. Results: The level of SNHG6 was elevated in Wilms' tumor tissues and cells, and SNHG6 played an oncogenic role to promote the proliferation and glycolysis and restrain the apoptosis of Wilms' tumor cells. MiR-429 was identified as a target of SNHG6, and miR-429 interference partly reversed the inhibitory effects induced by SNHG6 silencing on the malignant behaviors of Wilms' tumor cells. FRS2 mRNA bound to miR-429 in Wilms' tumor cells. SNHG6 upregulated the expression of FRS2 through acting as a sponge of miR-429. MiR-429-induced influences in Wilms' tumor cells were largely counteracted by the overexpression of FRS2. SNHG6 silencing suppressed the Wilms' tumor growth through miR-429/FRS2 axis in vivo. Conclusion: SNHG6 accelerated Wilms' tumor progression through regulating miR-429/FRS2 signaling in vitro and in vivo.	NA	Cancer Biother Radiopharm. 2021 Jan 22. doi: 10.1089/cbr.2020.3705.
3501	LncRNA	FOXD2-AS1	miR-760	E2F3	CCA cells and tissues	Cholangiocarcinoma	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33570683	Long Non-coding RNA FOXD2-AS1 Promotes Proliferation, Migration, and Invasion in Cholangiocarcinoma Through Regulating miR-760/E2F3 Axis.	BACKGROUND: Long non-coding RNA (lncRNA) has been testified to influence the initiation and evolution of sundry carcinomas. Recently, lncRNA FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) has been found to display vital regulating functions in various cancers. METHODS: qRT-PCR was used to verify the dysregulation of FOXD2-AS1 expression in CCA cells and tissues, and the correlation of FOXD2-AS1 expression with clinicopathological characteristics was investigated. The viability, migration, and invasion of CCA cells were verified through CCK-8 assay, colony formation experiment, wound healing assay, and transwell assay. The regulatory networks of FOXD2-AS1 were analyzed by Bioinformatic prediction and dual-luciferase reporter assay. RESULTS: We discovered that FOXD2-AS1 was significantly upregulated in CCA and its up-regulation was closely correlated with terminal TNM stage, lymph node metastasis and poor survival in the current research. In addition, it was revealed that FOXD2-AS1 was an independent prognostic factor. Functional tests uncovered that the cell viability, migration, and invasion could be restrained through downregulating the expression of FOXD2-AS1, while FOXD2-AS1 overexpression could facilitate the cell viability, migration, and invasion. Mechanistically, FOXD2-AS1 was founded to interact directly with miR-760 and the oncogene E2F3 was the downstream target of miR-760 through bioinformatic prediction and dual-luciferase reporter assays. Finally, we testified that FOXD2-AS1 could competitively sponge miR-760 and further upregulated the E2F3 expression to play a vital part in cholangiocarcinoma. CONCLUSIONS: This research revealed that lncRNA FOXD2-AS1 could enhance CCA malignant progression through regulating the miR-760/E2F3 axis and was expected to be a prognostic biomarker and therapeutic target for cholangiocarcinoma.	NA	Dig Dis Sci. 2021 Feb 11. doi: 10.1007/s10620-021-06876-9.
3502	LncRNA	HNF1A-AS1	miR-363	SERTAD3	BC cells and tissues	Breast Cancer	Homo sapiens (human)	qRT-PCR	33472456	Silencing long non-coding RNA HNF1A-AS1 inhibits growth and resistance to TAM of breast cancer cells via the microRNA-363/SERTAD3 axis.	Long non-coding RNAs (lncRNAs) can exert effects on drug resistance of cancer cells. This study investigated the role of lncRNA HNF1A-antisense 1 (HNF1A-AS1) in growth and Tamoxifen (TAM) sensitivity of breast cancer (BC) cells. HNF1A-AS1 expression was promoted in BC cells and tissues. BC cells with HNF1A-AS1 silencing were constructed to detect cell proliferation. TAM resistant cell line with HNF1A-AS1 silencing and parent cell line with overexpressed HNF1A-AS1 were constructed to measure drug resistance. Silencing HNF1A-AS1 reduced proliferation and TAM resistance of BC cells. The downstream microRNAs (miRs) of HNF1A-AS1 and its targets were figured out and their functions in TAM resistance of BC cells were identified. HNF1A-AS1 sponged miR-363 to promote SERTAD3 expression. Downregulation of miR-363 or upregulation of SERTAD3 stimulated TAM resistance of BC cells. The findings in vitro were reproduced in in vivo experiments. It could be concluded that silencing HNF1A-AS1 inhibited growth and drug resistance to TAM of BC cells through the miR-363/SERTAD3 axis and the inactivation of the TGF-β/Smad pathway.	NA	J Drug Target. 2021 May 17:1-12. doi: 10.1080/1061186X.2021.1878362.
3503	LncRNA	LINC00941	miR-205-5p	MYC	colon cancer tissues and cells	Colon Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down;	33654409	Novel lncRNA LINC00941 Promotes Proliferation and Invasion of Colon Cancer Through Activation of MYC.	PURPOSE: We conducted the study to elucidate how LncRNA LINC00941 affects colon cancer progression and its possible regulatory mechanism. METHODS: The expression level of LINC00941 in colon cancer tissues and cells was detected by qRT-PCR. The function of LINC00941 on colon cancer cell proliferation, migration, and invasion was detected by CCK-8 and Transwell assay respectively. The target interactions among LINC00941, miR-205-5p, and MYC were further confirmed by dual-luciferase reporter gene assays and RNA pull-down experiments. Meanwhile, in vivo experiments were carried out to study the role of LINC00941 in the xenotransplantation model. RESULTS: LINC00941 expression level was elevated in colon cancer tissues and cells. LINC00941 overexpression accelerated proliferation, migration, and invasion of colon cancer cells, while the LINC00941 knockdown showed the opposite results. In addition, LINC00941 regulated the expression of MYC by sponging miR-205-5p as a competitive endogenous RNA, and miR-205-5p knockdown reversed the tumor inhibition of LINC00941 knockdown on colon cancer cells. Xenograft model assay confirmed that LINC00941 silencing could inhibit colon cancer cell growth and metastasis. CONCLUSION: LINC00941 may markedly promote colon cancer progression by acting on the miR-205-5p/MYC axis as a ceRNA, which offers novel clues for lncRNA to guide the treatment and prognosis of colon cancer.	NA	Onco Targets Ther. 2021 Feb 22;14:1173-1186. doi: 10.2147/OTT.S293519. eCollection 2021.
3504	LncRNA	FENDRR	miR-4700-3p	FOXC2	MDR GC cell lines	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33869020	The FENDRR/FOXC2 Axis Contributes to Multidrug Resistance in Gastric Cancer and Correlates With Poor Prognosis.	The dysregulation of long non-coding RNAs (lncRNAs) and transcription factors (TFs) is closely related to the development and progression of drug resistance in cancer chemotherapy. However, their regulatory interactions in the multidrug resistance (MDR) of gastric cancer (GC) has largely remained unknown. In this study, we report a novel oncogenic role of lncRNA FENDRR in conferring MDR in GC by coordinated regulation of FOXC2 expression at the transcriptional and posttranscriptional levels. In vitro and in vivo experiments demonstrated that downregulation of FENDRR expression remarkably decreased drug resistant ability of GC MDR cells while upregulation of FENDRR expression produced the opposite effect. FENDRR overexpression was observed in MDR GC cell lines, patient-derived xenografts, and clinical samples. And the high levels of FENDRR expression were correlated with poor prognosis in GC patients. Regarding the mechanism, FENDRR was revealed to increase proto-oncogene FOXC2 transcription by performing an enhancer-like role in the nucleus and by sponging miR-4700-3p in the cytoplasm. Both FOXC2 and miR-4700-3p were shown to be functionally involved in the FENDRR-induced chemoresistance. In addition, there is a positive correlation between FENDRR and FOXC2 expression in clinic and the overexpressed FOXC2 indicated a poor prognosis in GC patients. Collectively, our findings provide a new perspective for the lncRNA-TF regulatory interaction involved in MDR, suggesting that targeting the FENDRR/FOXC2 axis may be an effective approach to circumvent GC chemoresistance.	NA	Front Oncol. 2021 Mar 22;11:634579. doi: 10.3389/fonc.2021.634579. eCollection 2021.
3505	LncRNA	LINC00514	miR-204-3p	KRAS	GC cells and tissues	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33888645	LINC00514 promotes gastric cancer cell growth and EMT progression via miR-204-3p/KRAS.	Long noncoding RNAs (LncRNAs) participate in tumor development and tumorigenesis. However, the mechanism, function and expression of LINC00514 in GC remain unknown. We showed that LINC00514 was upregulated in GC specimens compared with nontumor specimens. Overexpression of LINC00514 induced cell growth and EMT progression in GC cells. By using bioinformatics prediction, we found that miR-204-3p contained binding sequences for LINC00514. Luciferase reporter analysis noted that miR-204-3p overexpression decreased the luciferase expression under LINC00514-wild-type and KRAS-wild-type reporters but not that under mutant reporter. Ectopic LINC00514 expression decreased miR-204-3p expression. miR-204-3p expression was decreased in GC specimens compared with nontumor specimens and that LINC00514 was negatively correlated with miR-204-3p in GC specimens. Furthermore, KRAS was identified as a target gene for miR-204-3p according to TargetScan. Elevated miR-204-3p expression inhibited KRAS expression in HGC-27 cells, and ectopic expression of LINC00514 enhanced KRAS expression. Elevated LINC00514 expression enhanced cell growth and EMT progression by sponging KRAS. Our data indicated that LINC00514 may act as an oncogene and therapeutic target for GC.	NA	Aging (Albany NY). 2021 Apr 22;13(8):12007-12015. doi: 10.18632/aging.202905. Epub 2021 Apr 22.
3506	Circular RNA	CircNR3C2	miR-513a-3p	HRD1	breast cancer tissues/cell lines	Triple Negative Breast Cancer	Homo sapiens (human)	microarray;Immunoblotting;	33530981	CircNR3C2 promotes HRD1-mediated tumor-suppressive effect via sponging miR-513a-3p in triple-negative breast cancer.	BACKGROUND: E3 ubiquitin ligase HRD1 (HMG-CoA reductase degradation protein 1, alias synoviolin with SYVN1 as the official gene symbol) was found downregulated and acting as a tumor suppressor in breast cancer, while the exact expression profile of HRD1 in different breast cancer subtypes remains unknown. Recent studies characterized circular RNAs (circRNAs) playing an regulatory role as miRNA sponge in tumor progression, presenting a new viewpoint for the post-transcriptional regulation of cancer-related genes. METHODS: Examination of the expression of HRD1 protein and mRNA was implemented using public microarray/RNA-sequencing datasets and breast cancer tissues/cell lines. Based on public RNA-sequencing results, online databases and enrichment/clustering analyses were used to predict the specific combinations of circRNA/miRNA that potentially govern HRD1 expression. Gain-of-function and rescue experiments in vitro and in vivo were executed to evaluate the suppressive effects of circNR3C2 on breast cancer progression through HRD1-mediated proteasomal degradation of Vimentin, which was identified using immunoblotting, immunoprecipitation, and in vitro ubiquitination assays. RESULTS: HRD1 is significantly underexpressed in triple-negative breast cancer (TNBC) against other subtypes and has an inverse correlation with Vimentin, inhibiting the proliferation, migration, invasion and EMT (epithelial-mesenchymal transition) process of breast cancer cells via inducing polyubiquitination-mediated proteasomal degradation of Vimentin. CircNR3C2 (hsa_circ_0071127) is also remarkably downregulated in TNBC, negatively correlated with the distant metastasis and lethality of invasive breast carcinoma. Overexpressing circNR3C2 in vitro and in vivo leads to a crucial enhancement of the tumor-suppressive effects of HRD1 through sponging miR-513a-3p. CONCLUSIONS: Collectively, we elucidated a bona fide circNR3C2/miR-513a-3p/HRD1/Vimentin axis that negatively regulates the metastasis of TNBC, suggesting that circNR3C2 and HRD1 can act as potential prognostic biomarkers. Our study may facilitate the development of therapeutic agents targeting circNR3C2 and HRD1 for patients with aggressive breast cancer.	NA	Mol Cancer. 2021 Feb 2;20(1):25. doi: 10.1186/s12943-021-01321-x.
3507	LncRNA	H19	miR-675-5p	GATA2	EVT cells	NA	Homo sapiens (human)	RNA sequencing;	33513878	LncRNA H19-Derived miR-675-5p Accelerates the Invasion of Extravillous Trophoblast Cells by Inhibiting GATA2 and Subsequently Activating Matrix Metalloproteinases.	The invasion of extravillous trophoblast (EVT) cells into the maternal decidua, which plays a crucial role in the establishment of a successful pregnancy, is highly orchestrated by a complex array of regulatory mechanisms. Non-coding RNAs (ncRNAs) that fine-tune gene expression at epigenetic, transcriptional, and post-transcriptional levels are involved in the regulatory mechanisms of EVT cell invasion. However, little is known about the characteristic features of EVT-associated ncRNAs. To elucidate the gene expression profiles of both coding and non-coding transcripts (i.e., mRNAs, long non-coding RNAs (lncRNAs), and microRNAs (miRNAs)) expressed in EVT cells, we performed RNA sequencing analysis of EVT cells isolated from first-trimester placentae. RNA sequencing analysis demonstrated that the lncRNA H19 and its derived miRNA miR-675-5p were enriched in EVT cells. Although miR-675-5p acts as a placental/trophoblast growth suppressor, there is little information on the involvement of miR-675-5p in trophoblast cell invasion. Next, we evaluated a possible role of miR-675-5p in EVT cell invasion using the EVT cell lines HTR-8/SVneo and HChEpC1b; overexpression of miR-675-5p significantly promoted the invasion of both EVT cell lines. The transcription factor gene GATA2 was shown to be a target of miR-675-5p; moreover, small interfering RNA-mediated GATA2 knockdown significantly promoted cell invasion. Furthermore, we identified MMP13 and MMP14 as downstream effectors of miR-675-5p/GATA2-dependent EVT cell invasion. These findings suggest that miR-675-5p-mediated GATA2 inhibition accelerates EVT cell invasion by upregulating matrix metalloproteinases.	NA	Int J Mol Sci. 2021 Jan 27;22(3):1237. doi: 10.3390/ijms22031237.
3508	LncRNA	SNHG19	miR-137	E2F7	NSCLC tissues, plasma and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;luciferase assay;	33842336	LncRNA SNHG19 Promotes the Development of Non-Small Cell Lung Cancer via Mediating miR-137/E2F7 Axis.	OBJECTIVE: Non-small cell lung cancer (NSCLC) is a common malignant tumor, which has high incidence and low the 5-year survival rate. Long non-coding RNAs (lncRNAs) play critical roles in carcinoma occurrence and metastasis. Herein, our aim was to investigate the effects of lncRNA SNHG19 in NSCLC progression. MATERIALS AND METHODS: Long non-coding RNA Small Nucleolar RNA Host Gene 19 (lncRNA SNHG19) expression level was measured by bioinformatics and qRT-PCR. Edu, Transwell, and scratch assays were performed to explore the role of si-SNHG19 or SNHG19 on NSCLC progression. Luciferase assay was used to verify the relationship between SNHG19/E2F7 and miR-137. The experiment of Xenograft was used for exploring the function of SNHG19 in vivo. RESULTS: SNHG19 was upregulated in cancer tissues, patients plasma and cell lines of NSCLC. Knockdown of SNHG19 inhibited cell proliferation, migration, and invasion. Luciferase assay confirmed that SNHG19 regulated E2F7 expression via interacting with miR-137. Overexpression of SNHG19 accelerated NSCLC tumor progression via miR-137/E2F7 axis both in vitro and in vivo. CONCLUSIONS: Our results clarified the SNHG19 function for the first time, and SNHG19 promoted the progression of NSCLC, which was mediated by the miR-137/E2F7 axis. This study might provide new understanding and targets for NSCLC diagnosis and treatment.	NA	Front Oncol. 2021 Mar 25;11:630241. doi: 10.3389/fonc.2021.630241. eCollection 2021.
3509	LncRNA	HCP5	miR-29b-3p	DNMT3A	HCC tissues and cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	34148029	Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A.	Multiple studies have revealed that long non-coding RNA (lncRNAs) served as regulatory factors in modulating tumorigenesis of hepatocellular carcinoma (HCC). In the present study, we demonstrated that lncRNA HCP5 was overexpressed in HCC tissues and cell lines, and these findings were obvious even in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis, and invasion both in vitro and in vivo through promoting apoptosis and by inactivating the epithelial-mesenchymal transition (EMT) progress. Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, and served as a tumor suppressor of HCC to prevent cell proliferation, migration, and invasion. Subsequently, DNMT3A was identified as a downstream regulatory factor of miR-29b-3p, and acted as a participated element of HCC progression by activating AKT phosphorylation. Taken together, our study elucidated for the first time that HCP5 plays a crucial role in HCC via the HCP5/miR-29b-3p/DNMT3A/AKT axis and our findings demonstrated a novel diagnostic and therapeutic strategy with potentiality to treat HCC.	NA	Aging (Albany NY). 2021 Jun 18;13. doi: 10.18632/aging.203155.
3510	LncRNA	LINC01638	miR-523-5p	BATF3	LSCC cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	33714208	Long noncoding RNA LINC01638 contributes to laryngeal squamous cell cancer progression by modulating miR-523-5p/BATF3 axis.	Long noncoding RNA (lncRNA) plays a critical role in tumorigenesis. How lncRNA regulates laryngeal squamous cell carcinoma (LSCC) progression remains poorly understood. In the present study, we found that LINC01638 was highly expressed in LSCC tissues. And LINC01638 expression was positively correlated with clinical stage and lymph node metastasis. Patients with LINC01638 high expression displayed a low survival rate. Results from CCK8, colony formation, and transwell assays showed that LINC01638 knockdown suppressed the proliferation, migration and invasion of LSCC cells in vitro. Animal experiments indicated that LINC01638 silencing attenuated tumor growth in vivo. In terms of mechanism, LINC01638 was found to sponge miR-523-5p and promote BATF3 expression. In summary, our results demonstrated that LINC01638/miR-523-5p/BATF3 axis plays a crucial function in initiating LSCC development and may be a potential target for tumor therapy.	NA	Aging (Albany NY). 2021 Mar 10;13(6):8611-8619. doi: 10.18632/aging.202675. Epub 2021 Mar 10.
3511	LncRNA	PRNCR1	miR-377	CCND2	breast cancer cell lines	Breast Cancer	Homo sapiens (human)	RIP assay;Western blot;RNA pull-down;	33608112	LncRNA PRNCR1 Promotes Breast Cancer Proliferation and Inhibits Apoptosis by Modulating microRNA-377/CCND2/MEK/MAPK Axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) have recently become the vital gene regulators in diverse cancers. In our study, we purposed to inquiry into the mechanisms of lncRNA PRNCR1 in breast cancer via microRNA-377 (miR-377)/CCND2/MEK/MAPK axis. METHODS: PRNCR1 expression in breast cancer tissues was detected, and the correlation between PRNCR1 expression and prognostic survival was analyzed. The expressions of PRNCR1 and miR-377 in breast cancer cell lines were detected. Relationships among PRNCR1, miR-377 and CCND2 were confirmed by luciferase activity, RNA pull-down or RIP assays. Breast cancer cells were introduced with silenced PRNCR1 or restored miR-377 to explore their functions in malignant phenotype of breast cancer cells. The expression of MEK/MAPK pathway-related proteins was determined by western blot analysis. RESULTS: PRNCR1 was highly expressed and miR-377 was poorly expressed in patients with breast cancer, and patients with high expression of PRNCR1 had a poor prognosis. PRNCR1 silencing or miR-377 overexpression resulted in suppressed breast cancer cell proliferation ability, blocked cell cycle process and induced apoptosis. PRNCR1 regulated CCND2 expression by competitively binding to miR-377. CCND2 activated the MEK/MAPK pathway, and after treatment with Mirdametinib, the MEK/MAPK pathway was inhibited, which was found to retard breast cancer growth. CONCLUSION: Our study highlights that lncRNA PRNCR1 may competitively bind to miR-377, leading to upregulated CCND2, which in turn activated MEK/MAPK pathway to promote breast cancer growth.	NA	Arch Med Res. 2021 Feb 16:S0188-4409(21)00030-8. doi: 10.1016/j.arcmed.2021.01.007.
3512	Circular RNA	cirRNA_0074027	miR-525-3p	p53	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33760126	Circular RNA_0074027 participates in cell proliferation, apoptosis and metastasis of colorectal cancer cells through regulation of miR-525-3p.	The present study aimed to elucidate the biological function of circular RNAs (circRNA) 0074027 in colorectal cancer (CRC). The expression of circRNA-0074027 in CRC tissues and cells was determined by reverse transcription-quantitative PCR. The in vitro experiments, including Cell Counting Kit-8 (CCK-8) assay, 5-Ethynyl-2'-deoxyuridine assay, flow cytometry and Transwell assay, were applied to evaluate cell proliferation, apoptosis and metastasis ability respectively following downregulation of circRNA-0074027. The correlation between circRNA-0074027 and micro (mi)RNA-525-3p was determined via dual-luciferase reporter assay. Finally, western blotting was used to explore the possible regulatory mechanism. CircRNA-0074027 was upregulated in CRC tissues, while miR-525-3p expression was reduced. In addition, patients with CRC and circRNA-0074027 overexpression were more likely to have low tumor differentiation, lymph node metastasis and advanced TMN stage. Deletion of circRNA-0074027 could suppress cell proliferation and metastasis through up-regulating p53 expression and forbidding epithelial-mesenchymal transition signaling pathway. The addition of miRNA-525-3p inhibitors could reverse the anti-tumor effects induced by the deletion of circRNA-0074027. The downregulation of cirRNA_0074027 inhibited tumor progression via sponging miR-525-3p, which could be a promising treatment bio-marker for CRC.	NA	Mol Med Rep. 2021 May;23(5):324. doi: 10.3892/mmr.2021.11963. Epub 2021 Mar 24.
3513	LncRNA	OIP5-AS1	miR-140-5p	RhoA	CD4(+)IL-17(+) cell	Multiple Sclerosis	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33515560	OIP5-AS1 facilitates Th17 differentiation and EAE severity by targeting miR-140-5p to regulate RhoA/ROCK2 signaling pathway.	AIMS: Multiple sclerosis (MS) is one of the commonest neurologic disorders globally. LncRNA OIP5-AS1 has been found to be implicated in the etiology of MS. This study was to explore the roles and molecular mechanisms of OIP5-AS1 in the development of MS. MATERIALS AND METHODS: RT-qPCR assay was used to measure expressions of OIP5-AS1, miR-140-5p, IL-17A mRNA and RhoA mRNA. CD4(+)IL-17(+) cell proportion was determined by flow cytometry. IL-17A secretion was examined by ELISA assay. Cell inflammatory infiltration and demyelination were assessed by histological analyses. The interaction between miR-140-5p and OIP5-AS1 or RhoA 3'UTR was validated by bioinformatical analysis and luciferase reporter assay. Western blot assay was performed to detect protein expressions of ROCK2 and RhoA. An experimental autoimmune encephalomyelitis (EAE) models was established to explore the role of OIP5-AS1 in MS in vivo. KEY FINDINGS: OIP5-AS1 expression was enhanced in MS patients. Also, elevated OIP5-AS1 level was observed during T-helper 17 (Th17) differentiation. Moreover, OIP5-AS1 promoted Th17 differentiation in vitro and contributed to the development of EAE in vivo. Mechanical explorations revealed that OIP5-AS1 targeted miR-140-5p to regulate Th17 differentiation. Moreover, RhoA was a target of miR-140-5p and miR-140-5p inhibited the activation of RhoA/ROCK2 signaling. Also, RhoA upregulation abrogated the inhibitory effects of miR-140-5p on Th17 differentiation. SIGNIFICANCE: OIP5-AS1 contributed to EAE development by targeting miR-140-5p/RhoA and activating RhoA/ROCK2 signaling pathway, shedding light on the roles and molecular mechanisms of OIP5-AS1 in the development of MS and providing some candidate targets for the diagnose and treatment of MS.	NA	Life Sci. 2021 Jan 27:119108. doi: 10.1016/j.lfs.2021.119108.
3514	LncRNA	LINC01006	miR-28-5p	PAK2	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Cell proliferation assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33576457	Long non-coding RNA LINC01006 exhibits oncogenic properties in cervical cancer by functioning as a molecular sponge for microRNA-28-5p and increasing PAK2 expression.	As previously reported, long intergenic non-protein-coding RNA 1006 (LINC01006) plays crucial roles in prostate, pancreatic and gastric cancers. However, whether it plays important roles in cervical cancer remains unclear. The present study thus aimed to determine the precise role of LINC01006 in cervical cancer and elucidate its regulatory mechanisms. The expression of LINC01006 in cervical cancer was examined by reverse transcription-quantitative polymerase chain reaction. Cell proliferation assay, flow cytometric analysis, Transwell migration and invasion assays, and tumor xenograft model experiments were performed to elucidate the roles of LINC01006 in cervical cancer. Bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments were performed for mechanistic analyses. The expression of LINC01006 was found to be upregulated in cervical cancer and to be associated with a poor prognosis. The absence of LINC01006 inhibited the proliferation, migration and invasion of cervical cancer cells, whereas it promoted cell apoptosis in vitro. The downregulation of LINC01006 impeded tumor growth in vivo. LINC01006 was verified as an endogenous 'sponge' that competed for microRNA-28-5p (miR-28-5p), which resulted in the upregulation of the miR-28-5p target P21-activated kinase 2 (PAK2). Rescue experiments revealed that the suppression of miR-28-5p expression or the overexpression of PAK2 abrogated the effects of LINC01006 downregulation on malignant cellular functions in cervical cancer. On the whole, the present study demonstrates that LINC01006 exhibits tumor-promoting functions in cervical cancer via the regulation of the miR-28-5p/PAK2 axis. These findings may provide the basis for the identification of LINC01006-targeted clinical therapy.	NA	Int J Mol Med. 2021 Apr;47(4):46. doi: 10.3892/ijmm.2021.4879. Epub 2021 Feb 12.
3515	LncRNA	NEAT1	miR-483	STAT3	osteosarcoma cell lines and osteosarcoma tissues	Osteosarcoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33546665	The lncRNA NEAT1 promotes the epithelial-mesenchymal transition and metastasis of osteosarcoma cells by sponging miR-483 to upregulate STAT3 expression.	BACKGROUND: Osteosarcoma is one of the most prevalent primary bone tumours in adolescents. Accumulating evidence shows that aberrant expression of the long non-coding RNA (lncRNA) NEAT1 and microRNA-483 (miR-483) contribute to the epithelial-mesenchymal transition (EMT), invasion and metastasis of tumour cells. However, the potential regulatory effects of NEAT1 and miR-483 on the EMT of osteosarcoma remain elusive. METHODS: The expression of the NEAT1, miR-483, signal transducer and activator of transcription-1 (STAT1), STAT3, and EMT-associated markers was measured using qRT-PCR or western blotting. NEAT1 overexpression or knockdown was induced by lentivirus-mediated transfection. A luciferase reporter assay was employed to confirm the association between NEAT1/miR-483 and miR-483/STAT3. RNA immunoprecipitation (RIP) was also performed to verify the NEAT1 and miR-483 interaction. Wound healing and transwell assays were implemented to assess the migration and invasion of U2OS cells. Unilateral subcutaneous injection of U2OS into nude mice was performed to investigate tumour metastasis in vivo. RESULTS: The expression of miR-483 was downregulated in both osteosarcoma cell lines and osteosarcoma tissues. The overexpression of miR-483 suppressed the migration, invasion, and expression of EMT-associated proteins in U2OS cells, while simultaneous overexpression of STAT3 partially relieved this suppression. Mechanistically, miR-483 specifically targeted the 3' untranslated region (3'UTR) of STAT3 and repressed its expression. However, NEAT1 sponged miR-438, increased STAT3 expression, and repressed STAT1 expression, subsequently increasing the EMT of osteosarcoma cells. The knockdown of NEAT1 in transplanted U2OS cells impaired the liver and lung metastases of osteosarcoma in nude mice. Moreover, NEAT1 silencing inhibited the mesenchymal- epithelial transition (MET) of osteosarcoma at metastasis sites. CONCLUSIONS: The lncRNA NEAT1/miR-483/STAT3 axis plays a crucial role in regulating the metastasis of osteosarcoma and potentially represents one appealing therapeutic target for osteosarcoma treatment in the future.	NA	Cancer Cell Int. 2021 Feb 5;21(1):90. doi: 10.1186/s12935-021-01780-8.
3516	LncRNA	SNHG6	miR-204-5p	E2F1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA pull-down assay;Luciferase reporter assay;RNA pull-down;	33824472	LncRNA SNHG6 promotes G1/S-phase transition in hepatocellular carcinoma by impairing miR-204-5p-mediated inhibition of E2F1.	Emerging evidence suggests that long noncoding RNAs (lncRNAs) function as competitive endogenous RNA (ceRNA) targeting proteins and genes; however, the role of lncRNAs in hepatocellular carcinoma (HCC) is not well understood. We investigated the mechanism by which lncRNA SNHG6 promotes the development of HCC. RT-qPCR revealed upregulated lncRNA SNHG6 in the HCC setting. Elevated SNHG6 expression was indicative of poor prognosis in patients with HCC. SNHG6 overexpression resulted in increased cyclin D1, cyclin E1, and E2F1 expression both in vitro and in vivo. SNHG6 also promoted HCC cell proliferation by enhancing G1-S phase transition in vitro. Dual luciferase reporter assays, RIP, and RNA pull-down assays demonstrated SNHG6 competitively bound to miR-204-5p and inhibited its expression preventing miR-204-5p from targeting E2F1. Overexpression of miR-204-5p abolished the effect of SNHG6. Our data suggest that SNHG6 functions as a ceRNA that targets miR-204-5p resulting in an increased E2F1 expression and enhanced G1-S phase transition, thereby promoting the tumorigenesis of HCC.	NA	Oncogene. 2021 May;40(18):3217-3230. doi: 10.1038/s41388-021-01671-2. Epub 2021 Apr 6.
3517	LncRNA	LINC00265	miR-144-3p	CBX4	GC tissues and cell lines	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33464142	Long intergenic noncoding RNA00265 promotes proliferation of gastric cancer via the microRNA-144-3p/Chromobox 4 axis.	The expression and biological function of long intergenic noncoding RNA00265 (LINC00265) in gastric cancer (GC) have not yet been explored. This study aimed to detect LINC00265 expression in GC tissues and cell lines, investigate its roles in the proliferation of GC cells in vitro, and elucidate the regulatory mechanisms of LINC00265 action. It was found that LINC00265 expression was significantly upregulated in GC tissue samples and cell lines compared with their normal counterparts. Additionally, LINC00265 knockdown could inhibit GC cell proliferation in vitro. Further investigation revealed that LINC00265 acted as a competing endogenous RNA for microRNA-144-3p (miR-144-3p) and inhibition of miR-144-3p markedly counteracted LINC00265 knockdown-meditated suppression on GC cell proliferation. Additionally, Chromobox 4 (CBX4) was upregulated in GC and silencing CBX4 could reduce GC cell proliferation. Then, CBX4 mRNA was demonstrated to be a direct target of miR-144-3p in GC cells and LINC00265/miR-144-3p axis could regulate CBX4 expression. Taken together, LINC00265 may promote GC cell proliferation via the miR-144-3p/CBX4 axis.	NA	Bioengineered. 2021 Dec;12(1):1012-1025. doi: 10.1080/21655979.2021.1876320.
3518	LncRNA	miR143HG	miR-504	p53	GBM tissues	Glioblastoma	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;	33461388	LncRNA miR143HG inhibits the proliferation of glioblastoma cells by sponging miR-504.	AIM: It is known that miR-504 can target p53 to promote cancer progression. Our bioinformatics analysis revealed that miR-504 could bind miR-143 host gene (miR143HG), suggesting that miR143HG might also have crosstalk with p53 in cancer progression. This study aimed to analyze the function of miR143HG in glioblastoma (GBM). METHODS: This study selected 64 GBM patients. GBM and non-tumor tissues were obtained from the patients. RT-qPCR was used to analyze gene expression. Survival curve analysis was performed to analyze the prognostic values of miR143HG for GBM. The crosstalk between miR143HG and miR-504 was analyzed by overexpressing them in GBM cells, followed by RT-qPCRs to detect their expression. CCK-8 assay was used to detect the cell proliferation ability. RESULTS: We found that miR143HG was downregulated in GBM and predicted poor survival. The mRNA expression levels of miR143HG and p53 were positively correlated in GBM tissues. Bioinformatics analysis suggested that miR143HG could form base paring with miR-504, which has been reported to target p53. Overexpression experiments revealed that miR143HG overexpression upregulated the expression of p53, while miR-504 overexpression inhibited the effect of miR143HG overexpression on the expression of p53. Moreover, overexpression of miR143HG and p53 decreased GBM cell proliferation, while overexpression of miR-504 increased GBM cell proliferation. In addition, overexpression of miR-504 attenuated the effect of miR143HG overexpression on GBM cell proliferation. CONCLUSION: Therefore, miR143HG may decrease the proliferation of GBM cells by sponging miR-504 to upregulate p53.	NA	Int J Neurosci. 2021 Feb 2:1-9. doi: 10.1080/00207454.2020.1865950.
3519	Circular RNA	Circ_0077210	miR-92b-3p	CPEB3	HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33719338	Construction of circRNA-Based ceRNA Network to Reveal the Role of circRNAs in the Progression and Prognosis of Hepatocellular Carcinoma.	BACKGROUND: Circular RNAs (circRNAs) are now under hot discussion as novel promising biomarkers for patients with hepatocellular carcinoma (HCC). The purpose of our study is to identify several competing endogenous RNA (ceRNA) networks related to the prognosis and progression of HCC and to further investigate the mechanism of their influence on tumor progression. METHODS: First, we obtained gene expression data related to liver cancer from The Cancer Genome Atlas (TCGA) database (http://www.portal.gdc.cancer.gov/), including microRNA (miRNA) sequence, RNA sequence, and clinical information. A co-expression network was constructed through the Weighted Correlation Network Analysis (WGCNA) software package in R software. The differentially expressed messenger RNAs (DEmRNAs) in the key module were analyzed with the Database for Annotation Visualization and Integrated Discovery (DAVID) (https://david.ncifcrf.gov/summary.jsp) to perform functional enrichment analysis including Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The data of miRNA expression and clinical information downloaded from TCGA were utilized for survival analysis to detach the prognostic value of the DEmiRNAs of the key module. RESULTS: The 201 differentially expressed miRNAs (DEmiRNAs) and 3,783 DEmRNAs were preliminarily identified through differential expression analysis. The co-expression networks of DEmiRNAs and DEmRNAs were constructed with WGCNA. Further analysis confirmed four miRNAs in the most significant module (blue module) were associated with the overall survival (OS) of patients with liver cancer, including hsa-miR-92b-3p, hsa-miR-122-3p, hsa-miR-139-5p, and hsa-miR-7850-5p. DAVID was used for functional enrichment analysis of 286 co-expressed mRNAs. The GO analysis results showed that the top enriched GO terms were oxidation-reduction process, extracellular exosome, and iron ion binding. In KEGG pathway analysis, the top three enriched terms included metabolic pathways, fatty acid degradation, and valine, leucine, and isoleucine degradation. In addition, we intersected the miRNA-mRNA interaction prediction results with the differentially expressed and prognostic mRNAs. We found that hsa-miR-92b-3p can be related to CPEB3 and ACADL. By overlapping the data of predicted circRNAs by circBank and differentially expressed circRNAs of GSE94508, we screened has_circ_0077210 as the upstream regulatory molecule of hsa-miR-92b-3p. Hsa_circ_0077210/hsa-miR-92b-3p/cytoplasmic polyadenylation element binding protein-3 (CPEB3) and acyl-Coenzyme A dehydrogenase, long chain (ACADL) were validated in HCC tissue. CONCLUSION: Our research provides a mechanistic elucidation of the unknown ceRNA regulatory network in HCC. Hsa_circ_0077210 might serve a momentous therapeutic role to restrain the occurrence and development of HCC.	NA	Front Genet. 2021 Feb 26;12:626764. doi: 10.3389/fgene.2021.626764. eCollection 2021.
3520	Circular RNA	Circ_0077210	miR-92b-3p	ACADL	HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33719338	Construction of circRNA-Based ceRNA Network to Reveal the Role of circRNAs in the Progression and Prognosis of Hepatocellular Carcinoma.	BACKGROUND: Circular RNAs (circRNAs) are now under hot discussion as novel promising biomarkers for patients with hepatocellular carcinoma (HCC). The purpose of our study is to identify several competing endogenous RNA (ceRNA) networks related to the prognosis and progression of HCC and to further investigate the mechanism of their influence on tumor progression. METHODS: First, we obtained gene expression data related to liver cancer from The Cancer Genome Atlas (TCGA) database (http://www.portal.gdc.cancer.gov/), including microRNA (miRNA) sequence, RNA sequence, and clinical information. A co-expression network was constructed through the Weighted Correlation Network Analysis (WGCNA) software package in R software. The differentially expressed messenger RNAs (DEmRNAs) in the key module were analyzed with the Database for Annotation Visualization and Integrated Discovery (DAVID) (https://david.ncifcrf.gov/summary.jsp) to perform functional enrichment analysis including Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO). The data of miRNA expression and clinical information downloaded from TCGA were utilized for survival analysis to detach the prognostic value of the DEmiRNAs of the key module. RESULTS: The 201 differentially expressed miRNAs (DEmiRNAs) and 3,783 DEmRNAs were preliminarily identified through differential expression analysis. The co-expression networks of DEmiRNAs and DEmRNAs were constructed with WGCNA. Further analysis confirmed four miRNAs in the most significant module (blue module) were associated with the overall survival (OS) of patients with liver cancer, including hsa-miR-92b-3p, hsa-miR-122-3p, hsa-miR-139-5p, and hsa-miR-7850-5p. DAVID was used for functional enrichment analysis of 286 co-expressed mRNAs. The GO analysis results showed that the top enriched GO terms were oxidation-reduction process, extracellular exosome, and iron ion binding. In KEGG pathway analysis, the top three enriched terms included metabolic pathways, fatty acid degradation, and valine, leucine, and isoleucine degradation. In addition, we intersected the miRNA-mRNA interaction prediction results with the differentially expressed and prognostic mRNAs. We found that hsa-miR-92b-3p can be related to CPEB3 and ACADL. By overlapping the data of predicted circRNAs by circBank and differentially expressed circRNAs of GSE94508, we screened has_circ_0077210 as the upstream regulatory molecule of hsa-miR-92b-3p. Hsa_circ_0077210/hsa-miR-92b-3p/cytoplasmic polyadenylation element binding protein-3 (CPEB3) and acyl-Coenzyme A dehydrogenase, long chain (ACADL) were validated in HCC tissue. CONCLUSION: Our research provides a mechanistic elucidation of the unknown ceRNA regulatory network in HCC. Hsa_circ_0077210 might serve a momentous therapeutic role to restrain the occurrence and development of HCC.	NA	Front Genet. 2021 Feb 26;12:626764. doi: 10.3389/fgene.2021.626764. eCollection 2021.
3521	LncRNA	GAS6-AS2	miR-144-3p	MAPK6	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33459113	LncRNA GAS6-AS2 promotes non-small-cell lung cancer cell proliferation via regulating miR-144-3p/ MAPK6 axis.	The function of a new long non-coding RNA GAS6-AS2 in non-small cell lung cancer (NSCLC) is not fully understood. In this study, GAS6-AS2 was identified, and its roles as well as mechanisms in regulating proliferation of NSCLCs cells were investigated. qRT-PCR was used to analyze GAS6-AS2, miR-144-3p, and MAPK6 expression. Protein expression was detected by Western blotting. Cell Counting Kit-8 (CCK8) assay was used to examine the cell proliferation ability. The interaction between GAS6-AS2 and miR-144-3p was confirmed by dual-luciferase reporter assay and RNA pull down assay. A xenograft model was constructed to monitor the mice NSCLC tumor growth in vivo. GAS6-AS2 was up-regulated, while miR-144-3p was suppressed in NSCLC cells compared with normal lung cells. GAS6-AS2 suppression could inhibit the progression of NSCLC cells, and miR-144-3p could attenuate the effect. GAS6-AS2 could function as a competitive endogenous RNA (ceRNA) via direct sponging miR-144-3p-3p, which further regulating the expression of MAPK6. The knockdown of GAS6-AS2 could greatly suppress the tumor growth of NSCLC in vivo. GAS6-AS2 up-regulated MAPK6 by sponging miR-144-3p in NSCLC tissues and cells. Thus, GAS6-AS2 is an effective therapeutic target in NSCLC.	NA	Cell Cycle. 2021 Jan;20(2):179-193. doi: 10.1080/15384101.2020.1867782. Epub 2021 Jan 18.
3522	LncRNA	SChLAP1	miR-340-5p	EZH2	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qPCR;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	33589600	SChLAP1 promotes prostate cancer development through interacting with EZH2 to mediate promoter methylation modification of multiple miRNAs of chromosome 5 with a DNMT3a-feedback loop.	This study aimed to investigate the mechanism of SChLAP1 (second chromosome locus associated with prostate-1) on microRNA expression in prostate cancer. Differential expression of lncRNAs and microRNA prostate cancer cells were predicted by informatics and confirmed by qRT-PCR. SChLAP1-interacting proteins were characterized by RNA pull-down combined with western blotting, which was verified using RIP and qPCR analysis. Then ChIP assay and DNA pull-down were used to validate the binding of DNMT3a and HEK27me3 with miRNA gene promoters. Target genes of miRNAs were bioinformatically predicted and validated by dual-luciferase reporter assays. The tumorigenicity of prostate cancer cells was assessed using the cancer cell line-based xenograft (CDX) model. We found that SChLAP1 expression was significantly elevated in prostate cancer tissues and cell lines, which was negatively correlated with miR-340 expression. SChLAP1 directly binds with EZH2 and repressed multiple miRNA expression on chromosome 5 including the miR-340-3p in prostate cancer cells through recruiting H3K27me3 to mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p to suppress gene transcription. Moreover, DNMT3a was one of the common target genes of miR-340-5p/miR-143-3p/miR-145-5p in prostate cancer cells. And SChLAP1/EZH2 could also promote prostate cancer tumor development via the interaction of microRNA-DNMT3a signaling pathways in xenograft nude mice. Altogether, our results suggest that SChLAP1 enhanced the proliferation, migration, and tumorigenicity of prostate cancer cells through interacting with EZH2 to recruit H2K27me3 and mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p with a DNMT3a-feedback loop.	NA	Cell Death Dis. 2021 Feb 15;12(2):188. doi: 10.1038/s41419-021-03455-8.
3523	LncRNA	SChLAP1	miR-143-3p	EZH2	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qPCR;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	33589600	SChLAP1 promotes prostate cancer development through interacting with EZH2 to mediate promoter methylation modification of multiple miRNAs of chromosome 5 with a DNMT3a-feedback loop.	This study aimed to investigate the mechanism of SChLAP1 (second chromosome locus associated with prostate-1) on microRNA expression in prostate cancer. Differential expression of lncRNAs and microRNA prostate cancer cells were predicted by informatics and confirmed by qRT-PCR. SChLAP1-interacting proteins were characterized by RNA pull-down combined with western blotting, which was verified using RIP and qPCR analysis. Then ChIP assay and DNA pull-down were used to validate the binding of DNMT3a and HEK27me3 with miRNA gene promoters. Target genes of miRNAs were bioinformatically predicted and validated by dual-luciferase reporter assays. The tumorigenicity of prostate cancer cells was assessed using the cancer cell line-based xenograft (CDX) model. We found that SChLAP1 expression was significantly elevated in prostate cancer tissues and cell lines, which was negatively correlated with miR-340 expression. SChLAP1 directly binds with EZH2 and repressed multiple miRNA expression on chromosome 5 including the miR-340-3p in prostate cancer cells through recruiting H3K27me3 to mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p to suppress gene transcription. Moreover, DNMT3a was one of the common target genes of miR-340-5p/miR-143-3p/miR-145-5p in prostate cancer cells. And SChLAP1/EZH2 could also promote prostate cancer tumor development via the interaction of microRNA-DNMT3a signaling pathways in xenograft nude mice. Altogether, our results suggest that SChLAP1 enhanced the proliferation, migration, and tumorigenicity of prostate cancer cells through interacting with EZH2 to recruit H2K27me3 and mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p with a DNMT3a-feedback loop.	NA	Cell Death Dis. 2021 Feb 15;12(2):188. doi: 10.1038/s41419-021-03455-8.
3524	LncRNA	SChLAP1	miR-145-5p	EZH2	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qPCR;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	33589600	SChLAP1 promotes prostate cancer development through interacting with EZH2 to mediate promoter methylation modification of multiple miRNAs of chromosome 5 with a DNMT3a-feedback loop.	This study aimed to investigate the mechanism of SChLAP1 (second chromosome locus associated with prostate-1) on microRNA expression in prostate cancer. Differential expression of lncRNAs and microRNA prostate cancer cells were predicted by informatics and confirmed by qRT-PCR. SChLAP1-interacting proteins were characterized by RNA pull-down combined with western blotting, which was verified using RIP and qPCR analysis. Then ChIP assay and DNA pull-down were used to validate the binding of DNMT3a and HEK27me3 with miRNA gene promoters. Target genes of miRNAs were bioinformatically predicted and validated by dual-luciferase reporter assays. The tumorigenicity of prostate cancer cells was assessed using the cancer cell line-based xenograft (CDX) model. We found that SChLAP1 expression was significantly elevated in prostate cancer tissues and cell lines, which was negatively correlated with miR-340 expression. SChLAP1 directly binds with EZH2 and repressed multiple miRNA expression on chromosome 5 including the miR-340-3p in prostate cancer cells through recruiting H3K27me3 to mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p to suppress gene transcription. Moreover, DNMT3a was one of the common target genes of miR-340-5p/miR-143-3p/miR-145-5p in prostate cancer cells. And SChLAP1/EZH2 could also promote prostate cancer tumor development via the interaction of microRNA-DNMT3a signaling pathways in xenograft nude mice. Altogether, our results suggest that SChLAP1 enhanced the proliferation, migration, and tumorigenicity of prostate cancer cells through interacting with EZH2 to recruit H2K27me3 and mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p with a DNMT3a-feedback loop.	NA	Cell Death Dis. 2021 Feb 15;12(2):188. doi: 10.1038/s41419-021-03455-8.
3525	LncRNA	MEG3	miR-145-5p	RTKN	IRI-treated HK-2 cells	Kidney Ischemia-Reperfusion Injury	Homo sapiens (human)	qRT-PCR	33602903	c-MYC-induced long noncoding RNA MEG3 aggravates kidney ischemia-reperfusion injury through activating mitophagy by upregulation of RTKN to trigger the Wnt/β-catenin pathway.	Ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) is a life-threatening disease. The activation of mitophagy was previously identified to play an important role in IRI. Maternally expressed 3 (MEG3) can promote cerebral IRI and hepatic IRI. The present study was designed to study the role of MEG3 in renal IRI. Renal IRI mice models were established, and HK-2 cells were used to construct the in vitro models of IRI. Hematoxylin-eosin staining assay was applied to reveal IRI-triggered tubular injury. MitoTracker Green FM staining and an ALP kit were employed for detection of mitophagy. TdT-mediated dUTP-biotin nick-end labeling assay was used to reveal cell apoptosis. The results showed that renal cortex of IRI mice contained higher expression of MEG3 than that of sham mice. MEG3 expression was also elevated in HK-2 cells following IRI, suggesting that MEG3 might participate in the development of IRI. Moreover, downregulation of MEG3 inhibited the apoptosis of HK-2 cells after IRI. Mitophagy was activated by IRI, and the inhibition of MEG3 can restore mitophagy activity in IRI-treated HK-2 cells. Mechanistically, we found that MEG3 can bind with miR-145-5p in IRI-treated cells. In addition, rhotekin (RTKN) was verified to serve as a target of miR-145-5p. MEG3 upregulated RTKN expression by binding with miR-145-5p. Further, MEG3 activated the Wnt/β-catenin pathway by upregulation of RTKN. The downstream effector of Wnt/β-catenin pathway, c-MYC, served as the transcription factor to activate MEG3. In conclusion, the positive feedback loop of MEG3/miR-145-5p/RTKN/Wnt/β-catenin/c-MYC promotes renal IRI by activating mitophagy and inducing apoptosis, which might offer a new insight into the therapeutic methods for renal IRI in the future.	NA	Cell Death Dis. 2021 Feb 18;12(2):191. doi: 10.1038/s41419-021-03466-5.
3526	LncRNA	TRPM2-AS	miR-22-3p	GINS2	bladder tissues and cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA pull-down assay;luciferase assay;RNA pull-down;	33658791	TRPM2-AS Promotes Bladder Cancer by Targeting miR-22-3p and Regulating GINS2 mRNA Expression.	BACKGROUND: Bladder cancer (BLCA) refers to the malignancy growth that spreads from the bladder linings to the bladder muscles. However, the impact of miR-22-3p and lncRNA TRPM2-AS on this tumor has generated divergent views in the literature. This research aimed to study the effects of lncRNA TRPM2-AS on BLCA and its interaction with miR-22-3p and GINS2 mRNA. METHODS: qRT-PCR was employed to measure the expression of TRPM2-AS, miR-22-3p and GINS2 mRNA in bladder tissues and cells. The subcellular localization of TRPM2-AS in T24 and 5637 cell lines was identified using a cell fractionation system. Luciferase assay, RIP assay and RNA pull-down assay were later performed to validate the direct binding relationship between TRPM2-AS, miR-22-3p and GINS2 mRNA. Several experiments were conducted to determine the viability, proliferation, colony formation and apoptosis of the cell lines. RESULTS: Findings indicated that TRPM2-AS was significantly upregulated in BLCA tissues and cell lines. Apart from that, it was observed that TRPM2-AS knockdown significantly inhibited the viability, proliferation and colony formation of BCLA cells, but it promoted the apoptosis of the BCLA cells. A significant downstream target of TRPM2-AS, miR-22-3p was found to show a lower expression level in BLCA tissues and cell lines. However, the inhibition of miR-22-3p considerably enhanced BLCA cell phenotypes. As well as discovering that GINS2 mRNA was a downstream target of miR-22-3p and was significantly upregulated in BLCA, experimental results also indicated that the knockdown of GINS2 suppressed BLCA cell phenotypes. CONCLUSION: This research confirmed that TRPM2-AS could promote BCLA by binding to miR-22-3p to increase GINS2 expression. This novel interactome in BLCA cell lines might provide more insights into BLCA therapy.	NA	Onco Targets Ther. 2021 Feb 23;14:1219-1237. doi: 10.2147/OTT.S282151. eCollection 2021.
3527	Circular RNA	Circ_0081572	miR-378h	RORA	periodontitis tissues	Periodontitis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33524877	Circ_0081572 inhibits the progression of periodontitis through regulating the miR-378h/RORA axis.	OBJECTIVES: Revealing the role and mechanism of circ_0081572 in periodontitis progression. DESIGN: Quantitative real-time PCR (qRT-PCR) was applied to measure the expression of circ_0081572, microRNA (miR)-378h and retinoid acid-related orphan receptor A (RORA). Lipopolysaccharide (LPS) was used to treat periodontal ligament cells (PDLCs) to construct periodontitis cell model in vitro. Cell counting kit 8 (CCK8) assay and flow cytometry were used to measure cell viability and apoptosis. The caspase 3 activity was detected by Caspase 3 Activity Assay Kit. Western blot assay was performed to detect the expression of apoptosis-associated proteins and RORA. The inflammation response and oxidative stress were determined by detecting the levels of inflammatory cytokines and reactive oxygen species (ROS). The relationship between miR-378h and circ_0081572 or RORA was verified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay. RESULTS: Circ_0081572 was a stability circRNA with downregulated expression in the gingival tissues of periodontitis patients. Overexpression of circ_0081572 could alleviate LPS-induced PDLCs injury. Circ_0081572 could serve as a sponge for miR-378h. Furthermore, miR-378h could reverse the inhibition of circ_0081572 on LPS-induced PDLCs injury. In addition, RORA could be targeted by miR-378h, and its silencing could reverse the suppressive effect of miR-378h inhibitor and circ_0081572 overexpression on LPS-induced PDLCs injury. CONCLUSIONS: Our results suggested that circ_0081572 might prevent periodontitis by regulating the miR-378h /RORA axis.	NA	Arch Oral Biol. 2021 Apr;124:105053. doi: 10.1016/j.archoralbio.2021.105053. Epub 2021 Jan 23.
3528	LncRNA	APCDD1L-AS1	miR-1322	SIRT5	LUAD cells	Lung Cancer	Homo sapiens (human)	Cell transfection;Cell transfection;MTT assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Immunoblotting;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33516270	LncRNA APCDD1L-AS1 induces icotinib resistance by inhibition of EGFR autophagic degradation via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis in lung adenocarcinoma.	BACKGROUND: Epidermal growth factor receptor-tyrosinase kinase inhibitor (EGFR-TKI) resistance is the major obstacle in the treatment of lung adenocarcinoma (LUAD) patients harboring EGFR-sensitive mutations. However, the long non-coding RNAs (lncRNAs) related to EGFR-TKIs resistance and their functional mechanisms are still largely unknown. This study aimed to investigate the role and regulatory mechanism of lncRNA APCDD1L-AS1 in icotinib resistance of lung cancer. METHODS: Molecular approaches including qRT-PCR, MTT assay, colony formation, RNA interference and cell transfection, RNA immunoprecipitation (RIP), dual luciferase reporter assay, RNA fluorescence in situ hybridization, TUNEL assay, flow cytometry, immunoblotting, xenograft model and transcriptome sequencing were used to investigate the mechanism of APCDD1L-AS1 in icotinib resistance. RESULTS: A novel lncRNA, APCDD1L-AS1 was identified as the most significantly upregulated lncRNA in icotinib-resistant LUAD cells by the transcriptome sequencing and differential lncRNA expression analysis. We found that APCDD1L-AS1 not only promoted icotinib resistance, but also upregulated the protein expression level of EGFR. Mechanistically, APCDD1L-AS1 promoted icotinib resistance and EGFR upregulation by sponging with miR-1322/miR-1972/miR-324-3p to remove the transcription inhibition of SIRT5. Furthermore, SIRT5 elevated EGFR expression and activation by inhibiting the autophagic degradation of EGFR, finally promoting icotinib resistance. Consistently, the autophagy initiator rapamycin could decrease EGFR levels and increase the sensitivity of icotinib-resistant LUAD cells to icotinib. CONCLUSION: APCDD1L-AS1 could promote icotinib resistance by inhibiting autophagic degradation of EGFR via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis. The combination of autophagy initiator and EGFR-TKIs might serve as a potential new strategy for overcoming EGFR-TKIs resistance in LUAD patients.	NA	Biomark Res. 2021 Jan 30;9(1):9. doi: 10.1186/s40364-021-00262-3.
3529	LncRNA	APCDD1L-AS1	miR-1972	SIRT5	LUAD cells	Lung Cancer	Homo sapiens (human)	Cell transfection;Cell transfection;MTT assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Immunoblotting;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33516270	LncRNA APCDD1L-AS1 induces icotinib resistance by inhibition of EGFR autophagic degradation via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis in lung adenocarcinoma.	BACKGROUND: Epidermal growth factor receptor-tyrosinase kinase inhibitor (EGFR-TKI) resistance is the major obstacle in the treatment of lung adenocarcinoma (LUAD) patients harboring EGFR-sensitive mutations. However, the long non-coding RNAs (lncRNAs) related to EGFR-TKIs resistance and their functional mechanisms are still largely unknown. This study aimed to investigate the role and regulatory mechanism of lncRNA APCDD1L-AS1 in icotinib resistance of lung cancer. METHODS: Molecular approaches including qRT-PCR, MTT assay, colony formation, RNA interference and cell transfection, RNA immunoprecipitation (RIP), dual luciferase reporter assay, RNA fluorescence in situ hybridization, TUNEL assay, flow cytometry, immunoblotting, xenograft model and transcriptome sequencing were used to investigate the mechanism of APCDD1L-AS1 in icotinib resistance. RESULTS: A novel lncRNA, APCDD1L-AS1 was identified as the most significantly upregulated lncRNA in icotinib-resistant LUAD cells by the transcriptome sequencing and differential lncRNA expression analysis. We found that APCDD1L-AS1 not only promoted icotinib resistance, but also upregulated the protein expression level of EGFR. Mechanistically, APCDD1L-AS1 promoted icotinib resistance and EGFR upregulation by sponging with miR-1322/miR-1972/miR-324-3p to remove the transcription inhibition of SIRT5. Furthermore, SIRT5 elevated EGFR expression and activation by inhibiting the autophagic degradation of EGFR, finally promoting icotinib resistance. Consistently, the autophagy initiator rapamycin could decrease EGFR levels and increase the sensitivity of icotinib-resistant LUAD cells to icotinib. CONCLUSION: APCDD1L-AS1 could promote icotinib resistance by inhibiting autophagic degradation of EGFR via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis. The combination of autophagy initiator and EGFR-TKIs might serve as a potential new strategy for overcoming EGFR-TKIs resistance in LUAD patients.	NA	Biomark Res. 2021 Jan 30;9(1):9. doi: 10.1186/s40364-021-00262-3.
3530	LncRNA	APCDD1L-AS1	miR-324-3p	SIRT5	LUAD cells	Lung Cancer	Homo sapiens (human)	Cell transfection;Cell transfection;MTT assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Immunoblotting;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33516270	LncRNA APCDD1L-AS1 induces icotinib resistance by inhibition of EGFR autophagic degradation via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis in lung adenocarcinoma.	BACKGROUND: Epidermal growth factor receptor-tyrosinase kinase inhibitor (EGFR-TKI) resistance is the major obstacle in the treatment of lung adenocarcinoma (LUAD) patients harboring EGFR-sensitive mutations. However, the long non-coding RNAs (lncRNAs) related to EGFR-TKIs resistance and their functional mechanisms are still largely unknown. This study aimed to investigate the role and regulatory mechanism of lncRNA APCDD1L-AS1 in icotinib resistance of lung cancer. METHODS: Molecular approaches including qRT-PCR, MTT assay, colony formation, RNA interference and cell transfection, RNA immunoprecipitation (RIP), dual luciferase reporter assay, RNA fluorescence in situ hybridization, TUNEL assay, flow cytometry, immunoblotting, xenograft model and transcriptome sequencing were used to investigate the mechanism of APCDD1L-AS1 in icotinib resistance. RESULTS: A novel lncRNA, APCDD1L-AS1 was identified as the most significantly upregulated lncRNA in icotinib-resistant LUAD cells by the transcriptome sequencing and differential lncRNA expression analysis. We found that APCDD1L-AS1 not only promoted icotinib resistance, but also upregulated the protein expression level of EGFR. Mechanistically, APCDD1L-AS1 promoted icotinib resistance and EGFR upregulation by sponging with miR-1322/miR-1972/miR-324-3p to remove the transcription inhibition of SIRT5. Furthermore, SIRT5 elevated EGFR expression and activation by inhibiting the autophagic degradation of EGFR, finally promoting icotinib resistance. Consistently, the autophagy initiator rapamycin could decrease EGFR levels and increase the sensitivity of icotinib-resistant LUAD cells to icotinib. CONCLUSION: APCDD1L-AS1 could promote icotinib resistance by inhibiting autophagic degradation of EGFR via the miR-1322/miR-1972/miR-324-3p-SIRT5 axis. The combination of autophagy initiator and EGFR-TKIs might serve as a potential new strategy for overcoming EGFR-TKIs resistance in LUAD patients.	NA	Biomark Res. 2021 Jan 30;9(1):9. doi: 10.1186/s40364-021-00262-3.
3531	LncRNA	H19	miR-21	PTEN	airway smooth muscle cells	NA	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Flow Cytometry assay;	33536765	LncRNA H19 Inhibits Proliferation and Migration of Airway Smooth Muscle Cells Induced by PDGF-BB Through miR-21/PTEN/Akt Axis.	BACKGROUND: LncRNA H19 expression is down-regulated in patients with asthma. The hyperplasia of airway smooth muscle cells (ASMCs) promotes the development of airway remodeling in asthma. Therefore, we attempted to evaluate the regulatory function of H19 in the proliferation and migration of ASMCs. METHODS: The expressions of H19 and miR-21 were detected using qRT-PCR. PDGF-BB-induced abnormal proliferation and migration of ASMCs was used as the airway remodeling model in vitro. The expressions of H19 and miR-21 were modified by transfection with pcDNA3.1-H19 and miR-21 mimic, respectively. CCK-8 assay, flow cytometry-based cell cycle analysis was conducted to examine the proliferation ability of ASMCs. The migration ability was measured by transwell assay. Dual-luciferase reporter system was carried out to find the potential relationship between miR-21 and H19 or PTEN. Western blot was conducted to detect the expressions of PCNA, MMP-9, α-SMA, PTEN, and the phosphorylation level of Akt. RESULTS: LncRNA-H19 expression was decreased and microRNA-21 expression was increased in serum samples of children with asthma and PDGF-BB-stimulated ASMCs. Overexpression of H19 reduced the proliferation and migration ability of ASMCs with PDGF-BB treatment and these changes were reversed by miR-21 mimic. H19 promoted the protein level of PTEN via sponging miR-21. Overexpression of H19 suppressed miR-21-induced phosphorylation of Akt, and the suppression effect of H19 on phosphorylation of Akt was significantly reduced after transfecting shPTEN in ASMCs. CONCLUSION: In this study, overexpression of H19 suppressed the proliferation and migration of ASMCs induced by PDGF-BB via miR-21/PTEN/Akt axis, which could be a potential biomarker and target for treating hyperplasia of airway smooth muscle cells.	NA	J Asthma Allergy. 2021 Jan 28;14:71-80. doi: 10.2147/JAA.S291333. eCollection 2021.
3532	Circular RNA	Circ-PGAP3	miR-769-5p	p53	CC tissues	Cervical Cancer	Homo sapiens (human)	qRT-PCR;	33591461	The novel circular RNA circ-PGAP3 retards cervical cancer growth by regulating the miR-769-5p/p53 axis.	Cervical cancer (CC) is still an intractable disease that seriously affects women's health. Elucidating its pathogenesis will bring new targets for clinical treatment. Circular RNA (circRNA) is an endogenous RNA that has recently been reported to be closely related to cancer progression and development. In the current study, by performing in silico analysis and qRT-PCR assay, we found a circRNA derived from PGAP3, referred as circ-PGAP3 (hsa_circ_0106800, chr17:37843549-37844086), which was significantly downregulated in CC tissues. Low circ-PGAP3 was closely linked to poor prognosis. And overexpression of circ-PGAP3 significantly reduced CC cell proliferation in vitro and tumor growth in vivo. In terms of mechanism, circ-PGAP3 was transcriptionally elevated by p53, a well-recognized tumor suppressor, and circ-PGAP3 was located in the cytoplasm where sponged miR-769-5p to increase the levels of p53 and its downstream targets. Importantly, the regulatory feedback loop of circ-PGAP3/p53 was also confirmed in vivo. Overall, our data clearly expounded the tumor-inhibiting role of circ-PGAP3 in CC, circ-PGAP3 repressed CC tumorigenesis via regulating the miR-769-5p/p53 axis. Therefore, restoration of circ-PGAP3 may be a promising therapeutic target for this thorny disease.	NA	Hum Cell. 2021 May;34(3):878-888. doi: 10.1007/s13577-021-00493-4. Epub 2021 Feb 16.
3533	LncRNA	HOTAIRM1	miR-498	ABCE1	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33537917	LncRNA HOTAIRM1 knockdown inhibits cell glycolysis metabolism and tumor progression by miR-498/ABCE1 axis in non-small cell lung cancer.	BACKGROUND: Non-small cell lung cancer (NSCLC) is a major contributor of cancer-related mortality. Long non-coding RNAs (lncRNAs) are indicated to participate in the pathogenesis of NSCLC. OBJECTIVE: In this research, the effects of lncRNA HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1) on NSCLC progression and underlying mechanism were revealed. METHODS: The expression levels of HOTAIRM1 and microRNA-498 (miR-498) were detected by quantitative real time polymerase chain reaction (qRT-PCR) in NSCLC tissues, cells or exosomes. The protein expression of CD63, CD81, hexokinase 2 (HK2) and ATP binding cassette subfamily E member 1 (ABCE1) was determined by western blot. Cell viability, apoptosis, migration and invasion were investigated by cell counting kit-8 (CCK-8), flow cytometry, transwell migration and invasion assays, respectively. Cell glycolysis metabolism was revealed by glucose uptake and lactate production assays and western blot analysis. The binding relationship between miR-498 and HOTAIRM1 or ABCE1 was predicted by DIANA-LncBase v2 and starBase online database, and identified by dual-luciferase reporter assay. The effects of HOTAIRM1 on NSCLC growth in vivo were revealed by in vivo tumor formation assay. RESULTS: HOTAIRM1 expression was dramatically upregulated, whereas miR-498 expression was significantly downregulated in NSCLC tissues cells or exosomes as compared to control groups. Mechanistically, HOTAIRM1 knockdown repressed cell viability, migration, invasion and glycolysis metabolism, whereas induced cell apoptosis in NSCLC; however, miR-498 inhibitor hindered these effects. Functionally, HOTAIRM1 functioned as a sponge of miR-498 and miR-498 targeted ABCE1. In addition, HOTAIRM1 silencing inhibited NSCLC growth in vivo by downregulating ABCE1 and upregulating miR-498 expression. CONCLUSIONS: HOTAIRM1 knockdown repressed cell glycolysis metabolism and tumor development by reducing ABCE1 expression through sponging miR-498 in NSCLC, which provided a theoretical basis for further studying NSCLC progression.	NA	Genes Genomics. 2021 Feb;43(2):183-194. doi: 10.1007/s13258-021-01052-9. Epub 2021 Feb 3.
3534	LncRNA	H19	miR-675	p53	cSCC cells	Cutaneous Squamous Cell Carcinoma	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33649811	Roles of the H19/microRNA-675 axis in the proliferation and epithelial-mesenchymal transition of human cutaneous squamous cell carcinoma cells.	The long non-coding RNA (lncRNA) H19 and microRNA(miR)-675 were reported to serve an important role in the tumorigenesis and metastasis of numerous cancer types by promoting the epithelial-mesenchymal transition (EMT) process; however, the underlying mechanisms of action of H19 and miR-675 in cutaneous squamous cell carcinoma (cSCC) remain unknown. The mRNA expression levels of H19 and miR-675 were analyzed using reverse transcription-quantitative PCR, and Cell Counting Kit-8, wound healing and Transwell assays were performed to analyze the cell proliferation, migration and invasion of cSCC cells, respectively. The levels of cell apoptosis were also determined using a TUNEL assay. Protein expression levels of p53 and marker proteins related to the EMT process were analyzed using western blotting. In addition, a dual luciferase reporter assay was performed to determine the interactions between H19, miR-675 and p53. The results of the present study revealed that the expression levels of H19 and miR-675 were upregulated in cSCC tissues and cSCC cell lines. The knockdown of H19 or miR-675 expression inhibited cell proliferation, migration and invasion, but induced cell apoptosis. In addition, the expression levels of EMT-related markers were also downregulated. The overexpression of H19 upregulated the expression levels of its predicted target, miR-675, which subsequently promoted the EMT process and downregulated the expression levels of p53. Conversely, the genetic silencing of H19 or miR-675 inhibited proliferation and invasion in SCL1 and A431 cSCC cell lines. In conclusion, the findings of the present study provided novel insight into the potential role of H19 and miR-675 in the development, metastasis and progression of cSCC, which may help the development of treatments for cSCC.	NA	Oncol Rep. 2021 Apr;45(4):39. doi: 10.3892/or.2021.7990. Epub 2021 Mar 2.
3535	LncRNA	SNHG8	miR-1270	S100A11	OC tissues and cells	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33491301	lncRNA SNHG8 promotes ovarian cancer progression through serving as sponge for miR-1270 to regulate S100A11 expression.	BACKGROUND: Long non-coding RNA small nucleolar RNA host gene 8 (SNHG8) has been found correlated with cancer progression. This work was aimed to investigate the functions of SNHG8 in ovarian cancer (OC). METHODS: Expression level of SNHG8 in OC tissues and cells was analyzed using real time-quantitative polymerase chain reaction (RT-qPCR) method. The biological roles of SNHG8 in OC were analyzed through proliferation assay, wound healing assay, and transwell invasion assay. Furthermore, interactions of SNHG8 or S100 calcium binding protein A11 (S100A11) and microRNA-1270 (miR-1270) were explored. Moreover, the effects of SNHG8, miR-1270, and S100A11 on the overall survival of OC patients were investigated. RESULTS: SNHG8 has increased expression in OC tissues and cells compared with normal counterparts, and correlated with poorer overall survival of OC patients. OC cell proliferation, migration, and invasion abilities were enhanced by SNHG8 overexpression but inhibited by its knockdown. In addition, we showed that SNHG8 regulates OC progression through targeting the miR-1270 and S100A11. CONCLUSIONS: Our work indicated that SNHG8 regulates OC progression through miR-1270/S100A11 axis, which may provide novel therapeutic targets for OC.	NA	J Gene Med. 2021 Jan 25:e3315. doi: 10.1002/jgm.3315.
3536	Circular RNA	CircRasGEF1B	miR-21-3p	MITA	Siniperca chuatsi rhabdovirus-infected tissues and cells	NA	Homo sapiens (human)	FISH;FISH;	33441345	A Highly Conserved Circular RNA circRasGEF1B Enhances Antiviral Immunity by Regulating miR-21-3p/MITA Pathway in Lower Vertebrates.	Circular RNAs (circRNAs) represent a class of widespread, diverse, and covalently closed circRNAs that function as microRNA (miRNA) sponges and crucial regulators of gene expression in mammals. However, the regulation and function of circRNAs in lower vertebrates are still unknown. Here, we first discover a highly conserved circRNA termed circRasGEF1B, which displays a high conservation from mammals to fish and serves as key regulator in eliciting antiviral immunity in teleost fish. Results indicate that circRasGEF1B was highly expressed in Siniperca chuatsi rhabdovirus-infected tissues and cells. Functionally, miR-21-3p could inhibit cellular antiviral responses significantly, whereas circRasGEF1B counteract the effects of miR-21-3p. In mechanism, the results demonstrate that circRasGEF1B acts as a competing endogenous RNA (ceRNA) of miR-21-3p to relieve the repressive effect of miR-21-3p on its target MITA, then enhance the innate antiviral responses. Our results not only provide a novel insight into the functions of circRNAs in lower vertebrates, but broaden our understanding of circRNAs in viral infection.IMPORTANCE Siniperca chuatsi rhabdovirus (SCRV) is a typical fish RNA rhabdovirus, which is one of the most significant viral pathogens in teleost fish and can cause severe hemorrhagic septicemia in freshwater and marine fishes. Here, we discovered a highly conserved circRNAs called circRasGEF1B, which acts as a key regulator for innate antiviral responses upon SCRV infection. circRasGEF1B acts as an endogenous sponge of miR-21-3p that downregulates miR-21-3p expression levels. circRasGEF1B is able to bind to miR-21-3p directly and regulates MITA expression. To our knowledge, this report is the first to characterize circRNA-miRNA regulatory networks that exist in lower vertebrates.	NA	J Virol. 2021 Jan 13;95(7):e02145-20. doi: 10.1128/JVI.02145-20.
3537	LncRNA	XIST	miR-182-5p	PD-L1	MDA-MB-231 cells and BC tissues	Breast Cancer	Homo sapiens (human)	qRT-PCR	34149904	Long non-coding RNAs XIST and MALAT1 hijack the PD-L1 regulatory signaling pathway in breast cancer subtypes.	Long non-coding RNAs (lncRNAs) have attracted widespread attention as potential biological and pathological regulators. lncRNAs are involved in several biological processes in cancer. Triple negative breast cancer (TNBC) is characterized by strong heterogeneity and aggressiveness. At present, the implication of microRNAs (miRs) and lncRNAs in immunotherapy has been poorly studied. Nevertheless, the blockade of immune checkpoints, particularly that of the programmed cell-death protein-1/programmed cell-death ligand-1 (PD-L1) axis, is considered as a principle approach in breast cancer (BC) therapy. The present study aimed to investigate the interaction between immune-modulatory upstream signaling pathways of the PD-L1 transcript that could enhance personalized targeted therapy. MDA-MB-231 cells were transfected with miR-182-5p mimics followed by RNA extraction and cDNA synthesis using a reverse transcription kit, and the expression levels of the target genes were assessed by reverse transcription-quantitative PCR. Furthermore, the expression levels of target genes were measured in tissues derived from 41 patients with BC, including patients with luminal BC and TNBC, as well as their adjacent lymph nodes. The results revealed that the expression levels of miR-182-5p, PD-L1 and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) were upregulated in MDA-MB-231 cells and BC tissues. However, X-inactive specific transcript (XIST) expression was downregulated in cancer tissues and TNBC cells. Following co-transfection of cells with small interfering RNAs specific for each target gene and miR-182-5p antagomirs, the effect of miR-182-5p was abolished in the presence of lncRNAs. Therefore, the results of the present study indicated that although miR-182-5p exhibited an oncogenic effect, XIST exerted a dominant effect on the regulation of the PD-L1 signaling pathway via the inhibition of the oncogenic function of MALAT1.	NA	Oncol Lett. 2021 Aug;22(2):593. doi: 10.3892/ol.2021.12854. Epub 2021 Jun 7.
3538	LncRNA	CBR3-AS1	miR-25-3p	MEK4	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	microarray;Western blot;	33494806	LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway.	BACKGROUND: Adriamycin (ADR) resistance is one of the main obstacles to improving the clinical prognosis of breast cancer patients. Long noncoding RNAs (lncRNAs) can regulate cell behavior, but the role of these RNAs in the anti-ADR activity of breast cancer remains unclear. Here, we aim to investigate the imbalance of a particular long noncoding RNA, lncRNA CBR3 antisense RNA 1 (CBR3-AS1), and its role in ADR resistance. METHODS: Microarray analysis of ADR-resistant breast cancer cells was performed to identify CBR3-AS1. CCK-8 and colony formation assays were used to detect the sensitivity of breast cancer cells to ADR. Dual-luciferase reporter, RNA pulldown, IHC and western blot analyses were used to verify the relationship between the expression of CBR3-AS1, miRNA and target genes. For in vivo experiments, the effect of CBR3-AS1 on breast cancer resistance was observed in a xenograft tumor model. The role of CBR3-AS1 in influencing ADR sensitivity was verified by clinical breast cancer specimens from the TCGA, CCLE, and GDSC databases. RESULTS: We found that CBR3-AS1 expression was significantly increased in breast cancer tissues and was closely correlated with poor prognosis. CBR3-AS1 overexpression promoted ADR resistance in breast cancer cells in vitro and in vivo. Mechanistically, we identified that CBR3-AS1 functioned as a competitive endogenous RNA by sponging miR-25-3p. MEK4 and JNK1 of the MAPK pathway were determined to be direct downstream proteins of the CBR3-AS1/miR-25-3p axis in breast cancer cells. CONCLUSIONS: In summary, our findings demonstrate that CBR3-AS1 plays a critical role in the chemotherapy resistance of breast cancer by mediating the miR-25-3p and MEK4/JNK1 regulatory axes. The potential of CBR3-AS1 as a targetable oncogene and therapeutic biomarker of breast cancer was identified.	NA	J Exp Clin Cancer Res. 2021 Jan 25;40(1):41. doi: 10.1186/s13046-021-01844-7.
3539	LncRNA	CBR3-AS1	miR-25-3p	JNK1	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	microarray;Western blot;	33494806	LncRNA CBR3-AS1 regulates of breast cancer drug sensitivity as a competing endogenous RNA through the JNK1/MEK4-mediated MAPK signal pathway.	BACKGROUND: Adriamycin (ADR) resistance is one of the main obstacles to improving the clinical prognosis of breast cancer patients. Long noncoding RNAs (lncRNAs) can regulate cell behavior, but the role of these RNAs in the anti-ADR activity of breast cancer remains unclear. Here, we aim to investigate the imbalance of a particular long noncoding RNA, lncRNA CBR3 antisense RNA 1 (CBR3-AS1), and its role in ADR resistance. METHODS: Microarray analysis of ADR-resistant breast cancer cells was performed to identify CBR3-AS1. CCK-8 and colony formation assays were used to detect the sensitivity of breast cancer cells to ADR. Dual-luciferase reporter, RNA pulldown, IHC and western blot analyses were used to verify the relationship between the expression of CBR3-AS1, miRNA and target genes. For in vivo experiments, the effect of CBR3-AS1 on breast cancer resistance was observed in a xenograft tumor model. The role of CBR3-AS1 in influencing ADR sensitivity was verified by clinical breast cancer specimens from the TCGA, CCLE, and GDSC databases. RESULTS: We found that CBR3-AS1 expression was significantly increased in breast cancer tissues and was closely correlated with poor prognosis. CBR3-AS1 overexpression promoted ADR resistance in breast cancer cells in vitro and in vivo. Mechanistically, we identified that CBR3-AS1 functioned as a competitive endogenous RNA by sponging miR-25-3p. MEK4 and JNK1 of the MAPK pathway were determined to be direct downstream proteins of the CBR3-AS1/miR-25-3p axis in breast cancer cells. CONCLUSIONS: In summary, our findings demonstrate that CBR3-AS1 plays a critical role in the chemotherapy resistance of breast cancer by mediating the miR-25-3p and MEK4/JNK1 regulatory axes. The potential of CBR3-AS1 as a targetable oncogene and therapeutic biomarker of breast cancer was identified.	NA	J Exp Clin Cancer Res. 2021 Jan 25;40(1):41. doi: 10.1186/s13046-021-01844-7.
3540	LncRNA	ANRIL	miR-7-5p	IGF-1R	healthy/inflamed periodontal ligament tissues	NA	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33692995	Upregulating the Expression of LncRNA ANRIL Promotes Osteogenesis via the miR-7-5p/IGF-1R Axis in the Inflamed Periodontal Ligament Stem Cells.	BACKGROUND: Long non-coding RNA (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) is a base length of about 3.8 kb lncRNA, which plays an important role in several biological functions including cell proliferation, migration, and senescence. This study ascertained the role of lncRNA ANRIL in the senescence and osteogenic differentiation of inflamed periodontal ligament stem cells (iPDLSCs). METHODS: Healthy periodontal ligament stem cells (hPDLSCs) and iPDLSCs were isolated from healthy/inflamed periodontal ligament tissues, respectively. The proliferation abilities were determined by CCK-8, EdU assay, and flow cytometry (FCM). The methods of Western blot assay (WB), quantitative real-time polymerase chain reaction (qRT-PCR), alizarin red staining, alkaline phosphatase (ALP) staining, ALP activity detection, and immunofluorescence staining were described to determine the biological influences of lncRNA ANRIL on iPDLSCs. Senescence-associated (SA)-β-galactosidase (gal) staining, Western blot analysis, and qRT-PCR were performed to determine cell senescence. Dual-luciferase reporter assays were conducted to confirm the binding of lncRNA ANRIL and miR-7-5-p, as well as miR-7-5p and insulin-like growth factor receptor (IGF-1R). RESULTS: HPDLSCs and iPDLSCs were isolated and cultured successfully. LncRNA ANRIL and IGF-1R were declined, while miR-7-5p was upregulated in iPDLSCs compared with hPDLSCs. Overexpression of ANRIL enhanced the osteogenic protein expressions of OSX, RUNX2, ALP, and knocked down the aging protein expressions of p16, p21, p53. LncRNA ANRIL could promote the committed differentiation of iPDLSCs by sponging miR-7-5p. Upregulating miR-7-5p inhibited the osteogenic differentiation of iPDLSCs. Further analysis identified IGF-1R as a direct target of miR-7-5p. The direct binding of lncRNA ANRIL and miR-7-5p, miR-7-5p and the 3'-UTR of IGF-1R were verified by dual-luciferase reporter assay. Besides, rescue experiments showed that knockdown of miR-7-5p reversed the inhibitory effect of lncRNA ANRIL deficiency on osteogenesis of iPDLSCs. CONCLUSION: This study disclosed that lncRNA ANRIL promotes osteogenic differentiation of iPDLSCs by regulating the miR-7-5p/IGF-1R axis.	NA	Front Cell Dev Biol. 2021 Feb 22;9:604400. doi: 10.3389/fcell.2021.604400. eCollection 2021.
3541	LncRNA	CCDC26	miR-195-5p	PRR11	Myeloid Leukemia Cell (K562 and HL-60)	Myeloid Leukemia	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33439746	LncRNA CCDC26 Interacts with CELF2 Protein to Enhance Myeloid Leukemia Cell Proliferation and Invasion via the circRNA_ANKIB1/miR-195-5p/PRR11 Axis.	LncRNA CCDC26 is aberrantly expressed in myeloid leukemia (ML) and promotes myeloid leukemia progression, but the potential mechanism of CCDC26 in regulating ML progression is unclear. In this study, we observed that lncRNA CCDC26 was upregulated in both chronic and acute ML cell lines. LncRNA CCDC26 promoted the proliferation and invasion of K562 and HL-60 cells, which was determined by cell counting kit-8 test and Transwell invasion assay. Flow cytometry showed that lncRNA CCDC26 inhibited cell apoptosis. Bioinformatics and expression correlation analyses revealed that there was a potential interaction between CCDC26 and CUGBP Elav-like family member 2 (CELF2) protein, an RNA bind protein (RBP). Then the relationship between CCDC26 and the RBP CELF2 was identified by using RNA pull-down and RNA immunoprecipitation (RNA-IP) assays. Further analysis showed that overexpression of CCDC26 could noticeably upregulate circRNA_ANKIB1 expression via sponging CELF2. Subsequently, we found that overexpressed circRNA_ANKIB1 could significantly promote proline rich 11 (PRR11) protein expression by sponging miR-195a-5p. Moreover, PRR11 was also upregulated by CCDC26 and downregulated by CELF2. Mechanically, we uncovered that the miR-195a-5p inhibitor activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathways through upregulating PRR11 protein expression. Furthermore, the inhibitors of AKT, p65-NF-κB, or Bcl-2 could inhibit the effect of the miR-195a-5p inhibitor on ML cell behaviors. In conclusion, lncRNA CCDC26 could upregulate PRR11 protein expression by sponging miR-195a-5p, thereby activating the PI3K/AKT and NF-κB pathways to enhance ML cell proliferation and invasion and suppress cell apoptosis.	NA	Cell Transplant. 2021 Jan-Dec;30:963689720986080. doi: 10.1177/0963689720986080.
3542	LncRNA	LINC00461	miR-195	HOXA10	HNSCC cells	Head And Neck Squamous  Carcinoma 	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;RNA pull-down;	33869744	LINC00461 facilitates HNSCC development and reduces chemosensitivity by impairing miR-195-mediated inhibition of HOXA10.	Homeobox A10 (HOXA10) has been regarded to serve as an oncogene in head and neck squamous cell carcinoma (HNSCC). This study was intended to explore the interaction among the long intergenic noncoding RNA 00461 (LINC00461), microRNA (miR)-195, and HOXA10, and to investigate its role in epithelial-mesenchymal transition (EMT) and chemoresistance in HNSCC. The effects of LINC00461, miR-195, and HOXA10 on the EMT and chemoresistance of HNSCC cells were analyzed by comprehensive analysis of gain- and loss-of-function techniques. The intimate relationships among LINC00461, miR-195, and HOXA10 were investigated by several procedures such as RNA-binding protein immunoprecipitation, RNA pull-down, and dual-luciferase reporter assays. A xenotransplantation tumor model in nude mice was established for the assessment of the tumorigenic ability of the cells in vivo. Our findings indicated that LINC00461 was highly expressed in HNSCC and its overexpression induced EMT and precipitated the chemoresistance of HNSCC cells to cisplatin. The LINC00461 could bind to miR-195 while miR-195 targeted HOXA10 independently. Moreover, LINC00461 impaired miR-195-mediated inhibition of HOXA10 to induce EMT and increase the chemoresistance in HNSCC. Tumor weight and volume were reduced by lentivirus-mediated elevation of miR-195 by inhibition of HOXA10, which could be annulled by LINC00461 overexpression. LINC00461 downregulates the expression of miR-195 to subsequently upregulate the expression of HOXA10, thereby promoting EMT and enhancing chemoresistance in HNSCC.	NA	Mol Ther Oncolytics. 2021 Jan 20;21:74-86. doi: 10.1016/j.omto.2021.01.008. eCollection 2021 Jun 25.
3543	LncRNA	LINC00885	miR-432-5p	MACC1	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Cell migration and invasion assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33603486	Long Intergenic Non-Coding RNA LINC00885 Promotes Tumorigenesis of Cervical Cancer by Upregulating MACC1 Expression Through Serving as a Competitive Endogenous RNA for microRNA-432-5p.	PURPOSE: Long intergenic non-protein coding RNA 885 (LINC00885) has been well studied in breast cancer; however, its contribution in cervical cancer remains unclear. In this study, we aimed to determine the detailed functions of LINC00885 in cervical cancer and elucidate the underlying molecular regulation mechanism. METHODS: The expression status of LINC00885 in cervical cancer was determined using reverse transcription-quantitative polymerase chain reaction and by searching The Cancer Genome Atlas database. The detailed functions of LINC00885 in cervical cancer cells were confirmed using Cell Counting Kit 8 assay, flow cytometry analysis, Transwell cell migration and invasion assays, and tumor xenograft assay. Mechanistic experiments included bioinformatics prediction, RNA immunoprecipitation, luciferase reporter assay, and rescue experiments. RESULTS: LINC00885 was clearly overexpressed in cervical cancer, which was linked with unfavorable clinical outcomes. Functionally, LINC00885 deficiency suppressed cervical cancer cell proliferation, migration, and invasion but stimulated cell apoptosis in vitro. Furthermore, loss of LINC00885 restricted the growth of cervical cancer cells in vivo. Mechanistically, LINC00885 functioned as a competitive endogenous RNA for microRNA-432-5p (miR-432-5p) in cervical cancer. Furthermore, metastasis-associated colon cancer 1 (MACC1) was confirmed as the direct target of miR-432-5p, and LINC00885 could enhance MACC1 expression by sequestering miR-432-5p. Rescue experiments revealed that silencing of miR-432-5p or upregulation of MACC1 expression could effectively counteract the restrained aggressive properties of cervical cancer cells induced by LINC00885 deficiency. CONCLUSION: LINC00885 upregulated MACC1 expression in cervical cancer cells by sponging miR-432-5p, thereby promoting cancer progression. The LINC00885/miR-432-5p/MACC1 pathway may help in the identification of potential prognostic biomarkers and therapeutic targets in cervical cancer.	NA	Cancer Manag Res. 2021 Feb 12;13:1435-1447. doi: 10.2147/CMAR.S291778. eCollection 2021.
3544	LncRNA	H19	miR-532-3p	SIRT1	bone marrow mesenchymal stem cells (BMSCs)	Osteoporosis	Homo sapiens (human)	qRT-PCR	33577975	Estrogen promotes lncRNA H19 expression to regulate osteogenic differentiation of BMSCs and reduce osteoporosis via miR-532-3p/SIRT1 axis.	Osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) plays an essential role in bone formation. Its imbalance can lead to osteoporosis. Estrogen and long noncoding RNAs (lncRNAs) have been confirmed to participate in osteogenesis. However, the underlying mechanism remains unclear. The purpose of our study was to explore the function of lncRNA H19 in estrogen-induced osteogenic differentiation of BMSCs. The present research demonstrated that the expression levels of lncRNA H19 and SIRT1 were markedly downregulated in postmenopausal osteoporosis (PMOP), while miR-532-3p expression was obviously increased. Moreover, estrogen induced the osteogenic differentiation of BMSCs by upregulating lncRNA H19. Furthermore, our integrated experiments showed that lncRNA H19 caused a decrease in the expression of miR-532-3p, which was verified to target SIRT1 directly. Additionally, estrogen alleviated osteoporosis in OVX rats through lncRNA H19-mediated miR-532-3p/SIRT1 axis. Our findings imply that lncRNA H19 mediates estrogen-regulated osteogenic differentiation in BMSCs via miR-532-3p/SIRT1 signalling and may become a novel target for alleviating PMOP.	NA	Mol Cell Endocrinol. 2021 May 1;527:111171. doi: 10.1016/j.mce.2021.111171. Epub 2021 Feb 9.
3545	LncRNA	KCNQ1	miR-133b	EGFR	ESCC tissues and cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33909822	Long non-coding RNA KCNQ1 overlapping transcript 1 promotes the progression of esophageal squamous cell carcinoma by adsorbing microRNA-133b.	OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.	NA	Clinics (Sao Paulo). 2021 Apr 26;76:e2175. doi: 10.6061/clinics/2021/e2175. eCollection 2021.
3546	LncRNA	H19	miR-326	BCL-2	ALL tissues	Pediatric Acute Lymphoblastic Leukemia	Homo sapiens (human)	qRT-PCR;	33580459	Increased level of long non coding RNA H19 is correlated with the downregulation of miR-326 and BCL-2 genes in pediatric acute lymphoblastic leukemia, a possible hallmark for leukemogenesis.	Long non-coding RNAs (lncRNAs) and their role in competitive endogenous RNA (ceRNA) networks have emerged as fundamental debates in the biological processes of initiation and progression of cancer. This study aimed to identify and measure the expression levels of relevant ceRNA regulatory genes contributing to acute lymphoblastic leukemia (ALL). lncRNA H19 and BCL-2 mRNA were chosen based on in silico studies and their interactions with miR-326. Subsequently, the aforementioned coding/non-coding gene expression profiles were measured using qRT-PCR in 50 bone marrow samples, including 33 cases with pediatric ALL and 17 controls with no evidence of malignancy. lncRNA H19 was identified as an oncogenic factor which was noticeably increased in the newly diagnosed patients (P = 0.0019, AUC = 0.84) and negatively associated with miR-326 (r = -0.6, P = 0.02). Furthermore, a negative correlation was introduced between the transcriptional levels of miR-326 and the anti-apoptotic BCL-2 gene (r = -0.6, P = 0.028). The novel experimental and bioinformatic results achieved in this study may provide new insights into the molecular leukemogenesis of pediatric ALL.	NA	Mol Biol Rep. 2021 Feb;48(2):1531-1538. doi: 10.1007/s11033-021-06161-y. Epub 2021 Feb 12.
3547	LncRNA	CCR7	let-7e-5p	SNHG12	pulmonary arterial hypertension tissues	Pulmonary Arterial Hypertension	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Luciferase reporter assay;	33630421	CCR7 and its related molecules may be potential biomarkers of pulmonary arterial hypertension.	Pulmonary arterial hypertension (PAH) is a chronic progressive cardiovascular disease characterized by vascular remodeling and leading to right-heart failure. The purpose of this research was to further study the pathogenesis of PAH and to detect potential prognostic signatures. Differentially expressed genes (DEGs) selected from GSE38267 were mostly enriched in inflammation-related pathways, suggesting inflammation may be involved in the occurrence and development of PAH. Through the prediction and verification of related miRNAs and long noncoding RNAs using online databases and Gene Expression Omnibus (GEO) datasets, CCR7 and its related molecules, including hsa-let-7e-5p and SNHG12, were identified as possible targets. The expression levels of CCR7, hsa-let-7e-5p and SNHG12 were then verified by quantitative RT-PCR in vivo and in vitro. Further study showed that silencing of SNHG12 decreased the expression of CCR7 under hypoxia treatment in vitro. Dual-luciferase reporter assays were used to verify the relationship between hsa-let-7e-5p and SNHG12. Collectively, our research reveals that a long noncoding RNA-miRNA-mRNA interaction network may be involved in the pathogenesis of PAH and suggests SNHG12, hsa-let-7e-5p and CCR7 as potential biomarkers for PAH.	NA	FEBS Open Bio. 2021 Jun;11(6):1565-1578. doi: 10.1002/2211-5463.13130. Epub 2021 May 12.
3548	LncRNA	FAM83A-AS1	miR-495-3p	FAM83A	LUAD tissues and cells	Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;	33732373	FAM83A and FAM83A-AS1 both play oncogenic roles in lung adenocarcinoma.	Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD.	NA	Oncol Lett. 2021 Apr;21(4):297. doi: 10.3892/ol.2021.12558. Epub 2021 Feb 17.
3549	LncRNA	JPX	miR-5195-3p	VEGFA	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33613033	Long Non-Coding RNA JPX Contributes to Tumorigenesis by Regulating miR-5195-3p/VEGFA in Non-Small Cell Lung Cancer.	BACKGROUND: Lung cancer is the most frequently diagnosed cancer. Of all lung cancers, 80-85% are verified as non-small-cell lung cancer (NSCLC). Just proximal to X-inactive specific transcript (JPX), functions as lncRNA, contributed to tumor progression and suggested a poor prognosis in NSCLC. However, the pathogenesis of JPX involved in NSCLC is still unclear. METHODS: The expressions of JPX, miR-5195-3p, and Vascular endothelial growth factor A (VEGFA) were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Proliferation, colony number, apoptosis, invasion, and migration were analyzed by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, transwell, and wound healing assays, severally. The protein levels of VEGFA, E-cadherin, N-cadherin, and Vimentin were detected by Western blot assay. The interaction between JPX, miR-5195-3p and VEGFA was predicted by starBase, and then verified by the dual-luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull-down assay. The biological role of JPX on NSCLC tumor growth was assessed by the xenograft tumor model in vivo. RESULTS: JPX and VEGFA were upregulated, and miR-5195-3p was downregulated in NSCLC. JPX induced proliferation, colony number, invasion, migration, epithelial-mesenchymal transition (EMT), and inhibited apoptosis of NSCLC cells. JPX is directly bound to miR-5195-3p. JPX regulated NSCLC cell proliferation, apoptosis and EMT by modulating miR-5195-3p. miR-5195-3p hindered NSCLC cells proliferation, EMT and accelerated apoptosis by directly targeting VEGFA. JPX silencing hindered the cell growth of NSCLC in vivo. CONCLUSION: JPX facilitated proliferation, colony number, invasion, migration, EMT, and repressed apoptosis by miR-5195-3p/VEGFA axis, offering a possible therapeutic strategy for NSCLC.	NA	Cancer Manag Res. 2021 Feb 12;13:1477-1489. doi: 10.2147/CMAR.S255317. eCollection 2021.
3550	LncRNA	LINC01410	miR-506-3p	NOTCH2	glioma cells	Glioma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Western blot;Chromatin immunoprecipitation;Luciferase reporter assay;Rescue assay;RNA pull-down;	33712887	LncRNA LINC01410 Induced by MYC Accelerates Glioma Progression via Sponging miR-506-3p and Modulating NOTCH2 Expression to Motivate Notch Signaling Pathway.	Glioma is a common invasive cancer with unfavorable prognosis in patients. Long non-coding RNAs have been reported to participate in modulating diverse cellular processes. Here, we focused on exploring the role of long intergenic non-protein coding RNA 1410 (LINC01410) in glioma and its underlying mechanism. The expression levels and protein levels of genes were analyzed by quantitative real-time PCR (RT-qPCR) analysis and western blot. Loss-of-function assays were performed to assess the function of LINC01410 in glioma cells. The interactions among MYC, LINC01410, microRNA-506-3p (miR-506-3p) and notch receptor 2 (NOTCH2) were validated through Chromatin immunoprecipitation (ChIP), RNA Binding Protein immunoprecipitation (RIP), RNA pull-down and luciferase reporter assays. Our data supported that LINC01410 was up-regulated in glioma cells. Bioinformatics predictions and the integrated experiments identified that MYC activated LINC01410 transcription and LINC01410 promoted the levels of NOTCH2 through sponging miR-506-3p and further motivated Notch signaling pathway. Rescue assays validated that LINC01410 exerted its influential functions on glioma cell proliferation and apoptosis via enhancing NOTCH2 expression. Our studies identified that LINC01410 accelerates the progression of glioma through acting as a ceRNA for miR-506-3p and elevating NOTCH2 expression to further activate the Notch signaling pathway, which indicated that LINC01410 might act as a novel regulator of glioma progression.	NA	Cell Mol Neurobiol. 2021 Mar 13. doi: 10.1007/s10571-021-01042-1.
3551	LncRNA	KCNQ1OT1	miR-454	USP47	NPC cells (5-8F/DDP and SUNE-1/DDP)	Nasopharyngeal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;Luciferase reporter assay;	33576460	Long non-coding RNA KCNQ1OT1 promotes nasopharyngeal carcinoma cell cisplatin resistance via the miR-454/USP47 axis.	Long non-coding RNAs serve an essential role in drug resistance in various types of cancer, including lung, breast and bladder cancer. The present study aimed to investigate whether KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) was associated with cisplatin (DDP) resistance in nasopharyngeal carcinoma (NPC). KCNQ1OT1, microRNA (miR)-454 and ubiquitin specific peptidase 47 (USP47) expression levels were measured via reverse transcription-quantitative PCR. 5-8F/DDP and SUNE-1/DDP cell viability and chemosensitivity were assessed by performing Cell Counting Kit-8 assays. Colony forming and Transwell assays were conducted to assess the effect of the KCNQ1OT1/miR-454/USP47 axis on DDP resistance in NPC cells. The association between miR-454 and KCNQ1OT1 or USP47 was verified via bioinformatics analysis, dual-luciferase reporter assays and RIP assays. KCNQ1OT1 and USP47 expression levels were significantly upregulated, whereas miR-454 expression levels were significantly downregulated in DDP-resistant NPC cells compared with parental NPC cells. KCNQ1OT1 knockdown promoted chemosensitivity in DDP-resistant NPC cells (5-8F/DDP and SUNE-1/DDP), as indicated by significantly decreased cell proliferation, migration and invasion in the short hairpin RNA (sh)KCNQ1OT1 group compared with the sh-negative control (NC) group. Moreover, miR-454 was identified as a target of KCNQ1OT1. KCNQ1OT1 overexpression significantly reversed miR-454 overexpression-mediated effects on NPC cell viability and DDP resistance. Furthermore, the results indicated that miR-454 directly targeted USP47. Compared with the shNC group, USP47 knockdown significantly suppressed NPC cell viability and DDP resistance, which was significantly reversed by co-transfection with miR-454 inhibitor. Furthermore, compared with the shNC group, KCNQ1OT1 knockdown significantly downregulated USP47 expression, which was significantly counteracted by miR-454 knockdown. Collectively, the results of the present study indicated that KCNQ1OT1 enhanced DDP resistance in NPC cells via the miR-454/USP47 axis, suggesting a potential therapeutic target for patients with DDP-resistant NPC.	NA	Int J Mol Med. 2021 Apr;47(4):54. doi: 10.3892/ijmm.2021.4887. Epub 2021 Feb 12.
3552	Circular RNA	Circ_0077755	miR-182	Cx43	breast cancer cells	Breast Cancer	Homo sapiens (human)	microarray;	33514777	A risk progression breast epithelial 3D culture model reveals Cx43/hsa_circ_0077755/miR-182 as a biomarker axis for heightened risk of breast cancer initiation.	mRNA-circRNA-miRNAs axes have been characterized in breast cancer, but not as risk-assessment axes for tumor initiation in early-onset breast cancer that is increasing drastically worldwide. To address this gap, we performed circular RNA (circRNA) microarrays and microRNA (miRNA) sequencing on acini of HMT-3522 S1 (S1) breast epithelial risk-progression culture model in 3D and chose an early-stage population miRNome for a validation cohort. Nontumorigenic S1 cells form fully polarized epithelium while pretumorigenic counterparts silenced for gap junction Cx43 (Cx43-KO-S1) lose epithelial polarity, multilayer and mimic premalignant in vivo mammary epithelial morphology. Here, 121 circRNAs and 65 miRNAs were significantly dysregulated in response to Cx43 silencing in cultured epithelia and 15 miRNAs from the patient cohort were involved in epithelial polarity disruption. Focusing on the possible sponging activity of the validated circRNAs to their target miRNAs, we found all miRNAs to be highly enriched in cancer-related pathways and cross-compared their dysregulation to actual miRNA datasets from the cultured epithelia and the patient validation cohort. We present the involvement of gap junction in post-transcriptional axes and reveal Cx43/hsa_circ_0077755/miR-182 as a potential biomarker signature axis for heightened-risk of breast cancer initiation, and that its dysregulation patterns might predict prognosis along breast cancer initiation and progression.	NA	Sci Rep. 2021 Jan 29;11(1):2626. doi: 10.1038/s41598-021-82057-y.
3553	Circular RNA	CircPVT1	miR-145-5p	TBX15	ccRCC tissues and cells	Clear Cell Renal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;RNA sequencing;	33453148	CircPVT1 promotes progression in clear cell renal cell carcinoma by sponging miR-145-5p and regulating TBX15 expression.	Emerging evidence revealed that circular RNAs (circRNAs) play significant roles in regulating tumorigenesis and cancer progression. However, few circRNAs were well characterized in clear cell renal cell carcinoma (ccRCC). We found that circPVT1 was significantly upregulated in ccRCC tissues and positively associated with the clinical stage. The Area Under Curve of tissue and serum circPVT1 expression in ccRCC were 0.93 and 0.86, respectively. Importantly, we demonstrated that circPVT1 promoted ccRCC growth and metastasis in vitro and in vivo. We also found that circPVT1 directly binds to miRNA-145-5p via the Biotin-labelled miRNA pulldown assay and dual-luciferase reporter assay, and miR-145-5p inhibitor significantly attenuated the effect of circPVT1 knockdown on ccRCC cells. Moreover, through RNA sequencing and bioinformatics analysis, we demonstrated that TBX15 was regulated by the circPVT1/miR-145-5p axis and predicted poor prognosis in ccRCC. These findings suggest that circPVT1 promotes ccRCC growth and metastasis through sponging miR-145-5p and regulating downstream target TBX15 expression. The circPVT1/miR-145-5p/TBX15 axis might be a potential diagnostic marker and therapeutic target in ccRCC.	NA	Cancer Sci. 2021 Apr;112(4):1443-1456. doi: 10.1111/cas.14814. Epub 2021 Feb 10.
3554	LncRNA	SNHG3	miR-487a-3p	TRIM25	PCa tissues and cells(LNCaP and PC-3)	Prostate Cancer	Homo sapiens (human)	Western blot;	33416420	Long Noncoding RNA Small Nucleolar RNA Host Gene 3 Mediates Prostate Cancer Migration, Invasion, and Epithelial-Mesenchymal Transition by Sponging miR-487a-3p to Regulate TRIM25.	Background: Long noncoding RNA small nucleolar RNA host gene 3 (SNHG3) is related to the proliferation and metastasis of cancer cells. This study aims to reveal the role of SNHG3 in prostate cancer (PCa), which may help prevent PCa metastasis. Methods: SNHG3 plasmid, SNHG3 siRNA, miR-487a-3p mimic, miR-487a-3p inhibitor, TRIM25 plasmid, and TRIM25 siRNA were transfected or cotransfected into LNCaP and PC-3 cells. The proliferation, migration, and invasion of PCa cells were measured by Cell Counting Kit-8, wound-healing, and transwell assays, respectively. The expressions of SNHG3, miR-487a-3p, E-cadherin, N-cadherin, Snail, and TRIM25 in PCa tissues and cells were measured by quantitative reverse transcription polymerase chain reaction or western blot. Results: SNHG3 expression level was upregulated in PCa tissues and cells. SNHG3 overexpression and miR-487a-3p inhibitor promoted cell viability, migration, invasion, and N-cadherin and Snail levels, and inhibited E-cadherin level in LNCaP cells, while SNHG3 silencing and miR-487a-3p mimic had the opposite effects on PC-3 cells. The inhibitory effect of miR-487a-3p mimic on the migration, invasion, and epithelial-mesenchymal transition (EMT) of LNCaP cells was inversed by both SNHG3 and TRIM25 plasmids. Similarly, the function of miR-487a-3p inhibitor in PC-3 cells was also inversed by SNHG3 siRNA and TRIM25 siRNA. Conclusion: SNHG3 mediates PCa migration, invasion, and EMT by sponging miR-487a-3p to regulate TRIM25. The Clinical Trial Registration number: Y20180831.	NA	Cancer Biother Radiopharm. 2021 Jan 7. doi: 10.1089/cbr.2020.3988.
3555	LncRNA	CAR10	miR-892a	GJB2	NSCLC tissues	Non-Small Cell Lung Cancer	Homo sapiens (human)	RNA pull-down assay;Western blot;Immunohistochemistry;luciferase assay;RNA pull-down;	33664589	Long Non-Coding RNA CAR10 Facilitates Non-Small Cell Lung Cancer Cell Migration and Invasion by Modulating the miR-892a/GJB2 Pathway.	INTRODUCTION: Non-coding RNAs, including long non-coding (lnc)RNAs and microRNAs (miRs), play crucial roles in numerous malignant tumors, including non-small cell lung cancer (NSCLC). METHODS: The expression levels of chromatin-associated RNA Intergenic 10 (CAR10), gap junction protein beta 2 (GJB2) and miR-892a in NSCLC were evaluated by reanalyzing three Gene Expression Omnibus (GEO) datasets, and performing reverse transcription-quantitative PCR, immunohistochemistry staining and Western blot analysis, accordingly. Functionally, Transwell and Matrigel assays were performed to measure changes in the migration and invasion abilities of the A549 and H1299 cell lines. The targeted binding effects between CAR10 and miR-892a, as well as between miR-892a and GJB2 were confirmed by conducting dual-luciferase reporter and RNA pull-down assays, respectively. RESULTS: The present study demonstrated that CAR10 was upregulated in patients with NSCLC, which was also associated with a poor prognosis. Functionally, CAR10 was confirmed to be oncogenic and promoted NSCLC cell migration and invasion, using overexpression and knockdown Transwell assays. Furthermore, GJB2 expression was revealed to be upregulated and was positively correlated with CAR10 expression in NSCLC. A further mechanistic study revealed that GJB2 was a downstream target of CAR10, which induced the migration and invasive potential of the A549 and H1299 cell lines. More specifically, miR-892a was found to serve as a bridge between CAR10 and GJB2, via similar miRNA response elements. The RNA pull-down and luciferase assays indicated that miR-892a directly binds both CAR10 and GJB2. CONCLUSION: CAR10 promoted NSCLC cell migration and invasion by upregulating GJB2 and sponging miR-892a. These findings illustrated that the CAR10/miR-892a/GJB2 axis may be a novel molecular target for the treatment of NSCLC.	NA	Cancer Manag Res. 2021 Feb 25;13:1967-1979. doi: 10.2147/CMAR.S287386. eCollection 2021.
3556	LncRNA	SNHG1	miR-424-5p	FGF2	OS tissues and cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33732298	Long non-coding RNA small nucleolar RNA host gene 1 knockdown suppresses the proliferation, migration and invasion of osteosarcoma cells by regulating microRNA-424-5p/FGF2 in vitro.	The aim of the present study was to clarify the effect of long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) on the proliferation, migration and invasion of osteosarcoma (OS) cells and to explore the potential underlying mechanisms. The expression levels of SNHG1, microRNA (miR)-424-5p and fibroblast growth factor 2 (FGF2) in OS tissues and cells were detected using reverse transcription-quantitative polymerase chain reaction. OS cell proliferation, migration and invasion were analysed by MTT, wound healing and Transwell invasion assays, respectively. The targeting relationships between SNHG1 and miR-424-5p, as well as between miR-424-5p and FGF2, were confirmed using RNA-binding protein immunoprecipitation and/or dual-luciferase reporter gene assays. The results demonstrated that the expression levels of SNHG1 and FGF2 were upregulated, whereas the expression of miR-424-5p was downregulated in OS tissues and cells. The silencing of SNHG1 significantly inhibited the proliferation, migration and invasion of OS cells. Additionally, FGF2 was shown to be a target of miR-424-5p, which in turn, was a target of SNHG1. miR-424-5p silencing and FGF2 overexpression both reversed the suppressive effects of SNHG1 knockdown on the proliferation, migration and invasion of OS cells. Thus, the silencing of SNHG1 may inhibit the proliferation, migration and invasion of OS cells by regulating the miR-424-5p/FGF2 axis.	NA	Exp Ther Med. 2021 Apr;21(4):325. doi: 10.3892/etm.2021.9756. Epub 2021 Feb 5.
3557	LncRNA	CHRF	miR-182-5p	ATG7	H9C2 cells	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	Rescue assay;	33491285	LncRNA CHRF aggravates myocardial ischemia/reperfusion injury by enhancing autophagy via modulation of the miR-182-5p/ATG7 pathway.	Myocardial ischemia/reperfusion (I/R) injury is a very frequent cardiovascular disease and one of the leading causes of death. Abundant evidence has shown that long noncoding RNAs (lncRNAs) are crucial players in myocardial I/R injury. LncRNA cardiac hypertrophy-related factor (CHRF) has been revealed as an important modulator in cardiac disease. However, the function of CHRF in myocardial I/R injury is unclear. In our current work, we found that the expression of CHRF was upregulated in myocardial I/R injury models. Suppression of CHRF relieved myocardial I/R injury in vivo. In addition, in vitro silencing of CHRF enhanced cell viability and attenuated lactate dehydrogenase activity (LDH) as well as apoptosis in H9C2 cells treated with hypoxia/reoxygenation injury. Autophagy has been studied to play an important role in myocardial I/R injury. Thus, experiments related to autophagy were done, and the results showed that CHRF knockdown decreased autophagy. For the exploration of the regulatory mechanism, we found that CHRF sequestered and negatively regulated miR-182-5p to release its inhibition on ATG7. Findings from rescue assays revealed that ATG7 overexpression could suppress the effects of CHRF silence on cell viability, LDH level, apoptosis, and autophagy. To sum up, our results suggested that CHRF exacerbated myocardial I/R injury by enhancing autophagy via modulation of the miR-182-5p/ATG7 pathway. Therefore, this competing endogenous RNA axis may be a potential therapeutic biomarker for myocardial I/R injury.	NA	J Biochem Mol Toxicol. 2021 Apr;35(4):e22709. doi: 10.1002/jbt.22709. Epub 2021 Jan 24.
3558	LncRNA	PVT1	miR-23b-3p	EGR1	serum samples of DN patients and HG-induced HRMCs	NA	Homo sapiens (human)	qRT-PCR;RACE;Western blot;Luciferase reporter assay;	33408314	Knockdown of plasmacytoma variant translocation 1 (PVT1) inhibits high glucose-induced proliferation and renal fibrosis in HRMCs by regulating miR-23b-3p/early growth response factor 1 (EGR1).	Long noncoding RNAs (lncRNAs) have been reported to play critical role in the development of diabetic nephropathy (DN). However, the effects and mechanism of plasmacytoma variant translocation 1 (PVT1) remain poorly understood. The expression of PVT1, miR-23b-3p, early growth response factor 1 (EGR1), Fibronectin (FN), Collagen IV (Col IV), alpha smooth muscle actin (α-SMA), E-cadherin, and vimentin, transforming growth factor (TGF)-β1 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed by Cell Counting-8 (CCK-8) assay. Western blot assay was conducted to measure the protein levels of FN, Col IV, E-cadherin, α-SMA, vimentin, TGF-β1, and EGR1. The interaction between miR-23b-3p and PVT1 or EGR1 was predicted by starBase or TargetScan and confirmed by the dual luciferase reporter assay. The oxidative stress factors were analyzed by corresponding kits. We found that the expression of PVT1 and EGR1 was increased and miR-23b-3p was decreased in serum samples of DN patients and HG-induced HRMCs. Knockdown of PVT1 significantly inhibited HG-induced proliferation, extracellular matrix (ECM) accumulation, epithelial-mesenchymal transition (EMT), and oxidative stress in HRMCs, while these effects were abated by inhibiting miR-23b-3p. In addition, EGR1 was confirmed as downstream target of miR-23b-3p and miR-23b-3p could specially bind to PVT1. Besides, downregulation of PVT1 inhibited the progression of DN partially via upregulating miR-23b-3p and downregulating EGR1. In conclusion, our results suggested that PVT1 knockdown suppressed DN progression though functioning as ceRNA of miR-23b-3p to regulate EGR1 expression in vitro, providing potential value for the treatment of DN.	NA	Endocr J. 2021 May 28;68(5):519-529. doi: 10.1507/endocrj.EJ20-0642. Epub 2021 Jan 7.
3559	Circular RNA	CircHIPK3	miR-637	CDK6	vascular smooth muscle cells	Atherosclerosis	Homo sapiens (human)	ChIP;	33659023	Identification of Differently Expressed mRNAs in Atherosclerosis Reveals CDK6 Is Regulated by circHIPK3/miR-637 Axis and Promotes Cell Growth in Human Vascular Smooth Muscle Cells.	Atherosclerosis is the leading cause of heart disease and stroke, and one of the leading causes of death and disability worldwide. The phenotypic transformation of vascular smooth muscle cells (VSMCs) plays an important role in the pathological process of atherosclerosis. The present study aimed to identify differently expressed mRNAs in atherosclerosis by analyzing GSE6088 database. Our results revealed there were totally 467 increased and 490 decreased differential expressed genes (DEGs) in atherosclerosis. Bioinformatics analysis demonstrated that the DEGs substantially existed in pathways, including Glyoxylate and dicarboxylate metabolism, Tyrosine metabolism, Tryptophan metabolism, Beta-Alanine metabolism, Fatty acid biosynthesis and Starch and sucrose metabolism. Next, we constructed a protein-protein interaction (PPI) network to identify hub genes in atherosclerosis. Also, we identified CDK6 as a key regulator of atherosclerosis. In this study, we found that CDK6 knockdown suppressed HASMC and HUASMC cell proliferation. Circular RNA (CircRNA) is a non-coding RNA which is reported to have an unusual influence on tumorigenesis process and other aspects in the last few years. Previous studies showed circRNAs could act as miRNAs sponging in multiple biological processes. Bioinformatics prediction and luciferase analysis showed that CDK6 were targeted and regulated by circHIPK3/miR-637. Moreover, silencing circHIPK3 could also significantly induce the arrest and apoptosis of cell cycle. In conclusion, this study discovered the important regulatory role of circHIPK3 in the proliferation and apoptosis of VSMCs by influencing the miR-637/CDK6 axis.	NA	Front Genet. 2021 Feb 15;12:596169. doi: 10.3389/fgene.2021.596169. eCollection 2021.
3560	LncRNA	NONhsaT024778	miR-1290	Robo1	chordoma tissues and cell lines	Chordoma	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33767589	LncRNA-NONHSAT024778 promote the proliferation and invasion of chordoma cell by regulating miR-1290/Robo1 axis.	Chordoma is a malignant bone tumor originating from the embryonic remnants of the notochord. lncRNAs act as competing endogenous RNAs (ceRNAs) and play a critical role in tumor pathology. However, the biological role of lncRNA-NONHSAT024778 and the underlying molecular mechanism in chordoma remains unknown. qRT-PCR was used to analyze the expression changes of NONHSAT024778 and miR-1290 in chordoma tissues and cell lines. Bioinformatics analysis and luciferase reporter assay were applied to detect the targeting binding effect between NONHSAT024778 and miR-1290, and between Robo1 and miR-1290. The effect of NONHSAT024778 on chordoma cell proliferation and invasion and its regulation of miR-1290 by acting as a ceRNA were also investigated. An increased NONHSAT024778 expression was correlated with a decreased miR-1290 level in chordoma tissues. NONHSAT024778 knockdown suppressed the proliferation and invasion of chordoma cells. miR-1290 restored expression rescued the carcinogenic function of NONHSAT024778. Bioinformatics analysis showed that NONHSAT024778 acted as ceRNA to regulate Robo1 via sponging miR-1290 in chordoma cells, thereby promoting chordoma cell malignant progression. In vivo results confirmed the anti-tumor effects of NONHSAT024778 knockdown activating miR-1290 to inhibit the oncogene Robo1. NONHSAT024778 is substantially overexpressed, whereas miR-1290 is decreased in chordoma tissue. NONHSAT024778-miR-1290-Robo1 axis plays a critical role in chordoma tumorigenesis and might be a potential predictive biomarker for the diagnosis and therapeutic target among patients with chordoma.	NA	Int J Biol Sci. 2021 Feb 8;17(3):796-806. doi: 10.7150/ijbs.54091. eCollection 2021.
3561	LncRNA	DANCR	miR-185-5p	HMGA2	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;	33481014	Long non-coding RNA DANCR accelerates colorectal cancer progression via regulating the miR-185-5p/HMGA2 axis.	Long non-coding RNAs (lncRNAs) are crucial players in tumor progression. Herein, this work was designated to decipher the clinical significance, function and molecular mechanism of an lncRNA, differentiation antagonizing non-coding RNA (DANCR) in colorectal cancer (CRC). Quantitative real-time PCR (qRT-PCR) was adopted to examine DANCR, miR-185-5p and HMGA2 mRNA expressions in CRC tissues and cells. Both gain-of-function and loss-of-function cell models for DANCR were established, and then MTT, wound healing and Transwell, flow cytometry assays were carried out to detect the proliferation, migration, invasion, cell cycle and apoptosis of CRC cells. Dual luciferase reporter gene assay and RIP assay were utilized to validate the targeting relationships between DANCR and miR-185-5p. Western blot was employed for detecting high mobility group A2 (HMGA2) expressions in CRC cells. In this study, we demonstrated that the expression of DANCR was elevated in CRC tissues and cell lines, and its high expression was significantly associated with increased TNM stage and positive lymph node metastasis. DANCR overexpression promoted CRC cell proliferation, migration, invasion and cell cycle progression, but inhibited apoptosis; while knocking down DANCR caused the opposite effects. DANCR was further identified as a molecular sponge for miR-185-5p, and DANCR could indirectly increase the expression of HMGA2 via repressing miR-185-5p. In conclusion, DANCR/miR-185-5p/HMGA2 axis participated in the progression of CRC.	NA	J Biochem. 2021 Jan 22:mvab011. doi: 10.1093/jb/mvab011.
3562	Circular RNA	CircVAPA	miR-125b-5p	STAT3	GC tissues and cells	Gastric Cancer	Homo sapiens (human)	MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33642823	Circular RNA circVAPA promotes chemotherapy drug resistance in gastric cancer progression by regulating miR-125b-5p/STAT3 axis.	BACKGROUND: Gastric cancer (GC) is a prevalent malignancy, leading to a high incidence of cancer-associated death. Cisplatin (DDP)-based chemotherapy is the principal therapy for clinical GC treatment, but DDP resistance is a severe clinical challenge and the mechanism remains poorly understood. Circular RNAs (circRNAs) have been identified to play crucial roles in modulating the chemoresistance of gastric cancer cells. AIM: To explore the effect of circVAPA on chemotherapy resistance during GC progression. METHODS: The effect of circVAPA on GC progression and chemotherapy resistance was analyzed by MTT assay, colony formation assay, Transwell assay, wound healing assay, and flow cytometry analysis in GC cells and DDP resistant GC cell lines, and tumorigenicity analysis in nude mice in vivo. The mechanism was investigated by luciferase reporter assay, quantitative real-time PCR, and Western blot analysis. RESULTS: CircVAPA expression was up-regulated in clinical GC tissues compared with normal samples. CircVAPA depletion inhibited proliferation, migration, and invasion and increased apoptosis of GC cells. The expression of circVAPA, STAT3, and STAT3 downstream genes was elevated in DDP resistant SGC7901/DDP cell lines. CircVAPA knockdown attenuated the DDP resistance of GC cells. Mechanically, circVAPA was able to sponge miR-125b-5p, and miR-125b-5p could target STAT3 in the GC cells. MiR-125b-5p inhibitor reversed circVAPA depletion-enhanced inhibitory effect of DDP on GC cells, and STAT3 knockdown blocked circVAPA overexpression-induced proliferation of DDP-treated SGC7901/DDP cells. The depletion of STAT3 and miR-125b-5p inhibitor reversed circVAPA depletion-induced GC cell apoptosis. Functionally, circVAPA contributed to the tumor growth of SGC7901/DDP cells in vivo. CONCLUSION: CircVAPA promotes chemotherapy resistance and malignant progression in GC by miR-125b-5p/STAT3 signaling. Our findings present novel insights into the mechanism by which circVAPA regulates chemotherapy resistance of GC cells. CircVAPA and miR-125b-5p may be considered as the potential targets for GC therapy.	NA	World J Gastroenterol. 2021 Feb 14;27(6):487-500. doi: 10.3748/wjg.v27.i6.487.
3563	LncRNA	SLC16A1-AS1	miR-194	SOCS2	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qPCR;Luciferase reporter assay;	33603475	LncRNA SLC16A1-AS1 Suppresses Cell Proliferation in Cervical Squamous Cell Carcinoma (CSCC) Through the miR-194/SOCS2 Axis.	BACKGROUND: SLC16A1-AS1 has been characterized as an oncogenic long non-coding (lncRNA) in breast cancer and bladder cancer, while its role in cervical squamous cell carcinoma (CSCC) is unknown. METHODS: CSCC and non-tumor tissue samples were collected from 60 female patients, and qPCR was performed to detect the expression of SLC16A1-AS1, miR-194 and SOCS2. Luciferase reporter assay was performed to detect the interaction between SLC16A1-AS1 and miR-194. Colony formation assay was used to detect cell proliferation. RESULTS: SLC16A1-AS1 was down-regulated in CSCC and correlated with poor survival. Overexpression of SLC16A1-AS1 could inhibit the proliferation of cervical cancer cells. In addition, SLC16A1-AS1 could sponge miR-194 and increase the expression levels of SOCS2, ultimately inhibiting the proliferation of cervical cancer cells. CONCLUSION: SLC16A1-AS1 was downregulated in CSCC and suppressed cell proliferation in cervical squamous cell carcinoma (CSCC) through the miR-194/SOCS2 axis.	NA	Cancer Manag Res. 2021 Feb 11;13:1299-1306. doi: 10.2147/CMAR.S276629. eCollection 2021.
3564	Circular RNA	CircARFGEF1	miR-125a-3p	GLRX3	endothelial cell line	NA	Homo sapiens (human)	qRT-PCR	33539420	CircRNA ARFGEF1 functions as a ceRNA to promote oncogenic KSHV-encoded viral interferon regulatory factor induction of cell invasion and angiogenesis by upregulating glutaredoxin 3.	Circular RNAs (circRNAs) are novel single-stranded noncoding RNAs that can decoy other RNAs to inhibit their functions. Kaposi's sarcoma (KS), caused by oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV), is a highly angiogenic and invasive vascular tumor of endothelial origin commonly found in AIDS patients. We have recently shown that KSHV-encoded viral interferon regulatory factor 1 (vIRF1) induces cell invasion, angiogenesis and cellular transformation; however, the role of circRNAs is largely unknown in the context of KSHV vIRF1. Herein, transcriptome analysis identified 22 differentially expressed cellular circRNAs regulated by vIRF1 in an endothelial cell line. Among them, circARFGEF1 was the highest upregulated circRNA. Mechanistically, vIRF1 induced circARFGEF1 transcription by binding to transcription factor lymphoid enhancer binding factor 1 (Lef1). Importantly, upregulation of circARFGEF1 was required for vIRF1-induced cell motility, proliferation and in vivo angiogenesis. circARFGEF1 functioned as a competing endogenous RNAs (ceRNAs) by binding to and inducing degradation of miR-125a-3p. Mass spectrometry analysis demonstrated that glutaredoxin 3 (GLRX3) was a direct target of miR-125a-3p. Knockdown of GLRX3 impaired cell motility, proliferation and angiogenesis induced by vIRF1. Taken together, vIRF1 transcriptionally activates circARFGEF1, potentially by binding to Lef1, to promote cell oncogenic phenotypes via inhibiting miR-125a-3p and inducing GLRX3. These findings define a novel mechanism responsible for vIRF1-induced oncogenesis and establish the scientific basis for targeting these molecules for treating KSHV-associated cancers.	NA	PLoS Pathog. 2021 Feb 4;17(2):e1009294. doi: 10.1371/journal.ppat.1009294. eCollection 2021 Feb.
3565	Circular RNA	CircCDYL	miR-185-5p	TNRC6A	NSCLC tissues, plasma, and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	33531835	Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A.	AIM: A series of research reveal that circular RNA (circRNA) plays a vital role in regulating the development of tumor cells. In this research, we would explore the role and mechanism of circCDYL in non-small cell lung cancer (NSCLC). METHODS: RT-PCR was performed to detect the expression of circCDYL in NSCLC tissues, plasma, and cell lines. The tumor cell proliferation ability was evaluated by clone formation assay, and cell cycle determination. Flow cytometry was used to detect apoptosis in NSCLC cell lines. Western blot and RT-PCR were used to assess the expression of proteins and genes. Luciferase assay was performed to confirm the relationship of circRNA-miRNA-mRNA. RESULTS: The decreased level of circCDYL was observed in NSCLC patients' tissues and plasma, which was also downregulated in NSCLC cell lines. Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal. CONCLUSION: Here, we revealed that circCDYL inhibited proliferation and induced apoptosis in NSCLC cell lines via regulating ERK1/2 signal, and the mechanism of this progression may target miR-185-5p/TNRC6A, which provided a theoretical basis for clinical therapy.	NA	Cancer Manag Res. 2021 Jan 25;13:633-642. doi: 10.2147/CMAR.S280315. eCollection 2021.
3566	Circular RNA	Circ_0119872	miR-622	G3BP1	UM cells	Uveal Melanoma	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;RNA pull-down;	33579337	Circ_0119872 promotes uveal melanoma development by regulating the miR-622/G3BP1 axis and downstream signalling pathways.	BACKGROUND: The abnormal expression of circular RNAs (circRNAs) in uveal melanoma (UM) has been revealed, but the specific underlying molecular mechanism of their association with UM development has not been fully explored. METHODS: The levels of circ_0119872, G3BP1 and miR-622 in UM cell lines and tissues were determined by quantitative real-time PCR (qRT-PCR) and western blotting assays. In vitro and in vivo assays were performed to investigate the function of circ_0119872 in the tumorigenesis of UM cells. The relationships among circ_0119872, miR-622 and G3BP1 were predicted using bioinformatic tools and verified by RNA-FISH, RNA pull-down and dual-luciferase reporter assays. The effects of circ_0119872 on Wnt/β-catenin and mTOR signalling pathways were determined by gene set enrichment analysis (GSEA) and western blotting. RESULTS: We found that circ_0119872 is upregulated in UM cell lines and tissues. Moreover, overexpression of circ_0119872 promotes the malignancy of UM cells, while silencing of circ_0119872 inhibits it. In addition, circ_0119872 can directly interact with miR-622 as a miRNA sponge that regulates the expression of the miR-622 target gene G3BP1 as well as downstream Wnt/β-catenin and mTOR signalling pathways. CONCLUSIONS: Circ_0119872 may act as an oncogene in UM through a novel circ_0119872/miR-622/G3BP1 axis, activating the Wnt/β-catenin and mTOR signalling pathways, which in turn may provide potential biomarkers and therapeutic targets for the management of UM.	NA	J Exp Clin Cancer Res. 2021 Feb 12;40(1):66. doi: 10.1186/s13046-021-01833-w.
3567	LncRNA	MALAT1	miR-206	PTGS1	AIT tissues and Nthy-ori 3-1 cells	Autoimmune Thyroiditis	Homo sapiens (human)	ELISA;Flow cytometry assay;Western blot;Flow Cytometry assay;luciferase assay;	33452572	Ursolic acid ameliorates Nthy-ori 3-1 cells injury induced by IL-1β through limiting MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway.	RATIONALE: Ursolic acid (UA) has exhibited anti-inflammatory and anti-oxidative drug effects. OBJECTIVES: In the research, we assessed the effects of UA on Nthy-ori 3-1 cells stimulated by IL-1β and attempted to elucidate the mechanisms underlying the effects. METHODS: Autoimmune thyroiditis (AIT) was simulated using Nthy-ori 3-1 cells by IL-1β (10 μM) treatment. UA (20 μM) was applied to ameliorate the injury of Nthy-ori 3-1 cells. The target of UA was predicted by TCMSP, BATMAN, and GEO database. Targeted relationship between lncRNA MALAT1 and miR-206, as well as miR-206 and PTGS1, was predicted by bioinformatics software and identified by dual luciferase assays. Cytokines in the cell supernatant and the apoptosis of cells were detected by ELISAs and flow cytometry assays, respectively. Expression levels of NF-κB signaling pathway-related proteins were estimated by western blot. RESULTS: By enquiring TCMSP, BATMAN, and GEO database, PTGS1 was identified as a target of UA. Afterward, a ceRNA network among MALAT1, miR-206, and PTGS1 was constructed. The expression levels of MALAT1 and PTGS1 in AIT tissues were obviously enhanced. Moreover, the ceRNA network formed by MALAT1/miR-206/PTGS1 contributed to the damage of Nthy-ori 3-1 cells induced by IL-1β. However, UA ameliorated the Nthy-ori 3-1 cells injury induced by IL-1β through mediating the MALAT1/miR-206/PTGS1 ceRNA network and NF-κB signaling pathway. CONCLUSIONS: UA treatment significantly relieved the injury of Nthy-ori 3-1 cells via inhibiting the ceRNA mechanism of MALAT1/miR-206/PTGS1 and inflammatory pathways, insinuating that UA may be helpful for the treatment of AIT.	NA	Psychopharmacology (Berl). 2021 Apr;238(4):1141-1156. doi: 10.1007/s00213-021-05761-7. Epub 2021 Jan 16.
3568	LncRNA	Linc00963	miR-655	TRIM24	CRPC cells	Prostate Cancer	Homo sapiens (human)	Rescue assay;	33643926	Linc00963 Promote Cell Proliferation and Tumor Growth in Castration-Resistant Prostate Cancer by Modulating miR-655/TRIM24 Axis.	Previous studies have shown that both long intergenic non-coding RNA 00963 (Linc00963) and tripartite motif containing 24 (TRIM24) are activators of the PI3K/AKT pathway, and both are involved in the carcinogenesis and progression of prostate cancer. However, the regulatory mechanisms between Linc00963 and TRIM24 are still unclear. In this study, we aimed to elucidate the underlying relationship between Linc00963 and TRIM24 in castration-resistant prostate cancer (CRPC). We found that TRIM24, an established oncogene in CRPC, was positively correlated with Linc00963 in prostate cancer tissues. In addition, TRIM24 was positively regulated by Lin00963 in CRPC cells. Mechanistically, TRIM24 was the direct target of microRNA-655 (miR-655) in CRPC cells, and Linc00963 could competitively bind miR-655 and upregulate TRIM24 expression. Using gain- and loss-of- function assays and rescue assays, we identified that miR-655 inhibits TRIM24 expression and cell proliferation and colony forming ability in CRPC, and that Linc00963 promotes TRIM24 expression, cell proliferation, and colony forming ability of CRPC cells by directly suppressing miR-655 expression. We further identified that Linc00963 could promote tumor growth of CRPC cells by inhibiting miR-655 and upregulating TRIM24 axis in vivo. Taken together, our study reveals a new mechanism for the Linc00963/miR-655/TRIM24 competing endogenous RNA (ceRNA) network in accelerating cell proliferation in CRPC in vitro and in vivo, and suggests that Linc00963 could be considered a novel therapeutic target for CRPC.	NA	Front Oncol. 2021 Feb 11;11:636965. doi: 10.3389/fonc.2021.636965. eCollection 2021.
3569	LncRNA	EBLN3P	miR-224-5p	Rab10	osteosarcoma tissues and cells	Osteosarcoma	Homo sapiens (human)	Immunohistochemistry;luciferase assay;	33479458	LncRNA EBLN3P promotes the progression of osteosarcoma through modifying the miR-224-5p/Rab10 signaling axis.	The treatment of patients with advanced-stage osteosarcoma represents a major challenge, with very few treatments currently approved. Although accumulating evidence has demonstrated the importance of lncRNAs in osteosarcoma, the current knowledge on the functional roles and molecular mechanisms of lncRNA endogenous born avirus-like nucleoprotein (EBLN3P) is limited. At present, the expressions of EBLN3P and miR-224-5p in osteosarcoma tissues were quantified by reverse transcription-quantitative PCR assay, and the expression of Ras-related protein 10 (Rab10) in osteosarcoma tissues was quantified by immunohistochemistry and western-blotting. The bioinformatics prediction software ENCORI was used to predict the putative binding sites of EBLN3P, Rab10 and miR-224-5p. The regulatory role of EBLN3P or miR-224-5p on cell proliferation, migration and invasion ability were verified by Cell Counting Kit-8, wound healing and Transwell assays, respectively. The interaction among EBLN3P, miR-224-5p and Rab10 were testified by luciferase. The increased expression of EBLN3P and Rab10 and decreased expression of miR-224-5p were observed in osteosarcoma tissues and cell lines. Besides, the overexpression of EBLN3P or knockdown of miR-224-5p were revealed to promote the proliferation, migration and invasion of osteosarcoma cells. Bioinformatics analysis and luciferase assay revealed that EBLN3P could directly interacted with miR-224-5p to attenuate miR-224-5p binding to the Rab10 3'-untranslated region. Furthermore, the mechanistic investigations revealed activation of the miR-224-5p/Rab10 regulatory loop by knockdown of miR-372-3p or overexpression of Rab10, thereby confirming the in vitro role of EBLN3P in promoting osteosarcoma cell proliferation, migration and invasion. To the best of our knowledge, the present study is the first to demonstrate that EBLN3P may act as a competitive endogenous RNA to modulate Rab10 expression by competitive sponging to miR-224-5p, leading to the regulation of osteosarcoma progression, which indicates a possible new approach to osteosarcoma diagnosis and treatment.	NA	Sci Rep. 2021 Jan 21;11(1):1992. doi: 10.1038/s41598-021-81641-6.
3570	LncRNA	LINC00857	miR-150-5p	E2F3	PC tissues and cell lines	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33680969	m(6)A-Mediated Upregulation of LINC00857 Promotes Pancreatic Cancer Tumorigenesis by Regulating the miR-150-5p/E2F3 Axis.	The mortality and morbidity rates of pancreatic cancer (PC) have been increasing over the past two decades. Recent evidence indicates that long non-coding RNAs (lncRNAs) are usually dysregulated in the tumorigenesis and progression of PC. In the present study, we showed that the expression of LINC00857 was upregulated in PC and associated with poor prognosis based on the Gene Expression Profiling Interactive Analysis (GEPIA) database and validated in our PC tissues and cell lines. N(6)-Methyladenosine (m(6)A) was highly enriched within LINC00857 and enhanced its RNA stability. Knockdown of LINC00857 remarkably inhibited the proliferation and promoted the apoptosis of PC cells. Then, by using bioinformation analysis and verified experiments, we identified that LINC00857 functioned as a competing endogenous RNA (ceRNA) for sponging miR-150-5p, leading to the upregulation of its target E2F3 in PC cells. Taken above, our study revealed a potential ceRNA regulatory pathway in which LINC00857 modulates E2F3 expression by binding to miR-150-5p, ultimately promoting tumorigenesis in PC. LINC00857/miR-150-5p/E2F3 regulatory axis may be taken as an alternative therapeutic target for treating PC.	NA	Front Oncol. 2021 Feb 18;11:629947. doi: 10.3389/fonc.2021.629947. eCollection 2021.
3571	LncRNA	SNHG16	miR-488	ITGA6	osteosarcoma tissues and cell lines	Osteosarcoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;Rescue assay;	33598394	LncRNA SNHG16 promotes epithelial-mesenchymal transition by upregulating ITGA6 through miR-488 inhibition in osteosarcoma.	BACKGROUND: Osteosarcoma is a primary cause of cancer-associated death in children and adolescents worldwide. Long non-coding RNAs SNHG16 (lncRNA SNHG16) and integrin subunit-a 6 (ITGA6) are recently reported to be involved in the tumorigenesis of osteosarcoma by multiple mechanisms. However, the correlation between SNHG16 and ITGA6 in osteosarcoma remains undetermined. METHODS: Expression of miR-488, SNHG16 and ITGA6, as well as epithelial-mesenchymal transition (EMT) associated markers in osteosarcoma tissues and cell lines were examined by qRT-PCR or Western blotting. Effects of miR-488, SNHG16 and ITGA6 on cell migration, invasion were evaluated by wound-healing assay and transwell assay. Bioinformatics analysis and dual-luciferase reported assays were applied to assess the interaction among miR-488, SNHG16 and ITGA6. RNA immunoprecipitation (RIP) was also used to verify SNHG16 and miR-488 interaction. Finally, animal study was used to detect the effect of SNHG16 on osteosarcoma in vivo. RESULTS: SNHG16 and ITGA6 were significantly increased while miR-488 was decreased in osteosarcoma. ITGA6 was screened as a target gene of miR-488, and SNHG16 was sponged by miR-488 in osteosarcoma cells. MiR-488 overexpression and SNHG16 knockdown suppressed migration, invasion and EMT of osteosarcoma cells. Moreover, rescue assays proved that the influences of SNHG16 on osteosarcoma cells migration, invasion and EMT were dependent on miR-488 and ITGA6. In addition, the promotive effects of SNHG16 on osteosarcoma tumor growth and metastasis were further supported by xenograft tumor growth assay. CONCLUSION: SNHG16 promoted migration, invasion and EMT of osteosarcoma by sponging miR-488 to release ITGA6.	NA	J Bone Oncol. 2021 Jan 19;27:100348. doi: 10.1016/j.jbo.2021.100348. eCollection 2021 Apr.
3572	LncRNA	NKX2-1-AS1	miR-145-5p	SERPINE1	gastric cancer tissues	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;qRT-PCR;RIP assay;Western blot;FISH;luciferase assay;Luciferase reporter assay;	33512745	LncRNA NKX2-1-AS1 promotes tumor progression and angiogenesis via upregulation of SERPINE1 expression and activation of the VEGFR-2 signaling pathway in gastric cancer.	Long noncoding RNAs (lncRNAs) can compete with endogenous RNAs to modulate the gene expression and contribute to oncogenesis and tumor metastasis. lncRNA NKX2-1-AS1 (NKX2-1 antisense RNA 1) plays a pivotal role in cancer progression and metastasis; however, the contribution of aberrant expression of NKX2-1-AS1 and the mechanism by which it functions as a competing endogenous RNA (ceRNA) in gastric cancer (GC) remains elusive. NKX2-1-AS1 expression was detected in paired tumor and nontumor tissues of 178 GC patients by quantitative reverse transcription PCR (qRT-PCR). Using loss-of-function and gain-of-function experiments, the biological functions of NKX2-1-AS1 were evaluated both in vitro and in vivo. Further, to assess that NKX2-1-AS1 regulates angiogenic processes, tube formation and co-culture assays were performed. RNA binding protein immunoprecipitation (RIP) assay, a dual-luciferase reporter assay, quantitative PCR, Western blot, and fluorescence in situ hybridization (FISH) assays were performed to determine the potential molecular mechanism underlying this ceRNA. The results indicated that NKX2-1-AS1 expression was upregulated in GC cell lines and tumor tissues. Overexpression of NKX2-1-AS1 was significantly associated with tumor progression and enhanced angiogenesis. Functionally, NKX2-1-AS1 overexpression promoted GC cell proliferation, metastasis, invasion, and angiogenesis, while NKX2-1-AS1 knockdown restored these effects, both in vitro and in vivo. RIP and dual-luciferase assays revealed that the microRNA miR-145-5p is a direct target of NKX2-1-AS1 and that NKX2-1-AS1 serves as a ceRNA to sponge miRNA and regulate angiogenesis in GC. Moreover, serpin family E member 1 (SERPINE1) is an explicit target for miR-145-5p; besides, the NKX2-1-AS1/miR-145-5p axis induces the translation of SERPINE1, thus activating the VEGFR-2 signaling pathway to promote tumor progression and angiogenesis. NKX2-1-AS1 overexpression is associated with enhanced tumor cell proliferation, angiogenesis, and poor prognosis in GC. Collectively, NKX2-1-AS1 functions as a ceRNA to miR-145-5p and promotes tumor progression and angiogenesis by activating the VEGFR-2 signaling pathway via SERPINE1.	NA	Mol Oncol. 2021 Apr;15(4):1234-1255. doi: 10.1002/1878-0261.12911. Epub 2021 Feb 13.
3573	LncRNA	MEG3	miR-23b-3p	FOXO4	pituitary tumor cells (GH3 and MMQ)	Pituitary Adenoma	Homo sapiens (human)	Flow cytometry assay;Western blot;Flow Cytometry assay;	33649837	lncRNA MEG3 inhibits pituitary tumor development by participating in cell proliferation, apoptosis and EMT processes.	Pituitary tumors do not pose a threat to life but can cause visual disturbances and serious clinical syndromes, such as infertility and metabolic syndrome. Therefore, screening of key genes involved in the occurrence and development of pituitary tumors can provide new targets for the treatment of pituitary tumors. The aim of the present study was to investigate the molecular mechanism of long non-coding (lnc.) RNA maternally expressed 3 (MEG3) in cell proliferation, apoptosis and epithelial-mesenchymal transition (EMT) processes of pituitary tumor. Tissue samples were obtained from 34 patients who underwent surgical treatment of pituitary tumors. Pituitary tumor cells (GH3 and MMQ) were transfected with pcDNA3.1(+)-MEG3, short hairpin (sh)MEG3, microRNA (miR)-23-3p inhibitor or their controls using Lipofectamine(®) 2000. Reverse transcription-quantitative PCR and western blot analyses were used to detect the levels of MEG3, miR-23b-3p and FOXO4, as well as proliferation-, apoptosis- and EMT-associated genes and proteins. Cell Counting Kit-8 and flow cytometry assays were performed to detect proliferation and apoptosis, and Transwell assay was undertaken to assess invasion and migration. Luciferase reporter and RNA pulldown assays were performed to verify the binding between lncRNA MEG3, miR-23b-3p and FOXO4. Pearson's correlation analysis was used to analyze the correlation between expression levels of MEG3, miR-23b-3p and FOXO4. lncRNA MEG3 was expressed at lower levels in pituitary tumor tissues and cells. Overexpression of lncRNA MEG3 inhibited proliferation, invasion and migration and accelerated apoptosis of pituitary tumor cells. lncRNA MEG3 negatively regulated miR-23b-3p expression levels, while miR-23b-3p negatively regulated FOXO4 expression levels. Overexpression of lncRNA MEG3 inhibited the EMT process in pituitary tumor cells. miR-23-3p inhibitor rescued the effect of shMEG3 on proliferation, invasion, migration, apoptosis and the EMT process in pituitary tumor cells. lncRNA MEG3 inhibited pituitary tumor development by participating in cell proliferation, apoptosis and the EMT process, which may present a novel target for pituitary tumor treatment.	NA	Oncol Rep. 2021 Apr;45(4):40. doi: 10.3892/or.2021.7991. Epub 2021 Mar 2.
3574	LncRNA	H19	miR-29b-3p	HMGB1	lung cancer cell lines(293T, NCI-H1975, Calu-3 and 2BS)	Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33527767	The LncRNA H19/microRNA-29b-3p/HMGB1 signaling axis contributes to the regulation of lung cancer cell growth.	The long non-coding RNA (lncRNA) H19 acts as a competitive endogenous RNA (ceRNA) of miR-29b-3p and has been reported to exert pro-tumorigenic roles in several cancer types. However, the role of lncRNA H19 in lung cancer is not fully understood. Here, we investigated the role of the lncRNA H19/microRNA-29b-3p (miR-29b-3p)/high mobility group box 1 (HMGB1) signaling pathway in lung cancer cell growth using 293T, NCI-H1975, Calu-3 and 2BS cell lines. Cell viability was determined using a cell counting kit-8 (CCK-8) assay, while apoptosis and cell cycle distribution were assessed by flow cytometry. Cell migration was detected using a wound healing assay. Cell invasion was evaluated by transwell assay. The expression of lncRNA H19, miR-29b-3p, HMGB1, toll-like receptor 4 (TLR4), and matrix metallopeptidase 9 (MMP-9) was measured by fluorescence quantitative PCR or western blotting. We demonstrated that miR-29b-3p could directly bind to both lncRNA H19 and HMGB1 by dual-luciferase reporter assay. Three shRNAs targeting lncRNA H19 (shlncRNA H19) were designed, and shlncRNA H19-2 was selected to investigate the function of lncRNA H19 in tumor cell biology. Compared with controls, lung cancer cells expressing shlncRNA H19 exhibited decreased proliferation, cell-cycle arrest at the G1 phase, increased levels of cell apoptosis, and reduced migration and invasion. Moreover, shlncRNA H19 upregulated the expression of miR-29b-3p and reduced the protein expression of HMGB1, TLR4, and MMP-9 in lung cancer cells. Together, our data indicate that the lncRNA H19/miRNA-29b-3p/HMGB1 signaling axis is involved in the regulation of lung cancer cell growth.	NA	FEBS Open Bio. 2021 Feb 2. doi: 10.1002/2211-5463.13103.
3575	LncRNA	SNHG18	miR-211-5p	BRD4	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33500406	MKL1-induced lncRNA SNHG18 drives the growth and metastasis of non-small cell lung cancer via the miR-211-5p/BRD4 axis.	Megakaryocytic leukemia 1 (MKL1) is a key transcription factor involved in non-small cell lung cancer (NSCLC) growth and metastasis. Yet, its downstream target genes, especially long non-coding RNA (lncRNA) targets, are poorly investigated. In this study, we employed lncRNA array technology to identify differentially expressed lncRNAs in NSCLC cells with or without overexpression of MKL1. Candidate lncRNAs were further explored for their clinical significance and function in NSCLC. The results showed that MKL1 promoted the expression of lncRNA SNHG18 in NSCLC cells. SNHG18 upregulation in NSCLC specimens correlated with lymph node metastasis and reduced overall survival of NSCLC patients. SNHG18 expression served as an independent prognostic factor for NSCLC. Knockdown of SNHG18 blocked MKL1-induced growth and invasion of NSCLC cells in vitro. Animal studies validated the requirement for SNHG18 in NSCLC growth and metastasis. Moreover, overexpression of SNHG18 promoted NSCLC cell proliferation and invasion. Mechanically, SNHG18 exerted its prometastatic effects on NSCLC cells through repression of miR-211-5p and induction of BRD4. Clinical evidence indicated that SNHG18 expression was negatively correlated with miR-211-5p expression in NSCLC tissues. Altogether, SNHG18 acts as a lncRNA mediator of MKL1 in NSCLC. SNHG18 facilitates NSCLC growth and metastasis by modulating the miR-211-5p/BRD4 axis. Therefore, SNHG18 may be a potential therapeutic target for the treatment of NSCLC.	NA	Cell Death Dis. 2021 Jan 26;12(1):128. doi: 10.1038/s41419-021-03399-z.
3576	LncRNA	NEAT1	miR-34a	LDHA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33645623	Inhibition of lncRNA-NEAT1 sensitizes 5-Fu resistant cervical cancer cells through de-repressing the microRNA-34a/LDHA axis.	Cervical cancer is one of the most diagnosed malignancies among females. The 5-fluorouracil (5-Fu) is a widely used chemotherapeutic agent against diverse cancers. Despite the initially encouraging progresses, a fraction of cervical cancer patients developed 5-Fu resistance. We detected that NEAT1 was significantly upregulated in cervical cancer tissues and cell lines. Moreover, NEAT1 was positively associated with 5-Fu resistance. Furthermore, expression of NEAT1 was significantly upregulated in 5-Fu resistant CaSki cervical cancer cells. Knocking down NEAT1 by shRNA dramatically promoted the sensitivity of 5-Fu resistant CaSki cells. We observed a negative correlation between lncRNA-NEAT1 and miR-34a in cervical cancer patient tissues. Overexpression of miR-34a significantly sensitized 5-Fu resistant cells. Bioinformatical analysis uncovered that NEAT1 functions as a competitive endogenous RNA (ceRNA) of miR-34a in cervical cancer cells via sponging it at multiple sites to suppress expression of miR-34a. This negative association between NEAT1 and miR-34a was further verified in cervical cancer tissues. We found the 5-Fu resistant cells displayed significantly increased glycolysis rate. Overexpression of miR-34a suppressed cellular glycolysis rate and sensitized 5-Fu resistant cells through direct targeting the 3'UTR of LDHA, a glycolysis key enzyme. Importantly, knocking down NEAT1 successfully downregulated LDHA expressions and glycolysis rate of cervical cancer cells by upregulating miR-34a, a process could be further rescued by miR-34a inhibition. Finally, we demonstrated inhibition of NEAT1 significantly sensitized cervical cancer cells to 5-Fu through the miR-34a/LDHA pathway. In summary, this study suggests a new molecular mechanism for the NEAT1-mediated 5-Fu resistance via the miR-34a/LDHA-glycolysis axis.	NA	Biosci Rep. 2021 Mar 1:BSR20200533. doi: 10.1042/BSR20200533.
3577	Circular RNA	CircCOL5A1	miR-7-5p	Epac1	keloid tissues and fibroblasts	Keloid	Homo sapiens (human)	FISH;qPCR;RT-qPCR;RACE;Western blot;FISH;Flow Cytometry assay;Immunohistochemistry;	33553184	Circular RNA CircCOL5A1 Sponges the MiR-7-5p/Epac1 Axis to Promote the Progression of Keloids Through Regulating PI3K/Akt Signaling Pathway.	Keloids, as a result of abnormal wound healing in susceptible individuals, are characterized by the hyper-proliferation of fibroblasts and exaggerated deposition of extracellular matrix. Current surgical and therapeutic modalities provide limited satisfactory results. Growing evidence has highlighted the roles of circRNAs in acting as miRNA sponges. However, up to date, the regulatory mechanism of circRNAs in the pathological process of keloids has rarely been reported. In this study, cell proliferation, cell migration, flow cytometry, western blotting, fluorescence in situ hybridization, dual-luciferase activity, and immunohistochemistry assays were applied to explore the roles and mechanisms of the circCOL5A1/miR-7-5p/Epac1 axis in the keloid. The therapeutic potential of circCOL5A1 was investigated by establishing keloid implantation models. The RT-qPCR result revealed that circCOL5A1 expression was obviously higher in keloid tissues and keloid fibroblasts. Subsequent cellular experiments demonstrated that circCOL5A1 knockdown repressed the proliferation, migration, extracellular matrix (ECM) deposition, whereas promoted cell apoptosis, through the PI3K/Akt signaling pathway. Furthermore, RNA-fluorescence in situ hybridization (RNA-FISH) illustrated that both circCOL5A1 and miR-7-5p were located in the cytoplasm. The luciferase reporter gene assay confirmed that exact binding sites were present between circCOL5A1 and miR-7-5p, as well as between miR-7-5p and Epac1. Collectively, the present study revealed that circCOL5A1 functioned as competing endogenous RNA (ceRNA) by adsorbing miR-7-5p to release Epac1, which contributed to pathological hyperplasia of keloids through activating the PI3K/Akt signaling pathway. Our data indicated that circCOL5A1 might serve as a novel promising therapeutic target and represent a new avenue to understand underlying pathogenesis for keloids.	NA	Front Cell Dev Biol. 2021 Jan 21;9:626027. doi: 10.3389/fcell.2021.626027. eCollection 2021.
3578	Circular RNA	CircPVT1	miR-21-5p	Smad7	bone marrow-derived mesenchymal stem cells	Osteonecrosis	Homo sapiens (human)	RNA pull-down assay;Western blot;Immunohistochemistry;RNA pull-down;	33733589	CircPVT1 up-regulation attenuates steroid-induced osteonecrosis of the femoral head through regulating miR-21-5p-mediated Smad7/TGFβ signalling pathway.	Steroid-induced osteonecrosis of the femoral head (SIONFH) has been a common disease following corticosteroid therapy. Presently, we aim to explore the functions of circular RNA (circ) PVT1 in SIONFH rats and the underlying mechanism. Glucocorticoid (GC) was used to treat SD rats and bone marrow-derived mesenchymal stem cells (BMSCs) to construct SIONFH model in vitro and in vivo, respectively. The pathological injury of the femoral head in the SIONFH rats was detected via haematoxylin-eosin (HE) staining and immunohistochemistry (IHC). The osteogenic differentiation, proliferation and apoptosis of BMSCs were detected. Western blot was used to detect Smad7, Bax, Bcl2 and Smad2/3. The potential targets of circPVT1 and miR-21-5p were validated through luciferase reporter gene assay and RNA pull-down assay, respectively. We found that CircPVT1 was decreased in the femoral head of SIONFH rats and GC-treated BMSCs, while miR-21-5p was markedly up-regulated. Overexpressed circPVT1 attenuated the apoptosis and cell viability inhibition of BMSCs induced by GC, while miR-21-5p up-regulation had the opposite effects. What's more, the in vivo experiments confirmed that up-regulating circPVT1 repressed osteonecrosis in SIONFH rats through repressing apoptosis. Mechanistically, circPVT1 functioned as a ceRNA of miR-21-5p, which targeted at the 3'untranslated region of Smad7. CircPVT1 enhancing Smad7 and mitigating GC activated TGFβ/Smad2/3 pathway through inhibiting miR-21-5p. In conclusion, CircPVT1 exerts protective effects against SIONFH via modulating miR-21-5p-mediated Smad7/TGFβ pathway.	NA	J Cell Mol Med. 2021 May;25(10):4608-4622. doi: 10.1111/jcmm.16294. Epub 2021 Mar 18.
3579	LncRNA	ZFPM2-AS1	miR-515-5p	TUSC3	thyroid cancer tissues and cells	Thyroid Cancer	Homo sapiens (human)	ChIP;ELISA;Chromatin immunoprecipitation;Luciferase reporter assay;	33976749	ZFPM2-AS1 transcriptionally mediated by STAT1 regulates thyroid cancer cell growth, migration and invasion via miR-515-5p/TUSC3.	Objective: Our purpose was to study the roles and molecular mechanisms of long non-coding RNA (lncRNA) ZFPM2 Antisense RNA 1 (ZFPM2-AS1) in thyroid cancer. Methods: Firstly, the expression of ZFPM2-AS1, miR-515-5p and TUSC3 was detected in thyroid cancer tissues and cells. Secondary, their biological functions (proliferation, apoptosis, migration and invasion) were analyzed by a serious of functional experiments including cell counting kit-8 (CCK-8), clone formation, 5-Ethynyl-2'-deoxyuridine (EdU), enzyme-linked immunosorbent assay (ELISA), wound healing and Transwell assays. Thirdly, the mechanisms of STAT1/ZFPM2-AS1 and ZFPM2-AS1/miR-515-5p/TUSC were validated using chromatin immunoprecipitation (CHIP), pull-down and luciferase reporter assays. Results: ZFPM2-AS1 and TUSC were both highly expressed and miR-515-5p was down-regulated in thyroid cancer tissues as well as cells. Their knockdown weakened thyroid cancer cell growth, migration, and invasion. ZFPM2-AS1 was mainly distributed in the nucleus and cytoplasm of thyroid cancer cells. Mechanistically, up-regulation of ZFPM2-AS1 was induced by transcription factor STAT1 in line with CHIP and luciferase reporter assays. Furthermore, as a sponge of miR-515-5p, ZFPM2-AS1 decreased the ability of miR-515-5p to inhibit TUSC3 expression by pull-down, luciferase reporter and gain-and-loss assays, thereby promoting malignant progression of thyroid cancer. Conclusion: ZFPM2-AS1 acted as an oncogene in thyroid cancer, which was transcriptionally mediated by STAT1. Furthermore, ZFPM2-AS1 weakened the inhibitory effect of miR-515-5p on TUSC3. Thus, ZFPM2-AS1 could be an underlying biomarker for thyroid cancer.	NA	J Cancer. 2021 Apr 17;12(11):3393-3406. doi: 10.7150/jca.51437. eCollection 2021.
3580	LncRNA	MALAT1	miR-212	SOX6	LPS-treated MG-63 cells	Femoral Neck Fracture Healing	Homo sapiens (human)	CCK-8 assay;ELISA;microarray;qRT-PCR;	33725277	MALAT1 knockdown promoted cell viability and migration of LPS-treated MG-63 cells via sponging miR-212.	BACKGROUND: Most fractures could heal after treatment, around 5-10 % of patients still develop delayed union and nonunion. Evidence has increasingly shown that abnormal expression of long noncoding RNAs is closely related to the occurrence and development of various diseases including fracture healing. However, evidence regarding the effect of MALAT1 on fracture healing remains limited. OBJECTIVES: In this study, we attempt to explore the role of MALAT1 during the process of femoral neck fracture healing and elucidate the underlying mechanism of this disease. METHODS: We first detect the expression of lncRNAs in serums from 3 pairs of patients with delayed femoral neck fracture healing and healthy volunteers using lncRNA microarray. And the expression of long noncoding RNA MALAT1 in serums and LPS-treated MG-63 cells was measured using qRT-PCR. CCK-8 assay, cell migration and qRT-PCR were applied to the role of MALAT1 knockdown in LPS-treated MG-63 cells. ELISA was used for the measurement of inflammatory cytokines in serums of patients and healthy volunteers. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. RESULTS: MALAT1 expression was up-regulated in serum of patients with delayed union of femoral neck fracture. MALAT1 knockdown promoted cell viability and migration, reduced inflammation in LPS-treated MG-63 cells. The bioinformatics analysis showed MALAT1 acts as a molecular sponge for miR-212. And SOX6 was a target of miR-212. Besides, MALAT1 knockdown suppressed SOX6 expression via targeting miR-212 in LPS-treated MG-63 cells. CONCLUSIONS: These data suggest MALAT1 knockdown promoted the biological behavior of LPS-treated MG-63 cells via sponging miR-212, which may provide a new therapeutic avenue for delayed union of femoral neck fracture.	NA	Genes Genomics. 2021 May;43(5):523-531. doi: 10.1007/s13258-021-01038-7. Epub 2021 Mar 16.
3581	LncRNA	MALAT1	miR-146a	CXCR4	AML cells	Acute Myeloid Leukemia	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33382018	Long non-coding RNA MALAT1 modulate cell migration, proliferation and apoptosis by sponging microRNA-146a to regulate CXCR4 expression in acute myeloid leukemia.	OBJECTIVES: To investigate the role of Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in acute myeloid leukemia (AML) and analyze the potential regulatory network of MALAT1/miR-146a/ CXCR4. METHODS: The expressions of MALAT1, miR-146a and CXCR4 were performed by qRT-PCR and Western Blot. We conducted trans-well assay, CCK-8 assay and flow cytometry to evaluate the migration, proliferation and apoptosis of AML cells. Also by using luciferase reporter assay, we investigated the interaction between miR-146a and MALAT1 or CXCR4. RESULTS: Firstly, MALAT1 and CXCR4 were upregulated while miR-146a was downregulated in AML patients compared with healthy controls. We observed a negative correlation between miR-146a and MALAT1 or CXCR4, but a positive correlation between MALAT1 and CXCR4 in AML patients. MALAT1 knockdown inhibited migration and proliferation but induced apoptosis of HL-60 cells. MALAT1 restrained miR-146a expression by acting as a ceRNA. miR-146a regulated HL-60 cells migration, proliferation and apoptosis by directly targeting CXCR4 expression. Finally, we found that CXCR4 expression was downregulated by MALAT1 knockdown and partially restored by miR-146a abrogation. CONCLUSIONS: Our results showed that MALAT1 regulates migration, proliferation and apoptosis by sponging miR-146a to regulate CXCR4 expression in AML cells, providing novel insights into the role of MALAT1 as a therapeutic target in AML.	NA	Hematology. 2021 Dec;26(1):43-52. doi: 10.1080/16078454.2020.1867781.
3582	Circular RNA	Circ-PRKCH	miR-140-3p	ADAM10	LPS-evoked C-28/I2 cells	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33880996	Silencing of circ-PRKCH protects against lipopolysaccharide (LPS)-evoked chondrocyte damage and extracellular matrix loss by the miR-140-3p/ADAM10 axis.	Circular RNAs (circRNAs) have been implicated in the pathology of osteoarthritis (OA). Nevertheless, the precise actions of circRNA protein kinase C eta (circ-PRKCH, hsa_circ_0032131) on OA pathogenesis are still undiscovered. Cell viability and apoptosis were determined using Cell Counting-8 Kit (CCK-8) assay and flow cytometry, respectively. The levels of circ-PRKCH, microRNA (miR)-140- 3p and a-disintegrin and metallopeptidase domain 10 (ADAM10) mRNA were tested by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Targeted interplays among circ- PRKCH, miR-140-3p and ADAM10 were verified by dual-luciferase reporter assay. circ-PRKCH was up-regulated in OA tissues and lipopolysaccharide (LPS)-evoked C-28/I2 cells. circ-PRKCH knockdown alleviated LPS-evoked cell injury and extracellular matrix (ECM) loss in C-28/I2 cells. Mechanistically, circ-PRKCH acted as a miR-140-3p sponge. Moreover, the silencing of circ-PRKCH exerted a protective role in LPS-evoked C-28/I2 cells by up-regulating miR-140-3p. ADAM10 was a direct target of miR- 140-3p, and miR-140-3p overexpression mitigated LPS-evoked C-28/I2 cell injury and ECM loss by down-regulating ADAM10. Furthermore, circ-PRKCH mediated ADAM10 expression via sponging miR-140-3p in C-28/I2 cells. Our present study suggested that circ-PRKCH silencing alleviated LPSevoked chondrocyte injury and ECM loss partially through the miR-140-3p/ADAM10 axis.	NA	Gen Physiol Biophys. 2021 Mar;40(2):89-101. doi: 10.4149/gpb_2021001.
3583	LncRNA	LINC00960	miR-146a-5p	IRAK1	PDAC tissues and cell lines	Pancreatic Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33380238	Long intergenic non-protein coding RNA 960 regulates cancer cell viability, migration and invasion through modulating miR-146a-5p/interleukin 1 receptor associated kinase 1 axis in pancreatic ductal adenocarcinoma.	Long non-coding RNAs (lncRNAs) are considered as crucial regulatory factors in cancer biology. However, the biological function of long intergenic non-protein coding RNA 960 (LINC00960) in the tumorigenesis of pancreatic ductal adenocarcinoma (PDAC) is still unknown. The goal of this study is to investigate the role of LINC00960 in PDAC. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression levels of LINC00960 in PDAC tissues and cell lines. After transfection, the loss-of-function models of LINC00960 or interleukin 1 receptor-associated kinase 1 (IRAK1) were established with BxPC-3 cells and Colo357 cells, and the malignant phenotypes of BxPC-3 cells and Colo357 cells were detected by CCK-8 assay, BrdU assay and Transwell assay, respectively. The interactions among LINC00960, miR-146a-5p and IRAK1 were predicted by bioinformatics analysis, and verified by luciferase reporter assay, RNA immunoprecipitation assay and RNA pull-down assay. The regulatory functions of LINC00960 and miR-146a-5p on IRAK1 were detected by Western blot. We demonstrated that the LINC00960 expression was increased in PDAC tissues and cell lines. Knocking down LINC00960 or IRAK1 could repress the viability, migration, and invasion of BxPC-3 and Colo357 cells. LINC00960 functioned as a molecular sponge for miR-146a-5p, and IRAK1 was verified as a target gene of miR-146a-5p. Additionally, LINC00960 could up-regulate IRAK1 expression via repressing miR-146a-5p, and the oncogenic properties of LINC00960 were partly reversed by miR-146a-5p. Our findings reveal that LINC00960 is a promoter of PDAC progression through regulating miR-146a-5p/IRAK1axis.	NA	Bioengineered. 2021 Dec;12(1):369-381. doi: 10.1080/21655979.2020.1868742.
3584	LncRNA	LHFPL3-AS1	miR-362-5p	CHSY1	OSCC tissues and cell lines	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;	33833527	LncRNA LHFPL3-AS1 Promotes Oral Squamous Cell Carcinoma Growth and Cisplatin Resistance Through Targeting miR-362-5p/CHSY1 Pathway.	BACKGROUND: Oral squamous cell carcinoma (OSCC) is a common oral cancer. The current study aims to elucidate the potential roles of long noncoding RNA (lncRNA) LHFPL3-AS1 in OSCC development. METHODS: Gene expression was measured by qRT-PCR in tumor tissues and cell lines. Loss-of-function assays were performed to analyze the effects of LHFPL3-AS1 on malignant behaviors. Bioinformatics analysis was conducted to explore the downstream signaling pathway of LHFPL3-AS1 in OSCC. RESULTS: LHFPL3-AS1 was highly expressed in OSCC tissues and cell lines. LHFPL3-AS1 was upregulated in cisplatin-resistant tumor cell lines. LHFPL3-AS1 level was correlated with survival rate. LHFPL3-AS1 knockdown suppressed OSCC proliferation, migration and invasion. LHFPL3-AS1 downregulation reduced cisplatin resistance of OSCC cells. LHFPL3-AS1 was the competing endogenous RNA (ceRNA) for miR-194-5p to enhance CHSY1 expression. CONCLUSION: LHFPL3-AS1/miR-362-5p/CHSY1 signaling pathway plays essential roles in regulating OSCC development and cisplatin resistance.	NA	Onco Targets Ther. 2021 Mar 31;14:2293-2300. doi: 10.2147/OTT.S298679. eCollection 2021.
3585	Circular RNA	Circ_0001445	miR-127-5p	SNX5	Glioma cells	Glioma	Homo sapiens (human)	Cell transfection;Cell transfection;Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;luciferase assay;RNA sequencing;	33982667	Exosomal circRNA 0001445 promotes glioma progression through miRNA-127-5p/SNX5 pathway.	BACKGROUND: Glioma is one of the most wide-spreading brain cancers worldwide. Exosomes have emerged as essential regulators in intercellular communication, and exosomal circular RNAs (circRNAs) are critical for cancer progression. In this study, we aimed to investigate the role of exosomal circRNAs in glioma progression and associated mechanisms. METHODS: Exosomes derived from glioma cells were isolated and identified by transmission electron microscopy and nanoparticle tracking analysis (NTA). CCK-8, wound healing assays, transwell invasion assays, and flow cytometry assays were performed to assess glioma progression. RNA sequencing, RT-qPCR, western blotting, fluorescence in situ hybridization assay, luciferase assays, and cell transfection assay were performed to investigate related molecular mechanisms. RESULTS: The results demonstrated that exosomes derived from glioma cells promoted glioma progression. Also, exosomal circRNA 0001445 was taken up and upregulated in glioma cells treated with exosomes. In addition, exosomal circRNA 0001445 acted as a sponge for miRNA-127-5p to upregulate the expression of sorting nexin 5 (SNX5). Lastly, the effect of exosomal circRNA 0001445 was mediated by miRNA-127-5p/ SNX5 signaling pathway. CONCLUSION: These results demonstrated that exosomal circRNA 0001445 promoted glioma progression through miRNA-127-5p/SNX5 signaling pathway. This study provides a novel understanding of the molecular mechanism of glioma progression.	NA	Aging (Albany NY). 2021 May 12;13(9):13287-13299. doi: 10.18632/aging.203013. Epub 2021 May 12.
3586	LncRNA	AGAP2-AS1	miR-628-5p	KLF12	PTC tissues and cell ines	Papillary Thyroid Cancer 	Homo sapiens (human)	qRT-PCR	33604734	Long non-coding RNA AGAP2-AS1 promotes proliferation and metastasis in papillary thyroid cancer by miR-628-5p/KLF12 axis.	Long non-coding RNA (lncRNA) AGAP2-AS1 acts as an oncogene in several types of cancers. However, the role and mechanism of AGAP2-AS1 in papillary thyroid carcinoma (PTC) remain unclear. Thus, in this study, we aimed to explore the role of AGAP2-AS1 in PTC. Our results showed that AGAP2-AS1 was significantly upregulated in PTC tissues. Knockdown of AGAP2-AS1 inhibited the proliferation, migration and invasion of PTC cells. In vivo experiment showed that AGAP2-AS1 knockdown inhibited the tumorigenesis of PTC. MiR-628-5p was found to act as a target miRNA of AGAP2-AS1 in PTC. The expression level of miR-628-5p in PTC tissues was negatively associated with that of AGAP2-AS1. Inhibition of miR-628-5p attenuated the effects of AGAP2-AS1 knockdown on PTC. Moreover, miR-628-5p directly bound to the 3'UTR of KLF12 and inhibited the expression of KLF12. Knockdown of KLF12 enhanced the inhibitory effects of miR-628-5p on PTC cell proliferation and metastasis. In conclusion, these findings indicated that AGAP2-AS1 exerted an oncogenic role in PTC progression and metastasis. The effects of AGAP2-AS1 might be mediated by the regulation of miR-628-5p/KLF12 axis.	NA	J Bioenerg Biomembr. 2021 Apr;53(2):235-245. doi: 10.1007/s10863-021-09879-3. Epub 2021 Feb 18.
3587	LncRNA	AK020546	miR-350-3p	ErbB3	heart tissues	Cardiac Ischemia Reperfusion Injury	Homo sapiens (human)	qRT-PCR	33988127	LncRNA AK020546 protects against cardiac ischemia-reperfusion injury by sponging miR-350-3p.	Long non-coding RNAs (lncRNAs) have been implicated in the development of cardiovascular diseases. We observed that lncRNA AK020546 was downregulated following ischemia/reperfusion injury to the myocardium and following H(2)O(2) treatment in H9c2 cardiomyocytes. In vivo and in vitro studies showed that AK020546 overexpression attenuated the size of the ischemic area, reduced apoptosis among H9c2 cardiomyocytes, and suppressed the release of reactive oxygen species, lactic acid dehydrogenase, and malondialdehyde. AK020546 served as a competing endogenous RNA for miR-350-3p and activated the miR-350-3p target gene ErbB3. MiR-350-3p overexpression reversed the effects of AK020546 on oxidative stress injury and apoptosis in H9c2 cardiomyocytes. Moreover, ErbB3 knockdown alleviated the effects of AK020546 on the expression of ErbB3, Bcl-2, phosphorylated AKT, cleaved Caspase 3, and phosphorylated Bad. These findings suggest lncRNA AK020546 protects against ischemia/reperfusion and oxidative stress injury by sequestering miR-350-3p and activating ErbB3, which highlights its potential as a therapeutic target for ischemic heart diseases.	NA	Aging (Albany NY). 2021 May 13;13(10):14219-14233. doi: 10.18632/aging.203038. Epub 2021 May 13.
3588	LncRNA	BCAR4	miR-139-3p	ELAVL1	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	33602031	Long non-coding RNA BCAR4 aggravated proliferation and migration in esophageal squamous cell carcinoma by negatively regulating p53/p21 signaling pathway.	Long non-coding RNA breast cancer antiestrogen resistance 4 (lncRNA BCAR4) is an independent factor on the survival prognosis of patients with multiple cancers. However, the role of lncRNA BCAR4 in esophageal squamous cell cancer (ESCC) remains unknown. Here, we unraveled that lncRNA BCAR4 was upregulated in ESCC and predicted poor prognosis. Functionally, lncRNA BCAR4 knockdown induced cell apoptosis and G1/S arrest, while inhibited cell proliferation and migration in vitro; conversely, overexpressing lncRNA BCAR4 promoted proliferation and metastasis. Mechanistically, lncRNA BCAR4 sponged miR-139-3p to upregulate ELAVL1, thereby inhibiting p53/p21 pathway in ESCC cells. In conclusion, lncRNA BCAR4 promotes ESCC tumorigenesis via regulating p53/p21 signaling pathway and develops a brand-new biomarker and medicine target for ESCC.	NA	Bioengineered. 2021 Dec;12(1):682-696. doi: 10.1080/21655979.2021.1887645.
3589	LncRNA	BLACAT1	miR-29a-3p	DVL3	prostate cancer tissues and cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33641528	LncRNA BLACAT1 Promotes Proliferation, Migration and Invasion of Prostate Cancer Cells via Regulating miR-29a-3p/DVL3 Axis.	BACKGROUND: Long non-coding RNA bladder cancer associated transcript 1 (BLACAT1) is oncogenic in several types of cancers. However, little is known concerning its expression and function in prostate cancer. METHODS: Paired prostate cancer samples were collected, and the expression levels of BLACAT1, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR); BLACAT1 shRNAs were transfected into PC-3 and LNCaP cell lines, and proliferative ability was detected by cell counting kit-8 (CCK-8) assay; qRT-PCR and Western blot were used to analyze the changes of miR-29a-3p and DVL3; dual-luciferase reporter gene assay was used to determine the regulatory relationships between miR-29a-3p and BLACAT1, and miR-29a-3p and DVL3. RESULTS: BLACAT1 expression was significantly up-regulated in cancerous tissues of prostate cancer samples and positively correlated with the expression of DVL3, while negatively associated with miR-29a-3p. After the transfection of BLACAT1 shRNAs into prostate cancer cells, the proliferative ability and metastatic ability of cancer cells were significantly inhibited; BLACAT1 shRNAs could reduce the expression of DVL3 on both mRNA and protein expressions levels, the luciferase activity of BLACAT1 reporter was inhibited by miR-29a-3p, and DVL3 was validated as a target gene of miR-29a-3p. CONCLUSION: BLACAT1 expression is abnormally up-regulated in prostate cancer tissues. BLACAT1 can modulate the proliferative and metastatic ability of prostate cancer cells and have the potential to be the "ceRNA" to regulate the expression of DVL3 by sponging miR-29a-3p.	NA	Technol Cancer Res Treat. 2021 Jan-Dec;20:1533033820972342. doi: 10.1177/1533033820972342.
3590	LncRNA	BLACAT2	miR-193b-5p	METTL3	GC cells	Gastric Cancer	Homo sapiens (human)	Luciferase reporter assay;	33976730	Longnon-coding RNA BLACAT2 promotes gastric cancer progression via the miR-193b-5p/METTL3 pathway.	Gastric cancer is one of the leading prevalent and malignant cancers worldwide, especially in east Asia. However, the in-depth molecular mechanism underlying gastric cancer progression remains uncertain. Recently, studies have identified that long non-coding RNA (lncRNA) could play critical roles in the tumorigenesis of multiple types of cancer. Studies on long non-coding RNA BLACAT2 have proven that it participates in bladder cancer and colorectal cancer regulation and was identified as highly expressed using the cBioPortal for Cancer Genomics in gastric cancer. However, the precise function of lncRNA-BLACAT2 in the carcinogenesis and progression of gastric cancer remains largely unexplored. Our study discovered that lncRNA-BLACAT2 was significantly upregulated in gastric cancer. Different studies have illustrated that BLACAT2 promoted gastric cancer progression through regulating proliferation, migration, invasion, and apoptosis in terms of biological function. Furthermore, BLACAT2 was verified to perform its function through interaction with miR-193b-5p using a luciferase reporter assay. On the other hand, MiR-193b-5p specific inhibitor treatment reversed the inhibitory effect of BLACAT2 on cell biological functions. Additional studies also discovered that Methyltransferase Like 3 (METTL3) was the downstream target of miR-193b-5p. Subsequently, restoration of METTL3 eliminated the suppressive effect of proliferation or the promotive effect of apoptosis caused by BLACAT2 knockdown. To sum up, these experimental results demonstrated that BLACAT2 acted as an oncogene in gastric cancer progression through the regulation of the miR-193b-5p/METTL3 pathway, hence providing new insights regarding the pathogenesis of gastric cancer.	NA	J Cancer. 2021 Apr 2;12(11):3209-3221. doi: 10.7150/jca.50403. eCollection 2021.
3591	LncRNA	BX357664	miR-183a-3p	PTEN	GC cell lines	Gastric Cancer	Homo sapiens (human)	microarray;qPCR;RT-qPCR;	33607219	Long non-coding RNA BX357664 inhibits gastric cancer progression by sponging miR-183a-3p to regulate the PTEN expression and PI3K/AKT pathway.	Lately, long non-coding RNA (lncRNA) is recognized as a key regulator of gastric cancer (GC) which has aroused great interest in the fields of medicine, toxicology, and functional food. Studies related to LncRNA expression microarray data indicate that BX357664 is down-regulated in GC specimens. However, the expression pattern and molecular mechanism of BX357664 in GC have not been studied so far. The purpose of this study was to investigate the expression of lncRNA BX357664 in GC and its function in GC cell lines. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the level of BX357664 in 50 pairs of cancer tissues and adjacent non-cancer tissues collected from GC patients. It was found that BX357664 level was lowered in cancer specimens than adjacent non-cancer tissues and correlated with tumor size and TNM stage. Also, we used cell counting kit 8 (CCK8), cell clone formation assay and transwell assay, which affirmed that up-regulation of BX357664 inhibited the proliferation, migration, and invasion of GC cells, but promoted apoptosis. In the dual-luciferase report analysis, BX357664 acted as a miR-183-3p ceRNA to target and regulate the expression of PTEN and affect the PI3K/AKT pathway. These results indicate that BX357664 can inhibit the proliferation and metastasis of GC through the miR-183-3p/PTEN/PI3K/AKT pathway, which may serve as potential targets for the treatment of GC in the future.	NA	Food Chem Toxicol. 2021 Apr;150:112069. doi: 10.1016/j.fct.2021.112069. Epub 2021 Feb 17.
3592	LncRNA	CDKN2B-AS1	miR-133	GDNF	neural cells	NA	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;	34150056	Regulation of glial cell-derived neurotrophic factor in sevoflurane-induced neuronal apoptosis by long non-coding RNA CDKN2B-AS1 as a ceRNA to adsorb miR-133.	OBJECTIVE: To investigate the regulatory mechanism of sevoflurane-induced neuronal apoptosis through analyzing the expression of glial cell-derived neurotrophic factor (GDNF) mediated by miR-133, sponged by long non-coding RNA (lncRNA) CDKN2B-AS1. METHODS: An in vitro cell injury model was established by using different concentrations of sevoflurane and primary hippocampal neurons. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8); caspase-3 and caspase-9 activities were detected by colorimetry, and apoptotic cells were determined by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Fluorescence in situ hybridization (FISH) analysis was used to detect localized expression of CDKN2B antisense RNA 1 (CDKN2B-AS1), and dual-luciferase reporter assay was employed to verify the correlation of CDKN2B-AS1 and miR-133, and of miR-133 and GDNF. The expression of CDKN2B-AS1, miR-133, and GDNF mRNA in the cell injury model were measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Western blot was utilized to detect the expression of GDNF protein in the cell injury model. RESULTS: In the cell injury model, CDKN2B-AS1 was highly expressed in the cytoplasm, and CDKN2B-AS1 and GDNF were downregulated and miR-133 was upregulated as detected by qRT-PCR (all P<0.05). The connections between CDKN2B-AS1 and miR-133, and between miR-133 and GDNF were confirmed. That is, CDKN2B-AS1 regulated the expression of GDNF by adsorbing miR-133 (all P<0.05). In cells treated with sevoflurane, overexpression of CDKN2B-AS1 could inhibit caspase-3 and caspase-9 activities and the degree of apoptosis. miR-133 could partially alleviate the effect of overexpressing CDKN2B-AS1 on cells, and si-GDNF the effect of miR-133 inhibitor (all P<0.05). CONCLUSION: lncRNA CDKN2B-AS1 can up-regulate the expression of GDNF, inhibit neuronal apoptosis, and ease the toxic effect of sevoflurane on neural cells by acting as a sponge to adsorb miR-133.	NA	Am J Transl Res. 2021 May 15;13(5):4760-4770. eCollection 2021.
3593	LncRNA	CDKN2B-AS1	miR-424-5p	AKT3	ectopic, eutopic endometria and normal endometrial tissues.	Endometriosis 	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33820740	Effects of CDKN2B-AS1 on cellular proliferation, invasion and AKT3 expression are attenuated by miR-424-5p in a model of ovarian endometriosis.	RESEARCH QUESTION: Endometriosis is a common and complicated gynaecologic disease. Long non-coding RNA CDKN2B-AS1 plays a crucial role in the development and progression of several cancers. Whether CDKN2B-AS1 contributes to endometriosis, however, remains unknown. DESIGN: Cellular proliferation, invasion and DNA synthesis abilities were assessed by CCK8, transwell and 5-ethynyle-2'-deoxyuridine assays. The expression of epithelial-mesenchymal transition markers and three isoforms of AKT was detected using Western blot. Real-time polymerase chain reaction was used to determine the relative expression levels of CDKN2B-AS1 and candidate miRNAs in ectopic, eutopic endometria and normal endometrial tissues. The relationship between CDKN2B-AS1 and miRNA was determined by luciferase reporter assays. RESULTS: The relative expression level of CDKN2B-AS1 was up-regulated in eutopic and ectopic endometria. In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin. miR-424-5p was confirmed the target of CDKN2B-AS1 through bioinformatics tools and luciferase reporter assays. In addition, the enhanced effect of cellular phenotype of CDKN2B-AS1 overexpression was significantly attenuated by miR-424-5p overexpression. Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. Mechanistically, CDKN2B-AS1 acts as a ceRNA by sponging miR-424-5p and targets AKT3. CONCLUSIONS: The cellular mechanism of CDKN2B-AS1 in endometriosis was confirmed; CDKN2B-AS1 may be a potential target for ovarian endometriosis therapy.	NA	Reprod Biomed Online. 2021 Jun;42(6):1057-1066. doi: 10.1016/j.rbmo.2021.02.004. Epub 2021 Feb 12.
3594	Circular RNA	Circ_0000003	miR-330-3p	GLS	TSCC tissues and cell lines	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR	33649795	Circ_0000003 regulates glutamine metabolism and tumor progression of tongue squamous cell carcinoma via the miR-330-3p/GLS axis.	Various circular RNAs (circRNAs) have been shown to exert vital functions in tongue squamous cell carcinoma (TSCC). However, their roles in TSCC progression remain to be elucidated. This research aimed to investigate the role and mechanism of hsa_circ_0000003 (circ_0000003) in TSCC progression. Here, we found that circ_0000003 expression was upregulated in TSCC tissues and cell lines, and high circ_0000003 expression was correlated with advanced TNM stage, increased tumor size and poor patient survival. Circ_0000003 was revealed to facilitate cell proliferation, migration and invasion of TSCC cells. Mechanistically, we found that circ_0000003 acted as a competing endogenous RNA (ceRNA) that sponged miR-330-3p, thereby elevating glutaminase (GLS) expression. Accordingly, cell invasion, migration, glutamine consumption, α-ketoglutarate (α-KG) production and ATP production were significantly decreased by circ_0000003 knockdown in TSCC cells, and these effects were reversed by miR-330-3p inhibition. In conclusion, circ_0000003 facilitates TSCC cell proliferation, migration, invasion and glutamine catabolism by regulating the miR-330-3p/GLS pathway.	NA	Oncol Rep. 2021 Apr;45(4):45. doi: 10.3892/or.2021.7996. Epub 2021 Mar 2.
3595	Circular RNA	Circ_0000629	miR-1290	CDC73	BC tissues and cells	Bladder Cancer	Homo sapiens (human)	FISH;microarray;FISH;	33790645	Circular RNA_0000629 Suppresses Bladder Cancer Progression Mediating MicroRNA-1290/CDC73.	BACKGROUND: Recent studies showed circular RNAs (circRNAs) played regulatory roles in bladder cancer (BC). However, the relevance of circ_0000629, a newly identified circRNA, has not been determined yet. We aimed to characterize the function of circ_0000629 in BC and the relevant mechanism. METHODS: First, we downloaded circRNA-related microarrays GSE147985 and GSE92675 from the GEO database, followed by a validation in our clinically obtained samples. We then overexpressed circ_0000629 in T24 and SW780 cells and evaluated the effects of circ_0000629 on BC cell proliferatory, apoptotic, and metastatic abilities. We further detected the subcellular localization of circ_0000629 in T24 and SW780 cells by the fractionation and export assay and FISH experiments. Integrated microarray analyses and bioinformatics website prediction were utilized to screen out the downstream microRNA (miRNA)/mRNA. The effects of miR-1290 and CDC73 on BC cell growth and metastasis was verified by functional rescue experiments. In addition, mice xenografts were built to measure the effect of circ_0000629 on tumor growth in vivo. RESULTS: Circ_0000629 and CDC73 were reduced, and miR-1290 was significantly overexpressed in BC tissues and cells. Moreover, circ_0000629 significantly inhibited the development and metastasis of BC cells, but further overexpression of miR-1290 or knockdown of CDC73 attenuated the inhibitory effect of circ_0000629 on BC cells. Circ_0000629 localized in the cytoplasm and regulated CDC73 expression by sponging miR-1290. Further, overexpressed circ_0000629 reduced the BC tumor growth in vivo. CONCLUSION: Circ_0000629 promotes the expression of CDC73 by competitively binding to miR-1290, thereby inhibiting the growth and metastasis of BC cells.	NA	Cancer Manag Res. 2021 Mar 22;13:2701-2715. doi: 10.2147/CMAR.S292863. eCollection 2021.
3596	Circular RNA	Circ_0003266	miR-503-5p	PDCD4	CRC tissues / adjacent tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33726686	Circ_0003266 sponges miR-503-5p to suppress colorectal cancer progression via regulating PDCD4 expression.	BACKGROUND: Circular RNAs (circRNAs) feature prominently in tumor progression. However, the biological function and molecular mechanism of circ_0003266 in colorectal cancer (CRC) require further investigation. METHODS: Circ_0003266 expression in 46 pairs CRC tissues / adjacent tissues, and CRC cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR); after circ_0003266 was overexpressed or knocked down in CRC cells, cell proliferation, apoptosis, migration, and invasion were evaluated by the cell counting kit-8 (CCK-8), flow cytometry, and Transwell assays, respectively; the interaction among circ_0003266, miR-503-5p, and programmed cell death 4 (PDCD4) was confirmed using bioinformatics analysis and dual-luciferase reporter assay; PDCD4 protein expression in CRC cells was quantified using Western blot. RESULTS: Circ_0003266 was significantly lowly expressed in CRC tissues and cell lines. Circ_0003266 overexpression markedly repressed CRC cell proliferation, migration, and invasion, and accelerated the cell apoptosis, but its overexpression promoted the malignant phenotypes of CRC cells. PDCD4 was a direct target of miR-503-5p and circ_0003266 promoted PDCD4 expression by competitively sponging miR-503-5p. CONCLUSION: Circ_0003266 suppresses the CRC progression via sponging miR-503-5p and regulating PDCD4 expressions, which suggests that circ_0003266 may serve as a novel target for the treatment of CRC.	NA	BMC Cancer. 2021 Mar 16;21(1):284. doi: 10.1186/s12885-021-07997-0.
3597	Circular RNA	Circ_0005774	miR-192-5p	ULK1	AML cells (HL-60,NB4)	Acute Myeloid Leukemia	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33735626	Circular RNA circ_0005774 contributes to proliferation and suppresses apoptosis of acute myeloid leukemia cells via circ_0005774/miR-192-5p/ULK1 ceRNA pathway.	Circular RNAs (circRNAs) and microRNAs (miRNAs) have been emerging as new players in acute myeloid leukemia (AML). Hsa_circ_0005774 (circ_0005774) is an upregulated circRNA in pediatric AML, while its role is uncovered. Thus, we intended to measure the function and mechanism of circ_0005774 in AML leukemogenesis. Real time-quantitative PCR revealed that circ_0005774 was highly expressed in blood of pediatric AML patients and AML cells (HL-60 and NB4), accompanied with downregulated miRNA-192-5p (miR-192-5p) which was a crucial tumor-associated and leukemia-related miRNA. Circ_0005774 was abundant in miRNA response element according to CSCD software, and miR-192-5p was identified as a target of circ_0005774, as evidenced by RNA immunoprecipitation and dual-luciferase reporter assays. Cell viability assay, flow cytometry and western blotting were performed to measure cell functions. Accordingly, blocking circ_0005774 and/or overexpressing miR-192-5p could enhance apoptosis rate of HL-60 and NB4 cells, but suppress cell viability and cell cycle entrance, accompanied with depression of proliferation markers including proliferating cell nuclear antigen (PCNA), CyclinD1 and B cell lymphoma 2 (Bcl-2). Meanwhile, depleting miR-192-5p counteracted the role of circ_0005774 knockdown in AML cells. Uncoordinated 51-like kinase 1 (ULK1) was previously demonstrated to be associated with diagnosis, prognosis and therapeutic strategy for AML, and restoring ULK1 could abrogate miR-192-5p overexpression-induced effects in HL-60 and NB4 cells. Notably, ULK1 was a downstream target of miR-192-5p and indirectly modulated by circ_0005774. In conclusion, circ_0005774 knockdown repressed cell proliferation and promoted apoptosis of AML cells partially through regulating miR-192-5p/ULK1 axis.	NA	Biochem Biophys Res Commun. 2021 Apr 30;551:78-85. doi: 10.1016/j.bbrc.2021.02.058. Epub 2021 Mar 15.
3598	Circular RNA	Circ_0084927	miR-142-3p	ERC1	BC cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34150003	Circular RNA circ_0084927 regulates proliferation, apoptosis, and invasion of breast cancer cells via miR-142-3p/ERC1 pathway.	OBJECTIVE: We aimed to investigate the mechanism of circular RNA circ_0084927 in the progression of breast cancer (BC). METHODS: The levels of circ_0084927, miR-142-3p, and ELKS/RAB6-interacting/CAST family member-1 (ERC1) mRNA in the BC tissues and cells were detected by qRT-PCR. CCK8, colony formation, Transwell, and flow cytometry assays were performed to examine the cell proliferation, colony formation, cell invasion, and apoptosis, respectively, in the BC cells with regulated expressions of circ_0084927, miR-142-3p, and ERC1. RNase R treatment was employed to verify the circular structure of circ_0084927. Nucleocytoplasmic separation experiment, bioinformatics analysis, dual-luciferase reporter assay, and RNA immunoprecipitation were performed to investigate the ceRNA mechanism of circ_0084927. RESULTS: High levels of circ_0084927 and ERC1 and low levels of miR-142-3p were detected in the BC tissues and cells. Knockdown of circ_0084927 promoted apoptosis and inhibited proliferation, colony formation, and invasion of BC cells (all P<0.05), whereas overexpression of circ_0084927 in the BC cells achieved the opposite effects. miR-142-3p is the target of circ_0084927. Overexpression of miR-142-3p could inhibit BC cell proliferation, colony formation, and cell invasion and induce apoptosis of the BC cells (all P<0.05), and the effects of miR-142-3p knockout on the BC cells could be reversed by silencing circ_0084927. miR-142-3p could target ERC1. Both ERC1 silencing and circ_0084927 knockout in the BC cells could achieve the tumor-suppressing effect, and this effect could be more remarkable under simultaneous ERC1 silencing and circ_0084927 knockout (all P<0.05). CONCLUSION: Circ_0084927 can promote the progression of BC by regulating the miR-142-3p/ERC1 axis.	NA	Am J Transl Res. 2021 May 15;13(5):4120-4136. eCollection 2021.
3599	Circular RNA	Circ-0079593	miR-433	EGFR	melanoma cell line	Melanoma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33577032	Circ-0079593 promotes proliferation and migration of melanoma cells by sponging microRNA-433 and elevating EGFR expression.	OBJECTIVE: The aim of this study was to analyze the biological effects of circ-0079593 and its potential mechanism in the progression of melanoma. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to detect circ-0079593 expression in melanoma tissue samples and cell lines, and the relationship between circ-0079593 expression and prognosis of patients with melanoma was analyzed based on collected clinical information. Then, the melanoma cell line stably overexpressing circ-0079593 was constructed using lentiviral stable transfection technique, and then, Cell Counting Kit-8 (CCK-8) and transwell assays were carried out to detect the proliferation rate, migration, as well as invasion abilities of melanoma cells, respectively. In addition, the potential binding targets of circ-0079593 were searched through bioinformatics analysis, and the results were verified by Dual-Luciferase assay. RESULTS: It was found that, in comparison with the normal control group, circ-0079593 showed a significantly high expression in melanoma tissues and cell lines, which predicted a poor prognosis of melanoma patients. In vitro experiments showed that the overexpression of circ-0079593 remarkably enhanced proliferation rate, as well as invasion ability of melanoma cells. Moreover, bioinformatics data analysis revealed that there exist binding sites of microRNA-433 both in circ-0079593 and EGFR. Meanwhile, the results of the Luciferase assay confirmed that circ-0079593 probably bound to microRNA-433, as an endogenous competitive RNA (ceRNA), to regulate EGFR expression. At last, cell reverse experiments demonstrated that the overexpression of microRNA-433 could attenuate the capacity of melanoma cells to proliferate and migrate, while simultaneous overexpression of circ-0079593 partially restored those cell functions. CONCLUSIONS: In melanoma, circ-0079593 may serve as a cancer-promoting gene to accelerate the rates of cell proliferation and migration, which may exert its effects by elevating EGFR expression by binding to microRNA-433.	NA	Eur Rev Med Pharmacol Sci. 2021 Jan;25(2):779-786. doi: 10.26355/eurrev_202101_24639.
3600	Circular RNA	Circ-AASDH	miR-140-3p	E2F7	LUAD tissues and cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;RNA pull-down;	33569293	Circ-AASDH functions as the progression of early stage lung adenocarcinoma by targeting miR-140-3p to activate E2F7 expression.	BACKGROUND: Lung adenocarcinoma (LUAD), which is the most common subtype of non-small cell lung cancer, is a leading course of cancer-related mortality worldwide. Recently, circular RNA (CircRNAs) has become a hot spot in cancer research because of its important role in tumorigenesis and development and its superior stability. This study aims to clarify the role of circ-AASDH in LUAD and explore its competitive endogenous RNA mechanism. METHODS: The circ-AASDH, miR-140-3p and E2F transcription factor 7 (E2F7) mRNA expression levels were detected via qRT-PCR. CCK-8 and colony formation assay were used to evaluate the ability of cell proliferation. Transwell assay and wound healing assay were performed to measure the invasion and migration ability. Flow cytometry was used to detect the apoptosis of cells. Moreover, Sanger sequencing, RNaseR treatment and divergent primers were used to verify the circular structure. Luciferase reporter and RNA pull-down experiment were performed to characterize the ceRNA mechanism of circ-AASDH. The xenograft model of mice was established to investigate the tumorigenicity of circ-AASDH to LUAD in vivo. RESULTS: By screening for differentially expressed circRNAs, we found that circ-AASDH was highly expressed in LUAD tissues and cells and correlated with tumor size, clinical stage and poor prognosis. Transfection of si-circ-AASDH can inhibit the proliferation and migration of LUAD cells and promote apoptosis in vitro. In mechanism, circ-AASDH could be used as a sponge of miR-140-3p to weaken its inhibition on the expression of E2F7. Additionally, the overexpression of circ-AASDH could deduce the suppression of miR-140-3p on the malignant progression of LUAD cells. Besides, silencing of circ-AASDH inhibited cell proliferation and migration by regulating the expression of E2F7. Furthermore, overexpression of circ-AASDH can promote the growth of LUAD in vivo. CONCLUSIONS: Circ-AASDH/miR-140-3p/E2F7 regulating axis promoted the progression in LUAD. Our results provided ideas for understanding the biological mechanism of circ-AASDH and clarify potential therapeutic targets in LUAD.	NA	Transl Lung Cancer Res. 2021 Jan;10(1):57-70. doi: 10.21037/tlcr-20-1062.
3601	Circular RNA	Circ-ASPH	miR-599	AR	GM tissues and cells(LN229 and U87MG)	Glioma	Homo sapiens (human)	microarray;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;RNA pull-down;	33777211	Upregulation of circ-ASPH contributes to glioma cell proliferation and aggressiveness by targeting the miR-599/AR/SOCS2-AS1 signaling pathway.	Glioma (GM) is the most common type of malignant brain tumor with a high recurrence rate. Circular RNAs (circRNAs) play a key role in mediating tumorigenesis. However, the functions and mechanisms of circRNAs in GM are still not fully understood. A circRNA microarray was performed to identify differentially expressed circRNAs in GM and non-cancerous specimens. Reverse transcription-quantitative PCR was used to detect circ-aspartyl/asparaginyl β-hydroxylase (ASPH) expression in GM tissues and cells. The clinical importance of circ-ASPH was investigated using Kaplan-Meier analysis. The functions of circ-ASPH were investigated in LN229 and U87MG cells. Bioinformatics, RNA immunoprecipitation, RNA pull-down and luciferase reporter assays were used to explore the mechanisms of circ-ASPH in GM. circ-ASPH levels were upregulated in GM specimens and cells. The prognostic role of circ-ASPH was identified in patients with GM. Loss/gain of function assays demonstrated that circ-ASPH increased cell proliferation, migration and invasion in GM cells. Mechanistically, circ-ASPH counteracted microRNA (miR)-599-mediated androgen receptor (AR) suppression by acting as a sponge for miR-599. Rescue assays indicated that circ-ASPH facilitated cell progression by regulating AR expression. Moreover, AR activated long non-coding RNA suppressor of cytokine signaling 2-antisense RNA 1 (SOCS2-AS1) expression in GM cells. Taken together, circ-ASPH/miR-599/AR/SOCS2-AS1 signaling may be a promising biomarker/therapeutic target for GM.	NA	Oncol Lett. 2021 May;21(5):388. doi: 10.3892/ol.2021.12649. Epub 2021 Mar 17.
3602	Circular RNA	CircDtx1	miR-15a-5p	TRIF	teleost fish	NA	Homo sapiens (human)	FISH;FISH;	33735323	Circular RNA circDtx1 regulates IRF3-mediated antiviral immune responses through suppression of miR-15a-5p-dependent TRIF downregulation in teleost fish.	Circular RNAs (circRNAs) represent a class of widespread and diverse covalently closed circular endogenous RNAs that exert crucial functions in regulating gene expression in mammals. However, the function and regulation mechanism of circRNAs in lower vertebrates are still unknown. Here, we discovered a novel circRNA derived from Deltex E3 ubiquitin ligase 1 (Dtx1) gene, namely, circDtx1, which was related to the antiviral responses in teleost fish. Results indicated that circDtx1 played essential roles in host antiviral immunity and inhibition of SCRV replication. Our study also found a microRNA miR-15a-5p, which could inhibit antiviral immune response and promote viral replication by targeting TRIF. Moreover, we also found that the antiviral effect inhibited by miR-15a-5p could be reversed with the circDtx1. In mechanism, our data revealed that circDtx1 was a competing endogenous RNA (ceRNA) of TRIF by sponging miR-15a-5p, leading to activation of the NF-κB/IRF3 pathway, and then enhancing the innate antiviral responses. Our results indicated that circRNAs played a regulatory role in immune responses in teleost fish.	NA	PLoS Pathog. 2021 Mar 18;17(3):e1009438. doi: 10.1371/journal.ppat.1009438. eCollection 2021 Mar.
3603	Circular RNA	CircFAT1	miR-30e-5p	USP22	NSCLC tissues and cell lines(A549,H1299)	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33884267	circRNA circFAT1(e2) Elevates the Development of Non-Small-Cell Lung Cancer by Regulating miR-30e-5p and USP22.	BACKGROUND: As a newly discovered regulatory RNA, circular RNA (circRNA) has become a hot spot in many tumor pieces of research. In recent years, it has been discovered that circRNAs have multiple biological effects in different stages of cancer. However, the expression pattern and mechanism of circFAT1(e2) in non-small-cell lung cancer (NSCLC) are still unclear. METHODS: The expressions of circFAT1(e2) in NSCLC tissues and cell lines were studied. Functionally, CCK-8 and transwell experiments were performed in A549 and H1299. In addition, we also performed a dual-luciferase report analysis to clarify the mechanism of action of circFAT1(e2). RESULTS: circFAT1(e2) was significantly upregulated in NSCLC tissues and cell lines. circFAT1(e2) gene knockdown could significantly inhibit the proliferation, migration, and invasion of NSCLC cells. Loss of function testing found that circFAT1(e2) functioned as an oncogene in NSCLC cells. In addition, circFAT1(e2) acted as a ceRNA to spongy miR-30e-5p, which led to the increase in USP22 and promoted cell growth. CONCLUSIONS: The circFAT1(e2)-miR-30e-5p-USP22 axis is a crucial part of the progression of NSCLC. This study suggests that circFAT1(e2) may be an important potential of prognostic prediction and treatment targets for NSCLC patients.	NA	Biomed Res Int. 2021 Apr 2;2021:6653387. doi: 10.1155/2021/6653387. eCollection 2021.
3604	Circular RNA	Circ-KIAA0907	miR-96-5p	UNC13C	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RACE;RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33715625	Circ-KIAA0907 inhibits the progression of oral squamous cell carcinoma by regulating the miR-96-5p/UNC13C axis.	BACKGROUND: Circular RNA (circRNA) plays an important role in regulating cell biological function and has been shown to be involved in cancer progression, including oral squamous cell carcinoma (OSCC). Circ-KIAA0907 has been found to play an anti-cancer role in OSCC, so it is worth exploring more functions and new mechanisms of circ-KIAA0907 in OSCC progression. METHODS: Quantitative real-time PCR (qRT-PCR) was used to detect the expression of circ-KIAA0907, microRNA (miR)-96-5p, and unc-13 homolog C (UNC13C). Transwell assay, flow cytometry, and colony formation assay were employed to measure the migration, invasion, apoptosis, and radiosensitivity of cells. Besides, glucose uptake, lactate production, and extracellular acidification rate (ECAR) were determined to evaluate the glycolysis ability of cells. Dual-luciferase reporter assay and RIP assay were performed to confirm the interactions among circ-KIAA0907, miR-96-5p, and UNC13C. And RNA pull-down assay was used to verify the binding degree of miR-96-5p to its targets. Moreover, UNC13C protein level was examined using western blot (WB) analysis. OSCC xenograft models were constructed to perform in vivo experiments. RESULTS: Circ-KIAA0907 was a stability circRNA with lowly expression in OSCC. Overexpressed circ-KIAA0907 could inhibit migration, invasion, and glycolysis, while promoting apoptosis and radiosensitivity in OSCC cells. In the terms of mechanism, circ-KIAA0907 could sponge miR-96-5p to regulate UNC13C expression. MiR-96-5p overexpression could reverse the inhibitory effect of circ-KIAA0907 on OSCC progression, and UNC13C knockdown also could overturn the suppressive effect of miR-96-5p inhibitor on OSCC progression. Animal experiments revealed that circ-KIAA0907 could reduce the tumor growth of OSCC by regulating the miR-96-5p/UNC13C axis. CONCLUSION: Our study suggests that circ-KIAA0907 restrains OSCC progression via the miR-96-5p/UNC13C axis, indicating that it may be a potential target for OSCC treatment.	NA	World J Surg Oncol. 2021 Mar 14;19(1):75. doi: 10.1186/s12957-021-02184-8.
3605	Circular RNA	CircKRT1	miR-495-3p	PDL1	OSCC tissues and cells	Oral Squamous Cell Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33675276	CircKRT1 drives tumor progression and immune evasion in oral squamous cell carcinoma by sponging miR-495-3p to regulate PDL1 expression.	Regulatory functions of circRNAs by targeting the micro RNA (miRNA)/mRNA axis have been increasingly found in oral squamous cell carcinoma (OSCC). CircRNA keratin 1 (CircKRT1) and miR-495-3p were dysregulated in OSCC. Programmed death ligand 1 (PDL1) was an important immunotherapeutic molecule in OSCC. Our objective was to explore whether circKRT1 could regulate cancer progression and immune evasion in OSCC by affecting the miR-495-3p/PDL1 axis. RNA expression was examined by quantitative real-time polymerase chain reaction. All protein levels were detected by western blot. OSCC cell growth was assessed by CCK-8 and colony formation assays. Cell migratory and invasive abilities were evaluated by transwell assay. CD8(+) T-cell cytotoxicity was determined via lactate dehydrogenase assay. CD8(+) T-cell percentage and apoptosis were analyzed by flow cytometry. Target screening was performed by Veen Diagram and RNA pull-down assay. Target binding was verified using dual-luciferase reporter and RNA immunoprecipitation assays. A xenograft in mice was conducted for in vivo experiment. CircKRT1 and PDL1 were highly expressed in OSCC tissues and cells. CircKRT1 knockdown repressed OSCC cell growth, migration, invasion, epithelial-mesenchymal transition, and CD8(+) T-cell apoptosis, but enhanced CD8(+) T cytotoxicity and percentage. The inhibitory effects of circKRT1 downregulation on OSCC progression and immune evasion were related to PDL1 expression inhibition. CircKRT1 sponged miR-495-3p and miR-495-3p targeted PDL1. OSCC progression and immune evasion were regulated by circKRT1 via the miR-495-3p/PDL1 axis. CircKRT1 also facilitated OSCC progression in vivo by regulating miR-495-3p and PDL1. This study clarified that circKRT1 worked as a miR-495-3p sponge to regulate PDL1, consequently affecting cancer progression and immune evasion in OSCC.	NA	Cell Biol Int. 2021 Mar 6. doi: 10.1002/cbin.11581.
3606	Circular RNA	CircMETTL3	miR-31-5p	CDK1	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33867838	CircMETTL3, upregulated in a m6A-dependent manner, promotes breast cancer progression.	Growing evidence indicates N6-methyladenosine (m6A) has biological function in oncogenesis. METTL3, the catalytic component, is the most important part of methyltransferase complex and plays a crucial role in cancers. However, the biological function of circRNAs derived from METTL3 in breast cancer and the underlying molecular mechanism remains unclear. Herein, we report circMETTL3, which has not been explored in breast cancer, and it is markedly upregulated in breast cancer. Moreover, we uncovered that circMETTL3 could facilitate cell proliferation, migration and invasion in breast cancer. Mechanism investigation showed that circMETTL3 might act as a competing endogenous RNA (ceRNA) of miR-31-5p and upregulate its target cyclin-dependent kinases (CDK1). Moreover, m6A modification of circMETTL3 might affect its expression. Taken together, our results elucidate that circMETTL3 promotes breast cancer progression through circMETTL3/miR-31-5p/CDK1 axis. Moreover, METTL3, the host gene of circMETTL3, may regulate circMETTL3 expression in an m6A-dependent manner, while circMETTL3 has no effect on METTL3 expression, providing a new relationship between the circRNA and the corresponding host gene. Thus, it may serve as a new therapeutic target for breast cancer.	NA	Int J Biol Sci. 2021 Mar 15;17(5):1178-1190. doi: 10.7150/ijbs.57783. eCollection 2021.
3607	Circular RNA	CircMMP11	miR-625-5p	ZEB2	breast cancer cells	Breast Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase report assay;RNA pull-down;	33632213	CircMMP11 regulates proliferation, migration, invasion, and apoptosis of breast cancer cells through miR-625-5p/ZEB2 axis.	BACKGROUND: Circular RNAs (circRNAs) have been demonstrated to play significant roles in regulating gene expression in tumorigenesis, including breast cancer (BC). This study was designed to explore the role and underlying molecular mechanisms of circMMP11 in BC. METHODS: The real-time quantitative polymerase chain reaction (RT-qPCR) assay was used for examining expression of circMMP11, microRNA-625-5p (miR-625-5p), and Zinc finger E-box binding homeobox-2 (ZEB2). The protein expression of ZEB2, Vimentin, and E-cadherin was assessed by western blot assay. The proliferation ability of BC cells was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and colony-forming assays. The transwell assay was used to measure migration and invasion of BC cells. The apoptotic cells were examined by flow cytometry assay. The interaction association among circMMP11, miR-625-5p, and ZEB2 was confirmed by RNA pull-down and dual-luciferase report assays. A xenograft experiment was established to clarify the role of circMMP11 silencing in vivo. RESULTS: We found that circMMP11 and ZEB2 were overexpressed in BC tissues and cells compared with controls. The suppression of circMMP11 or ZEB2 repressed proliferation, migration, and invasion while induced apoptosis of BC cells. Additionally, miR-625-5p, interacted with ZEB2, was a target of circMMP11 in BC cells. CircMMP11 regulated the expression of ZEB2 by targeting miR-625-5p. Knockdown of circMMP11-mediated effects on BC cells could be abolished by overexpression of ZEB2. Consistently, silencing of circMMP11 impeded the tumor growth in vivo. CONCLUSIONS: CircMMP11/miR-625-5p/ZEB2 axis affected proliferation, migration, invasion, and apoptosis of BC cells through the mechanism of competing endogenous RNAs (ceRNA), indicating that circMMP11 was an oncogenic circRNA in BC.	NA	Cancer Cell Int. 2021 Feb 25;21(1):133. doi: 10.1186/s12935-021-01816-z.
3608	Circular RNA	CircNEIL3	miR-432-5p	ADAR1	PDAC tissues and cell lines	Pancreatic Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;RIP assay;RNA immunoprecipitation;FISH;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;RNA sequencing;	33750389	CircNEIL3 regulatory loop promotes pancreatic ductal adenocarcinoma progression via miRNA sponging and A-to-I RNA-editing.	BACKGROUND: A growing number of studies have focused on investigating circRNAs as crucial regulators in the progression of multiple cancer types. Nevertheless, the biological effects and underlying mechanisms of circRNAs in pancreatic ductal adenocarcinoma (PDAC) remain unclear. METHODS: Differentially expressed circRNAs between cancerous tissue and adjacent normal tissues were identified by RNA sequencing in PDAC. Subsequently, in vitro and in vivo functional experiments were performed to investigate the functional roles of circNEIL3 in PDAC tumour growth and metastasis. Furthermore, RNA pull-down, dual-luciferase reporter assays, RNA immunoprecipitation (RIP) assays, fluorescent in situ hybridization (FISH) and Sanger sequencing assays were performed to examine the circular interaction among circNEIL3, miR-432-5p and adenosine deaminases acting on RNA 1 (ADAR1). RESULTS: CircNEIL3 was upregulated in PDAC and promoted the progression of PDAC cells both in vitro and in vivo. Mechanistically, circNEIL3 was shown to regulate the expression of ADAR1 by sponging miR-432-5p to induce RNA editing of glioma-associated oncogene 1 (GLI1), ultimately influencing cell cycle progression and promoting epithelial-to-mesenchymal transition (EMT) in PDAC cells. Moreover, we discovered that the circNEIL3/miR-432-5p/ADAR1 axis was correlated with the PDAC clinical stage and overall survival of PDAC patients, while ADAR1 may reduce the biogenesis of circNEIL3. CONCLUSIONS: Our findings reveal that circNEIL3 facilitates the proliferation and metastasis of PDAC through the circNEIL3/miR-432-5p/ADAR1/GLI1/cell cycle and EMT axis and that its expression is regulated by ADAR1 through a negative feedback loop. Therefore, circNEIL3 may serve as a prognostic marker and a therapeutic target for PDAC.	NA	Mol Cancer. 2021 Mar 9;20(1):51. doi: 10.1186/s12943-021-01333-7.
3609	Circular RNA	CircUBAP2	miR-4756	IFIT1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33707417	Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis.	Cancer-associated fibroblasts (CAFs) are commonly acquired activated extracellular matrix (ECM)-producing myofibroblasts, a phenotypes with multiple roles in hepatic fibrogenesis and carcinogenesis via crosstalk with cohabitating stromal/cancer cells. Here, we discovered a mechanism whereby CAF-derived cytokines enhance hepatocellular carcinoma (HCC) progression and metastasis by activating the circRNA-miRNA-mRNA axis in tumor cells. CAFs secreted significantly higher levels of CXCL11 than normal fibroblasts (NFs), and CXCL11 also had comparatively higher expressions in HCC tissues, particularly in metastatic tissues, than para-carcinoma tissues. Both CAF-derived and experimentally introduced CXCL11 promoted HCC cell migration. Likewise, CAFs promoted tumor migration in orthotopic models, as shown by an increased number of tumor nodules, whereas CXCL11 silencing triggered a decrease of it. CXCL11 stimulation upregulated circUBAP2 expression, which was significantly higher in HCC tissues than para-carcinoma tissues. Silencing circUBAP2 reversed the effects of CXCL11 on the expression of IL-1β/IL-17 and HCC cell migration. Further downstream, the IFIT1 and IFIT3 levels were significantly upregulated in HCC cells upon CXCL11 stimulation, but downregulated upon circUBAP2 silencing. IFIT1 or IFIT3 silencing reduced the expression of IL-17 and IL-1β, and attenuated the migration capability of HCC cells. Herein, circUBAP2 counteracted miR-4756-mediated inhibition on IFIT1/3 via sponging miR-4756. miR-4756 inhibition reversed the effects induced by circUBAP2 silencing on the IL-17 and IL-1β levels and HCC cell migration. In orthotopic models, miR-4756 inhibition also reversed the effects on metastatic progression induced by silencing circUBAP2.	NA	Cell Death Dis. 2021 Mar 11;12(3):260. doi: 10.1038/s41419-021-03545-7.
3610	Circular RNA	CircUBAP2	miR-4756	IFIT3	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33707417	Cancer-associated fibroblast-derived CXCL11 modulates hepatocellular carcinoma cell migration and tumor metastasis through the circUBAP2/miR-4756/IFIT1/3 axis.	Cancer-associated fibroblasts (CAFs) are commonly acquired activated extracellular matrix (ECM)-producing myofibroblasts, a phenotypes with multiple roles in hepatic fibrogenesis and carcinogenesis via crosstalk with cohabitating stromal/cancer cells. Here, we discovered a mechanism whereby CAF-derived cytokines enhance hepatocellular carcinoma (HCC) progression and metastasis by activating the circRNA-miRNA-mRNA axis in tumor cells. CAFs secreted significantly higher levels of CXCL11 than normal fibroblasts (NFs), and CXCL11 also had comparatively higher expressions in HCC tissues, particularly in metastatic tissues, than para-carcinoma tissues. Both CAF-derived and experimentally introduced CXCL11 promoted HCC cell migration. Likewise, CAFs promoted tumor migration in orthotopic models, as shown by an increased number of tumor nodules, whereas CXCL11 silencing triggered a decrease of it. CXCL11 stimulation upregulated circUBAP2 expression, which was significantly higher in HCC tissues than para-carcinoma tissues. Silencing circUBAP2 reversed the effects of CXCL11 on the expression of IL-1β/IL-17 and HCC cell migration. Further downstream, the IFIT1 and IFIT3 levels were significantly upregulated in HCC cells upon CXCL11 stimulation, but downregulated upon circUBAP2 silencing. IFIT1 or IFIT3 silencing reduced the expression of IL-17 and IL-1β, and attenuated the migration capability of HCC cells. Herein, circUBAP2 counteracted miR-4756-mediated inhibition on IFIT1/3 via sponging miR-4756. miR-4756 inhibition reversed the effects induced by circUBAP2 silencing on the IL-17 and IL-1β levels and HCC cell migration. In orthotopic models, miR-4756 inhibition also reversed the effects on metastatic progression induced by silencing circUBAP2.	NA	Cell Death Dis. 2021 Mar 11;12(3):260. doi: 10.1038/s41419-021-03545-7.
3611	Circular RNA	CircWAC	miR-142	WWP1	TNBC cells and tissues	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33648498	CircWAC induces chemotherapeutic resistance in triple-negative breast cancer by targeting miR-142, upregulating WWP1 and activating the PI3K/AKT pathway.	BACKGROUND: Chemotherapeutic resistance is the main cause of clinical treatment failure and poor prognosis in triple-negative breast cancer (TNBC). There is no research on chemotherapeutic resistance in TNBC from the perspective of circular RNAs (circRNAs). METHODS: TNBC-related circRNAs were identified based on the GSE101124 dataset. Quantitative reverse transcription PCR was used to detect the expression level of circWAC in TNBC cells and tissues. Then, in vitro and in vivo functional experiments were performed to evaluate the effects of circWAC in TNBC. RESULTS: CircWAC was highly expressed in TNBC and was associated with worse TNBC patient prognosis. Subsequently, it was verified that downregulation of circWAC can increase the sensitivity of TNBC cells to paclitaxel (PTX) in vitro and in vivo. The expression of miR-142 was negatively correlated with circWAC in TNBC. The interaction between circWAC and miR-142 in TNBC cells was confirmed by RNA immunoprecipitation assays, luciferase reporter assays, pulldown assays, and fluorescence in situ hybridization. Mechanistically, circWAC acted as a miR-142 sponge to relieve the repressive effect of miR-142 on its target WWP1. In addition, the overall survival of TNBC patients with high expression of miR-142 was significantly better than that of patients with low expression of miR-142, and these results were verified in public databases. MiR-142 regulated the expression of WWP1 and the activity of the PI3K/AKT pathway. It was confirmed that WWP1 is highly expressed in TNBC and that the prognosis of patients with high WWP1 expression is poor. CONCLUSIONS: CircWAC/miR-142/WWP1 form a competing endogenous RNA (ceRNA) network to regulate PI3K/AKT signaling activity in TNBC cells and affect the chemosensitivity of cells.	NA	Mol Cancer. 2021 Mar 1;20(1):43. doi: 10.1186/s12943-021-01332-8.
3612	Circular RNA	Circ-Zfp644	miR-93-5p	Limk1	CH cells	Cardiac Hypertrophy	Homo sapiens (human)	RIP assay;RNA pull-down assay;Luciferase reporter assay;Rescue assay;RNA pull-down;	33559936	Circ-Zfp644 acts as a pro-hypertrophic mediator in an Ang-II induced in vitro myocardial hypertrophy model.	Cardiac hypertrophy (CH) is a common risk factor for heart failure and even sudden cardiac death. Molecules have emerged as vital regulators in cardiac disorders. LIM domain kinase 1 (Limk1) is reported as a pro-fibrotic mediator in patients with permanent atrial fibrillation and it has also been suggested to aggravate cardiac dysfunction in rats with chronic heart failure. The present study observed that Limk1 was significantly upregulated in the in vitro model of CH induced by angiotensin II (Ang-II). Interestingly, silencing Limk1 led to inhibition of the hypertrophic phenotypes in Ang-II-treated cardiomyocytes. Next, through a series of mechanistic assays including RIP assay, RNA pull-down assay, and luciferase reporter assay, miR-93-5p was verified to target Limk1. Furthermore, circ-Zfp644 was validated as the sponge of miR-93-5p. Circ-Zfp644 functioned as a ceRNA to upregulate Limk1 expression via sequestering miR-93-5p in Ang-II-treated cardiomyocytes. Finally, a range of rescue assays revealed that circ-Zfp644 stimulated hypertrophic effects in Ang-II-treated cardiomyocytes via upregulating Limk1 while miR-93-5p exerted the opposite effects via its inhibition on Limk1. On the whole, the present study revealed that circ-Zfp644 aggravated CH through modulating the miR-93-5p/Limk1 axis. The findings observed on the in vitro model of CH provided new potential for developing CH treatment.	NA	Cell Biol Int. 2021 Jun;45(6):1260-1268. doi: 10.1002/cbin.11569. Epub 2021 Mar 25.
3613	LncRNA	DANCR	miR-1225-3p	ErbB2	SPCA1 and A549 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA pull-down assay;Western blot;luciferase assay;Luciferase reporter assay;RNA pull-down;	33577030	Long non-coding RNA DANCR promoted non-small cell lung cancer cells metastasis via modulating of miR-1225-3p/ErbB2 signal.	OBJECTIVE: Currently, we aimed to illustrate the role of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) and erb-b2 receptor tyrosine kinase 2 (ErbB2) in non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: Expression of DANCR, microRNA-1225-3p (miR-1225-3p) and ErbB2 mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) assays. The clinical value of DANCR was checked by a ROC curve analysis, a Kaplan-Meier analysis and a Pearson Chi-Square test. Transwell chamber assays were performed to determine the migration and invasion ability changes of SPCA1 and A549 cells. The protein expression of ErbB2 was tested by Western blot assays. The targeted binding effect between miR-1225-3p and DANCR or ErbB2 was confirmed by a Dual-Luciferase reporter assay and an RNA pull-down assay, respectively. RESULTS: In the current study, it was found that DANCR was upregulated and correlated with poor prognosis in patients with NSCLC. DANCR promoted NSCLC cells migration and invasion via upregulation of ErbB2. DANCR regulated ErbB2 at posttranscriptional level. Mechanically, it was illustrated that miR-1225-3p negatively regulated ErbbB2 and it-mediated migration and invasion via directly targeting in NSCLC cells. Meanwhile, it was showed that DANCR interacted with miR-1225-3p in a reciprocal suppression manner. Even further, through a RIP assay and a luciferase assay, we showed that DANCR interacted with miR-1225-3p through a microRNA response element (MRE-1225-3p) via directly binding. Finally, it was demonstrated that DANCR served as a miR-1225-3p sponge to promote ErbB2 expression and to facilitate ErbB2-mediated migration and invasion in NSCLC cells. CONCLUSIONS: In the current study, it was illustrated that DNACR promoted ErbB2-mediated migration and invasion via working as a ceRNA of miR-1225-3p in NSCLC cells.	NA	Eur Rev Med Pharmacol Sci. 2021 Jan;25(2):758-769. doi: 10.26355/eurrev_202101_24637.
3614	LncRNA	DDX11-AS1	miR-34a-3p	TRAF5	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33752668	Silenced lncRNA DDX11-AS1 or up-regulated microRNA-34a-3p inhibits malignant phenotypes of hepatocellular carcinoma cells via suppression of TRAF5.	BACKGROUND: Studies have discussed long noncoding RNA DDX11-AS1 (DDX11-AS1)-mediated downstream mechanism in hepatocellular carcinoma (HCC). The goal of this study was to investigate the regulatory mechanism of DDX11-AS1-mediated microRNA-34a-3p (miR-34a-3p)/tumor necrosis factor receptor-associated factor 5 (TRAF5) axis on HCC cells. METHODS: DDX11-AS1, miR-34a-3p and TRAF5 expression levels in HCC were detected. The correlation of DDX11-AS1, miR-34a-3p and TRAF5 in HCC patients was analyzed by Pearson test. HCC cells were transfected with corresponding plasmid/oligonucleotide, and cell proliferation, migration, invasion, apoptosis and tumor formation ability were detected. Bioinformatics software, dual luciferase report experiment and RNA-pull down experiment analysis were applied to verify the targeting relationship between DDX11-AS1, miR-34a-3p and TRAF5. RESULTS: Elevated DDX11-AS1 and TRAF5 and reduced miR-34a-3p exhibited in HCC. Silenced DDX11-AS1 or up-regulated miR-34a-3p inhibited the proliferation, migration, invasion, promoted apoptosis of HCC cells and repressed the tumor growth in nude mice. In addition, DDX11-AS1 bound to miR-34a-3p to target TRAF5. Silencing TRAF5 or elevating miR-34a-3p expression mitigated up-regulated DDX11-AS1-mediated promotion of tumor growth. CONCLUSION: Silenced DDX11-AS1 or up-regulated miR-34a-3p inhibits HCC cell growth via elevation of TRAF5, which could be of great benefit to find early diagnostic markers for HCC patients.	NA	Cancer Cell Int. 2021 Mar 22;21(1):179. doi: 10.1186/s12935-021-01847-6.
3615	LncRNA	DLEU2	miR-369-3p	TRIM2	A549 cells and lung tissues	Idiopathic Pulmonary Fibrosis	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33760118	Knockdown of long non-coding RNA DLEU2 suppresses idiopathic pulmonary fibrosis by regulating the microRNA-369-3p/TRIM2 axis.	Idiopathic pulmonary fibrosis (IPF) is the most common form of idiopathic interstitial pneumonia with an increasing incidence. In the present study, Genome Expression Omnibus (GEO) datasets (GSE10667, GSE24206 and GSE32537) were applied to identify lncRNA DLEU2 in IPF. Through prediction using starBase, TargetScan, miRTarBase and miRDB, tripartite motif containing 2 (TRIM2) and prostaglandin F2 receptor inhibitor (PTGFRN) were found to be upregulated in IPF. DLEU2 expression, the mRNA expression of TRIM2 and PTGFRN, and miR-369-3p expression in A549 cells and lung tissues were detected by RT-qPCR. The protein expression of TRIM2 and PTGFRN in lung tissues and A549 cells was detected by western blot analysis. The proliferation and migration of A549 cells was respectively detected by CCK-8 assay and wound healing assay. The expression of collagen I, α-smooth muscle actin (SMA) and E-cadherin was detected by immunofluorescence assay in A549 cells, and collagen I expression was detected by immunohistochemistry assay in lung tissues. The expression of collagen I, α-SMA and E-cadherin was also detected by western blot analysis in A549 cells and lung tissues. Dual-luciferase reporter assay was used to confirm the association between DLEU2 and miR-369-3p, and miR-369-3p and TRIM2. As a result, DLEU2 expression was found to be upregulated in IPF and in transforming growth factor (TGF)-β1-stimulated A549 cells. The silencing of DLEU2 inhibited the TGF-β1-induced proliferation, migration and epithelial-mesenchymal transition (EMT) of A549 cells and bleomycin (BLM)-induced pulmonary fibrosis in mice. TRIM2 expression was increased and miR-369-3p expression was decreased in the lung tissues of mice with BLM-induced fibrosis and in TGF-β1-stimulated A549 cells. DLEU2 directly targeted miR-369-3p. The effect of the silencing of DLEU2 on TGF-β1-stimulated A549 cells was suppressed by the silencing of miR-369-3p. TRIM2 was the target protein of miR-369-3p. On the whole, the present study demonstrates that the silencing of DLEU2 suppressed IPF by upregulating miR-369-3p expression and downregulating TRIM2 expression.	NA	Int J Mol Med. 2021 May;47(5):80. doi: 10.3892/ijmm.2021.4913. Epub 2021 Mar 24.
3616	LncRNA	DNAJC3-AS1	miR-27a-3p	PRDM14	clear cell RCC tissues and in cell lines	Renal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Western blot;Luciferase reporter assay;	33629299	LncRNA DNAJC3-AS1 functions as oncogene in renal cell carcinoma via regulation of the miR-27a-3p/PRDM14 axis.	OBJECTIVE: Renal cancer (RCC) is one of the most common urological malignancies worldwide. Although great advances have been made in the diagnosis and management of RCC, its prognosis remains unsatisfactory. Long noncoding RNAs (lncRNAs) have been found to be essential factors in the initiation and development of cancer. The current study aimed to measure the expression and functions of lncRNA DNAJC3-AS1 in the progression of clear cell RCC (ccRCC). PATIENTS AND METHODS: The expression of lncRNA DNAJC3-AS1 was detected in 30 pairs of ccRCC tissues and in cell lines by RT-PCR, and its prognostic association with ccRCC was evaluated by the Kaplan-Meier method. The proliferation, migration, invasion and apoptosis of ccRCC cells were measured after silencing DNAJC3-AS1. The interaction between DNAJC3-AS1, miR-27a-3p and PRDM14 was identified by Dual-Luciferase reporter assay. The protein levels were measured by Western blotting. RESULTS: The expression of DNAJC3-AS1 was upregulated in ccRCC tissues and cell lines compared to their normal counterparts. In vitro, silencing DNAJC3-AS1 reduced the proliferation, migration and invasion of ccRCC cells. Downregulation of DNAJC3-AS1 also led to the apoptosis of ccRCC cells. Moreover, we also found that DNAJC3-AS1 acted as a sponge of miR-27a-3p and identified PRDM14 as a target of miR-27a-3p. CONCLUSIONS: LncRNA DNAJC3-AS1 acts as an oncogene and plays an essential role in the tumorigenesis of ccRCC, possibly via the regulation of the miR-27a-3p/PRDM14 axis.	NA	Eur Rev Med Pharmacol Sci. 2021 Feb;25(3):1291-1301. doi: 10.26355/eurrev_202102_24833.
3617	LncRNA	DNM3OS	miR-193a-3p	MAP3K3	OC tissues and cell lines	Ovarian Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34027641	DNM3OS Facilitates Ovarian Cancer Progression by Regulating miR-193a-3p/MAP3K3 Axis.	PURPOSE: Long non-coding RNAs (lncRNAs) are essential regulators in the development of ovarian cancer (OC). Nonetheless, the function of lncRNA DNM3 opposite strand/antisense RNA (DNM3OS) in OC remains unclear. This work aimed to investigate the biological roles and underlying mechanisms of DNM3OS in OC. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction was conducted to examine DNM3OS, microRNA (miR)-193a-3p, and mitogen-activated protein kinase 3 (MAP3K3) mRNA expression in OC tissues and cell lines. Kaplan-Meier survival analysis was employed to analyze the relationship between DNM3OS expression and the prognosis of OC patients. Cell counting kit-8, 5-ethynyl-2'-deoxyuridine, and transwell experiments were conducted to monitor cell proliferation, migration, and invasion, respectively. Western blot was applied to examine epithelial-mesenchymal transition associated protein (E-cadherin and N-cadherin) expression. Luciferase reporter gene and RNA immunoprecipitation experiments were performed to confirm the relationships among DNM3OS, miR-193a-3p, and MAP3K3. Pearson's correlation analysis was adopted to analyze the correlations among DNM3OS, miR-193a-3p, and MAP3K3 mRNA. RESULTS: DNM3OS expression was remarkably increased in OC tissues and cell lines, which was associated with the unfavorable prognosis of the patients. DNM3OS overexpression enhanced OC cell proliferation, migration, and invasion; suppressed E-cadherin protein expression; and facilitated N-cadherin protein expression, while the transfection of miR-193a-3p mimics had the opposite effects. DNM3OS directly interacted with miR-193a-3p, and miR-193a-3p targeted MAP3K3 by directly binding to 3'UTR. DNM3OS could up-regulate the expression of MAP3K3 via repressing miR-193a-3p expression. CONCLUSION: DNM3OS, as an oncogenic lncRNA, increases the malignancy of OC cells via regulation of an miR-193a-3p/MAP3K3 axis.	NA	Yonsei Med J. 2021 Jun;62(6):535-544. doi: 10.3349/ymj.2021.62.6.535.
3618	LncRNA	DUXAP8	miR-448	WTAP	PC tissue and cells	Pancreatic Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33625109	Long Noncoding RNA DUXAP8 Promotes Pancreatic Carcinoma Cell Migration and Invasion Via Pathway by miR-448/WTAP/Fak Signaling Axis.	OBJECTIVES: Pancreatic carcinoma (PC) has become the fourth leading cause of cancer deaths. Long noncoding RNA DUXAP8 has also been reported to play a regulatory role in PC progression. However, its molecular mechanism in PC is not fully elucidated. METHODS: Quantitative real-time polymerase chain reaction was used to detect the levels of DUXAP8, microRNA (miR)-448, Wilms tumor 1-associating protein (WTAP), focal adhesion kinase (Fak), and matrix metallopeptidase 2/9. Western blotting was carried out to detect matrix metallopeptidase 2/9, WTAP, Fak, and p-Fak. The interaction between DUXAP8 and miR-448 as well as WTAP and miR-448 was validated by bioinformatics and dual-luciferase reporter assays. Transwell assay was used to analyze cell invasion and migration. 3-[4,5-Dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay was used to analyze cell proliferation. RESULTS: DUXAP8 was upregulated, whereas miR-448 was downregulated in PC tissue and cells. Meanwhile, DUXAP8 knockdown or miR-448 overexpression inhibited migration, invasion, and proliferation of PC cells. DUXAP8 directly targeted miR-448, and miR-448 directly bound to WTAP. Downregulation of miR-448 reversed the inhibition of migration and invasion of PC cells by DUXAP8 knockdown. CONCLUSIONS: DUXAP8 sponges miR-448 to modulate migration, invasion, and proliferation of PC cells, indicating a novel mechanistic role of DUXAP8 in the regulation of PC progression.	NA	Pancreas. 2021 Mar 1;50(3):317-326. doi: 10.1097/MPA.0000000000001751.
3619	LncRNA	FDNCR	miR-543-3p	DCN	granulosa cells	NA	Homo sapiens (human)	qRT-PCR	33767918	lncRNA FDNCR promotes apoptosis of granulosa cells by targeting the miR-543-3p/DCN/TGF-β signaling pathway in Hu sheep.	Long non-coding RNAs (lncRNAs) regulate the development of follicles and reproductive diseases, but the mechanisms by which lncRNAs regulate ovarian functions and fertility remain elusive. We profiled the expression of lncRNAs in ovarian tissues of Hu sheep with different prolificacy and identified 21,327 lncRNAs. Many of the lncRNAs were differentially expressed in different groups. We further characterized an lncRNA that was predominantly expressed in the ovaries of the low prolificacy Fec(B+) (LPB+) group and mainly present in granulosa cells (GCs), and the expression of this lncRNA decreased during follicular development, which we named follicular development-associated lncRNA (FDNCR). Next, we found that FDNCR directly binds miR-543-3p, and decorin (DCN) was identified as a target of miR-543-3p. FDNCR overexpression promoted GC apoptosis through increased expression of DCN, which could be attenuated by miR-543-3p. Furthermore, miR-543-3p increased and FDNCR reduced the expression of transforming growth factor-β (TGF-β) pathway-related genes, including TGF-β1 and inhibin beta A (INHBA), which were upregulated upon DCN silencing. Our results demonstrated that FDNCR sponges miR-543-3p in GCs and prevents miR-543-3p from binding to the DCN 3' UTR, resulting in DCN transactivation and TGF-β pathway inhibition and promotion of GC apoptosis in Hu sheep. These findings provide insights into the mechanisms underlying prolificacy in sheep.	NA	Mol Ther Nucleic Acids. 2021 Mar 1;24:223-240. doi: 10.1016/j.omtn.2021.02.030. eCollection 2021 Jun 4.
3620	LncRNA	FGD5-AS1	miR-944	MACC1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Luciferase reporter assay;MTT assay;	33550920	Long Noncoding RNA FGD5-AS1 Knockdown Decrease Viability, Migration, and Invasion of Non-Small Cell Lung Cancer (NSCLC) Cells by Regulating the MicroRNA-944/MACC1 Axis.	OBJECTIVE: Long noncoding RNA FGD5 antisense RNA 1 (FGD5-AS1) participates in the regulation of non-small cell lung cancer (NSCLC) progression, but the underlying mechanisms are not fully revealed. This study aimed to determine the regulatory mechanism of FGD5-AS1 on the viability, migration, and invasion of NSCLC cells. METHODS: QRT-PCR was performed to measure the expression of FGD5-AS1, microRNA-944 (miR-944), and MACC1 in NSCLC. The correlation between FGD5-AS1 and clinicopathological features of NSCLC patients was analyzed. The viability of NSCLC cells were detected using MTT assay, and the migration and invasion were measured by transwell assay. Additionally, dual-luciferase reporter assay was used to demonstrate the interactions among FGD5-AS1, miR-944, and MACC1. Furthermore, exosomes were isolated from NSCLC cells and identified by transmission electron microscopy (TEM) and western blot. Then, the macrophages treated with exosomes were co-cultured with NSCLC cells to assess the effect of exosomes containing lower FGD5-AS1 level on NSCLC. RESULTS: The expression of FGD5-AS1 and MACC1 was increased in NSCLC, but miR-944 expression was decreased. FGD5-AS1 expression had significantly correlation with TNM stage and metastasis in NSCLC patients. FGD5-AS1 knockdown decreased the viability, migration, and invasion of NSCLC cells. Additionally, FGD5-AS1 and MACC1 were both targeted by miR-944 with the complementary binding sites at 3' UTR. In the feedback experiments, miR-944 inhibition or MACC1 overexpression reversed the reduction effect of FGD5-AS1 knockdown on the tumorigenesis of NSCLC. Moreover, silencing of FGD5-AS1 suppressed macrophages M2 polarization, and eliminated the promoting effects of exosomes mediated macrophages on NSCLC cell migration and invasion. CONCLUSIONS: FGD5-AS1 knockdown attenuated viability, migration, and invasion of NSCLC cells by regulating the miR-944/MACC1 axis, providing a new therapeutic target for NSCLC.	NA	Technol Cancer Res Treat. 2021 Jan-Dec;20:1533033821990090. doi: 10.1177/1533033821990090.
3621	LncRNA	FGD5-AS1	miR-493-5p	DDX5	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33550957	Silencing of Long Non-Coding RNA FGD5-AS1 Inhibits the Progression of Non-Small Cell Lung Cancer by Regulating the miR-493-5p/DDX5 Axis.	BACKGROUND: Long non-coding RNA FGD5 antisense RNA 1 (FGD5-AS1), identified to be a carcinogenic lncRNA, exhibits a regulatory role in some malignancies including non-small cell lung cancer (NSCLC). The aim of the present research is to decipher the function and underlying mechanism of FGD5-AS1 in progression of NSCLC. METHODS: Expression of FGD5-AS1, miR-493-5p and DEAD-box protein 5 (DDX5) in NSCLC tissues and cells was quantified utilizing qRT-PCR. Cell proliferation was assessed by CCK-8 method. Scratch healing test and Transwell assay were used for assaying cell migration and invasion. Expressions of DDX5 and epithelial-mesenchymal transition (EMT)-related proteins were examined by Western blot. Additionally, targeting relationships between FGD5-AS1 and miR-493-5p, miR-493-5p and DDX5 were verified by dual-luciferase reporter gene assay. RESULTS: Expression of FGD5-AS1 in NSCLC tissues and cell lines was up-regulated. Expression of FGD5-AS1 was in association with enlarged tumor size and lymph node metastasis of the patients. Knockdown of FGD5-AS1 led to the inhibition of proliferation, migration, invasion and EMT of NSCLC cells. FGD5-AS1 directly targeted miR-493-5p, while DDX5 was the target of miR-493-5p in NSCLC cells. Additionally, FGD5-AS1 could positively regulate the expression of DDX5 via suppressing miR-493-5p. CONCLUSION: FGD5-AS1 facilitates the proliferation, migration, invasion and EMT of NSCLC cells by sponging miR-493-5p and up-regulating DDX5.	NA	Technol Cancer Res Treat. 2021 Jan-Dec;20:1533033821990007. doi: 10.1177/1533033821990007.
3622	LncRNA	FOXD3-AS1	miR-128-3p	LIMK1	CC tissues and cell ines	Cervical Cancer 	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33760158	FOXD3-AS1/miR-128-3p/LIMK1 axis regulates cervical cancer progression.	Long non-coding RNA forkhead box D3 antisense RNA 1 (FOXD3-AS1) functions as an oncogenic regulator in several types of cancer, including breast cancer, glioma and cervical cancer. However, the effects and mechanisms underlying FOXD3-AS1 in cervical cancer (CC) are not completely understood. The present study aimed to investigate the biological functions and potential molecular mechanisms underlying FOXD3-AS1 in CC progression. Reverse transcription-quantitative PCR was performed to detect FOXD3-AS1, microRNA (miR)-128-3p and LIM domain kinase 1 (LIMK1) expression levels in CC tissues and cells. Immunohistochemical staining and western blotting were conducted to assess LIMK1 protein expression levels in CC tissues and cells, respectively. Cell Counting Kit-8 and BrdU assays were used to determine the role of FOXD3-AS1 in regulating cell proliferation. CC cell migration and invasion were assessed by performing Transwell assays. Dual-luciferase reporter assays were conducted to verify the binding between miR-128-3p and FOXD3-AS1. FOXD3-AS1 expression was significantly increased in CC tissues and cell lines compared with adjacent healthy tissues and normal cervical epithelial cells, respectively. High FOXD3-AS1 expression was significantly associated with poor differentiation of tumor tissues, increased tumor size and positive lymph node metastasis. FOXD3-AS1 overexpression significantly increased CC cell proliferation, migration and invasion compared with the negative control (NC) group, whereas FOXD3-AS1 knockdown resulted in the opposite effects compared with the small interfering RNA-NC group. Moreover, the results demonstrated that FOXD3-AS1 targeted and negatively regulated miR-128-3p, which indirectly upregulated LIMK1 expression. Therefore, the present study demonstrated that FOXD3-AS1 upregulated LIMK1 expression via competitively sponging miR-128-3p in CC cells, promoting CC progression.	NA	Oncol Rep. 2021 May;45(5):62. doi: 10.3892/or.2021.8013. Epub 2021 Mar 24.
3623	LncRNA	GAS5	miR-222-3p	TIMP3	MPP cells	Mycoplasma Pneumoniae Pneumonia	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;MTT assay;Luciferase reporter assay;MTT assay;	33760178	Long non-coding RNA GAS5 protects against Mycoplasma pneumoniae pneumonia by regulating the microRNA-222-3p/TIMP3 axis.	Mycoplasma pneumoniae pneumonia (MPP) is a type of pneumonia induced by M. pneumoniae (MP) infection. The present study investigated the effect of long non-coding RNA growth arrest-specific 5 (GAS5) in MPP and the underlying molecular mechanism of this. The expression of GAS5, microRNA-222-3p, (miR-222-3p) and tissue inhibitor of metalloproteinases-3 (TIMP3) in MPP was investigated using reverse transcription-quantitative PCR. Lipid-associated membrane protein (LAMP)-induced THP-1 cells were used to model MPP. The viability of LAMP-induced THP-1 cells was analyzed using an MTT assay. Expression levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α) pro-inflammatory cytokines, and the anti-inflammatory cytokine heme oxygenase-1 (HO-1) in LAMP-induced THP-1 cells were measured by ELISA. A dual-luciferase reporter assay assessed the associations among GAS5, miR-222-3p and TIMP3. The expression of GAS5 and TIMP3 was downregulated in MPP. Expression of miR-222-3p was upregulated. GAS5-overexpression increased the viability of LAMP-induced THP-1 cells. GAS5 upregulation decreased the levels of IL-1β, IL-6, TNF-α and HO-1 levels in LAMP-induced THP-1 cells. GAS5 directly interacted with miR-222-3p. TIMP3 was a target of miR-222-3p. miR-222-3p upregulation or TIMP3-knockdown reversed the promotion effect on cell viability as well as the inhibitory effect on inflammation caused by GAS5-overexpression in LAMP-induced THP-1 cells. GAS5-overexpression increased the viability and decreased the inflammation of LAMP-induced THP-1 cells by regulating the miR-222-3p/TIMP3 axis. These results demonstrated a potential therapeutic target for MPP treatment.	NA	Mol Med Rep. 2021 May;23(5):380. doi: 10.3892/mmr.2021.12019. Epub 2021 Mar 24.
3624	LncRNA	H19	miR-29b	COL1A1	OSF tissues	Oral Submucous Fibrosis	Homo sapiens (human)	qRT-PCR	33672311	Targeting lncRNA H19/miR-29b/COL1A1 Axis Impedes Myofibroblast Activities of Precancerous Oral Submucous Fibrosis.	Oral submucous fibrosis (OSF) is known as a potentially malignant disorder, which may result from chemical irritation due to areca nuts (such as arecoline). Emerging evidence suggests that fibrogenesis and carcinogenesis are regulated by the interaction of long noncoding RNAs (lncRNAs) and microRNAs. Among these regulators, profibrotic lncRNA H19 has been found to be overexpressed in several fibrosis diseases. Here, we examined the expression of H19 in OSF specimens and its functional role in fibrotic buccal mucosal fibroblasts (fBMFs). Our results indicate that the aberrantly overexpressed H19 contributed to higher myofibroblast activities, such as collagen gel contractility and migration ability. We also demonstrated that H19 interacted with miR-29b, which suppressed the direct binding of miR-29b to the 3'-untranslated region of type I collagen (COL1A1). We showed that ectopic expression of miR-29b ameliorated various myofibroblast phenotypes and the expression of α-smooth muscle actin (α-SMA), COL1A1, and fibronectin (FN1) in fBMFs. In OSF tissues, we found that the expression of miR-29b was downregulated and there was a negative correlation between miR-29b and these fibrosis markers. Lastly, we demonstrate that arecoline stimulated the upregulation of H19 through the transforming growth factor (TGF)-β pathway. Altogether, this study suggests that increased TGF-β secretion following areca nut chewing may induce the upregulation of H19, which serves as a natural sponge for miR-29b and impedes its antifibrotic effects.	NA	Int J Mol Sci. 2021 Feb 23;22(4):2216. doi: 10.3390/ijms22042216.
3625	LncRNA	H19	miR-20a-5p	Tgfbr2	skeletal muscle fibrosis	Myoblast Fibrogenesis	Homo sapiens (human)	qRT-PCR	33615521	Long non-coding RNA H19 promotes myoblast fibrogenesis via regulating the miR-20a-5p-Tgfbr2 axis.	Emerging evidence has indicated long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, including fibrosis. Here, we report that lncRNA H19 is able to promote skeletal muscle fibrosis. lnc-H19 was identified to be highly expressed in skeletal muscle fibrosis in vivo and in vitro; while lnc-H19 knockdown attenuated fibrosis in vitro. The knockdown of lnc-H19 was proved to inhibit the activation of the TGFβ/Smad pathway in C2C12 myoblasts by sponging miR-20a-5p to regulate Tgfbr2 expression through the competing endogenous RNA function. Our study elucidates the roles of the lnc-H19-miR-20a-5p-Tgfbr2 axis in regulating the TGFβ/Smad pathway of myoblast fibrogenesis, which might provide a promising therapeutic target for skeletal muscle fibrosis.	NA	Clin Exp Pharmacol Physiol. 2021 Jun;48(6):921-931. doi: 10.1111/1440-1681.13489. Epub 2021 Mar 21.
3626	LncRNA	H19	miR-675-5p	PFKFB3	cancer-associated fibroblasts	Oral Squamous Cell Cancer	Homo sapiens (human)	RNA sequencing;	33762576	Glycolysis reprogramming in cancer-associated fibroblasts promotes the growth of oral cancer through the lncRNA H19/miR-675-5p/PFKFB3 signaling pathway.	As an important component of the tumor microenvironment, cancer-associated fibroblasts (CAFs) secrete energy metabolites to supply energy for tumor progression. Abnormal regulation of long noncoding RNAs (lncRNAs) is thought to contribute to glucose metabolism, but the role of lncRNAs in glycolysis in oral CAFs has not been systematically examined. In the present study, by using RNA sequencing and bioinformatics analysis, we analyzed the lncRNA/mRNA profiles of normal fibroblasts (NFs) derived from normal tissues and CAFs derived from patients with oral squamous cell carcinoma (OSCC). LncRNA H19 was identified as a key lncRNA in oral CAFs and was synchronously upregulated in both oral cancer cell lines and CAFs. Using small interfering RNA (siRNA) strategies, we determined that lncRNA H19 knockdown affected proliferation, migration, and glycolysis in oral CAFs. We found that knockdown of lncRNA H19 by siRNA suppressed the MAPK signaling pathway, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) and miR-675-5p. Furthermore, the lncRNA H19/miR-675-5p/PFKFB3 axis was involved in promoting the glycolysis pathway in oral CAFs, as demonstrated by a luciferase reporter system assay and treatment with a miRNA-specific inhibitor. Our study presents a new way to understand glucose metabolism in oral CAFs, theoretically providing a novel biomarker for OSCC molecular diagnosis and a new target for antitumor therapy.	NA	Int J Oral Sci. 2021 Mar 25;13(1):12. doi: 10.1038/s41368-021-00115-7.
3627	LncRNA	HCG18	miR-106a-5p	PPP2R2A	PTC tissues and cells	Papillary Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33798913	LncRNA-HCG18 regulates the viability, apoptosis, migration, invasion and epithelial-mesenchymal transition of papillary thyroid cancer cells via regulating the miR-106a-5p/PPP2R2A axis.	The incidence of papillary thyroid cancer (PTC) has experienced a rapid increase in recent years. Long non-coding RNA-homo sapiens HLA complex group (HCG) 18 plays a regulatory role in cancers, but its role in PTC remained unknown. This study determined the expressions of HCG18, microRNA (miR)-106a-5p, and protein phosphatase 2 regulatory subunit B alpha (PPP2R2A) in PTC tissues and cells by qRT-PCR. ENCORI predicted the targeting relation between HCG18 and miR-106a-5p. TargetScan v7.2 predicted the targeting relation between miR-106a-5p and PPP2R2A. Dual-luciferase reporter assay was performed to validate the two targeting relations. The viability, migration, and invasion of PTC cells were detected by Cell Counting Kit-8, wound healing assay, and Transwell assay, respectively. The expressions of matrix metalloproteinase 2 (MMP-2), MMP-9, E-cadherin, N-cadherin, and Vimentin in TPC-1 and MDA-T68 cells were assessed by qRT-PCR and Western blot. It was found that HCG18 was down-regulated in PTC. Overexpressing HCG18 suppressed viability, migration, and invasion, promoted apoptosis, and inhibited miR-106a-5p expression in PTC cells. HCG18 interacted with miR-106a-5p, the expression of which was upregulated in PTC. Upregulating miR-106a-5p expression by lentivirus infection promoted viability, migration and invasion and inhibited apoptosis of PTC cells, reversed the effect of HCG18 on the biological behaviors of PTC cells, and promoted the expressions of MMP-2, MMP-9, E-cadherin, and Vimentin and downregulated E-cadherin expression in PTC cells. PPP2R2A, a direct target of miR-106a-5p, was downregulated in PTC, and HCG18 promoted PPP2R2A expression in PTC cells by sponging miR-106a-5p. Furthermore, PPP2R2A reversed the effects of miR-106a-5p on PTC cells. In conclusion, HCG18 suppressed viability, migration, invasion and epithelial-mesenchymal transition and promoted apoptosis of PTC cells via regulating the miR-106a-5p/PPP2R2A axis.	NA	Pathol Res Pract. 2021 May;221:153395. doi: 10.1016/j.prp.2021.153395. Epub 2021 Mar 4.
3628	LncRNA	HEIH	miR-193a-5p	CDK8	NPC tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33577031	Long non-coding RNA HEIH modulates CDK8 expression by inhibiting miR-193a-5p to accelerate nasopharyngeal carcinoma progression.	OBJECTIVE: Nasopharyngeal carcinoma (NPC) is the commonest malignant tumor. In this article, we aimed to examine the molecular role of lncRNA HEIH in the progression of NPC. PATIENTS AND METHODS: We assessed the expression of HEIH, miR-193a-5p and CDK8 in NPC tissues and cells by real-time PCR. The cell proliferation, invasion and migration of SUNE-1 cells were examined by CCK-8 and transwell assay. Western blot assay was adopted to measure the protein expression level of CDK8. Dual-Luciferase reporter assay was adopted to evaluate the correlation between HEIH, miR-193a-5p and CDK8. RESULTS: We discovered that HEIH was high expressed and miR-193a-5p was reduced in both NPC tissues and cells. The upregulation of HEIH facilitated cell proliferation, migration and invasion of SUNE-1 cells. In addition, overexpression of miR-193a-5p restrained cell progression of SUNE-1 cells. Moreover, HEIH was proved to be a molecular sponge of miR-193a-5p in NPC. Besides that, CDK8 was found to be a direct target gene of miR-193a-5p in NPC. Furthermore, CDK8 knockdown suppressed cell progression of SUNE-1 cells. CONCLUSIONS: Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8.	NA	Eur Rev Med Pharmacol Sci. 2021 Jan;25(2):770-778. doi: 10.26355/eurrev_202101_24638.
3629	LncRNA	HOTAIR	miR-126	SDF-1	SS tissues and SW982 cells	Synovial Sarcoma	Homo sapiens (human)	Western blot;	33868482	Long non-coding RNA HOTAIR promotes the progression of synovial sarcoma through microRNA-126/stromal cell-derived factor-1 regulation.	The long non-coding RNA (lncRNA) HOTAIR is an oncogene, that has been reported to be aberrantly expressed in multiple types of malignant tumor tissues. However, its expression and association with synovial sarcoma (SS) remains unclear. The present study aimed to elucidate the expression level of HOTAIR in SS tissues and also identify its role. Reverse transcription-quantitative PCR was used to detect the expression level of HOTAIR and microRNA (miR)-126 in 54 tissue samples from patients with SS, in 10 tissue samples from synovium tissues of normal patients, and in SW982 cells. The protein expression level was measured using western blot analysis and cellular immunofluorescence. Cellular proliferation, invasion and migration were assessed using MTT, Transwell and wound healing assays, respectively. HOTAIR was expressed at high levels in SS tissues. In contrast, miR-126 was expressed at low levels in SS tissues, and was negatively correlated with HOTAIR expression. HOTAIR knockdown in SW982 cells inhibited cellular proliferation in vitro, but also significantly increased the ratio of cells in the G(1)/G(0) phase of the cell cycle, and decreased the ratio of cells in the G(2)/S phase. In addition, HOTAIR knockdown inhibited the invasion and migration of the SW982 cells, as observed in the Transwell and wound healing assays. Furthermore, HOTAIR knockdown increased miR-126 expression level and decreased the expression level of stromal cell-derived factor-1 (SDF-1) at the protein level. On the other hand, while miR-126-mimic decreased the protein expression level of SDF-1, miR-126-inhibitor increased its expression level in SW982 cells. Notably, HOTAIR knockdown or SDF-1 knockout significantly decreased the protein expression levels of CDK1, CDK2, cyclin D1, MMP-9, vimentin and N-cadherin, and significantly increased the protein expression levels of p21, p53 and E-cadherin in SW982 cells. HOTAIR was highly expressed in SS tissues, wherein it could promote the proliferation, invasion and migration of SS cells by increasing the expression of SDF-1 via miR-126 inhibition.	NA	Oncol Lett. 2021 Jun;21(6):444. doi: 10.3892/ol.2021.12705. Epub 2021 Apr 6.
3630	LncRNA	HOTAIRM1	miR-133b-3p	TGFb	glioma stem-like cells	Glioma	Homo sapiens (human)	qRT-PCR	33816233	HOTAIRM1 Promotes Malignant Progression of Transformed Fibroblasts in Glioma Stem-Like Cells Remodeled Microenvironment via Regulating miR-133b-3p/TGFβ Axis.	Recent studies have reported that cancer associated fibroblasts (CAFs) and glioma stem-like cells (GSCs) played active roles in glioma progression in tumor microenvironment (TME). Long non-coding RNAs (lncRNAs) have been found to be closely associated with glioma development in recent years, however, their molecular regulatory mechanisms on CAFs in GSCs remodeled TME kept largely unelucidated. Our study found that GSCs could induce malignant transformation of fibroblasts (t-FBs) based on dual-color fluorescence tracing orthotopic model. Associated with poor prognosis, Lnc HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1) was highly expressed in high-grade gliomas and t-FBs. Depleting HOTAIRM1 inhibited the proliferation, invasion, migration, and even tumorigenicity of t-FB. Conversely, overexpression of HOTAIRM1 promoted malignancy phenotype of t-FB. Mechanistically, HOTAIRM1 directly bound with miR-133b-3p, and negatively regulated the latter. MiR-133b-3p partly decreased the promotion effect of HOTAIRM1 on t-FBs. Furthermore, transforming growth factor-β (TGFβ) was verified to be a direct target of miR-133b-3p. HOTAIRM1 can modulate TGFβ via competing with miR-133b-3p. Collectively, HOTAIRM1/miR-133b-3p/TGFβ axis was involved in modulating t-FBs malignancy in TME remodeled by GSCs, which had the potential to serve as a target against gliomas.	NA	Front Oncol. 2021 Mar 19;11:603128. doi: 10.3389/fonc.2021.603128. eCollection 2021.
3631	LncRNA	HOTTIP	miR-148a-3p	AKT2	OC tissues and cell lines	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33710684	LncRNA HOTTIP inhibits cell pyroptosis by targeting miR-148a-3p/AKT2 axis in ovarian cancer.	Long noncoding RNA HOTTIP is a crucial regulator in multiple types of cancer, including ovarian cancer (OC). However, the biological roles and underlying mechanisms of HOTTIP in OC have rarely been studied. Hence, this study aimed to investigate the functional correlation between HOTTIP and pyroptosis in OC progression. The expression of HOTTIP in OC tissues and cell lines was characterized by quantitative real-time PCR. Cell proliferation was evaluated using Cell Counting Kit-8 and clone formation assays. Western blot was performed to quantify protein levels. A dual-luciferase reporter assay was used to analyze the molecular interaction among HOTTIP, miR-148a-3p, and AKT2. The expression of HOTTIP was significantly upregulated in OC tissue samples and cell lines. The silencing of HOTTIP led to the inhibition of cell proliferation and NLRP1 inflammasome-mediated pyroptosis. In addition, HOTTIP increased AKT2 expression by negatively regulating miR-148a-3p and then inhibited ASK1/JNK signaling. Further rescue experiments revealed that downregulation of miR-148a-3p and overexpression of AKT2 obviously diminished the effects of HOTTIP downregulation in OC cells. Thus, our study elucidated a novel pyroptosis-related mechanism by which HOTTIP participated in OC progression, which might provide a theoretical reference for clinical treatment.	NA	Cell Biol Int. 2021 Mar 12. doi: 10.1002/cbin.11588.
3632	LncRNA	HOXA11-AS	miR-98	PBX3	NPC cells	Nasopharyngeal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33968209	HOXA11-AS induces cisplatin resistance by modulating the microRNA-98/PBX3 axis in nasopharyngeal carcinoma.	Long non-coding RNA homeobox A11-antisense RNA (HOXA11-AS) has been implicated in cisplatin (DDP) resistance in multiple types of cancer. The purpose of the present study was to investigate the role of HOXA11-AS in DDP-resistant nasopharyngeal carcinoma (NPC) cells. The expression levels of HOXA11-AS were examined using reverse transcription-quantitative PCR. Cell viability was measured using a Cell Counting Kit-8 assay, and a TUNEL assay was utilized to assess cell apoptosis. The expression levels of apoptosis-related factors (Bax and Bcl-2) were detected by western blot analysis. The interaction between microRNA-98 (miR-98) and HOXA11-AS or pre-B-cell leukemia homeobox 3 (PBX3) was demonstrated using bioinformatics analysis, dual-luciferase reporter assays and RNA immunoprecipitation assays. HOXA11-AS and PBX3 expressions levels were upregulated, whereas miR-98 levels were downregulated in DDP-resistant NPC tissues. Patients with NPC with high HOXA11-AS expression had a low survival rate. Knockdown of HOXA11-AS enhanced the DDP sensitivity of DDP-resistant NPC (5-8F/DDP and SUNE1/DDP) cells, which was demonstrated by the accelerated apoptosis. In addition, HOXA11-AS inhibited the expression levels of miR-98 through direct interaction. Furthermore, miR-98 inhibition counteracted the inductive effect of HOXA11-AS-knockdown on the DDP sensitivity of NPC cells. PBX3 was a target of miR-98 and was positively modulated by HOXA11-AS. Overexpression of PBX3 reversed the suppressive effect of HOXA11-AS silencing on the DDP resistance of NPC cells. The data demonstrated that HOXA11-AS enhanced DDP resistance in NPC via the miR-98/PBX3 axis, providing a potential therapeutic target for patients with DDP-resistant NPC.	NA	Oncol Lett. 2021 Jun;21(6):493. doi: 10.3892/ol.2021.12754. Epub 2021 Apr 26.
3633	LncRNA	HOXA-AS3	miR-29a-3p	LTbR	GC cells and tissues	Gastric Cancer	Homo sapiens (human)	qPCR;Western blot;	33602223	LncRNA HOXA-AS3 promotes gastric cancer progression by regulating miR-29a-3p/LTβR and activating NF-κB signaling.	BACKGROUND: Gastric cancer (GC) is among the most common and deadliest cancers globally. Many long non-coding RNAs (lncRNAs) are key regulators of GC pathogenesis. This study aimed to define the role of HOXA-AS3 in this oncogenic context. METHODS: Levels of HOXA-AS3 expression in GC were quantified via qPCR. The effects of HOXA-AS3 knockdown on GC cells function were evaluated in vitro using colony formation assays, wound healing assays and transwell assays. Subcutaneous xenograft and tail vein injection tumor model systems were generated in nude mice to assess the effects of this lncRNA in vivo. The localization of HOXA-AS3 within cells was confirmed by subcellular fractionation, and predicted microRNA (miRNA) targets of this lncRNA and its ability to modulate downstream NF-κB signaling in GC cells were evaluated via luciferase-reporter assays, immunofluorescent staining, and western blotting. RESULTS: GC cells and tissues exhibited significant HOXA-AS3 upregulation (P < 0.05), and the levels of this lncRNA were found to be correlated with tumor size, lymph node status, invasion depth, and Helicobacter pylori infection status. Knocking down HOXA-AS3 disrupted GC cell proliferation, migration, and invasion in vitro and tumor metastasis in vivo. At a mechanistic level, we found that HOXA-AS3 was able to sequester miR-29a-3p, thereby regulating the expression of LTβR and modulating NF-κB signaling in GC. CONCLUSION: HOXA-AS3/miR-29a-3p/LTβR/NF-κB regulatory axis contributes to the progression of GC, thereby offering novel target for the prognosis and treatment of GC.	NA	Cancer Cell Int. 2021 Feb 18;21(1):118. doi: 10.1186/s12935-021-01827-w.
3634	LncRNA	hsa_circ_0000700	miR-1229	PRRG4	ECA-109 and TE-1 cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33854621	Circular RNA hsa_circ_0000700 promotes cell proliferation and migration in Esophageal Squamous Cell Carcinoma by sponging miR-1229.	Accumulating evidence has demonstrated that circular RNAs (circRNAs) are involved in the pathogenesis of cancer, including that of esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the role of hsa_circ_0000700 in ESCC. hsa_circ_0000700, miR-1229, and related functional gene expression was measured by RT-qPCR. To characterize the functions of hsa_circ_0000700 and miR-1229, ESCC cells were infected with hsa_circ_0000700-specific siRNA, miR-1229 mimics, and an inhibitor alone or in combination. Cell Counting Kit-8 (CCK8), colony formation, EdU, flow cytometry, and Transwell assays were employed to evaluate cell proliferation, apoptosis, and migration. Luciferase reporter and RNA immunoprecipitation assays were used to confirm the targeting relationship between hsa_circ_0000700 and miR-1229. Finally, a competing endogenous RNAs (ceRNA) network was built for hsa_circ_0000700, and miR-1229 targets were analyzed by bioinformatics. circ_0000700 expression was significantly upregulated in ESCC cell lines. Actinomycin D and RNase R treatment confirmed that circ_0000700 was more stable than its linear CDH9 mRNA form. Moreover, a cytoplasmic and nuclear fractionation assay suggested that circ_0000700 was mainly distributed in the cytoplasm of ECA-109 and TE-1 cells. In vitro, the proliferative and migratory capacities of ECA-109 and TE-1 cells were inhibited by knocking down circ_0000700 expression. Additionally, miR-1229 silencing reversed the circ_0000700-specific siRNA-induced attenuation of malignant phenotypes. Mechanistically, circ_0000700 was identified as a sponge of miR-1229 and could activate PRRG4, REEP5, and PSMB5 indirectly to promote ESCC progression. In summary, our results suggest that hsa_circ_0000700 functions as an oncogenic factor by sponging miR-1229 in ESCC.	NA	J Cancer. 2021 Mar 5;12(9):2610-2623. doi: 10.7150/jca.47112. eCollection 2021.
3635	LncRNA	hsa_circ_0000700	miR-1229	REEP5	ECA-109 and TE-1 cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33854621	Circular RNA hsa_circ_0000700 promotes cell proliferation and migration in Esophageal Squamous Cell Carcinoma by sponging miR-1229.	Accumulating evidence has demonstrated that circular RNAs (circRNAs) are involved in the pathogenesis of cancer, including that of esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the role of hsa_circ_0000700 in ESCC. hsa_circ_0000700, miR-1229, and related functional gene expression was measured by RT-qPCR. To characterize the functions of hsa_circ_0000700 and miR-1229, ESCC cells were infected with hsa_circ_0000700-specific siRNA, miR-1229 mimics, and an inhibitor alone or in combination. Cell Counting Kit-8 (CCK8), colony formation, EdU, flow cytometry, and Transwell assays were employed to evaluate cell proliferation, apoptosis, and migration. Luciferase reporter and RNA immunoprecipitation assays were used to confirm the targeting relationship between hsa_circ_0000700 and miR-1229. Finally, a competing endogenous RNAs (ceRNA) network was built for hsa_circ_0000700, and miR-1229 targets were analyzed by bioinformatics. circ_0000700 expression was significantly upregulated in ESCC cell lines. Actinomycin D and RNase R treatment confirmed that circ_0000700 was more stable than its linear CDH9 mRNA form. Moreover, a cytoplasmic and nuclear fractionation assay suggested that circ_0000700 was mainly distributed in the cytoplasm of ECA-109 and TE-1 cells. In vitro, the proliferative and migratory capacities of ECA-109 and TE-1 cells were inhibited by knocking down circ_0000700 expression. Additionally, miR-1229 silencing reversed the circ_0000700-specific siRNA-induced attenuation of malignant phenotypes. Mechanistically, circ_0000700 was identified as a sponge of miR-1229 and could activate PRRG4, REEP5, and PSMB5 indirectly to promote ESCC progression. In summary, our results suggest that hsa_circ_0000700 functions as an oncogenic factor by sponging miR-1229 in ESCC.	NA	J Cancer. 2021 Mar 5;12(9):2610-2623. doi: 10.7150/jca.47112. eCollection 2021.
3636	LncRNA	hsa_circ_0000700	miR-1229	PSMB5	ECA-109 and TE-1 cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33854621	Circular RNA hsa_circ_0000700 promotes cell proliferation and migration in Esophageal Squamous Cell Carcinoma by sponging miR-1229.	Accumulating evidence has demonstrated that circular RNAs (circRNAs) are involved in the pathogenesis of cancer, including that of esophageal squamous cell carcinoma (ESCC). The current study aimed to investigate the role of hsa_circ_0000700 in ESCC. hsa_circ_0000700, miR-1229, and related functional gene expression was measured by RT-qPCR. To characterize the functions of hsa_circ_0000700 and miR-1229, ESCC cells were infected with hsa_circ_0000700-specific siRNA, miR-1229 mimics, and an inhibitor alone or in combination. Cell Counting Kit-8 (CCK8), colony formation, EdU, flow cytometry, and Transwell assays were employed to evaluate cell proliferation, apoptosis, and migration. Luciferase reporter and RNA immunoprecipitation assays were used to confirm the targeting relationship between hsa_circ_0000700 and miR-1229. Finally, a competing endogenous RNAs (ceRNA) network was built for hsa_circ_0000700, and miR-1229 targets were analyzed by bioinformatics. circ_0000700 expression was significantly upregulated in ESCC cell lines. Actinomycin D and RNase R treatment confirmed that circ_0000700 was more stable than its linear CDH9 mRNA form. Moreover, a cytoplasmic and nuclear fractionation assay suggested that circ_0000700 was mainly distributed in the cytoplasm of ECA-109 and TE-1 cells. In vitro, the proliferative and migratory capacities of ECA-109 and TE-1 cells were inhibited by knocking down circ_0000700 expression. Additionally, miR-1229 silencing reversed the circ_0000700-specific siRNA-induced attenuation of malignant phenotypes. Mechanistically, circ_0000700 was identified as a sponge of miR-1229 and could activate PRRG4, REEP5, and PSMB5 indirectly to promote ESCC progression. In summary, our results suggest that hsa_circ_0000700 functions as an oncogenic factor by sponging miR-1229 in ESCC.	NA	J Cancer. 2021 Mar 5;12(9):2610-2623. doi: 10.7150/jca.47112. eCollection 2021.
3637	Circular RNA	hsa_circ_0003340	miR-615-5p	PDX1	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33854374	CircRNA circ-OGDH (hsa_circ_0003340) Acts as a ceRNA to Regulate Glutamine Metabolism and Esophageal Squamous Cell Carcinoma Progression by the miR-615-5p/PDX1 Axis.	BACKGROUND: Circular RNA hsa_circ_0003340 (circ-OGDH) has been uncovered to be involved in esophageal squamous cell carcinoma (ESCC) progression. However, the mechanism by which circ-OGDH regulates ESCC progression is unclear. METHODS: Expression levels of circ-OGDH, microRNA (miR)-615-5p, and PDX1 (pancreatic and duodenal homeobox 1) mRNA were evaluated with quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, apoptosis, migration, invasion, and cell cycle progression of ESCC cells were analyzed by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide), colony formation, flow cytometry, and transwell assays. Measurement of glutamine consumption, α-KG (α-ketoglutarate) production, and ATP (Adenosine Triphosphate) content using corresponding kits. Protein levels were analyzed by Western blotting. The targeting relationship between circ-OGDH or PDX1 and miR-615-5p was verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. The function of circ-OGDH in ESCC was confirmed by animal experiments. RESULTS: Circ-OGDH was upregulated in ESCC. Circ-OGDH inhibition reduced ESCC growth in vivo and accelerated cell apoptosis, cell cycle arrest, repressed cell proliferation, migration, invasion, and reduced cell glutamine metabolism in ESCC cells in vitro. MiR-615-5p was downregulated in ESCC, while PDX1 had an opposite result. Circ-OGDH sponged miR-615-5p to regulate PDX1 expression. MiR-615-5p inhibitor neutralized the repressive effect of circ-OGDH knockdown on malignancy and glutamine metabolism of ESCC cells. PDX1 overexpression counteracted the inhibitory impact of miR-615-5p mimic on malignancy and glutamine metabolism of ESCC cells. CONCLUSION: Circ-OGDH sponged miR-615-5p to elevate PDX1 expression, thus elevating glutamine metabolism and promoting tumor growth in ESCC. The study offered evidence to support circ-OGDH as a promising target for ESCC therapy.	NA	Cancer Manag Res. 2021 Apr 7;13:3041-3053. doi: 10.2147/CMAR.S290088. eCollection 2021.
3638	Circular RNA	hsa_circ_0053063	miR-330-3p	PDCD4	BC tissues and cell lines	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;	33744861	Hsa_circ_0053063 inhibits breast cancer cell proliferation via hsa_circ_0053063/hsa-miR-330-3p/PDCD4 axis.	Breast cancer (BC) is one of the most common malignancies and its mortality is the highest among females. Circular RNAs (circRNAs), a novel group of non-coding RNAs, play an important regulatory role in angiogenesis and cancer progression. Hsa_circ_0053063 is a circRNA generated from several exons of HADHA. The potential role of hsa_circ_0053063 in BC remains unknown and needs to be explored. Hsa_circ_0053063 was mainly located in the cytoplasm and activated in BC tissues and cell lines. The binding position between hsa_circ_0053063 and miR-330-3p was confirmed by luciferase reporter assay. Moreover, hsa_circ_0053063 inhibited cell viability, proliferation, and progression of BC through the negative regulation of miR-330-3p. Programmed cell death 4 (PDCD4) is a direct target of miR-330-3p. Besides, the over-expression of miR-330-3p promoted cell progression by directly targeting and regulating PDCD4. Mechanistically, hsa_circ_0053063 activated PDCD4 by targeting miR-330-3p to inhibit BC progression. In conclusion, hsa_circ_0053063 inhibits breast cancer cell proliferation via hsa_circ_0053063/hsa-miR-330-3p/PDCD4 axis, which may provide a new therapeutic target for BC patients.	NA	Aging (Albany NY). 2021 Mar 19;13(7):9627-9645. doi: 10.18632/aging.202707. Epub 2021 Mar 19.
3639	Circular RNA	hsa_circ_0065336	miR-505-3p	PTPN11	THP-1 cells	Invasive Trichosporon Asahii Infection	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;RNA sequencing;	33750466	Comprehensive circRNA-microRNA-mRNA network analysis revealed the novel regulatory mechanism of Trichosporon asahii infection.	BACKGROUND: Invasive Trichosporon asahii (T. asahii) infection frequently occurs with a high mortality in immunodeficient hosts, but the pathogenesis of T. asahii infection remains elusive. Circular RNAs (circRNAs) are a type of endogenous noncoding RNA that participate in various disease processes. However, the mechanism of circRNAs in T. asahii infection remains completely unknown. METHODS: RNA sequencing (RNA-seq) was performed to analyze the expression profiles of circRNAs, microRNAs (miRNAs), and mRNAs in THP-1 cells infected with T. asahii or uninfected samples. Some of the RNA-seq results were verified by RT-qPCR. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were used to analyze the differentially expressed mRNAs. A circRNA-miRNA-mRNA network was constructed and verified by dual-luciferase reporter assay and overexpression experiments. RESULTS: A total of 46 circRNAs, 412 mRNAs and 47 miRNAs were differentially expressed at 12 h after T. asahii infection. GO and KEGG analyses showed that the differentially expressed mRNAs were primarily linked to the leukocyte migration involved in the inflammatory response, the Toll-like receptor signaling pathway, and the TNF signaling pathway. A competing endogenous RNA (ceRNA) network was constructed with 5 differentially expressed circRNAs, 5 differentially expressed miRNAs and 42 differentially expressed mRNAs. Among them, hsa_circ_0065336 was found to indirectly regulate PTPN11 expression by sponging miR-505-3p. CONCLUSIONS: These data revealed a comprehensive circRNA-associated ceRNA network during T. asahii infection, thus providing new insights into the pathogenesis of the T. asahii-host interactions.	NA	Mil Med Res. 2021 Mar 9;8(1):19. doi: 10.1186/s40779-021-00311-w.
3640	Circular RNA	hsa_circ_0072309	miR-607	FTO	NSCLC tissue and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	microarray;Luciferase reporter assay;	33879631	Circular RNA hsa_circ_0072309 promotes tumorigenesis and invasion by regulating the miR-607/FTO axis in non-small cell lung carcinoma.	Emerging evidence has demonstrated that circular RNAs (circRNAs) are abnormally expressed in non-small cell lung carcinoma (NSCLC). However, the contributions of circRNAs to the tumorigenesis of lung adenocarcinoma (LUAD), one of the subtypes of NSCLC, remain unclear. Based on a microarray assay, we found that hsa_circ_0072309 was significantly upregulated in NSCLC compared with matched normal samples. Moreover, functional experiments demonstrated that hsa_circ_0072309 promotes the proliferation, migration, and invasion of NSCLC cells. In vitro precipitation of circRNAs, luciferase reporter assays, and biotin-coupled microRNA capture assays were carried out to investigate the mechanisms by which hsa_circ_0072309 regulates NSCLC. Through the above work, we found that hsa_circ_0072309 interacted with miR-607 via its miRNA response element to upregulate the expression of FTO, an m6A demethylase and downstream target of miR-607, thus promoting tumorigenesis of NSCLC. In total, our findings indicated the oncogenic role of hsa_circ_0072309 in NSCLC and provide a potential target for treatment.	NA	Aging (Albany NY). 2021 Apr 20;13(8):11629-11645. doi: 10.18632/aging.202856. Epub 2021 Apr 20.
3641	LncRNA	LINC00263	miR-147a	CAPN2	various other types of cancer cells	Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;RNA sequencing;	33731671	hnRNPK-regulated LINC00263 promotes malignant phenotypes through miR-147a/CAPN2.	Malignant characteristics of cancers, represented by rapid cell proliferation and high metastatic potential, are a major cause of high cancer-related mortality. As a multifunctional RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK) is closely associated with cancer progression in various types of cancers. In this study, we sought to identify hnRNPK-regulated long intergenic non-coding RNAs (lincRNAs) that play a critical role in the regulation of cancer malignancy. We found that hnRNPK controlled malignant phenotypes including invasiveness, proliferation, and clonogenicity. RNA sequencing and functional studies revealed that LINC00263, a novel target of hnRNPK, is involved in the oncogenic functions of hnRNPK. Knockdown of LINC00263 mitigated the malignant capabilities. Conversely, increased malignant phenotypes were observed in LINC00263-overexpressing cells. Since LINC00263 was mainly localized in the cytosol and highly enriched in Argonaute 2-immunoprecipitation (Ago2-IP), we hypothesized that LINC00263 acts as a competitive endogenous RNA (ceRNA), and thus sought to identify LINC00263-associated microRNAs. Using small RNA sequencing followed by antisense oligonucleotide pull-down, miR-147a was selected for further study. We found that miR-147a negatively regulates LINC00263 via direct interaction, thus suppressing malignant capabilities. Moreover, knockdown of hnRNPK and LINC00263 upregulated miR-147a, indicating that LINC00263 serves as a ceRNA for miR-147a. By analyzing RNA sequencing data and miRNA target prediction, calpain 2 (CAPN2) was identified as a putative target of miR-147a. Ago2-IP and luciferase reporter assay revealed that miR-147a suppressed CAPN2 expression by directly binding to the 3'UTR of CAPN2 mRNA. In addition, we found that the weakened malignant capabilities following knockdown of hnRNPK or LINC00263 were restored by miR-147a inhibition or CAPN2 overexpression. Furthermore, our findings were validated in various other types of cancer cells including lung cancer, colorectal cancer, neuroblastoma, and melanoma. Collectively, we demonstrate that hnRNPK-regulated LINC00263 plays an important role in cancer malignancy by acting as a miR-147a decoy and thus upregulating CAPN2.	NA	Cell Death Dis. 2021 Mar 17;12(4):290. doi: 10.1038/s41419-021-03575-1.
3642	LncRNA	LINC00263	miR-147a	CAPN2	various other types of cancer cells	Colorectal Cancer	Homo sapiens (human)	Luciferase reporter assay;RNA sequencing;	33731671	hnRNPK-regulated LINC00263 promotes malignant phenotypes through miR-147a/CAPN2.	Malignant characteristics of cancers, represented by rapid cell proliferation and high metastatic potential, are a major cause of high cancer-related mortality. As a multifunctional RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK) is closely associated with cancer progression in various types of cancers. In this study, we sought to identify hnRNPK-regulated long intergenic non-coding RNAs (lincRNAs) that play a critical role in the regulation of cancer malignancy. We found that hnRNPK controlled malignant phenotypes including invasiveness, proliferation, and clonogenicity. RNA sequencing and functional studies revealed that LINC00263, a novel target of hnRNPK, is involved in the oncogenic functions of hnRNPK. Knockdown of LINC00263 mitigated the malignant capabilities. Conversely, increased malignant phenotypes were observed in LINC00263-overexpressing cells. Since LINC00263 was mainly localized in the cytosol and highly enriched in Argonaute 2-immunoprecipitation (Ago2-IP), we hypothesized that LINC00263 acts as a competitive endogenous RNA (ceRNA), and thus sought to identify LINC00263-associated microRNAs. Using small RNA sequencing followed by antisense oligonucleotide pull-down, miR-147a was selected for further study. We found that miR-147a negatively regulates LINC00263 via direct interaction, thus suppressing malignant capabilities. Moreover, knockdown of hnRNPK and LINC00263 upregulated miR-147a, indicating that LINC00263 serves as a ceRNA for miR-147a. By analyzing RNA sequencing data and miRNA target prediction, calpain 2 (CAPN2) was identified as a putative target of miR-147a. Ago2-IP and luciferase reporter assay revealed that miR-147a suppressed CAPN2 expression by directly binding to the 3'UTR of CAPN2 mRNA. In addition, we found that the weakened malignant capabilities following knockdown of hnRNPK or LINC00263 were restored by miR-147a inhibition or CAPN2 overexpression. Furthermore, our findings were validated in various other types of cancer cells including lung cancer, colorectal cancer, neuroblastoma, and melanoma. Collectively, we demonstrate that hnRNPK-regulated LINC00263 plays an important role in cancer malignancy by acting as a miR-147a decoy and thus upregulating CAPN2.	NA	Cell Death Dis. 2021 Mar 17;12(4):290. doi: 10.1038/s41419-021-03575-1.
3643	LncRNA	LINC00263	miR-147a	CAPN2	various other types of cancer cells	Neuroblastoma	Homo sapiens (human)	Luciferase reporter assay;RNA sequencing;	33731671	hnRNPK-regulated LINC00263 promotes malignant phenotypes through miR-147a/CAPN2.	Malignant characteristics of cancers, represented by rapid cell proliferation and high metastatic potential, are a major cause of high cancer-related mortality. As a multifunctional RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK) is closely associated with cancer progression in various types of cancers. In this study, we sought to identify hnRNPK-regulated long intergenic non-coding RNAs (lincRNAs) that play a critical role in the regulation of cancer malignancy. We found that hnRNPK controlled malignant phenotypes including invasiveness, proliferation, and clonogenicity. RNA sequencing and functional studies revealed that LINC00263, a novel target of hnRNPK, is involved in the oncogenic functions of hnRNPK. Knockdown of LINC00263 mitigated the malignant capabilities. Conversely, increased malignant phenotypes were observed in LINC00263-overexpressing cells. Since LINC00263 was mainly localized in the cytosol and highly enriched in Argonaute 2-immunoprecipitation (Ago2-IP), we hypothesized that LINC00263 acts as a competitive endogenous RNA (ceRNA), and thus sought to identify LINC00263-associated microRNAs. Using small RNA sequencing followed by antisense oligonucleotide pull-down, miR-147a was selected for further study. We found that miR-147a negatively regulates LINC00263 via direct interaction, thus suppressing malignant capabilities. Moreover, knockdown of hnRNPK and LINC00263 upregulated miR-147a, indicating that LINC00263 serves as a ceRNA for miR-147a. By analyzing RNA sequencing data and miRNA target prediction, calpain 2 (CAPN2) was identified as a putative target of miR-147a. Ago2-IP and luciferase reporter assay revealed that miR-147a suppressed CAPN2 expression by directly binding to the 3'UTR of CAPN2 mRNA. In addition, we found that the weakened malignant capabilities following knockdown of hnRNPK or LINC00263 were restored by miR-147a inhibition or CAPN2 overexpression. Furthermore, our findings were validated in various other types of cancer cells including lung cancer, colorectal cancer, neuroblastoma, and melanoma. Collectively, we demonstrate that hnRNPK-regulated LINC00263 plays an important role in cancer malignancy by acting as a miR-147a decoy and thus upregulating CAPN2.	NA	Cell Death Dis. 2021 Mar 17;12(4):290. doi: 10.1038/s41419-021-03575-1.
3644	LncRNA	LINC00263	miR-147a	CAPN2	various other types of cancer cells	Melanoma	Homo sapiens (human)	Luciferase reporter assay;RNA sequencing;	33731671	hnRNPK-regulated LINC00263 promotes malignant phenotypes through miR-147a/CAPN2.	Malignant characteristics of cancers, represented by rapid cell proliferation and high metastatic potential, are a major cause of high cancer-related mortality. As a multifunctional RNA-binding protein, heterogeneous nuclear ribonucleoprotein K (hnRNPK) is closely associated with cancer progression in various types of cancers. In this study, we sought to identify hnRNPK-regulated long intergenic non-coding RNAs (lincRNAs) that play a critical role in the regulation of cancer malignancy. We found that hnRNPK controlled malignant phenotypes including invasiveness, proliferation, and clonogenicity. RNA sequencing and functional studies revealed that LINC00263, a novel target of hnRNPK, is involved in the oncogenic functions of hnRNPK. Knockdown of LINC00263 mitigated the malignant capabilities. Conversely, increased malignant phenotypes were observed in LINC00263-overexpressing cells. Since LINC00263 was mainly localized in the cytosol and highly enriched in Argonaute 2-immunoprecipitation (Ago2-IP), we hypothesized that LINC00263 acts as a competitive endogenous RNA (ceRNA), and thus sought to identify LINC00263-associated microRNAs. Using small RNA sequencing followed by antisense oligonucleotide pull-down, miR-147a was selected for further study. We found that miR-147a negatively regulates LINC00263 via direct interaction, thus suppressing malignant capabilities. Moreover, knockdown of hnRNPK and LINC00263 upregulated miR-147a, indicating that LINC00263 serves as a ceRNA for miR-147a. By analyzing RNA sequencing data and miRNA target prediction, calpain 2 (CAPN2) was identified as a putative target of miR-147a. Ago2-IP and luciferase reporter assay revealed that miR-147a suppressed CAPN2 expression by directly binding to the 3'UTR of CAPN2 mRNA. In addition, we found that the weakened malignant capabilities following knockdown of hnRNPK or LINC00263 were restored by miR-147a inhibition or CAPN2 overexpression. Furthermore, our findings were validated in various other types of cancer cells including lung cancer, colorectal cancer, neuroblastoma, and melanoma. Collectively, we demonstrate that hnRNPK-regulated LINC00263 plays an important role in cancer malignancy by acting as a miR-147a decoy and thus upregulating CAPN2.	NA	Cell Death Dis. 2021 Mar 17;12(4):290. doi: 10.1038/s41419-021-03575-1.
3645	LncRNA	LINC00284	miR-211-3p	MAFG	OSCC tissues and cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Rescue assay;	33618612	Silencing of LINC00284 inhibits cell proliferation and migration in oral squamous cell carcinoma by the miR-211-3p/MAFG axis and FUS/KAZN axis.	Oral squamous cell carcinoma (OSCC) is one of the most common malignancies worldwide. Emerging evidence has suggested that long noncoding RNAs (lncRNAs) play vital roles in various biological processes of cancers, such as cell proliferation, migration, invasion, and apoptosis. As reported previously, long intergenic non-protein coding RNA 284 (LINC00284) is an important regulator in multiple cancers. However, the biological role, as well as regulatory mechanism of LINC00284 in OSCC, has not been investigated. In our study, RT-qPCR results indicated that LINC00284 was significantly upregulated in OSCC tissues and cells. Moreover, loss-of-function experiments demonstrated that LINC00284 downregulation suppressed cell proliferation and migration and facilitated cell apoptosis. Mechanistically, we found that LINC00284 sponged microRNA 211-3p (miR-211-3p) to upregulate MAF bZIP transcription factor G (MAFG) expression in OSCC cells. Additionally, LINC00284 interacted with FUS protein to increase KAZN mRNA stability. Functional assays showed that either MAFG or KAZN overexpression promoted the malignant behaviors of OSCC cells. Through a series of rescue assays, we found that the inhibitory effect of silencing LINC00284 on OSCC cells can be reversed by upregulated MAFG and KAZN. Overall, silencing LINC00284 inhibits the malignant characteristics of OSCC cells by downregulating MAFG and inhibiting the binding of FUS to KAZN mRNA.	NA	Cancer Biol Ther. 2021 Feb 1;22(2):149-163. doi: 10.1080/15384047.2021.1877864. Epub 2021 Feb 22.
3646	LncRNA	LINC00461	miR-219-5p	COX-2	EC patient tissues and cell lines	Endometrial Cancer	Homo sapiens (human)	qRT-PCR	33573388	LINC00461 Promoted Endometrial Carcinoma Growth and Migration by Targeting MicroRNA-219-5p/Cyclooxygenase-2 Signaling Axis.	Endometrial carcinoma (EC) ranks as the most common female genital cancer in developed countries. Lately, more and more long noncoding RNAs (lncRNAs) have been identified as vital regulators in numerous physiological and pathological processes, including EC. However, the expression pattern and precise functions of different lncRNAs in EC remain unclear. In this study, we reported LINC00461 was upregulated in EC patient tissues and cell lines. In addition, LINC00461 knockdown could remarkably suppress cell proliferation, cell cycle progression, cell migration, and promote cell apoptosis in EC cells. We discovered LINC00461 could sponge microRNA-219-5p (miR-219-5p) and suppress its expression, thereby upregulating expression level of miR-219-5p's target, cyclooxygenase-2 (COX-2). In vivo animal models, LINC00461 knockdown inhibited tumor growth by increasing miR-219-5p level and reducing COX-2 expression, thus confirming LINC00461 functions as an oncogene in EC. In this study, a novel regulatory role of LINC00461/miR-219-5p/COX-2 axis was systematically investigated in context of EC, with the aim to provide promising intervention targets for EC therapy from bench to clinic. [Formula: see text].	NA	Cell Transplant. 2021 Jan-Dec;30:963689721989616. doi: 10.1177/0963689721989616.
3647	LncRNA	LINC00488	miR-376a-3p	PON2	thyroid cancer cell lines (BCPAP, BHP5-16, TPC-1 and CGTH-W3)	Thyroid Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	33600548	Long non-coding RNA LINC00488 facilitates thyroid cancer cell progression through miR-376a-3p/PON2.	OBJECTIVE: Long non-coding RNAs (lncRNAs) recently have been identified as influential indicators in a variety of malignancies. The aim of the present study was to identify a functional lncRNA LINC00488 and its effects on thyroid cancer in the view of cell proliferation and apoptosis. METHODS: In order to evaluate the effects of LINC00488 on the cellular process of thyroid cancer, we performed a series of in vitro experiments, including cell counting kit-8 (CCK-8) assay, EdU (5-ethynyl-2'-deoxyuridine) assay, flow cytometry, transwell chamber assay, Western blot and RT-qPCR. The target gene of LINC00488 was then identified by bioinformatics analysis (DIANA and TargetScan). Finally, a series of rescue experiments was conducted to validate the effect of LINC00488 and its target genes on proliferation, migration, invasion and apoptosis of thyroid cancer. RESULTS: Our findings revealed that LINC00488 was highly expressed in thyroid cancer cell lines (BCPAP, BHP5-16, TPC-1 and CGTH-W3) and promoted the proliferation, migration and invasion, while inhibited the apoptosis of thyroid cancer cells (BCPAP and TPC-1). The results of bioinformatics analysis and dual luciferase reporter gene assay showed that LINC00488 could directly bind to miR-376a-3p and down-regulated the expression level of miR-376a-3p. In addition, Paraoxonase-2 (PON2) was a target gene of miR-376a-3p and negatively regulated by miR-376a-3p. Rescue experiment indicated that LINC00488 might enhance PON2 expression by sponging miR-376a-3p in thyroid cancer. CONCLUSION: Taken together, our study revealed that lncRNA LINC00488 acted as an oncogenic gene in the progression of thyroid cancer via regulating miR-376a-3p/PON2 axis, which indicated that LINC00488-miR-376a-3p-PON2 axis could serve as novel biomarkers or potential targets for the treatment of thyroid cancer.	NA	Biosci Rep. 2021 Mar 26;41(3):BSR20201603. doi: 10.1042/BSR20201603.
3648	LncRNA	LINC00518	miR-33a-3p	HIF-1a	CMM cells	Cutaneous Melanoma	Homo sapiens (human)	qRT-PCR	33664256	Long noncoding RNA LINC00518 induces radioresistance by regulating glycolysis through an miR-33a-3p/HIF-1α negative feedback loop in melanoma.	The long noncoding RNA, LINC00518, is highly expressed in various types of cancers and is involved in cancer progression. Although LINC00518 promotes the metastasis of cutaneous malignant melanoma (CMM), the mechanism underlaying its effects on CMM radiosensitivity remains unclear. In this study, LINC00518 expression was significantly upregulated in CMM samples, and LINC00518 levels were associated with poor prognosis of patients with CMM. Knockdown of LINC00518 in CMM cells significantly inhibited cell invasion, migration, proliferation, and clonogenicity. LINC00518-mediated invasion, migration, proliferation, and clonogenicity were negatively regulated by the microRNA, miR-33a-3p, in vitro, which increased sensitivity to radiotherapy via inhibition of the hypoxia-inducible factor 1α (HIF-1α)/lactate dehydrogenase A glycolysis axis. Additionally, HIF-1α recognized the miR-33a-3p promoter region and recruited histone deacetylase 2, which decreased the expression of miR-33a-3p and formed an LINC00518/miR-33a-3p/HIF-1α negative feedback loop. Furthermore, signaling with initially activated glycolysis and radioresistance in CMM cells was impaired by Santacruzamate A, a histone deacetylase inhibitor, and 2-deoxy-D-glucose, a glycolytic inhibitor. Lastly, knockdown of LINC00518 expression sensitized CMM cancer cells to radiotherapy in an in vivo subcutaneously implanted tumor model. In conclusion, LINC00518 was confirmed to be an oncogene in CMM, which induces radioresistance by regulating glycolysis through an miR-33a-3p/HIF-1α negative feedback loop. Our study, may provide a potential strategy to improve the treatment outcome of radiotherapy in CMM.	NA	Cell Death Dis. 2021 Mar 4;12(3):245. doi: 10.1038/s41419-021-03523-z.
3649	LncRNA	LINC00520	miR-577	CCNE2	NSCLC tissue and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33728585	SP1-induced overexpression of LINC00520 facilitates non-small cell lung cancer progression through miR-577/CCNE2 pathway and predicts poor prognosis.	Long noncoding RNAs (lncRNAs) have gained much attention in the past few years. Long intergenic non-protein coding RNA 520 (LINC00520) was one of the newly discovered lncRNA which has been demonstrated to be dysregulated in several cancers. So far, the function and mechanism of LINC00520 in non-small cell lung cancer (NSCLC) are unclear. In this paper, our group first showed that LINC00520 level was elevated in non-small cell lung cancer (NSCLC) tissue and cells. In addition, SP1 could bind directly to the promoter region of LINC00520 and thus promote its transcription. Increased LINC00520 was distinctly correlated with advanced tumor stage and shorter survival time in NSCLC patients. Further functional investigations provided evidences that forced down regulation of LINC00520 inhibited NSCLC cell proliferation, invasion, metastasis and EMT, while contributing to cells apoptosis. Mechanistically, we found that LINC00520 serving as a competing endogenous RNA to be involved in the modulation of miR-577 expressions, and thus affected the expression of CCNE2 which was a target gene of miR-577. Moreover, in NSCLC cells with si-LINC00520, up regulation of CCNE2 led to an increase of cell growth and invasion. Taken together, LINC00520 displayed its tumor-promotive roles through modulating the miR-577/CCNE2 axis, highlighting a potential therapeutic strategy for NSCLC patients.	NA	Hum Cell. 2021 May;34(3):952-964. doi: 10.1007/s13577-021-00518-y. Epub 2021 Mar 11.
3650	LncRNA	LINC00662	miR-103a-3p	PDK4	CC cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Rescue assay;	33819358	LINC00662 modulates cervical cancer cell proliferation, invasion, and apoptosis via sponging miR-103a-3p and upregulating PDK4.	Cervical cancer (CC) is one of the most common cancers among women with high recurrence rates all over the world. Recently, the molecular mechanism of CC has been gradually uncovered in accumulating reports. This study aimed to investigate the function and upstream regulation mechanism of pyruvate dehydrogenase kinase 4 (PDK4) in CC cells, which was verified as an oncogene in several cancers. Through RT-qPCR assay, we discovered that PDK4 was highly expressed in CC cells. Then, it was demonstrated in function assays that PDK4 facilitated CC cell proliferation and invasion, but inhibited CC cell apoptosis. Next, we sought to determine the upstream genes of PDK4, and miR-103a-3p was identified to target PDK4. Then, through bioinformatics tools and a range of mechanism assays, long intergenic non-protein coding RNA 662 (LINC00662) was verified as the sponge of miR-103a-3p. Moreover, LINC00662 positively modulated PDK4 expression via competitively binding to miR-103a-3p in CC cells. Subsequently, rescue assays demonstrated that LINC00662 accelerated CC cell proliferation and inhibited cell apoptosis through upregulating PDK4. Furthermore, forkhead box A1 (FOXA1) was verified to activate transcription of both LINC00662 and PDK4. Taken together, our study revealed a novel ceRNA pattern of LINC00662/miR-103a-3p/PDK4 with FOXA1 as a transcription factor of LINC00662 and PDK4 in CC cells.	NA	Mol Carcinog. 2021 Jun;60(6):365-376. doi: 10.1002/mc.23294. Epub 2021 Apr 5.
3651	LncRNA	LINC00857	miR-1306	Vimentin	colorectal cancer tissue samples and cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33833823	Long Noncoding RNA LINC00857 Promotes Proliferation, Migration, and Invasion of Colorectal Cancer Cell through miR-1306/Vimentin Axis.	Colorectal cancer is a commonly diagnosed cancer and the leading cause of cancer-related death which still increasing in many countries. The lack of biomarkers for early detection and clinic treatment results in high morbidity and mortality. The novel role of long noncoding RNA LINC00857 on cell proliferation migration and invasion was explored in this article. The expression level of LINC00857 in colorectal cancer tissue samples and cells was determined notably higher than normal tissue samples and cells. Silence LINC00857 can significantly inhibit colorectal cancer cell viability and metastasis in vitro. Moreover, LINC00857 depletion caused cell accumulation in the G0/G1 phase. In addition, we recognized the novel LINC00857-miR-1306-vimentin axis and demonstrated it by dual-luciferase reporter assay. And this signaling axis could be considered as the target for colorectal cancer treatment. In conclusion, LINC00857 can promote colorectal cancer progress by sponging miR-1306 and upregulate vimentin to accelerate the epithelial-mesenchymal transition process.	NA	Comput Math Methods Med. 2021 Mar 23;2021:5525763. doi: 10.1155/2021/5525763. eCollection 2021.
3652	LncRNA	LINC00857	miR-340-5p	TGFA	PAAD tissues and cells	Pancreatic Cancer	Homo sapiens (human)	luciferase assay;	33661995	LncRNA LINC00857 strengthens the malignancy behaviors of pancreatic adenocarcinoma cells by serving as a competing endogenous RNA for miR-340-5p to upregulate TGFA expression.	BACKGROUND: Pancreatic adenocarcinoma (PAAD) is a pancreatic disease with a high mortality rate in the world. This present research intends to identify the function of lncRNA LINC00857/miR-340-5p/Transforming growth factor alpha (TGFA) in the progression of PAAD. METHODS: Bioinformatics analysis was used to explore the differentially expressed lncRNA/miRNA/mRNA and analyze the relationship between lncRNA/miRNA/mRNA expression and prognosis of PAAD by enquiring TCGA, GEO and GTEX. KEGG pathway analysis and GO enrichment analysis were implemented to annotate the crucial genes regulated by LINC00857. The biological behaviors of PAAD cells were detected by CCK-8, colony formation and transwell assays. Interactive associations between LINC00857 and miR-340-5p, as well as miR-340-5p and TGFA were analyzed by dual luciferase assay. RESULTS: By enquiring TCGA database, we got that LINC00857 was highly expressed in patients with PAAD and positively associated with worse prognosis in PAAD patients. Moreover, LINC00857 upregulation promoted the proliferation and clone formation abilities of PAAD cells. Afterwards, the downstream miRNA and mRNA targets of LINC00857 were picked up to construct a ceRNA network. Further study revealed that TGFA expression was positively regulated by LINC00857 and negatively regulated by miR-340-5p. Besides that, the inhibitory effect of miR-340-5p on PAAD cells growth and movement can be blocked by LINC00857 upregulation. While, the malignant behavior of PAAD cells induced by TGFA overexpression can be eliminated by LINC00857 knockdown. CONCLUSIONS: Upregulation of LINC00857 improved growth, invasion and migration abilities of PAAD cells by modulation of miR-340-5p/TGFA, affording potential targets and biomarkers for the clinical diagnosis and treatment.	NA	PLoS One. 2021 Mar 4;16(3):e0247817. doi: 10.1371/journal.pone.0247817. eCollection 2021.
3653	LncRNA	LINC00936	miR-425-3p	ZC3H12A	GC tissues and cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33756228	Elevated linc00936 or silenced microRNA-425-3p inhibits immune escape of gastric cancer cells via elevation of ZC3H12A.	OBJECTIVE: Gastric cancer (GC) is a malignant tumor originated from gastric mucosa. Without effective therapy, this study was to investigate the mechanism of long intergenic noncoding RNA 00936 (linc00936)/microRNA-425-3p (miR-425-3p)/monocyte chemotactic protein-induced protein 1 (ZC3H12A) axis mediating immune escape of GC cells. METHODS: Peripheral blood samples, GC tissues and adjacent tissues were collected. The levels of CD3(+), CD4(+), and CD8(+) in peripheral blood were detected. The expression levels of linc00936, miR-425-3p and ZC3H12A in GC tissues and cells were detected. The correlation between the expression of linc00936 in the tissues and the levels of CD3(+), CD4(+) and CD8(+) in the peripheral blood of GC patients was analyzed. Cytokine-induced killer (CIK) cells were induced, and co-incubated with GC cells. BGC-823 and MKN-45 cells were screened and transfected with linc00936- or miR-425-3p-related oligonucleotides to figure out their roles in immune escape, migration, apoptosis and the cytotoxicity of CIK cells in GC cells. RESULTS: Elevated miR-425-3p and reduced linc00936, and ZC3H12A expression levels were found in GC tissues and cells. Linc00936 expression was positively correlated with CD3(+) and CD4(+), and negatively correlated with CD8(+) in peripheral blood of patients with GC. Up-regulating linc00936 or down-regulating miR-425-3p inhibited immune escape, migration, promoted apoptosis of GC cells, as well induced CIK cell cytotoxicity to GC cells. Down-regulated linc00936 or elevated miR-425-3p facilitated immune escape, migration, depressed apoptosis of GC cells, and reduced the cytotoxicity of CIK cells to GC cells. CONCLUSION: The study concludes that up-regulated linc00936 or silenced miR-425-3p inhibits immune escape of GC cells via elevation of ZC3H12A.	NA	Int Immunopharmacol. 2021 Jun;95:107559. doi: 10.1016/j.intimp.2021.107559. Epub 2021 Mar 20.
3654	LncRNA	LINC01116	miR-744-5p	TGF-b1	glioma tissues and cells	Glioma	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	34150180	Knocking down LINC01116 can inhibit the regulation of TGF-β through miR-774-5p axis and inhibit the occurrence and development of glioma.	BACKGROUND: Many studies have shown that non-coding RNAs (ncRNAs), including long non-coding RNA (LncRNA) and micro RNA (miRNA), play a crucial regulatory role in glioma. LINC01116 is a newly discovered LncRNA, and the relationship between LncRNA and glioma is still under exploration. METHOD: LncRNAs with potential differences were screened through GEO database, and the expressions of LINC01116 and miR-744-5p/TGF-β1 in glioma tissues were tested using qRT-PCR. Changes in proliferation and migration/invasion of glioma were tested using CCK-8 and transwell assay. The expression changes of TGF-β1 were tested using qRT-PCR and Western blot. Targeted binding among LINC01116, miR-744-5p and TGF-β1 was verified using double luciferase reporter, RNA Immunoprecipitation (PIR) and RNA pull-down experiments. The effect of LINC01116 on tumor growth was determined by tumor allografting test. RESULTS: GEO database and clinical research revealed that the expression level of LINC01116 in glioma increased, and the elevation of LINC01116 was closely related to the adverse prognosis of clinical patients. Functional experiments showed that the inhibition of LINC01116 could up-regulate miR-744-5p-mediated proliferation and metastasis of glioma cells. Western blot analysis and qRT-PCR analysis showed that LINC01116 regulated TGF-β1 by mediating miR-744-5p. Further cell behavior experiments showed that LINC01116 acted as miR-744-5p sponge to inhibit proliferation and metastasis caused by TGF-β1. Finally, the analysis of animal models in vivo showed that LINC01116 could regulate the tumor growth of glioma. CONCLUSION: LncRNA LINC01116 acts as an oncogene and promotes TGF-β1 mediated proliferation and metastasis by acting as competitive endogenous RNA (ceRNA) in glioma.	NA	Am J Transl Res. 2021 May 15;13(5):5702-5719. eCollection 2021.
3655	LncRNA	LINC01116	miR-744-5p	UBE2L3	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Rescue assay;	33726770	Long non-coding RNA LINC01116 acts as an oncogene in prostate cancer cells through regulation of miR-744-5p/UBE2L3 axis.	BACKGROUND: Long non-coding RNA (lncRNA) has been confirmed to exert a critical effect on the progression of tumors, including prostate cancer. Previous literature has demonstrated LINC01116 involves in activities of multiple cancers. However, the underlying role of LINC01116 in prostate cancer remains unclear. METHODS: qRT-PCR measured the expression of LINC01116 in prostate cancer cells. EdU experiment was used to detect cell proliferation. Transwell assays detected cell migration and invasion. Immunofluorescence staining and western blot assays were utilized to measure EMT progress. The binding relationship between RNAs was confirmed by a series of mechanism assays. In addition, rescue experiments were conducted to verify the relationship among RNAs. RESULTS: LINC01116 was found to be highly expressed in prostate cancer cells. Functional assays indicated that inhibition of LINC01116 could suppress cell proliferation, migration, invasion and EMT progress. Also, miR-744-5p was proven to bind with LINC01116. Moreover, UBE2L3 was verified as the target gene of miR-744-5p. In rescue assays, we discovered that inhibited miR-744-5p or overexpressed UBE2L3 could offset the suppressive influence of silencing LINC01116 on prostate cancer cells. CONCLUSION: Our study suggested that lncRNA LINC01116 acted as an oncogene in prostate cancer and accelerated prostate cancer cell growth through regulating miR-744-5p/UBE2L3 axis.	NA	Cancer Cell Int. 2021 Mar 16;21(1):168. doi: 10.1186/s12935-021-01843-w.
3656	LncRNA	LINC01291	miR-625-5p	IGF-1R	melanoma tumors and cells	Melanoma	Homo sapiens (human)	Cell migration and invasion assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33674778	Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression.	Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291's role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.	NA	Cancer Gene Ther. 2021 Mar 5. doi: 10.1038/s41417-021-00313-9.
3657	LncRNA	LINC01296	miR-141-3p	ZEB1	NSCLC, CRC tissues and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;Western blot;	33854632	LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process.	Purpose: Tumor metastasis seriously affects the survival of patients. In recent years, some studies confirmed that long non-coding RNA (lncRNA) played an essential role in tumor progression. A few studies reported that LINC01296 acted as an oncogenic regulator of cancer. However, its in-depth specific biological mechanism in tumor metastasis is still unknown. Methods: Real-time quantitative PCR (qPCR) was performed to detect the expression of LINC01296 and miR-141-3p in NSCLC, CRC tissues and cell lines, and the dual luciferase report was used to evaluate the relationship between LINC01296, miR-141-3p and ZEB1/ZEB2 relationship. Western blot experiments are used to detect changes in protein levels. Transwell and wound healing measures migration and invasion capabilities. Results: In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis. We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. Conclusions: The report revealed a new mechanism by which LINC01296 regulates the EMT process through miR-141-3p/ZEB1-ZEB2 axis and affects cancer metastasis.	NA	J Cancer. 2021 Mar 5;12(9):2723-2734. doi: 10.7150/jca.55626. eCollection 2021.
3658	LncRNA	LINC01296	miR-141-3p	ZEB2	NSCLC, CRC tissues and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;Western blot;	33854632	LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process.	Purpose: Tumor metastasis seriously affects the survival of patients. In recent years, some studies confirmed that long non-coding RNA (lncRNA) played an essential role in tumor progression. A few studies reported that LINC01296 acted as an oncogenic regulator of cancer. However, its in-depth specific biological mechanism in tumor metastasis is still unknown. Methods: Real-time quantitative PCR (qPCR) was performed to detect the expression of LINC01296 and miR-141-3p in NSCLC, CRC tissues and cell lines, and the dual luciferase report was used to evaluate the relationship between LINC01296, miR-141-3p and ZEB1/ZEB2 relationship. Western blot experiments are used to detect changes in protein levels. Transwell and wound healing measures migration and invasion capabilities. Results: In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis. We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. Conclusions: The report revealed a new mechanism by which LINC01296 regulates the EMT process through miR-141-3p/ZEB1-ZEB2 axis and affects cancer metastasis.	NA	J Cancer. 2021 Mar 5;12(9):2723-2734. doi: 10.7150/jca.55626. eCollection 2021.
3659	LncRNA	LINC01296	miR-141-3p	ZEB1	NSCLC, CRC tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	qPCR;Western blot;	33854632	LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process.	Purpose: Tumor metastasis seriously affects the survival of patients. In recent years, some studies confirmed that long non-coding RNA (lncRNA) played an essential role in tumor progression. A few studies reported that LINC01296 acted as an oncogenic regulator of cancer. However, its in-depth specific biological mechanism in tumor metastasis is still unknown. Methods: Real-time quantitative PCR (qPCR) was performed to detect the expression of LINC01296 and miR-141-3p in NSCLC, CRC tissues and cell lines, and the dual luciferase report was used to evaluate the relationship between LINC01296, miR-141-3p and ZEB1/ZEB2 relationship. Western blot experiments are used to detect changes in protein levels. Transwell and wound healing measures migration and invasion capabilities. Results: In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis. We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. Conclusions: The report revealed a new mechanism by which LINC01296 regulates the EMT process through miR-141-3p/ZEB1-ZEB2 axis and affects cancer metastasis.	NA	J Cancer. 2021 Mar 5;12(9):2723-2734. doi: 10.7150/jca.55626. eCollection 2021.
3660	LncRNA	LINC01296	miR-141-3p	ZEB2	NSCLC, CRC tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	qPCR;Western blot;	33854632	LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process.	Purpose: Tumor metastasis seriously affects the survival of patients. In recent years, some studies confirmed that long non-coding RNA (lncRNA) played an essential role in tumor progression. A few studies reported that LINC01296 acted as an oncogenic regulator of cancer. However, its in-depth specific biological mechanism in tumor metastasis is still unknown. Methods: Real-time quantitative PCR (qPCR) was performed to detect the expression of LINC01296 and miR-141-3p in NSCLC, CRC tissues and cell lines, and the dual luciferase report was used to evaluate the relationship between LINC01296, miR-141-3p and ZEB1/ZEB2 relationship. Western blot experiments are used to detect changes in protein levels. Transwell and wound healing measures migration and invasion capabilities. Results: In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis. We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. Conclusions: The report revealed a new mechanism by which LINC01296 regulates the EMT process through miR-141-3p/ZEB1-ZEB2 axis and affects cancer metastasis.	NA	J Cancer. 2021 Mar 5;12(9):2723-2734. doi: 10.7150/jca.55626. eCollection 2021.
3661	LncRNA	LINC01564	miR-107	PHGDH	hepatocellular carcinoma cell	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33742121	Energy stress-induced linc01564 activates the serine synthesis pathway and facilitates hepatocellular carcinogenesis.	Cancer cells undergo metabolic adaption to sustain their survival and growth under metabolic stress conditions, yet the underlying mechanism remains largely unclear. It is also not known if lncRNAs contribute to this metabolic adaption of cancer cells. Here we show that linc01564 is induced in response to glucose deprivation by the transcription factor ATF4. Linc01564 functions to facilitate hepatocellular carcinoma cell survival under glucose deprivation by activating the serine synthesis pathway. Mechanistically, linc01564 acts as a competing endogenous RNA for miR-107/103a-3p and attenuates the inhibitory effect of miR-107/103a-3p on PHGDH, the rate-limiting enzyme of the serine synthesis pathway, thereafter leading to increased PHGDH expression. Furthermore, linc01564 is able to promote hepatocellular carcinogenesis via PHGDH. Together, these findings suggest that linc01564 is an important player in the regulation of metabolic adaption of cancer cells and also implicate linc01564 as a potential therapeutic target for cancer.	NA	Oncogene. 2021 Apr;40(16):2936-2951. doi: 10.1038/s41388-021-01749-x. Epub 2021 Mar 19.
3662	LncRNA	LINC01564	miR-103a-3p	PHGDH	hepatocellular carcinoma cell	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33742121	Energy stress-induced linc01564 activates the serine synthesis pathway and facilitates hepatocellular carcinogenesis.	Cancer cells undergo metabolic adaption to sustain their survival and growth under metabolic stress conditions, yet the underlying mechanism remains largely unclear. It is also not known if lncRNAs contribute to this metabolic adaption of cancer cells. Here we show that linc01564 is induced in response to glucose deprivation by the transcription factor ATF4. Linc01564 functions to facilitate hepatocellular carcinoma cell survival under glucose deprivation by activating the serine synthesis pathway. Mechanistically, linc01564 acts as a competing endogenous RNA for miR-107/103a-3p and attenuates the inhibitory effect of miR-107/103a-3p on PHGDH, the rate-limiting enzyme of the serine synthesis pathway, thereafter leading to increased PHGDH expression. Furthermore, linc01564 is able to promote hepatocellular carcinogenesis via PHGDH. Together, these findings suggest that linc01564 is an important player in the regulation of metabolic adaption of cancer cells and also implicate linc01564 as a potential therapeutic target for cancer.	NA	Oncogene. 2021 Apr;40(16):2936-2951. doi: 10.1038/s41388-021-01749-x. Epub 2021 Mar 19.
3663	LncRNA	LincIN	miR-7	HOXB13	ESCC tissues and cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33693959	Upregulated long non-coding RNA LincIN promotes tumor progression via the regulation of nuclear factor 90/microRNA-7/HOXB13 in esophageal squamous cell carcinoma.	Long non-coding RNA LincIN has been reported to be overexpressed and to be involved in the metastasis of breast cancer. However, the expression and role of LincIN in esophageal squamous cell carcinoma (ESCC) remain unsolved. In the present study, LincIN expression was examined in ESCC by RT-qPCR, and the roles of LincIN in ESCC were determined using cell growth, migration and invasion assays. In addition, the effects of LincIN on nuclear factor 90 (NF90) and microRNA/miR (miR)-7 were examined by RNA immunoprecipitation assay, RT-qPCR, dual-luciferase reporter assay and western blot analysis. The results revealed that LincIN expression was significantly increased in ESCC tissues and cell lines. The increased expression of LincIN was positively associated with invasion depth, lymph node metastasis, TNM stage and a poor prognosis. Functional assays revealed that the overexpression of LincIN promoted ESCC cell growth, migration and invasion. Mechanistic analysis revealed that LincIN physically bound to NF90, enhanced the binding between NF90 and primary miR-7 (pri-miR-7), and further enhanced the inhibitory effects of NF90 on miR-7 biogenesis. Therefore, LincIN downregulated miR-7 expression in ESCC. The expression of miR-7 inversely correlated with that of LincIN in ESCC tissues. By downregulating miR-7, LincIN increased the expression of HOXB13, a target of miR-7. The overexpression of miR-7 or the depletion of HOXB13 both attenuated the tumor-promoting roles of LincIN in ESCC cell growth, migration and invasion. On the whole, the findings of the present study suggest that LincIN is overexpressed and plays an oncogenic role in ESCC via the regulation of the NF90/miR-7/HOXB13 axis. Thus, LincIN may prove to be a promising prognostic biomarker and therapeutic target for ESCC.	NA	Int J Mol Med. 2021 May;47(5):78. doi: 10.3892/ijmm.2021.4911. Epub 2021 Mar 11.
3664	LncRNA	LIPE-AS1	miR-195-5p	MAPK	CC tissues and cells	Cervical Cancer	Homo sapiens (human)	RT-PCR;RIP assay;Western blot;Flow Cytometry assay;	33898314	LncRNA LIPE-AS1 Predicts Poor Survival of Cervical Cancer and Promotes Its Proliferation and Migration via Modulating miR-195-5p/MAPK Pathway.	Aims: A growing number of studies have unveiled that long non-coding RNA (lncRNA) is conductive to cervical cancer (CC) development. However, the effect of LIPE-AS1 is remained to be studied in CC. Main Methods: Reverse transcription-polymerase chain reaction (RT-PCR) was employed to measure LIPE-AS1 expression in CC tissues and the adjacent normal tissues. Additionally, we conducted gain- and loss-of functional experiments of LIPE-AS1 and adopted CCK8 assay, BrdU assay, and in vivo tumor formation experiment to test the proliferation of CC cells (HCC94 and HeLa). Besides, the apoptosis, invasion, and epithelial-mesenchymal transformation (EMT) of CC cells were estimated using flow cytometry, transwell assay, and western blot, respectively. Further, LIPE-AS1 downstream targets were analyzed through bioinformatics, and the binding relationships between LIPE-AS1 and miR-195-5p were verified via dual-luciferase activity experiment and RNA Protein Immunoprecipitation (RIP) assay. Moreover, rescue experiments were conducted to confirm the effects of LIPE-AS1 and miR-195-5p in regulating CC development and the expressions of MAPK signaling pathway related proteins were detected by RT-PCR, western blot, and immunofluorescence. Key Findings: LIPE-AS1 was over-expressed in CC tissues (compared to normal adjacent tissues) and was notably related to tumor volume, distant metastasis. Overexpressing LIPE-AS1 accelerated CC cell proliferation, migration and EMT, inhibited apoptosis; while LIPE-AS1 knockdown had the opposite effects. The mechanism studies confirmed that LIPE-AS1 sponges miR-195-5p as a competitive endogenous RNA (ceRNA), which targets the 3'-untranslated region (3'-UTR) of MAP3K8. LIPE-AS1 promoted the expression of MAP3K8 and enhanced ERK1/2 phosphorylation, which were reversed by miR-195-5p. Significance: LIPE-AS1 regulates CC progression through the miR-195-5p/MAPK signaling pathway, providing new hope for CC diagnosis and treatment.	NA	Front Oncol. 2021 Apr 9;11:639980. doi: 10.3389/fonc.2021.639980. eCollection 2021.
3665	LncRNA	lnc865	miR-29b-2-5p	STAT3	TGFβ1-stimulated fibroblast L929 cells	Pulmonary Fibrosis	Homo sapiens (human)	qRT-PCR	33929970	Acetyl oxygen benzoate engeletin ester promotes KLF4 degradation leading to the attenuation of pulmonary fibrosis via inhibiting TGFβ1-smad/p38MAPK-lnc865/lnc556-miR-29b-2-5p-STAT3 signal pathway.	Pulmonary fibrosis is a common pulmonary interstitial disease of pathogenesis without effective drugs for treatment. Therefore, discovering new and effective drugs is urgently needed. In the present study, we prepared a novel compound named acetyl oxygen benzoate engeletin ester (AOBEE), investigated its effect on experimental pulmonary fibrosis, and proposed a long non-coding RNA (lncRNA)-mediated mechanism of its action. Bleomycin-induced pulmonary fibrosis in mice exhibited that AOBEE improved forced vital capacity (FVC) and alveolar structure and inhibited α-SMA, vimentin, and collagen expression. TGFβ1-stimulated fibroblast L929 cells showed that AOBEE reduced these fibrotic proteins expression and inhibited the activated-fibroblast proliferation and migration. Whole transcriptome sequencing was performed to screen out lncRNA-lnc865 and lnc556 with high expression under bleomycin treatment, but AOBEE caused a considerable decrease in lnc865 and lnc556. Mechanistic study elucidated that AOBEE alleviated pulmonary fibrosis through lnc865- and lnc556-mediated mechanism, in which both lnc865 and lnc556 sponged miR-29b-2-5p to target signal transducer and activator of transcription 3 (STAT3). Further signal pathway inhibitors and the Cignal Finder 45-pathway reporter array illustrated that the up- and downstream pathways were TGFβ1-smad2/3 and p38MAPK, and Krüppel-like factor 4 (KLF4), respectively. In conclusion, AOBEE promoted KLF4 degradation leading to the attenuation of pulmonary fibrosis by inhibiting TGFβ1-smad/p38MAPK-lnc865/lnc556-miR-29b-2-5p-STAT3 signal pathway. We hope this work will provide valuable information to design new drugs and therapeutic targets of lncRNAs for pulmonary fibrosis treatment.	NA	Aging (Albany NY). 2021 Apr 30;13(10):13807-13821. doi: 10.18632/aging.202975. Epub 2021 Apr 30.
3666	LncRNA	lnc556	miR-29b-2-5p	STAT3	TGFβ1-stimulated fibroblast L929 cells	Pulmonary Fibrosis	Homo sapiens (human)	qRT-PCR	33929970	Acetyl oxygen benzoate engeletin ester promotes KLF4 degradation leading to the attenuation of pulmonary fibrosis via inhibiting TGFβ1-smad/p38MAPK-lnc865/lnc556-miR-29b-2-5p-STAT3 signal pathway.	Pulmonary fibrosis is a common pulmonary interstitial disease of pathogenesis without effective drugs for treatment. Therefore, discovering new and effective drugs is urgently needed. In the present study, we prepared a novel compound named acetyl oxygen benzoate engeletin ester (AOBEE), investigated its effect on experimental pulmonary fibrosis, and proposed a long non-coding RNA (lncRNA)-mediated mechanism of its action. Bleomycin-induced pulmonary fibrosis in mice exhibited that AOBEE improved forced vital capacity (FVC) and alveolar structure and inhibited α-SMA, vimentin, and collagen expression. TGFβ1-stimulated fibroblast L929 cells showed that AOBEE reduced these fibrotic proteins expression and inhibited the activated-fibroblast proliferation and migration. Whole transcriptome sequencing was performed to screen out lncRNA-lnc865 and lnc556 with high expression under bleomycin treatment, but AOBEE caused a considerable decrease in lnc865 and lnc556. Mechanistic study elucidated that AOBEE alleviated pulmonary fibrosis through lnc865- and lnc556-mediated mechanism, in which both lnc865 and lnc556 sponged miR-29b-2-5p to target signal transducer and activator of transcription 3 (STAT3). Further signal pathway inhibitors and the Cignal Finder 45-pathway reporter array illustrated that the up- and downstream pathways were TGFβ1-smad2/3 and p38MAPK, and Krüppel-like factor 4 (KLF4), respectively. In conclusion, AOBEE promoted KLF4 degradation leading to the attenuation of pulmonary fibrosis by inhibiting TGFβ1-smad/p38MAPK-lnc865/lnc556-miR-29b-2-5p-STAT3 signal pathway. We hope this work will provide valuable information to design new drugs and therapeutic targets of lncRNAs for pulmonary fibrosis treatment.	NA	Aging (Albany NY). 2021 Apr 30;13(10):13807-13821. doi: 10.18632/aging.202975. Epub 2021 Apr 30.
3667	LncRNA	LOXL1-AS1	miR-525-5p	HSPA9	thymoma and thymic carcinoma cells	Thymic Cancer	Homo sapiens (human)	qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33907842	LOXL1-AS1 promotes thymoma and thymic carcinoma progression by regulating miR-525-5p-HSPA9.	Due to the lack of specific symptoms in early thymic epithelial tumours (TETs), patients are mostly in the advanced stage at the time of presentation. The aim of the present study was to explore the mechanism by which the long noncoding RNA (lncRNA) LOXL1-AS1 affects thymoma and thymic carcinoma progression by targeting the miR-525-5p-HSPA9 axis. Bioinformatics was used to analyse the process of LOXL1-AS1 targeting miR-525-5p-HSPA9 and its expression characteristics in TET. The relationships between LOXL1-AS1, miR-525-5p, HSPA9 and prognosis were analysed. The dual luciferase reporter assay was applied to verify targeting. The gene was knocked down or overexpressed by plasmid transfection. Cell counting kit 8 (CCK-8) assay, flow cytometry and Transwell assay were used to detect cell viability, apoptosis and invasion ability, respectively. Proteins and RNAs were examined by western blot analysis and qPCR, respectively. A tumour-burdened assay was used to perform in vivo verification. LOXL1-AS1 and HSPA9 were overexpressed in thymoma and thymic carcinoma; high levels of LOXL1-AS1 and HSPA9 were associated with poor prognosis, and there was a significant positive correlation between their levels. Downregulation of miR-525-5p expression was also associated with poor prognosis of patients. Clinical trials also demonstrated the same trends. miR-525-5p inhibited the expression of HSPA9 protein by targeting the 3'-untranslated region (UTR) of HSPA9 mRNA. LOXL1-AS1 promoted the expression of HSPA9 as a sponge targeting miR-525-5p. Animal experiment results also showed that knockdown of miR-525-5p promoted cancer by promoting the expression of HSPA9. In conclusion, LOXL1-AS1 and HSPA9 are highly expressed in thymoma and thymic carcinoma; miR-525-5p is expressed at low levels in thymoma and thymic carcinoma; and downregulation of miR-525-5p is associated with poor prognosis. In summary, this study demonstrates that LOXL1-AS1 acts as a sponge that targets miR-525-5p to promote HSPA9 expression, thereby promoting the growth and invasion and inhibiting apoptosis of thymoma and thymic carcinoma cells.	NA	Oncol Rep. 2021 Jun;45(6):117. doi: 10.3892/or.2021.8068. Epub 2021 Apr 28.
3668	LncRNA	MALAT1	miR-146b-5p	NUMB	intestinal epithelial cells	Crohns Disease	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qRT-PCR;RIP assay;Luciferase reporter assay;	33677577	MALAT1 maintains the intestinal mucosal homeostasis in Crohn's disease via the miR-146b-5p-CLDN11/NUMB pathway.	BACKGROUND & AIMS: Intestinal homeostasis disorder is critical for developing Crohn's disease (CD). Maintaining mucosal barrier integrity is essential for intestinal homeostasis, preventing intestinal injury and complications. Among the remarkably altered long non-coding RNAs (lncRNAs) in CD, we aimed to investigate whether metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) modulated CD and consequent disruption of intestinal homeostasis. METHODS: Microarray analyses on intestinal mucosa of CD patients and controls were performed to identify dysregulated lncRNAs. MALAT1 expression was investigated via qRT-PCR and its distribution in intestinal tissues was detected using BaseScope. Intestines from MALAT1 knockout mice with colitis were investigated using histological, molecular and biochemical approaches. Effects of intestinal epithelial cells transfected with MALAT1 lentiviruses and Smart Silencer, on monolayer permeability and apical junction complex (AJC) proteins were analysed. MiR-146b-5p were confirmed as a critical MALAT1 mediator in cells transfected with miR-146b-5p mimic/inhibitor and in colitis mice administered with agomir-146b-5p/antagomir-146b-5p. Interaction between MALAT1 and miR-146b-5p was predicted via bioinformatics and validated using Dual-luciferase reporter assay and Ago2-RIP. RESULTS: MALAT1 was aberrantly downregulated in the intestine mucosa of CD patients and mice with experimental colitis. MALAT1 knockout mice were hypersensitive to DSS-induced experimental colitis. MALAT1 regulated intestinal mucosal barrier and regained intestinal homeostasis by sequestering miR-146b-5p and maintaining the expression of the AJC proteins NUMB and CLDN11. CONCLUSIONS: Downregulation of MALAT1 contributed to the pathogenesis of CD by disrupting AJC. Thus, a specific MALAT1-miR-146b-5p-NUMB/CLDN11 pathway that plays a vital role in maintaining intestinal mucosal homeostasis may serve as a novel target for CD treatment.	NA	J Crohns Colitis. 2021 Mar 2:jjab040. doi: 10.1093/ecco-jcc/jjab040.
3669	LncRNA	MALAT1	miR-146b-5p	CLDN11	intestinal epithelial cells	Crohns Disease	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qRT-PCR;RIP assay;Luciferase reporter assay;	33677577	MALAT1 maintains the intestinal mucosal homeostasis in Crohn's disease via the miR-146b-5p-CLDN11/NUMB pathway.	BACKGROUND & AIMS: Intestinal homeostasis disorder is critical for developing Crohn's disease (CD). Maintaining mucosal barrier integrity is essential for intestinal homeostasis, preventing intestinal injury and complications. Among the remarkably altered long non-coding RNAs (lncRNAs) in CD, we aimed to investigate whether metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) modulated CD and consequent disruption of intestinal homeostasis. METHODS: Microarray analyses on intestinal mucosa of CD patients and controls were performed to identify dysregulated lncRNAs. MALAT1 expression was investigated via qRT-PCR and its distribution in intestinal tissues was detected using BaseScope. Intestines from MALAT1 knockout mice with colitis were investigated using histological, molecular and biochemical approaches. Effects of intestinal epithelial cells transfected with MALAT1 lentiviruses and Smart Silencer, on monolayer permeability and apical junction complex (AJC) proteins were analysed. MiR-146b-5p were confirmed as a critical MALAT1 mediator in cells transfected with miR-146b-5p mimic/inhibitor and in colitis mice administered with agomir-146b-5p/antagomir-146b-5p. Interaction between MALAT1 and miR-146b-5p was predicted via bioinformatics and validated using Dual-luciferase reporter assay and Ago2-RIP. RESULTS: MALAT1 was aberrantly downregulated in the intestine mucosa of CD patients and mice with experimental colitis. MALAT1 knockout mice were hypersensitive to DSS-induced experimental colitis. MALAT1 regulated intestinal mucosal barrier and regained intestinal homeostasis by sequestering miR-146b-5p and maintaining the expression of the AJC proteins NUMB and CLDN11. CONCLUSIONS: Downregulation of MALAT1 contributed to the pathogenesis of CD by disrupting AJC. Thus, a specific MALAT1-miR-146b-5p-NUMB/CLDN11 pathway that plays a vital role in maintaining intestinal mucosal homeostasis may serve as a novel target for CD treatment.	NA	J Crohns Colitis. 2021 Mar 2:jjab040. doi: 10.1093/ecco-jcc/jjab040.
3670	LncRNA	MALAT1	miR-135b-5p	GPNMB	SK-N-SH and SK-N-BE cells	Parkinsons Disease	Homo sapiens (human)	qRT-PCR	33726823	Long non-coding RNA MALAT1 regulates cell proliferation and apoptosis via miR-135b-5p/GPNMB axis in Parkinson's disease cell model.	BACKGROUNDS: Parkinson's disease (PD) is a common age-related neurodegenerative disorder worldwide. This research aimed to investigate the effects and mechanism underlying long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PD. METHODS: SK-N-SH and SK-N-BE cells were treated with MPP(+) to establish the MPP(+)-stimulated cell model of PD, and MALAT1 expression was determined. Then, the effects of MALAT1 depletion on cell proliferation and apoptosis were determined in the MPP(+)-stimulated cell model of PD. Besides, the correlations between microRNA-135b-5p (miR-135b-5p) and MALAT1 or glycoprotein nonmetastatic melanoma protein B (GPNMB) in MPP(+)-stimulated cell model of PD were explored. RESULTS: MALAT1 was increasingly expressed and downregulation of MALAT1 promoted cell proliferation while inhibited apoptosis in MPP(+)-stimulated cells. Besides, miR-135b-5p was a target of MALAT1 and directly targeted to GPNMB. Further investigation indicated that suppression of MALAT1 regulated cell proliferation and apoptosis by miR-135b-5p/GPNMB axis. CONCLUSION: Our findings reveal that MALAT1/miR-135b-5p/GPNMB axis regulated cell proliferation and apoptosis in MPP(+)-stimulated cell model of PD, providing a potential biomarker and therapeutic target for PD.	NA	Biol Res. 2021 Mar 16;54(1):10. doi: 10.1186/s40659-021-00332-8.
3671	LncRNA	MALAT1	miR-195a-5p	HMGA1	oxygen-glucose deprivation/reoxygenation (OGD/R) cell model	Ogd/R-Induced Injury	Homo sapiens (human)	qRT-PCR	33750458	LncRNA MALAT1 aggravates oxygen-glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis.	BACKGROUND: This study aimed to investigate the potential role and molecular mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in cerebral ischemia/reperfusion injury. RESULTS: Using an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model, we determined that the expression of MALAT1 was significantly increased during OGD/R. MALAT1 knockdown reversed OGD/R-induced apoptosis and ER stress. Mechanistically, MALAT1 promoted OGD/R-induced neuronal injury through sponging miR-195a-5p to upregulating high mobility group AT-hook1 (HMGA1). CONCLUSIONS: Collectively, these data demonstrate the mechanism underlying the invovlvement of MALAT1 in cerebral ischemia/reperfusion injury, thus providing translational evidence that MALAT1 may serve as a novel biomarker and therapeutic target for ischemic stroke.	NA	Biol Res. 2021 Mar 9;54(1):8. doi: 10.1186/s40659-021-00331-9.
3672	LncRNA	MALAT1	miR-145-5p	HMGA2	thymic cancer cell lines	Thymic Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34122636	si-MALAT1 attenuates thymic cancer cell proliferation and promotes apoptosis via the miR-145-5p/HMGA2 pathway.	Metastasis-associated-lung-adenocarcinoma-transcript-1 (MALAT1) is a long non-coding RNA that is considered a potential tumor marker. The present study aimed to investigate the effect and mechanism of MALAT1 on cell proliferation and apoptosis in thymic cancer cells. IU-TAB-1, A549, HCT-116 and 293T cells were screened by reverse transcription-quantitative PCR to assess high-mobility group AT-hook 2 (HMGA2) expression in various types of cancer cells and were transfected with small interfering (si)RNA targeting MALAT1 (si-MALAT1). Cell proliferation was evaluated by Cell Counting Kit-8 assay. Cell apoptosis and cell cycle were examined using flow cytometry. The protein expression of cyclin D1, cyclin E, Bax, Bcl-2 and HMGA2 was determined by western blot analysis, while the associations between MALAT1 and microRNA (miR)-145-5p and between HMGA2 and miR-145-5p were determined by luciferase reporter assay. Among the four cell lines evaluated, IU-TAB-1 showed the highest expression of MALAT1; thus, IU-TAB-1 cells were selected for subsequent experiments. Compared with the findings in the control group, si-MALAT1 significantly decreased the cell proliferation of IU-TAB-1 cells, whereas the apoptosis levels and number of cells in G(2) phase were increased. The protein expression levels of cyclin D1, cyclin E, Bcl-2 and HMGA2 were significantly decreased in the si-MALAT1 group compared with those in the control group, while Bax levels were significantly increased. After treatment with si-MALAT1 in combination with miR-145-5p mimics or inhibitors, cell proliferation and apoptosis were respectively enhanced and inhibited in IU-TAB-1 cells. miR-145-5p inhibited the luciferase activity of IU-TAB-1 cells transfected with the MALAT1 or HMGA2 3' untranslated region. In conclusion, si-MALAT1 significantly attenuated cell proliferation and apoptosis via the miR-145-5p/HMGA2 pathway in thymic cancer cells.	NA	Oncol Lett. 2021 Aug;22(2):585. doi: 10.3892/ol.2021.12846. Epub 2021 Jun 3.
3673	LncRNA	MLK7-AS1	miR-375-3p	YWHAZ	NSCLC tissues and cell lines(H1299,A549)	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33968726	Long Noncoding RNA MLK7-AS1 Promotes Non-Small-Cell Lung Cancer Migration and Invasion via the miR-375-3p/YWHAZ Axis.	Long noncoding RNAs act essential regulators in lung cancer tumorigenesis. Our research aimed to investigate the potential function and molecular mechanisms of MLK7-AS1 in NSCLC (non-small-cell lung cancer). QRT-PCR results indicated that the MLK7-AS1 expression level was upregulated in NSCLC cells and tissues. MLK7-AS1 strengthened cell migration and invasion in H1299 and A549 cells. Luciferase reporter assay found that MLK7-AS1 functioned as an endogenous sponge for miR-375-3p. Transwell assay results showed that miR-375-3p suppressed cell migration and invasion in H1299 and A549 cells. YWHAZ was confirmed as a target gene of miR-375-3p by Targetscan. YWHAZ overexpression promoted the invasion of H1299 and A549 cells. MLK7-AS1 upregulated YWHAZ expression and enhanced H1299 and A549 cell invasion by sponging miR-375-3p. MLK7-AS1 improved the metastasis ability of A549 in vivo. In conclusion, MLK7-AS1 was identified as a novel oncogenic RNA in NSCLC and can function as a potential therapeutic target for NSCLC treatment.	NA	Front Oncol. 2021 Apr 22;11:626036. doi: 10.3389/fonc.2021.626036. eCollection 2021.
3674	LncRNA	MNX1-AS1	miR-370	FoxM1	LSCC cell	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	Rescue assay;	33882027	LncRNA MNX1-AS1 drives aggressive laryngeal squamous cell carcinoma progression and serves as a ceRNA to target FoxM1 by sponging microRNA-370.	Long non-coding RNA (LncRNA) MNX1 antisense RNA 1(MNX1-AS1) is associated with the pathology of numerous cancers. But, the role and underlying pathways of MNX1-AS1 in the regulation of laryngeal squamous cell carcinoma (LSCC) is not known. We demonstrated remarkably elevated levels of MNX1-AS1 in the LSCC tissues, which was correlated with poor disease prognosis. Moreover, MNX1-AS1-silencing strongly suppressed LSCC cell proliferation, migration, and invasion. We also demonstrated that MNX1-AS1 sequesters that activity of miR-370, thereby releasing Forkhead Box ml (FoxM1) from the inhibitory actions of MNX1-AS1. Furthermore, the positive correlation of MNX1-AS1 and FoxM1 as well as the converse correlation between miR-370 and MNX1-AS1 (or FoxM1) were revealed in LSCC tissues using experiments. Based on rescue assays, FoxM1 overexpression or miR-370 downregulation partially recovered the inhibitory effect of MNX1-AS1 silencing on LSCC cells. Moreover, knockdown of MNX1-AS1 retarded tumor growth in nude mice model. In summary, these findings verified that MNX1-AS1 modulated LSCC progression by competitively binding with miR-370 to regulate FoxM1.	NA	Aging (Albany NY). 2021 Mar 19;13(7):9900-9910. doi: 10.18632/aging.202746. Epub 2021 Mar 19.
3675	LncRNA	MTX2-6	miR-574-5p	SMAD4	ESCC tissues and cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	33869216	LncRNA MTX2-6 Suppresses Cell Proliferation by Acting as ceRNA of miR-574-5p to Accumulate SMAD4 in Esophageal Squamous Cell Carcinoma.	Esophageal squamous cell carcinoma (ESCC) has been one of the key causes of cancer deaths worldwide. It has been found that long non-coding RNA (lncRNA) is related to the generation and progression of various cancers (including ESCC). However, there are still many lncRNAs related to ESCC whose functions and molecular mechanisms have not been clearly elucidated. In this study, we first reported that lncRNA MTX2-6 was significantly downregulated in ESCC tissues and cell lines. The decreased expression of MTX2-6 is closely related to larger tumor and worse prognosis of ESCC patients. Through a series of functional experiments, we detected that overexpressed MTX2-6 inhibited cell proliferation and promoted cell apoptosis of ESCC in vitro and in vivo. Further studies showed that MTX2-6 exerts as a competing endogenous RNA (ceRNA) by binding miR-574-5p and elevates the expression of SMAD4 in ESCC. In summary, our results clarify the tumor suppressor roles of MTX2-6/miR-574-5p/SMAD4 axis in the progression of ESCC and provide emerging therapeutic targets for ESCC patients.	NA	Front Cell Dev Biol. 2021 Mar 23;9:654746. doi: 10.3389/fcell.2021.654746. eCollection 2021.
3676	LncRNA	NARL	miR-217-5p	NOD1	spleen 	NA	Homo sapiens (human)	FISH;FISH;	33581111	The Long noncoding RNA NARL regulates immune responses via microRNA-mediated NOD1 downregulation in teleost fish.	Increasing evidence shows that the long non-coding RNA (lncRNA) is a major regulator and participates in the regulation of various physiological and pathological processes, such as cell proliferation, differentiation, metastasis, and apoptosis. Unlike mammals, however, the study of lncRNA in lower invertebrates is just beginning and the extent of lncRNA-mediate regulation remains unclear. Here, we for the first time identify a lncRNA, termed NOD1 antibacterial and antiviral-related lncRNA (NARL), as a key regulator for innate immunity in teleost fish. We found that NOD1 plays an important role in the antibacterial and antiviral process in fish, and that the microRNA miR-217-5p inhibits NOD1 expression and thus weakens the NF-κB and the IRF3-driven signaling pathway. Furthermore, our results indicated that NARL functions as a competing endogenous RNA (ceRNA) for miR-217-5p to regulate protein abundance of NOD1; thus, invading microorganisms are eliminated and immune responses are promoted. Our study also demonstrates the regulation mechanism that lncRNA NARL can competitive adsorption miRNA to regulate the miR-217-5p/NOD1 axis is widespread in teleost fish. Taken together, our results reveal that NARL in fish is a critical positive regulator of innate immune responses to viral and bacterial infection by suppressing a feedback to NOD1-NF-κB/ IRF3-mediated signaling.	NA	J Biol Chem. 2021 Feb 10;296:100414. doi: 10.1016/j.jbc.2021.100414.
3677	LncRNA	NBR2	miR-22	TCF7	hepatoblastoma tissue and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33651649	LncRNA NBR2 aggravates hepatoblastoma cell malignancy and promotes cell proliferation under glucose starvation through the miR-22/TCF7 axis.	Hepatoblastoma (HB) is the most commonly seen pediatric liver malignancy. With frequent mutations in CTNNB1 gene that encodes β-catenin, hepatoblastoma has been considered as a Wnt/β-catenin-activated malignant tumor. Altered glucose metabolism upon nutrient deprivation (glucose starvation) might also be a critical event in hepatoblastoma carcinogenesis. The present study provides a lncRNA NBR2/miR-22/TCF7 axis modulating proliferation, invasion, migration, and apoptosis of hepatoblastoma cells upon glucose starvation through Wnt and downstream TCF7 signaling pathways. The expression of NBR2 is significantly increased within hepatoblastoma tissue samples; moreover, under incubation with 0 mM glucose (glucose starvation), NBR2 expression is significantly upregulated. NBR2 silencing not only inhibited hepatoblastoma cell viability, invasion, and migration under normal culture condition but also promoted the cell apoptosis under glucose starvation. NBR2 silencing in hepatoblastoma cells also decreased TCF7 mRNA expression and TCF7 protein levels, as well as the protein levels of the cell cycle, glucose entrapment, and EMT markers. miR-22 is directly bound to both NBR2 and TCF7; lncRNA NBR2 counteracted miR-22-mediated repression on TCF7 via acting as a ceRNA. The effects of NBR2 silencing on TCF7 expression, hepatoblastoma cell phenotype, and cell cycle, glucose entrapment, and EMT markers were all significantly reversed by miR-22 inhibition. In conclusion, lncRNA NBR2 aggravates hepatoblastoma cell malignancy through competing with TCF7 for miR-22 binding, therefore counteracting miR-22-mediated repression on TCF7. LncRNA NBR2 might be a promising target to inhibit hepatoblastoma cell proliferation under glucose starvation.	NA	Cell Cycle. 2021 Mar-Mar;20(5-6):575-590. doi: 10.1080/15384101.2021.1885236. Epub 2021 Mar 2.
3678	LncRNA	NEAT1	miR-196a-5p	S100A9	LL37-treated HaCaT cells	Rosacea	Homo sapiens (human)	qRT-PCR	33678493	Long non-coding RNA NEAT1 functions as a competing endogenous RNA to regulate S100A9 expression by sponging miR-196a-5p in rosacea.	BACKGROUND: Rosacea is a complex, chronic, and recurrent dermatologic condition that adversely affects quality of life and self-esteem. However, clinical relevance and molecular mechanisms underlying NEAT1 influence in rosacea remain unclear. OBJECTIVE: The present study aims to investigate the dynamics and influences of lncRNAs, miRNAs, and mRNAs in rosacea patients, and to explore the impacts of NEAT1 treatments on miR-196a-5p and S100A9 expression in LL37-treated HaCaT cells. METHODS: RNA-sequencing of skin tissues from rosacea patients and integrative analyses facilitated comprehensive exploration of lncRNA, mRNA, and miRNA networks. We identified differentially expressed lncRNAs in paired rosacea afflicted and non-lesioned tissues by hub lncRNAs in the ceRNA network. The role of NEAT1 in LL37-treated HaCaT cells was identified by in vitro experiments. RESULTS: There were 237 lncRNAs, 38 miRNAs, and 1784 mRNAs in lesioned skin compared to non-lesioned skin in six rosacea patients. NEAT1 was upregulated in rosacea skin and in LL37-treated HaCaT cells. Moreover, inflammatory damage was able to be reduced in vitro after knockdown of NEAT1. Finally, NEAT1 was able to directly interact with miR-196a-5p, and downregulating miR-196a-5p was efficient in reversing the influence of NEAT1 siRNA on S100A9. CONCLUSION: We have completed the first genome-wide lncRNA profiling of paired lesioned and non-lesioned samples from rosacea afflicted patients. The NEAT1/miR-196a-5p/S100A9 axis may have played an important role in the dynamics underlying inflammatory responses of rosacea. NEAT1 may have functioned as a competing endogenous RNA which regulated inflammatory responses in rosacea by sponging miR-196a-5p and upregulating S100A9 expression.	NA	J Dermatol Sci. 2021 Apr;102(1):58-67. doi: 10.1016/j.jdermsci.2021.02.005. Epub 2021 Feb 27.
3679	LncRNA	NEAT1	miR-139	JAK3	airway smooth muscle cell	Asthma	Homo sapiens (human)	ELISA;Western blot;luciferase assay;	33590796	LncRNA NEAT1 promotes airway smooth muscle cell inflammation by activating the JAK3/STAT5 pathway through targeting of miR-139.	Background Asthma is a chronic inflammatory heterogeneous respiratory disease. Previous studies showed that the lncRNA NEAT1 (nuclear paraspeckle assembly transcript 1) might play an important role in the pathogenesis of asthma, but its potential mechanism in airway smooth muscle cell (ASMC) inflammation remains largely unknown and needs further investigation.Methods We performed cellular immunofluorescence to identify the features of ASMCs and detected the expression levels of lncRNA NEAT1, miR-139, TNF-α, IL-6, IL-8 and IL-1β by quantitative real-time PCR (Q-PCR) and ELISA. Western blotting (WB) was used to measure the protein expression of the related genes, and bioinformatics as well as dual luciferase assays were used to validate the interaction between lncRNA NEAT1 and miR-139 and the interaction between miR-139 and the 3'-UTR of JAK3.Results The expression of lncRNA NEAT1 was increased in the ASMCs of asthma patients, but miR-139 was decreased. Overexpression of lncRNA NEAT1 promoted the expression of the inflammatory cytokines such as TNF-α, IL-6, IL-8 and IL-1β in ASMCs. LncRNA NEAT1 was able to target miR-139 to activate the JAK3/STAT5 signaling pathway and induced the expression of these inflammatory cytokines in ASMCs. Overexpression of miR-139 or suppression of the JAK3/STAT5 signaling pathway reversed the inflammatory effect of lncRNA NEAT1.Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.	NA	Exp Lung Res. 2021 Apr-May;47(4):161-172. doi: 10.1080/01902148.2021.1876792. Epub 2021 Feb 16.
3680	LncRNA	NEAT1	miR-500a-3p	XBP-1	gastric cancer tissue and cell lines	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33982777	lncRNA NEAT1 regulates gastric carcinoma cell proliferation, invasion and apoptosis via the miR-500a-3p/XBP-1 axis.	Gastric cancer is a serious malignant tumor. Despite progression in gastric cancer research in recent years, the specific molecular mechanism underlying the pathogenesis of the disease is not completely understood. Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) affects the proliferation and metastasis of multiple types of tumor cells in colorectal cancer and breast cancer but its specific role in gastric cancer requires further investigation. The aim of the present study was to analyze the role of NEAT1 in gastric cancer. The expression of endoplasmic reticulum stress marker proteins and apoptosis-related proteins in gastric cancer tissue and cell lines was analyzed using western blotting. The targeting relationship of NEAT1 and miR-500a-3p was analyzed using dual-luciferase reporter assay. Cell proliferation was analyzed using CCK8 assay and colony formation assay while cell invasion was detected using Transwell assay. Cell apoptosis was analyzed using TUNEL staining and LC3 expression through immunofluorescent staining (IF). The results showed that lncRNA NEAT1-overexpression gastric cancer cells were established to determine its effects on cell proliferation, invasion, apoptosis, autophagy and endoplasmic reticulum stress. Subsequently, microRNA (miR)-500a was overexpressed in lncRNA NEAT1-overexpression cells. Compared with the vector group, lncRNA NEAT1 overexpression significantly inhibited gastric cancer cell proliferation and invasion, but significantly promoted cell apoptosis. Furthermore, the results indicated that lncRNA NEAT1 targeted and downregulated the expression of miR-500a-3p, and miR-500a-3p targeted X-box binding protein-1 (XBP-1) mRNA. lncRNA NEAT1 overexpression-mediated inhibition of gastric cancer cell proliferation and invasion was significantly reversed by miR-500a-3p overexpression. Furthermore, compared with the vector group, the expression levels of endoplasmic reticulum stress-related proteins (XBP-1S/XBP-1U ratio and 78-kDa glucose-regulated protein) and apoptosis-related proteins (Bax and cleaved-caspase-3) were significantly upregulated by lncRNA NEAT1 overexpression; however, miR-500a-3p overexpression reversed lncRNA NEAT1 overexpression-mediated effects on protein expression. The present study demonstrated that lncRNA NEAT1 inhibited gastric cancer cell proliferation and invasion, and promoted apoptosis by regulating the miR-500a-3p/XBP-1 axis.	NA	Mol Med Rep. 2021 Jul;24(1):503. doi: 10.3892/mmr.2021.12142. Epub 2021 May 13.
3681	LncRNA	NEAT1	miR-141-3p	KLF12	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RACE;Western blot;	33820555	Long non-coding RNA NEAT1 transported by extracellular vesicles contributes to breast cancer development by sponging microRNA-141-3p and regulating KLF12.	OBJECTIVE: Breast cancer (BC) remains a public-health issue on a global scale. Long non-coding RNAs (lncRNAs) play functional roles in BC. This study focuses on effects of NEAT1 on BC cell invasion, migration and chemotherapy resistance via microRNA (miR)-141-3p and KLF12. METHODS: After extraction and identification of serum extracellular vesicles (EVs), NEAT1 expression in EVs was detected and its association with clinical characteristics of BC patients was analyzed. Besides, the gain-of function was performed to investigate the roles of NEAT1 and miR-141-3p in BC, and levels of NEAT1, miR-141-3p, KLF12 and MDR1 after EV treatment were detected by RT-qPCR and Western blot analysis. Furthermore, the in vitro findings were confirmed via lung metastases in nude mice. RESULTS: NEAT1 expression in serum EVs was high and related to lymph node metastasis, progesterone receptor, estrogen receptor and Ki-67 in BC patients. After EV treatment, NEAT1 and KLF12 levels were increased, miR-141-3p expression was decreased, the abilities of proliferation, invasion, migration and in vivo metastasis were enhanced, and the sensitivity of cells to cisplatin, paclitaxel and 5-fluorouracil was decreased. After NEAT1 interference, NEAT1 and KLF12 levels in BC cells treated with EVs were decreased, miR-141-3p expression was increased, cell proliferation, invasion, migration and in vivo metastasis were decreased, and drug resistance sensitivity was increased. NEAT1 can bind to miR-141-3p and upregulates KLF12 expression. CONCLUSIONS: EVs inhibit the regulation of KLF12 by miR-141-3p by transporting NEAT1 to BC cells, thus promoting BC cell invasion, migration, and chemotherapy resistance.	NA	Cell Biosci. 2021 Apr 5;11(1):68. doi: 10.1186/s13578-021-00556-x.
3682	LncRNA	NEAT1	miR-31-5p	POU2F1	septic RAW264.7 cells	Sepsis 	Homo sapiens (human)	qRT-PCR	33710444	LncRNA NEAT1 Promotes Inflammatory Response in Sepsis via the miR-31-5p/POU2F1 Axis.	Sepsis is considered to be a systemic inflammatory response, which results in organ dysfunction. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) involved in sepsis progression has been reported. However, the underlying mechanism of NEAT1 in sepsis-induced inflammatory response remains to be revealed. In this study, NEAT1 and POU domain class 2 transcription factor 1 (POU2F1) were highly expressed in LPS-induced septic RAW264.7 cells, opposite to miR-31-5p expression. Furthermore, we found that NEAT1 silencing inhibited LPS-induced inflammatory response and cell proliferation, and promoted cell apoptosis. Subsequently, we found that miR-31-5p interacted with NEAT1 and targeted the 3'UTR of POU2F1, and in LPS-induced RAW264.7 cells, the inhibition of NEAT1 silencing was reversed by miR-31-5p knockdown, while POU2F1 downregulation could cover the functions of miR-31-5p knockdown. In a word, this study indicates that NEAT1 inhibits the LPS-induced progression of sepsis in RAW264.7 cells by modulating miR-31-5p/POU2F1 axis, suggesting that NEAT1 will be the potential therapeutic target for sepsis.	NA	Inflammation. 2021 Mar 12. doi: 10.1007/s10753-021-01436-9.
3683	LncRNA	NOP14-AS1	miR-665	HMGB3	TSCC tissues and cell lines	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33814931	LncRNA NOP14-AS1 Promotes Tongue Squamous Cell Carcinoma Progression by Targeting MicroRNA-665/HMGB3 Axis.	PURPOSE: The expression profile, clinical effects, and detailed roles of NOP14 antisense RNA 1 (NOP14-AS1) in tongue squamous cell carcinoma (TSCC) remain ambiguous and need to be further explored. Thus, this work was initiated to offer further solid evidence regarding the expression and roles of NOP14-AS1 in TSCC. Furthermore, additional efforts were exerted to reveal the molecular events by which NOP14-AS1 affects the malignant behaviours of TSCC. METHODS: NOP14-AS1 expression was detected in TSCC tissues and cell lines using quantitative reverse transcription-polymerase chain reaction. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and xenograft tumor model analysis were performed to assess the malignant biological behaviors of TSCC cells after NOP14-AS1 depletion. Mechanistic studies were performed using bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation, and rescue experiments. RESULTS: NOP14-AS1 upregulation was identified in TSCC tissues and cell lines. Patients with TSCC exhibiting a high NOP14-AS1 expression faced shorter overall survival than those with a low NOP14-AS1 expression. Functionally, NOP14-AS1 depletion facilitated apoptosis and impeded cell proliferation, migration, and invasion in TSCC. In vivo, the growth of TSCC cells was hindered by NOP14-AS1 depletion. Mechanically, NOP14-AS1 functioned as a competing endogenous RNA by sponging microRNA-665 (miR-665), thereby overexpressing the target high mobility group box 3 (HMGB3) of miR-665. Lastly, rescue experiments confirmed that the introduction of HMGB3 overexpression plasmid or miR-665 inhibitor could abrogate the inhibition of aggressive phenotypes triggered by NOP14-AS1 knockdown. CONCLUSION: NOP14-AS1 executed pro-oncogenic activities in TSCC cells by targeting the miR-665/HMGB3 axis. The NOP14-AS1/miR-665/HMGB pathway may be a valuable prognostic indicator and therapeutic target for preventing TSCC.	NA	Cancer Manag Res. 2021 Mar 26;13:2821-2834. doi: 10.2147/CMAR.S293322. eCollection 2021.
3684	LncRNA	OIP5-AS1	miR-381-3p	HMGB3	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33821219	Exosomal-mediated transfer of OIP5-AS1 enhanced cell chemoresistance to trastuzumab in breast cancer via up-regulating HMGB3 by sponging miR-381-3p.	BACKGROUND: Long noncoding RNA OPA-interacting protein 5 antisense transcript 1 (OIP5-AS1) was confirmed to involve in the malignancy of breast cancer. However, whether exosomal OIP5-AS1 is implicated in trastuzumab resistance remains unclear. METHODS: The IC(50) value of cells to trastuzumab, cell proliferation, migration, and apoptosis was analyzed by cell counting kit-8 assay, colony formation assay, transwell assay, or flow cytometry, respectively. The expression of OIP5-AS1 and microRNA (miR)-381-3p was detected using quantitative real-time polymerase chain reaction. Exosomes were isolated by ultracentrifugation and qualified by nanoparticle tracking analysis software. Western blot was used to detect the protein levels of tumor susceptibility gene 101 (TSG101), CD81, CD63, or high-mobility group protein B3 (HMGB3). The interaction between miR-381-3p and OIP5-AS1 or HMGB3 was confirmed by dual-luciferase reporter assay and pull-down assay. In vivo experiments were conducted using murine xenograft models. RESULTS: OIP5-AS1 was elevated in trastuzumab-resistant breast cancer cells, and OIP5-AS1 knockdown rescued trastuzumab sensitivity. Extracellular OIP5-AS1 was packaged into exosomes, which were secreted by trastuzumab-resistant cells, and could be absorbed by trastuzumab-sensitive cells in breast cancer. Importantly, intercellular transfer of OIP5-AS1 via exosomes enhanced trastuzumab resistance in vitro. OIP5-AS1 was a sponge of miR-381-3p; besides, miR-381-3p targeted HMGB3. Murine xenograft analysis showed exosomal OIP5-AS1 induced trastuzumab resistance in vivo. Exosomal OIP5-AS1 was dysregulated in the serum of breast cancer patients and might be a promising diagnostic biomarker in trastuzumab resistance. CONCLUSION: Intercellular transfer of OIP5-AS1 by exosomes enhanced trastuzumab resistance in breast cancer via miR-381-3p/HMGB3 axis, indicating a potential therapeutic strategy to boost the effectiveness of trastuzumab in resistant breast cancer patients.	NA	Open Med (Wars). 2021 Mar 30;16(1):512-525. doi: 10.1515/med-2021-0249. eCollection 2021.
3685	LncRNA	OIP5-AS1	miR-128-3p	CCNG1	OC tissues and cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33760168	Long non-coding RNA OIP5-AS1 facilitates the progression of ovarian cancer via the miR-128-3p/CCNG1 axis.	Long non-coding RNA (LncRNA) o-phthalaldehyde-interacting protein 5 antisense transcript 1 (OIP5-AS1) serves major roles in the progression of various types of cancer. The present study investigated its biological function in ovarian cancer (OC) and its mechanisms. The levels of OIP5-AS1, microRNA-128-3p (miR-128-3p) and cyclin G1 (CCNG1) were examined by reverse transcription-quantitative PCR. Cell viability, apoptosis, migration and invasion were detected to analyze cellular progression. Glycolytic metabolism was assessed by detecting the levels of glucose consumption and lactate production. CCNG1 and hexokinase 2 protein levels were measured by western blotting. Dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down assays were performed to affirm the interaction between two molecules. OIP5-AS1 was found to be upregulated in OC tissues and cells. Knockdown of OIP5-AS1 suppressed cell viability, migration, invasion and glycolysis while promoting apoptosis in OC cells. OIP5-AS1 interacted with miR-128-3p and functioned as an oncogene by sequestering miR-128-3p. In addition, CCNG1 was a target gene for miR-128-3p and miR-128-3p regulated the CCNG1-induced effects on OC cells by downregulating CCNG1. OIP5-AS1 upregulated the expression of CCNG1 via targeting miR-128-3p. OIP5-AS1 knockdown also inhibited tumor growth of OC in vivo by modulating the expression of miR-128-3p and CCNG1. Collectively, these data illustrated that the oncogenic role of OIP5-AS1 in OC was associated with the miR-128-3p/CCNG1 axis at least in part. OIP5-AS1 might be a probable diagnostic and therapeutic biomarker for the treatment of OC patients.	NA	Mol Med Rep. 2021 May;23(5):388. doi: 10.3892/mmr.2021.12027. Epub 2021 Mar 24.
3686	LncRNA	POU3F3	miR-650	MGMT	melanoma cells	Melanoma	Homo sapiens (human)	qRT-PCR	33816296	LncRNA POU3F3 Contributes to Dacarbazine Resistance of Human Melanoma Through the MiR-650/MGMT Axis.	Background: Alkylating agents are critical therapeutic options for melanoma, while dacarbazine (DTIC)-based chemotherapy showed poor sensitivity in clinical trials. Long non-coding RNAs (lncRNAs) were highlighted in the progression of malignant tumors in recent years, whereas little was known about their involvement in melanoma. Methods: The functional role and molecular mechanism of lncRNA POU3F3 were evaluated on DTIC-resistant melanoma cells. Further studies analyzed its clinical role in the disease progression of melanoma. Results: We observed elevated the expression of lncRNA POU3F3 in the DTIC-resistant melanoma cells. Gain-of-function assays showed that the overexpression of lncRNA POU3F3 maintained cell survival with DTIC treatment, while the knockdown of lncRNA POU3F3 restored cell sensitivity to DTIC. A positive correlation of the expression O6-methylguanine-DNA-methyltransferase (MGMT) was observed with lncRNA POU3F3 in vitro and in vivo. Bioinformatic analyses predicted that miR-650 was involved in the lncRNA POU3F3-regulated MGMT expression. Molecular analysis indicated that lncRNA POU3F3 worked as a competitive endogenous RNA to regulate the levels of miR-650, and the lncRNA POU3F3/miR-650 axis determined the transcription of MGMT in melanoma cells to a greater extent. Further clinical studies supported that lncRNA POU3F3 was a risk factor for the disease progression of melanoma. Conclusion: LncRNA POU3F3 upregulated the expression of MGMT by sponging miR-650, which is a crucial way for DTIC resistance in melanoma. Our results indicated that lncRNA POU3F3 was a valuable biomarker for the disease progression of melanoma.	NA	Front Oncol. 2021 Mar 17;11:643613. doi: 10.3389/fonc.2021.643613. eCollection 2021.
3687	LncRNA	POU6F2-AS1	miR-34c-5p	KCNJ4	LADC tissues and cell lines(Calu-3,NCI-H460)	Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;	33999092	Long noncoding RNA POU6F2-AS1 regulates lung cancer aggressiveness through sponging miR-34c-5p to modulate KCNJ4 expression.	It has been extensively reported that long noncoding RNAs (lncRNAs) were closely associated with multiple malignancies. The aim of our study was to investigate the effects and mechanism of lncRNA POU6F2-AS1 in lung adenocarcinoma (LADC).The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets provided us the information of LADC clinical samples. High-regulation of POU6F2-AS1 was presented in LADC tissues compared with adjacent normal tissues, which was correlated with poor outcome of LADC patients. Functional experiments in Calu-3 and NCI-H460 cells showed that POU6F2-AS1 significantly promoted LADC cell proliferation, colony formation, invasion and migration. Moreover, through online prediction, luciferase reporter assay and Pearson's correlation analysis, we found that POU6F2-AS1 may act as a competing endogenous RNA (ceRNA) of miR-34c-5p and facilitated the expression of potassium voltage-gated channel subfamily J member 4 (KCNJ4). The promoting effect of cell aggressiveness induced by POU6F2-AS1 was enhanced by KCNJ4, whilst was abrogated due to the overexpression of miR-34c-5p. Collectively, POU6F2-AS1 might function as a ceRNA through sponging miR-34c-5p to high-regulate KCNJ4 in LADC, which indicates that POU6F2-AS1 might be a promising therapeutic target with significant prognostic value for LADC treatment.	NA	Genet Mol Biol. 2021 May 14;44(2):e20200050. doi: 10.1590/1678-4685-GMB-2020-0050. eCollection 2021.
3688	Pseudogene	PPIAP22	miR-197-3p	PPIA	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33790943	A Critical Role of Peptidylprolyl Isomerase A Pseudogene 22/microRNA-197-3p/Peptidylprolyl Isomerase A Axis in Hepatocellular Carcinoma.	The burden of hepatocellular carcinoma (HCC) worldwide is increasing over time, while the underlying molecular mechanism of HCC development is still under exploration. Pseudogenes are classified as a special type of long non-coding RNAs (lncRNAs), and they played a vital role in regulating tumor-associated gene expression. Here, we report that a pseudogene peptidylprolyl isomerase A pseudogene 22 (PPIAP22) and its parental gene peptidylprolyl isomerase A (PPIA) were upregulated in HCC and were associated with the clinical outcomes of HCC. Further investigation revealed that PPIAP22 might upregulate the expression of PPIA through sponging microRNA (miR)-197-3p, behaving as competing endogenous RNA (ceRNA). PPIA could participate in the development of HCC by regulating mRNA metabolic process and tumor immunity based on the functional enrichment analysis. We also found a strong correlation between the expression levels of PPIA and the immune cell infiltration or the expression of chemokines, especially macrophage, C-C motif chemokine ligand 15 (CCL15), and C-X-C motif chemokine ligand 12 (CXCL12). Our findings demonstrate that the PPIAP22/miR-197-3p/PPIA axis plays a vital role in the progression of HCC by increasing the malignancy of tumor cells and regulating the immune cell infiltration, especially macrophage, through CCL15-CCR1 or CXCL12-CXCR4/CXCR7 pathways.	NA	Front Genet. 2021 Mar 15;12:604461. doi: 10.3389/fgene.2021.604461. eCollection 2021.
3689	LncRNA	PRR34-AS1	miR-498	TOMM20	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	FISH;qPCR;RT-qPCR;Western blot;FISH;Luciferase reporter assay;	33609562	PRR34-AS1 sponges miR-498 to facilitate TOMM20 and ITGA6 mediated tumor progression in HCC.	BACKGROUND: The researches on PRR34 antisense RNA 1 (PRR34-AS1) have been limited. Both translocase of outer mitochondrial membrane 20 (TOMM20) and integrin subunit alpha 6 (ITGA6) have been proven to facilitate cancer progression. Whether TOMM20 or ITGA6 affects hepatocellular carcinoma (HCC) progression has never been investigated. Some studies showed that microRNA 498 (miR-498) can suppress HCC progression. Additionally, the influence of ceRNA network (including PRR34-AS1, miR-498, and TOMM20 or ITGA6) on HCC progression has not been inquired into yet. METHODS: The knockdown or overexpression efficiency was validated via RT-qPCR. Also, RT-qPCR was applied to detect the expression of PRR34-AS1, miR-498, TOMM20, and ITGA6. Cell proliferation in HCC was tested via EdU and colony formation assays. Transwell assays presented the migratory and invasive capabilities of HCC cells. Subcellular fractionation and FISH assays showed the subcellular localization of PRR34-AS1. RNA pull down and luciferase reporter assays were performed to explore whether miR-498 combines with PRR34-AS1, TOMM20 or ITGA6. Western blot was conducted to detect protein expression. Rescue experiments were conducted to verify the relationship among PRR34-AS1, miR-498, TOMM20, and ITGA6. RESULTS: The expressions of PRR34-AS1, TOMM20, and ITGA6 were markedly high in HCC cell lines while miR-498 was lowly expressed. PRR34-AS1, TOMM20, and ITGA6 promoted HCC progression while miR-498 suppressed cell proliferation, migration, and invasion in HCC. Furthermore, PRR34-AS1, TOMM20, and ITGA6 combined with miR-498. CONCLUSION: PRR34-AS1 facilitates HCC progression by regulating miR-498/TOMM20/ITGA6 axis.	NA	Exp Mol Pathol. 2021 Jun;120:104620. doi: 10.1016/j.yexmp.2021.104620. Epub 2021 Feb 17.
3690	LncRNA	PRR34-AS1	miR-498	ITGA6	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	FISH;qPCR;RT-qPCR;Western blot;FISH;Luciferase reporter assay;	33609562	PRR34-AS1 sponges miR-498 to facilitate TOMM20 and ITGA6 mediated tumor progression in HCC.	BACKGROUND: The researches on PRR34 antisense RNA 1 (PRR34-AS1) have been limited. Both translocase of outer mitochondrial membrane 20 (TOMM20) and integrin subunit alpha 6 (ITGA6) have been proven to facilitate cancer progression. Whether TOMM20 or ITGA6 affects hepatocellular carcinoma (HCC) progression has never been investigated. Some studies showed that microRNA 498 (miR-498) can suppress HCC progression. Additionally, the influence of ceRNA network (including PRR34-AS1, miR-498, and TOMM20 or ITGA6) on HCC progression has not been inquired into yet. METHODS: The knockdown or overexpression efficiency was validated via RT-qPCR. Also, RT-qPCR was applied to detect the expression of PRR34-AS1, miR-498, TOMM20, and ITGA6. Cell proliferation in HCC was tested via EdU and colony formation assays. Transwell assays presented the migratory and invasive capabilities of HCC cells. Subcellular fractionation and FISH assays showed the subcellular localization of PRR34-AS1. RNA pull down and luciferase reporter assays were performed to explore whether miR-498 combines with PRR34-AS1, TOMM20 or ITGA6. Western blot was conducted to detect protein expression. Rescue experiments were conducted to verify the relationship among PRR34-AS1, miR-498, TOMM20, and ITGA6. RESULTS: The expressions of PRR34-AS1, TOMM20, and ITGA6 were markedly high in HCC cell lines while miR-498 was lowly expressed. PRR34-AS1, TOMM20, and ITGA6 promoted HCC progression while miR-498 suppressed cell proliferation, migration, and invasion in HCC. Furthermore, PRR34-AS1, TOMM20, and ITGA6 combined with miR-498. CONCLUSION: PRR34-AS1 facilitates HCC progression by regulating miR-498/TOMM20/ITGA6 axis.	NA	Exp Mol Pathol. 2021 Jun;120:104620. doi: 10.1016/j.yexmp.2021.104620. Epub 2021 Feb 17.
3691	LncRNA	PVT1	miR-612	CENP-H	EC tissues and cells	Endometrial Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Immunohistochemistry;luciferase assay;	33948369	The PVT1/miR-612/CENP-H/CDK1 axis promotes malignant progression of advanced endometrial cancer.	Our previous study introduced the oncogenic role of the long non-coding RNA plasmacytoma variant translocation 1 (PVT1) in endometrial cancer (EC). In this study, we aimed to construct a PVT1-centered competing endogenous RNA (ceRNA) network to outline a regulatory axis that might promote the malignant progression of advanced EC. Raw Uterine Corpus Endometrial Carcinoma (UCEC) datasets were collected from The Cancer Genome Atlas (TCGA) database and used for construction of the PVT1-centered ceRNA network. The ceRNA binding sites were established using dual-luciferase assays. FISH assays displayed the co-location of PVT1 and miR-612 in EC cells. Immunohistochemistry, in situ hybridization, qRT-PCR, and western blots were used to assess the expression of miR-612 and CENP-H in EC tissues, and their functions on biological behaviours were examined by a series of in vitro and in vivo assays. Molecule interactions were illustrated by co-transfection assays. The bioinformatics analysis showed that PVT1/miR-612/CENP-H/CDK1 axis played a vital role in the malignant progression of advanced EC. MiR-612 was downregulated in EC tissues and acted as a tumour suppressor to inhibit cell proliferation, migration, invasion, and promote cell apoptosis. CENP-H was found overexpressed in EC tissues, and the expression level was correlated to diagnosis and prognosis of EC. Hyperactivated CENP-H promoted cell proliferation, migration, invasion, and inhibited cell apoptosis. Overexpressed CENP-H prevented the anti-tumour effects observed with upregulated miR-612; knockdown of miR-612 also suppressed the anti-tumour effects of downregulated PVT1. Knockdown of PVT1 together with upregulated miR-612 exerted the strongest anti-tumour effects in nude mice. These effects were mediated by CDK1 through modulation of the Akt/mTOR signaling pathway. In conclusion, the PVT1/miR-612/CENP-H/CDK1 axis promoted the malignant progression of advanced EC and could serve as a promising target for potential treatments.	NA	Am J Cancer Res. 2021 Apr 15;11(4):1480-1502. eCollection 2021.
3692	LncRNA	PVT1	miR-186-5p	CXCL13	primary cultured astrocyte	Neuropathic Pain	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Immunohistochemistry;Luciferase activity assay;RNA immunoprecipitation;	33742328	Downregulating lncRNA PVT1 Relieves Astrocyte Overactivation Induced Neuropathic Pain Through Targeting miR-186-5p/CXCL13/CXCR5 Axis.	Spinal cord injury (SCI) is one of the main causes leading to neuropathic pain. Here, we aim to explore the molecular mechanism and function of lncRNA PVT1 in neuropathic pain induced by SCI. The expression of lncRNA PVT1, microRNA (miR) - 186-5p was measured via quantitative reverse transcription PCR (qRT-PCR), and the activation of astrocytes (labeled by GFAP) was detected by immunohistochemistry. Western blot was conducted to detect the expression of chemokine ligand 13 (CXCL13), chemokine receptor 5 (CXCR5), cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS) and glial fibrillary acidic protein (GFAP) in spinal cord injury lesions. The levels of inflammatory cytokines (including IL-1β and IL-6) and MDA in tissues were examined via Enzyme-linked immunosorbent assay (ELISA). In vitro experiments were also conducted in primary cultured astrocyte to explore the response of astrocyte to lipopolysaccharide (LPS). What's more, the PVT1-miR-186-5p interaction was verified via the dual luciferase activity assay and RNA immunoprecipitation (RIP) assay. The results demonstrated that the levels of PVT1, CXCL13 and CXCR5 were upregulated, while miR-186-5p were decreased in SCI rats' spinal cord and LPS-mediated astrocytes. In the SCI model, PVT1 depletion significantly alleviated neuropathic pain, astrocytic activation and reduced the expression of neuroinflammatory factors and proteins. The relevant mechanism studies confirmed that PVT1 is a competitive endogenous RNA (ceRNA) of miR-186-5p, targets and inhibits its expression and promotes the expression of CXCL13/CXCR5, while miR-186-5p targets CXCL13. In conclusion, inhibition of lncRNA PVT1 alleviates neuropathic pain in SCI rats by upregulating miR-186-5p and down-regulating CXCL13/CXCR5. The PVT1/miR-186-5p/CXCL13/CXCR5 axis can be used as a new therapeutic target for neuropathic pain.	NA	Neurochem Res. 2021 Jun;46(6):1457-1469. doi: 10.1007/s11064-021-03287-0. Epub 2021 Mar 19.
3693	LncRNA	PVT1	miR-186-5p	CXCR5	primary cultured astrocyte	Neuropathic Pain	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Immunohistochemistry;Luciferase activity assay;RNA immunoprecipitation;	33742328	Downregulating lncRNA PVT1 Relieves Astrocyte Overactivation Induced Neuropathic Pain Through Targeting miR-186-5p/CXCL13/CXCR5 Axis.	Spinal cord injury (SCI) is one of the main causes leading to neuropathic pain. Here, we aim to explore the molecular mechanism and function of lncRNA PVT1 in neuropathic pain induced by SCI. The expression of lncRNA PVT1, microRNA (miR) - 186-5p was measured via quantitative reverse transcription PCR (qRT-PCR), and the activation of astrocytes (labeled by GFAP) was detected by immunohistochemistry. Western blot was conducted to detect the expression of chemokine ligand 13 (CXCL13), chemokine receptor 5 (CXCR5), cyclooxygenase-2 (COX2), inducible nitric oxide synthase (iNOS) and glial fibrillary acidic protein (GFAP) in spinal cord injury lesions. The levels of inflammatory cytokines (including IL-1β and IL-6) and MDA in tissues were examined via Enzyme-linked immunosorbent assay (ELISA). In vitro experiments were also conducted in primary cultured astrocyte to explore the response of astrocyte to lipopolysaccharide (LPS). What's more, the PVT1-miR-186-5p interaction was verified via the dual luciferase activity assay and RNA immunoprecipitation (RIP) assay. The results demonstrated that the levels of PVT1, CXCL13 and CXCR5 were upregulated, while miR-186-5p were decreased in SCI rats' spinal cord and LPS-mediated astrocytes. In the SCI model, PVT1 depletion significantly alleviated neuropathic pain, astrocytic activation and reduced the expression of neuroinflammatory factors and proteins. The relevant mechanism studies confirmed that PVT1 is a competitive endogenous RNA (ceRNA) of miR-186-5p, targets and inhibits its expression and promotes the expression of CXCL13/CXCR5, while miR-186-5p targets CXCL13. In conclusion, inhibition of lncRNA PVT1 alleviates neuropathic pain in SCI rats by upregulating miR-186-5p and down-regulating CXCL13/CXCR5. The PVT1/miR-186-5p/CXCL13/CXCR5 axis can be used as a new therapeutic target for neuropathic pain.	NA	Neurochem Res. 2021 Jun;46(6):1457-1469. doi: 10.1007/s11064-021-03287-0. Epub 2021 Mar 19.
3694	Circular RNA	PVT1	miR-145	Talin1	ADS endometrial tissue and cells	Adenomyosis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33728345	Elevated Circular RNA PVT1 Promotes Eutopic Endometrial Cell Proliferation and Invasion of Adenomyosis via miR-145/Talin1 Axis.	Several theories on the origin of adenomyosis (ADS) have been proposed, of which the most widely accepted is the fundamental pathogenic role of uterine eutopic endometrium. Emerging evidence suggests that circular RNAs participate in the multiple tumorgenesis. The vital importance of circular RNA PVT1 (circPVT1) in the pathological progress like malignancies has been well documented. Nevertheless, its underlying correlation with ADS remains elusive yet. The purpose of this study was to investigate the expression pattern, regulatory effect, and internal mechanism of circPVT1 in ADS. qRT-PCR was performed to detect the relative mRNA expression of circPVT1, miR-145, and Talin1 in ADS endometrial tissue and cells. The protein level of Talin1 was measured by Western blot and immunochemistry. Immunofluorescence was used to identify the primary endometrial epithelial and stromal cells. circPVT1 knockdown in vitro was achieved by transfecting with specific lentivirus vector CCK-8, and colony formation assays were utilized to assess cell proliferation; meanwhile, the transwell assay was employed for evaluating cell invasion ability. By conducting bioinformatics, dual-luciferase reporter assay, or RNA immunoprecipitation (RIP) experiment, the interaction between miR-145 and circPVT1 or Talin1 was verified. Rescue experiments further determined the regulatory effect of circPVT1/miR-145/Talin1 axis. We found both circPVT1 and Talin1 were markedly upregulated in ADS endometrial tissue and cells, whereas miR-145 was decreased. Elevated expression of circPVT1 was closely related to the severity of dysmenorrhea, menorrhagia, and uterine enlargement of patients with ADS. Knockdown of circPVT1 inhibited adenomyotic epithelial and stromal cell proliferation and invasion. Further mechanistic experiments revealed that circPVT1 negatively regulated miR-145 through serving as a molecular sponge. And the facilitating effect of circPVT1 was partially reversed by miR-145. Talin1 was demonstrated to be a down target of miR-145 and indirectly affected by circPVT1. Our findings unveiled that enhanced circPVT1 may be involved in the pathogenesis of ADS via stimulating endometrial cell proliferation and invasion. The establishment of circPVT1/miR-145/Talin1 pathway might present a novel therapeutic insight for ADS.	NA	Biomed Res Int. 2021 Feb 27;2021:8868700. doi: 10.1155/2021/8868700. eCollection 2021.
3695	LncRNA	RHPN1-AS1	miR-485-5p	TPX2	OC tissues and cell ines	Ovarian Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33907841	RHPN1-AS1 promotes ovarian carcinogenesis by sponging miR-485-5p and releasing TPX2 mRNA.	Long non-coding RNAs (lncRNAs) play a crucial role in cancer development. However, researchers have yet to identify the underlying association between lncRNAs and ovarian cancer (OC). The aim of the present study was to examine the effect of lncRNA RHPN1-AS1 (RHPN1-AS1) on OC cells and tissues. Reverse transcriptase-quantitative PCR (RT-qPCR) was utilized to quantify RHPN1-AS1, miR-485-5p, and TPX2 mRNA expression in samples with OC. Luciferase-reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull-down assay were then employed to validate the target relationship among RHPN1-AS1, miR-485-5p and TPX2. Cell Counting Kit-8, BrdU, wound-healing, cell-adhesion, and flow cytometry assays were also employed to assess cell viability, proliferation, migration, adhesion and apoptosis, respectively, in SKOV3 and OVCAR3 cell lines. Findings revealed that RHPN1-AS1 demonstrated a higher expression level in OC cell lines and tissues. In addition, RHPN1-AS1 enhanced the adhesion, proliferation and migration of OC cell lines but decreased apoptosis of OC cells. It was also observed that the relationship between RHPN1-AS1 and miR-485-5p was negative and that RHPN1-AS1 could sponge miR-485-5p to regulate the proliferation, apoptosis, adhesion, and migration abilities of OC cells. Moreover, TPX2 was targeted by miR-485-5p and was significantly overexpressed in OC cell lines and tissues. Experimental investigations also revealed that TPX2 promoted the proliferation, adhesion, and migration of OC cells but suppressed the apoptosis of SKOV3 and OVCAR3 cells. In summary, RHPN1-AS1 played a tumor promotive role by sponging miR-485-5p to increase TPX2 expression in OC tumorigenesis.	NA	Oncol Rep. 2021 Jun;45(6):111. doi: 10.3892/or.2021.8062. Epub 2021 Apr 28.
3696	LncRNA	RMST	miR-204-5p	VCAM1	brain microvascular endothelial cells	Ischemic Stroke	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33607153	Long non-coding RNA RMST promotes oxygen-glucose deprivation-induced injury in brain microvascular endothelial cells by regulating miR-204-5p/VCAM1 axis.	AIMS: Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in the pathogenesis of ischemic stroke, including lncRNA rhabdomyosarcoma 2-associated transcript (RMST). We aimed to elucidate the role and molecular mechanism of RMST in ischemic stroke. MATERIALS AND METHODS: The in vitro ischemic stroke model was established by treating brain microvascular endothelial cells with oxygen-glucose deprivation (OGD). The expression of RMST, miR-204-5p and vascular cell adhesion molecule 1 (VCAM1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The interaction between miR-204-5p and RMST or VCAM1 was confirmed using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Cell viability, migration and apoptosis were assessed by Cell Counting Kit-8 (CCK-8), wound healing assay and flow cytometry, respectively. Lactic dehydrogenase (LDH) leakage rate was determined by LDH activity assay kit. The protein level of VCAM1 was analyzed by western blot (WB) assay. KEY FINDINGS: RMST was upregulated in OGD-treated HBMEC and bEnd.3 cells. MiR-204-5p was a direct target of RMST, and miR-204-5p inhibition abated the inhibitory effect of RMST knockdown on OGD-induced injury via inhibiting cell viability and migration and promoting apoptosis in HBMEC and bEnd.3 cells. Moreover, VCAM1 was identified as a direct target of miR-204-5p, and VCAM1 alleviated the effect of miR-204-5p on reduction of OGD-induced injury in HBMEC and bEnd.3 cells. In addition, RMST regulated VCAM1 expression via sponging miR-204-5p. SIGNIFICANCE: RMST knockdown attenuated OGD-induced injury of HBMEC and bEnd.3 cells via regulating miR-204-5p/VCAM1 axis, indicating a possible therapeutic strategy for future ischemic stroke therapy.	NA	Life Sci. 2021 Feb 16:119244. doi: 10.1016/j.lfs.2021.119244.
3697	LncRNA	RP11-279C4.1	miR-1273g-3p	CBX3	glioma tissues and cell lines	Glioma	Homo sapiens (human)	qRT-PCR;Rescue assay;	33694060	The LncRNA RP11-279C4.1 Enhances the Malignant Behaviour of Glioma Cells and Glioma Stem-Like Cells by Regulating the miR-1273g-3p/CBX3 Axis.	Glioma is the most common type of solid tumour affecting the central nervous system, and the survival rate of patients with glioma is low. However, the mechanism associated with glioma progression remains unclear. Growing evidence suggests that lncRNAs play essential roles in the initiation and progression of tumours, including gliomas. In the present study, we identified and verified the expression of the novel lncRNA RP11-279C4.1 by analyzing the TANRIC database and performing qRT-PCR assays, the results of which revealed its upregulation in glioma tissues and cell lines. The results of multiple functional experiments demonstrated that RP11-279C4.1 knockdown inhibited glioma malignant phenotypes, including cell proliferation, migration, invasion and cell self-renew ability in vitro. In addition, RP11-279C4.1 downregulation suppressed tumour growth in vivo. Mechanistically, RP11-279C4.1 induced CBX3 activation via competitively sponging miR-1273g-3p, and rescue assay results confirmed the importance of the RP11-279C4.1/miR-1273g-3p/CBX3 axis. Overall, the results of our present study demonstrated that RP11-279C4.1 functions as an oncogene that promotes tumour progression by modulating the miR-1273g-3p/CBX3 axis in glioma, suggesting that RP11-279C4.1 may be a novel therapeutic target for glioma.	NA	Mol Neurobiol. 2021 Mar 10. doi: 10.1007/s12035-021-02337-6.
3698	LncRNA	SChLAP1	miR-524-5p	HMGA2	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR	33846810	Long non-coding RNA SChLAP1 regulates the proliferation of triple negative breast cancer cells via the miR-524-5p/HMGA2 axis.	Long non-coding RNA (lncRNA) second chromosome locus associated with prostate-1 (SChLAP1), also named LINC00913, has been reported to accelerate the carcinogenesis of prostate cancer. The aim of this study was to explore the role and mechanism of SChLAP1 in triple negative breast cancer (TNBC). The expression of SChLAP1 in TNBC tissues and cells was determined by reverse transcription quantitative PCR. The effects of SChLAP1 on the growth of TNBC cells was evaluated by detecting cell viability, colony formation and apoptosis. The present study determined that SChLAP1 was upregulated in TNBC tissues and was associated with the long-distant lymph node metastasis of patients with TNBC. Knockdown of SChLAP1 significantly inhibited cell viability and colony formation, and triggered apoptosis of TNBC cells. Bioinformatics analysis suggested that SChLAP1 acted as a sponge of microRNA (miR)-524-5p and negatively modulated the expression of miR-524-5p. An inverse correlation was also identified between the expression levels of SChLAP1 and miR-524-5p in TNBC tissues. Furthermore, the results demonstrated that SChLAP1 interacted with miR-524-5p, and subsequently regulated the expression level of High Mobility Group AT-Hook 2 (HMGA2) in TNBC cells. It was also found that the overexpression of HMGA2 rescued the suppressed viability of TNBC cells induced by SChLAP1 knockdown. In conclusion, the present findings demonstrated that SChLAP1 modulated the malignant tumor behaviors of TNBC cells by regulating HMGA2 and subsequently restraining miR-524-5p.	NA	Mol Med Rep. 2021 Jun;23(6):446. doi: 10.3892/mmr.2021.12085. Epub 2021 Apr 13.
3699	LncRNA	SENP3-EIF4A1	miR-195-5p	CCNE1	TNBC tissues and cell lines	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33791304	Long Non-coding RNA SENP3-EIF4A1 Functions as a Sponge of miR-195-5p to Drive Triple-Negative Breast Cancer Progress by Overexpressing CCNE1.	Triple-negative breast cancer (TNBC) has high malignancy and limited treatment, so novel molecular therapeutic targets are urgently needed. Cyclin E1 (CCNE1) promotes progression in breast cancer, but its role and inherent mechanisms in TNBC are yet to be elucidated. Competing endogenous RNA (ceRNA) may be a potential mechanism. CCNE1 was selected though bioinformatics and clinical samples, and cell lines were utilized to verify CCNE1 expression by qRT-PCR and western blot. Predicting tools provided potential miR-195-5p and SENP3-EIF4A1 and tested from multilevel. Functional experiments were conducted in vitro and in vivo. Luciferase reporter assay and RNA immunoprecipitation experiments were implemented to ensure the interaction between miR-195-5p and SENP3-EIF4A1/CCNE1 in TNBC. Bioinformatics found DNA hypermethylation of miR-195-5p and preliminarily verified. Mechanistically, SENP3-EIF4A1-miR-195-5p-associated ceRNA could drive TNBC progress though regulating CCNE1. DNA hypermethylation of miR-195-5p might be another reason. In summary, SENP3-EIF4A1-miR-195-5p-CCNE1 axis promotes TNBC progress and may contribute to the novel diagnosis and treatment of TNBC.	NA	Front Cell Dev Biol. 2021 Mar 15;9:647527. doi: 10.3389/fcell.2021.647527. eCollection 2021.
3700	LncRNA	SLCO4A1-AS1	miR-876-3p	RBBP6	ALL cells	Acute Lymphocytic Leukemia	Homo sapiens (human)	qPCR;RT-qPCR;RNA pull-down assay;Western blot;Flow Cytometry assay;Rescue assay;RNA pull-down;	33683013	The lncRNA SLCO4A1-AS1/miR-876-3p/RBBP6 axis regulates cell proliferation and apoptosis in acute lymphocytic leukemia via the JNK signaling pathway.	INTRODUCTION: Acute lymphocytic leukemia (ALL) is a hematologic malignancy caused by the clonal proliferation of immature lymphocytes. Long noncoding RNAs (lncRNAs) have been reported as critical regulators in several cancers, including ALL. LncRNA SLCO4A1 antisense RNA 1 (SLCO4A1-AS1) has been revealed to be implicated in tumorigenesis of several cancers. Our study focused on the role of SLCO4A1-AS1 in ALL. METHODS: RT-qPCR, Western blot analysis, CCK-8, EdU, and Flow cytometry analysis were used to explore the biological function of SLCO4A1-AS1 in ALL cellular processes. Luciferase reporter and RNA pull-down assays were applied to explore the mechanism of SLCO4A1-AS1 in ALL cells. RESULTS: SLCO4A1-AS1 was upregulated in ALL tissues and cell lines. We found that suppression of SLCO4A1-AS1 suppressed ALL cell proliferation and facilitated cell apoptosis. Our result confirmed that SLCO4A1-AS1 acted as a ceRNA by sponging microRNA 876-3p (miR-876-3p) to upregulate retinoblastoma binding protein 6 (RBBP6) expression in ALL cells. Moreover, SLCO4A1-AS1 activated the JNK signaling pathway by upregulating RBBP6. Rescue assays revealed that the activation of the JNK signaling or overexpression of RBBP6 revered the suppressive effect of SLCO4A1-AS1 knockdown on growth of ALL cells. CONCLUSION: SLCO4A1-AS1 promoted cell growth of ALL by the miR-876-3p/RBBP6 axis to activate the JNK signaling pathway.	NA	Int J Lab Hematol. 2021 Mar 8. doi: 10.1111/ijlh.13501.
3701	LncRNA	SNHG11	miR-184	CDC25A	GC samples and cell lines(SGC-7901,MKN-28)	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33816469	Assessing the Regulatory Functions of LncRNA SNHG11 in Gastric Cancer Cell Proliferation and Migration.	The aim of this study was to assess the regulatory functions of SNHG11 in gastric cancer (GC) cell proliferation and migration. Dual-luciferase reporter assay and bioinformatics prediction [starBase (http://starbase.sysu.edu.cn/) and TargetScan (http://www.targetscan.org)] indicated that SNHG11 functions as a miR-184 sponge that can directly act on CDC25A. Compared with normal healthy gastric tissue and mucosal epithelial cell GES-1, SNHG11 and CDC25A expressions were dramatically increased in GC samples and cell lines, whereas microRNA-184 (miR-184) levels were reduced. SNHG11 silencing led to increased miR-184 and reduced CDC25A, whereas miR-184 downregulation recovered the expression of CDC25A. Additionally, miR-184 upregulation also played a role in regulating CDC25A ablation. Then, SNHG11 was silenced or miR-184 was upregulated in two GC cells (SGC-7901 and MKN-28). SNHG11 silencing and miR-184 upregulation caused a notable decrease in GC cell growth and proliferation and increased the apoptotic level of GC cells. Furthermore, SNHG11 silencing and miR-184 upregulation contributed to a decreased migration capacity of GC cells. Downregulated miR-184 expression in SNHG11 silenced GC cells showed that miR-184 inhibition reversed the effect of SNHG11 silencing on the growth, proliferation, apoptosis, and migration of GC cells. Moreover, in vivo xenograft experiments demonstrated that SNHG11 knockdown can inhibit tumor growth. These observations confirmed that SNHG11 acts as an oncogene, whereas miR-194 served as a tumor suppressor in GC development. SNHG11 may provide a new biomarker for GC diagnosis, treatment, and prognosis.	NA	Front Cell Dev Biol. 2021 Mar 18;9:620476. doi: 10.3389/fcell.2021.620476. eCollection 2021.
3702	LncRNA	SNHG14	miR-206	SOX9	HCC cell line SMCC7721	Hepatocellular Carcinoma	Homo sapiens (human)	RIP assay;Western blot;Flow Cytometry assay;RNA pull-down;	33782806	LncRNA SNHG14 Sponges miR-206 to Affect Proliferation, Apoptosis, and Metastasis of Hepatocellular Carcinoma Cells by Regulating SOX9.	OBJECTIVE: To explore how lncRNA SNHG14 modulates the biological features of hepatocellular carcinoma (HCC) cells by regulating SOX9 via mediating miR-206. METHODS: HCC tissues were collected to perform the quantitative reverse transcriptase polymerase chain reaction to determine the expressions of SNHG14, miR-206, and SOX9. HCC cell line SMCC7721 was selected for co-transfection by si-SNHG14/miR-206 inhibitor/si-SOX9, followed by the measurement of cell proliferation using Cell Count Kit-8 (CCK-8) assay and clone formation assay. The migration and invasion were evaluated by wound healing test and Transwell assay. The apoptotic rate was determined by flow cytometry. Levels of the apoptosis-related proteins were measured through Western blotting. RESULTS: SNHG14 and SOX9 were up-regulated in HCC tumor tissues compared with adjacent normal tissues, with decreased miR-206 expression. Moreover, SNHG14 expression was significantly associated with the TNM stage, lymphatic metastasis, and histological differentiation of HCC patients. Besides, inverse correlations between SNHG14 and miR-206, as well as between miR-206 and SOX9, were noted. The dual luciferase reporter gene assay, RIP, and RNA pull-down experiments also revealed the targeting relationship between SNHG14 and miR-206 or between miR-206 and SOX9. Silencing SNHG14 and SOX9 inhibited the proliferation, invasion, and migration of HCC cells, with increased apoptosis, which was all abolished by silencing miR-206. CONCLUSION: Inhibition of SNHG14 suppresses SOX9 by up-regulating miR-206, to further inhibit the proliferation, migration, and invasion of HCC cells with the promoted apoptosis, which is a novel target for the treatment of HCC.	NA	Dig Dis Sci. 2021 Mar 29. doi: 10.1007/s10620-021-06920-8.
3703	LncRNA	SNHG15	miR-188-5p	DAAM1	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33742497	SNHG15 facilitated malignant behaviors of oral squamous cell carcinoma through targeting miR-188-5p/DAAM1.	BACKGROUND: Long non-coding RNA (lncRNA) small nucleolar RNA host gene 15 (SNHG15) has been discovered and demonstrated to have significant function in multiple cancers. Nevertheless, how it participates in the progression of oral squamous cell carcinoma (OSCC) and its potential regulatory system are still unclear. METHODS: RT-qPCR detected the expression of SNHG15, miR-188-5p, and DAAM1. RNA pull down, RT-qPCR, and bioinformatics were used for finding and selecting downstream targets of SNHG15. RESULTS: SNHG15 presented a high expression in OSCC cells. Moreover, inhibition of SNHG15 exhibited repressive influence on proliferative, migrated, and invasive abilities but induce apoptosis of OSCC cells. Through the search of bioinformatics and RNA pull down assays, we confirmed that miR-188-5p was one target of SNHG15 in OSCC cells. Additionally, miR-188-5p could hamper the growth of OSCC cells. Moreover, it was manifested that DAAM1 was down-regulated by miR-188-5p. DAAM1 was up-regulated in OSCC cells. Furthermore, it exerted oncogenic function in the course of OSCC. Eventually, overexpression of DAAM1 offsets the effects of down-regulation of SNHG15 on the development of OSCC. CONCLUSION: To summarize, our study certified that SNHG15 contributed to the process of OSCC via sponging miR-188-5p to elevate DAAM1 expression. SNHG15 might offer novel sight to improve the results of treatment for OSCC.	NA	J Oral Pathol Med. 2021 Mar 20. doi: 10.1111/jop.13169.
3704	LncRNA	SNHG4	miR-590-3p	CDK1	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33744866	lncRNA SNHG4 modulates colorectal cancer cell cycle and cell proliferation through regulating miR-590-3p/CDK1 axis.	Colorectal cancer (CRC) is a prevalent malignancy worldwide. The development of genome sequencing technology has allowed the discovery that epigenetic regulation might play a critical role in CRC tumorigenesis. In the present study, we found that the long noncoding RNA (lncRNA) SNHG4 was dramatically increased in CRC tissue samples and cell lines based on both publicly available and experimental data. SNHG4 knockdown suppressed the viability and colony formation capacity of CRC cells. The expression of CDK1 was considerably increased in CRC tissue samples and cells and had a positive correlation with the expression of SNHG4 in CRC. SNHG4 silencing not only caused S phase cell cycle arrest but also significantly downregulated the CDK1, cyclin B1, and cyclin A2 protein levels in CRC cells. miR-590-3p simultaneously bound to SNHG4 and CDK1. miR-590-3p functioned to inhibit CDK1 expression. miR-590-3p overexpression exerted the same effects on the CRC cell phenotype as SNHG4 knockdown. The effects of si-SNHG4 on CRC cells were significantly reversed by anti-miR-590-3p, indicating that SNHG4 relieved the miR-590-3p-induced inhibition of CDK1 by acting as a competing endogenous RNA (ceRNA). In vivo, SNHG4 silencing inhibited subcutaneously transplanted tumor growth and decreased cell cycle marker levels, whereas miR-590-3p inhibition exerted the opposite effects. The in vivo effects of SNHG4 silencing were also reversed by miR-590-3p inhibition. The SNHG4/miR-590-3p/CDK1 axis influences the cell cycle to modulate CRC cell proliferation and subcutaneously transplanted tumor growth. Further application of this axis still requires analysis using more animal models and clinical investigations.	NA	Aging (Albany NY). 2021 Mar 19;13(7):9838-9858. doi: 10.18632/aging.202737. Epub 2021 Mar 19.
3705	LncRNA	SNHG6	miR-26a-5p	ARPP19	NPC tissues and cell	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA pull-down assay;RNA pull-down;	33744438	LncRNA SNHG6 accelerates nasopharyngeal carcinoma progression via modulating miR-26a-5p/ARPP19 axis.	OBJECTIVES: Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. DESIGN: Prospective feasibility study. SETTING: The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital. Long noncoding RNAs (lncRNAs) have been reported to be involved in multiple cancer progression, yet the biological role of lncRNA SNHG6 in nasopharyngeal carcinoma (NPC) is still unclear. This research aims to explore the molecular mechanism of SNHG6 in the development and progression of NPC. RT-qPCR assay was used to examine the expression of SNHG6, miR-26a-5p, and ARPP19 in NPC. CCK-8 and transwell assays were employed to detect NPC cell viability, migration, and invasion. The interaction between miR-26a-5p and SNHG6 or ARPP19 was determined by the luciferase reporter, RIP and RNA pull-down assays. We observed that SNHG6 expression was enhanced in NPC tissues and cells. SNHG6 deletion attenuated NPC cell viability and metastasis. MiR-26a-5p was predicted and validated to interact with SNHG6, and miR-26a-5p expression was markedly elevated in NPC after SNHG6 silence. Moreover, miR-26a-5p inhibitor rescued the suppressive effect of SNHG6 depletion on NPC cell viability, migration and invasion. Besides, ARPP19 was a target of SNHG6 and positively regulated by SNHG6. ARPP19 overexpression neutralized the repressive effect of SNHG6 knockdown on NPC progression. Our results indicated that SNHG6 regulated NPC progression through modulating miR-26a-5/ARPP19 axis, which might provide new insights into NPC diagnosis and treatment.	NA	Bioorg Med Chem Lett. 2021 May 15;40:127955. doi: 10.1016/j.bmcl.2021.127955. Epub 2021 Mar 17.
3706	LncRNA	SNHG7	miR-122-5p	FOXK2	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33738672	LncRNA SNHG7 Promotes the HCC Progression Through miR-122-5p/FOXK2 Axis.	Hepatocellular carcinoma (HCC) is a malignant tumor with high mortality and severe complication in China. Numerous studies have shown that long noncoding RNAs (lncRNAs) are involved in the regulation of various processes in cancer cells. Our research aimed to investigate the underlying mechanism of the lncRNA small nucleolar RNA host gene 7 (SNHG7) in HCC development. The expression of SNHG7, microRNA-122-5p (miR-122-5p), and Forkhead box K2 (FOXK2) was assessed via quantitative real-time polymerase chain reaction. 3-(4,5) -dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT) and transwell assays were performed to measure cell viability, migration, and invasion, respectively. The relative protein levels were detected by Western blot. The relationships between miR-122-5p and SNHG7 or FOXK2 were predicted by online software and then confirmed by dual-luciferase reporter assay. Animal experiments were conducted to clarify the effects of SNHG7 on proliferation in vivo. To begin with, SNHG7 was upregulated, while miR-122-5p was downregulated in HCC tissues and cells. Downregulation of SNHG7 inhibited cell growth and metastasis. Interestingly, SNHG7 could abolish the effects of miR-122-5p on HCC cells. Furthermore, miR-122-5p targeted FOXK2 and miR-122-5p recovered the effects of FOXK2 downregulation on cell growth and metastasis in HCC cells. Besides, SNHG7 facilitated HCC tumor growth in vivo through the miR-122-5p/FOXK2 axis. The lncRNA SNHG7 boosted the development of HCC by regulating FOXK2 through sponging miR-122-5p.	NA	Dig Dis Sci. 2021 Mar 18. doi: 10.1007/s10620-021-06918-2.
3707	LncRNA	SNHG8	miR-588	ATG7	CRC tissues / adjacent tissues and cell lines	Colorectal Cancer	Homo sapiens (human)	Western blot;	34122628	Long non-coding RNA SNHG8 promotes autophagy as a ceRNA to upregulate ATG7 by sponging microRNA-588 in colorectal cancer.	Colorectal cancer (CRC) is the third most common cancer worldwide. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 8 (SNHG8) acts as an oncogene in different types of cancer, including prostate, breast and ovarian cancer. SNHG8 promotes the tumorigenesis of CRC; however, its underlying molecular mechanism remains unclear. The present study aimed to explore the mechanism of SNHG8 on CRC development via various assays, including western blot, pull-down, PCR and immunofluorescence assays. The results of the present study demonstrated that SNHG8 expression was substantially upregulated in primary tumor tissues from The Cancer Genome Atlas dataset. Western blot and immunofluorescence analyses demonstrated that SNHG8 facilitated cell proliferation and autophagy in CRC cells. Notably, the function of SNHG8 in enhancing autophagy was dependent on autophagy-related gene 7 (ATG7). In addition, western blot analysis indicated that the effect of SNHG8 on autophagy in CRC cells was dependent on the miR-588/ATG7 axis. Taken together, the results of the present study suggest that SNHG8 promotes autophagy in CRC cells.	NA	Oncol Lett. 2021 Aug;22(2):577. doi: 10.3892/ol.2021.12838. Epub 2021 Jun 2.
3708	LncRNA	ST8SIA6-AS1	miR-338-3p	NONO	HCC cell	Hepatocellular Carcinoma	Homo sapiens (human)	FISH;qPCR;RT-qPCR;RIP assay;Western blot;FISH;Luciferase reporter assay;	33722502	ST8SIA6-AS1 promotes the development of hepatocellular carcinoma cells through miR-338-3p/NONO Axis.	BACKGROUND: Increasing studies have shown a vital fact that long non-coding RNAs (lncRNAs) play a considerable regulatory role in hepatocellular carcinoma (HCC) progression. However, whether ST8 alpha-N-acetyl-neuraminide alpha-2, 8-sialyltransferase 6 antisense RNA 1 (ST8SIA6-AS1) affects the development of HCC is unclear. METHODS: The target genes in HCC cell lines were quantified via utilzing quantitative real-time polymerase chain reaction (RT-qPCR) analysis and western blot. Effects of ST8SIA6-AS1 on proliferative, apoptosis and migratory ability of HCC cells were proved by a series of function experiments. The cellular distribution of ST8SIA6-AS1 was examined through fluorescent in situ hybridization (FISH) assay and subcellular fractionation experiments. RNA pulldown assay was implemented to explore the target of ST8SIA6-AS1. RNA Binding Protein Immunoprecipitation (RIP) and luciferase reporter assays were performed to identify the specific relationships between miR-338-3p and ST8SIA6-AS1/ non-POU domain containing octamer binding (NONO). RESULTS: The expression of ST8SIA6-AS1 was apparently elevated in HCC cell. Silenced ST8SIA6-AS1 reduced proliferative, migratory and invasive ability of HCC cells. Moreover, ST8SIA6-AS1 targeted miR-338-3p to modulate the expression of NONO in HCC cells. CONCLUSIONS: ST8SIA6-AS1 enhances the progression of HCC via miR-338-3p/NONO axis in vitro.	NA	Dig Liver Dis. 2021 Mar 12:S1590-8658(21)00078-5. doi: 10.1016/j.dld.2021.02.012.
3709	LncRNA	TMPO-AS1	miR-1179	TRIM37	breast cancer cell lines(MDA-MB-231,MCF7)	Breast Cancer	Homo sapiens (human)	qRT-PCR	33981362	Long non-coding RNA TMPO-AS1 facilitates chemoresistance and invasion in breast cancer by modulating the miR-1179/TRIM37 axis.	Breast cancer has become the most common female tumor in the world. Although great progress has been made in the past decade, the treatment of advanced breast cancer remains unsatisfactory. An increasing number of reports have indicated that long non-coding RNAs (lncRNAs) have a pivotal role in chemoresistance as potential oncogenes in numerous types of cancer. However, the precise mechanisms underlying the action of lncRNAs in breast cancer resistance to chemotherapy have yet to be fully elucidated. In the present study, the function and molecular mechanisms of the lncRNA TMPO-antisense RNA 1 (AS1) in terms of its resistance to docetaxel (DOC) were explored in the MDA-MB-231 and MCF7 breast cancer cell lines. The results obtained suggested that TMPO-AS1 was markedly upregulated in DOC-resistant breast cancer cells compared with the sensitive breast cancer cells. Functionally, TMPO-AS1-knockdown sensitized MDA-231/DOC and MCF-7/DOC cells to DOC and suppressed cell invasion, with increased rates of DOC-induced apoptosis. Mechanistically, TMPO-AS1-downregulation induced DOC-sensitivity in breast cancer cells via depleting tripartite motif-containing protein 37 (TRIM37) by sponging microRNA (miR)-1179. Taken together, the present study has revealed the existence of a novel TMPO-AS1/miR-1179/TRIM37 molecular axis conferring DOC resistance of breast cancer cells, thereby suggesting a promising novel therapeutic target for breast cancer.	NA	Oncol Lett. 2021 Jul;22(1):500. doi: 10.3892/ol.2021.12761. Epub 2021 Apr 28.
3710	LncRNA	TRAF3IP2-AS1	miR-200a-3p	PTEN	tRCC tissues and cells	Renal Cancer	Homo sapiens (human)	FISH;qRT-PCR;RNA immunoprecipitation;Western blot;FISH;Immunohistochemistry;luciferase assay;RNA immunoprecipitation;	33741027	Low expression of TRAF3IP2-AS1 promotes progression of NONO-TFE3 translocation renal cell carcinoma by stimulating N(6)-methyladenosine of PARP1 mRNA and downregulating PTEN.	BACKGROUND: NONO-TFE3 translocation renal cell carcinoma (NONO-TFE3 tRCC) is one subtype of RCCs associated with Xp11.2 translocation/TFE3 gene fusions RCC (Xp11.2 tRCCs). Long non-coding RNA (lncRNA) has attracted great attention in cancer research. The function and mechanisms of TRAF3IP2 antisense RNA 1 (TRAF3IP2-AS1), a natural antisense lncRNA, in NONO-TFE3 tRCC remain poorly understood. METHODS: FISH and qRT-PCR were undertaken to study the expression, localization and clinical significance of TRAF3IP2-AS1 in Xp11.2 tRCC tissues and cells. The functions of TRAF3IP2-AS1 in tRCC were investigated by proliferation analysis, EdU staining, colony and sphere formation assay, Transwell assay and apoptosis analysis. The regulatory mechanisms among TRAF3IP2-AS1, PARP1, PTEN and miR-200a-3p/153-3p/141-3p were investigated by luciferase assay, RNA immunoprecipitation, Western blot and immunohistochemistry. RESULTS: The expression of TRAF3IP2-AS1 was suppressed by NONO-TFE3 fusion in NONO-TFE3 tRCC tissues and cells. Overexpression of TRAF3IP2-AS1 inhibited the proliferation, migration and invasion of UOK109 cells which were derived from cancer tissue of patient with NONO-TFE3 tRCC. Mechanistic studies revealed that TRAF3IP2-AS1 accelerated the decay of PARP1 mRNA by direct binding and recruitment of N(6)-methyladenosie methyltransferase complex. Meanwhile, TRAF3IP2-AS1 competitively bound to miR-200a-3p/153-3p/141-3p and prevented those from decreasing the level of PTEN. CONCLUSIONS: TRAF3IP2-AS1 functions as a tumor suppressor in NONO-TFE3 tRCC progression and may serve as a novel target for NONO-TFE3 tRCC therapy. TRAF3IP2-AS1 expression has the potential to serve as a novel diagnostic and prognostic biomarker for NONO-TFE3 tRCC detection.	NA	J Hematol Oncol. 2021 Mar 19;14(1):46. doi: 10.1186/s13045-021-01059-5.
3711	LncRNA	TRHDE-AS1	miR-181a-5p	PTEN	HS tissues and HSFs	Hypertrophic Scar	Homo sapiens (human)	RACE;	33675502	LncRNA TRHDE-AS1 inhibit the scar fibroblasts proliferation via miR-181a-5p/PTEN axis.	Hypertrophic scar (HS), a fibroproliferative disorder caused by abnormal wound healing after skin injury, which is characterized by excessive deposition of extracellular matrix and invasive growth of fibroblasts. Recent studies have shown that some non-coding RNA implicated the formation of HS, but the mechanism remains unclear. In this study, we found that lncRNA TRHDE-AS1 was downregulated in HS tissues and HSFs, and the level of lncRNA TRHDE-AS1 negatively correlated with the level of miR-181a-5p in HS tissue and HSFs. Overexpressed lncRNA TRHDE-AS1 significantly suppressed miR-181a-5p level, while promoted HSFs apoptosis and inhibited HSFs proliferation. Further study shown that PTEN was a direct target of miR-181a-5p, and lncRNA TRHDE-AS1 served as a molecular sponge for miR-181a-5p to regulate the expression of PTEN. Overexpression of PTEN could eliminate lncRNA TRHDE-AS1-mediated proliferation suppression of HSFs. In conclusion, our study suggested that lncRNA TRHDE-AS1/miR-181a-5p/PTEN axis plays an important role in promoting hypertrophic scar formation, which may be effectively used as a therapeutic target for hypertrophic scar treatment.	NA	J Mol Histol. 2021 Apr;52(2):419-426. doi: 10.1007/s10735-021-09968-y. Epub 2021 Mar 6.
3712	LncRNA	TUG1	miR-188-3p	FGF5	Min6 cells	Type 2 Diabetes Mellitus	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qRT-PCR;Chromatin immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;	33660806	SP1-induced lncRNA TUG1 regulates proliferation and apoptosis in islet cells of type 2 diabetes mellitus via the miR-188-3p/FGF5 axis.	OBJECTIVE: To elucidate the role of TUG1 in the onset of type 2 diabetes mellitus (T2DM) and the potential mechanism. MATERIALS AND METHODS: Relative levels of TUG1 and SP1 in high-fat diet animal model and high-glucose cell model were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and their correlation was analyzed. Potential binding sites in the promoter sequences of TUG1 and SP1 were predicted using the JASPAR. Their interaction was further confirmed by chromatin immunoprecipitation (ChIP) and Dual-Luciferase reporter assay. The influences of TUG1 on proliferative and apoptotic potentials in Min6 cells were examined by Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) assay and flow cytometry, respectively. Subsequently, the interaction in the TUG1/miR-188-3p /FGF5 axis was similarly explored by Dual-Luciferase reporter assay. RESULTS: SP1 and TUG1 were downregulated in high-fat and high-glucose models, and they displayed a positive correlation. TUG1 bound E2 region in SP1 promoters. Knockdown of TUG1 inhibited proliferative rate and induced apoptosis in high-glucose-treated Min6 cells. Furthermore, the TUG1 / miR-188-3p /FGF5 axis was identified to be responsible for regulating Min6 cell functions. CONCLUSIONS: SP1 induces TUG1 downregulation in T2DM cell models, which further regulates proliferative and apoptotic potentials in islet cells by activating the miR-188-3p/FGF5 axis.	NA	Eur Rev Med Pharmacol Sci. 2021 Feb;25(4):1959-1966. doi: 10.26355/eurrev_202102_25096.
3713	LncRNA	TUG1	miR-494-3p	E-cadherin	HK-2 cell	Acute Kidney Injury	Homo sapiens (human)	ELISA;RT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	33663500	LncRNA TUG1 regulates the development of ischemia-reperfusion mediated acute kidney injury through miR-494-3p/E-cadherin axis.	BACKGROUND: Acute kidney injury (AKI) results from renal dysfunction caused by various causes, resulting in high mortality. The underlying mechanisms of ischemia-reperfusion (I/R) induced AKI is very complicated and needed for further research. Here, we sought to found out the functions of lncRNA TUG1 in I/R-induced AKI. METHODS: In vivo model was constructed by I/R-induced mice and in vitro model was constructed by hypoxia/reoxygenation (H/R)-induced HK-2 cell. Kidney tissue damage was evaluated through H&E staining in mice. Cell flow cytometry was used to detect the degree of apoptosis. TUG1, miR-494-3p and E-cadherin were determined both by RT-PCR and western blot. Dual luciferase assay was employed to validate the relationships between TUG1, miR-494-3p and E-cadherin. Inflammatory factors including IL-1β, TNFɑ and IL-6 were evaluated by ELISA. RESULTS: lncRNA TUG1 was decreased while miR-494-3p was elevated in vivo and in vitro. Overexpression of TUG1 or transfection with miR-494-3p inhibitor significantly alleviated cell apoptosis. MiR-494-3p directly targeted E-cadherin and TUG1 suppressed cell apoptosis via serving as a miR-494-3p sponge to disinhibit E-cadherin. CONCLUSION: lncRNA TUG1 alleviated I/R-induced AKI through targeting miR-494-3p/E-cadherin.	NA	J Inflamm (Lond). 2021 Mar 4;18(1):12. doi: 10.1186/s12950-021-00278-4.
3714	LncRNA	TUG1	miR-199a-3p	MSI2	Ewings sarcoma cells	Ewings Sarcoma	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33780263	LncRNA TUG1 promotes Ewing's sarcoma cell proliferation, migration, and invasion via the miR-199a-3p-MSI2 signaling pathway.	The aim of this study was to investigate the roles and potential mechanisms of long non-coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in the proliferation, migration, and invasion of Ewing's sarcoma cells. RT-qPCR was used to detect the expression of TUG1, microRNA-199a-3p (miR-199a-3p), and musashi2 (MSI2) in Ewing's sarcoma tissues and cell lines. Kaplan-Meier overall survival curves showed the survival rates of Ewing's sarcoma patients with high and low expression of TUG1. The association between the expressions of TUG1/MSI2 and miR-199a-3p in Ewing's sarcoma tissues was assessed by Pearson's correlation analysis. Cell proliferation, migration, and invasion were detected by CCK-8 assay and Transwell assay, respectively. The protein level of MSI2 was determined using western blotting. The interaction between TUG1/MSI2 and miR-199a-3p was validated by the dual-luciferase reporter assay. The levels of TUG1 and MSI2 were increased, while the level of miR-199a-3p was decreased in Ewing's sarcoma tissues and cells. High expression of TUG1 or MSI2 indicated a decreased overall survival rate of Ewing's sarcoma patients. TUG1/MSI2 level was negatively correlated with miR-199a-3p level. While TUG1 level was positively correlated with MSI2 level. In Ewing's sarcoma cells, knockdown of TUG1/MSI2 or overexpression of miR-199a-3p inhibited cell proliferation, migration, and invasion, whereas the overexpression of TUG1/MSI2 presented the opposite results. TUG1 functioned as a competing endogenous RNA to regulate MSI2 expression by sponging miR-199a-3p. Finally, miR-199a-3p inhibitor or MSI2 overexpression counteracted the TUG1 knockdown-mediated inhibitory effect on Ewing's sarcoma cell proliferation, migration, and invasion. TUG1 promotes proliferation, migration, and invasion of Ewing's sarcoma cells via sequestering miR-199a-3p to enhance the MSI2 expression, suggesting that TUG1 might be a potential target for treating Ewing's sarcoma.	NA	Neoplasma. 2021 May;68(3):590-601. doi: 10.4149/neo_2021_201110N1198. Epub 2021 Mar 30.
3715	LncRNA	UCA1	miR-185-5p	HOXA13	LSCC tissues and cell lines	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;	33629307	Long non-coding RNA UCA1 mediates proliferation and metastasis of laryngeal squamous cell carcinoma cells via regulating miR-185-5p/HOXA13 axis.	OBJECTIVE: LncRNA urothelial cancer associated 1 (UCA1) is involved in the development of laryngeal squamous cell carcinoma (LSCC), however, its specific mechanism is not fully clear. PATIENTS AND METHODS: Quantitative reverse transcription-PCR (RT-qPCR) was conducted to determine the expressions of lncRNA-UCA1, miR-185-5p and homeobox A13 (HOXA13) in LSCC tissues and cell lines. Cell Counting Kit-8 assay, colony formation assay, wound healing assay, Transwell and flow cytometry, DIANA-LncBase V2, as well as Starbase, Targetscan, and Dual-Luciferase reporter gene system were conducted to detect and confirm the crosstalk networks among lncRNA-UCA1, miR-185-5p, and HOXA13. RESULTS: The levels of UCA1 and HOXA13 were significantly higher and the expression of miR-185-5p was reduced in LSCC tissues and cell lines. Moreover, miR-185-5p was predicted as a target gene for lncRNA UCA1, while HOXA13 was the target gene for miR-185-5p. UCA1 siRNA inhibited the proliferation and invasion of LSCC cells, moreover, the proliferation and invasion of LSCC cells were suppressed by miR-185-5p mimics but were enhanced by miR-185-5p inhibitor. UCA1 siRNA and overexpressed HOXA13 reversed the promotive effects of miR-185-5p inhibitor and inhibitory effects of miR-185-5p mimics on cell proliferation and metastasis, respectively. CONCLUSIONS: The current findings reveal the important role of lncRNA UCA1/miR-185-5p/HOXA13 regulatory network in LSCC cells, and potentially provide new insights into the pathogenesis of LSCC.	NA	Eur Rev Med Pharmacol Sci. 2021 Feb;25(3):1366-1378. doi: 10.26355/eurrev_202102_24845.
3716	LncRNA	VIM-AS1	miR-655	ZEB1	bladder cancer cell lines	Bladder Cancer	Homo sapiens (human)	Immunoblotting;	33902589	The VIM-AS1/miR-655/ZEB1 axis modulates bladder cancer cell metastasis by regulating epithelial-mesenchymal transition.	BACKGROUND: Invasive bladder tumors cause a worse prognosis in patients and remain a clinical challenge. Epithelial-mesenchymal transition (EMT) is associated with bladder cancer metastasis. In the present research, we attempted to demonstrate a novel mechanism by which a long noncoding RNA (lncRNA)-miRNA-mRNA axis regulates EMT and metastasis in bladder cancer. METHODS: Immunofluorescence (IF) staining was used to detect Vimentin expression. The protein expression of ZEB1, Vimentin, E-cadherin, and Snail was investigated by using immunoblotting assays. Transwell assays were performed to detect the invasive capacity of bladder cancer cells. A wound healing assay was used to measure the migratory capacity of bladder cancer cells. RESULTS: Herein, we identified lncRNA VIM-AS1 as a highly- expressed lncRNA in bladder cancer, especially in metastatic bladder cancer tissues and high-metastatic bladder cancer cell lines. By acting as a ceRNA for miR-655, VIM-AS1 competed with ZEB1 for miR-655 binding, therefore eliminating the miR-655-mediated suppression of ZEB1, finally promoting EMT in both high- and low-metastatic bladder cancer cells and enhancing cancer cell metastasis. CONCLUSIONS: In conclusion, the VIM-AS1/miR-655/ZEB1 axis might be a promising target for improving bladder cancer metastasis via an EMT-related mechanism.	NA	Cancer Cell Int. 2021 Apr 26;21(1):233. doi: 10.1186/s12935-021-01841-y.
3717	Circular RNA	VRK1	miR-221-3P	PTEN	PE placenta tissues and HTR-8/SVneo cells	Pre-Eclampsia	Homo sapiens (human)	microarray;	33738906	Circular RNA VRK1 facilitates pre-eclampsia progression via sponging miR-221-3P to regulate PTEN/Akt.	Pre-eclampsia (PE) is a worldwide pregnancy-related disorder. It is mainly characterized by defect migration and invasion of trophoblast cells. Recently, circular RNAs (circRNAs) have been believed to play a vital role in PE. The expression patterns and the biological functions of circRNAs in PE remain elusive. Here, we performed a circRNA microarray to identify putative PE-related circRNAs. Bioinformatics analyses were used to screen the circRNAs which have potential relationships with pre-eclampsia, and we identified a novel circRNA (circVRK1) that was up-regulated in PE placenta tissues. By using HTR-8/SVneo cells, circVRK1 knockdown significantly enhanced cell migration and invasion abilities, as well as epithelial-mesenchymal transition (EMT). Mechanistically, we found that circVRK1 and PTEN could function as the ceRNAs to miR-221-3p. Overexpression of miR-221-3p promoted cell migration, invasion and EMT via regulating PTEN. The cotransfection of miR-221-3p inhibitor or PTEN reversed the effect from circVRK1 knockdown. Moreover, the circVRK1/miR-221-3p/PTEN axis greatly regulated Akt phosphorylation. In general, circVRK1 suppresses trophoblast cell migration, invasion and EMT, by acting as a ceRNA to miR-221-3p to regulate PTEN, and further inhibit PI3K/Akt activation. The purpose of this paper is to open wide insights to investigate the onset of PE and provide new potential therapeutic targets in PE.	NA	J Cell Mol Med. 2021 Mar 18. doi: 10.1111/jcmm.16454.
3718	LncRNA	XIST	miR-302a-3p	USP8	primary ligament fibroblasts	NA	Homo sapiens (human)	RT-PCR;Western blot;Luciferase reporter assay;	33748113	METTL3 Regulates Ossification of the Posterior Longitudinal Ligament via the lncRNA XIST/miR-302a-3p/USP8 Axis.	The prevalence of ossification of the posterior longitudinal ligament (OPLL) is increasing, and currently there is no effective medical treatment for OPLL. Methyltransferase like 3 (METTL3), one of the components of the N (6)-methyladenosine (m(6)A) methyltransferase complex, regulates gene expression via modification of mRNA. Although METTL3 has been implicated in a variety of diseases, its role in OPLL remains to be elucidated. Primary ligament fibroblasts were used in this study. To investigate the role of METTL3 in OPLL, METTL3 was silenced or overexpressed. m(6)A RNA methylation was measured by commercially available kits. Luciferase reporter assay was performed to investigate the binding of miR-302a-3p and METTL3, and the binding of miR-302a-3p and USP8. Quantitative RT-PCR and western blots were used to evaluate mRNA and protein expression, respectively. OPLL increases METTL3 and its m(6)A modification. Overexpressing METTL3 significantly promoted osteogenic differentiation of primary ligament fibroblasts. Mechanism study showed that METTL3 increased m(6)A methylation of long non-coding RNA (lncRNA) X-inactive specific transcript (XIST). Further study showed that lncRNA XIST regulates osteogenic differentiation of primary ligament fibroblasts via miR-302a-3p, which targets ubiquitin-specific protease 8 (USP8). METTL3 enhanced osteogenic differentiation of primary ligament fibroblasts via the lncRNA XIST/miR-302a-3p/USP8 axis. The findings highlight the importance of METTL3-mediated m(6)A methylation of XIST in OPLL and provide new insights into therapeutic strategies for OPLL.	NA	Front Cell Dev Biol. 2021 Mar 5;9:629895. doi: 10.3389/fcell.2021.629895. eCollection 2021.
3719	LncRNA	XIST	miR-16-5p	WEE1	NSCLC tissue and cell	Non-Small Cell Lung Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	33583218	Knockdown of lncRNA X inactive specific transcript (XIST) radiosensitizes non-small cell lung cancer (NSCLC) cells through regulation of miR-16-5p/WEE1 G2 checkpoint kinase (WEE1) axis.	Long non-coding RNA (lncRNA) X inactive specific transcript (XIST) is reported to play an oncogenic role in non-small cell lung cancer (NSCLC). However, the role of XIST in regulating the radiosensitivity of NSCLC cells remains unclear. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of XIST and miR-16-5p in NSCLC in tissues and cells, and Western blot was used to assess the expression of WEE1 G2 checkpoint kinase (WEE1). Cell counting kit-8 (CCK-8), colony formation and flow cytometry assays were used to determine cell viability and apoptosis after NSCLC cells were exposed to different doses of X-rays. The interaction between XIST and miR-16-5p was confirmed by StarBase database, qRT-PCR and dual-luciferase reporter gene assays. TargetScan database was used to predict WEE1 as a target of miR-16-5p, and their targeting relationship was further validated by Western blot, qRT-PCR and dual-luciferase reporter gene assays. XIST was highly expressed in both NSCLC tissue and cell lines, and knockdown of XIST repressed NSCLC cell viability and cell survival, and facilitated apoptosis under the irradiation. MiR-16-5p was a target of XIST, and rescue experiments demonstrated that miR-16-5p inhibitors could reverse the role of XIST knockdown on radiosensitivity in NSCLC cells. WEE1 was validated as a target gene of miR-16-5p, and WEE1 could be negatively regulated by XIST. XIST promotes the radioresistance of NSCLC cells by regulating the expressions of miR-16-5p and WEE1, which can be a novel target for NSCLC therapy.	NA	Int J Immunopathol Pharmacol. 2021 Jan-Dec;35:2058738420966087. doi: 10.1177/2058738420966087.
3720	Circular RNA	ZNF609	miR-1224-3p	PLK1	Glioma tissues and cell lines	Glioma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33976745	Circular RNA ZNF609 promotes the malignant progression of glioma by regulating miR-1224-3p/PLK1 signaling.	Objective: Previous studies have demonstrated that circular RNAs (circRNAs) play vital roles in pathological process of various diseases, including tumors. This study aimed at exploring the role and mechanism of circRNA RNA ZNF609 (circ-ZNF609) in the occurrence and development of glioma. Materials and methods: Real-time quantitative PCR (qRT-PCR) was applied to measure the expression of circ-ZNF609, miRNA-1224-3p (miR-1224-3p) and Polo-like kinase 1 (PLK1) in glioma tissues and cell lines. Furthermore, the association between circ-ZNF609 and clinical features of glioma was analyzed. CCK8 assay, EdU assay and Transwell assay were conducted to detect the effect of circ-ZNF609, miR-1224-3p and PLK1 on proliferation, migration and invasion in glioma cells. Then, we investigated the underlying mechanism of circ-ZNF609 by bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation (RIP), qRT-PCR and western blotting assay. Results: Circ-ZNF609 was confirmed prominently upregulated in glioma. Inhibition of circ-ZNF609 could obviously suppress glioma cell proliferation, migration and invasion, while overexpression of circ-ZNF609 promoted glioma growth and metastasis. In vivo, xenotransplanted tumor model also showed that overexpression of circ-ZNF609 could promote in vivo glioma growth. Mechanistically, circ-ZNF609 could promote PLK1 expression via binding to miR-1224-3p, circ-ZNF609/miR-1224-3p/PLK1 was shown responsible for circ-ZNF609 promoting glioma growth and metastasis. Conclusion: Together, our results revealed that circ-ZNF609 elevates glioma growth and metastasis via enforcing PLK1 expression by competitively binding miR-1224-3p, suggesting that circ-ZNF609 might be an underlying therapeutic target for glioma.	NA	J Cancer. 2021 Apr 12;12(11):3354-3366. doi: 10.7150/jca.54934. eCollection 2021.
3721	LncRNA	ZXF1	miR-378a-3p	PCDHA3	EEC cells	Endometrioid Endometrial Cancer	Homo sapiens (human)	qRT-PCR	33751805	LncRNA-ZXF1 regulates P21 expression in endometrioid endometrial carcinoma by managing ubiquitination-mediated degradation and miR-378a-3p/PCDHA3 axis.	Long noncoding RNAs (lncRNAs) have a profound effect on biological processes in various malignancies. However, few studies have investigated their functions and specific mechanisms in endometrial cancer. In this study, we focused on the role and mechanism of lncRNA-ZXF1 in endometrial cancer. Bioinformatics and in viro and in vivo experiments were used to explore the expression and function of lncRNA-ZXF1. We identified lncRNA-ZXF1 altered the migration and invasion of endometrioid endometrial cancer (EEC) cells. Furthermore, our results suggest that lncRNA-ZXF1 regulates EEC cell proliferation. This regulation may be achieved by the lncRNA-ZXF1-mediated alteration in the expression of P21 through two mechanisms. One is that lncRNA-ZXF1 functions as a molecular sponge of miR-378a-3p to regulate PCDHA3 expression and then modulate the expression of P21. The other is that lncRNA-ZXF1 inhibits CDC20-mediated degradation of ubiquitination by directly binding to P21. To the best of our knowledge, this study is the first to explore lncRNA-ZXF1 functioning as a tumor-suppressing lncRNA in EEC. LncRNA-ZXF1 may become therapeutic, diagnostic, and prognostic indicator in the future.	NA	Mol Oncol. 2021 Mar 9. doi: 10.1002/1878-0261.12940.
3722	LncRNA	NEAT1	miR-211-5p	MAPK1	PC-12 cells	Spinal Cord Injury	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	34151707	Knockdown of long non-coding RNA NEAT1 relieves the inflammatory response of spinal cord injury through targeting miR-211-5p/MAPK1 axis.	Spinal cord injury (SCI) is a refractory disease often accompanied by inflammation. Long non-coding RNA NEAT1 (lncRNA NEAT1) was reported to be involved in the expression of the inflammasomes, while the regulatory effect of NEAT1 on SCI was poorly investigated. Herein, we carried out further studies on the pathogenesis of SCI. PC-12 cells were incubated with lipopolysaccharide (LPS) to induce inflammation. Western blotting assay was used to measure the protein expression levels. RNA expression levels were analyzed using RT-qPCR. Cell counting kit 8 and flow cytometry assays were used to separately determine the cell viability and apoptosis rate. The targeted relationships were verified by luciferase reporter and RNA pull-down assays. It was found that LPS induced inflammation in the PC-12 cells, leading to significantly higher cell apoptosis rate and lower viability, and the expression level of NEAT1 was elevated by LPS. However, knockdown of NEAT1 partially reversed the effects of LPS. Subsequently, the potential interaction between NEAT1 and miR-211-5p was validated and miR-211-5p inhibitor was further confirmed to antagonize the effects of NEAT knockdown. The downstream target gene of miR-211-5p was predicted and verified to be MAPK1. In addition, overexpression of MAPK1 was proved to antagonize the effects of NEAT1 knockdown. Taken together, the knockdown of NEAT1 remarkably alleviated the inflammation of SCI via miR-211-5p/MAPK1 axis.	NA	Bioengineered. 2021 Dec;12(1):2702-2712. doi: 10.1080/21655979.2021.1930925.
3723	LncRNA	ZEB1-AS1	miR-335-5p	APOC1	colorectal cancer cells	Colorectal Cancer Liver Metastases	Homo sapiens (human)	qRT-PCR	34081622	Construction of a novel mRNA-miRNA-lncRNA network and identification of potential regulatory axis associated with prognosis in colorectal cancer liver metastases.	Liver metastasis is a leading cause of death in patients with colorectal cancer (CRC). Increasing evidence demonstrates that competing endogenous RNA (ceRNA) networks play important roles in malignant cancers. The purpose of this study was to identify molecular markers and build a ceRNA network as a significant predictor of colorectal liver metastases (CRLM). By integrated bioinformatics analysis, we found that apolipoprotein C1 (APOC1) was upregulated in CRLM and associated with prognosis in patients with CRC and thereby established an APOC1-dependent ceRNA network. By survival analysis, expression analysis, and correlation analysis of each element in the ceRNA network, we identified that ZEB1-AS1, miR-335-5p and APOC1 regulated each other. We further experimentally confirmed that ZEB1-AS1 promoted a CRC progression via regulating the expression of miR-335-5p that controlled the expression of APOC1. Our findings indicate that the ZEB1-AS1-miR-335-5p-APOC1 ceRNA regulatory network is significantly valuable for better prognosis of patients with CRC and as a new therapeutic target for the treatment of CRLM.	NA	Aging (Albany NY). 2021 Jun 3;13(11):14968-14988. doi: 10.18632/aging.203049. Epub 2021 Jun 3.
3724	LncRNA	XIST	miR-130a	STAT3	C28/I2 cells	Osteoarthritis Chondrocytes	Homo sapiens (human)	qRT-PCR;RACE;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34120462	Kaempferol attenuates the effects of XIST/miR-130a/STAT3 on inflammation and extracellular matrix degradation in osteoarthritis.	Aim: To investigate whether kaempferol exhibited protective effects on osteoarthritis chondrocytes by modulating the XIST/miR-130a/STAT3 axis. Methods: qRT-PCR and western blot assays were used for gene and protein determination. Dual luciferase reporter and RNA immunoprecipitation assays were employed to study the interaction between miRNA and lncRNA or genes. Results: Kaempferol decreased proinflammatory cytokine production and extracellular matrix degradation in C28/I2 cells. Additionally, kaempferol ameliorated XIST expression and enhanced miR-130a expression. XIST interacted with miR-130a, and STAT3 was identified as a target of miR-130a. Knockdown of XIST expression suppressed proinflammatory cytokine production and extracellular matrix degradation in C28/I2 cells. Overexpression of STAT3 rescued the effects of XIST knockdown. Conclusion: Kaempferol inhibited inflammation and extracellular matrix degradation by modulating the XIST/miR-130a/STAT3 axis in chondrocytes.	NA	Future Med Chem. 2021 Jun 14. doi: 10.4155/fmc-2021-0127.
3725	LncRNA	XIST	miR-335	BCL2L2	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34090463	Long non-coding RNA XIST regulates ovarian cancer progression via modulating miR-335/BCL2L2 axis.	BACKGROUND: X inactivation-specific transcript (XIST) is the long non-coding RNA (lncRNA) related to cancer, which is involved in the development and progression of various types of tumor. However, up to now, the exact role and molecular mechanism of XIST in the progression of ovarian cancer are not clear. We studied the function of XIST in ovarian cancer cells and clinical tumor specimens. METHODS: RT-qPCR was performed to detect the expression levels of miR-335 and BCL2L2 in ovarian cancer cells and tissues. MTT and transwell assays were carried out to detect cell proliferation, migration, and invasion abilities. Western blot was performed to analyze the expression level of BCL2L2. The interaction between miR-335 and XIST/BCL2L2 was confirmed using a luciferase reporter assay. RESULTS: The inhibition of XIST can inhibit the proliferation invasion and migration of human ovarian cancer cells. In addition, the miR-335/BCL2L2 axis was involved in the functions of XIST in ovarian cancer cells. These results suggested that XIST could regulate tumor proliferation and invasion and migration via modulating miR-335/BCL2L2. CONCLUSION: XIST might be a carcinogenic lncRNA in ovarian cancer by regulating miR-335, and it can serve as a therapeutic target in human ovarian cancer.	NA	World J Surg Oncol. 2021 Jun 5;19(1):165. doi: 10.1186/s12957-021-02274-7.
3726	LncRNA	XIST	miR-23b-3p	STX17	perinatal mouse ovaries	Perinatal Oocyte Loss	Homo sapiens (human)	qRT-PCR	34035229	Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries.	The fecundity of female mammals is resolved by the limited size of the primordial follicle (PF) pool formed perinatally. The establishment of PF pool is accompanied by a significant programmed oocyte death. Long non-coding RNAs (lncRNA) are central modulators in regulating cell apoptosis or autophagy in multiple diseases, however, the significance of lncRNAs governing perinatal oocyte loss remains unknown. Here we find that Yin-Yang 1 (YY1) directly binds to the lncRNA X-inactive-specific transcript (Xist) promoter and facilitates Xist expression in the perinatal mouse ovaries. Xist is highly expressed in fetal ovaries and sharply downregulated along with the establishment of PF pool after birth. Gain or loss of function analysis reveals that Xist accelerates oocyte autophagy, mainly through binding to pre-miR-23b or pre-miR-29a in the nucleus and preventing the export of pre-miR-23b/pre-miR-29a to the cytoplasm, thus resulting in decreased mature of miR-23b-3p/miR-29a-3p expression and upregulation miR-23b-3p/miR-29a-3p co-target, STX17, which is essential for timely control of the degree of oocyte death in prenatal mouse ovaries. Overall, these findings identify Xist as a key non-protein factor that can control the biogenesis of miR-23b-3p/miR-29a-3p, and this YY1-Xist-miR-23b-3p/miR-29a-3p-STX17 regulatory axis is responsible for perinatal oocyte loss through autophagy.	NA	Cell Death Dis. 2021 May 25;12(6):540. doi: 10.1038/s41419-021-03831-4.
3727	LncRNA	XIST	miR-29a-3p	STX17	perinatal mouse ovaries	Perinatal Oocyte Loss	Homo sapiens (human)	qRT-PCR	34035229	Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries.	The fecundity of female mammals is resolved by the limited size of the primordial follicle (PF) pool formed perinatally. The establishment of PF pool is accompanied by a significant programmed oocyte death. Long non-coding RNAs (lncRNA) are central modulators in regulating cell apoptosis or autophagy in multiple diseases, however, the significance of lncRNAs governing perinatal oocyte loss remains unknown. Here we find that Yin-Yang 1 (YY1) directly binds to the lncRNA X-inactive-specific transcript (Xist) promoter and facilitates Xist expression in the perinatal mouse ovaries. Xist is highly expressed in fetal ovaries and sharply downregulated along with the establishment of PF pool after birth. Gain or loss of function analysis reveals that Xist accelerates oocyte autophagy, mainly through binding to pre-miR-23b or pre-miR-29a in the nucleus and preventing the export of pre-miR-23b/pre-miR-29a to the cytoplasm, thus resulting in decreased mature of miR-23b-3p/miR-29a-3p expression and upregulation miR-23b-3p/miR-29a-3p co-target, STX17, which is essential for timely control of the degree of oocyte death in prenatal mouse ovaries. Overall, these findings identify Xist as a key non-protein factor that can control the biogenesis of miR-23b-3p/miR-29a-3p, and this YY1-Xist-miR-23b-3p/miR-29a-3p-STX17 regulatory axis is responsible for perinatal oocyte loss through autophagy.	NA	J Cell Mol Med. 2021 Jun 11. doi: 10.1111/jcmm.16653.
3728	LncRNA	XIST	miR-23b-3p	STX17	perinatal mouse ovaries	Perinatal Oocyte Loss	Mus musculus (mouse)	qRT-PCR	34035229	Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries.	The fecundity of female mammals is resolved by the limited size of the primordial follicle (PF) pool formed perinatally. The establishment of PF pool is accompanied by a significant programmed oocyte death. Long non-coding RNAs (lncRNA) are central modulators in regulating cell apoptosis or autophagy in multiple diseases, however, the significance of lncRNAs governing perinatal oocyte loss remains unknown. Here we find that Yin-Yang 1 (YY1) directly binds to the lncRNA X-inactive-specific transcript (Xist) promoter and facilitates Xist expression in the perinatal mouse ovaries. Xist is highly expressed in fetal ovaries and sharply downregulated along with the establishment of PF pool after birth. Gain or loss of function analysis reveals that Xist accelerates oocyte autophagy, mainly through binding to pre-miR-23b or pre-miR-29a in the nucleus and preventing the export of pre-miR-23b/pre-miR-29a to the cytoplasm, thus resulting in decreased mature of miR-23b-3p/miR-29a-3p expression and upregulation miR-23b-3p/miR-29a-3p co-target, STX17, which is essential for timely control of the degree of oocyte death in prenatal mouse ovaries. Overall, these findings identify Xist as a key non-protein factor that can control the biogenesis of miR-23b-3p/miR-29a-3p, and this YY1-Xist-miR-23b-3p/miR-29a-3p-STX17 regulatory axis is responsible for perinatal oocyte loss through autophagy.	NA	Cell Death Dis. 2021 May 25;12(6):540. doi: 10.1038/s41419-021-03831-4.
3729	LncRNA	XIST	miR-29a-3p	STX17	perinatal mouse ovaries	Perinatal Oocyte Loss	Mus musculus (mouse)	qRT-PCR	34035229	Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries.	The fecundity of female mammals is resolved by the limited size of the primordial follicle (PF) pool formed perinatally. The establishment of PF pool is accompanied by a significant programmed oocyte death. Long non-coding RNAs (lncRNA) are central modulators in regulating cell apoptosis or autophagy in multiple diseases, however, the significance of lncRNAs governing perinatal oocyte loss remains unknown. Here we find that Yin-Yang 1 (YY1) directly binds to the lncRNA X-inactive-specific transcript (Xist) promoter and facilitates Xist expression in the perinatal mouse ovaries. Xist is highly expressed in fetal ovaries and sharply downregulated along with the establishment of PF pool after birth. Gain or loss of function analysis reveals that Xist accelerates oocyte autophagy, mainly through binding to pre-miR-23b or pre-miR-29a in the nucleus and preventing the export of pre-miR-23b/pre-miR-29a to the cytoplasm, thus resulting in decreased mature of miR-23b-3p/miR-29a-3p expression and upregulation miR-23b-3p/miR-29a-3p co-target, STX17, which is essential for timely control of the degree of oocyte death in prenatal mouse ovaries. Overall, these findings identify Xist as a key non-protein factor that can control the biogenesis of miR-23b-3p/miR-29a-3p, and this YY1-Xist-miR-23b-3p/miR-29a-3p-STX17 regulatory axis is responsible for perinatal oocyte loss through autophagy.	NA	J Cell Mol Med. 2021 Jun 11. doi: 10.1111/jcmm.16653.
3730	LncRNA	XIST	miR-146a-5p	STAT3	endothelial cells	Lps-Induced Acute Lung Injury	Homo sapiens (human)	qRT-PCR	34114724	STAT3-activated lncRNA XIST accelerates the inflammatory response and apoptosis of LPS-induced acute lung injury.	Acute lung injury (ALI) is a severe lung respiratory failure characterized by high morbidity and mortality. Novel findings demonstrated the critical roles of long non-coding RNA (lncRNA) in ALI. Here, we tried to investigate the roles and potential mechanism of lncRNA X-inactive specific transcript (XIST) in ALI. Results illustrated that lncRNA XIST was up-regulated in the lipopolysaccharide (LPS)-induced ALI mice models and pulmonary endothelial cells. Biofunctional assays unveiled that knockdown of XIST repressed the inflammatory response and apoptosis in LPS-induced endothelial cells. Mechanistically, XIST acted as the miR-146a-5p sponge to positively regulate STAT3. Moreover, STAT3 combined the promoter region of XIST to accelerate the transcription, constituting the positive feedback loop of XIST/miR-146a-5p/STAT3 in ALI. Collectively, these findings suggested that XIST knockdown attenuates the LPS-induced ALI, providing a potential therapeutic target.	NA	Hum Cell. 2021 May 12:1-11. doi: 10.1007/s13577-021-00542-y.
3731	LncRNA	XIST	miR-16-5p	NA	lung tissues of septic rats, lipopolysaccharide-stimulated cells	Sepsis-Induced Lung Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;MTT assay;RIP assay;RNA pull-down assay;Western blot;Luciferase reporter assay;MTT assay;RNA pull-down;	33978928	Down-regulation of long non-coding RNA XIST aggravates sepsis-induced lung injury by regulating miR-16-5p.	This study aims to explain the role and related mechanisms of long non-coding RNA (lncRNA) X inactive specific transcript (XIST) in sepsis-induced acute lung injury (ALI). The in vivo septic models and in vitro septic model were established. In animal models, the lung injury of the rats was evaluated after XIST was overexpressed. In cell models, the effects of XIST and microRNA (miR)-16-5p on ALI was detected by MTT assay, Western blot and ELISA. The interaction between XIST and miR-16-5p was investigated by bioinformatics analysis, dual-luciferase reporter assay, RIP assay and RNA pull-down assay. We found that XIST expression was down-regulated in lung tissues of septic rats and lipopolysaccharide-stimulated cells, while the expression of miR-16-5p was up-regulated. Down-regulation of XIST significantly promoted pulmonary edema, increased the levels of TNF-α, IL-1β and malondialdehyde, inhibited the cell viability and decreased the level of superoxide dismutase. Mechanistically, it was confirmed that XIST could sponge miR-16-5p, and thus repress its expression, and the transfection of miR-16-5p mimics could reverse the effects of XIST over-expression in the cell model. Collectively, it is concluded that XIST reduces sepsis-induced ALI via regulating miR-16-5p.	NA	J Diabetes Investig. 2021 Jun 17. doi: 10.1111/jdi.13617.
3732	LncRNA	UCA1	miR-624-3p	VEGF	human retinal endothelial cells	Diabetic Retinopathy	Homo sapiens (human)	microarray;RT-PCR;Luciferase reporter assay;	34137197	Long noncoding RNA UCA1 promotes high glucose-induced human retinal endothelial cells angiogenesis via regulating miR-624-3p/VEGF-C.	AIMS/INTRODUCTION: Emerging evidences have indicated that lncRNAs play important roles in the development and progression of Diabetic retinopathy (DR). It is reported that UCA1 was highly expressed in diabetic lymphoendothelial cells and influences glucose metabolism in rats with DR. The aim of the present study was to explore the role of UCA1 in the mechanism of DR. METHODS: Gene expression analyses in fibrovascular membranes excised from patients with DR using public microarray datasets (GSE60436). RT-PCR was performed to detect UCA1, miR-624-3p and VEGF-C expressions in blood of patients and human retinal endothelial cells (HRECs). Moreover, CCK-8, transwell assay, and tube formation assay were used to identify biological effects of UCA1 on HRECs proliferation, migration ability and angiogenesis in vitro. RESULTS: UCA1 and VEGF-C was elevated in DR patients and high glucose-induced HRECs cell lines, while miR-624-3p was decreased. UCA1 inhibition inhibited proliferation, angiogenesis and migration of HRECs cells under high glucose condition. Luciferase reporter assay indicated that UCA1 could sponge with miR-624-3p, which could directly target at VEGF-C. Finally, we proved a pathway that UCA1 promoted cell proliferation, migration and angiogenesis through sponging with miR-624-3p thereby upregulating VEGF-C in high glucose-induced HRECs. CONSLUSIONS: We identified UCA1 as an important factor associated with DR, which could regulate the expression of VEGF-C by sponging miR-624-3p in human retinal endothelial cells. Our results pay the way for further studies on diagnostic and therapeutic studies related to UCA1 in DR patients.	NA	Biosci Rep. 2021 Jun 25;41(6):BSR20201389. doi: 10.1042/BSR20201389.
3733	LncRNA	UCA1	miR-613	NA	HL-60 and U-937 cells	Acute Leukemia	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33969374	LncRNA UCA1 elevates the resistance of human leukemia cells to daunorubicin by the PI3K/AKT pathway via sponging miR-613.	Acute leukemia is a hematological malignant tumor. Long non-coding RNA urothelial cancer-associated 1 (UCA1) is involved in the chemo-resistance of diverse cancers, but it is unclear whether UCA1 is associated with the sensitivity of acute leukemia cells to daunorubicin (DNR). DNR (100 nM) was selected for functional analysis. The viability, cell cycle progression, apoptosis, and invasion of treated acute leukemia cells (HL-60 and U-937) were evaluated by cell counting kit-8 (CCK-8) assay, flow cytometry assay, or transwell assay. Protein levels were detected with Western blot analysis. Expression patterns of UCA1 and miR-613 were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between UCA1 and microRNA-613 (miR-613) was verified by dual-luciferase reporter assay. We observed that UCA1 expression was elevated in HL-60 and U-937cells. DNR constrained viability, cell cycle progression, invasion, and facilitated apoptosis of HL-60 and U-937 cells in a dose-dependent manner, but these impacts mediated by DNR were reverted after UCA1 overexpression. MiR-613 was down-regulated in HL-60 and U-937 cells, and UCA1 was verified as a miR-613 sponge. MiR-613 inhibitor reversed DNR treatment-mediated effects on viability, cell cycle progression, apoptosis, and invasion of HL-60 and U-937 cells, but these impacts mediated by miR-613 inhibitor were counteracted after UCA1 inhibition. Notably, the inactivation of the PI3K/AKT pathway caused by DNR treatment was reversed after miR-613 inhibitor introduction, but this influence mediated by miR-613 inhibitor was offset after UCA1 knockdown. In conclusion, UCA1 up-regulation facilitated the resistance of acute leukemia cells to DNR via the PI3K/AKT pathway by sponging miR-613.	NA	Life Sci. 2021 Jul 15;277:119569. doi: 10.1016/j.lfs.2021.119569. Epub 2021 May 4.
3734	LncRNA	UCA1	miR-495	SP1	CRC tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;luciferase assay;	33961855	lncRNA UCA1 induced by SP1 and SP3 forms a positive feedback loop to facilitate malignant phenotypes of colorectal cancer via targeting miR-495.	AIMS: Long noncoding RNA (LncRNA) urothelial cancer associated 1 (UCA1) was dysregulated in colorectal cancers (CRC) and promoted tumor progression of CRC. The aims of this study are to further investigate the underlying mechanism. MAIN METHODS: Short hairpin RNAs (shRNAs) were applied for gene knockdown. microRNA mimic and pcDNA-UCA1 plasmids were transfected for miR-495 and UCA1 overexpression, respectively. MTT was applied to determine cell viability and sensitivity of 5-fluorouracil (FU). Transwell assays were performed to evaluate cell migration/invasion. Angiogenesis was evaluated by tube formation. Western blotting and quantitative PCR were utilized for protein and mRNA detection, respectively. The interaction of UCA1, miR-495 and SP1/SP3 were explored by dual-luciferase assay. RNA pulldown was adopted to determine the UCA1/miR-495 interaction. KEY FINDINGS: UCA1 was significantly upregulated in CRC tissues. UCA1 enhanced cell proliferation, migration/invasion, angiogenesis, epithelial-mesenchymal transition, and resistance to 5-FU in CRC cell lines. MiR-495 was inversely correlated to the expression of UCA1. The results indicated that UCA1 sponged miR-495, leading to the disinhibition of SP1/SP3 expression. SP1/SP3 induced the expression of DNA methyltransferases and, in turn, contributed to UCA1 mediated tumor-promoting actions. Reduction of SP1/SP3 exerted anti-cancer effects, which can be reversed by forced expression of UCA1. SIGNIFICANCE: UCA1-miR-495-SP1/SP3 axis is dysregulated in CRC and contributed to malignant phenotypes of CRC. UCA1-SP1/SP3 may form a positive feedback loop in CRC.	NA	PLoS One. 2021 Jun 7;16(6):e0252761. doi: 10.1371/journal.pone.0252761. eCollection 2021.
3735	LncRNA	UCA1	miR-495	SP3	CRC tissues	Colorectal Cancer	Homo sapiens (human)	Western blot;luciferase assay;	33961855	lncRNA UCA1 induced by SP1 and SP3 forms a positive feedback loop to facilitate malignant phenotypes of colorectal cancer via targeting miR-495.	AIMS: Long noncoding RNA (LncRNA) urothelial cancer associated 1 (UCA1) was dysregulated in colorectal cancers (CRC) and promoted tumor progression of CRC. The aims of this study are to further investigate the underlying mechanism. MAIN METHODS: Short hairpin RNAs (shRNAs) were applied for gene knockdown. microRNA mimic and pcDNA-UCA1 plasmids were transfected for miR-495 and UCA1 overexpression, respectively. MTT was applied to determine cell viability and sensitivity of 5-fluorouracil (FU). Transwell assays were performed to evaluate cell migration/invasion. Angiogenesis was evaluated by tube formation. Western blotting and quantitative PCR were utilized for protein and mRNA detection, respectively. The interaction of UCA1, miR-495 and SP1/SP3 were explored by dual-luciferase assay. RNA pulldown was adopted to determine the UCA1/miR-495 interaction. KEY FINDINGS: UCA1 was significantly upregulated in CRC tissues. UCA1 enhanced cell proliferation, migration/invasion, angiogenesis, epithelial-mesenchymal transition, and resistance to 5-FU in CRC cell lines. MiR-495 was inversely correlated to the expression of UCA1. The results indicated that UCA1 sponged miR-495, leading to the disinhibition of SP1/SP3 expression. SP1/SP3 induced the expression of DNA methyltransferases and, in turn, contributed to UCA1 mediated tumor-promoting actions. Reduction of SP1/SP3 exerted anti-cancer effects, which can be reversed by forced expression of UCA1. SIGNIFICANCE: UCA1-miR-495-SP1/SP3 axis is dysregulated in CRC and contributed to malignant phenotypes of CRC. UCA1-SP1/SP3 may form a positive feedback loop in CRC.	NA	ASN Neuro. 2021 Jan-Dec;13:17590914211003247. doi: 10.1177/17590914211003247.
3736	LncRNA	TUG1	miR-29c-3p	SIRT1	cell line HK-2	Renal Epithelial Cells Injury	Homo sapiens (human)	qRT-PCR	34097717	LncRNA TUG1/miR-29c-3p/SIRT1 axis regulates endoplasmic reticulum stress-mediated renal epithelial cells injury in diabetic nephropathy model in vitro.	Long non-coding RNAs (lncRNAs) are important regulators in diabetic nephropathy. In this study, we investigated the potential role of lncRNA TUG1 in regulating endoplasmic reticulum stress (ERS)-mediated apoptosis in high glucose induced renal tubular epithelial cells. Human renal tubular epithelial cell line HK-2 was challenged with high glucose following transfection with lncRNA TUG1, miR-29c-3p mimics or inhibitor expression plasmid, either alone or in combination, for different experimental purposes. Potential binding effects between TUG1 and miR-29c-3p, as well as between miR-29c-3p and SIRT1 were verified. High glucose induced apoptosis and ERS in HK-2 cells, and significantly decreased TUG1 expression. Overexpressed TUG1 could prevent high glucose-induced apoptosis and alleviated ERS via negatively regulating miR-29c-3p. In contrast, miR-29c-3p increased HK-2 cells apoptosis and ERS upon high glucose-challenge. SIRT1 was a direct target gene of miR-29c-3p in HK-2 cells, which participated in the effects of miR-29c-3p on HK-2 cells. Mechanistically, TUG1 suppressed the expression of miR-29c-3p, thus counteracting its function in downregulating the level of SIRT1. TUG1 regulates miR-29c-3p/SIRT1 and subsequent ERS to relieve high glucose induced renal epithelial cells injury, and suggests a potential role for TUG1 as a promising diagnostic marker of diabetic nephropathy.	NA	World J Surg Oncol. 2021 Jun 5;19(1):163. doi: 10.1186/s12957-021-02279-2.
3737	LncRNA	TUG1	miR-200a-3p	NLRP3	SH-SY5Y and SK-N-SH cells	Cerebral Ischemia-Reperfusion Injury	Homo sapiens (human)	qRT-PCR	33853366	LncRNA TUG1 Demethylated by TET2 Promotes NLRP3 Expression, Contributes to Cerebral Ischemia/Reperfusion Inflammatory Injury.	LncRNA TUG1 has not yet been reported in cerebral ischemia/reperfusion (I/R) injury. Methylcytosine dioxygenase TET2 is involved in ischemic damage. This study aimed to investigate the effects of TUG1 demethylated by TET2 on I/R-induced inflammatory response and identified its possible mechanisms.We found that TUG1 expression was significantly upregulated in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced SH-SY5Y and SK-N-SH cells. Using the middle cerebral artery occlusion (MCAO) mice, we observed a similar effect. We also found that I/R injury could downregulate miR-200a-3p and upregulate NLRP3 and TET2. The knockdown of TUG1 could alleviate OGD/R-induced inflammatory response through upregulating miR-200a-3p and downregulating NLRP3 and other pro-inflammatory molecules. miR-200a-3p inhibition can partially reverse the effects of TUG1 silencing. Further experiments confirmed that TUG1 sponged miR-200a-3p to diminish miR-200a-3p and promote NLRP3 dependent inflammatory responses. Mechanically, knockdown of TET2 induced low levels of TUG1 and high levels of miR-200a-3p in both SK-N-SH and SH-SY5Y cells. IL-18, IL-1β, NLRP3, Caspase-1, and GSDMD-N were highly downregulated in OGD/R-induced SK-N-SH and SH-SY5Y cells after TET2 knockdown. TUG1 overexpression could reverse this effect. All the data indicated that TET2 could demethylate TUG1 and contribute to the inflammatory response. In additional experiments using the MCAO mice model, we confirmed knockdown of TET2 attenuated I/R-induced inflammatory response and brain injuries via decreasing TUG1 and increasing miR-200a-3p to inhibit NLRP3 expression. The demethylation of TUG1 by TET2 might aggravate I/R-induced inflammatory injury via modulating NLRP3 by miR-200a-3p. Our data confirmed that TET2 contributed to I/R-induced inflammatory response via the demethylation of TUG1 and regulated TUG1/miR-200a-3p/NLRP3 pathway.	NA	Front Oncol. 2021 Jun 1;11:652835. doi: 10.3389/fonc.2021.652835. eCollection 2021.
3738	LncRNA	TTN-AS1	miR-107	HMGA1	gallbladder carcinoma tissues and cell lines	Gallbladder Cancer	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;Luciferase reporter assay;MTT assay;	34090483	LncRNA TTN-AS1 acts as a tumor promoter in gallbladder carcinoma by regulating miR-107/HMGA1 axis.	BACKGROUND: The incidence of gallbladder carcinoma (GBM) in China has increased in recent years. Here, the functional mechanism of lncRNA TTN-AS1 in GBC was preliminary elucidated. METHODS: The expression levels of lncRNA TTN-AS1, miR-107, and HMGA1 in tissues and cell lines were assessed by RT-qPCR. Cell proliferation was measured by MTT assays. Cell invasion and migration abilities were evaluated by Transwell assays. The relationship between miR-107 and lncRNA TTN-AS1 or HMGA1 was confirmed by luciferase reporter assay. RESULTS: Upregulation of lncRNA TTN-AS1 and downregulation of miR-107 were detected in GBC. Furthermore, the expressions between TTN-AS1 and miR-107 were mutually inhibited in GBC. Functionally, lncRNA TTN-AS1 promoted cell viability and motility in GBC by sponging miR-107. In addition, miR-107 directly targets HMGA1. And HMGA1 can be positively regulated by lncRNA TTN-AS1 in GBC. Furthermore, HMGA1 promoted GBC progression by interacting with lncRNA TTN-AS1/miR-107 axis. CONCLUSION: LncRNA TTN-AS1 acted as a tumor promoter in GBC by sponging miR-107 and upregulating HMGA1.	NA	Exp Ther Med. 2021 Aug;22(2):843. doi: 10.3892/etm.2021.10275. Epub 2021 Jun 6.
3739	LncRNA	TTN-AS1	miR-16-1-3p	TFAP4	OS cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	34141611	Silencing of the Long Non-Coding RNA TTN-AS1 Attenuates the Malignant Progression of Osteosarcoma Cells by Regulating the miR-16-1-3p/TFAP4 Axis.	OBJECTIVES: Osteosarcoma (OS) is a type of bone malignancy. This study attempted to explore the effect of long non-coding RNA TTN-AS1 (TTN-AS1) on OS and to determine its molecular mechanisms. METHODS: The expression of TTN-AS1, microRNA-16-1-3p (miR-16-1-3p), and transcription factor activating enhancer binding protein 4 (TFAP4) in OS was assessed using qRT-PCR. The OS cell proliferation, migration, and invasion were measured using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and transwell assays. N-cadherin and MMP-2 protein level was determined with western blot. Interactions between TTN-AS1 and miR-16-1-3p or TFAP4 and miR-16-1-3p were confirmed using the dual-luciferase reporter assay. Additionally, an OS xenograft tumor model was constructed to assess the effect of TTN-AS1 on tumor growth. RESULTS: TTN-AS1 and TFAP4 expression was increased in OS, while miR-16-1-3p expression was decreased. TTN-AS1 silencing restrained OS cell proliferation, migration, invasion, N-cadherin and MMP-2 protein expression, and hindered tumor growth. MiR-16-1-3p overexpression retarded the malignant behavior of OS cells. TTN-AS1 played a carcinostatic role by down-regulating miR-16-1-3p in the OS cells. Moreover, miR-16-1-3p inhibition or TFAP4 elevation weakened the suppressive effect of TTN-AS1 silencing on OS cell tumor progression. CONCLUSION: TTN-AS1 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of OS cells via mediating the miR-16-1-3p/TFAP4 axis. TTN-AS1 may be a critical target for improving OS.	NA	Hum Cell. 2021 Jul;34(4):1244-1254. doi: 10.1007/s13577-021-00541-z. Epub 2021 May 17.
3740	LncRNA	TPT1-AS1	miR-324-5p	CDK16	thermally injured cells	Thermal Injury	Homo sapiens (human)	RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34149889	Long non-coding RNA TPT1-AS1 alleviates cell injury and promotes the production of extracellular matrix by targeting the microRNA-324-5p/CDK16 axis in human dermal fibroblasts after thermal injury.	Long non-coding RNAs (lncRNAs) are associated with the healing of burn wounds in the dermis. The present study aimed to probe the role and regulatory network of the lncRNA TPT1 antisense RNA 1 (TPT1-AS1) in human dermal fibroblasts (HDFs) following thermal injury. A model of thermally injured cells was constructed with HDFs. The levels of TPT1-AS1, microRNA (miR)-324-5p and cyclin-dependent kinase (CDK)16 were determined through reverse transcription-quantitative PCR. Cell viability, cell cycle distribution, cell apoptosis rate and extracellular matrix (ECM) synthesis were assessed with a series of in vitro gain-of-function experiments and MTT, flow cytometry and western blot analyses. The binding ability of miR-324-5p and TPT1-AS1 (or the 3' untranslated region of CDK16) was identified via bioinformatics analysis and luciferase reporter assay. It was found that TPT1-AS1 and CDK16 were downregulated, but miR-324-5p was upregulated, in the HDFs after thermal injury. TPT1-AS1 elevation induced cell viability and ECM synthesis but attenuated cell cycle arrest at the G(0)/G(1) stage and decreased the cell apoptosis rate of thermally injured HDFs. In addition, TPT1-AS1 sponged miR-324-5p to modulate CDK16 expression. Moreover, silencing CDK16 weakened the impacts of TPT1-AS1 upregulation on cell function and ECM synthesis in heat-treated HDFs. In summary, TPT1-AS1 relieved cell injury and induced ECM synthesis by sponging miR-324-5p and targeting CDK16 in the HDFs after thermal injury, implying a protective role for TPT1-AS1 in the burn wound healing process.	NA	Cell Mol Biol Lett. 2021 Jun 8;26(1):27. doi: 10.1186/s11658-021-00264-x.
3741	LncRNA	TPT1-AS1	miR-3156-5p	CASP2	breast cancer cell	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33999360	Long non-coding RNA TPT1-AS1 sensitizes breast cancer cell to paclitaxel and inhibits cell proliferation by miR-3156-5p/caspase 2 axis.	Long non-coding RNAs (lncRNAs) are key modulators during cancer progression. Application of using lncRNA expression to evaluate patient prognosis and sensitivity to treatment is highly anticipated, yet the expression and mechanism of many lncRNAs remain unknown. Herein, we projected for the investigation of TPT1-AS1 function in breast cancer. TPT1-AS1 was assessed by bioinformatic analysis of publicly available datasets and quantitative real-time PCR (qRT-PCR). Cell sensitivity to paclitaxel and cell proliferation was measured by flow cytometry and CCK-8. Interaction among TPT1-AS1, microRNA (miRNA, miR)-3156-5p and Caspase 2 (CASP2) was studied by bioinformatic analysis, qRT-PCR, western blot as well as dual luciferase reporter assay. Herein, TPT1-AS1 was significantly diminished in breast cancer from publicly available datasets and our collected samples. In breast cancer cells, TPT1-AS1 overexpression repressed cell proliferation and sensitized breast cancer cells to paclitaxel. RegRNA 2.0 predicted a potential interaction between TPT1-AS1 and miR-3156-5p which was confirmed by qRT-PCR as well as dual luciferase reporter assay. CASP2, a proapoptotic gene, was corroborated to be targeted by miR-3156-5p. Meanwhile, TPT1-AS1 upregulated CASP2 in breast cancer cells, and its biological function was reversed by CASP2 knockdown. Collectively, TPT1-AS1 diminished cell proliferation and sensitized cells to chemotherapy by sponging miR-3156-5p and upregulating CASP2, acting as a biomarker for patients with breast cancer.	NA	Cell Death Dis. 2021 May 15;12(5):499. doi: 10.1038/s41419-021-03756-y.
3742	LncRNA	TP73-AS1	miR-654-3p	AKT3	endothelial cells	Atherosclerosis	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34103010	LncRNA TP73-AS1 promotes oxidized low-density lipoprotein-induced apoptosis of endothelial cells in atherosclerosis by targeting the miR-654-3p/AKT3 axis.	BACKGROUND: Although lncRNA TP73-AS1 has been shown to play important roles in various human diseases, its function in atherosclerosis (AS) remains unclear. METHODS: Human aortic endothelial cells (HAECs) were treated with 50 μg/ml oxidized low-density lipoprotein (ox-LDL) to establish an atherosclerotic cell model. The expression of TP73-AS1, miR-654-3p and AKT3 was detected by qRT-PCR. Cell functions were evaluated CCK-8 assay and flow cytometry. The protein levels of apoptosis-related proteins were evaluated by western blot. The binding relationship among TP73-AS1, miR-654-3p and AKT3 was determined by bioinformatics analysis and luciferase reporter assay. RESULTS: TP73-AS1 was upregulated and miR-654-3p was downregulated in ox-LDL treated HAECs. TP73-AS1 silencing and miR-654-3p mimics decreased the viability and inhibited apoptosis of ox-LDL treated HAECs, decreased the expression levels of c-caspase-9, c-caspase-3 and Bax, and increased Bcl-2 expression. In addition, miR-654-3p inhibitor significantly reversed the inhibitory effects of si-TP73-AS1 on cell viability and apoptosis. TP73-AS1 could positively regulate AKT3 through directly sponging miR-654-3p. CONCLUSION: TP73-AS1 promoted apoptosis of ox-LDL stimulated endothelial cells by targeting the miR-654-3p/AKT3 axis, suggesting that TP73-AS1 might be a potential target for AS treatment.	NA	J Gastrointest Oncol. 2021 Apr;12(2):423-432. doi: 10.21037/jgo-21-147.
3743	LncRNA	SOX2OT	miR-194-5p	SOX5	CRC tissue and cells	Colorectal Cancer	Homo sapiens (human)	ISH;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;Rescue assay;	33993197	A novel lncRNA SOX2OT promotes the malignancy of human colorectal cancer by interacting with miR-194-5p/SOX5 axis.	Long noncoding RNAs (lncRNAs) show emerging roles in colorectal cancer (CRC) development and are considered to be involved in the potential mechanism of tumor malignancy. While Sox2 overlapping transcript (SOX2OT) has been implicated in the progression of multiple cancers, its role in CRC remains to be explored. In this study, in situ hybridization (ISH) and qRT-PCR were performed to establish the functional relationships between SOX2OT and CRC deranged in CRC tissue and cells. Subsequently, SOX2OT shRNAs vectors were transfected into CRC cells to performed loss-of-function assays to detect the potential role of SOX2OT on proliferation and metastasis in vitro and vivo. The results showed SOX2OT was an oncogene that was up-regulated in human CRC tissues and cell lines. SOX2OT silencing suppressed cell proliferation, migration, and invasion in CRC cells in vitro, and inhibited tumorigenesis in the mouse xenografts. Bioinformatic predictive analysis coupled with the dual-luciferase reporter, RNA immunoprecipitation (RIP), and functional rescue assay elucidated the mechanistic network of the SOX2OT-miR-194-5p-SOX5 axis in CRC. Mechanistically, SOX2OT acted as a competing endogenous RNA (ceRNA) to upregulate SOX5 by sponging miR-194-5p. Downregulated SOX2OT boosted miR-194-5p expression, thus decreased the protein level of SOX5, which suppresses tumorgenesis of CRC.	NA	Oncol Lett. 2021 Jul;22(1):565. doi: 10.3892/ol.2021.12826. Epub 2021 May 29.
3744	LncRNA	SOX2OT	miR-194-5p	SOX5	CRC tissue and cells	Colorectal Cancer	Mus musculus (mouse)	ISH;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;Rescue assay;	33993197	A novel lncRNA SOX2OT promotes the malignancy of human colorectal cancer by interacting with miR-194-5p/SOX5 axis.	Long noncoding RNAs (lncRNAs) show emerging roles in colorectal cancer (CRC) development and are considered to be involved in the potential mechanism of tumor malignancy. While Sox2 overlapping transcript (SOX2OT) has been implicated in the progression of multiple cancers, its role in CRC remains to be explored. In this study, in situ hybridization (ISH) and qRT-PCR were performed to establish the functional relationships between SOX2OT and CRC deranged in CRC tissue and cells. Subsequently, SOX2OT shRNAs vectors were transfected into CRC cells to performed loss-of-function assays to detect the potential role of SOX2OT on proliferation and metastasis in vitro and vivo. The results showed SOX2OT was an oncogene that was up-regulated in human CRC tissues and cell lines. SOX2OT silencing suppressed cell proliferation, migration, and invasion in CRC cells in vitro, and inhibited tumorigenesis in the mouse xenografts. Bioinformatic predictive analysis coupled with the dual-luciferase reporter, RNA immunoprecipitation (RIP), and functional rescue assay elucidated the mechanistic network of the SOX2OT-miR-194-5p-SOX5 axis in CRC. Mechanistically, SOX2OT acted as a competing endogenous RNA (ceRNA) to upregulate SOX5 by sponging miR-194-5p. Downregulated SOX2OT boosted miR-194-5p expression, thus decreased the protein level of SOX5, which suppresses tumorgenesis of CRC.	NA	Oncol Lett. 2021 Jul;22(1):565. doi: 10.3892/ol.2021.12826. Epub 2021 May 29.
3745	LncRNA	SNHG7	miR-625	NA	ESCC tumor tissues and ESCC cell lines, adjacent normal tissues and HET1A cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	34012636	Long non-coding RNA small nucleolar RNA host gene 7 facilitates the proliferation, migration, and invasion of esophageal cancer cells by regulating microRNA-625.	BACKGROUND: Esophageal cancer (EC) is a highly aggressive malignant tumor, of which esophageal squamous cell carcinoma (ESCC) constitutes the main subtype. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) has been extensively studied in many tumors and has been confirmed to be an oncogene; however, it has yet to be investigated in an ESCC study. Therefore, this study intended to uncover the role of SNHG7 in ESCC. METHODS: Quantitative real-time polymerase chain reaction was applied to measure the expression levels of SNHG7 and miR-625 in ESCC tumor tissues and cell lines. Cell Counting Kit-8 assay, 5-Ethynyl-2'-deoxyuridine assay, scratch assay, and Transwell assay were conducted to assess the proliferation, migration, and invasion ESCC cell. We verified the interaction between SNHG7 and miR-625 by performing the dual luciferase reporter gene experiment. RESULTS: Compared to that in adjacent normal tissues and HET1A cell lines, the expression level of SNHG7 in ESCC tumor tissues and ESCC cell lines was up-regulated, while the expression level of miR-625 was down-regulated. ESCC cell proliferation, migration, and invasion were significantly promoted by SNHG7 overexpression but inhibited by silencing of SNHG7. Further, luciferase reporter gene experiments confirmed that SNHG7 interacted with miR-625, and rescue experiments showed that SNHG7 promoted the malignant phenotype by inhibiting miR-625. CONCLUSIONS: SNHG7 is up-regulated in ESCC tumor tissues and cell lines, while miR-625 is expressed at a low level. SNHG7 is able to facilitate the proliferation, migration, and invasion of ESCC cells by targeting miR-625.	NA	Kaohsiung J Med Sci. 2021 Jun 21. doi: 10.1002/kjm2.12411.
3746	LncRNA	SNHG7	miR-138-5p	EZH2	glioma cells	Glioma	Homo sapiens (human)	Western blot;	34113393	lncRNA SNHG7 promotes cell proliferation in glioma by acting as a competing endogenous RNA and sponging miR-138-5p to regulate EZH2 expression.	Glioma is the most common type of primary brain cancer in adults. Accumulating studies have reported that long non-coding RNAs (lncRNAs) serve a significant role in the initiation and development of glioma. lncRNA small nucleolar RNA host gene 7 (SNHG7) has been previously demonstrated to serve a role in numerous glioma biological processes, including cell proliferation, invasion and migration. The present study aimed to investigate the role of SNHG7 in glioma through reverse transcription-quantitative PCR, western blotting and cell function assays. The results revealed that SNHG7 expression was upregulated in glioma tissues and cell lines, while microRNA (miR)-138-5p expression was downregulated. Moreover, the knockdown of SNHG7 expression decreased the proliferation of glioma cells. Mechanistic studies demonstrated that SNHG7 downregulated miR-138-5p expression, which subsequently affected the expression levels of its target gene, enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). In conclusion, the results of the present study suggested that SNHG7 may act as a competing endogenous RNA to sponge miR-138-5p and modulate EZH2 expression. Thus, SNHG7 may enhance glioma proliferation via modulating the miR-138-5p/EZH2 signaling axis.	NA	J Mol Histol. 2021 Jun 10. doi: 10.1007/s10735-021-09985-x.
3747	LncRNA	SNHG3	miR-485-5p	LCMX1B	glioma cells	Glioma	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34153159	Long noncoding RNA SNHG3 promotes glioma tumorigenesis by sponging miR-485-5p to upregulate LMX1B expression.	LIM homeobox transcription factor 1-beta (LMX1B) has recently been found to be highly expressed in advanced gliomas and is associated with poor survival. However, the regulatory molecular mechanism of LMX1B expression in gliomas remains unclear. In this study, bioinformatics analysis showed that miR-485-5p may be the potential upstream regulator of LMX1B, and long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) may function as a competitive endogenous RNA to sponge miR-485-5p. In addition, the expression of SNHG3 and LMX1B in advanced glioma tissues was significantly upregulated, while the expression of miR-485-5p was significantly downregulated. SNHG3 overexpression reduced the expression of miR-485-5p; increased the expression of LMX1B; and promoted the proliferation, migration, and invasion of glioma cells. In contrast, miR-485-5p overexpression reduced the expression of LMX1B and inhibited cell proliferation, migration, and invasion. The luciferase reporter assay and RNA immunoprecipitation assay further confirmed the interaction between SNHG3 and miR-485-5p and between miR-485-5p and LMX1B. In addition, subcutaneous and orthotropic xenograft models confirmed that lncRNA SNHG3 silencing or miR-485-5p overexpression significantly reduced the growth of glioma xenografts and prolonged survival time. These results indicate that lncRNA SNHG3 can regulate the expression of LMX1B by sponging miR-485-5p, thereby promoting the proliferation, migration, and invasion of glioma cells. This study provides the first evidence that the SNHG3/miR-485-5p/LMX1B axis is involved in glioma tumorigenesis and highlights the potential of SNHG3 and miR-485-5p as therapeutic targets for glioma.	NA	BMC Pulm Med. 2021 Jun 6;21(1):191. doi: 10.1186/s12890-021-01552-0.
3748	LncRNA	SNHG16	miR-218-5p	LASP1	trophoblast cells	Preeclampsia	Homo sapiens (human)	qPCR;RT-qPCR;RNA pull-down assay;Flow Cytometry assay;RNA pull-down;	34110517	LncRNA SNHG16 regulates trophoblast functions by the miR-218-5p/LASP1 axis.	Altered placental development and function lead to placental diseases such as preeclampsia (PE) which is mainly characterized by insufficient trophoblast invasion and abnormally invasive placenta disorders. Long noncoding RNAs (lncRNAs) are widely reported to function as crucial players in the pathogenesis of PE. The present investigation clarified the role of lncRNA small nucleolar RNA host gene 16 (SNHG16) in PE. RT-qPCR was used to measure gene expression. The proliferation of trophoblast cells was examined using CCK-8 and EdU assays. Trophoblast migration and invasion were assessed using wound healing and transwell assays. The apoptosis was estimated by flow cytometry. Luciferase reporter and RNA pull-down assays were performed to explore the molecular mechanisms in trophoblast cells. We found that SNHG16 was downregulated in placenta from patients with PE. Moreover, SNHG16 depletion significantly inhibited trophoblast cell proliferation, migration, and invasion and stimulated apoptosis, while SNHG16 overexpression exerted an opposite effect. Subsequently, we confirmed that SNHG16 acted as a competing RNA (ceRNA) of miR-218-5p that was verified to directly target LASP1. Both miR-218-5p depletion and LASP1 upregulation antagonized the effect of SNHG16 knockdown on HTR-8/SVneo cell functions. In conclusion, SNHG16 facilitates trophoblast cell migration and invasion by the miR-218-5p/LASP1 axis.	NA	Cell Signal. 2021 Aug;84:110013. doi: 10.1016/j.cellsig.2021.110013. Epub 2021 Apr 23.
3749	LncRNA	SNHG16	miR-128-3p	HMGB3	lung tissues	Acute Lung Injury	Homo sapiens (human)	ELISA;Western blot;Immunohistochemistry;	34092219	Down-regulation of SNHG16 alleviates the acute lung injury in sepsis rats through miR-128-3p/HMGB3 axis.	BACKGROUND: Long noncoding RNAs contribute to various inflammatory diseases, including sepsis. We explore the role of small nucleolar RNA host gene 16 (SNHG16) in sepsis-mediated acute lung injury (ALI) and inflammation. METHODS: A sepsis-induced ALI rat model was constructed by the cecal ligation and perforation method. The profiles of SNHG16, miR-128-3p, and high-mobility group box 3 (HMGB3) were monitored by quantitative reverse transcription PCR and Western blot. The pathologic changes of lung tissues were evaluated by Hematoxylin-Eosin staining, immunohistochemistry, and dry and wet method. Meanwhile, the pro-inflammatory factors and proteins were determined by ELISA and Western blot. In contrast, a sepsis model in BEAS-2B was induced with lipopolysaccharide (LPS) to verify the effects of SNHG16/miR-128-3p/HMGB3 on lung epithelial cell viability and apoptosis. RESULTS: As a result, SNHG16 and HMGB3 were up-regulated, while miR-128-3p was down-regulated in sepsis-induced ALI both in vivo and in vitro. Inhibiting SNHG16 reduced the apoptosis and inflammation in the sepsis-induced ALI model. Overexpressing SNHG16 promoted LPS-mediated lung epithelial apoptosis and inhibited cell viability and inflammation, while miR-128-3p had the opposite effects. Mechanistically, SNHG16 targeted miR-128-3p and attenuated its expression, while miR-128-3p targeted the 3' untranslated region of HMGB3. CONCLUSIONS: Overall, down-regulating SNHG16 alleviated the sepsis-mediated ALI by regulating miR-128-3p/HMGB3.	NA	Int J Cardiol. 2021 Jul 1;334:30. doi: 10.1016/j.ijcard.2021.04.057. Epub 2021 Apr 30.
3750	LncRNA	SNHG16	miR-128-3p	HMGB3	lung tissues	Acute Lung Injury	Rattus (rat)	ELISA;Western blot;Immunohistochemistry;	34092219	Down-regulation of SNHG16 alleviates the acute lung injury in sepsis rats through miR-128-3p/HMGB3 axis.	BACKGROUND: Long noncoding RNAs contribute to various inflammatory diseases, including sepsis. We explore the role of small nucleolar RNA host gene 16 (SNHG16) in sepsis-mediated acute lung injury (ALI) and inflammation. METHODS: A sepsis-induced ALI rat model was constructed by the cecal ligation and perforation method. The profiles of SNHG16, miR-128-3p, and high-mobility group box 3 (HMGB3) were monitored by quantitative reverse transcription PCR and Western blot. The pathologic changes of lung tissues were evaluated by Hematoxylin-Eosin staining, immunohistochemistry, and dry and wet method. Meanwhile, the pro-inflammatory factors and proteins were determined by ELISA and Western blot. In contrast, a sepsis model in BEAS-2B was induced with lipopolysaccharide (LPS) to verify the effects of SNHG16/miR-128-3p/HMGB3 on lung epithelial cell viability and apoptosis. RESULTS: As a result, SNHG16 and HMGB3 were up-regulated, while miR-128-3p was down-regulated in sepsis-induced ALI both in vivo and in vitro. Inhibiting SNHG16 reduced the apoptosis and inflammation in the sepsis-induced ALI model. Overexpressing SNHG16 promoted LPS-mediated lung epithelial apoptosis and inhibited cell viability and inflammation, while miR-128-3p had the opposite effects. Mechanistically, SNHG16 targeted miR-128-3p and attenuated its expression, while miR-128-3p targeted the 3' untranslated region of HMGB3. CONCLUSIONS: Overall, down-regulating SNHG16 alleviated the sepsis-mediated ALI by regulating miR-128-3p/HMGB3.	NA	Int J Cardiol. 2021 Jul 1;334:30. doi: 10.1016/j.ijcard.2021.04.057. Epub 2021 Apr 30.
3751	LncRNA	SNHG16	miR-1303-p	STARD9	ccRCC cells	Clear Cell Renal Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;Rescue assay;	33901578	SNHG16 promotes cell proliferation and inhibits cell apoptosis via regulation of the miR-1303-p/STARD9 axis in clear cell renal cell carcinoma.	Clear cell renal cell carcinoma (ccRCC) is a common subtype of renal cell carcinoma (RCC) and causes many deaths. Numerous medical studies have suggested that long noncoding RNAs (lncRNAs) exert their biological functions on ccRCC. Herein, functions of lncRNA SNHG16 in ccRCC cells and the mechanism mediated by SNHG16 were investigated. The expression levels of SNHG16 and its downstream genes in ccRCC cells and RCC tissues were examined utilizing reverse transcription quantitative polymerase chain reaction analyses. Cell counting kit-8 and 5-Ethynyl-2'-deoxyuridine assays were performed to evaluate the proliferation of ccRCC cells, and flow cytometry analyses were employed to determine the apoptosis of ccRCC cells. Western blot analysis was applied to examine protein levels associated with cell proliferation and apoptosis. The combination between SNHG16 and miRNA as well as miRNA and its target gene were explored by luciferase reporter, RNA pull down, and RNA immunoprecipitation assays. The significant upregulation of SNHG16 was observed in RCC tissues and ccRCC cells. SNHG16 downregulation inhibited the proliferation and promoted the apoptosis of ccRCC cells. In addition, SNHG16 served as a competing endogenous RNA for miR-1301-3p, and STARD9 was a target gene of miR-1301-3p in ccRCC cells. SNHG16 upregulated STARD9 expression by binding with miR-1301-3p in ccRCC cells. Rescue assays validated that SNHG16 promoted ccRCC cell promotion and induced ccRCC cell apoptosis by upregulating STARD9 expression. In conclusions, SNHG16 promotes ccRCC cell proliferation and suppresses ccRCC cell apoptosis via interaction with miR-1301-3p to upregulate STARD9 expression in ccRCC cells.	NA	Acta Biochim Biophys Sin (Shanghai). 2021 May 21;53(6):719-728. doi: 10.1093/abbs/gmab034.
3752	LncRNA	SNHG15	miR-346	NA	NA	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	qRT-PCR	33933513	The circulating LncRNA SNHG15/miR-346 axis may be a potential biomarker of cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury.	unknown	NA	Oral Dis. 2021 Apr 29. doi: 10.1111/odi.13893.
3753	LncRNA	SNHG14	miR-495-3p	HIPK1	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR	33856026	Long non-coding RNA SNHG14 aggravates LPS-induced acute kidney injury through regulating miR-495-3p/HIPK1.	Acute kidney injury (AKI) is a complex syndrome with an abrupt decrease of kidney function, which is associated with high morbidity and mortality. Sepsis is the common cause of AKI. Mounting evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in the development and progression of sepsis-induced AKI. In this study, we aimed to illustrate the function and mechanism of lncRNA SNHG14 in lipopolysaccharide (LPS)-induced AKI. We found that SNHG14 was highly expressed in the plasma of sepsis patients with AKI. SNHG14 inhibited cell proliferation and autophagy and promoted cell apoptosis and inflammatory cytokine production in LPS-stimulated HK-2 cells. Functionally, SNHG14 acted as a competing endogenous RNA (ceRNA) to negatively regulate miR-495-3p expression in HK-2 cells. Furthermore, we identified that HIPK1 is a direct target of miR-495-3p in HK-2 cells. We also revealed that the SNHG14/miR-495-3p/HIPK1 interaction network regulated HK-2 cell proliferation, apoptosis, autophagy, and inflammatory cytokine production upon LPS stimulation. In addition, we demonstrated that the SNHG14/miR-495-3p/HIPK1 interaction network regulated the production of inflammatory cytokines (TNF-α, IL-6, and IL-1β) via modulating NF-κB/p65 signaling in LPS-challenged HK-2 cells. In conclusion, our findings suggested a novel therapeutic axis of SNHG14/miR-495-3p/HIPK1 to treat sepsis-induced AKI.	NA	Neuropsychiatr Dis Treat. 2021 Jun 4;17:1793-1799. doi: 10.2147/NDT.S311499. eCollection 2021.
3754	LncRNA	SLCO4A1-AS1	miR-7855-p	SETD7	LSCC tissues and cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	Flow Cytometry assay;Luciferase reporter assay;	33914996	SLCO4A1-AS1 regulates laryngeal squamous cell carcinoma cell phenotypes via the Wnt pathway.	AIM: Long non-coding RNAs were widely reported to regulate laryngeal squamous cell carcinoma (LSCC), a prevalent tumor in the head and neck. We aimed to investigate the role of solute carrier organic anion transporter family member 4A1 antisense RNA 1 (SLCO4A1-AS1) in LSCC. MATERIALS & METHODS: CCK-8 and colony formation assays were conducted to examine the viability and proliferation of LSCC cells. The apoptosis of LSCC cells was evaluated using flow cytometry and TUNEL assays. The distribution of SLCO4A1-AS1 in LSCC cells was detected by subcellular fractionation assay. The interaction between molecules was confirmed using luciferase reporter assay. RESULTS: SLCO4A1-AS1 was overexpressed in LSCC tissues and cells. Furthermore, silenced SLCO4A1-AS1 repressed the proliferation and facilitated apoptosis of LSCC cells. Mechanistical investigation revealed that SLCO4A1-AS1 was a competing endogenous RNA (ceRNA) to upregulate SETD7 by binding with miR-7855-p. Additionally, SLCO4A1-AS1 positively regulated the Wnt/β-catenin signaling pathway by upregulating SETD7. Rescue experiments demonstrated that SLCO4A1-AS1 promoted LSCC proliferation and inhibited LSCC apoptosis by upregulation of SETD7 and activation of the Wnt/β-catenin pathway. CONCLUSION: SLCO4A1-AS1 promotes proliferation and inhibits apoptosis of LSCC cells by upregulation of SETD7 in a miR-7855-5p dependent way to activate the Wnt/β-catenin pathway.	NA	Cancer Biother Radiopharm. 2021 Apr 20. doi: 10.1089/cbr.2020.4395.
3755	LncRNA	SAMMSON	miR-130a	NA	vascular smooth muscle cell	Intracranial Aneurysm	Homo sapiens (human)	qPCR;RT-qPCR;RNA pull-down assay;RNA pull-down;	34113109	LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm.	BACKGROUND: MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Therefore, we further studied the crosstalk between SAMMSON and miR-130a in IA. METHODS: SAMMSON and miR-130a expression were measured using RT-qPCR. SAMMSON subcellular location was analyzed with nuclear fractionation assay. Their direct interaction was explored with RNA pull-down assay. The role of SAMMSON in miR-130a maturation was studied with overexpression analysis. VSMC cell proliferation was analyzed with BrdU assay. RESULTS: SAMMSON and premature miR-130a were deregulated in IA, while mature miR-130a was upregulated in IA. SAMMSON is localized in both the nucleus and cytoplasm, and direct interaction between SAMMSON and miR-130a was observed. SAMMSON overexpression suppressed miR-130a maturation in VSMCs and reduced the enhancing effects of miR-130a on VSMC cell proliferation. CONCLUSION: SAMMSON is overexpressed in IA and suppresses VSMC proliferation via inhibiting miR-130a maturation.	NA	Neuropsychiatr Dis Treat. 2021 Jun 4;17:1793-1799. doi: 10.2147/NDT.S311499. eCollection 2021.
3756	LncRNA	RP11-89K21.1	miR-146a-5p	RHPN2	LUAD tissues and pair-matched adjacent normal tissues	Lung Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33877886	Long Noncoding RNA RP11-89K21.1 Interacts with miR-146a/b-5p to Promote Proliferation and Gefitinib Resistance Through Regulating RHPN2 and RhoA/ROCK Pathway in Lung Adenocarcinoma.	Background: Long noncoding RNAs (lncRNAs) have major roles in lung adenocarcinoma (LUAD). lncRNA RP11-89K21.1 was reported to be abnormally expressed in LUAD, yet its biological functions in LUAD progression remain unclear. Materials and Methods: The 40 LUAD tissues and pair-matched adjacent normal tissues were enrolled in this study. Quantitative real-time polymerase chain reaction was performed to detect the expression of lncRNA, miRNA, and mRNA in LUAD samples and cell lines. Loss-of-function assays were used to evaluate the effects of RP11-89K21.1 on LUAD cell proliferation and gefitinib resistance. Bioinformatics analysis, luciferase reporter assay, and Western blot were employed to explore the regulatory relationships among RP11-89K21.1, miR-146a/b-5p, and RHPN2. Results: The authors identified that RP11-89K21.1 was highly expressed in LUAD tissues and cell lines. Moreover, upregulated RP11-89K21.1 was strongly associated with unfavorable overall survival of patients with LUAD. Knockdown of RP11-89K21.1 significantly suppressed proliferation and sensitized cell to gefitinib. Mechanistically, RP11-89K21.1 could directly bind miR-146a-5p and miR-146b-5p and decrease their expression to upregulate RHPN2, and subsequently activated RhoA/ROCK pathway. More importantly, overexpression of RHPN2 reversed regulatory effects of RP11-89K21.1 knockdown on cell proliferation and gefitinib resistance. Conclusions: These observations provide new insights into the role of RP11-89K21.1 in regulating LUAD tumorigenesis, suggesting that RP11-89K21.1 is a potential therapeutic target for LUAD treatment.	NA	Cancer Biother Radiopharm. 2021 Apr 20. doi: 10.1089/cbr.2020.4395.
3757	LncRNA	RP11-89K21.1	miR-146b-5p	RHPN2	LUAD tissues and pair-matched adjacent normal tissues	Lung Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33877886	Long Noncoding RNA RP11-89K21.1 Interacts with miR-146a/b-5p to Promote Proliferation and Gefitinib Resistance Through Regulating RHPN2 and RhoA/ROCK Pathway in Lung Adenocarcinoma.	Background: Long noncoding RNAs (lncRNAs) have major roles in lung adenocarcinoma (LUAD). lncRNA RP11-89K21.1 was reported to be abnormally expressed in LUAD, yet its biological functions in LUAD progression remain unclear. Materials and Methods: The 40 LUAD tissues and pair-matched adjacent normal tissues were enrolled in this study. Quantitative real-time polymerase chain reaction was performed to detect the expression of lncRNA, miRNA, and mRNA in LUAD samples and cell lines. Loss-of-function assays were used to evaluate the effects of RP11-89K21.1 on LUAD cell proliferation and gefitinib resistance. Bioinformatics analysis, luciferase reporter assay, and Western blot were employed to explore the regulatory relationships among RP11-89K21.1, miR-146a/b-5p, and RHPN2. Results: The authors identified that RP11-89K21.1 was highly expressed in LUAD tissues and cell lines. Moreover, upregulated RP11-89K21.1 was strongly associated with unfavorable overall survival of patients with LUAD. Knockdown of RP11-89K21.1 significantly suppressed proliferation and sensitized cell to gefitinib. Mechanistically, RP11-89K21.1 could directly bind miR-146a-5p and miR-146b-5p and decrease their expression to upregulate RHPN2, and subsequently activated RhoA/ROCK pathway. More importantly, overexpression of RHPN2 reversed regulatory effects of RP11-89K21.1 knockdown on cell proliferation and gefitinib resistance. Conclusions: These observations provide new insights into the role of RP11-89K21.1 in regulating LUAD tumorigenesis, suggesting that RP11-89K21.1 is a potential therapeutic target for LUAD treatment.	NA	Cancer Biother Radiopharm. 2021 Apr 20. doi: 10.1089/cbr.2020.4395.
3758	LncRNA	RBM5-AS1	miR-132	PRC2	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	Cell Biol Int. 2021 May 21. doi: 10.1002/cbin.11649.
3759	LncRNA	RBM5-AS1	miR-132	EZH2	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	
3760	LncRNA	RBM5-AS1	miR-132	SUZ12	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	
3761	LncRNA	RBM5-AS1	miR-132	EED	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	Cell Biol Int. 2021 May 21. doi: 10.1002/cbin.11649.
3762	LncRNA	RBM5-AS1	miR-212	PRC2	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	Cell Biol Int. 2021 May 21. doi: 10.1002/cbin.11649.
3763	LncRNA	RBM5-AS1	miR-212	EZH2	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	
3764	LncRNA	RBM5-AS1	miR-212	SUZ12	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	
3765	LncRNA	RBM5-AS1	miR-212	EED	HCC tissues,Hep3B and HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34019714	LncRNA RBM5-AS1 promotes cell proliferation and invasion by epigenetically silencing miR-132/212 in hepatocellular carcinoma cells.	Hepatocellular carcinoma (HCC) is regarded as one of the most common malignancies worldwide leading to cancer-related death. Long non-coding RNAs (lncRNAs) are a critical modulator affecting HCC progression. Whereas, the pathogenesis of lncRNA RBM5-AS1 in the development of HCC remains unclear. qRT-PCR or western blot assays were applied to detect the expression of genes and proteins, respectively. The proliferation and metastasis abilities were assessed using CCK-8, EdU and transwell assays. RNA immunoprecipitation (RIP) experiment was employed to validate the molecular interactions. RBM5-AS1 is highly expressed in HCC tissues and cell lines, especially in Hep3B and HepG2 cells. RBM5-AS1 knockdown dramatically restrains cell proliferation, invasion and migration of HCC cells. Importantly, RBM5-AS1 acts as an epigenetic regulator to elevate the H3K27me3 level of miR-132/212 promoter regions via recruiting PRC2 (EZH2, SUZ12, EED), and eventually reducing miR-132/212 expressions. The recovery experiments demonstrated that downregulation of miR-132/212 markedly eliminate the anti-tumor effects mediated by RBM5-AS1 silencing in HCC cells. The data of this work illustrates that RBM5-AS1 acts as an epigenetic regulator to promote the HCC progression by repressing miR-132/212 expressions, which would provide a new insight for understanding the action mechanism of RBM5-AS1 in HCC development. This article is protected by copyright. All rights reserved.	NA	Cell Biol Int. 2021 May 21. doi: 10.1002/cbin.11649.
3766	LncRNA	RAET1E-AS1	miR-145-5p	WNT11	adipose-derived stem cells	Asc Dysfunction	Homo sapiens (human)	RT-PCR;RNA sequencing;	34051854	The whole profiling and competing endogenous RNA network analyses of noncoding RNAs in adipose-derived stem cells from diabetic, old, and young patients.	BACKGROUND: Mesenchymal stem cells including adipose-derived stem cells (ASCs) have a considerable potential in the field of translational medicine. Unfortunately, multiple factors (e.g., older age, co-existing diabetes, and obesity) may impair cellular function, which hinders the overall effectiveness of autologous stem cell therapy. Noncoding RNAs-including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs)-have been shown to play important roles in stem cell biology. However, the overall diabetes-related and aging-related expression patterns and interactions of these RNAs in ASCs remain unknown. METHOD: The phenotypes and functions of ASCs isolated from diabetic (D-ASCs), old (O-ASCs), and young (Y-ASCs) donors were evaluated by in vitro assays. We conducted high-throughput RNA sequencing (RNA-seq) in these ASCs to identify the differentially expressed (DE) RNAs. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) analyses were performed to investigate mRNAs with significant differences among groups. The lncRNA- or circRNA-associated competing endogenous RNA (ceRNA) networks were constructed based on bioinformatics analyses and real-time polymerase chain reaction (RT-PCR) results. The miR-145-5p mimics were transfected into O-ASCs and verified by PCR. RESULTS: ASCs from diabetic and old donors showed inferior migration ability and increased cellular senescence. Furthermore, O-ASCs have decreased capacities for promoting endothelial cell angiogenesis and fibroblast migration, compared with Y-ASCs. The DE miRNAs, mRNAs, lncRNAs, and circRNAs were successfully identified by RNA-seq in O-ASCs vs. Y-ASCs and D-ASCs vs. O-ASCs. GO and KEGG analyses demonstrated that DE mRNAs were significantly enriched in aging and cell senescence terms separately. PPI networks revealed critical DE mRNAs in the above groups. RNAs with high fold changes and low p values were validated by PCR. ceRNA networks were constructed based on bioinformatics analyses and validated RNAs. Additionally, the lncRNA RAET1E-AS1-miR-145-5p-WNT11/BMPER axis was validated by PCR and correlation analyses. Finally, the overexpression of miR-145-5p was found to rejuvenate O-ASCs phenotype and augment the functionality of these cells. CONCLUSION: Our research may provide insights regarding the underlying mechanisms of ASC dysfunction; it may also offer novel targets for restoring therapeutic properties in ASCs.	NA	Stem Cell Res Ther. 2021 May 29;12(1):313. doi: 10.1186/s13287-021-02388-5.
3767	LncRNA	RAET1E-AS1	miR-145-5p	BMPER	adipose-derived stem cells	Asc Dysfunction	Homo sapiens (human)	RT-PCR;RNA sequencing;	34051854	The whole profiling and competing endogenous RNA network analyses of noncoding RNAs in adipose-derived stem cells from diabetic, old, and young patients.	BACKGROUND: Mesenchymal stem cells including adipose-derived stem cells (ASCs) have a considerable potential in the field of translational medicine. Unfortunately, multiple factors (e.g., older age, co-existing diabetes, and obesity) may impair cellular function, which hinders the overall effectiveness of autologous stem cell therapy. Noncoding RNAs-including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs)-have been shown to play important roles in stem cell biology. However, the overall diabetes-related and aging-related expression patterns and interactions of these RNAs in ASCs remain unknown. METHOD: The phenotypes and functions of ASCs isolated from diabetic (D-ASCs), old (O-ASCs), and young (Y-ASCs) donors were evaluated by in vitro assays. We conducted high-throughput RNA sequencing (RNA-seq) in these ASCs to identify the differentially expressed (DE) RNAs. Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and protein-protein interaction (PPI) analyses were performed to investigate mRNAs with significant differences among groups. The lncRNA- or circRNA-associated competing endogenous RNA (ceRNA) networks were constructed based on bioinformatics analyses and real-time polymerase chain reaction (RT-PCR) results. The miR-145-5p mimics were transfected into O-ASCs and verified by PCR. RESULTS: ASCs from diabetic and old donors showed inferior migration ability and increased cellular senescence. Furthermore, O-ASCs have decreased capacities for promoting endothelial cell angiogenesis and fibroblast migration, compared with Y-ASCs. The DE miRNAs, mRNAs, lncRNAs, and circRNAs were successfully identified by RNA-seq in O-ASCs vs. Y-ASCs and D-ASCs vs. O-ASCs. GO and KEGG analyses demonstrated that DE mRNAs were significantly enriched in aging and cell senescence terms separately. PPI networks revealed critical DE mRNAs in the above groups. RNAs with high fold changes and low p values were validated by PCR. ceRNA networks were constructed based on bioinformatics analyses and validated RNAs. Additionally, the lncRNA RAET1E-AS1-miR-145-5p-WNT11/BMPER axis was validated by PCR and correlation analyses. Finally, the overexpression of miR-145-5p was found to rejuvenate O-ASCs phenotype and augment the functionality of these cells. CONCLUSION: Our research may provide insights regarding the underlying mechanisms of ASC dysfunction; it may also offer novel targets for restoring therapeutic properties in ASCs.	NA	Stem Cell Res Ther. 2021 May 29;12(1):313. doi: 10.1186/s13287-021-02388-5.
3768	Circular RNA	PVT1	miR-200a	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Homo sapiens (human)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3769	Circular RNA	PVT1	miR-125b	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Homo sapiens (human)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3770	Circular RNA	PVT1	miR-200a	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Mus musculus (mouse)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3771	Circular RNA	PVT1	miR-125b	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Mus musculus (mouse)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3772	Circular RNA	PVT1	miR-200a	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Rattus (rat)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3773	Circular RNA	PVT1	miR-125b	NA	MI tissues and H/R-triggered cardiomyocytes	Mi And H/R Injury	Rattus (rat)	microarray;Flow Cytometry assay;	34097926	Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.	Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.	NA	J Mol Cell Cardiol. 2021 Jun 4:S0022-2828(21)00113-9. doi: 10.1016/j.yjmcc.2021.05.019.
3774	LncRNA	PVT1	miR-17-5p	NA	septic AKI patients serum, LPS-stimulated HK-2 cells	Sepsis-Induced Acute Kidney Injury	Homo sapiens (human)	CCK-8 assay;ELISA;qRT-PCR;RIP assay;RNA pull-down assay;Western blot;RNA pull-down;	34089461	LncRNA PVT1 accelerates LPS-induced septic acute kidney injury through targeting miR-17-5p and regulating NF-κB pathway.	BACKGROUND: Long noncoding RNA PVT1 is associated with diverse human diseases, including acute kidney injury (AKI). However, our understandings of PVT1 on septic AKI are limited. METHODS: The septic AKI model was constructed through lipopolysaccharide (LPS) treatment. PVT1 and miR-17-5p levels were measured using qRT-PCR analysis. The concentrations of inflammatory cytokines were determined with ELISA kits. Cell viability and apoptosis were assessed using CCK-8 assay and flow-cytometric analysis, respectively. Protein levels were examined using western blot assay. The targeting association between miR-17-5p and PVT1 was verified by dual-luciferase reporter, RIP and RNA pull-down assays. RESULTS: PVT1 level was elevated and miR-17-5p level was declined in septic AKI patients' serum and LPS-stimulated HK-2 cells. Cell viability was suppressed and cell apoptosis and inflammation were promoted after LPS treatment. PVT1 knockdown or miR-17-5p elevation restored LPS-mediated HK-2 cell injury. MiR-17-5p was sponged by PVT1, and its inhibition weakened the impact of PVT1 deficiency on LPS-mediated injury of HK-2 cells. In addition, PVT1 knockdown inactivated NF-κB pathway mediated by LPS treatment, but miR-17-5p inhibition further reversed this effect. CONCLUSION: PVT1 knockdown promoted cell viability, suppressed inflammatory response and apoptosis by regulating miR-17-5p expression and NF-κB pathway in LPS-stimulated HK-2 cells.	NA	Int Urol Nephrol. 2021 Jun 5. doi: 10.1007/s11255-021-02905-8.
3775	LncRNA	PVT1	miR-21-5p	ZFP36L2	cardiomyocytes	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	34131106	ZFP36L2 regulates myocardial ischemia/reperfusion injury and attenuates mitochondrial fusion and fission by LncRNA PVT1.	Among several leading cardiovascular disorders, ischemia-reperfusion (I/R) injury causes severe manifestations including acute heart failure and systemic dysfunction. Recently, there has been increasing evidence suggesting that alterations in mitochondrial morphology and dysfunction also play an important role in the prognosis of cardiac disorders. Long non-coding RNAs (lncRNAs) form major regulatory networks altering gene transcription and translation. While the role of lncRNAs has been extensively studied in cancer and tumor biology, their implications on mitochondrial morphology and functions remain to be elucidated. In this study, the functional roles of Zinc finger protein 36-like 2 (ZFP36L2) and lncRNA PVT1 were determined in cardiomyocytes under hypoxia/reoxygenation (H/R) injury in vitro and myocardial I/R injury in vivo. Western blot and qRT-PCR analysis were used to assess the levels of ZFP36L2, mitochondrial fission and fusion markers in the myocardial tissues and cardiomyocytes. Cardiac function was determined by immunohistochemistry, H&E staining, and echocardiogram. Ultrastructural analysis of mitochondrial fission was performed using transmission electron microscopy. The mechanistic model consisting of PVT1 with ZFP36L2 and microRNA miR-21-5p with E3 ubiquitin ligase MARCH5 was assessed by subcellular fraction, RNA pull down, FISH, and luciferase reporter assays. These results identified a novel regulatory axis involving PVT1, miR-21-5p, and MARCH5 that alters mitochondrial morphology and function during myocardial I/R injury. Using an in vivo I/R injury mouse model and in vitro cardiomyocytes H/R model, we demonstrated that ZFP36L2 directly associates with PVT1 and alters mitochondrial fission and fusion. PVT1 also interactes with miR-21-5p and suppresses its expression and activity. Furthermore, we identified MARCH5 as a modifier of miR-21-5p, and its effect on mitochondrial fission and fusion are directly proportional to PVT1 expression during H/R injury. Our findings show that manipulation of PVT1-miR-21-5p-MARCH5-mediated mitochondrial fission and fusion via ZFP36L2 may be a novel therapeutic approach to regulate myocardial I/R injury.	NA	Cell Death Dis. 2021 Jun 15;12(6):614. doi: 10.1038/s41419-021-03876-5.
3776	LncRNA	PVT1	miR-21-5p	ZFP36L2	cardiomyocytes	Myocardial Ischamia Reperfusion Injury Injury	Mus musculus (mouse)	FISH;qRT-PCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	34131106	ZFP36L2 regulates myocardial ischemia/reperfusion injury and attenuates mitochondrial fusion and fission by LncRNA PVT1.	Among several leading cardiovascular disorders, ischemia-reperfusion (I/R) injury causes severe manifestations including acute heart failure and systemic dysfunction. Recently, there has been increasing evidence suggesting that alterations in mitochondrial morphology and dysfunction also play an important role in the prognosis of cardiac disorders. Long non-coding RNAs (lncRNAs) form major regulatory networks altering gene transcription and translation. While the role of lncRNAs has been extensively studied in cancer and tumor biology, their implications on mitochondrial morphology and functions remain to be elucidated. In this study, the functional roles of Zinc finger protein 36-like 2 (ZFP36L2) and lncRNA PVT1 were determined in cardiomyocytes under hypoxia/reoxygenation (H/R) injury in vitro and myocardial I/R injury in vivo. Western blot and qRT-PCR analysis were used to assess the levels of ZFP36L2, mitochondrial fission and fusion markers in the myocardial tissues and cardiomyocytes. Cardiac function was determined by immunohistochemistry, H&E staining, and echocardiogram. Ultrastructural analysis of mitochondrial fission was performed using transmission electron microscopy. The mechanistic model consisting of PVT1 with ZFP36L2 and microRNA miR-21-5p with E3 ubiquitin ligase MARCH5 was assessed by subcellular fraction, RNA pull down, FISH, and luciferase reporter assays. These results identified a novel regulatory axis involving PVT1, miR-21-5p, and MARCH5 that alters mitochondrial morphology and function during myocardial I/R injury. Using an in vivo I/R injury mouse model and in vitro cardiomyocytes H/R model, we demonstrated that ZFP36L2 directly associates with PVT1 and alters mitochondrial fission and fusion. PVT1 also interactes with miR-21-5p and suppresses its expression and activity. Furthermore, we identified MARCH5 as a modifier of miR-21-5p, and its effect on mitochondrial fission and fusion are directly proportional to PVT1 expression during H/R injury. Our findings show that manipulation of PVT1-miR-21-5p-MARCH5-mediated mitochondrial fission and fusion via ZFP36L2 may be a novel therapeutic approach to regulate myocardial I/R injury.	NA	Cell Death Dis. 2021 Jun 15;12(6):614. doi: 10.1038/s41419-021-03876-5.
3777	LncRNA	PVT1	miR-551b	FGFR1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	34113122	LncRNA PVT1 Facilitates Proliferation, Migration and Invasion of NSCLC Cells via miR-551b/FGFR1 Axis.	BACKGROUND: Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) plays a crucial role in non-small cell lung cancer (NSCLC). Nonetheless, regulatory effects of PVT1 on functions of NSCLC cells remain blurry. METHODS: Relative expression levels of PVT1, miR-551b and FGFR1 mRNA in tumor tissues and cells were examined employing quantitative real-time polymerase chain reaction (qRT-PCR); CCK-8 and BrdU assays were utilized for measuring cell viability and proliferation of H1299 and A549 cells; cell migration and invasion were detected deploying Transwell assay; dual-luciferase assay was used for the validation of binding sequence between PVT1 and miR-551b. FGFR1 expression in protein level was quantified employing Western blot. RESULTS: PVT1 was highly expressed in NSCLC tissues and cell lines, whereas miR-551b expression was down-regulated. Overexpression of PVT1 potentiated viability, proliferation, migration and invasion of NSCLC cells while miR-551b inhibited the biological behaviors mentioned above. MiR-551b was predicted and then confirmed as a direct downstream target of PVT1. Meanwhile, a negative correlation was observed between PVT1 expression and miR-551b expression in NSCLC tissues. Besides, PVT1 could increase FGFR1 expression by repressing miR-551b expression. CONCLUSION: PVT1 promotes the proliferation, migration and invasion of NSCLC cells by indirectly mediating FGFR1 via targeting miR-551b.	NA	Onco Targets Ther. 2021 Jun 2;14:3555-3565. doi: 10.2147/OTT.S273794. eCollection 2021.
3778	LncRNA	PVT1	miR-124-3p	NA	head and neck squamous cell carcinoma cells	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	34033197	lncRNA PVT1 promotes cetuximab resistance of head and neck squamous cell carcinoma cells by inhibiting miR-124-3p.	BACKGROUND: Cetuximab has been widely used in the clinical treatment of head and neck squamous cell carcinoma (HNSCC). However, whether long non-coding RNA plasmacytoma variant translocation 1 (lncRNA PVT1) is correlated with cetuximab resistance remains unclear. METHODS: Western blot and qRT-PCR were performed to quantify the levels of genes and proteins, respectively. Cell functions were measured using Cell Counting Kit-8 (CCK-8), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and flow cytometry assays. The methylation level was tested using methylation-specific PCR (MSP). RESULTS: PVT1 was upregulated and positively correlated with the poor prognosis of HNSCC. PVT1 overexpression markedly promoted the survival and weakened the cetuximab sensitivity of HNSCC cells, while miR-124-3p overexpression showed opposite effects. Mechanistically, the silence of PVT1 indirectly promoted miR-124-3p expression by reducing its promoter methylation. Importantly, miR-124-3p overexpression impeded the regulatory roles of PVT1 overexpression. CONCLUSION: PVT1 decreased the sensitivity of HNSCC cells to cetuximab by enhancing methylation-mediated inhibition of miR-124-3p, which might provide a new insight for the cetuximab chemoresistance of HNSCC.	NA	Head Neck. 2021 May 25. doi: 10.1002/hed.26742.
3779	LncRNA	PVT1	miR-199a-5p	caveolin1	lung cancer cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33902331	Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial-Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer.	PM2.5 plays an important role in the physiological and pathological progression of lung cancer. Lentinan exerts antitumor activity in many kinds of human cancers. Plasmacytoma variant translocation 1 (PVT1) exerts antitumor activity in many kinds of human cancers. However, the role and underlying molecular mechanism of PVT1 in the role of lentinan in PM2.5-exposed lung cancer are still largely unknown. Our study confirmed that PM2.5 exposure induced the production of inflammatory factors, epithelial-mesenchymal transition (EMT) and migration of lung cancer cells. Lentinan exerted antitumor effects by inhibiting the production of inflammatory factors, EMT, and migration of lung cancer cells. Lentinan suppressed PM2.5 exposure-induced cellular progression by inhibiting the PM2.5 exposure-induced elevation of PVT1 expression. PVT1 absorbed miR-199a, and miR-199a inhibited caveolin1 expression and thus formed the PVT1/miR-199a/caveolin1 signaling pathway in lung cancer cells. Our study revealed that silencing of the PVT1/miR-199a/caveolin1 signaling pathway affected the role of lentinan in PM2.5-exposed lung cancer cells. Thus, this study first investigated the role of lentinan in PM2.5-exposed lung cancer cells and further displayed the underlying molecular mechanism, providing a potential treatment for PM2.5-exposed lung cancer.	NA	DNA Cell Biol. 2021 May;40(5):683-693. doi: 10.1089/dna.2020.6338. Epub 2021 Apr 23.
3780	LncRNA	PVT1	miR-24	KLF6	LPS-induced cardiac fibroblasts	Myocardial Injury	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;	33907980	PVT1 knockdown inhibited the biological behavior of LPS-induced cardiac fibroblasts by regulating miR-24.	BACKGROUND: The heart is one of the target organs vulnerable to sepsis. About 50% of sepsis patients will suffer from myocardial injury and cardiac dysfunction, which will aggravate the sepsis and affect its prognosis. OBJECTIVES: Here, we attempt to investigate the function of long non coding RNA PVT1 in LPS-induced cardiac fibroblasts in vitro, and explore its potential mechanism. METHODS: The expression of PVT1 in LPS-induced cardiac fibroblasts was detected by qRT-PCR. CCK-8 assay, cell migration, qRT-PCR and western blotting analysis were applied to evaluating the effect of PVT1 knockdown on LPS-induced cardiac fibroblasts. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. RESULTS: PVT1 expression was up-regulated in LPS-induced cardiac fibroblasts. And knockdown of PVT1 inhibited cell viability and migration, alleviated inflammation cytokines production of LPS-treated cardiac fibroblasts. The bioinformatics analysis predicted PVT1 negatively regulates miR-24 and KLF6 is a direct target of miR-24. CONCLUSIONS: In a word, we observed PVT1 expression level was up-regulated in LPS- treated cardiac fibroblasts. PVT1 knockdown could alleviate LPS-induced biological behavior of cardiac fibroblasts through sponging miR-24 in vitro.	NA	Genes Genomics. 2021 Apr 27. doi: 10.1007/s13258-021-01104-0.
3781	LncRNA	PSMG3AS1	miR-613	SphK1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33849377	LncRNA PSMG3AS1 promotes proliferation of non-small cell lung cancer cells by sponging miR-613 to upregulate SphK1.	PSMG3-AS1 is a characterized oncogenic lncRNA in breast cancer, while its role in other cancers remains unclear. This study was to investigate the role and underlying mechansim of PSMG3-AS1 in non-small cell lung cancer (NSCLC). In this study, we found that PSMG3-AS1 could interact with miR-613. The expression of PSMG3-AS1 was upregulated in NSCLC, while the expression of miR-613 was downregulated in NSCLC. However, PSMG3-AS1 and miR-613 were not significantly correlated with each other. In NSCLC cells, PSMG3-AS1 and miR-613 overexpression failed to regulate the expression of each other. Interestingly, PSMG3-AS1 overexpression led to upregulated SphK1, a downstream target of miR-613. In addition, PSMG3-AS1 overexpression reduced the inhibitory effects of miR-613 on NSCLC cell proliferation. Therefore, PSMG3-AS1 may promote the proliferation of NSCLC cells by sponging miR-613 to upregulate SphK1.	NA	Cell Cycle. 2021 May;20(9):829-838. doi: 10.1080/15384101.2021.1900499. Epub 2021 Apr 14.
3782	LncRNA	PRNCR1	miR-326	FSCN1	OSCC tissues	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Luciferase reporter assay;	33928608	LncRNA PRNCR1 aggravates the malignancy of oral squamous cell carcinoma by regulating miR-326/FSCN1 axis.	OBJECTIVE: The important regulatory mechanism of lncRNA PRNCR1 has been emphasized in malignant tumors. However, the role of lncRNA PRNCR1 remains unclear in oral squamous cell carcinoma (OSCC). The purpose of this study is to reveal the role of lncRNA PRNCR1 in OSCC. PATIENTS AND METHODS: RT-qPCR was used to detect mRNA expression. The functional mechanism of lncRNA PRNCR1 in OSCC was investigated by CCK-8, transwell and Luciferase reporter assays. RESULTS: LncRNA PRNCR1 was upregulated in OSCC and promoted cell proliferation, migration and invasion. LncRNA PRNCR1 directly binds to miR-326. The mutual inhibition between the expressions of lncRNA PRNCR1 and miR-326 was identified in OSCC. In addition, miR-326 restrained cell proliferation, migration and invasion in OSCC. Further, miR-326 directly targets FSCN1. FSCN1 expression was positively regulated by lncRNA PRNCR1 in OSCC. And FSCN1 promoted the progression of OSCC and aggravated the carcinogenic effect of lncRNA PRNCR1 in OSCC. CONCLUSIONS: LncRNA PRNCR1 promotes the progression of OSCC by functioning as a miR-326 'sponge' to upregulate FSCN1 expression.	NA	Eur Rev Med Pharmacol Sci. 2021 Apr;25(8):3226-3234. doi: 10.26355/eurrev_202104_25731.
3783	Circular RNA	Prkcsh	miR-488	Ccl2	multiple nerve cells	Spinal Cord Injury	Homo sapiens (human)	qRT-PCR	34100450	Down-regulating Circular RNA Prkcsh suppresses the inflammatory response after spinal cord injury.	Circular RNAs (circRNAs) are a class of conserved, endogenous non-coding RNAs that are involved in transcriptional and post-transcriptional gene regulation and are highly enriched in the nervous system. They participate in the survival and differentiation of multiple nerve cells, and may even promote the recovery of neurological function after stroke. However, their role in the inflammatory response after spinal cord injury remains unclear. In the present study, we established a mouse model of T9 spinal cord injury using the modified Allen's impact method, and identified 16,013 circRNAs and 960 miRNAs that were differentially expressed after spinal cord injury. Of these, the expression levels of circPrkcsh were significantly different between injured and sham-treated mice. We then treated astrocytes with tumor necrosis factor-α in vitro to simulate the inflammatory response after spinal cord injury. Our results revealed an elevated expression of circPrkcsh with a concurrent decrease in miR-488 expression in injured cells. We also found that circPrkcsh regulated the expression of the inflammation-related gene Ccl2. Furthermore, in tumor necrosis factor-α-treated astrocytes, circPrkcsh knockdown decreased the expression of Ccl2 by upregulating miR-488 expression, and reduced the secretion of inflammatory cytokines in vitro. These findings suggest that differentially expressed circRNAs participate in the inflammatory response after spinal cord injury and act as the regulators of certain microRNAs. Furthermore, circPrkcsh may be used as an miR-488 sponge to regulate Ccl2 expression, which might provide a new potential therapy for SCI. The study was approved by the Animal Ethics Committee of Shandong University of China (approval No. KYLL-20170303) on March 3, 2017.	NA	Neural Regen Res. 2022 Jan;17(1):144-151. doi: 10.4103/1673-5374.314114.
3784	Circular RNA	Prkcsh	miR-488	Ccl2	multiple nerve cells	Spinal Cord Injury	Rattus (rat)	qRT-PCR	34100450	Down-regulating Circular RNA Prkcsh suppresses the inflammatory response after spinal cord injury.	Circular RNAs (circRNAs) are a class of conserved, endogenous non-coding RNAs that are involved in transcriptional and post-transcriptional gene regulation and are highly enriched in the nervous system. They participate in the survival and differentiation of multiple nerve cells, and may even promote the recovery of neurological function after stroke. However, their role in the inflammatory response after spinal cord injury remains unclear. In the present study, we established a mouse model of T9 spinal cord injury using the modified Allen's impact method, and identified 16,013 circRNAs and 960 miRNAs that were differentially expressed after spinal cord injury. Of these, the expression levels of circPrkcsh were significantly different between injured and sham-treated mice. We then treated astrocytes with tumor necrosis factor-α in vitro to simulate the inflammatory response after spinal cord injury. Our results revealed an elevated expression of circPrkcsh with a concurrent decrease in miR-488 expression in injured cells. We also found that circPrkcsh regulated the expression of the inflammation-related gene Ccl2. Furthermore, in tumor necrosis factor-α-treated astrocytes, circPrkcsh knockdown decreased the expression of Ccl2 by upregulating miR-488 expression, and reduced the secretion of inflammatory cytokines in vitro. These findings suggest that differentially expressed circRNAs participate in the inflammatory response after spinal cord injury and act as the regulators of certain microRNAs. Furthermore, circPrkcsh may be used as an miR-488 sponge to regulate Ccl2 expression, which might provide a new potential therapy for SCI. The study was approved by the Animal Ethics Committee of Shandong University of China (approval No. KYLL-20170303) on March 3, 2017.	NA	Neural Regen Res. 2022 Jan;17(1):144-151. doi: 10.4103/1673-5374.314114.
3785	LncRNA	PRKCQ-AS1	miR-545-5p	STAT1	HaCaT cells	Psoriasis	Homo sapiens (human)	qRT-PCR	34080300	Transcriptome wide analysis of long non-coding RNA-associated ceRNA regulatory circuits in psoriasis.	Long non-coding RNAs (lncRNAs) play critical roles in regulating immune-associated diseases and chronic inflammatory disorders. Here, we found that lncRNAs involve in the pathogenesis of psoriasis through integrative analysis of RNA-seq data sets from a psoriasis cohort. Then, lncRNA-protein-coding genes (PCGs) co-expression network analysis demonstrated that lncRNAs extensively interact with IFN-γ signalling pathway-associated genes. Further, we validated 3 lncRNAs associate with IFN-γ signalling pathway activation upon IFN-γ stimulated in HaCaT cells, and loss of function experiments indicate their functional roles in the activation of inflammatory cytokine genes. Additionally, microRNA target screening analysis showed that lncRNAs may regulate JAK/STAT pathway activity through complete endogenous RNA (ceRNA) mechanism. Further experimental validation of PRKCQ-AS1/STAT1/miR-545-5p regulatory circuitry showed that lncRNAs regulate the expression of JAK/STAT signalling pathway genes through competing for miR-545-5p. In summary, our results demonstrated that dysregulation of lncRNA-JAK/STAT pathway axis promotes the inflammation level in psoriasis and thus provide potential therapeutic targets for psoriasis treatments.	NA	J Cell Mol Med. 2021 Jun 2. doi: 10.1111/jcmm.16703.
3786	LncRNA	PP7080	miR-601	SIRT1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Luciferase activity assay;	33955831	Long noncoding RNA PP7080 promotes hepatocellular carcinoma development by sponging mir-601 and targeting SIRT1.	Hepatocellular carcinoma (HCC) is the most common primary liver malignancy in adults, ranking the second leading cause of cancer-related death. To date, the underlying mechanisms of HCC pathogenesis are still unclear. Recently, more and more studies have reported that long noncoding RNAs (lncRNAs) are involved in the occurrence and development of HCC. This study aims to investigate the expressions, clinical significance and roles of lncRNA PP7080 in HCC. We analyzed the transcriptome data of HCC cancer tissue (n = 369) and normal tissue (n = 50) in the TCGA database. We used the qRT-PCR method to detect the expression levels of lncRNA PP7080 in 40 pairs of HCC and adjacent tissues. The survival curve was drawn by KM-plotter. The changes of migration, invasion and proliferation of HCC cells were detected by transwall, CCK8 and colony forming assays, respectively. For the interaction between genes, we performed the luciferase activity assay to analyze. The expression of lncRNA PP7080 and miR-601 in cancer tissues of 40 cancer patients was analyzed by Pearson correlation. LncRNA PP7080 was highly expressed in HCC and predicted a poor prognosis. Luciferase activity assay identified lncRNA PP7080 as a molecular sponge for miR-601 in HCC cells. LncRNA PP7080 promoted HCC cells proliferation, migration and invasion by miR-601/SIRT1 signal axis. These results revealed lncRNA PP7080 effect in regulating miR-601/SIRT1 signal axis in the progression of HCC, indicating the important role of miR-601 in HCC pathogenesis.	NA	Bioengineered. 2021 Dec;12(1):1599-1610. doi: 10.1080/21655979.2021.1920323.
3787	LncRNA	PINK1-AS	miR-200a	NA	GC cells	Gastric Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33958720	LncRNA PINK1-AS promotes Gαi1-driven gastric cancer tumorigenesis by sponging microRNA-200a.	Gastric cancer (GC) is one of the leading causes of human mortality around the world. We have previously shown that Gαi1 (the inhibitory subunit 1 of the heterotrimeric guanine nucleotide-binding protein) recruitment to ligand-activated receptor tyrosine kinases (RTKs) is essential for signaling. Testing its role in GC cancer-promoting functions, we found that Gαi1 is upregulated in human GC, correlating with poor overall survival. In established and primary human GC cells, Gαi1 shRNA (small hairpin RNA) or knockout produced significant anti-GC cell activity, proliferation and migration was inhibited, and apoptosis was activated. Conversely, ectopic Gαi1 overexpression promoted proliferation and migration of GC cells in vitro. By examining the tumor-suppressive miRNA microRNA-200a (miR-200a), we found that miR-200a directly silenced Gαi1 to induce anti-GC cell activity. The expression of miR-200a was downregulated in human GC, correlating with upregulation of a novel miR-200a-targeting long non-coding RNA (LncRNA), PINK1 (PTEN Induced Kinase 1)-AS. RNA immunoprecipitation, RNA-pull down, and RNA fluorescence in situ hybridization assays confirmed that PINK1-AS directly binds to miR-200a. Silencing PINK1-AS in GC cells led to miR-200a accumulation, Gαi1 downregulation, and inhibition of GC cell progression in vitro, whereas PINK1-AS upregulation produced the converse results. Significantly, anti-GC cell activity induced by PINK1-AS shRNA was ameliorated by the expression of miR-200a antisense or the 3'-UTR (untranslated region)-depleted Gαi1. In vivo, the growth of subcutaneous MGC-803 xenografts in nude mice was inhibited by PINK1-AS shRNA, but accelerated by PINK1-AS overexpression. Patient-derived GC xenograft growth in nude mice was largely inhibited after intratumoral injection of PINK1-AS shRNA lentivirus. In conclusion, PINK1-AS promotes Gαi1-driven GC progression by sponging miR-200a.	NA	Oncogene. 2021 Jun;40(22):3826-3844. doi: 10.1038/s41388-021-01812-7. Epub 2021 May 6.
3788	LncRNA	PCNAP1	miR-340-5p	ATF7	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	34007276	LncRNA PCNAP1 Promotes Hepatoma Cell Proliferation through Targeting miR-340-5p and is Associated with Patient Survival.	Hepatocellular carcinoma (HCC) is one of the most common malignancies and causes poor outcome. Dysregulation of long noncoding RNA (lncRNA) is involved in HCC. Upregulation of the lncRNA PCNAP1 has been reported to promote HBV-infectious HCC growth, but its clinical significance and underlying mechanisms in HCC development remain unclear. Here, we report that PCNAP1 expression is increased in both HBV-infectious and noninfectious HCC tissues compared with matched normal tissues, and its upregulation correlates with poor survival rates of HCC patients. Furthermore, we found that PCNAP1 promotes HCC cell proliferation through acting as a competitive endogenous RNA (ceRNA) to sponge miR-340-5p, which has been reported to directly inhibit ATF7 expression in HCC cells. Moreover, the PCNAP1/miR-340-5p/ATF7 signaling associates with the poor survival rates of HCC patients. Collectively, our findings suggest that the PCNAP1/miR-340-5p/ATF7 signaling may be a potential biomarker for the prognosis of HCC patients and a potential therapeutic target for HCC.	NA	J Oncol. 2021 Apr 28;2021:6627173. doi: 10.1155/2021/6627173. eCollection 2021.
3789	LncRNA	PAXIP1-AS1	miR-6744-5p	PCBP2	OC cell lines.	Ovarian Cancer	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;	34108034	H3K27ac-induced lncRNA PAXIP1-AS1 promotes cell proliferation, migration, EMT and apoptosis in ovarian cancer by targeting miR-6744-5p/PCBP2 axis.	We aimed to explore role of lncRNA PAX-interacting protein 1-antisense RNA1 (PAXIP1-AS1) in ovarian cancer (OC). RT-qPCR analysis identified upregulation of PAXIP1-AS1 in OC cell lines. Functionally, PAXIP1-AS1 knockdown inhibited cell proliferation, accelerated cell apoptosis, and suppressed cell migration and epithelial-mesenchymal transition (EMT) process. Upregulation of PAXIP1-AS1 was induced by CBP-mediated H3K27 acetylation (H3K27ac) via bioinformatic analysis and ChIP assay. Furthermore, PAXIP1-AS1 served as a competing endogenous RNA (ceRNA) to regulate PCBP2 expression by sponging microRNA-6744-5p (miR-6744-5p). Restoration experiments showed that overexpressed PCBP2 rescued effects of silenced PAXIP1-AS1 on cell proliferation, apoptosis, migration and EMT. Overall, lncRNA PAXIP1-AS1 activated by H3K27ac functioned as a tumor promoter in OC via mediating miR-6744-5p/PCBP2 axis, which provided promising insight into exploration on OC therapy.	NA	J Ovarian Res. 2021 Jun 9;14(1):76. doi: 10.1186/s13048-021-00822-z.
3790	LncRNA	PART 1	miR-20b-5p	BAMBI	OS tissues and cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;	33850885	LncRNA prostate androgen-regulated transcript 1 (PART 1) functions as an oncogene in osteosarcoma via sponging miR-20b-5p to upregulate BAMBI.	BACKGROUND: Osteosarcoma (OS) is an aggressive bone cancer that most commonly affects adolescents and children. Emerging studies have shown that long noncoding RNA (lncRNA) performs essential roles in the occurrence and development of many tumors. Prostate androgen-regulated transcript 1 (PART 1) has been reported as a tumor oncogene; despite this, the mechanisms underlying its involvement in OS are unclear. METHODS: OS and paired normal tissue samples were obtained, and gene expressions were detected by real time-quantitative polymerase chain reaction (RT-qPCR). The functions of PART 1 in OS cell proliferation, invasion, and migration were determined by Cell Counting Kit-8 (CCK-8) and Transwell assays. Furthermore, the binding sites of PART 1 and miR-20b-5p as well as those between miR-20b-5p and bone morphogenic protein and activin membrane-bound inhibitor homolog (BAMBI) were verified by bioinformatics analysis and dual-luciferase reporter assay. RESULTS: Our study found obvious overexpression of PART 1 in OS tissues and cells. Furthermore, PART 1 overexpression facilitated OS cell proliferation, invasion, and migration. Further mechanistic investigations revealed that PART 1 could sponge to miR-20b-5p, which was expressed at a low level in OS tissues and cells. Importantly, miR-20b-5p overexpression inhibited OS cell proliferation, invasion, and migration. Additionally, BAMBI was confirmed as a downstream gene of miR-20b-5p, and its expression was reversely modulated by miR-20b-5p and positively modulated by PART 1. Rescue experiments suggested that BAMBI was involved in PART 1-mediated promotion of OS progression. CONCLUSIONS: PART 1 serves as a competing endogenous RNA to promote OS tumorigenesis via its regulation of the miR-20b-5p/BAMBI axis, which may provide a promising therapeutic biomarkers for OS patients.	NA	Ann Transl Med. 2021 Mar;9(6):488. doi: 10.21037/atm-21-658.
3791	LncRNA	PAHRF	miR-23a-3p	MST1	human pulmonary artery smooth muscle cells	Pulmonary Arterial Hypertension	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase activity assay;	34126237	The lncRNA PAHRF functions as a competing endogenous RNA to regulate MST1 expression by sponging miR-23a-3p in pulmonary arterial hypertension.	BACKGROUND: Emerging evidence has shown that long non-coding RNA (lncRNA) plays important roles in the development of pulmonary arterial hypertension (PAH). However, some new lncRNAs in patients with PAH are still lacking research. Herein, we examined the expression and role of lncRNA (pulmonary arterial hypertension related factor, PAHRF) in PAH. METHODS: LncRNA PAHRF expression and localization were analyzed by realtime PCR and fluorescence in situ hybridization. Proliferation and apoptosis were detected by MTT, CCK-8, EDU staining, JC-1 assay, flow cytometry and western blotting. Luciferase activity assay was used to identify PAHRF/ miR-23a-3p/serine/threonine kinase 4 (STK4/MST1) interaction. RESULTS: LncRNA PAHRF was down-regulated in both the PAs of PAH patients and hypoxic human pulmonary artery smooth muscle cells (PASMCs). The overexpression of PAHRF inhibited the proliferation and promoted the apoptosis of PASMCs. Similarly, we also found PAHRF overexpression decreased the proliferation under hypoxia condition. Knockdown of PAHRF exerted the opposite effects. Luciferase activity assay proved molecular binding between PAHRF and hsa-miR-23a-3p. Moreover, MST1 was confirmed to be the putative target gene and regulated by PAHRF/miR-23a-3p. In addition, we explored the molecular mechanism regulating the expression of miR-23a-3p, and found that lncRNA PAHRF acted as an endogenous sponge for miR-23a-3p, and silencing lncRNA PAHRF could up-regulate the expression of miR-23a-3p. On the contrary, PAHRF-overexpressing plasmid inhibited the expression of miR-23a-3p in hypoxia. CONCLUSIONS: Our present study reveals a novel PAH regulating model that is composed of PAHRF, miR-23a-3p, and MST1. The aim of this study is probably going to provide a new explanation and give a further understanding of the occurrence of vascular remodeling in PAH from the perspective competing endogenous RNA hypothesis.	NA	Vascul Pharmacol. 2021 Jun 11:106886. doi: 10.1016/j.vph.2021.106886.
3792	LncRNA	OIP5-AS1	miR-34b-5p	HuR	colon cancer cells	Colon Cancer	Homo sapiens (human)	qRT-PCR	34021273	Molecular mechanism of miR-34b-5p and RNA binding protein HuR binding to lncRNA OIP5-AS1 in colon cancer cells.	Colon cancer (CC) is a leading cause of cancer-related death. Long non-coding RNA OIP5-AS1 (lncRNA OIP5-AS1) expression pattern has been studied in many cancers. We aimed to identify the mechanism of lncRNA OIP5-AS1 in CC development. OIP5-AS1 expression pattern in CC tissues and cells was detected and the relation between OIP5-AS1 level and CC prognosis was analyzed. The proliferation, migration and invasion of CC cells were detected after silencing or overexpression of OIP5-AS1. Tumor xenograft in nude mice was established to verify the effect of OIP5-AS1 in vivo. The interaction between HuR protein and OIP5-AS1 and the interaction of miR-34b-5p with HuR and OIP5-AS1 were measured. OIP5-AS1 was highly expressed in CC and associated with poor prognosis. Silencing OIP5-AS1 inhibited CC cell malignant behaviors and inhibited the growth rate and tumor weight. In the mechanism, HuR bound to OIP5-AS1 and stabilized OIP5-AS1 expression. Both miR-34-5p and HuR bind to OIP5 and oppositely affect its expression. miR-34b-5p inhibited the proliferation and invasion of CC cells by inhibiting OIP5-AS1 and PI3K/Akt pathway. miR-34b-5p inhibited CC growth by inhibiting OIP5-AS1. Collectively, miR-34b-5p targets HuR and miR-34b-5p binds to OIP5-AS1 with HuR, thus inhibiting OIP5-AS1 and PI3K/Akt pathway and CC progression.	NA	Cancer Gene Ther. 2021 May 21. doi: 10.1038/s41417-021-00342-4.
3793	LncRNA	OIP5-AS1	miR-217	MTDH	BCa tissues and cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33928606	Long noncoding RNA OIP5-AS1 exhibits oncogenic activity in bladder cancer through miR-217 and MTDH.	OBJECTIVE: The aim of this study was to investigate the role of long non-coding Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in bladder cancer (BCa), and the mechanism of OIP5-AS1/microRNA-217 (miR-217)/metadherin (MTDH) in promoting the progression of BCa. PATIENTS AND METHODS: OIP5-AS1, miR-217 and MTDH expressions in BCa tissues and cells were detected by qRT-PCR or Western blot. CCK-8 and transwell assays were used to determine the proliferation and invasion of BCa cells. The correlation between OIP5-AS1 and miR-217, miR-217 and MTDH, and OIP5-AS1 and MTDH were studied by Luciferase reporter assay and Spearman correlation analysis. Statistical analysis of test data was performed using t-test. RESULTS: OIP5-AS1 was upregulated in BCa tissues and cells, and OIP5-AS1 knockdown could inhibit the proliferation and invasion of BCa cells. MiR-217 was a direct-acting target of OIP5-AS1, and MTDH was a target of miR-217. OIP5-AS1 knockdown inhibits human BCa cell proliferation and invasion through miR-217/MTDH axis. CONCLUSIONS: This study systematically explored the effect of OIP5-AS1 in human BCa. MiR-217/MTDH pathway mediated the promotion of OIP5-AS1 in BCa cells proliferation and invasion. OIP5-AS1, as an oncogene, could be used as a biomarker for the treatment of BCa.	NA	Eur Rev Med Pharmacol Sci. 2021 Apr;25(8):3211-3220. doi: 10.26355/eurrev_202104_25729.
3794	LncRNA	OIP5-AS1	miR-129-5p	IGF2BP2	glioblastoma cells	Glioblastoma	Homo sapiens (human)	qRT-PCR	34132932	Long non-coding RNA OIP5-AS1 inhibition upregulates microRNA-129-5p to repress resistance to temozolomide in glioblastoma cells via downregulating IGF2BP2.	OBJECTIVE: Long non-coding RNAs (lncRNAs) and miRNAs (miRNAs) participate in tumors, while the effects of lncRNA OIP5 antisense RNA 1 (OIP5-AS1) and miR-129-5p on glioblastoma (GBM) remain to be further studied. We aim to explore the role of OIP5-AS1/miR-129-5p/insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) axis in GBM progression. METHODS: OIP5-AS1, miR-129-5p and IGF2BP2 expression in tissues was determined. Temozolomide (TMZ)-resistant GBM cells were established and transfected with relative plasmid to alter OIP5-AS1, IGF2BP2 or miR-129-5p expression. Then, the viability, proliferation, apoptosis and in vivo tumor growth were assessed. The subcellular localization of OIP5-AS1 was determined, and the binding relationships between OIP5-AS1 and miR-129-5p, and between miR-129-5p and IGF2BP2 were confirmed. RESULTS: OIP5-AS1 and IGF2BP2 were upregulated whereas miR-129-5p was downregulated in GBM. OIP5-AS1 silencing or miR-129-5p overexpression inhibited GBM cell chemoresistance to TMZ and proliferation, and promoted cell apoptosis. MiR-129-5p downregulation or IGF2BP2 upregulation reversed the role of OIP5-AS1 silencing on GBM cells. OIP5-AS1 sponged miR-129-5p and miR-129-5p targeted IGF2BP2. CONCLUSION: OIP5-AS1 inhibition upregulated miR-129-5p to repress resistance to TMZ in GBM cells via downregulating IGF2BP2.	NA	Cell Biol Toxicol. 2021 Jun 16. doi: 10.1007/s10565-021-09614-z.
3795	LncRNA	OIP5-AS1	miR-30c-5p	NA	human umbilical vascular endothelial cells	Atherosclerosis	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33867356	LncRNA OIP5-AS1 accelerates ox-LDL-treated HUVECs injury by NF-κB pathway via miR-30c-5p.	BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) could induce endothelial injury and played a vital role in the progression and development of atherosclerosis. This study aimed to investigate the role of Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in ox-LDL-induced human umbilical vascular endothelial cells (HUVECs) injury and the potential mechanisms. METHODS: Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The levels of lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were detected by corresponding detection kits, respectively. Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of OIP5-AS1 or microRNA-30c-5p (miR-30c-5p) in HUVECs. Binding between OIP5-AS1 and miR-30c-5p was predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Western blot was used to analyze p-IκB, IκB, p-p65 and p65 levels. RESULTS: In HUVECs, exposure to ox-LDL led to a decrease in cell viability and an increase in LDH release and apoptosis with concomitant enhancement of oxidative stress, as evidenced by increased ROS and MDA generation, as well as decreased SOD activity and NO levels, while OIP5-AS1 knockdown or miR-30c-5p upregulation could rescue these effects above. Mechanically, OIP5-AS1 functioned as a sponge of miR-30c-5p. OIP5-AS1-induced injury and apoptosis, oxidative stress and activation of NF-κB pathway were reversed by miR-30c-5p in ox-LDL-treated HUVECs. CONCLUSION: OIP5-AS1 contributed to ox-LDL-treated HUVECs injury by activation of NF-κB pathway via miR-30c-5p.	NA	Clin Hemorheol Microcirc. 2021 Apr 13. doi: 10.3233/CH-211130.
3796	LncRNA	NR2F2-AS1	miR-106b	PLEKHO2	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	34070923	The miR-106b/NR2F2-AS1/PLEKHO2 Axis Regulates Migration and Invasion of Colorectal Cancer through the MAPK Pathway.	Increasing numbers of miRNAs have been observed as oncogenes or tumor suppressors in colorectal cancer (CRC). It was recently reported that hsa-miR-106b-5p (miR-106b) promoted CRC cell migration and invasion. However, there were also studies showing contradictory results. Therefore, in the present study, we further explore the role of miR-106b and its downstream networks in the carcinogenesis of CRC. We observed that the expression of miR-106b is significantly increased in Pan-Cancer and CRC tissues compared with normal tissues from The Cancer Genome Atlas (TCGA) database. Furthermore, we used Transwell, Cell Counting Kit-8, and colony formation assays to clarify that miR-106b promotes the migratory, invasive, and proliferative abilities of CRC cells. For the first time, we systematically screened the target mRNAs and lncRNAs of miR-106b using TCGA database and the bioinformatics algorithms. Dual-luciferase reporter assay confirmed that NR2F2-AS1 and PLEKHO2 are the direct targets of miR-106b. Furthermore, NR2F2-AS1 acts as a competing endogenous RNA (ceRNA) to regulate PLEKHO2 expression by sponging miR-106b. The results of Gene set enrichment analysis (GSEA) and Western blot indicated that they play important roles in CRC progression by regulating MAPK pathway. Thus, miR-106b/NR2F2-AS1/PLEKHO2/MAPK signaling axis may suggest the potential usage in CRC treatment.	NA	Int J Mol Sci. 2021 May 30;22(11):5877. doi: 10.3390/ijms22115877.
3797	Circular RNA	Circ_0003012	miR-298-3p	Smoc2	the hippocampus of the mice	Alzheimers Disease	Homo sapiens (human)	RACE;RNA sequencing;	34093124	CircRNA-ceRNA Network Revealing the Potential Regulatory Roles of CircRNA in Alzheimer's Disease Involved the cGMP-PKG Signal Pathway.	Background: Alzheimer's disease (AD) is a chronic progressive neurodegenerative disease. The characteristic pathologies include extracellular senile plaques formed by β-amyloid protein deposition, neurofibrillary tangles formed by hyperphosphorylation of tau protein, and neuronal loss with glial cell hyperplasia. Circular RNAs (circRNAs) are rich in miRNA-binding sites (miRNA response elements, MREs), which serve as miRNA sponges or competitive endogenous RNAs (ceRNAs). Although several research groups have identified dysregulated circRNAs in the cerebral cortex of SAMP8 mice or APP/PS1 mice using deep RNA-seq analysis, we need to further explore circRNA expression patterns, targets, functions and the signaling pathways involved in the pathogenesis of AD and in particular the hippocampal circRNA expression profiles in AD. Methods: We used deep RNA sequencing to investigate circRNA-ceRNA network patterns in the hippocampus of APP/PS1 mice. Results: In our study, 70 dysregulated circRNAs, 39 dysregulated miRNAs and 121 dysregulated mRNAs were identified between the APP/PS1 group and the wild-type group at 8 months in the hippocampus of the mice. Through correlation analysis, we identified 11 dysregulated circRNAs, 7 dysregulated miRNAs and 8 dysregulated mRNAs forming 16 relationships in the circRNA-miRNA-mRNA regulatory network. Gene ontology (GO) analysis indicated that the dysregulated circRNAs were most enriched in biological metabolic processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the dysregulation of circRNAs was enriched in the cGMP-PKG signaling pathway, cAMP signaling pathway, Hippo signaling pathway, platelet activation, long-term potentiation and axon guidance. In addition, our findings preliminarily verified that the novel_circ_0003012/mmu-miR-298-3p/Smoc2 signaling axis may regulate the pathophysiology of AD by affecting the cGMP-PKG signaling pathway. Conclusions: These newly identified circRNAs in networks and signaling pathways reveal potential diagnostic or therapeutic targets for AD.	NA	Front Mol Neurosci. 2021 May 21;14:665788. doi: 10.3389/fnmol.2021.665788. eCollection 2021.
3798	Circular RNA	Circ_0003012	miR-298-3p	Smoc2	the hippocampus of the mice	Alzheimers Disease	Mus musculus (mouse)	RACE;RNA sequencing;	34093124	CircRNA-ceRNA Network Revealing the Potential Regulatory Roles of CircRNA in Alzheimer's Disease Involved the cGMP-PKG Signal Pathway.	Background: Alzheimer's disease (AD) is a chronic progressive neurodegenerative disease. The characteristic pathologies include extracellular senile plaques formed by β-amyloid protein deposition, neurofibrillary tangles formed by hyperphosphorylation of tau protein, and neuronal loss with glial cell hyperplasia. Circular RNAs (circRNAs) are rich in miRNA-binding sites (miRNA response elements, MREs), which serve as miRNA sponges or competitive endogenous RNAs (ceRNAs). Although several research groups have identified dysregulated circRNAs in the cerebral cortex of SAMP8 mice or APP/PS1 mice using deep RNA-seq analysis, we need to further explore circRNA expression patterns, targets, functions and the signaling pathways involved in the pathogenesis of AD and in particular the hippocampal circRNA expression profiles in AD. Methods: We used deep RNA sequencing to investigate circRNA-ceRNA network patterns in the hippocampus of APP/PS1 mice. Results: In our study, 70 dysregulated circRNAs, 39 dysregulated miRNAs and 121 dysregulated mRNAs were identified between the APP/PS1 group and the wild-type group at 8 months in the hippocampus of the mice. Through correlation analysis, we identified 11 dysregulated circRNAs, 7 dysregulated miRNAs and 8 dysregulated mRNAs forming 16 relationships in the circRNA-miRNA-mRNA regulatory network. Gene ontology (GO) analysis indicated that the dysregulated circRNAs were most enriched in biological metabolic processes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the dysregulation of circRNAs was enriched in the cGMP-PKG signaling pathway, cAMP signaling pathway, Hippo signaling pathway, platelet activation, long-term potentiation and axon guidance. In addition, our findings preliminarily verified that the novel_circ_0003012/mmu-miR-298-3p/Smoc2 signaling axis may regulate the pathophysiology of AD by affecting the cGMP-PKG signaling pathway. Conclusions: These newly identified circRNAs in networks and signaling pathways reveal potential diagnostic or therapeutic targets for AD.	NA	Front Mol Neurosci. 2021 May 21;14:665788. doi: 10.3389/fnmol.2021.665788. eCollection 2021.
3799	LncRNA	NORAD	miR-26a	TGFbR1	HSF cells	Hypertrophic Scar	Homo sapiens (human)	ELISA;qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33857357	LncRNA NORAD regulates scar hypertrophy via miRNA-26a mediating the regulation of TGFβR1/2.	BACKGROUND: Transforming growth factor-β (TGF-β) pathway presents dysregulation in pathological scarring and mediates hypertrophic scar (HS) formation. OBJECTIVES: The study aims to analyze the potential mechanism of long non-coding RNA NORAD (LncRNA NORAD) and microRNA (miR-26a) regulation of the TGF-β pathway in hypertrophic scar fibroblasts (HSFs). MATERIAL AND METHODS: Hypertrophic scar tissues were collected and assayed for LncRNA NORAD, miR-26a, transforming growth factor β receptor I (TGF-βR1) and TGF-βR2, with enzyme-linked immunosorbent assay (ELISA) or qualitative polymerase chain reaction (qPCR). LncRNA NORAD interfering plasmids were transfected into HSFs and induced with TGF-β1. Cell Counting Kit-8 (CCK-8) assays were performed to assess HSF proliferation, and flow cytometry to analyze apoptosis and the cell cycle. TGF-βR1, TGF-βR2, Smad2, and p-Smad2 levels were detected using western blot (WB). The related proteins (p21, cyclin D1 and cyclin-dependent kinase 4 (CDK4)) regulating the cell cycle, and apoptosis-related proteins (caspase-3 and Bcl-2) were also detected using WB. The binding sites of miRNA-26a and LncRNA NORAD, TGF-βR2, or UBE3A were predicted using Starbase and confirmed with dual luciferase reporter assay. RNA immunoprecipitation (RIP) was utilized to explore the interplay of miR-26a with its target genes. RESULTS: LncRNA NORAD is decreased, miR-26a is increased and TGF-β receptors show abnormal expression in scar tissue. LncRNA NORAD knockdown inhibits proliferation of HSF cells induced by TGF-β1 treatment. In addition, cell apoptotic levels are markedly increased and cell numbers in G0/G1 phase are increased. Moreover, the TGF-β/Smad pathway is regulated by decreasing endogenous LncRNA NORAD levels, possibly by affecting the relative levels of TGF-βR1. p21 is notably upregulated, while cyclin D1 and CDK4 are downregulated. Apoptosis-related proteins are significantly affected. LncRNA NORAD may act as a sponge, binding miR-26a and changing its expression. Finally, RIP shows that miR-26a targets the 3'UTRs of TGF-βR2 and UBE3A. CONCLUSIONS: LncRNA NORAD regulates HSF proliferation via miR-26a mediating the regulation of TGF-βR2/R1. LncRNA NORAD/miR-26a could be a potential target for treating HS.	NA	Adv Clin Exp Med. 2021 Apr;30(4):395-403. doi: 10.17219/acem/133482.
3800	LncRNA	NORAD	miR-26a	TGFbR2	HSF cells	Hypertrophic Scar	Homo sapiens (human)	ELISA;qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33857357	LncRNA NORAD regulates scar hypertrophy via miRNA-26a mediating the regulation of TGFβR1/2.	BACKGROUND: Transforming growth factor-β (TGF-β) pathway presents dysregulation in pathological scarring and mediates hypertrophic scar (HS) formation. OBJECTIVES: The study aims to analyze the potential mechanism of long non-coding RNA NORAD (LncRNA NORAD) and microRNA (miR-26a) regulation of the TGF-β pathway in hypertrophic scar fibroblasts (HSFs). MATERIAL AND METHODS: Hypertrophic scar tissues were collected and assayed for LncRNA NORAD, miR-26a, transforming growth factor β receptor I (TGF-βR1) and TGF-βR2, with enzyme-linked immunosorbent assay (ELISA) or qualitative polymerase chain reaction (qPCR). LncRNA NORAD interfering plasmids were transfected into HSFs and induced with TGF-β1. Cell Counting Kit-8 (CCK-8) assays were performed to assess HSF proliferation, and flow cytometry to analyze apoptosis and the cell cycle. TGF-βR1, TGF-βR2, Smad2, and p-Smad2 levels were detected using western blot (WB). The related proteins (p21, cyclin D1 and cyclin-dependent kinase 4 (CDK4)) regulating the cell cycle, and apoptosis-related proteins (caspase-3 and Bcl-2) were also detected using WB. The binding sites of miRNA-26a and LncRNA NORAD, TGF-βR2, or UBE3A were predicted using Starbase and confirmed with dual luciferase reporter assay. RNA immunoprecipitation (RIP) was utilized to explore the interplay of miR-26a with its target genes. RESULTS: LncRNA NORAD is decreased, miR-26a is increased and TGF-β receptors show abnormal expression in scar tissue. LncRNA NORAD knockdown inhibits proliferation of HSF cells induced by TGF-β1 treatment. In addition, cell apoptotic levels are markedly increased and cell numbers in G0/G1 phase are increased. Moreover, the TGF-β/Smad pathway is regulated by decreasing endogenous LncRNA NORAD levels, possibly by affecting the relative levels of TGF-βR1. p21 is notably upregulated, while cyclin D1 and CDK4 are downregulated. Apoptosis-related proteins are significantly affected. LncRNA NORAD may act as a sponge, binding miR-26a and changing its expression. Finally, RIP shows that miR-26a targets the 3'UTRs of TGF-βR2 and UBE3A. CONCLUSIONS: LncRNA NORAD regulates HSF proliferation via miR-26a mediating the regulation of TGF-βR2/R1. LncRNA NORAD/miR-26a could be a potential target for treating HS.	NA	Adv Clin Exp Med. 2021 Apr;30(4):395-403. doi: 10.17219/acem/133482.
3801	LncRNA	NKILA	miR-140-5p	CLDN2	HK2 cells	Acute Kidney Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33932903	LncRNA NKILA knockdown promotes cell viability and represses cell apoptosis, autophagy and inflammation in lipopolysaccharide-induced sepsis model by regulating miR-140-5p/CLDN2 axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) play vital roles in human diseases, including sepsis-induced acute kidney injury (AKI). Here, we aimed to investigate the functions of lncRNA NKILA in sepsis-engendered AKI. METHODS: HK2 cells stimulated with LPS were used to mimic sepsis-induced AKI in vitro. qRT-PCR was conducted for lncRNA NKILA and miR-140-5p levels. Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis were employed to analyze cell viability and apoptosis. Western blot assay was utilized to measured protein levels. ELISA kits were used to examine the concentrations of IL-6, IL-1β and TNF-α. Dual-luciferase reporter assay was utilized to analyze the relationships among lncRNA NKILA, miR-140-5p and claudin 2 (CLDN2). RESULTS: LPS restrained HK2 cell viability and accelerated cell apoptosis and autophagy. LncRNA NKILA was increased in LPS-treated HK2 cells. LncRNA NKILA silencing reversed the promotional influence of LPS on cell progression in HK2 cells. miR-140-5p inhibition ameliorated lncRNA NKILA knockdown-mediated cell injury in LPS-mediated HK2 cells. CLDN2 was the target of miR-140-5p. MiR-140-5p elevation promoted cell viability and suppressed cell apoptosis, autophagy and inflammation in LPS-induced HK2 cells, with CLDN2 elevation overturned the effects. CONCLUSION: LncRNA NKILA silencing protected HK2 cells from LPS-induced impairments by reducing CLDN2 through sponging miR-140-5p.	NA	Biochem Biophys Res Commun. 2021 Jun 25;559:8-14. doi: 10.1016/j.bbrc.2021.04.074. Epub 2021 Apr 28.
3802	LncRNA	NEAT1	miR-140	RhoA	NA	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	qRT-PCR	34060267	Long non-coding NEAT1 weakens the protective role of sevoflurane on myocardial ischemia/reperfusion injury by mediating the microRNA-140/RhoA axis.	The function of long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) has been revealed in injury caused by myocardial ischemia/reperfusion (I/R), however, its association with Sevoflurane (Sev), an anesthetic effective for regulating inflammation and oxidative stress, is not yet clear in I/R injury. The aim of this study was to functionally validate and elucidate the mechanism-of-action for Sev-mediated NEAT1 in myocardial I/R injury. Firstly, reduced NEAT1 was revealed in myocardial I/R injured mice treated with Sev. Moreover, restoration of NEAT1 could repress the alleviating role of Sev in cardiac function, infarct size and myocardial apoptosis in mice, while miR-140 was remarkably enhanced in myocardial tissues from mice treated with Sev. Furthermore, miR-140 was suggested and authenticated as a downstream biomolecule of NEAT1 with the help of a bioinformatics tool. Interestingly, miR-140 inhibitor played the same role as NEAT1 overexpression on the cardiac function, infarct size and apoptosis of mice. Finally, it was manifested that RhoA was a putative target of miR-140, which functioned importantly in the Sev/miR-140-mediated myocardial I/R injury. All in all, NEAT1 knockdown contributed to Sev-mediated myocardial I/R injury alleviation via the miR-140/RhoA axis.	NA	J Biol Regul Homeost Agents. 2021 Jun 1;35(3). doi: 10.23812/20-653-A.
3803	LncRNA	NEAT1	miR-148b-3p	ICAM-1	human umbilical vein endothelial cells	Inflammatory Responses In Coronary Slow Flow	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34135616	LncRNA NEAT1 Promote Inflammatory Responses in Coronary Slow Flow Through Regulating miR-148b-3p/ICAM-1 Axis.	BACKGROUND: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown. PATIENTS AND METHODS: Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5-Ethynyl-2'-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay. RESULTS: This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis. CONCLUSION: This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.	NA	J Inflamm Res. 2021 Jun 9;14:2445-2463. doi: 10.2147/JIR.S312583. eCollection 2021.
3804	LncRNA	NEAT1	miR-150-5p	DRP1	HK-2 cells	Diabetic Nephropathy	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qPCR;RT-qPCR;RACE;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33914383	LncRNA NEAT1 accelerates renal tubular epithelial cell damage by modulating mitophagy via miR-150-5p-DRP1 axis in diabetic nephropathy.	NEW FINDINGS: What is the central question of this study Diabetic nephropathy (DN) is a severe complication of diabetes correlated with a higher mortality rate in diabetic patients. Renal tubular injury participates in the pathogenesis of DN. We aimed to uncover the biological function of the NEAT1-miR-150-5p-DRP1 axis in an in vitro model of DN and elaborate the potential mechanisms. What is the main finding and its importance NEAT1 facilitated high glucose-induced damage in HK-2 cells by reducing mitophagy via the miR-150-5p-DRP1 axis, which sheds light on DN pathogenesis and reveals a potential treatment for DN. ABSTRACT: Diabetic nephropathy (DN) is a severe complication in diabetic patients, with a high mortality rate. Renal tubular injury is involved in the pathogenesis of DN. In this study, we aimed to uncover the regulatory roles of the NEAT1-miR-150-5p-DRP1 axis in an in vitro model of DN and its possible mechanisms. High glucose-challenged HK-2 cells were used as an in vitro DN model. NEAT1, miR-150-5p and DRP1 levels were assessed by RT-qPCR. Cell viability was determined by the MTT assay. MitoSOX Red and JC-1 were used to evaluate intracellular production of reactive oxygen species and mitochondrial membrane potential, respectively. Lactate dehydrogenase release and superoxide dismutase activity were assessed with commercial kits. The protein levels of DRP1, p62, BECN1(beclin 1) and BNIP3 were determined by western blotting. The interaction between NEAT1 (DRP1) and miR-150-5p was verified by a dual-luciferase reporter assay and an RNA immunoprecipitation assay. Our results showed that in response to high glucose the NEAT1 and DRP1 levels were upregulated, whereas the miR-150-5p level was downregulated in HK-2 cells. Knockdown of NEAT1 or DRP1 in high glucose-challenged HK-2 cells inhibited excessive reactive oxygen species production and lactate dehydrogenase release, increased cell viability, mitochondrial membrane potential and superoxide dismutase activity and enhanced mitophagy. Inhibition of miR-150-5p resulted in the opposite results. Mechanistically, NEAT1 sponged miR-150-5p to increase the DRP1 level. Moreover, silencing of NEAT1 or DRP1 could counteract miR-150-5p inhibition-induced deleterious effects. Collectively, our findings indicate that NEAT1 facilitates high glucose-induced damage in HK-2 cells by suppressing mitophagy via the miR-150-5p-DRP 1 axis, which sheds light on a novel mechanism of DN.	NA	Exp Physiol. 2021 Apr 29. doi: 10.1113/EP089547.
3805	LncRNA	NEAT1	miR-146b	NA	HFL1 cells	Infantile Pneumonia	Homo sapiens (human)	qPCR;	33978942	LncRNA NEAT1 Regulates Infantile Pneumonia by Sponging miR-146b.	This study designed to investigate the potential role of lncRNA NEAT1/miR-146b in infantile pneumonia. In this study, 58 children with pneumonia and 58 healthy children collected for routine examination from December 2016 to January 2019. The lncRNA NEAT1 and miR-146b expression levels were detected by qPCR in both groups. The pneumonia model was established by inducing human embryonic lung fibroblasts HFL1 with LPS, and then transfected with lncRNA NEAT1 inhibition and miR-146b over-expression vector to observe the effect on cell viability and apoptosis after induction. Starbase predicted the binding site between lncRNA NEAT1 and miR-146b, and the targeted relationship between them was detected by dual luciferase reporter gene. The relative expression of lncRNA NEAT1 in serum of infantile pneumonia was up-regulated. Knocking down lncRNA NEAT1 promotes cell growth and reduces apoptosis in LPS-induced HFL1 cells. Results showed that the fluorescence activity of lncRNA NEAT1 obviously reduced when combined with miR-146b. In conclusion, the relative expression of miR-146b in serum of infantile pneumonia decreased, and over-expressing it could promote LPS-induced cell viability and reduce apoptosis. Taken together, this study demonstrated that the lncRNA NEAT1 regulates infantile pneumonia by sponging miR-146b.	NA	Mol Biotechnol. 2021 May 12. doi: 10.1007/s12033-021-00331-w.
3806	LncRNA	NEAT1	miR-411-5p	PTEN	HTR8/SVneo cells	Preeclampsia	Homo sapiens (human)	Dual-luciferase reporter assay;RNA pull-down assay;Luciferase reporter assay;RNA pull-down;	33876722	Interference with lncRNA NEAT1 promotes the proliferation, migration, and invasion of trophoblasts by upregulating miR-411-5p and inhibiting PTEN expression.	Background: Preeclampsia (PE) is an idiopathic hypertensive disorder of pregnancy, which is related to abnormal placental villi development. Our previous study has found that lncRNA NEAT1 promotes apoptosis of trophoblasts, but the role of NEAT1 in proliferation, migration, and invasion is still unclear. This study explores the role of NEAT1 in proliferation, migration, and invasion of trophoblasts.Methods: NEAT1 and miR-411-5p levels were detected by quantitative real-time PCR. Colony formation assay detected cell proliferation and transwell assay detected cell migration and invasion. Dual-luciferase reporter assay detected the binding between NEAT1 and miR-411-5p as well as the binding between miR-411-5p and PTEN. RNA pull-down assay detected the combination between NEAT1 and miR-411-5p.Result: NEAT1 was increased and miR-411-5p was reduced in PE patients and human trophoblasts (HTR8/SVneo cells) that were induced with H(2)O(2). Interference with NEAT1 promoted cell proliferation, migration, and invasion, and the miR-411-5p inhibitor reversed the effect of siRNA-NEAT1. The expression of PTEN was promoted in PE patients and HTR8/SVneo cells that were induced with H(2)O(2), while the miR-411-5p mimic inhibited PTEN expression, and the plasmid-mediated PTEN overexpression reversed the effect of the miR-411-5p mimic. Besides, under H(2)O(2) induction, the miR-411-5p mimic promoted cell proliferation, migration, and invasion, and the plasmid-mediated PTEN overexpression reversed the effect of the miR-411-5p mimic.Conclusion: Interference with lncRNA NEAT1 promoted the proliferation, migration, and invasion of trophoblasts and alleviated the development of PE, which was partly mediated by upregulating miR-411-5p and inhibiting PTEN expression.	NA	Immunopharmacol Immunotoxicol. 2021 Jun;43(3):334-342. doi: 10.1080/08923973.2021.1910834. Epub 2021 Apr 20.
3807	LncRNA	NEAT1	miR-16-5p	BRD4	lung tissues	Lung Injury	Homo sapiens (human)	qRT-PCR	33962228	LncRNA NEAT1 inhibition upregulates miR-16-5p to restrain the progression of sepsis-induced lung injury via suppressing BRD4 in a mouse model.	OBJECTIVE: Long non-coding RNAs (lncRNAs) are known to sponge microRNAs (miRNAs) to regulate biological processes. However, the role of nuclear paraspeckle assembly transcript 1 (NEAT1) binding miR-16-5p in sepsis-induced lung injury remains largely unknown. We aim to explore the effect of NEAT1 sponging miR-16-5p on sepsis-induced lung injury via regulating bromodomain containing 4 (BRD4). METHODS: A mouse model of sepsis-induced lung injury was established. Expression of NEAT1, miR-16-5p and BRD4 was determined. The pulmonary edema, myeloperoxidase (MPO) activity, pathological changes, levels of inflammatory factors, cell viability and apoptosis in mouse lung tissues were evaluated. The binding relationships between NEAT1 and miR-16-5p, and between miR-16-5p and BRD4 were confirmed. RESULTS: NEAT1 and BRD4 were upregulated while miR-16-5p was downregulated in sepsis-induced lung injury. NEAT1 inhibition or miR-16-5p elevation suppressed pulmonary edema, MPO activity, pathological changes, inflammation and apoptosis, and promoted cell viability in mouse lung tissues. NEAT1 bound with miR-16-5p and miR-16-5p targeted BRD4. CONCLUSION: NEAT1 inhibition upregulates miR-16-5p to repress the progression of sepsis-induced lung injury via downregulating BRD4.	NA	Int Immunopharmacol. 2021 May 4;97:107691. doi: 10.1016/j.intimp.2021.107691.
3808	LncRNA	NEAT1	miR-16-5p	BRD4	lung tissues	Lung Injury	Mus musculus (mouse)	qRT-PCR	33962228	LncRNA NEAT1 inhibition upregulates miR-16-5p to restrain the progression of sepsis-induced lung injury via suppressing BRD4 in a mouse model.	OBJECTIVE: Long non-coding RNAs (lncRNAs) are known to sponge microRNAs (miRNAs) to regulate biological processes. However, the role of nuclear paraspeckle assembly transcript 1 (NEAT1) binding miR-16-5p in sepsis-induced lung injury remains largely unknown. We aim to explore the effect of NEAT1 sponging miR-16-5p on sepsis-induced lung injury via regulating bromodomain containing 4 (BRD4). METHODS: A mouse model of sepsis-induced lung injury was established. Expression of NEAT1, miR-16-5p and BRD4 was determined. The pulmonary edema, myeloperoxidase (MPO) activity, pathological changes, levels of inflammatory factors, cell viability and apoptosis in mouse lung tissues were evaluated. The binding relationships between NEAT1 and miR-16-5p, and between miR-16-5p and BRD4 were confirmed. RESULTS: NEAT1 and BRD4 were upregulated while miR-16-5p was downregulated in sepsis-induced lung injury. NEAT1 inhibition or miR-16-5p elevation suppressed pulmonary edema, MPO activity, pathological changes, inflammation and apoptosis, and promoted cell viability in mouse lung tissues. NEAT1 bound with miR-16-5p and miR-16-5p targeted BRD4. CONCLUSION: NEAT1 inhibition upregulates miR-16-5p to repress the progression of sepsis-induced lung injury via downregulating BRD4.	NA	Int Immunopharmacol. 2021 May 4;97:107691. doi: 10.1016/j.intimp.2021.107691.
3809	LncRNA	NCK1-AS1	miR-22-3p	BCL9	gastric cancer tissues and cells	Gastric Cancer	Homo sapiens (human)	RIP assay;Western blot;	33974352	LncRNA NCK1-AS1 exerts oncogenic property in gastric cancer by targeting the miR-22-3p/BCL9 axis to activate the Wnt/β-catenin signaling.	Long noncoding RNAs (lncRNAs) exert crucial effects on the development of many malignancies, including gastric cancer. Herein, we investigated the role of lncRNA noncatalytic region of tyrosine kinase adaptor protein 1 (NCK1) divergent transcript (NCK1-DT, also known as NCK1-AS1) in gastric cancer. Reverse transcription quantitative polymerase chain reaction demonstrated that NCK1-AS1 exhibited high expression in gastric cancer tissues and cells. In vitro assays including MTT, colony formation, Transwell, wound healing and sphere formation assays indicated that NCK1-AS1 depletion inhibited cell proliferation, migration, invasion and stemness maintenance. Luciferase reporter and RIP assays suggested that NCK1-AS1 functioned as a competitive endogenous RNA (ceRNA) for miR-22-3p to positively modulate BCL9 expression. BCL9 was a target gene of miR-22-3p. According to western blot analysis and TOP/FOP flash assay, NCK1-AS1 activated the Wnt/β-catenin signaling via the miR-22-3p/BCL9 axis. Furthermore, rescue experiments verified that NCK1-AS1 affected cellular processes by activating the Wnt/β-catenin signaling pathway via the miR-22-3p/BCL9 axis. Tumor xenograft model validated that NCK1-AS1 promoted tumor growth in vivo via the Wnt/β-catenin signaling by upregulating BCL9 expression. Overall, NCK1-AS1 functions as an oncogene and promotes gastric cancer progression via the miR-22-3p/BCL9-Wnt/β-catenin signaling pathway.	NA	Environ Toxicol. 2021 May 11. doi: 10.1002/tox.23160.
3810	Circular RNA	NALCN	miR-493-3p	PTEN	glioma cells	Glioma	Homo sapiens (human)	RNA sequencing;	34112159	CircRNA NALCN acts as an miR-493-3p sponge to regulate PTEN expression and inhibit glioma progression.	BACKGROUND: An increasing number of studies have shown that circular RNAs (circRNAs) play important roles in the regulation of tumor progression. Therefore, we explored the expression characteristics, function, and related mechanism of the newly identified circNALCN in glioma. METHODS: RNA sequencing was used to analyze the expression profiles of circRNAs in brain tissue from five glioma cases and four normal controls. Quantitative real-time polymerase chain reaction was implemented to examine the levels of circNALCN, miR-493-3p, and phosphatase and tensin homolog (PTEN). Cell counting kit 8 assays were performed to analyze cell proliferation, and cell migration was assessed by the wound healing test and Transwell assay. Dual-luciferase reporter, fluorescence in situ hybridization, and RNA pulldown assays were performed to confirm the role of circNALCN as an miR-493-3p sponge, weakening the inhibitory effect of miR-493-3p on target PTEN expression. RESULTS: The downregulated expression of circNALCN was observed in both glioma tissues and cell lines. CircNALCN expression was negatively correlated with World Health Organization grade and overall survival in patients with glioma. Functionally, the overexpression of circNALCN significantly inhibited the proliferation and migration of glioma cells, whereas miR-493-3p mimics counteracted these effects. The mechanistic analysis demonstrated that circNALCN acted as a competing endogenous RNA for miR-493-3p to relieve the repressive effects of miR-493-3p on its target, PTEN, suppressing glioma tumorigenesis. CONCLUSIONS: CircNALCN inhibits the progression of glioma through the miR-493-3p/PTEN axis, providing a developable biomarker and therapeutic target for glioma patients.	NA	Cancer Cell Int. 2021 Jun 10;21(1):307. doi: 10.1186/s12935-021-02001-y.
3811	LncRNA	ZSCAN16-AS1	miR-181c-5p	SPAG9	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34097562	ZSCAN16-AS1 expedites hepatocellular carcinoma progression via modulating the miR-181c-5p/SPAG9 axis to activate the JNK pathway.	Hepatocellular carcinoma (HCC) is generally known as one of the most common cancers in the world. Nowadays, interventional therapies such as transcatheter arterial chemoembolization (TACE) have emerged as an efficient therapy for HCC patients. Accumulating evidence has unveiled that long non-coding RNAs (lncRNAs) are crucial regulators in HCC progression. Nonetheless, the biological function of lncRNA zinc finger and SCAN domain containing 16 antisense RNA 1 (ZSCAN16-AS1) in HCC has not been systematically clarified. RT-qPCR was used to test ZSCAN16-AS1 expression in HCC cells. The biological functions of RP11-757 G1.5 on HCC cell proliferation, migration, invasion and apoptosis were investigated by colony formation, EdU, CCK-8 and transwell assays, as well as flow cytometry analysis. RNA immunoprecipitation (RIP), RNA pull-down and luciferase reporter assays were utilized to explore the specific mechanism of ZSCAN16-AS1. ZSCAN16-AS1 was significantly up-regulated in HCC cells. ZSCAN16-AS1 silence inhibited HCC cell proliferation, migration and invasion, while it accelerated HCC cell apoptosis. ZSCAN16-AS1 worked as a competing endogenous RNA (ceRNA) to regulate sperm associated antigen 9 (SPAG9) expression through sponging miR-181 c-5p. Moreover, SPAG9 could activate the c-Jun-N-terminal kinase (JNK) pathway. Taken together, our study elucidated that ZSCAN16-AS1 expedited HCC progression via modulating the miR-181 c-5p/SPAG9 axis to activate the JNK pathway, which might be a highly potential HCC therapy and treatment target.	NA	Cell Cycle. 2021 Jun 7:1-13. doi: 10.1080/15384101.2021.1919828.
3812	LncRNA	MTORT1	miR-26a-5p	CREB1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34141617	Regulatory Mechanisms and Functional Roles of Hypoxia-Induced Long Non-Coding RNA MTORT1 in Breast Cancer Cells.	Long non-coding RNAs (lncRNAs) have been found to participate in multiple genetic pathways in cancer. Also, mitochondria-associated lncRNAs have been discovered to modulate mitochondrial function and metabolism. Previously, we identified oxygen-responsive lncRNAs in MCF-7 breast cancer cells under different oxygen concentrations. Among them, a novel mitochondria-encoded lncRNA, mitochondrial oxygen-responsive transcript 1 (MTORT1), was chosen for further investigation. Nuclear, cytoplasmic, and mitochondrial fractionation assays were performed to evaluate the endogenous expression levels of MTORT1 in breast cancer cells. In vitro proliferation and migration assays were conducted to investigate the functions of MTORT1 in breast cancer cells by knockdown of MTORT1. RNA immunoprecipitation and luciferase reporter assays were used to examine the physical binding between MTORT1 and microRNAs. Our results showed that MTORT1 had low endogenous expression levels in breast cancer cells and was mainly located in the mitochondria. Knockdown of MTORT1 enhanced cell proliferation and migration, implying a tumor suppressor role of this novel mitochondrial lncRNA. MTORT1 served as sponge of miR-26a-5p to up-regulate its target genes, CREB1 and STK4. Our findings shed some light on the characterization, function, and regulatory mechanism of the novel hypoxia-induced mitochondrial lncRNA MTORT1, which functions as a microRNA sponge and may inhibit breast cancer progression. These data suggest that MTORT1 may be a candidate for therapeutic targeting of breast cancer progression.	NA	Front Oncol. 2021 Jun 1;11:663114. doi: 10.3389/fonc.2021.663114. eCollection 2021.
3813	LncRNA	MTORT1	miR-26a-5p	STK4	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34141617	Regulatory Mechanisms and Functional Roles of Hypoxia-Induced Long Non-Coding RNA MTORT1 in Breast Cancer Cells.	Long non-coding RNAs (lncRNAs) have been found to participate in multiple genetic pathways in cancer. Also, mitochondria-associated lncRNAs have been discovered to modulate mitochondrial function and metabolism. Previously, we identified oxygen-responsive lncRNAs in MCF-7 breast cancer cells under different oxygen concentrations. Among them, a novel mitochondria-encoded lncRNA, mitochondrial oxygen-responsive transcript 1 (MTORT1), was chosen for further investigation. Nuclear, cytoplasmic, and mitochondrial fractionation assays were performed to evaluate the endogenous expression levels of MTORT1 in breast cancer cells. In vitro proliferation and migration assays were conducted to investigate the functions of MTORT1 in breast cancer cells by knockdown of MTORT1. RNA immunoprecipitation and luciferase reporter assays were used to examine the physical binding between MTORT1 and microRNAs. Our results showed that MTORT1 had low endogenous expression levels in breast cancer cells and was mainly located in the mitochondria. Knockdown of MTORT1 enhanced cell proliferation and migration, implying a tumor suppressor role of this novel mitochondrial lncRNA. MTORT1 served as sponge of miR-26a-5p to up-regulate its target genes, CREB1 and STK4. Our findings shed some light on the characterization, function, and regulatory mechanism of the novel hypoxia-induced mitochondrial lncRNA MTORT1, which functions as a microRNA sponge and may inhibit breast cancer progression. These data suggest that MTORT1 may be a candidate for therapeutic targeting of breast cancer progression.	NA	Front Oncol. 2021 Jun 1;11:663114. doi: 10.3389/fonc.2021.663114. eCollection 2021.
3814	LncRNA	MST1P2	miR-133b	NA	Hela and SIHA cells,cervical cancer tissues	Cervical Cancer	Homo sapiens (human)	Cell apoptosis assay;qPCR;RT-qPCR;luciferase assay;	34034626	Long noncoding RNA MST1P2 promotes cervical cancer progression by sponging with microRNA miR-133b.	Long noncoding RNA (lnc RNA) is aberrant expressed in many kinds of tumors and may be concerned with the occurrence and progression of tumors. Lnc RNA MST1P2 is increased in cervical cancer (CC), but its mechanism in CC has not been clarified. In this study, RT-qPCR was employed to analyze Lnc MST1P2 and miR-133b expression. CCK8 and cell apoptosis assay detect the proliferation optical density (OD) value and apoptosis rate. Cell metastasis was evaluated by Wound-healing assay and Transwell assay. Dual-Luciferase assay analyzed the relationship between Lnc MST1P2 and miR-133b. In vivo experiment was performed by establishing xenograft animal model. We found that Lnc MST1P2 is obviously overexpression in CC tissues and cells. Si-Lnc MST1P2 obviously repressed cell growth, cell migration, and cell invasion in Hela and SIHA cells. Moreover, Si-Lnc MST1P2 suppressed CC tumorigenesis in vivo. Dual-Luciferase assay and RT-qPCR assay further proved that Lnc MST1P2 has a negative regulation to miR-133b. miR-133b up-regulation inhibited cell viability and metastasis of Hela and SIHA cells. miR-133b inhibition notably decreased the anti-cancer effect of si-Lnc MST1P2. LncRNA MST1P2 serves as a Cervical Cancer oncogene by sponging with miR-133b.	NA	Bioengineered. 2021 Dec;12(1):1851-1860. doi: 10.1080/21655979.2021.1921550.
3815	LncRNA	MIR205HG	miR-2114-3p	TWIST2	OS tissues	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33949284	MIR205 host gene (MIR205HG) drives osteosarcoma metastasis via regulating the microRNA 2114-3p (miR-2114-3p)/twist family bHLH transcription factor 2 (TWIST2) axis.	Osteosarcoma (OS) is an aggressive malignant tumor with a high rate of lung metastasis and a lack of therapeutic targets. Although the anomalous expression of long non-coding RNA (lncRNA) has been extensively documented in human cancer, its contribution to OS metastasis remains poorly understood. In this study, we found that MIR205 host gene (MIR205HG) was significantly elevated in human OS tissues, especially in metastatic OS tissues. Stable knockdown of MIR205HG inhibited OS cell invasion and lung metastatic foci formation, but did not affect cell viability. The vast majority of MIR205HG was situated in the cytosol, and served as a competing endogenous RNA (ceRNA) that directly bound to microRNA 2114-3p (miR-2114-3p), resulting in increased twist family bHLH transcription factor 2 (TWIST2) level. Pre-clinically, high MIR205HG was linked with dismal overall and relapse-free survival. Functionally, the attenuated cell invasion caused by MIR205HG knockdown was effectively rescued by miR-2114-3p silencing or TWIST2 overexpression. Overall, our findings suggest that the previously uncharacterized regulatory axis of MIR205HG/miR-2114-3p/TWIST2 plays a critical role in promoting OS metastasis, which implies a potential therapeutic target in OS patients with metastasis.	NA	Bioengineered. 2021 Dec;12(1):1576-1586. doi: 10.1080/21655979.2021.1920326.
3816	LncRNA	MIR17HG	miR-138-5p	HK1	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	34145399	LncRNA MIR17HG promotes colorectal cancer liver metastasis by mediating a glycolysis-associated positive feedback circuit.	Glycolysis plays a crucial role in reprogramming the metastatic tumor microenvironment. A series of lncRNAs have been identified to function as oncogenic molecules by regulating glycolysis. However, the roles of glycolysis-related lncRNAs in regulating colorectal cancer liver metastasis (CRLM) remain poorly understood. In the present study, the expression of the glycolysis-related lncRNA MIR17HG gradually increased from adjacent normal to CRC to the paired liver metastatic tissues, and high MIR17HG expression predicted poor survival, especially in patients with liver metastasis. Functionally, MIR17HG promoted glycolysis in CRC cells and enhanced their invasion and liver metastasis in vitro and in vivo. Mechanistically, MIR17HG functioned as a ceRNA to regulate HK1 expression by sponging miR-138-5p, resulting in glycolysis in CRC cells and leading to their invasion and liver metastasis. More interestingly, lactate accumulated via glycolysis activated the p38/Elk-1 signaling pathway to promote the transcriptional expression of MIR17HG in CRC cells, forming a positive feedback loop, which eventually resulted in persistent glycolysis and the invasion and liver metastasis of CRC cells. In conclusion, the present study indicates that the lactate-responsive lncRNA MIR17HG, acting as a ceRNA, promotes CRLM through a glycolysis-mediated positive feedback circuit and might be a novel biomarker and therapeutic target for CRLM.	NA	Oncogene. 2021 Jun 18. doi: 10.1038/s41388-021-01859-6.
3817	LncRNA	MIR143HG	miR-1275	ILK	airway granulation fibroblasts	Airway Hyperplastic Stenosis	Homo sapiens (human)	microarray;	34118875	β-elemene alleviates airway stenosis via the ILK/Akt pathway modulated by MIR143HG sponging miR-1275.	BACKGROUND: We have previously found that β-elemene could inhibit the viability of airway granulation fibroblasts and prevent airway hyperplastic stenosis. This study aimed to elucidate the underlying mechanism and protective efficacy of β-elemene in vitro and in vivo. METHODS: Microarray and bioinformatic analysis were used to identify altered pathways related to cell viability in a β-elemene-treated primary cell model and to construct a β-elemene-altered ceRNA network modulating the target pathway. Loss of function and gain of function approaches were performed to examine the role of the ceRNA axis in β-elemene's regulation of the target pathway and cell viability. Additionally, in a β-elemene-treated rabbit model of airway stenosis, endoscopic and histological examinations were used to evaluate its therapeutic efficacy and further verify its mechanism of action. RESULTS: The hyperactive ILK/Akt pathway and dysregulated LncRNA-MIR143HG, which acted as a miR-1275 ceRNA to modulate ILK expression, were suppressed in β-elemene-treated airway granulation fibroblasts; β-elemene suppressed the ILK/Akt pathway via the MIR143HG/miR-1275/ILK axis. Additionally, the cell cycle and apoptotic phenotypes of granulation fibroblasts were altered, consistent with ILK/Akt pathway activity. In vivo application of β-elemene attenuated airway granulation hyperplasia and alleviated scar stricture, and histological detections suggested that β-elemene's effects on the MIR143HG/miR-1275/ILK axis and ILK/Akt pathway were in line with in vitro findings. CONCLUSIONS: MIR143HG and ILK may act as ceRNA to sponge miR-1275. The MIR143HG/miR-1275/ILK axis mediates β-elemene-induced cell cycle arrest and apoptosis of airway granulation fibroblasts by modulating the ILK/Akt pathway, thereby inhibiting airway granulation proliferation and ultimately alleviating airway stenosis.	NA	Cell Mol Biol Lett. 2021 Jun 12;26(1):28. doi: 10.1186/s11658-021-00261-0.
3818	LncRNA	MEG3	miR-149-3p	FOXP3	EC cells	Esophageal Cancer	Homo sapiens (human)	qRT-PCR	34140005	Long non-coding RNA MEG3 mediates the miR-149-3p/FOXP3 axis by reducing p53 ubiquitination to exert a suppressive effect on regulatory T cell differentiation and immune escape in esophageal cancer.	BACKGROUND: Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) has been implicated in the progression of esophageal cancer (EC). However, the specific mechanism of the involvement of MEG3 in EC development in relation to the regulation of immune escape remains uncertain. Thus, the aim of the current study was to investigate the effect of MEG3 on EC via microRNA-149-3p (miR-149-3p). METHODS: Gain- and loss-of-function experiments were initially performed in EC cells in addition to the establishment of a 4-nitroquinoline 1-oxide-induced EC mouse model aimed at evaluating the respective roles of forkhead box P3 (FOXP3), MEG3, miR-149-3p, mouse double minute 2 homolog (MDM2) and p53 in T cell differentiation and immune escape observed in EC. RESULTS: EC tissues were found to exhibit upregulated FOXP3 and MDM2 while MEG3, p53 and miR-149-3p were all downregulated. FOXP3 was confirmed to be a target gene of miR-149-3p with our data suggesting it reduced p53 ubiquitination and degradation by means of inhibiting MDM2. P53 was enriched in the promoter of miR-149-3p to upregulate miR-149-3p. The overexpression of MEG3, p53 or miR-149-3p or silencing FOXP3 was associated with a decline in CD25(+)FOXP3(+)CD4(+) T cells, IL-10(+)CD4(+) T cells and IL-4(+)CD4(+) T cells in spleen tissues, IL-4, and IL-10 levels as well as C-myc, N-myc and Ki-67 expression in EC mice. CONCLUSION: Collectively, MEG3 decreased FOXP3 expression and resulted in repressed regulatory T cell differentiation and immune escape in EC mice by upregulating miR-149-3p via MDM2-mediated p53.	NA	J Transl Med. 2021 Jun 17;19(1):264. doi: 10.1186/s12967-021-02907-1.
3819	LncRNA	MEG3	miR-149-3p	FOXP3	EC cells	Esophageal Cancer	Mus musculus (mouse)	qRT-PCR	34140005	Long non-coding RNA MEG3 mediates the miR-149-3p/FOXP3 axis by reducing p53 ubiquitination to exert a suppressive effect on regulatory T cell differentiation and immune escape in esophageal cancer.	BACKGROUND: Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) has been implicated in the progression of esophageal cancer (EC). However, the specific mechanism of the involvement of MEG3 in EC development in relation to the regulation of immune escape remains uncertain. Thus, the aim of the current study was to investigate the effect of MEG3 on EC via microRNA-149-3p (miR-149-3p). METHODS: Gain- and loss-of-function experiments were initially performed in EC cells in addition to the establishment of a 4-nitroquinoline 1-oxide-induced EC mouse model aimed at evaluating the respective roles of forkhead box P3 (FOXP3), MEG3, miR-149-3p, mouse double minute 2 homolog (MDM2) and p53 in T cell differentiation and immune escape observed in EC. RESULTS: EC tissues were found to exhibit upregulated FOXP3 and MDM2 while MEG3, p53 and miR-149-3p were all downregulated. FOXP3 was confirmed to be a target gene of miR-149-3p with our data suggesting it reduced p53 ubiquitination and degradation by means of inhibiting MDM2. P53 was enriched in the promoter of miR-149-3p to upregulate miR-149-3p. The overexpression of MEG3, p53 or miR-149-3p or silencing FOXP3 was associated with a decline in CD25(+)FOXP3(+)CD4(+) T cells, IL-10(+)CD4(+) T cells and IL-4(+)CD4(+) T cells in spleen tissues, IL-4, and IL-10 levels as well as C-myc, N-myc and Ki-67 expression in EC mice. CONCLUSION: Collectively, MEG3 decreased FOXP3 expression and resulted in repressed regulatory T cell differentiation and immune escape in EC mice by upregulating miR-149-3p via MDM2-mediated p53.	NA	J Transl Med. 2021 Jun 17;19(1):264. doi: 10.1186/s12967-021-02907-1.
3820	LncRNA	MCM3AP-AS1	miR-138-5p	SIRT1	CHON-001 and ATDC5 cells	Osteoarthritis	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	33942704	Long non-coding RNA MCM3AP-AS1 protects chondrocytes ATDC5 and CHON-001 from IL-1β-induced inflammation via regulating miR-138-5p/SIRT1.	Osteoarthritis (OA) is a chronic inflammatory joint disease. Increased apoptosis of chondrocytes contributes to cartilage degradation in OA pathogenesis. The function of lncRNA MCM3AP-AS1 in regulating the viability of chondrocytes still awaits further elaboration. In this work, MCM3AP-AS1, miR-138-5p and SIRT1 mRNA expression levels in OA and normal cartilage tissues were detected by qRT-PCR. Besides, chondrocyte cell lines, CHON-001 and ATDC5 induced by interleukin-1β (IL-1β) were used to initiate the inflammatory response environment of OA. CCK-8 assay was used to examine the cell multiplication; meanwhile, transwell assay was utilized to detect migration. Western blot was adopted to determine SIRT1 expression in chondrocyte. Enzyme-linked immunosorbent assay (ELISA) was performed to evaluate inflammatory factor levels. In addition, the binding sites between MCM3AP-AS1 and miR-138-5p, miR-138-5p and 3'UTR of SIRT1 were validated by dual-luciferase reporter assay, RIP assay or RNA pull-down assay. It was found that MCM3AP-AS1 was declined in OA cartilage tissues, positively interrelated with SIRT1 expression while negatively correlated with miR-138-5p. MCM3AP-AS1 up-regulation enhanced the viability and migration of CHON-001 and ATDC5 cells while restraining the apoptosis and inflammatory response. Additionally, miR-138-5p overexpression counteracted the effects on chondrocytes caused by MCM3AP-AS1 overexpression. MCM3AP-AS1 could adsorb miR-138-5p, and SIRT1 was verified as a target of miR-138-5p, and SIRT1 could be up-regulated by overexpression of MCM3AP-AS1 indirectly. In conclusion, MCM3AP-AS1 has the potential to be the 'ceRNA' to regulate miR-138-5p and SIRT1 in chondrocytes, and to participate in the pathogenesis of OA.	NA	Bioengineered. 2021 Dec;12(1):1445-1456. doi: 10.1080/21655979.2021.1905247.
3821	LncRNA	MALAT1	miR-188-5p	NA	MM cells	Multiple Myeloma	Gallus gallus (chicken)	ChIP;	34107898	Global investigation of estrogen-responsive genes regulating lipid metabolism in the liver of laying hens.	BACKGROUND: Estrogen plays an essential role in female development and reproductive function. In chickens, estrogen is critical for lipid metabolism in the liver. The regulatory molecular network of estrogen in chicken liver is poorly understood. To identify estrogen-responsive genes and estrogen functional sites on a genome-wide scale, we determined expression profiles of mRNAs, lncRNAs, and miRNAs in estrogen-treated ((17β-estradiol)) and control chicken livers using RNA-Sequencing (RNA-Seq) and studied the estrogen receptor α binding sites by ChIP-Sequencing (ChIP-Seq). RESULTS: We identified a total of 990 estrogen-responsive genes, including 962 protein-coding genes, 11 miRNAs, and 17 lncRNAs. Functional enrichment analyses showed that the estrogen-responsive genes were highly enriched in lipid metabolism and biological processes. Integrated analysis of the data of RNA-Seq and ChIP-Seq, identified 191 genes directly targeted by estrogen, including 185 protein-coding genes, 4 miRNAs, and 2 lncRNAs. In vivo and in vitro experiments showed that estrogen decreased the mRNA expression of PPARGC1B, which had been reported to be linked with lipid metabolism, by directly increasing the expression of miR-144-3p. CONCLUSIONS: These results increase our understanding of the functional network of estrogen in chicken liver and also reveal aspects of the molecular mechanism of estrogen-related lipid metabolism.	NA	BMC Genomics. 2021 Jun 9;22(1):428. doi: 10.1186/s12864-021-07679-y.
3822	LncRNA	MALAT1	miR-30e	UPF1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	34036905	Molecular mechanism of the canonical oncogenic lncRNA MALAT1 in gastric cancer.	Many experimental shreds of evidence have shown that lncRNA MALAT1 is related to proliferation ability, invasion and migration ability, autophagy ability, and chemoresistance in gastric cancer. Moreover, MALAT1 is related to metastasis and patient prognosis in gastric cancer. This review aims to reveal the biological functions and specific mechanisms of MALAT1 in gastric cancer. METHODS: After a comprehensive and systematic search in PubMed, various molecular mechanisms of MALAT1 in mediating gastric carcinogenesis are collated and summarized. RESULTS: MALAT1-mediated gastric cancer is involved in a variety of molecular mechanisms. For example, MALAT1 can enhance the proliferation ability of gastric cancer cells by inhibiting the expressions of miR-122, miR-1297, miR-22-3p, miR-202, etc. MALAT1 enhances the metastasis and invasion of gastric cancer by participating in EMT process, PI3-Akt and other pathways. MALAT1 enhances the proliferation and invasion of gastric cancer by inhibiting the function of tumor suppressor gene PCDH10. MALAT1 can increase the autophagy ability of gastric cancer cells by inhibiting miR-183 and increasing the level of autophagy markers. MALAT1 enhances chemical resistance by inhibiting UPF1 and miR-30e levels. CONCLUSIONS: MALAT1 is tightly linked to gastric carcinogenesis through various molecular mechanisms. Moreover, MALAT1 is also closely associated with chemoresistance and poor prognosis in gastric cancer patients, suggesting the possibility of its use as a clinical therapeutic target and a promising independent risk factor for predicting patient prognosis.	NA	Curr Med Chem. 2021 May 21. doi: 10.2174/0929867328666210521213352.
3823	LncRNA	MAFG-AS1	miR-574-5p	SOD2	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33989902	LncRNA MAFG-AS1 affects the tumorigenesis of breast cancer cells via the miR-574-5p/SOD2 axis.	Amounting evidence suggested that long non coding RNAs (lncRNAs) played vital roles in the progression of various cancers. The aim of this study is to examine the biological roles and underlying mechanisms of lncRNA MAFG-AS1 in the tumorigenesis of breast cancer (BC) cells. Here we showed that downregulation of MAFG-AS1 inhibited the viability, migration, and invasion of BC cells. Mechanism investigation showed that inhibition of MAFG-AS1 induced apoptosis via the intrinsic apoptotic pathway and overexpression of Bcl-2 could inhibited it. Further, MAFG-AS1 acts as a sponge of miR-574-5p which directly binds to SOD2 mRNA. Re-expression of SOD2 using a 3'-UTR mutant SOD2 reversed the effects of silencing of MAFG-AS1 on BC cells. Finally, downregulation of MAFG-AS1 inhibited the growth of tumour in vivo. Together, MAFG-AS1 acts as an oncogene via regulation of miR-574-5p/SOD2 axis in BC cells.	NA	Biochem Biophys Res Commun. 2021 Jun 30;560:119-125. doi: 10.1016/j.bbrc.2021.04.133. Epub 2021 May 11.
3824	LncRNA	LYRM4-AS1	miR-6515-5p	GRPR	Bone Marrow Mesenchymal Stem Cells	Osteoarthritis	Homo sapiens (human)	Western blot;Flow Cytometry assay;	34124036	Exosomes Isolated From Bone Marrow Mesenchymal Stem Cells Exert a Protective Effect on Osteoarthritis via lncRNA LYRM4-AS1-GRPR-miR-6515-5p.	OBJECTIVES: The aim of this study was to investigate the effects of exosomes isolated from human bone marrow mesenchymal stem cells (BMSCs) on osteoarthritis (OA) and a competitive endogenous RNA (ceRNA) network. METHODS: Exosomes were isolated from human BMSCs and characterized by transmission electron microscopy (TEM), Nanosight (NTA), and western blotting. Chondrocytes were treated with interleukin-1β (IL-1β) and then transfected with exosomes. Cell viability and apoptosis were determined using Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. Cells with IL-1β and exosomes were sequenced, and differentially expressed lncRNAs (DE-lncRNAs) and miRNAs (DE-miRNAs) were identified. Thereafter, a ceRNA network (LYRM4-AS1-GRPR-miR-6515-5p) was chosen for further validation. RESULTS: TEM, NTA, and western blotting showed that exosomes were successfully isolated, and PKH67 staining showed that exosomes could be taken up by IL-1β-induced chondrocytes. Compared with the control group, IL-1β significantly decreased cell viability and promoted apoptosis (P < 0.05), while exosomes reversed the changes induced by IL-1β. For MMP3, AKT, and GRPR, IL-1β upregulated their expression, while exosomes downregulated their expression. For PTEN, there was no significant difference in PTEN expression between the control and IL-1β groups; however, exosomes markedly upregulated PTEN expression. By sequencing, 907 DE-lncRNAs and 25 DE-miRNAs were identified, and a ceRNA network was constructed. The dual-luciferase reporter gene indicated that LYRM4-AS1, miR-6515-5, and GRPR interacted with each other. The results of cell experiments showed that LYRM4-AS1 regulated the growth of IL-1β-induced chondrocytes by GRPR/miR-6515-5p. CONCLUSION: Exosomes may alleviate OA inflammation by regulating the LYRM4-AS1/GRPR/miR-6515-5p signaling pathway.	NA	Front Cell Dev Biol. 2021 May 28;9:644380. doi: 10.3389/fcell.2021.644380. eCollection 2021.
3825	LncRNA	Loc680254	miR-30d-3p	Psrc1	Schwann cells	Sciatic Nerve Injury	Rattus (rat)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3826	LncRNA	Loc680254	miR-671	Psrc1	Schwann cells	Sciatic Nerve Injury	Rattus (rat)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3827	LncRNA	Loc680254	miR-3473	Ska1	Schwann cells	Sciatic Nerve Injury	Rattus (rat)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3828	LncRNA	Loc680254	miR-3594-5p	Ska1	Schwann cells	Sciatic Nerve Injury	Rattus (rat)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3829	LncRNA	Loc680254	miR-30d-3p	Psrc1	Schwann cells	Sciatic Nerve Injury	Homo sapiens (human)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3830	LncRNA	Loc680254	miR-671	Psrc1	Schwann cells	Sciatic Nerve Injury	Homo sapiens (human)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3831	LncRNA	Loc680254	miR-3473	Ska1	Schwann cells	Sciatic Nerve Injury	Homo sapiens (human)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3832	LncRNA	Loc680254	miR-3594-5p	Ska1	Schwann cells	Sciatic Nerve Injury	Homo sapiens (human)	qRT-PCR	34115425	Loc680254 regulates Schwann cell proliferation through Psrc1 and Ska1 as a microRNA sponge following sciatic nerve injury.	Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.	NA	Glia. 2021 Jun 11. doi: 10.1002/glia.24045.
3833	LncRNA	lncRNA-p21	miR-181	SIRT1	MLE-12 cells	Lps-Induced Acute Lung Injury	Homo sapiens (human)	Luciferase reporter assay;	33891698	Exosomal lncRNA-p21 derived from mesenchymal stem cells protects epithelial cells during LPS-induced acute lung injury by sponging miR-181.	Long noncoding RNAs (lncRNAs) act as essential regulators of various diseases. However, the functions of lncRNAs in sepsis-induced acute lung injury (SALI) remain unclear. Here, we found that lipopolysaccharide could upregulate lncRNA-p21 expression in mesenchymal stem cells (MSCs) in a time- and dose-dependent manner and that lncRNA-p21 was packaged into exosomes. Furthermore, we demonstrated that treatment with exosomal lncRNA-p21 could increase the expression of sirtuin 1 (SIRT1) to protect MLE-12 cells from apoptosis during sepsis. Moreover, we identified SIRT1 as a direct target of miR-181 and found that the level of SIRT1 was negatively correlated with the level of miR-181. The luciferase reporter assay also confirmed the negative correlation between the levels of miR-181 and lncRNA-p21. Our results showed that the lncRNA-p21-induced downregulation of miR-181 might suppress epithelial cell apoptosis and alleviate lung tissue injury by upregulating SIRT1 expression, suggesting the potential therapeutic effects of lncRNA-p21 on SALI. In conclusion, we found that the novel lncRNA-p21/miR-181/SIRT1 pathway may play an important role in the progression of SALI, and MSC-derived exosomes may be a new therapeutic strategy for this disease.	NA	Acta Biochim Biophys Sin (Shanghai). 2021 May 21;53(6):748-757. doi: 10.1093/abbs/gmab043.
3834	LncRNA	LncMyoD	miR-370-3p	ACADSB	C2C12 cell line	Development Of Skeletal Muscle	Homo sapiens (human)	qRT-PCR	33920575	LncMyoD Promotes Skeletal Myogenesis and Regulates Skeletal Muscle Fiber-Type Composition by Sponging miR-370-3p.	The development of skeletal muscle is a highly ordered and complex biological process. Increasing evidence has shown that noncoding RNAs, especially long-noncoding RNAs (lncRNAs) and microRNAs, play a vital role in the development of myogenic processes. In this study, we observed that lncMyoD regulates myogenesis and changes myofiber-type composition. miR-370-3p, which is directly targeted by lncMyoD, promoted myoblast proliferation and inhibited myoblast differentiation in the C2C12 cell line, which serves as a valuable model for studying muscle development. In addition, the inhibition of miR-370-3p promoted fast-twitch fiber transition. Further analysis indicated that acyl-Coenzyme A dehydrogenase, short/branched chain (ACADSB) is a target gene of miR-370-3p, which is also involved in myoblast differentiation and fiber-type transition. Furthermore, our data suggested that miR-370-3p was sponged by lncMyoD. In contrast with miR-370-3p, lncMyoD promoted fast-twitch fiber transition. Taken together, our results suggest that miR-370-3p regulates myoblast differentiation and muscle fiber transition and is sponged by lncMyoD.	NA	Genes (Basel). 2021 Apr 17;12(4):589. doi: 10.3390/genes12040589.
3835	LncRNA	Lnc-CTSLP8	miR-199a-5p	CTSL1	ovarian cancer cells	Ovarian Cancer	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Immunoblotting;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33933142	The lnc-CTSLP8 upregulates CTSL1 as a competitive endogenous RNA and promotes ovarian cancer metastasis.	BACKGROUND: Ovarian cancer is highly lethal and has a poor prognosis due to metastasis. Long non-coding RNAs (lncRNAs) are key regulators of tumor development, but their role in ovarian cancer metastasis remains unclear. METHODS: The expression of lnc-CTSLP8 in ovarian cancer was analyzed in public databases (TCGA and GEO) and validated via qRT-PCR. Lnc-CTSLP8 overexpression and knockout cell lines were constructed using a lentiviral vector and the CRISP/Cas9 system. Cell proliferation, colony formation, migration, and invasion were analyzed. An ovarian orthotopic tumor mouse model was used for the in vivo study. Changes in autophagosomes, autolysosomes, and mitochondria in ovarian cancer cells were observed via transmission electron microscopy. EMT markers were detected by immunoblotting and immunofluorescence assays. RNA immunoprecipitation, RNA pull-down, and dual luciferase reporter assays were performed to confirm the interaction between lnc-CTSLP8 and miR-199a-5p. RESULTS: A novel pseudogene, lnc-CTSLP8, was identified in ovarian cancer, with significantly elevated expression in metastatic tumor tissues compared to primary ovarian tumors. When overexpressed, lnc-CTSLP8 promoted ovarian cancer in vitro and in vivo by acting as a sponge for miR-199a-5p. Autophagy and EMT in ovarian cancer were also enhanced by lnc-CTSLP8. Mechanistically, lnc-CTSLP8 upregulated CTSL1 as a competitive endogenous RNA and exhibited oncogenic effects. Moreover, CTSL1 inhibitor treatment and miR-199a-5p overexpression abrogated the effects of lnc-CTSLP8 overexpression. CONCLUSIONS: lnc-CTSLP8 acts as a ceRNA in ovarian cancer and represents a potential therapeutic target for metastatic ovarian cancer.	NA	J Exp Clin Cancer Res. 2021 May 1;40(1):151. doi: 10.1186/s13046-021-01957-z.
3836	LncRNA	Lnc-CTSLP8	miR-199a-5p	CTSL1	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Immunoblotting;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33933142	The lnc-CTSLP8 upregulates CTSL1 as a competitive endogenous RNA and promotes ovarian cancer metastasis.	BACKGROUND: Ovarian cancer is highly lethal and has a poor prognosis due to metastasis. Long non-coding RNAs (lncRNAs) are key regulators of tumor development, but their role in ovarian cancer metastasis remains unclear. METHODS: The expression of lnc-CTSLP8 in ovarian cancer was analyzed in public databases (TCGA and GEO) and validated via qRT-PCR. Lnc-CTSLP8 overexpression and knockout cell lines were constructed using a lentiviral vector and the CRISP/Cas9 system. Cell proliferation, colony formation, migration, and invasion were analyzed. An ovarian orthotopic tumor mouse model was used for the in vivo study. Changes in autophagosomes, autolysosomes, and mitochondria in ovarian cancer cells were observed via transmission electron microscopy. EMT markers were detected by immunoblotting and immunofluorescence assays. RNA immunoprecipitation, RNA pull-down, and dual luciferase reporter assays were performed to confirm the interaction between lnc-CTSLP8 and miR-199a-5p. RESULTS: A novel pseudogene, lnc-CTSLP8, was identified in ovarian cancer, with significantly elevated expression in metastatic tumor tissues compared to primary ovarian tumors. When overexpressed, lnc-CTSLP8 promoted ovarian cancer in vitro and in vivo by acting as a sponge for miR-199a-5p. Autophagy and EMT in ovarian cancer were also enhanced by lnc-CTSLP8. Mechanistically, lnc-CTSLP8 upregulated CTSL1 as a competitive endogenous RNA and exhibited oncogenic effects. Moreover, CTSL1 inhibitor treatment and miR-199a-5p overexpression abrogated the effects of lnc-CTSLP8 overexpression. CONCLUSIONS: lnc-CTSLP8 acts as a ceRNA in ovarian cancer and represents a potential therapeutic target for metastatic ovarian cancer.	NA	J Exp Clin Cancer Res. 2021 May 1;40(1):151. doi: 10.1186/s13046-021-01957-z.
3837	LncRNA	Lnc-APUE	miR-20b	E2F1	HCC tissues	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33854885	LncRNA Lnc-APUE is Repressed by HNF4α and Promotes G1/S Phase Transition and Tumor Growth by Regulating MiR-20b/E2F1 Axis.	Many long noncoding RNAs (lncRNAs) have been annotated, but their functions remain unknown. The authors found a novel lnc-APUE (lncRNA accelerating proliferation by upregulating E2F1) that is upregulated in different cancer types, including hepatocellular carcinoma (HCC), and high lnc-APUE level is associated with short recurrence-free survival (RFS) of HCC patients. Gain- and loss-of-function analyses showed that lnc-APUE accelerated G1/S transition and tumor cell growth in vitro and allows hepatoma xenografts to grow faster in vivo. Mechanistically, lnc-APUE binds to miR-20b and relieves its repression on E2F1 expression, resulting in increased E2F1 level and accelerated G1/S phase transition and cell proliferation. Consistently, lnc-APUE level is positively associated with the expression of E2F1 and its downstream target genes in HCC tissues. Further investigations disclose that hepatocyte nuclear factor 4 alpha (HNF4α) binds to the lnc-APUE promoter, represses lnc-APUE transcription, then diminishes E2F1 expression and cell proliferation. HNF4α expression is reduced in HCC tissues and low HNF4α level is correlated with high lnc-APUE expression. Collectively, a HNF4α/lnc-APUE/miR-20b/E2F1 axis in which HNF4α represses lnc-APUE expression and keeps E2F1 at a low level is identified. In tumor cells, HNF4α downregulation leads to lnc-APUE upregulation, which prevents the inhibition of miR-20b on E2F1 expression and thereby promotes cell cycle progression and tumor growth.	NA	Adv Sci (Weinh). 2021 Feb 1;8(7):2003094. doi: 10.1002/advs.202003094. eCollection 2021 Apr.
3838	LncRNA	LINC02086	miR-770-5p	SLC26A2	LSCC cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	34130645	Identifying prognostic lncRNAs based on a ceRNA regulatory network in laryngeal squamous cell carcinoma.	PURPOSE: Growing evidence demonstrates that long non-coding RNAs (lncRNAs) play a crucial role as competing endogenous RNAs (ceRNAs) in tumor occurrence. The lncRNAs' functions and clinical significance in laryngeal squamous cell carcinoma (LSCC) remain unclear. The study aims to reveal the lncRNA-associated ceRNA regulatory network of LSCC and clarify its clinical relevance. METHODS: Here, we obtained LSCC transcriptome data from The Cancer Genome Atlas (TCGA) database and identified the differential expression profile of lncRNAs, miRNAs, and mRNAs by the EdgeR R package. The function enrichment analysis of mRNAs was performed using clusterProfiler R package and GSEA3.0. Then, we constructed a ceRNA network and prognosis model based on lncRNAs through bioinformatic methods. Moreover, we explored the functions of prognosis-related lncRNA in LSCC by CCK-8 and transwell assay. RESULTS: 1961 lncRNAs, 69 miRNAs, and 2224 mRNAs were identified as differentially expressed genes in LSCC tissues. According to the transcriptome differential expression profile, a ceRNA network containing 61 lncRNAs, 21 miRNAs, and 77 mRNAs was established. Then, four lncRNAs (AC011933.2, FAM30A, LINC02086, LINC02575) were identified from the ceRNA network to build a prognosis model for LSCC patients. And we found that LINC02086 and LINC02575 promoted the proliferation, migration, and invasion of LSCC cells while AC011933.2 and FAM30A inhibited these biological functions in vitro. Furthermore, we validated that LINc02086/miR-770-5p/SLC26A2 axis promoted migration in LSCC. CONCLUSION: Four lncRNAs of the ceRNA network were abnormally expressed and related to patient prognosis in LSCC. They played a significant role in the progress of LSCC via affecting the proliferation and metastasis of tumor cells.	NA	BMC Cancer. 2021 Jun 15;21(1):705. doi: 10.1186/s12885-021-08422-2.
3839	LncRNA	LINC01605	miR-493-3p	AKT1	human dermal fibroblast (HDF) cells	Hypertrophic Scar	Homo sapiens (human)	qRT-PCR	34011185	Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts.	Activated M2 macrophages are involved in hypertrophic scar (HS) formation via manipulating the differentiation of fibroblasts to myofibroblasts having the proliferative capacity and biological function. However, the function of exosomes derived from M2 macrophages in HS formation is unclear. Thus, this study aims to investigate the role of exosomes derived by M2 in the formation of HS. To understand the effect of exosomes derived from M2 macrophages on formation of HS, M2 macrophages were co-cultured with human dermal fibroblast (HDF) cells. Cell Counting Kit-8 assay was performed to evaluate HDF proliferation. To evaluate the migration and invasion of HDFs, wound-healing and transwell invasion assays were performed, respectively. To investigate the interaction between LINC01605 and miR-493-3p, a dual-luciferase reporter gene assay was adopted; consequently, an interaction between miR-493-3p and AKT1 was detected. Our results demonstrated that exosomes derived from M2 macrophages promoted the proliferation, migration, and invasion of HDFs. Additionally, we found that long noncoding RNA LINC01605, enriched in exosomes derived from M2 macrophages, promoted fibrosis of HDFs and that GW4869, an inhibitor of exosomes, could revert this effect. Mechanistically, LINC01605 promoted fibrosis of HDFs by directly inhibiting the secretion of miR-493-3p, and miR-493-3p down-regulated the expression of AKT1. Exosomes derived from M2 macrophages promote the proliferation and migration of HDFs by transmitting LINC01605, which may activate the AKT signaling pathway by sponging miR-493-3p. Our results provide a novel approach and basis for further investigation of the function of M2 macrophages in HS formation.	NA	Int J Immunopathol Pharmacol. 2021 Jan-Dec;35:20587384211016724. doi: 10.1177/20587384211016724.
3840	LncRNA	LINC01518	miR-216b-5p	NA	human Tenon capsule fibroblast (HTF) cells,situ human glaucoma tissues	Glaucoma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33993456	Long Noncoding RNA LINC01518 Modulates Proliferation and Migration in TGF-β1-Treated Human Tenon Capsule Fibroblast Cells Through the Regulation of hsa-miR-216b-5p.	In this study, we investigated the expression and functions of long noncoding RNAs (LncRNAs) of LINC01518 in an in vitro model of TGF-β1-treated human Tenon capsule fibroblast (HTF) cells. qRT-PCR was used to examine LINC01518 expression in in situ human glaucoma tissues, and in vitro HTF cells treated with TGF-β1. Lentivirus-mediated LINC01518 knockdown was performed in HTF cells to investigate its effect on TGF-β1-induced cell proliferation, migration and autophagy signaling pathway. The potential ceRNA candidate of LINC01518, hsa-miR-216b-5p, was probed by dual-luciferase assay and qRT-PCR. Hsa-miR-216b-5p was also knocked down in LINC01518-downregulated HTF cells to investigate the function of this lncRNA-miRNA epigenetic axis in TGF-β1-treated HTF cells. LINC01518 was upregulated in human glaucoma tissues and cultured HTF cells. LINC01518 downregulation significantly suppressed TGF-β1-induced cell proliferation, migration and autophagy signaling pathway in HTF cells. Hsa-miR-216b-5p was confirmed to be a ceRNA target of LINC01518. Knocking down hsa-miR-216b-5p reversed the suppressing effects of LINC01518 downregulation in TGF-β1-treated HTF cells. Our study demonstrated that LINC01518 is a functional factor in regulating proliferation and migration in TGF-β1-treated HTF cells, and hsa-miR-216b -5p may also be involved. Targeting the epigenetic axis of LINC01518/hsa-miR-216b-5p may provide new insight into the pathological development of human glaucoma.	NA	Neuromolecular Med. 2021 May 15. doi: 10.1007/s12017-021-08662-2.
3841	LncRNA	LINC01503	miR-615-3p	CCND1	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	34149919	Upregulation of LINC01503 promotes cervical cancer progression by targeting the miR-615-3p/CCND1 axis.	Mounting evidence indicates that long non-coding RNAs influence the progression of cervical cancer, but the precise function of LINC01503 in the pathogenesis of the disease remains unknown. Here, we found higher levels of LINC01503 in cervical cancer tissues. High LINC01503 expression was associated with enhanced progression of cervical cancer as indicated by advanced FIGO stage, increased metastasis of tumor cells to lymph nodes, and invasion into deeper cervical tissues. LINC01503 inhibition markedly suppressed the invasion and proliferative ability of tumor cells. Mechanistically, LINC01503 was demonstrated to negatively modulate the expression of miR-615-3p in cervical cancer. CCND1 was found to be a target of miR-615-3p. Rescue experiments indicated that LINC01503 inhibition suppressed the invasion and proliferative ability of the tumor cells, a phenomenon that was reversed following miR-615-3p inhibition or CCND1 overexpression. Collectively, these data indicate that LINC01503 enhances the progression of cervical cancer cells via interaction with miR-615-3p/CCND1 axis.	NA	J Cancer. 2021 Jun 1;12(15):4552-4560. doi: 10.7150/jca.54148. eCollection 2021.
3842	LncRNA	LINC01278	miR-500b-5p	ACTG2	HEK293T cells	Aortic Dissection	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;Luciferase reporter assay;	33910387	LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.	Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. We integrated the mRNA microarray data set with GSE52093 to determine the differentially expressed genes. Bioinformatic analysis, including Gene Expression Omnibus 2R, Venn diagram analysis, gene ontology, pathway enrichment, and protein-protein interaction networks were used to identify the target lncRNA, microRNA, and mRNA involved in AD. Subsequently, we validated the bioinformatics data using techniques in molecular biology in human tissues and VSMCs. Linc01278, microRNA-500b-5p, and ACTG2 played an important role in the vascular smooth muscle contraction pathway. Linc01278 and ACTG2 were downregulated and miR-500b-5p was upregulated in AD tissues. Molecular markers of VSMC phenotypic switching, including SM22α, SMA, calponin, and MYH11, were downregulated in AD tissues. Plasmid-based overexpression and RNA interference-mediated downregulation of linc01278 weakened and enhanced VSMC proliferation and phenotypic switching, respectively. Dual-luciferase reporter assays confirmed that linc01278 regulated miR-500b-5p that directly targeted ACTG2 in HEK293T cells. Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD.	NA	J Am Heart Assoc. 2021 May 4;10(9):e018062. doi: 10.1161/JAHA.120.018062. Epub 2021 Apr 29.
3843	LncRNA	LINC01272	miR-876	ITGB2	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;	34093798	LINC01272/miR-876/ITGB2 axis facilitates the metastasis of colorectal cancer via epithelial-mesenchymal transition.	Background: At the time of diagnosis, colorectal cancer (CRC) patients are usually in an advanced stage of disease, which is accompanied by metastasis. Long noncoding RNAs (lncRNAs) play critical regulatory roles in cancer biology. However, the contributions of lncRNA LINC01272 to CRC remain elusive. Methods: Bioinformatics and the survminer R package were used to predict intermolecular correlations and prognostic indicators. Quantitative real-time PCR was used to examine molecular expression. In vitro experiments, including migration assays, invasion assays, and wound healing assays, were used to investigate the effects of LINC01272, ITGB2 and miR-876 on CRC cell migration and invasion abilities. Furthermore, a dual-luciferase reporter gene assay was performed to explore the potential mechanism by which LINC01272 contributes to CRC. Results: We found that LINC01272 was highly expressed in multiple cancers and closely related to core epithelial-mesenchymal transition (EMT) factors and that high levels of LINC01272 are associated with a poor prognosis in CRC patients. qRT-PCR revealed that LINC01272 was highly expressed and negatively associated with miR-876 in CRC. Additionally, LINC01272 or ITGB2 silencing reduced, while miR-876 overexpression promoted, the invasiveness and metastatic capacity of CRC cells in vitro. Moreover, LINC01272 potentially targeted miR-876, and miR-876 potentially targeted ITGB2. Conclusion: LINC01272 was highly expressed in CRC and predicted a poor prognosis. LINC01272 promoted EMT and metastasis by regulating miR-876/ITGB2 to act as an oncogene in CRC. LINC01272 may be a promising prognostic biomarker and therapeutic target for the treatment of CRC patients in the future.	NA	J Cancer. 2021 May 5;12(13):3909-3919. doi: 10.7150/jca.55666. eCollection 2021.
3844	LncRNA	LINC01132	miR-431-5p	SOX9	EOC cells	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34132375	Silencing of the long noncoding RNA LINC01132 alleviates the oncogenicity of epithelial ovarian cancer by regulating the microRNA-431-5p/SOX9 axis.	To date, the role of lncRNA long intergenic non-protein-coding RNA 1132 (LINC01132) expression in epithelial ovarian cancer (EOC) has not been explored. Thus, LINC01132 expression in EOC was assessed and the regulatory activity of LINC01132 on the malignant behaviours of EOC cells was investigated. Additionally, the molecular events that occurred downstream of LINC01132 in EOC cells were also revealed. In the present study, LINC01132 expression in EOC was verified by employing RT-qPCR. The effects of LINC01132 on the aggressive behaviours of EOC cells were revealed utilizing multiple functional experiments. The targeting interaction among LINC01132, microRNA-431-5p (miR-431-5p) and SRY-box 9 (SOX9) was demonstrated by RNA immunoprecipitation and luciferase reporter assay. Herein, LINC01132 was overexpressed in EOC and was significantly associated with poor patient prognosis. Functionally, cell experiments revealed that LINC01132 depletion produced cancer-suppressive effects in EOC cells and regulated cell proliferation, migration, invasion and apoptosis in vitro. Additionally, the loss of LINC01132 attenuated tumour growth in vivo. Mechanistically, LINC01132 acted as a competing endogenous RNA by sequestering miR-431-5p and consequently overexpressing SOX9 in EOC cells, forming a LINC01132/miR-431-5p/SOX9 axis. In rescue experiments, miR-431-5p inhibition or SOX9 reintroduction eliminated the anti-tumour effects of LINC01132 silencing on the pathological behaviours of EOC cells. Generally, LINC01132 exhibited oncogenic activities in EOC cells by regulating the outcome of the miR-431-5p/SOX9 axis, providing an effective target for EOC diagnosis, therapy and prognosis evaluation.	NA	Int J Mol Med. 2021 Aug;48(2):151. doi: 10.3892/ijmm.2021.4984. Epub 2021 Jun 16.
3845	LncRNA	LINC01125	miR-19b-3p	TNFAIP3	lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33928340	Discovery of a novel linc01125 isoform in serum exosomes as a promising biomarker for NSCLC diagnosis and survival assessment.	A non-invasive method to distinguish potential lung cancer patients would improve lung cancer prevention. We employed the RNA-sequencing analysis to profile serum exosomal long non-coding RNAs (lncRNAs) from non-small cell lung cancer (NSCLC) patients and pneumonia controls, and then determined the diagnostic and prognostic value of a promising lncRNA in four datasets. We identified 90 dysregulated lncRNAs for NSCLC and found the most significant lncRNA was a novel isoform of linc01125. Serum exosomal linc01125 could distinguish NSCLC cases from disease-free and tuberculosis controls, with the area under the curve values as 0.662 [95% confidence interval (CI) = 0.614-0.711] and 0.624 (95% CI = 0.522-0.725), respectively. High expression of exosomal linc01125 was also correlated with an unfavorable overall survival of NSCLC (hazard ratio = 1.48, 95% CI = 1.05-2.08). Clinic treatment decreased serum exosomal linc01125 in NSCLC patients (P = 0.036). Linc01125 functions to inhibit cancer growth and metastasis via acting as a competing endogenous RNA to up-regulate tumor necrosis factor alpha-induced protein 3 (TNFAIP3) expression by sponging miR-19b-3p. Notably, the oncogenic transformation of 16HBE led to decreased linc01125 in cells but increased linc01125 in cell-derived exosomes. The expression of linc01125 in total exosomes was highly correlated with that in tumor-associated exosomes in serum. Moreover, lung cancer cells were capable of releasing linc01125 into exosomes in vitro and in vivo. Our analyses suggest serum exosomal linc01125 as a promising biomarker for non-invasively diagnosing NSCLC and predicting the prognosis of NSCLC.	NA	Carcinogenesis. 2021 Jun 21;42(6):831-841. doi: 10.1093/carcin/bgab034.
3846	LncRNA	LINC01116	miR-744-5p	HOXB8	pituitary adenoma cells	Pituitary Adenoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;Rescue assay;	34098015	LINC01116 boosts the progression of pituitary adenoma via regulating miR-744-5p/HOXB8 pathway.	Pituitary adenoma (PA) is one of the common intracranial tumors. In order to optimize status quo, seeking out potential biomarkers for pituitary adenoma diagnosis and treatment is urgent and important. Long non-coding RNAs (lncRNAs) have been related with progression of various cancers. Based on this reason and unknown role of long intergenic non-protein coding RNA 1116 (LINC01116) in pituitary adenoma, we aimed to explore the function and molecular mechanism of LINC01116 in pituitary adenoma. The RT-qPCR analysis showed that LINC01116 was abnormally overexpressed in pituitary adenoma cells. Down-regulated LINC01116 effectively suppressed cell proliferation and migration as well as epithelial-mesenchymal transition (EMT) progression in pituitary adenoma. Additionally, LINC01116 could competitively sponge miR-744-5p as shown by RIP, RNA pull down and luciferase reporter assays. Similarly, we also proved that homeobox B8 (HOXB8) was the target gene of miR-744-5p in pituitary adenoma cells. In the end, the rescue assays unmasked that HOXB8 could effectually reverse inhibition effect of LINC016 knockdown on pituitary adenoma cells proliferation, migration and EMT, further suggesting that LINC01116 expedited the pituitary adenoma progression by up-regulating HOXB8. Taken together, LINC01116 boosted the progression of pituitary adenoma cells via regulating miR-744-5p/HOXB8 pathway.	NA	Mol Cell Endocrinol. 2021 Jun 4:111350. doi: 10.1016/j.mce.2021.111350.
3847	LncRNA	LINC01116	miR-744-5p	CDCA4	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	34090440	Long non-coding RNA LINC01116 is activated by EGR1 and facilitates lung adenocarcinoma oncogenicity via targeting miR-744-5p/CDCA4 axis.	BACKGROUND: Lung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer. Nevertheless, the link between long non-coding RNA (lncRNA) LINC01116 and LAD remains poorly investigated. METHODS: QRT-PCR and western blot were applied for quantifying the expression of RNAs and proteins. Both functional experiments assays in vitro and xenografts model in vivo were implemented for analyzing LINC01116 function in LAD while molecular relationship among RNAs was investigated via mechanism experiments. RESULTS: LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1. LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells. MiR-744-5p could bind to LINC01116. MiR-744-5p inhibitor reversed the inhibitory effects of silencing LINC01116 on LAD malignant behaviors. In addition, cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p. Silencing LINC01116 elicited decline in CDCA4 mRNA and protein levels. Moreover, CDCA4 up-regulation could counteract the biological effects of LINC01116 knockdown on LAD cells. CONCLUSION: Our data revealed that LINC01116 promoted malignant behaviors of LAD cells by targeting miR-744-5p/CDCA4 axis, implying the theoretical potential of LINC01116 as a novel target for LAD treatment.	NA	Cancer Cell Int. 2021 Jun 5;21(1):292. doi: 10.1186/s12935-021-01994-w.
3848	LncRNA	LINC00963	miR-320a	XBP1	SUDHL4 cell line	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qPCR;Western blot;	34112145	The regulation of miR-320a/XBP1 axis through LINC00963 for endoplasmic reticulum stress and autophagy in diffuse large B-cell lymphoma.	BACKGROUND: This study incorporates fundamental research referring to considerable amounts of gene-sequencing data and bioinformatics tools to analyze the pathological mechanisms of diffuse large B-cell lymphoma (DLBCL). METHODS: A lncRNA-miRNA-mRNA ceRNA network of DLBCL was constructed through database analysis combining GTEx and TCGA. qPCR was used to detect the expression of LINC00963 and miR-320a in DLBCL cell lines. After LINC00963 or miR-320a overexpression in vitro, western blot was performed to assess the protein levels of UPR sensors (GRP78, p-IRE1, IRE1, active ATF6, ATF4 and XBP1), along with apoptosis markers (Bcl-2, Bax, caspase 3) and autophagy indicators (Beclin1, LC3II, LC3I and p62). Additionally, the expression of LC3 was analyzed through immunofluorescence (IF) assay.  RESULTS: Following LINC00963 overexpression in vitro, SUDHL4 cell line showed a marked increase in the level of UPR-related GRP78, p-IRE1 and spliced XBP-1/XBP-1(s), apoptosis-related Bax and cleaved caspase 3, as well as autophagy-related Beclin1 and LC3II, whereas miR-320a mimic greatly diminished the effects of LINC00963 overexpression. Moreover, LINC00963 targeted miR-320a while miR-320a bound to the 3'UTR of XBP1. It was also found that LINC00963 overexpression resulted in significantly delayed tumor growth in a xenograft model of DLBCL.  CONCLUSION: Mechanistically, LINC00963/miR-320a regulated XBP1-apoptosis pathway and autophagy, implying the therapeutic potential of this pathway for selective targeting. The data presented here illustrated the mechanism of LINC00963/miR-320a/XBP1 in DLBCL for the first time.	NA	Cancer Cell Int. 2021 Jun 10;21(1):305. doi: 10.1186/s12935-021-01992-y.
3849	LncRNA	LINC00963	miR-130a-3p	HSPA8	luminal A and B tumor tissues, two luminal A cell lines (MCF7 and T47D)	Breast Cancer	Homo sapiens (human)	qRT-PCR;	34043149	The potential roles of lncRNAs DUXAP8, LINC00963, and FOXD2-AS1 in luminal breast cancer based on expression analysis and bioinformatic approaches.	Numerous studies have demonstrated that lncRNAs participate in regulatory networks of different cancers. Dysregulation of various lncRNAs such as DUXAP8, LINC00963, and FOXD2-AS1 has been reported in the development of various cancers. The aim of this study was investigation of the importance and potential roles of DUXAP8, LINC00963, and FOXD2-AS1 in ER(+) breast cancer (BC). We examined the expression levels of DUXAP8, LINC00963, and FOXD2-AS1 in 71 luminal A and B tumor tissues and two luminal A cell lines (MCF7 and T47D) compared with adjacent non-tumor tissues and MCF10A cell line by qRT-PCR assay, respectively. For identifying the relation between three lncRNAs and luminal BC, bioinformatic analyses were performed using some databases and software including GENEVESTIGATOR software, GEPIA2, DAVID, REVIGO, STRING, lncATLAS, Kaplan-Meier plotter, starBase, and miRNet tool. The results showed the significant upregulation of all three lncRNAs in luminal A and B tumor specimens and cell lines. Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR(+)) and p53 protein expression in luminal BC patients, respectively. Based on bioinformatic analyses, DUXAP8 can be considered as a prognostic biomarker for patients with luminal BC. DUXAP8, LINC00963, and FOXD2-AS1 are involved in several cancer-associated signaling pathways and multiple cancer-related processes. In addition, bioinformatic analyses indicated that LINC00963/hsa-mir-130a-3p/HSPA8 axis might have potential regulatory role in BC. In conclusion, dysregulation of DUXAP8, LINC00963, and FOXD2-AS1 can play roles in the development of luminal BC. They may exert their functions through involvement in some cancer signaling pathways and processes. In addition, they may interact with miRNAs like predicted interaction of LINC00963 with miR-130a-3p.	NA	Hum Cell. 2021 Jul;34(4):1227-1243. doi: 10.1007/s13577-021-00539-7. Epub 2021 May 27.
3850	LncRNA	LINC00958	miR-510-5p	NA	ESCC cells	OEsophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	34003875	LINC00958 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition of oesophageal squamous cell carcinoma cells.	Oesophageal cancer is one of the deadliest cancers in the world. Oesophageal squamous cell carcinoma (ESCC) is the most prevalent histological type of oesophageal cancer. Oesophageal cancer has a poor prognosis because of its invasiveness. Thus, it is especially important to seek effective treatment methods. Research indicates that long non-coding RNAs (lncRNAs) play a significant role in the occurrence and development of oesophageal cancer. The aim of this study was to describe the role of LINC00958 in ESCC. Bioinformatics and real-time quantitative polymerase chain reaction (RT-qPCR) methods were utilized to predict and verify the expression of LINC00958 in ESCC. Related functional experiments, including cell proliferation, migration and invasion, were performed. In addition, a western blot and a dual luciferase reporter gene experiment were used to study the detailed carcinogenic mechanism of LINC00958. The results indicated there was a high expression of LINC00958 in ESCC, which promoted proliferation, migration, invasion and Epithelial-Mesenchymal Transition (EMT) of ESCC cells, and this effect may be via regulating miR-510-5p.	NA	PLoS One. 2021 May 18;16(5):e0251797. doi: 10.1371/journal.pone.0251797. eCollection 2021.
3851	LncRNA	LINC00922	miR-361-3p	CLDN1	OC tissues and cells	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34116704	The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p.	BACKGROUND: Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC. METHODS: LINC00922 expression in OC tissues and cells was identified by a comprehensive strategy of data miming, computational biology and quantitative real-time polymerase chain reaction (RT-qPCR) experiment. In vitro CCK-8, wound healing, transwell invasion, western blotting and in vivo tumorigenesis assays LINC00922 were conducted to evaluate the functions of LINC00992. Subsequently, bioinformatics technology and dual luciferase reporter assay were performed to confirm the between miR-361-3p and LINC00922 or CLDN1. Finally, rescue experiments were performed to confirm whether LINC00922 effect functions of OC cells through regulation of miR-361-3p. RESULTS: LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. Mechanically, LINC00922 could competitively bind with miR-361-3p to relieve the repressive effect of miR-361-3p on its target gene CLDN1 in OC cells. In addition, silencing miR-361-3p promoted OC cell proliferation, migration, invasion, EMT and Wnt/β-catenin signaling, while LINC00922 knockdown inhibited Wnt/β-catenin signaling by upregulating miR-361-3p. Rescue experiments revealed that LINC00922 knockdown inhibited OC cell proliferation, migration, invasion and EMT by regulating miR-361-3p. CONCLUSION: This study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC.	NA	J Ovarian Res. 2021 Jun 11;14(1):77. doi: 10.1186/s13048-021-00828-7.
3852	LncRNA	LINC00908	miR-671-5p	NA	DLBCL tissues and cell lines	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;luciferase assay;Luciferase reporter assay;RNA immunoprecipitation;	33958893	LINC00908 Promotes Diffuse Large B-Cell Lymphoma Development by Down-Regulating miR-671-5p.	INTRODUCTION: Emerging evidence has revealed that long noncoding RNA (lncRNA) play important role in almost all kinds of human cancers. LINC00908 has been reported to be involved in the development of prostate cancer, colorectal cancer and gastric cancer which was functioned as an oncogene. However, the potential biology role and molecular mechanism of LINC00908 in diffuse large B-cell lymphoma are still unclear. METHODS: LINC00908 and miR-671-5p expression were evaluated in DLBCL tissues and cell lines using RT-qPCR. CCK-8 and transwell assay were used to analyze the in vitro role of LINC00908 in DLBCL progression. The xenograft model was used to explore the in vivo role of LINC00908 in DLBCL growth. The physical interaction between LINC00908 and miR-671-5p was confirmed using bioinformatics analysis and a dual luciferase assay, RIP and RNA pull down. RESULTS: The expression of LINC00908 was markedly up-regulated in diffuse large B-cell lymphoma tissues and cell lines, and the decreased expression of LINC00908 significantly inhibited diffuse large B-cell lymphoma cell proliferation and invasion. Then, we revealed that LINC00908 directly interacted with miR-671-5p, which was down-regulated in diffuse large B-cell lymphoma cells and highly expressed with LINC00908 knockdown. Moreover, luciferase reporter assays and RNA immunoprecipitation (RIP) assay further proved that miR-671-5p is a direct target of LINC00908 in diffuse large B-cell lymphoma cells. Rescue experiments were also performed, and we confirmed that LINC00908 acts as an oncogene role in diffuse large B-cell lymphoma through miR-671-5p. Finally, the influence of LINC00908 silence significantly inhibited diffuse large B-cell lymphoma growth in vivo. CONCLUSION: LINC00908 promotes malignancy of diffuse large B-cell lymphoma through regulating miR-671-5p.	NA	Cancer Manag Res. 2021 Apr 30;13:3589-3599. doi: 10.2147/CMAR.S299715. eCollection 2021.
3853	LncRNA	LINC00473	miR-502-3p	KMT5A	pituitary adenoma (PA) cells	Pituitary Adenoma	Homo sapiens (human)	CCK-8 assay;Flow cytometry assay;qRT-PCR;Flow Cytometry assay;RNA sequencing;	34091587	LncRNA LINC00473 is involved in the progression of invasive pituitary adenoma by upregulating KMT5A via ceRNA-mediated miR-502-3p evasion.	Long noncoding RNAs (lncRNAs) and their crosstalks with other RNAs have been revealed to be closely related to tumorigenesis and development, but their role in invasive pituitary adenoma (IPA) remains largely unclear. In our study, LINC00473 was identified as the most upregulated lncRNA in IPA by whole transcriptome RNA sequencing (RNA-Seq). Further, its related signaling pathway LINC00473/miR-502-3p/KMT5A was obtained by constructing a competing endogenous RNA (ceRNA) regulatory network. Their expression in IPA and non-invasive pituitary adenoma (NIPA) tissues was verified by qRT-PCR. Then the effects and mechanisms of LINC00473 and its ceRNA network on the proliferation of pituitary adenoma (PA) cells were confirmed by gene overexpression or silencing techniques combined with CCK-8 assay, EdU staining, flow cytometry assay, and double luciferase reporter gene assay in PA cell lines AtT-20 and GT1-1 in vitro and in a xenograft model in vivo. LINC00473 is overexpressed in IPA and can promote PA cells proliferation. Mechanistically, overexpression of LINC00473 restricts miR-502-3p through the ceRNA mechanism, upregulates KMT5A expression, and promotes the expression of cyclin D1 and CDK2, which is conducive to the cell cycle process, thereby promoting the proliferation of PA cells, involving IPA progression.	NA	Cell Death Dis. 2021 Jun 5;12(6):580. doi: 10.1038/s41419-021-03861-y.
3854	LncRNA	LINC00473	miR-424-5p	wnt3a	HTR-8/SVneo cells	Preeclampsia	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34109708	Long intergenic noncoding RNA 00473 promoting migration and invasion of trophoblastic cell line HTR-8/SVneo via regulating miR-424-5p-mediated wnt3a/β-catenin signaling pathway.	BACKGROUND: Preeclampsia (PE) is a serious obstetric complication. Recent studies point out that the functions of long intergenic noncoding RNA 00473 (linc00473), miR-424-5p, and Wnt/β-catenin signaling pathway were involved in the invasion and migration of extravillous trophoblast. Here, we investigated the role and mechanism of linc00473 in HTR-8/SVneo trophoblastic cell line and its role in PE. METHOD: The expression levels of linc00473 and miR-424-5p in placental tissues and the transfection efficiency of miR-424-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). HTR-8/SVneo cell invasion and proliferation were determined by transwell and Cell Counting Kit-8 (CCK-8) assays. The protein expressions of wnt3a, p-GSK3β, GSK3β, active β-catenin, and total β-catenin were detected by Western blot. The apoptosis and migration of HTR-8/SVneo cells were detected by flow cytometry and wound healing assays. The targeting relationships between linc00473, miR-424-5p, and wnt3a were predicted by ENCORI database and TargetScan V7.2 and were determined using dual-luciferase reporter assay. RESULTS: The expression level of linc00473 was low and miR-424-5p was high in placenta of PE patients. Linc00473 can target miR-424-5p, while miR-424-5p target wnt3a. High expression of linc00473 and wnt3a promoted cell proliferation, migration, invasion, and inhibited cell apoptosis. However, miR-424-5p mimic inhibited HTR-8/SVneo cells proliferation, migration, invasion, while promoted cell apoptosis, partially reversed the effect of linc00473, while wnt3a overexpression partially counteracted the effect of miR-424-5p mimic. CONCLUSION: Linc00473 mediates the regulation of Wnt/β-catenin signaling pathway by miR-424-5p to affect the invasion and migration ability of trophoblastic cell line HTR-8/SVneo. It indicated that linc00473 is involved in PE and could be a therapeutic target.	NA	J Obstet Gynaecol Res. 2021 Jun 9. doi: 10.1111/jog.14870.
3855	LncRNA	LINC00473	miR-16-5p	CCND2	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33993193	Long intergenic non-coding RNA 00473 promotes proliferation and migration of gastric cancer via the miR-16-5p/CCND2 axis and by regulating AQP3.	Gastric cancer (GC) is one of the most common malignancies worldwide, but its molecular mechanisms remain unclear. Increasing evidence indicates that long non-coding RNAs (LncRNAs) play a pivotal role in various cancers recently. Our present study focused on exploring the function of long intergenic non-coding RNA 00473 (LINC00473) in GC. In this study, we found that LINC00473 expression was aberrantly increased in tumor tissues compared with the paired para-cancerous tissues. The expression of high LINC00473 in GC was notably correlated with a higher risk of lymphatic metastasis, a higher incidence of vascular cancer embolus, and advanced TNM stage. Further experiments showed that the overexpression of LINC00473 could promote the proliferation and metastasis of GC cells both in vitro and in vivo. The apoptosis of GC cells increased significantly by the decrease of LINC00473. Mechanistically, LINC00473 could sponge miR-16-5p in the cytoplasm and relieve its suppression of CCND2. Moreover, AQP3 was found to be a significant downstream target gene for LINC00473 through RNA transcriptome sequencing, as demonstrated by qRT-PCR and western blot. Overexpression of LINC00473 can partially reverse the effects of AQP3 decrease on GC proliferation and metastasis. LINC00473 regulated AQP3 expression through CREB was confirmed by western blot. Our research indicates that LINC00473/miR-16-5p/CCND2 axis plays a role in the proliferation of GC and modulates AQP3 to influence GC cell metastasis, making it a potential therapeutic target for GC.	NA	Cell Death Dis. 2021 May 15;12(5):496. doi: 10.1038/s41419-021-03775-9.
3856	LncRNA	LINC00473	miR-15a-5p	LITAF	Wish and JAR cells	Pre-Eclampsia	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;RNA pull-down;	33908139	LINC00473 downregulation facilitates trophoblast cell migration and invasion via the miR-15a-5p/LITAF axis in pre-eclampsia.	More and more evidence has identified that long non-coding RNAs (lncRNAs) are involved in various biological process of numerous diseases. It has been reported that long intergenic non-protein coding RNA 473 (LINC00473) was associated with pre-eclampsia (PE) development. However, role and molecular mechanism of LINC00473 in PE remains elusive. Therefore, we designed this research to figure out the specific biological function of LINC00473 in trophoblasts. Firstly, we testified expressions of LINC00473 in trophoblasts of PE with RT-qPCR analysis. Then, to probe biological function of LINC00473 in trophoblasts of PE, CCK-8 assay, trans-well assays and western blot analysis were conducted in Wish and JAR cells. As for verifying interaction of microRNA-15a-5p (miR-15a-5p) and LINC00473 or lipopolysaccharide induced TNF factor (LITAF), RNA pull-down and luciferase reporter assays were carried out. Finally, rescue experiments were conducted to probe regulatory pattern of the LINC00473/miR-15a-5p/LITAF axis in trophoblasts of PE. As a result, LINC00473 presented a significant upregulation in trophoblasts of PE. Moreover, LINC00473 knockdown induced trophoblast viability, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in trophoblasts. Additionally, miR-15a-5p interacted with LINC00473 and miR-15a-5p was negatively regulated by LINC00473 in trophoblasts. Simultaneously, miR-15a-5p negatively modulated LITAF in trophoblasts. Moreover, LITAF overexpression or miR-15a-5p downregulation reversed the promotive impact of silenced LINC00473 on trophoblast viability, migration, invasion and EMT. In conclusion, LINC00473 regulated migration and invasion in trophoblasts via the miR-15a-5p/LITAF axis. Our study may provide a novel insight for clinical treatment of PE.	NA	Environ Toxicol. 2021 Apr 28. doi: 10.1002/tox.23157.
3857	LncRNA	LINC00467	miR-494-3p	STAT3	PC tissues and cells	Prostate Cancer	Mus musculus (mouse)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	34094954	LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis.	BACKGROUND: The long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression. METHODS: We used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial-mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis. RESULTS: We established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo. CONCLUSIONS: Our study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.	NA	Front Oncol. 2021 May 19;11:661431. doi: 10.3389/fonc.2021.661431. eCollection 2021.
3858	LncRNA	LINC00467	miR-494-3p	STAT3	PC tissues and cells	Prostate Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	34094954	LINC00467 Promotes Prostate Cancer Progression via M2 Macrophage Polarization and the miR-494-3p/STAT3 Axis.	BACKGROUND: The long non-coding RNA LINC00467 plays a vital role in many malignancies. Nevertheless, the role of LINC00467 in prostate carcinoma (PC) is unknown. Herein, we aimed to explore the mechanism by which LINC00467 regulates PC progression. METHODS: We used bioinformatics analyses and RT-qPCR to investigate the expression of LINC00467 in PC tissues and cells. The function of LINC00467 in the progression of PC was confirmed by loss-of-function experiments. PC cell proliferation was assessed by CCK-8 and EdU assays. The cell cycle progression of PC cells was examined by flow cytometry. Moreover, Transwell assays were used to investigate the migration and invasion of PC cells. Western blot assays were used to detect the expression of factors associated with epithelial-mesenchymal transition. The interactions of LINC00467 with prostate cancer progression and M2 macrophage polarization were confirmed by RT-qPCR. The subcellular localization of LINC00467 was investigated via the fractionation of nuclear and cytoplasmic RNA. Bioinformatics data analysis was used to predict the correlation of LINC00467 expression with miR-494-3p expression. LINC00467/miR-494-3p/STAT3 interactions were identified by using a dual-luciferase reporter system. Finally, the influence of LINC00467 expression on PC progression was investigated with an in vivo nude mouse model of tumorigenesis. RESULTS: We established that LINC00467 expression was upregulated in PC tissues and cells. Downregulated LINC00467 expression inhibited PC cell growth, cell cycle progression, migration, and invasion. Downregulated LINC00467 expression similarly inhibited PC cell migration via M2 macrophage polarization. Western blot analysis showed that LINC00467 could regulate the STAT3 pathway. We established that LINC00467 is mainly localized to the cytoplasm. Bioinformatics analysis and rescue experiments indicated that LINC00467 promotes PC progression via the miR-494-3p/STAT3 axis. Downregulated LINC00467 expression was also able to suppress PC tumor growth in vivo. CONCLUSIONS: Our study reveals that LINC00467 promotes prostate cancer progression via M2 macrophage polarization and the miR-494-3p/STAT3 axis.	NA	Front Oncol. 2021 May 19;11:661431. doi: 10.3389/fonc.2021.661431. eCollection 2021.
3859	LncRNA	LINC00184	miR-23b-3p	ANXA2	cholangiocarcinoma cells	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;RNA pull-down;	33913242	Long noncoding RNA LINC00184 facilitates the proliferation, metastasis, and adenine metabolism of cholangiocarcinoma via modulating hsa-miR-23b-3p/ANXA2 axis.	The purpose of this article was to probe the mechanism underlying long noncoding RNA (lncRNA)-LINC00184 in cholangiocarcinoma development and to investigate the effects of LINC00184 on cholangiocarcinoma. We used bioinformatics to analyze the expression of LINC00184, microRNA (miR)-23b-3p and ANXA2 in cholangiocarcinoma tissues. The levels of LINC00184, miR-23b-3p, and ANXA2 were detected by qRT-PCR. Cell proliferation was tested by CCK8. Transwell assay was used to detect cell invasion and migration. The target connection between LINC00184, miR-23b-3p, or ANXA2 was probed by luciferase reporter assay. RNA pull-down method was employed to test the relationship among LINC00184/miR-23b-3p/ANXA2 in cholangiocarcinoma cells. The Pearson correlation coefficient analyzed was applied to analyze the correlation among LINC00184, miR-23b-3p, and ANXA2. LC-MS/M analysis was used to explore whether the changes of adenine metabolism was affected by LINC00184 in cholangiocarcinoma cells. We discovered that LINC00184 expression was heightened in cholangiocarcinoma patients and cells. Knockdown of LINC00184 repressed cell proliferation, invasion, migration and adenine metabolism in cholangiocarcinoma cells. miR-23b-3p was regarded as a target of LINC00184 and its depletion perversed the inhibitive influence of LINC00184 silencing on cholangiocarcinoma cells. ANXA2 was a target of miR-23b-3p and was negatively modulated by miR-23b-3p. Moreover, ANXA2 was positively modulated by LINC00184 via sponging miR-23b-3p. In short, silencing of LINC00184 suppressed cell proliferation, invasion and migration through over-expression of miR-23b-3p and reducing of ANXA2 in cholangiocarcinoma cells. These findings contribute to understanding the influences of LINC00184, miR-23b-3p, and ANXA2 on cholangiocarcinoma and provide basis for cholangiocarcinoma treatment.	NA	Environ Toxicol. 2021 Apr 29. doi: 10.1002/tox.23154.
3860	LncRNA	KCNQ1OT1	miR-26a-5p	ATG12	the serum of MI patients,I/R mouse, H/R-induced cell model	Myocardial Infarction	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	34089766	LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction.	BACKGROUND: As a dominant cardiovascular disease, myocardial infarction (MI) causes a considerable mortality globally. KCNQ1 overlapping transcript 1 (KCNQ1OT1) was reported to be overexpressed in MI patients. However, the detailed mechanisms remain unclear. METHODS: We analyzed the expression of KCNQ1OT1 in the serum of MI patients, and built ischemia/reperfusion (I/R) mouse and H/R-induced cell model. TTC staining was used to evaluate infarct size in mice. TUNEL was employed to assess cell apoptosis. QRT-PCR was performed to detect the expression of KCNQ1OT1 and miR-26a-5p. The formation of autophagosomes in cells was detected by immunofluorescence. Caspase3 activity was detected by the Caspase-3 Assay Kit. Autophagy and apoptosis-related proteins were assessed by western blotting. Luciferase reporter assay was used to assess the binding relationship of KCNQ1OT1 and miR-26a-5p and miR-20a-5p/ATG12. RESULTS: KCNQ1OT1 was up-regulated while miR-26a-5p was decreased in MI patients, I/R mouse and H/R-induced cell model. KCNQ1OT1 knockdown inhibited cell autophagy and protected cardiomyocytes from apoptosis by up-regulating miR-26a-5p. Either KCNQ1OT1 knockdown or miR-26a-5p mimics caused inhibition of autophagy related 12 homolog (ATG12), which was the direct target of miR-26a-5p. In vivo, KCNQ1OT1 promoted cardiomyocytes apoptosis via miR-26a-5p/ATG12 pathway. CONCLUSION: KCNQ1OT1/miR-26a-5p/ATG12 axis regulated cardiomyocyte autophagy and apoptosis, both in vivo and in vitro. These data supported that KCNQ1OT1 inhibition might be a promising therapeutic option for protection after MI.	NA	Int J Cardiol. 2021 Jun 2:S0167-5273(21)00910-4. doi: 10.1016/j.ijcard.2021.05.053.
3861	LncRNA	KCNQ1OT1	miR-26a-5p	ATG12	the serum of MI patients,I/R mouse, H/R-induced cell model	Myocardial Infarction	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;	34089766	LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction.	BACKGROUND: As a dominant cardiovascular disease, myocardial infarction (MI) causes a considerable mortality globally. KCNQ1 overlapping transcript 1 (KCNQ1OT1) was reported to be overexpressed in MI patients. However, the detailed mechanisms remain unclear. METHODS: We analyzed the expression of KCNQ1OT1 in the serum of MI patients, and built ischemia/reperfusion (I/R) mouse and H/R-induced cell model. TTC staining was used to evaluate infarct size in mice. TUNEL was employed to assess cell apoptosis. QRT-PCR was performed to detect the expression of KCNQ1OT1 and miR-26a-5p. The formation of autophagosomes in cells was detected by immunofluorescence. Caspase3 activity was detected by the Caspase-3 Assay Kit. Autophagy and apoptosis-related proteins were assessed by western blotting. Luciferase reporter assay was used to assess the binding relationship of KCNQ1OT1 and miR-26a-5p and miR-20a-5p/ATG12. RESULTS: KCNQ1OT1 was up-regulated while miR-26a-5p was decreased in MI patients, I/R mouse and H/R-induced cell model. KCNQ1OT1 knockdown inhibited cell autophagy and protected cardiomyocytes from apoptosis by up-regulating miR-26a-5p. Either KCNQ1OT1 knockdown or miR-26a-5p mimics caused inhibition of autophagy related 12 homolog (ATG12), which was the direct target of miR-26a-5p. In vivo, KCNQ1OT1 promoted cardiomyocytes apoptosis via miR-26a-5p/ATG12 pathway. CONCLUSION: KCNQ1OT1/miR-26a-5p/ATG12 axis regulated cardiomyocyte autophagy and apoptosis, both in vivo and in vitro. These data supported that KCNQ1OT1 inhibition might be a promising therapeutic option for protection after MI.	NA	Int J Cardiol. 2021 Jun 2:S0167-5273(21)00910-4. doi: 10.1016/j.ijcard.2021.05.053.
3862	LncRNA	KCNQ1OT1	miR-126-5p	TRPS1	CHON-001 cells	Osteoarthritis	Homo sapiens (human)	MTT assay;qRT-PCR;RACE;Western blot;MTT assay;	34108052	Long non-coding RNA KCNQ1OT1 promotes cell viability and migration as well as inhibiting degradation of CHON-001 cells by regulating miR-126-5p/TRPS1 axis.	BACKGROUND: Osteoarthritis (OA) is defined as a degenerative disease. Pivotal roles of long non-coding RNA (lncRNAs) in OA are widely elucidated. Herein, we intend to explore the function and molecular mechanism of lncRNA KCNQ1OT1 in CHON-001 cells. METHODS: Relative expression of KCNQ1OT1, miR-126-5p and TRPS1 was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined by MTT assay. The migratory ability of chondrocytes was assessed by transwell assay. Western blot was used to determine relative protein expression of collagen II, MMP13 and TRPS1. Dual-luciferase reporter (DLR) assay was applied to test the target of lncRNA KCNQ1OT1 or miR-126-5p. RESULTS: Relative expression of KCNQ1OT1 and TRPS1 was reduced, whereas miR-126-5p was augmented in cartilage tissues of post-traumatic OA patients compared to those of subjects without post-traumatic OA. Increased KCNQ1OT1 or decreased miR-126-5p enhanced cell viability and migration, and repressed extracellular matrix (ECM) degradation in CHON-001 cells. MiR-126-5p was the downstream target of KCNQ1OT1, and it could directly target TRPS1. There was an inverse correlation between KCNQ1OT1 and miR-126-5p or between miR-126-5p and TRPS1. Meantime, there was a positive correlation between KCNQ1OT1 and TRPS1. The promoting impacts of KCNQ1OT1 on cell viability and migration as well as the suppressive impact of KCNQ1OT1 on ECM degradation were partially abolished by miR-126-5p overexpression or TRPS1 knockdown in CHON-001 cells. CONCLUSIONS: Overexpression of KCNQ1OT1 attenuates the development of OA by sponging miR-126-5p to target TRPS1. Our findings may provide a possible therapeutic strategy for human OA in clinic.	NA	Adv Rheumatol. 2021 Jun 9;61(1):31. doi: 10.1186/s42358-021-00187-3.
3863	LncRNA	KCNQ1OT1	miR-30e-3p	NLRP3	HMC3 cells	Neuroinflammation And Neuronal Apoptosis	Homo sapiens (human)	RACE;RNA sequencing;	33932142	Identification of crucial noncoding RNAs and mRNAs in hypertrophic scars via RNA sequencing.	Hypertrophic scarring (HS) is a dermal fibroproliferative disorder characterized by excessive deposition of collagen and other extracellular matrix components. The aim of this study is to explore crucial long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) associated with HS and provide a better understanding of the molecular mechanism of HS. To investigate the lncRNA, circRNA and mRNA expression profiles, we performed RNA sequencing of human HS and normal skin tissues. After the identification of differentially expressed mRNAs (DEmRNAs), lncRNAs (DElncRNAs) and circRNAs (DEcircRNAs), we performed functional enrichment of DEmRNAs. Further on, we constructed DElncRNA/DEcircRNA-DEmRNA coexpression networks and competing endogenous RNA regulatory networks, and performed functional analyses of the DEmRNAs in the constructed networks. In total, 487 DEmRNAs, 92 DElncRNAs and 17 DEcircRNAs were identified. DEmRNAs were significantly enriched in processes such as collagen fibril organization, extracellular matrix-receptor interaction and the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. In addition, we detected 580 DElncRNA-DEmRNA and 505 DEcircRNA-DEmRNA coexpression pairs. The competing endogenous RNA network contained 18 circRNA-microRNA (miRNA) pairs, 18 lncRNA-miRNA pairs and 409 miRNA-mRNA pairs, including 10 circRNAs, 5 lncRNAs, 15 miRNAs and 160 mRNAs. We concluded that MIR503HG/hsa-miR-204-3p/ACAN, MIR503HG/hsa-miR-431-5p/TNFRSF9, MEG3/hsa-miR-6884-5p/ADAMTS14, AC000035.1-ADAMTS14 and hsa_circ_0069865-COMP/ADAM12 interaction pairs may play a central role in HS.	NA	FEBS Open Bio. 2021 Jun;11(6):1673-1684. doi: 10.1002/2211-5463.13167. Epub 2021 May 12.
3864	LncRNA	JPX	miR-18a-5p	HIF-1a	nucleus pulposus cells	Intervertebral Disc Degeneration	Homo sapiens (human)	RNA pull-down assay;luciferase assay;RNA pull-down;	34111667	LncRNA JPX regulates proliferation and apoptosis of nucleus pulposus cells by targeting the miR-18a-5p/HIF-1α/Hippo-YAP pathway.	With the aggravation of global aging, the rapid rise in the obesity rate, and the increasing number of patients with intervertebral disc degeneration (IDD), the principles and mechanism of this disease remain unclear. This study explored the molecular mechanism of IDD treatment through interactions of the lncRNA-miRNA-mRNA-signaling pathways and the effects on the proliferation and apoptosis of human nucleus pulposus cells (HNPCs) cultured in vitro. Our study revealed that lncRNA JPX is expressed at low levels in HNPCs under normoxic conditions. Luciferase and RNA pull-down assays were used to verify that lncRNA JPX directly bound to miR-18a-5p and influenced HNPC proliferation and apoptosis. Subsequently, a luciferase assay confirmed the direct binding of miR-18a-5p to HIF-1α and demonstrated a negative correlation between miR-18a-5p and HIF-1α. In addition, the HIF-1α antagonist reversed the inhibition of the Hippo-YAP pathway by the miR-18a-5p inhibitor. In conclusion, overexpression of lncRNA JPX upregulated HIF-1α by inhibiting the expression of miR-18a-5p, thereby inhibiting the Hippo-YAP pathway. By inhibiting this pathway, JPX overexpression promoted the proliferation of HNPCs and decreased their apoptosis. Therefore, the lncRNA JPX is a potential new target.	NA	Biochem Biophys Res Commun. 2021 Jun 7;566:16-23. doi: 10.1016/j.bbrc.2021.05.075.
3865	LncRNA	INHBA-AS1	miR-141-3p	MCL1	human hypertrophic scar fibroblasts	Hypertrophic Scar	Homo sapiens (human)	qPCR;RT-qPCR;RACE;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33977869	Silencing of long noncoding INHBA antisense RNA1 suppresses proliferation, migration, and extracellular matrix deposition in human hypertrophic scar fibroblasts via regulating microRNA-141-3p/myeloid cell leukemia 1 axis.	Long noncoding RNAs (lncRNAs) play vital roles in the progression of hypertrophic scar (HS). We aimed to explore the effect of lncRNA INHBA Antisense RNA1 (INHBA-AS1) in the formation of HS and identify the potential mechanisms. INHBA-AS1 and microRNA (miR)-141-3p expression in human HS fibroblasts (hHSFs) was determined using RT-qPCR. LncBase online database predicted that miR-141-3p could be a putative target of INHBA-AS1, and the interaction of them was verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Subsequently, following INHBA-AS1 silencing, cell proliferation and migration were evaluated using CCK-8, wound healing and Transwell assays. And rescue experiments were conducted to analyze the impact of INHBA-AS1 and miR-141-3p on HS formation. Immunofluorescence assay was employed to examine the expression of extracellular matrix (ECM)-related proteins. Then, StarBase database predicated that myeloid cell leukemia 1 (MCL1) was a potential target of miR-141-3p, which was verified with luciferase reporter- and RIP assays. Finally, cell function and ECM deposition were determined after MCL1-downregulation. INHBA-AS1 was significantly elevated while miR-141-3p was notably reduced in hHSFs. And it was confirmed that miR-141-3p was directly targeted by INHBA-AS1. Moreover, INHBA-AS1 silencing markedly attenuated the proliferation, migration and ECM accumulation of hHSFs, which were restored after miR-141-3p silencing. Additionally, MCL1 was confirmed as a direct target of miR-141-3p, and MCL1-knockdown remarkably alleviated the proliferation, migration and ECM accumulation of hHSFs. INHBA-AS1-knockdown suppresses the formation of HS by regulating miR-141-3p/MCL1 pathway, suggesting a promising therapeutic target for HS treatment.	NA	Bioengineered. 2021 Dec;12(1):1663-1675. doi: 10.1080/21655979.2021.1919013.
3866	LncRNA	IGF2-AS	miR-3126-5p	KLK4	bone marrow mesenchymal stem cells	Osteogenic Differentiation	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qPCR;RT-qPCR;RT-PCR;Western blot;Luciferase reporter assay;	34101307	LncRNA IGF2-AS promotes the osteogenic differentiation of bone marrow mesenchymal stem cells by sponging miR-3126-5p to upregulate KLK4.	BACKGROUND: Osteoporosis (OP) is a bone disease with a reduced amount and quality of bone. This study was designed to explore the role and mechanism of lncRNA IGF2-AS in the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). METHODS: Human lncRNA and miRNA microarray analyses were performed to detect the differential expression levels of lncRNAs and miRNAs in undifferentiated and osteogenically differentiated BMSCs. LncRNA IGF2-AS, miR-3126-5p, and KLK4 levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The osteogenic differentiation of BMSCs was assessed by alkaline phosphatase (ALP) staining and Alizarin Red staining (ARS). Protein levels of Osterix (Osx), osteocalcin (OCN), and runt-related transcription factor 2 (RUNX2) were examined by RT-PCR and western blot assays. The binding relationship between miR-3126-5p and lncRNA IGF2-AS or KLK4 was predicted by TargetScan (http://www.targetscan.org/vert_72/) and then verified with a dual-luciferase reporter assay. RESULTS: LncRNA IGF2-AS and KLK4 were highly expressed and miR-3126-5p was weakly expressed in osteogenically differentiated BMSCs. Moreover, lncRNA IGF2-AS overexpression enhanced the osteogenic differentiation of BMSCs. In contrast, lncRNA IGF2-AS knockdown showed the opposite trend. Moreover, miR-3126-5p overexpression abolished the lncRNA IGF2-AS-mediated osteogenic differentiation of BMSCs. LncRNA IGF2-AS functions as a sponge of miR-3126-5p to regulate KLK4 expression. CONCLUSION: LncRNA IGF2-AS enhances the osteogenic differentiation of BMSCs by modulating the miR-3126-5p/KLK4 axis, suggesting a promising therapeutic target for bone-related diseases.	NA	J Gene Med. 2021 Jun 7:e3372. doi: 10.1002/jgm.3372.
3867	LncRNA	IGF2-AS	miR-520g	CDH2	trophoblast cells	Recurrent Miscarriage	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;RT-qPCR;RNA immunoprecipitation;Western blot;	34109707	Long non-coding RNA IGF2-AS promotes trophoblast cell proliferation, migration, and invasion by regulating miR-520g/N-cadherin axis.	BACKGROUND: Recurrent miscarriage (RM) is a distressing reproductive issue worldwide. Dysfunction of trophoblasts can trigger numerous unfavorable pregnant outcomes such as RM, stillbirth, and fetal malformation. METHODS: In this text, the roles and molecular basis of long non-coding RNA insulin growth factor 2 antisense (IGF2-AS) in the development of trophoblast cells were further investigated. IGF2-AS, microRNA-520g (miR-520g), and N-cadherin levels were measured by RT-qPCR assay. Cell viability, the number of colonies, cell apoptosis, migration, and invasion were measured by CCK-8 assay, colony formation assay, flow cytometry, transwell migration, and invasion assays, respectively. The relative proteins expression was detected by western blot. RESULTS: The interaction between miR-520g and IGF2-AS or N-cadherin was tested by bioinformatics prediction analysis, and confirmed by dual-luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay. Our data revealed that IGF2-AS and N-cadherin levels were notably decreased, and miR-520g was strikingly increased in the placentas from RM patients. IGF2-AS overexpression promoted cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and hampered cell apoptosis in trophoblast cells, while IGF2-AS deletion exhibited opposite results. Moreover, miR-520g was a target gene of IGF2-AS and negatively regulated by IGF2-AS. MiR-520g inhibitor enhanced the proliferation, migration, and invasion capability of trophoblast cells, suppressed cell apoptosis, and promoted the EMT process. Moreover, the effects of IGF2-AS overexpression on trophoblast cells were reversed by miR-520g upregulation. CONCLUSIONS: These findings indicated that IGF2-AS facilitated trophoblast cell proliferation, migration, invasion, EMT, and suppressed cell apoptosis by regulating miR-520g/N-cadherin axis, providing potential biomarkers for RM.	NA	J Obstet Gynaecol Res. 2021 Jun 9. doi: 10.1111/jog.14886.
3868	Circular RNA	hsa_circ_0049055	miR-345-5p	FZD8	PTC cells	Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34108309	circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility via functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8).	Circular RNA 40S ribosomal protein S28 (circRPS28; hsa_circ_0049055) is upregulated in papillary thyroid carcinoma (PTC) patients. However, its role remained uncovered in the progression of PTC. Above all, expression of circRPS28 was determined in PTC samples by real-time quantitative PCR and circRPS28 was highly expressed in tumor tissues and cells. Besides, circRPS28 was predominantly distributed in the cytoplasm. Functional experiments were launched using colony formation assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2-deoxyuridine (EdU) assay, transwell assays, scratch wound assay, and flow cytometry. As a result, blocking circRPS28 restrained PTC cell viability, EdU positive cell rate, colony formation number, wounding healing rate, and numbers of migration and invasion cells, accompanied with apoptosis rate promotion. These effects paralleled with low B-cell lymphoma (Bcl)-2 level and high Bcl-2-associated X protein (Bax), matrix metalloproteinase-2 (MMP2), and MMP9 levels, as analyzed by western blotting. Overexpressing microRNA (miR)-345-5p exerted similar roles to circRPS28 silencing. Notably, dual-luciferase reporter assay and RNA immunoprecipitation confirmed the target relationship between circRPS28 and miR-345-5p, miR-345-5p and frizzled family receptor 8 (FZD8). Downregulating miR-345-5p abrogated effects of circRPS28 blockage in PTC cells, and restoring FZD8 counteracted miR-345-5p roles, either. Furthermore, xenograft tumor model was established in mice, and exhausting circRPS28 delayed the growth of PTC cells in vivo by regulating miR-345-5p and FZD8. In conclusion, we demonstrated that blocking circRPS28 and/or promoting miR-345-5p suppressed PTC cell growth and motility via regulating FZD8. This study might suggest a novel circRPS28/miR-345-5p/FZD8 competing endogenous RNA pathway in PTC.	NA	Endocr J. 2021 Jun 10. doi: 10.1507/endocrj.EJ21-0072.
3869	Circular RNA	hsa_circ_0044234	miR-135b-5p	GATA3	breast cancer cells	Breast Cancer	Homo sapiens (human)	microarray;qPCR;RT-qPCR;	34126989	Circular RNA hsa_circ_0044234 as distinct molecular signature of triple negative breast cancer: a potential regulator of GATA3.	BACKGROUND: Circular RNAs (circRNAs) have been implicated in the initiation and development of breast cancer as functional non-coding RNAs (ncRNA). The roles of circRNAs as the competing endogenous RNAs (ceRNAs) to sponge microRNAs (miRNAs) have also been indicated. However, the functions of circRNAs in breast cancer have not been totally elucidated. This study aimed to explore the clinical implications and possible roles of circ_0044234 in carcinogenesis of the most problematic BC subtype, triple negative breast cancer (TNBC), which are in desperate need of biomarkers and targeted therapies. METHODS: The importance of circ_0044234 as one of the most dysregulated circRNAs in TNBC was discovered through microarray expression profile analysis. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to confirm the downregulation of circ_0044234 in triple negative tumors and cell lines versus non-triple negative ones. The bioinformatics prediction revealed that circ_0044234 could act as an upstream sponge in the miR-135b/GATA3 axis, two of the most dysregulated transcripts in TNBC. RESULTS: Our experimental investigation of circ_0044234 expressions in various BC subtypes as well as cell lines reveals that TNBC expresses circ_0044234 at a substantially lower level than non-TNBC. The ROC curve analysis indicates that it could be applied as a discriminative biomarker to identify TNBC from other BC subtypes. Moreover, circ_0044234 expression could be an independent prognostic biomarker in BC. Interestingly, a substantial inverse expression correlation was detected between circ_0044234 and miR-135b-5p as well as between miR-135b-5p and GATA3 in breast tumors. CONCLUSIONS: The possible clinical usefulness of circ_0044234 as a promising distinct biomarker and upcoming therapeutic target for TNBC have been indicated in this research. Our comprehensive approach revealed the potential circ_0044234/miR135b-5p/GATA3 ceRNA axis in TNBC.	NA	Cancer Cell Int. 2021 Jun 14;21(1):312. doi: 10.1186/s12935-021-02015-6.
3870	Circular RNA	hsa_circ_0042823	miR-877-5p	FOXM1	AMC-HN-8 cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;	34124974	Hsa_circ_0042823 accelerates cancer progression via miR-877-5p/FOXM1 axis in laryngeal squamous cell carcinoma.	BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumour of the head and neck. Our previous study reveals that the circular RNA (circRNA) hsa_circ_0042823 is abnormally expressed in LSCC, suggesting that hsa_circ_0042823 is closely associated with LSCC. Here, we attempted to explore the molecular mechanism of hsa_circ_0042823 in LSCC. METHODS: Quantitative real-time PCR and western blot were performed to assess the expression of gene and protein in human laryngeal carcinoma cells, TU212 and TU686. MTT and transwell assays were performed to examine cell proliferation, migration and invasion. The relationship among hsa_circ_0042823, miR-877-5p and forkhead box M1 (FOXM1) was verified by luciferase reporter assay. Finally, we constructed a subcutaneous tumour mouse model to analyse in vivo growth of LSCC cells following knockdown of hsa_circ_0042823. RESULTS: Compared with normal human bronchial epithelial cells (HBECs), hsa_circ_0042823 was highly expressed in the LSCC cell lines (AMC-HN-8 and TU686). Further studies demonstrated that hsa_circ_0042823 interacted with miR-877-5p, and FOXM1 was the target of miR-877-5p. Hsa_circ_0042823 promoted the expression of FOXM1 via its ceRNA activity on miR-877-5p. Hsa_circ_0042823 overexpression promoted proliferation, migration and invasion of AMC-HN-8 cells through regulating miR-877-5p/FOXM1 axis. Additionally, inhibition of hsa_circ_0042823 inhibited growth of LSCC in vivo via miR-877-5p/FOXM1 axis. CONCLUSIONS: Hsa_circ_0042823/miR-877-5p/FOXM1 axis participates in the progression of LSCC. This work demonstrates that hsa_circ_0042823 accelerates cancer progression by regulating miR-877-5p/FOXM1 axis in LSCC. Therefore, this study may provide new insights into the pathogenesis of LSCC.KEY MESSAGESHsa_circ_0042823 promotes FOXM1 expression by sponging miR-877-5p.Hsa_circ_0042823 promotes proliferation, migration, invasion of LSCC cells.Hsa_circ_0042823 knockdown inhibits tumour growth of LSCC via miR-877-5p/FOXM1 axis.	NA	Ann Med. 2021 Dec;53(1):960-970. doi: 10.1080/07853890.2021.1934725.
3871	Circular RNA	hsa_circ_0042823	miR-877-5p	FOXM1	AMC-HN-8 cells	Laryngeal Squamous Cell Cancer	Mus musculus (mouse)	Western blot;Luciferase reporter assay;	34124974	Hsa_circ_0042823 accelerates cancer progression via miR-877-5p/FOXM1 axis in laryngeal squamous cell carcinoma.	BACKGROUND: Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumour of the head and neck. Our previous study reveals that the circular RNA (circRNA) hsa_circ_0042823 is abnormally expressed in LSCC, suggesting that hsa_circ_0042823 is closely associated with LSCC. Here, we attempted to explore the molecular mechanism of hsa_circ_0042823 in LSCC. METHODS: Quantitative real-time PCR and western blot were performed to assess the expression of gene and protein in human laryngeal carcinoma cells, TU212 and TU686. MTT and transwell assays were performed to examine cell proliferation, migration and invasion. The relationship among hsa_circ_0042823, miR-877-5p and forkhead box M1 (FOXM1) was verified by luciferase reporter assay. Finally, we constructed a subcutaneous tumour mouse model to analyse in vivo growth of LSCC cells following knockdown of hsa_circ_0042823. RESULTS: Compared with normal human bronchial epithelial cells (HBECs), hsa_circ_0042823 was highly expressed in the LSCC cell lines (AMC-HN-8 and TU686). Further studies demonstrated that hsa_circ_0042823 interacted with miR-877-5p, and FOXM1 was the target of miR-877-5p. Hsa_circ_0042823 promoted the expression of FOXM1 via its ceRNA activity on miR-877-5p. Hsa_circ_0042823 overexpression promoted proliferation, migration and invasion of AMC-HN-8 cells through regulating miR-877-5p/FOXM1 axis. Additionally, inhibition of hsa_circ_0042823 inhibited growth of LSCC in vivo via miR-877-5p/FOXM1 axis. CONCLUSIONS: Hsa_circ_0042823/miR-877-5p/FOXM1 axis participates in the progression of LSCC. This work demonstrates that hsa_circ_0042823 accelerates cancer progression by regulating miR-877-5p/FOXM1 axis in LSCC. Therefore, this study may provide new insights into the pathogenesis of LSCC.KEY MESSAGESHsa_circ_0042823 promotes FOXM1 expression by sponging miR-877-5p.Hsa_circ_0042823 promotes proliferation, migration, invasion of LSCC cells.Hsa_circ_0042823 knockdown inhibits tumour growth of LSCC via miR-877-5p/FOXM1 axis.	NA	Ann Med. 2021 Dec;53(1):960-970. doi: 10.1080/07853890.2021.1934725.
3872	Circular RNA	hsa_circ_0035292	miR-146b-3p	CXCR1	WI-38 cells	Acute Inflammation And Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34151690	The role of circTMOD3 in regulating LPS-induced acute inflammation and injury in human lung fibroblast WI-38 cells.	Circular RNAs (circRNAs) have been implicated in the molecular etiology of pediatric pneumonia. Here, we investigated the precise action of circRNA tropomodulin 3 (circTMOD3, hsa_circ_0035292) in cell injury and inflammation induced by lipopolysaccharide (LPS). Methods: Cell viability was gauged by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis and cycle distribution were assessed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was used to measure interleukin-6 (IL-6), IL-1β and tumor necrosis factor alpha (TNF-α) production. The levels of circTMOD3, microRNA (miR)-146b-3p, and C-X-C motif chemokine receptor 1 (CXCR1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Ribonuclease (RNase) R, Actinomycin D and subcellular localization assays were done to characterize circTMOD3. The direct relationship between miR-146b-3p and circTMOD3 or CXCR1 was confirmed by dual-luciferase reporter assays. Results: Our data showed that LPS induced the expression of circTMOD3 in WI-38 cells. CircTMOD3 was resistant to RNase R and was mainly present in the cytoplasm. Silencing endogenous circTMOD3 alleviated WI-38 cell injury and inflammation triggered by LPS. Mechanistically, circTMOD3 directly targeted miR-146b-3p, and CXCR1 was a direct and functional target of miR-146b-3p. CircTMOD3 regulated LPS-induced cell inflammation and injury by targeting miR-146b-3p, and miR-146b-3p-mediated suppression of CXCR1 impacted LPS-evoked cytotoxicity and inflammation. Furthermore, circTMOD3 functioned as a competing endogenous RNA (ceRNA) for miR-146b-3p to induce CXCR1 expression. Conclusion: Our findings demonstrated the regulation of circTMOD3 in LPS-induced cell injury and inflammation at least partially via miR-146b-3p-independent modulation of CXCR1.	NA	Exp Lung Res. 2021 Jun 20:1-12. doi: 10.1080/01902148.2021.1940376.
3873	Circular RNA	hsa_circ_0025721	miR-4428	CXCL8	CD8 T cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33955785	Identification of an immune signature to predict poor clinical outcome in cervical cancer.	Aim: To explore tumor immune microenvironment and identify immune prognostic-related circRNAs in cervical cancer. Materials & methods: RNA-seq in combination with bioinformatics were performed to establish a prognostic risk model and a circRNAs-miRNAs-CXCL8 network. Results: High-risk group correlated with poor survival outcome, and had lower PD-1 immunogenicity. Additionally, CXCL8 could distinguish normal tissue, low- and high-risk tumor tissues, the expression of which showed an increasing trend among the three groups. RNA-seq and bioinformatics indicated that circRNAs like hsa_circ_0025721 might upregulate CXCL8 through sponging miRNAs including hsa-miR-4428. Conclusion: We constructed an immune risk model related with CD8 T cells to predict the cervical cancer patients' prognosis and explored the abnormal expression mechanism of CXCL8 through the ceRNA mechanism.	NA	Epigenomics. 2021 Jun;13(11):891-907. doi: 10.2217/epi-2020-0437. Epub 2021 May 6.
3874	Circular RNA	hsa_circ_0000117	miR-337-3p	STAT3	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;Rescue assay;	33896365	Circular RNA hsa_circ_0000117 accelerates the proliferation and invasion of gastric cancer cells by regulating the microRNA-337-3p/signal transducer and activator of transcription 3 axis.	Circular RNA hsa_circ_0000117 is reportedly increased in Gastric cancer (GC), however, its role is unexplored. Hsa_circ_0000117 expression and function in GC was investigated using standard cell phenotypic and expression assays. Pull-down and luciferase reporter assays also elucidated hsa_circ_0000117 mechanisms. In the present study, we observed increased hsa_circ_0000117 and signal transducer and activator of transcription 3 (STAT3) expression, while microRNA-337-3p (miR-337-3p) was decreased in GC cells. Depleted hsa_circ_0000117 decreased GC proliferation and invasion. Hsa_circ_0000117 was also identified as a miR-337-3p sponge. Also, STAT3 was identified as a miR-337-3p target. Similarly, rescue assays indicated STAT3 overexpression (or miR-337-3p inhibition) reversed hsa_circ_0000117 effects in GC progression. Thus, our data suggested hsa_circ_0000117 exhibited oncogene properties in combination with the hsa_circ_0000117/miR-337-3p/STAT3 axis in GC, potentially providing a new therapeutic target for GC.Abbreviations GC: gastric cancer; STAT3: Signal transducer and activator of transcription 3; circRNA: Circular RNA; miRNA: microRNA; DMEM: Dulbecco's modified Eagle's medium; FBS: fetal bovine serum; PVDF: polyvinylidene fluoride; CCK-8: Cell counting kit-8; qRT-PCR: Quantitative real-time PCR; SDS-PAGE: sodium dodecyl sulfate polyacrylamide gel electrophoresis; TNM: TNM Classification of Malignant Tumors; mTOR: mechanistic target of rapamycin; ANOVA: one-way analysis of variance.	NA	Bioengineered. 2021 Dec;12(1):1381-1390. doi: 10.1080/21655979.2021.1918992.
3875	LncRNA	HOXA11-AS	miR-124	NA	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR	34117619	Suppression of lncRNA HOXA11-AS/miR-124 Axis Inhibits Glioma Progression.	Our aim was to clarify the regulations of lncRNA HOXA11-AS (HOXA11-AS) played on the progression of glioma as well as to investigate the mechanisms by which HOXA11-AS modulated development of glioma. This study confirmed the regulations of miR-124 and HOXA11-AS on the progression of glioma. Here, HOXA11-AS was overexpressed and miR-124 was underexpressed in glioma. Expression of miR-124 was negatively related to that of HOXA11-AS. Silencing of HOXA11-AS suppressed cell proliferation, invasion, and promoted apoptosis in glioma cells in vitro. Moreover, inhibition of HOXA11-AS expression repressed glioma xenograft tumor growth. Expression of miR-124 was repressed by HOXA11-AS functioning as sponge. In addition, miR-124 knockdown partially abolished the inhibitory roles of HOXA11-AS downregulation in glioma cells. Conclusively, this study suggested that silencing of HOXA11-AS restrained proliferation, invasion, induced apoptosis of glioma cells, and repressed xenograft growth via modulating miR-124 expression and thus inhibited glioma progression.	NA	Cell Biochem Biophys. 2021 Jun 11. doi: 10.1007/s12013-021-01007-7.
3876	LncRNA	HCP5	miR-128	HMGA2	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33993846	HCP5 contributes to cisplatin resistance in gastric cancer through miR-128/HMGA2 axis.	The long non-coding RNA HLA complex P5 (HCP5) is extensively related to cancer chemoresistance, while its function in gastric cancer (GC) has not been well elucidated yet. Here, the role and mechanism of HCP5 in regulating the chemoresistance of GC to cisplatin (DDP) was investigated. Our results revealed that HCP5 was increased in GC patients and indicated a poor prognosis. HCP5 knockdown weakens DDP resistance and reduced apoptosis of GC cells. miR-128 was decreased in GC patients and sponged by HCP5. HMGA2 was targeted by miR-128 and was increased in GC patients. HCP5 aggravated the resistance of GC cells to DDP in vitro by elevating HMGA2 expression via sponging miR-128. HCP5 silencing inhibited GC cells growth, resistance to DDP, and Ki-67 expression in vivo. In summary, HCP5 contributed to DDP resistance in GC cells through miR-128/HMGA2 axis, providing a promising therapeutic target for GC chemoresistance.	NA	Cell Cycle. 2021 Jun;20(11):1080-1090. doi: 10.1080/15384101.2021.1924948. Epub 2021 May 16.
3877	LncRNA	HCP5	miR-128	NA	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33994812	Knockdown of Long Non-Coding RNA HCP5 Increases Radiosensitivity Through Cellular Senescence by Regulating microRNA-128 in Gliomas.	INTRODUCTION: Glioma is the most common malignant brain tumor in adults. Radiation is a key therapy in glioma. However, the radioresistance of glioma was a big challenge. HLA complex P5 (HCP5) has been reported dysregulated in several types of malignant tumor, including glioma. The role of HCP5 in the radiosensitivity of glioma is so far unknown. The present study aimed to investigate the effect of HCP5 on radiosensitivity in gliomas. METHODS: The levels of HCP5 and microRNA (miR)-128 were detected using qRT-PCR. The cell growth curve was used to show the cell proliferation and evaluate the radiosensitivity of glioma cells following exposure to X-ray. Senescence-associated β-galactosidase (SA-β-Gal) staining was used to test the cellular senescence. Luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to determine the correlation between HCP5 and miR-128. RESULTS: HCP5 level of glioma cells was significantly higher than human astrocytes, whereas miR-128 level was lower in glioma cells. Besides, the HCP5 expression was increased in glioma tissues compared to normal brain tissues (NBTs). Knockdown of HCP5 inhibited cell proliferation and increased radiosensitivity in glioma cells. MiR-128 was predicted to be a target of HCP5. It was demonstrated that HCP5 directly bound to miR-128 and regulated its expression in glioma cells. Furthermore, the effects of HCP5 knockdown on radiosensitivity of glioma cells were attenuated by the inhibitor of miR-128. CONCLUSION: These findings suggested that interaction between lncRNA HCP5 and microRNA-128 could regulate the radiosensitivity of glioma cells by intervening in cellular senescence. This might be used as the potential radio-sensitization targets for glioma therapy.	NA	Cancer Manag Res. 2021 May 7;13:3723-3737. doi: 10.2147/CMAR.S301333. eCollection 2021.
3878	LncRNA	HBL1	NA	PRC2	pluripotent stem cells	Cardiogenesis	Homo sapiens (human)	ChIP;	34027990	LncRNA HBL1 is required for genome-wide PRC2 occupancy and function in cardiogenesis from human pluripotent stem cells.	Polycomb Repressive Complex 2 (PRC2) deposits H3K27me3 on chromatin to silence transcription. PRC2 broadly interacts with RNAs. Currently, the role of RNA- PRC2 interaction in human cardiogenesis remains elusive. Here, we found human-specific Heart Brake LncRNA 1 (HBL1) interacted with two PRC2 subunits, JARID2 and EED, in human pluripotent stem cells (hPSCs). Loss-of-JARID2, EED or HBL1 significantly enhanced cardiac differentiation from hPSCs. HBL1 depletion disrupted genome-wide PRC2 occupancy and H3K27me3 chromatin modification on essential cardiogenic genes, and broadly enhanced cardiogenic gene transcription in undifferentiated hPSCs and later-on differentiation. Additionally, ChIP-seq revealed reduced EED-occupancy on 62 overlapped cardiogenic genes in HBL1-/- and JARID2-/- hPSCs, indicating the epigenetic state of cardiogenic genes was determined by HBL1 and JARID2 at pluripotency stage. Furthermore, after cardiac development occurred, the cytosolic and nuclear fractions of HBL1 could crosstalk via a conserved "microRNA-1-JARID2" axis to modulate cardiogenic gene transcription. Overall, our findings delineate the indispensable role of HBL1 in guiding PRC2 function during early human cardiogenesis, and expand the mechanistic scope of lncRNA(s) that cytosolic and nuclear portions of HBL1 could coordinate to orchestrate human cardiogenesis.	NA	Development. 2021 May 24:dev.199628. doi: 10.1242/dev.199628.
3879	LncRNA	H19	miR-19b	SOX9	HSF cells	Healing	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;	34045678	Adipose mesenchymal stem cell-derived exosomes accelerate skin wound healing via the lncRNA H19/miR-19b/SOX9 axis.	It has been reported that adipose mesenchymal stem cells (ADSCs) accelerate wound healing. Moreover, exosomes, which serve as paracrine factors, play a vital role in wound healing. However, the mechanism remains unclear. This research aimed to determine the roles of exosomes derived from ADSCs (ADSC-Exos) in wound skin tissue repair. Flow cytometry and electron microscopy were carried out to identify ADSCs and ADSC-Exos, respectively; RT-qPCR was performed to assess the lncRNA H19 (H19), microRNA19b (miR-19b) and SRY-related high-mobility-group box 9 (SOX9) levels; Western blotting was carried out to evaluate collagen and β-catenin expression; CCK-8, scratch and transwell assays were conducted to evaluate human skin fibroblast (HSF) cell proliferation, migration and invasion, respectively; the potential binding sites between H19 and miR-19b, miR-19b and SOX9 were detected by dual-luciferase reporter gene assay and RIP assay; and H&E staining was conducted to observe skin wound tissues. ADSC-Exos accelerated the proliferation, migration and invasion of HSF cells via H19. H19 acts as a molecular sponge towards miR-19b, which targets SOX9. ADSC-Exos inhibited miR-19b expression via H19, resulting in accelerated HSF proliferation, migration and invasion. ADSC-Exos upregulated SOX9 to activate the Wnt/β-catenin pathway, resulting in accelerated HSF cell proliferation, migration and invasion, and ADSC-Exos promoted skin wound healing via H19 in mice.The high expression of H19 in ADSC-Exos may upregulate SOX9 expression via miR-19b to accelerate wound healing of skin tissues. Our study may provide novel perspectives for therapy to accelerate skin wound healing.	NA	Lab Invest. 2021 May 27. doi: 10.1038/s41374-021-00611-8.
3880	LncRNA	GATA6-AS1	miR-4530	GATA6	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33992085	Long non-coding RNA GATA6-AS1 upregulates GATA6 to regulate the biological behaviors of lung adenocarcinoma cells.	BACKGROUND: Lung adenocarcinoma (LUAD) is known to be one of the leading causes of cancer-related deaths globally. In recent decades, long non-coding RNAs (lncRNAs) have been indicated to exert pivotal regulating functions in multiple biological behaviors in the initiation and development of LUAD. However, the functional mechanism of lncRNA GATA binding protein 6 antisense RNA 1 (GATA6-AS1) in LUAD has not been explored. METHODS: In the current study, GATA6-AS1 expression in LUAD tissues was revealed. Meanwhile, GATA6-AS1 expression in LUAD cells was investigated via RT-qPCR analysis. After A549 and H1975 cells were transfected with GATA6-AS1 overexpression plasmids, EdU and colony formation assays, TUNEL assays and flow cytometry analyses, as well as wound healing and Transwell assays were conducted to detect cell proliferation, apoptosis, migration and invasion. Afterwards, bioinformatic tools, western blot analyses, dual-luciferase reporter assays, and RNA immunoprecipitation (RIP) assays were performed to investigate the correlation of microRNA-4530 (miR-4530), GATA6-AS1 and GATA6. RESULTS: We found that GATA6-AS1 expression was low-expressed in LUAD tissues and cells. Furthermore, the upregulation of GATA6-AS1 suppressed the proliferative, migration and invasion abilities, as well as promoted apoptotic rate of A549 and H1975 cells. Moreover, the mechanistic investigations revealed that GATA6-AS1 upregulated the expression of its cognate sense gene GATA6 by binding with miR-4530, thereby modulating the malignant progression of LUAD cells. CONCLUSIONS: GATA6-AS1 repressed LUAD cell proliferation, migration and invasion, and promoted cell apoptosis via regulation of the miR-4530/GATA6 axis, indicating GATA6-AS1 as a new prognostic biomarker for LUAD.	NA	BMC Pulm Med. 2021 May 15;21(1):166. doi: 10.1186/s12890-021-01521-7.
3881	LncRNA	Gas5	NA	Creb5	renal fibrosis tissue	Renal Fibrosis	Homo sapiens (human)	RACE;	33876672	LncRNA Gas5 regulates Fn1 deposition via Creb5 in renal fibrosis.	Aim: Although studies on lncRNAs in renal fibrosis have focused on target genes and functions of lncRNAs, a comprehensive interaction analysis of lncRNAs is lacking. Materials & methods: Differentially expressed genes in renal fibrosis were screened, and the interaction between lncRNAs and miRNAs was searched. Results: We constructed a ceRNA network associated with renal fibrosis, by which we found the transcription factor Creb5, a target gene of lncRNA Gas5 that might regulate extracellular Fn1 deposition. Conclusion: Our study not only provides a theoretical basis for the ceRNA regulation mechanism of Gas5 but also provides experimental evidence supporting the use of Gas5 targeting in the treatment of renal fibrosis.	NA	Epigenomics. 2021 May;13(9):699-713. doi: 10.2217/epi-2020-0449. Epub 2021 Apr 20.
3882	LncRNA	FGD5-AS1	miR-497-5p	SEPT2	LSCC cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	34003510	The LncRNA FGD5-AS1/miR-497-5p axis regulates septin 2 (SEPT2) to accelerate cancer progression and increase cisplatin-resistance in laryngeal squamous cell carcinoma.	Aberrant expression or mutation of the Septin gene family is closely associated with cancer progression, and septin 2 (SEPT2) exerts its tumor-promoting effects in multiple cancers, but its role in regulating laryngeal squamous cell carcinoma (LSCC) progression and drug resistance has not been investigated. Based on the published data, the present study identified that SEPT2 promoted cancer progression and increased cisplatin-resistance in LSCC, and a novel LncRNA FGD5-AS1/miR-497-5p axis was crucial for this process. Mechanistically, SEPT2 tended to be enriched in LSCC tissues and cells, and knock-down of SEPT2 inhibited cell proliferation, viability, migration, and tumorigenesis in LSCC cells in vitro and in vivo. Aside from that, SEPT2 overexpression increased cisplatin resistance in LSCC cells. Next, by conducting the dual-luciferase reporter gene system assay, we identified that the LncRNA FGD5-AS1/miR-497-5p axis regulated SEPT2 in LSCC. Specifically, LncRNA FGD5-AS1 sponged miR-497-5p to upregulate SEPT2 in LSCC cells in a competing endogenous RNA (ceRNA) mechanisms-dependent manner. Interestingly, upregulated LncRNA FGD5-AS1 and downregulated miR-497-5p were observed in LSCC tissues and cells, and LncRNA FGD5-AS1 ablation inhibited cancer progression. Also, LncRNA FGD5-AS1 overexpression increased cisplatin-resistance in LSCC by modulating the miR-497-5p/SEPT2 axis. Collectively, we conclude that targeting the LncRNA FGD5-AS1/miR-497-5p/SEPT2 signaling cascade may be an alternative strategy to treat LSCC in the clinic.	NA	Mol Carcinog. 2021 Jul;60(7):469-480. doi: 10.1002/mc.23305. Epub 2021 May 18.
3883	LncRNA	FGD5-AS1	miR-506-3p	RAB3D	OSA cells	Osteosarcoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33891267	Long non-coding RNA FGD5-AS1 enhances osteosarcoma cell proliferation and migration by targeting miR-506-3p/RAB3D axis.	Osteosarcoma (OSA), the malignant bone tumor, predominantly affecting children and adolescents, threatens the life and life quality of the patients. An increasing number of studies have indicated the role of long non-coding RNA (lncRNA) dysregulation in cancer biology. Herein, the study was aimed to explore the role of FGD5 antisense RNA 1 (FGD5-AS1), a lncRNA, in OSA. Expression levels of FGD5-AS1, miR-506-3p and RAB3D mRNA were quantified utilizing qRT-PCR. The expression of RAB3D protein was examined employing Western blot. A series of functional experiments including CCK-8 assay, BrdU assay, wound healing assay, Transwell assay were performed for studying the effects of FGD5-AS1 on the malignancy of OSA cell lines 143B and HOS. The binding site between miR-506-3p and FGD5-AS1 was identified and validated by luciferase reporter assay and RNA immunoprecipitation assay. It was demonstrated that the expression of FGD5-AS1 was up-regulated in OSA tissues and cell lines, and its high expression is associated with higher Enneking stage and poorer histological differentiation. Gain-of-function and loss-of-function studies suggested that FGD5-AS1 facilitated OSA cells proliferation and migration. The promoting effects of FGD5-AS1 overexpression on OSA cell proliferation and migration could be counteracted by miR-506-3p. Moreover, FGD5-AS1 competitively adsorbed miR-506-3p to repress its expression so as to up-regulate the expression of RAB3D. These results indicate that FGD5-AS1 is capable of expediting OSA cell proliferation and migration via sponging miR-506-3p to up-regulate RAB3D.	NA	Hum Cell. 2021 Jul;34(4):1255-1265. doi: 10.1007/s13577-021-00536-w. Epub 2021 Apr 23.
3884	LncRNA	DLEU1	miR-320b	PRPS1	CRC tissues	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;	34113562	LncRNA DLEU1 Contributes to the Growth and Invasion of Colorectal Cancer via Targeting miR-320b/PRPS1.	Growing evidences suggest that long non-coding RNAs (lncRNAs) are closely correlated to the development of human cancer, such as colorectal cancer (CRC). A previous report suggested that DLEU1 accelerated CRC development. However, DLEU1's underlying mechanism in CRC remains unclear. In our study, the level of DLEU1 in CRC tissues is investigated by qRT-PCR. Our data exhibited that DLEU1 level was observably increased in CRC tissues and CRC cell lines and was closely associated with bad prognosis of CRC patients. CRC cell proliferation was repressed by sh-LncRNA DLEU1, whereas cell apoptosis was markedly stimulated. Moreover, knockdown of DLEU1 inhibited cell migration and invasion. Mechanistically, through interacting with miR-320b in CRC, DLEU1 promoted the level of PRPS1 which was a target of miR-320b. The rescue experiment confirmed that knockdown of DLEU1 repressed cell proliferation, migration and invasion while stimulated cell apoptosis via miR-320b/phosphoribosyl pyrophosphate synthetase 1 (PRPS1) axis. Meanwhile, the data of xenograft model exhibited that inhibition of DLEU1 suppressed tumor growth in vivo. In summary, DLEU1 knockdown may repress PRPS1 expression via miR-320b, and then repress cell proliferation, migration and invasion while stimulate cell apoptosis. Our research may provide a novel target for the treatment of CRC.	NA	Front Oncol. 2021 May 25;11:640276. doi: 10.3389/fonc.2021.640276. eCollection 2021.
3885	LncRNA	DANCR	miR-338-3p	B4GALT3	neuroblastoma tissues and cells	Neuroblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34050113	Long noncoding RNA differentiation antagonizing nonprotein coding RNA promotes the proliferation, invasion and migration of neuroblastoma cells via targeting β-1, 4-galactosyltransferase III by sponging miR-338-3p.	Neuroblastoma is a common malignant tumor in children, and patients often have a poor prognosis. Long noncoding RNAs (lncRNAs) are involved in the regulation of neuroblastoma progression. However, the regulatory effect of lncRNA differentiation antagonizing nonprotein coding RNA (DANCR) on neuroblastoma is still not clear. The expression levels of DANCR, miR-338-3p and β-1, 4-galactosyltransferase III (B4GALT3) were determined by quantitative real-time PCR. 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide, flow cytometry and transwell assays were used to evaluate the proliferation, apoptosis, migration and invasion abilities of neuroblastoma cells. Moreover, western blot analysis was performed to assess the levels of B4GALT3 and the proliferation, apoptosis and migration-related proteins. Besides, a dual-luciferase reporter assay was used to verify the interactions among DANCR, miR-338-3p and B4GALT3. Mice xenograft models were used to ascertain the effect of DANCR on neuroblastoma tumor growth in vivo. Our results revealed that DANCR was highly expressed in neuroblastoma tissues and cells, and its silencing impeded the progression of neuroblastoma cells. DANCR could interact with miR-338-3p. Knockdown of miR-338-3p recovered the inhibitory effect of DANCR knockdown on neuroblastoma progression. B4GALT3 was a target of miR-338-3p. B4GALT3 overexpression reversed the suppression effect of DANCR silencing on neuroblastoma progression. In-vivo experiments further confirmed that DANCR silencing inhibited neuroblastoma tumor growth. Our results indicated that DANCR promoted B4GALT3 expression to increase the proliferation, migration and invasion of neuroblastoma cells via sponging miR-338-3p, which provided a theoretical basis for the targeted therapy of neuroblastoma.	NA	Neuroreport. 2021 May 27. doi: 10.1097/WNR.0000000000001664.
3886	LncRNA	DANCR	miR-1306-5p	PLK1	NCM460 cells	Sepsis	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34003569	LncRNA DANCR improves the dysfunction of the intestinal barrier and alleviates epithelial injury by targeting the miR-1306-5p/PLK1 axis in sepsis.	Intestinal barrier dysfunction often occurs in various acute or chronic pathological conditions and has been identified as an important clinical problem. Herein, we explored the biological role and molecular mechanism of Polo-like kinase 1 (PLK1) and differentiation antagonizing non-protein coding RNA (DANCR) in intestinal barrier dysfunction caused by sepsis. RT-qPCR analysis was used to examine PLK1, miR-1306-5p, and DANCR expression in NCM460 cells after LPS treatment. TUNEL assay and Western blot analysis were performed to explore PLK1 function in cell apoptosis and intestinal barrier in vitro. Hematoxylin and eosin staining, Western blot analysis, and TUNEL assay were used to investigate DANCR function in the intestinal barrier and cell apoptosis in vivo. The interaction between miR-1306-5p and PLK1 (or DANCR) was validated by luciferase reporter assay. As a result, PLK1 overexpression decreased cell apoptosis and promoted intestinal barrier function. Moreover, DANCR was validated as a sponge of miR-1306-5p to target PLK1. In addition, we found that DANCR overexpression decreased intestinal mucosal permeability and colon mucosa epithelial cell apoptosis in vivo. Conclusively, DANCR improved intestinal barrier dysfunction and alleviated epithelial injury by targeting the miR-1306-5p/PLK1 axis in sepsis.	NA	Cell Biol Int. 2021 May 18. doi: 10.1002/cbin.11633.
3887	LncRNA	DANCR	miR-145-5p	NRAS	colorectal cancer tissues	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;	33956301	Assessment of lncRNA DANCR, miR-145-5p and NRAS axis as biomarkers for the diagnosis of colorectal cancer.	Recent evidence reveals that miRNA sponges neutralize miRNAs activity by binding to miRNAs and sequester them from their relevant targets to regulate expression. The detailed mechanisms of sponge RNAs in colorectal cancer remain to be exactly determined. In this study DANCR, miR-145-5p, NRAS axis was evaluated and the diagnostic value of these targets was assessed in colorectal cancer patients. A case-control study was carried out on 40 samples of tumor tissues and 40 adjacent tissues. Total RNA was extracted, and then, the expression level of DANCR, miR-145-5p and NRAS was evaluated using qRT-PCR. In addition, the sensitivity and specificity of these markers were evaluated by receiver operating characteristic (ROC) curve analysis. Our results revealed that the expression level of DANCR was significantly upregulated in colorectal cancer tissues (p < 0.001). It was demonstrated that DANCR could regulate NRAS expression by sponging miR-145-5 in colorectal cancer patients. Furthermore, the mean expression of miR-145-5p (p < 0.001) and NRAS (p < 0.001) was significantly different between tumor and normal tissue. A significant correlation was observed between DANCR and miR-145-5p (p = 0.001), and also between miR-145-5p and NRAS (p < 0.001). Sensitivity and specificity value for DANCR, miR-145-5p and NRAS were (0.875 and 0.725), (0.875 and 0.745), and (0.877 and 0.694), respectively. According to the values of sensitivities and specificity of DANCR, miR-145-5p and NRAS, confirmed with ROC curve analysis, these biomarkers may be useful in the screening and differentiating between tumor and control sample in colorectal neoplasm.	NA	Mol Biol Rep. 2021 Apr;48(4):3541-3547. doi: 10.1007/s11033-021-06373-2. Epub 2021 May 6.
3888	LncRNA	DANCR	miR-185-5p	LASP1	PC3 and C4-2 cells	Prostate Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Immunohistochemistry;Luciferase reporter assay;	33885171	Long non-coding DANCR targets miR-185-5p to upregulate LIM and SH3 protein 1 promoting prostate cancer via the FAK/PI3K/AKT/GSK3β/snail pathway.	BACKGROUND: Long non-coding RNA differentiation antagonizing non-protein coding RNA (DANCR) acts as an oncogene in different cancers, although its roles in prostate cancer are not fully reported. We aimed to explore its mechanism in facilitating the malignancy of prostate cancer. METHODS: The expression of DANCR, microRNA (miR)-185-5p and LIM and SH3 protein 1 (LASP1) in 40 pairs of prostate cancer tissues and normal tissues, five prostate cancer cell lines and one epithelial cell line was assessed by a quantitative real-time polymerase chain reaction, western blotting and immunohistochemistry, respectively. In transfected PC3 and C4-2 cells, cell proliferation, migration, invasion, cell cycle distribution and epithelial-mesenchymal transition (EMT) protein expression were tested via cell counting kit-8, wound healing, transwell, flow cytometry and western blot assays, respectively. The interactions between DANCR, miR-185-5p and LASP1 were verified by a dual-luciferase reporter assay. Rescue experiments were conducted to determine the roles of DANCR on the malignant properties of PC3 and C4-2 cells. The involvement of the signaling pathway was examined using a p-FAK inhibitor. RESULTS: DANCR and LASP1 expression was enhanced, whereas miR-185-5p expression was diminished in prostate cancer tissues and cell lines. Knockdown of DANCR suppressed cell proliferation, migration, invasion, G1-S transition and expression of EMT proteins of the transfected PC3 and C4-2 cells. DANCR sponged miR-185-5p to upregulate LASP1 expression. DANCR-miR-185-5p-LASP1 axis activates the FAK/PI3K/AKT/GSK3β/Snail pathway to promote the malignant properties of PC3 and C4-2 cells. CONCLUSIONS: These findings suggest that DANCR exerts oncogenic roles in prostate cancer via the miR-185-5p/LASP1 axis activating the FAK/PI3K/AKT/GSK3β/Snail pathway. It can be a potential biomarker in the diagnosis and monitoring of prostate cancer.	NA	J Gene Med. 2021 Apr 22:e3344. doi: 10.1002/jgm.3344.
3889	LncRNA	CYTOR	miR-103	RAB10	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	34110382	Long noncoding RNA CYTOR triggers gastric cancer progression by targeting miR-103/RAB10.	Growing evidence has indicated that the long noncoding RNA (lncRNA) CYTOR is involved in the initiation and progression of malignancies, including gastric cancer. Nevertheless, the mechanisms of CYTOR in gastric cancer development are not fully understood. In the present study, we aimed to clarify the association of CYTOR, miR-103, and RAB10 in gastric cancer progression. We found that CYTOR expression was increased in metastatic gastric cancer biopsies compared with that in primary samples. CYTOR expression was significantly positively correlated with the invasiveness, lymph node metastasis, and advanced stages of gastric cancer. In addition, downregulation of CYTOR expression hampered cell proliferation and migration but induced cell apoptosis. Furthermore, CYTOR sponged miR-103 and diminished miR-103 expression, thus rescuing oncogene RAB10 expression. Knockdown of CYTOR suppressed tumor growth in human BGC823 mouse models. These findings suggest that the CYTOR/miR-103/RAB10 axis is a novel signaling pathway that facilitates gastric cancer progression. CYTOR-targeted interventions provide a rationale to improve therapies targeting gastric cancer progression.	NA	Acta Biochim Biophys Sin (Shanghai). 2021 Jun 10:gmab071. doi: 10.1093/abbs/gmab071.
3890	LncRNA	CRNDE	NA	YAP1	myocardial tissues and HL-1 cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;	33988471	LncRNA CRNDE inhibits cardiomyocytes apoptosis by YAP1 in myocardial ischaemia/reperfusion injury.	BACKGROUND: Cardiomyocytes apoptosis is the basic pathological process of myocardial ischaemia/reperfusion (MI/R) injury, so inhibiting apoptosis of cardiomyocytes can effectively improve MI/R injury. Long non-coding RNA colorectal neoplasia differentially expressed (lncRNA CRNDE) can inhibit cell apoptosis, but its specific role in MI/R injury has not been studied. The aim of this study is to explore the specific effect of lncRNA CRNDE on cardiomyocytes apoptosis. METHODS: MI/R model in vivo and hypoxia/re-oxygenation (H/R) model in vitro were constructed. Apoptotic levels were assessed by TUNEL staining assay. QRT-PCR was used to validate lncRNA CRNDE level in myocardial tissues and HL-1 cells. The protein expressions of YAP1, Bcl-2 and cleaved caspase-3 were detected by western blot analysis. Flow cytometry was used to determine the apoptosis rate of cardiomyocytes. RIP assay was used to detect the interaction between lncRNA CRNDE and YAP1. RESULTS: The extent of cardiomyocytes apoptosis was significantly increased, and the levels of lncRNA CRNDE, YAP1 and Bcl-2 were down-regulated, while cleaved caspase-3 expression was up-regulated in MI/R mice and H/R-treated HL-1 cells. The expressions of YAP1 and Bcl-2 were decreased, while the expression of cleaved caspase-3 was increased after the knockdown of lncRNA CRNDE. Furthermore, lncRNA CRNDE could bind to YAP1 and regulated the protein level of YAP1 by ubiquitination and proteasomal degradation pathway. After transfection of Si-YAP1 in the H/R-treated HL-1 cells transfected with pc-DNA CRNDE, the protein level of Bcl-2 was decreased, while cleaved caspase-3 expression and the apoptosis rate were increased. CONCLUSION: Our study suggested that lncRNA CRNDE could regulate YAP1 level by ubiquitination and proteasomal degradation pathway, thus inhibiting cardiomyocytes apoptosis in MI/R injury.	NA	Autoimmunity. 2021 Jun;54(4):204-212. doi: 10.1080/08916934.2021.1913580. Epub 2021 May 14.
3891	Circular RNA	CircSPAG16	NA	PIP5K1a	human bronchial epithelial BEAS-2B cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	34081812	CircSPAG16 suppresses cadmium-induced transformation of human bronchial epithelial cells by decoying PIP5K1α to inactivate Akt.	Circular RNAs (circRNAs) have been implicated to have important regulatory functions in chemical carcinogenesis via sponging microRNAs to regulate gene expression. Our study revealed a novel mechanism of circRNA in cadmium carcinogenesis through directly binding with protein. Here, we used cadmium-transformed human bronchial epithelial BEAS-2B cells to study the involvement and mechanism of circRNA in lung carcinogenesis caused by cadmium. By high-throughput sequencing, circSPAG16 was identified to be the most significantly downregulated circRNA in cadmium-transformed cells. CircSPAG16 was downregulated at Week 8, 12, 16, and 20 during cadmium-induced cell transformation. In addition, circSPAG16 overexpression prevented cadmium-induced transformation of BEAS-2B cells. Mechanistically, circSPAG16 inhibited the function of phosphatidylinositol 4-phosphate 5-kinase type-1 α (PIP5K1α) by binding with it. We demonstrated that PIP5K1α acted as an oncogene to activate Akt and promoted cancer hallmarks including proliferation, migration, invasion, and anchorage-independent growth in cadmium-transformed cells. CircSPAG16 overexpression inactivates PIP5K1α/Akt signaling in the transformed cells. Furthermore, PIP5K1α overexpression significantly rescued the inhibitory effects of circSPAG16 overexpression on pAkt and cancer hallmarks in cadmium-transformed cells. Collectively, our results revealed that circSPAG16 could prevent cadmium-induced transformation through binding with PIP5K1α to inactivate Akt. These results provide a novel regulatory mechanism of circRNA into carcinogenesis induced by cadmium.	NA	Mol Carcinog. 2021 Jun 3. doi: 10.1002/mc.23325.
3892	Circular RNA	CircRNA-17828	miR-6631-5p	DUSP6	broilers model	Tracheal Injury	Homo sapiens (human)	Immunohistochemistry;Luciferase reporter assay;RNA sequencing;	34098264	Hydrogen sulfide exposure induces pyroptosis in the trachea of broilers via the regulatory effect of circRNA-17828/miR-6631-5p/DUSP6 crosstalk on ROS production.	Hydrogen sulfide (H(2)S) is an air pollutant to cause tracheal injury. Pyroptosis is responsible for tissue injury through reactive oxygen species (ROS) production. Competitive endogenous RNAs (ceRNAs) chelate microRNAs and reduce their inhibitory effect on other transcripts, thus affecting ROS levels and pyroptosis. However, it is not clear how H(2)S regulates pyroptosis via the ceRNA axis. Therefore, we established a broilers model of H(2)S exposure for 42 days to assess pyroptosis and obtain a ceRNA network by immunohistochemistry and RNA sequencing. We detected pyroptosis induced by H(2)S and verified circRNA-IGLL1-17828/miR-6631-5p/DUSP6 axis by a double luciferase reporter assay. We also measured ROS levels and the expression of pyroptotic indicators such as (Caspase1) Casp-1, Interleukin 1β (IL-1β) and Interleukin 1β (IL-18). miR-6631-5p knockdown decreased pyroptotic indicators induced by H(2)S. Overexpression of miR-6631-5p or DUSP6 knockdown stimulated ROS generation and upregulated pyroptotic indicators. N-acetyl-(L)-cysteine (NAC) decreased pyroptotic indicators and ROS levels both induced by miR-6631-5p. Moreover, circRNA-IGLL1-17828, participated in intermolecular competition as a ceRNA of DUSP6. In conclusion, circRNA-IGLL1-17828/miR-6631-5p/DUSP6 crosstalk regulated H(2)S-induced pyroptosis in broilers trachea via ROS generation. This is the first study to reveal regulation mechanism of circRNA-related CeRNAs on pyroptosis induced by H(2)S, providing important reference for environmental toxicology.	NA	J Hazard Mater. 2021 May 21;418:126172. doi: 10.1016/j.jhazmat.2021.126172.
3893	Circular RNA	CircRNA_0026344	miR-21	Smad7	HBE cells	Cigarette Smoke-Induced Pulmonary Fibrosis	Homo sapiens (human)	microarray;qRT-PCR;RACE;RNA pull-down assay;RNA pull-down;	33961985	CircRNA_0026344 via exosomal miR-21 regulation of Smad7 is involved in aberrant cross-talk of epithelium-fibroblasts during cigarette smoke-induced pulmonary fibrosis.	For smoking-induced pulmonary fibrosis (PF), a serious disease endangering human health, there is no effective clinical treatment. Aberrant epithelium-fibroblast cross-talk is involved in formation of the excessive extracellular matrix (ECM) that contributes to PF. Circular RNAs have been associated with various pulmonary diseases. However, the mechanisms of circRNAs in PF are not clear. Herein, our goals were to investigate the involvement of circRNA_0026344 in the aberrant epithelium-fibroblast cross-talk induced by cigarette smoke (CS) and to define its mechanism. Chronic exposure (16 weeks) of BALB/c mice to 500 mg/m(3) CS induced lung injury and fibrosis in lung tissues. From HBE cells, circRNA_0026344 was selected by microarray analysis and verified as that with the most severe down-regulation caused by cigarette smoke extract (CSE). The regulatory relationship between circRNA_0026344 and miR-21 was assessed by use of bioinformatics, RNA pull-down assays, and qRT-PCR. We found that miR-21 binding sites were present in circRNA_0026344 and, in HBE cells, it could act as a sponge for miR-21. When pcDNA3.0-circRNA_0026344, a high expression plasmid of circRNA_0026344, was transfected into HBE cells, the CSE-induced up-regulation of miR-21 levels was reversed. In MRC-5 cells, HBE-secreted exosomal miR-21 decreased levels of Smad7 and activated the TGF-β1/Smad3 pathway. By using the Targetscan database, the presence of species-conserved miR-21 binding sites in the Smad7 3'UTR region were predicted. We verified, by use of a luciferase reporter gene, that miR-21 bound to the 3'UTR region of Smad7 mRNA to inhibit its transcription. In conclusion, the results reveal that, in CS-induced pulmonary fibrosis, circRNA_0026344, via exosomal miR-21 regulation of Smad7, is involved in aberrant cross-talk of epithelium-fibroblasts. These results will be useful for the discovery of early biomarkers and for providing therapeutic targets for smoking-induced pulmonary fibrosis.	NA	Toxicol Lett. 2021 Sep 1;347:58-66. doi: 10.1016/j.toxlet.2021.04.017. Epub 2021 May 4.
3894	Circular RNA	Circ-RANBP9	miR-5787	LAMA2	laryngeal cancer tissues and cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33850881	Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance.	BACKGROUND: Laryngeal cancer (LC) is a common malignant tumor of the head and neck. As circular RNAs (circRNAs) and other non-coding RNAs are involved in various malignant processes, we analyzed circRNAs to better understand LC and explored specific tumor markers. METHODS: High-throughput sequence was performed to analyze the differential circular RNAs in four coupled laryngeal cancers and para-cancerous tissues. The differential expression of selected circ-RANBP9 in laryngeal cancer tissues and cells was verified by RT-qPCR assay. CCK8, EDU, Transwell and wound healing assays were used to confirm the biological function of circ-RANBP9 in laryngeal cancer. Western blot assay was performed to identify the effects of circ-RANBP9 having on the epithelial to mesenchymal transition process. One-way AN0VA was used to analyze the correlation between the expression of circ-RANBP9 and clinicopathological parameters of the included patients. Kaplan-Meier analysis was used to investigate whether the expression level of circ-RANBP9 correlated with survival in LC patients. Bioinformatic analyses were also conducted to predict the functions and possible signaling pathways of the targeted mRNAs of circ-RANBP9 via co-expression and competing endogenous RNA network. RESULTS: We found a transcript from RNA sequence data, termed hsa_circ_0001578, which is a circRNA spliced from RANBP9. Circ-RANBP9 was downregulated in the LC cell lines tissues, relating to a better prognosis. Circ-RANBP9 was found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. For the diagnostic value of circ-RANBP9, the sensitivity and the specificity were 0.979 and 0.553, respectively. Circ-RANBP9 downregulation was significantly correlated with differentiation (P=0.031), T-stage (P=0.018), lymphatic metastasis (P=0.046), and clinical stage (P=0.003). Circ-RANBP9 was involved in insulin-like growth factor receptor binding, cell polarity, focal adhesion, and MAPK signaling pathways. CeRNA analysis identified the possible involvement of circ-RANBP9 in the ECM-receptor interaction, cAMP, calcium, and Wnt signaling pathways by harboring miRNA genes. CONCLUSIONS: Circ-RANBP9 was confirmed to play important roles in inhibiting laryngeal cancers. Circ-RANBP9 was also validated to be associated with the clinicopathological parameters and diagnostic value, suggesting that circ-RANBP9 is a promising biomarker for LC prognosis and early diagnosis.	NA	Ann Transl Med. 2021 Mar;9(6):484. doi: 10.21037/atm-21-567.
3895	Circular RNA	Circ-RANBP9	miR-4746-3p	LAMA2	laryngeal cancer tissues and cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33850881	Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance.	BACKGROUND: Laryngeal cancer (LC) is a common malignant tumor of the head and neck. As circular RNAs (circRNAs) and other non-coding RNAs are involved in various malignant processes, we analyzed circRNAs to better understand LC and explored specific tumor markers. METHODS: High-throughput sequence was performed to analyze the differential circular RNAs in four coupled laryngeal cancers and para-cancerous tissues. The differential expression of selected circ-RANBP9 in laryngeal cancer tissues and cells was verified by RT-qPCR assay. CCK8, EDU, Transwell and wound healing assays were used to confirm the biological function of circ-RANBP9 in laryngeal cancer. Western blot assay was performed to identify the effects of circ-RANBP9 having on the epithelial to mesenchymal transition process. One-way AN0VA was used to analyze the correlation between the expression of circ-RANBP9 and clinicopathological parameters of the included patients. Kaplan-Meier analysis was used to investigate whether the expression level of circ-RANBP9 correlated with survival in LC patients. Bioinformatic analyses were also conducted to predict the functions and possible signaling pathways of the targeted mRNAs of circ-RANBP9 via co-expression and competing endogenous RNA network. RESULTS: We found a transcript from RNA sequence data, termed hsa_circ_0001578, which is a circRNA spliced from RANBP9. Circ-RANBP9 was downregulated in the LC cell lines tissues, relating to a better prognosis. Circ-RANBP9 was found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. For the diagnostic value of circ-RANBP9, the sensitivity and the specificity were 0.979 and 0.553, respectively. Circ-RANBP9 downregulation was significantly correlated with differentiation (P=0.031), T-stage (P=0.018), lymphatic metastasis (P=0.046), and clinical stage (P=0.003). Circ-RANBP9 was involved in insulin-like growth factor receptor binding, cell polarity, focal adhesion, and MAPK signaling pathways. CeRNA analysis identified the possible involvement of circ-RANBP9 in the ECM-receptor interaction, cAMP, calcium, and Wnt signaling pathways by harboring miRNA genes. CONCLUSIONS: Circ-RANBP9 was confirmed to play important roles in inhibiting laryngeal cancers. Circ-RANBP9 was also validated to be associated with the clinicopathological parameters and diagnostic value, suggesting that circ-RANBP9 is a promising biomarker for LC prognosis and early diagnosis.	NA	Ann Transl Med. 2021 Mar;9(6):484. doi: 10.21037/atm-21-567.
3896	Circular RNA	Circ-RANBP9	miR-4757-5p	LAMA2	laryngeal cancer tissues and cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33850881	Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance.	BACKGROUND: Laryngeal cancer (LC) is a common malignant tumor of the head and neck. As circular RNAs (circRNAs) and other non-coding RNAs are involved in various malignant processes, we analyzed circRNAs to better understand LC and explored specific tumor markers. METHODS: High-throughput sequence was performed to analyze the differential circular RNAs in four coupled laryngeal cancers and para-cancerous tissues. The differential expression of selected circ-RANBP9 in laryngeal cancer tissues and cells was verified by RT-qPCR assay. CCK8, EDU, Transwell and wound healing assays were used to confirm the biological function of circ-RANBP9 in laryngeal cancer. Western blot assay was performed to identify the effects of circ-RANBP9 having on the epithelial to mesenchymal transition process. One-way AN0VA was used to analyze the correlation between the expression of circ-RANBP9 and clinicopathological parameters of the included patients. Kaplan-Meier analysis was used to investigate whether the expression level of circ-RANBP9 correlated with survival in LC patients. Bioinformatic analyses were also conducted to predict the functions and possible signaling pathways of the targeted mRNAs of circ-RANBP9 via co-expression and competing endogenous RNA network. RESULTS: We found a transcript from RNA sequence data, termed hsa_circ_0001578, which is a circRNA spliced from RANBP9. Circ-RANBP9 was downregulated in the LC cell lines tissues, relating to a better prognosis. Circ-RANBP9 was found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. For the diagnostic value of circ-RANBP9, the sensitivity and the specificity were 0.979 and 0.553, respectively. Circ-RANBP9 downregulation was significantly correlated with differentiation (P=0.031), T-stage (P=0.018), lymphatic metastasis (P=0.046), and clinical stage (P=0.003). Circ-RANBP9 was involved in insulin-like growth factor receptor binding, cell polarity, focal adhesion, and MAPK signaling pathways. CeRNA analysis identified the possible involvement of circ-RANBP9 in the ECM-receptor interaction, cAMP, calcium, and Wnt signaling pathways by harboring miRNA genes. CONCLUSIONS: Circ-RANBP9 was confirmed to play important roles in inhibiting laryngeal cancers. Circ-RANBP9 was also validated to be associated with the clinicopathological parameters and diagnostic value, suggesting that circ-RANBP9 is a promising biomarker for LC prognosis and early diagnosis.	NA	Ann Transl Med. 2021 Mar;9(6):484. doi: 10.21037/atm-21-567.
3897	Circular RNA	Circ-RANBP9	miR-3131	LAMA2	laryngeal cancer tissues and cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33850881	Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance.	BACKGROUND: Laryngeal cancer (LC) is a common malignant tumor of the head and neck. As circular RNAs (circRNAs) and other non-coding RNAs are involved in various malignant processes, we analyzed circRNAs to better understand LC and explored specific tumor markers. METHODS: High-throughput sequence was performed to analyze the differential circular RNAs in four coupled laryngeal cancers and para-cancerous tissues. The differential expression of selected circ-RANBP9 in laryngeal cancer tissues and cells was verified by RT-qPCR assay. CCK8, EDU, Transwell and wound healing assays were used to confirm the biological function of circ-RANBP9 in laryngeal cancer. Western blot assay was performed to identify the effects of circ-RANBP9 having on the epithelial to mesenchymal transition process. One-way AN0VA was used to analyze the correlation between the expression of circ-RANBP9 and clinicopathological parameters of the included patients. Kaplan-Meier analysis was used to investigate whether the expression level of circ-RANBP9 correlated with survival in LC patients. Bioinformatic analyses were also conducted to predict the functions and possible signaling pathways of the targeted mRNAs of circ-RANBP9 via co-expression and competing endogenous RNA network. RESULTS: We found a transcript from RNA sequence data, termed hsa_circ_0001578, which is a circRNA spliced from RANBP9. Circ-RANBP9 was downregulated in the LC cell lines tissues, relating to a better prognosis. Circ-RANBP9 was found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. For the diagnostic value of circ-RANBP9, the sensitivity and the specificity were 0.979 and 0.553, respectively. Circ-RANBP9 downregulation was significantly correlated with differentiation (P=0.031), T-stage (P=0.018), lymphatic metastasis (P=0.046), and clinical stage (P=0.003). Circ-RANBP9 was involved in insulin-like growth factor receptor binding, cell polarity, focal adhesion, and MAPK signaling pathways. CeRNA analysis identified the possible involvement of circ-RANBP9 in the ECM-receptor interaction, cAMP, calcium, and Wnt signaling pathways by harboring miRNA genes. CONCLUSIONS: Circ-RANBP9 was confirmed to play important roles in inhibiting laryngeal cancers. Circ-RANBP9 was also validated to be associated with the clinicopathological parameters and diagnostic value, suggesting that circ-RANBP9 is a promising biomarker for LC prognosis and early diagnosis.	NA	Ann Transl Med. 2021 Mar;9(6):484. doi: 10.21037/atm-21-567.
3898	Circular RNA	Circ-RANBP9	miR-611	LAMA2	laryngeal cancer tissues and cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33850881	Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance.	BACKGROUND: Laryngeal cancer (LC) is a common malignant tumor of the head and neck. As circular RNAs (circRNAs) and other non-coding RNAs are involved in various malignant processes, we analyzed circRNAs to better understand LC and explored specific tumor markers. METHODS: High-throughput sequence was performed to analyze the differential circular RNAs in four coupled laryngeal cancers and para-cancerous tissues. The differential expression of selected circ-RANBP9 in laryngeal cancer tissues and cells was verified by RT-qPCR assay. CCK8, EDU, Transwell and wound healing assays were used to confirm the biological function of circ-RANBP9 in laryngeal cancer. Western blot assay was performed to identify the effects of circ-RANBP9 having on the epithelial to mesenchymal transition process. One-way AN0VA was used to analyze the correlation between the expression of circ-RANBP9 and clinicopathological parameters of the included patients. Kaplan-Meier analysis was used to investigate whether the expression level of circ-RANBP9 correlated with survival in LC patients. Bioinformatic analyses were also conducted to predict the functions and possible signaling pathways of the targeted mRNAs of circ-RANBP9 via co-expression and competing endogenous RNA network. RESULTS: We found a transcript from RNA sequence data, termed hsa_circ_0001578, which is a circRNA spliced from RANBP9. Circ-RANBP9 was downregulated in the LC cell lines tissues, relating to a better prognosis. Circ-RANBP9 was found to inhibit the proliferation, migration, and invasion ability of LC, exerting a suppressive role in the epithelial to mesenchymal transition process as well. For the diagnostic value of circ-RANBP9, the sensitivity and the specificity were 0.979 and 0.553, respectively. Circ-RANBP9 downregulation was significantly correlated with differentiation (P=0.031), T-stage (P=0.018), lymphatic metastasis (P=0.046), and clinical stage (P=0.003). Circ-RANBP9 was involved in insulin-like growth factor receptor binding, cell polarity, focal adhesion, and MAPK signaling pathways. CeRNA analysis identified the possible involvement of circ-RANBP9 in the ECM-receptor interaction, cAMP, calcium, and Wnt signaling pathways by harboring miRNA genes. CONCLUSIONS: Circ-RANBP9 was confirmed to play important roles in inhibiting laryngeal cancers. Circ-RANBP9 was also validated to be associated with the clinicopathological parameters and diagnostic value, suggesting that circ-RANBP9 is a promising biomarker for LC prognosis and early diagnosis.	NA	Ann Transl Med. 2021 Mar;9(6):484. doi: 10.21037/atm-21-567.
3899	Circular RNA	CircPVT1	miR-30d	HuR	LUSC cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down;RNA sequencing;	34112238	CircPVT1 promotes proliferation of lung squamous cell carcinoma by binding to miR-30d/e.	BACKGROUND: Circular RNAs (circRNAs) are a new type of extensive non-coding RNAs that regulate the activation and progression of different human diseases, including cancer. However, information on the underlying mechanisms and clinical significance of circRNAs in lung squamous cell carcinoma (LUSC) remains scant. METHODS: The expression profile of RNAs in 8 LUSC tissues, and 9 healthy lung tissues were assayed using RNA sequencing (RNA-seq) techniques. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to profile the expression of circPVT1 and its relationship with the prognosis of LUSC, i.e., survival analysis. Moreover, in vitro and in vivo experiments were performed to evaluate the impacts of circPVT1 on the growth of tumors. RNA pull-down tests, mass spectrometry, dual-luciferase reporter assessment, and RNA immune-precipitation tests were further conducted to interrogate the cross-talk between circPVT1, HuR, or miR-30d/e in LUSC. RESULTS: Our data showed that circPVT1 was upregulated in LUSC tissues, serum, and cell lines. LUSC patients with higher circPVT1 expression exhibited shorter survival rates. The in vivo and in vitro data revealed that circPVT1 promotes the proliferation of LUSC cells. Additionally, mechanistic analysis showed that HuR regulated circPVT1. On the other hand, circPVT1 acted as a competing endogenous RNA (ceRNA) of miR-30d and miR-30e in alleviating the suppressive influences of miR-30d and miR-30e on its target cyclin F (CCNF). CONCLUSION: CircPVT1 promotes LUSC progression via HuR/circPVT1/miR-30d and miR-30e/CCNF cascade. Also, it acts as a novel diagnostic biomarker or treatment target of individuals diagnosed with LUSC.	NA	J Exp Clin Cancer Res. 2021 Jun 10;40(1):193. doi: 10.1186/s13046-021-01976-w.
3900	Circular RNA	CircPVT1	miR-30e	HuR	LUSC cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down;RNA sequencing;	34112238	CircPVT1 promotes proliferation of lung squamous cell carcinoma by binding to miR-30d/e.	BACKGROUND: Circular RNAs (circRNAs) are a new type of extensive non-coding RNAs that regulate the activation and progression of different human diseases, including cancer. However, information on the underlying mechanisms and clinical significance of circRNAs in lung squamous cell carcinoma (LUSC) remains scant. METHODS: The expression profile of RNAs in 8 LUSC tissues, and 9 healthy lung tissues were assayed using RNA sequencing (RNA-seq) techniques. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to profile the expression of circPVT1 and its relationship with the prognosis of LUSC, i.e., survival analysis. Moreover, in vitro and in vivo experiments were performed to evaluate the impacts of circPVT1 on the growth of tumors. RNA pull-down tests, mass spectrometry, dual-luciferase reporter assessment, and RNA immune-precipitation tests were further conducted to interrogate the cross-talk between circPVT1, HuR, or miR-30d/e in LUSC. RESULTS: Our data showed that circPVT1 was upregulated in LUSC tissues, serum, and cell lines. LUSC patients with higher circPVT1 expression exhibited shorter survival rates. The in vivo and in vitro data revealed that circPVT1 promotes the proliferation of LUSC cells. Additionally, mechanistic analysis showed that HuR regulated circPVT1. On the other hand, circPVT1 acted as a competing endogenous RNA (ceRNA) of miR-30d and miR-30e in alleviating the suppressive influences of miR-30d and miR-30e on its target cyclin F (CCNF). CONCLUSION: CircPVT1 promotes LUSC progression via HuR/circPVT1/miR-30d and miR-30e/CCNF cascade. Also, it acts as a novel diagnostic biomarker or treatment target of individuals diagnosed with LUSC.	NA	J Exp Clin Cancer Res. 2021 Jun 10;40(1):193. doi: 10.1186/s13046-021-01976-w.
3901	Circular RNA	CircMYH9	miR-761	HDGF	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33992597	Use Chou's 5-steps rule to study how Baicalin suppresses the malignant phenotypes and induces the apoptosis of colorectal cancer cells.	Baicalin is a traditional Chinese herb purified from the root of Scutellaria baicalensis Georgi. In this study, we further analyzed the molecular mechanism behind the anti-tumor activity of Baicalin in colorectal cancer (CRC). The establishment of circular RNA (circRNA)/microRNA (miRNA)/messenger RNA (mRNA) axis was predicted by bioinformatic databases and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Baicalin dose-dependently reduced the expression of circRNA myosin heavy chain 9 (circMYH9) in CRC cells. Baicalin exposure suppressed the malignant phenotypes of CRC cells, which were largely reversed by the overexpression of circMYH9. CircMYH9 functioned as a molecular sponge for miR-761. CircMYH9 overexpression protected CRC cells from Baicalin-induced injury partly through down-regulating miR-761. MiR-761 interacted with the 3' untranslated region (3' UTR) of hepatoma-derived growth factor (HDGF) mRNA. CircMYH9 up-regulated HDGF expression partly through sponging miR-761 in CRC cells. MiR-761 silencing counteracted the anti-tumor activity of Baicalin partly through up-regulating HDGF in CRC cells. Baicalin suppresses xenograft tumor growth in vivo, and this suppressive effect was partly reversed by the overexpression of circMYH9. In conclusion, Baicalin exhibited an anti-tumor activity in CRC cells partly through down-regulating circMYH9 and HDGF and up-regulating miR-761.	NA	Arch Biochem Biophys. 2021 Jul 15;705:108919. doi: 10.1016/j.abb.2021.108919. Epub 2021 May 13.
3902	Circular RNA	CircMTO1	miR-219a-5p	Smad2	human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR	34113391	circMTO1 sponges microRNA-219a-5p to enhance gallbladder cancer progression via the TGF-β/Smad and EGFR pathways.	Circular mitochondrial translation optimization 1 homologue (circMTO1) has been reported to regulate the tumorigenesis of different types of cancer; however, the role of circMTO1 in gallbladder cancer (GBC) remains unknown. The present study aimed to identify the potential miRNAs and target genes of circMTO1 during GBC progression, and clarify the regulatory mechanism between circMTO1 and miRNAs or target genes. The present study performed MTT and Transwell assays, and Annexin V staining to assess cell viability, migration and apoptosis, respectively. In addition, a lymphatic vessel formation assay was performed to assess tube formation of human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells. The results demonstrated that circMTO1 knockdown significantly attenuated the viability and migration of GBC cells and tube formation of HDLECs, and promoted apoptosis, indicating a tumor-promoting role of circMTO1. In addition, transfection with microRNA (miRNA/miR)-219a-5p inhibitor rescued short hairpin RNA-circMTO1-inhibited tumorigenesis of GBC cells, suggesting that miR-219a-5p acts as a downstream effector for circMTO1. Mechanistically, transfection with miR-219a-5p mimic suppressed the expression levels of Smad2/4 and epidermal growth factor receptor. Analysis of The Cancer Genome Atlas datasets revealed that circMTO1 expression was associated with overall survival and the stage of patients with GBC. Taken together, the results of the present study provide novel insight for the role of circMTO1-induced GBC tumorigenesis via regulation of miR-219a-5p expression.	NA	Oncol Lett. 2021 Jul;22(1):563. doi: 10.3892/ol.2021.12824. Epub 2021 May 27.
3903	Circular RNA	CircMTO1	miR-219a-5p	Smad4	human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR	34113391	circMTO1 sponges microRNA-219a-5p to enhance gallbladder cancer progression via the TGF-β/Smad and EGFR pathways.	Circular mitochondrial translation optimization 1 homologue (circMTO1) has been reported to regulate the tumorigenesis of different types of cancer; however, the role of circMTO1 in gallbladder cancer (GBC) remains unknown. The present study aimed to identify the potential miRNAs and target genes of circMTO1 during GBC progression, and clarify the regulatory mechanism between circMTO1 and miRNAs or target genes. The present study performed MTT and Transwell assays, and Annexin V staining to assess cell viability, migration and apoptosis, respectively. In addition, a lymphatic vessel formation assay was performed to assess tube formation of human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells. The results demonstrated that circMTO1 knockdown significantly attenuated the viability and migration of GBC cells and tube formation of HDLECs, and promoted apoptosis, indicating a tumor-promoting role of circMTO1. In addition, transfection with microRNA (miRNA/miR)-219a-5p inhibitor rescued short hairpin RNA-circMTO1-inhibited tumorigenesis of GBC cells, suggesting that miR-219a-5p acts as a downstream effector for circMTO1. Mechanistically, transfection with miR-219a-5p mimic suppressed the expression levels of Smad2/4 and epidermal growth factor receptor. Analysis of The Cancer Genome Atlas datasets revealed that circMTO1 expression was associated with overall survival and the stage of patients with GBC. Taken together, the results of the present study provide novel insight for the role of circMTO1-induced GBC tumorigenesis via regulation of miR-219a-5p expression.	NA	Oncol Lett. 2021 Jul;22(1):563. doi: 10.3892/ol.2021.12824. Epub 2021 May 27.
3904	Circular RNA	CircMTO1	miR-219a-5p	EGFR	human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR	34113391	circMTO1 sponges microRNA-219a-5p to enhance gallbladder cancer progression via the TGF-β/Smad and EGFR pathways.	Circular mitochondrial translation optimization 1 homologue (circMTO1) has been reported to regulate the tumorigenesis of different types of cancer; however, the role of circMTO1 in gallbladder cancer (GBC) remains unknown. The present study aimed to identify the potential miRNAs and target genes of circMTO1 during GBC progression, and clarify the regulatory mechanism between circMTO1 and miRNAs or target genes. The present study performed MTT and Transwell assays, and Annexin V staining to assess cell viability, migration and apoptosis, respectively. In addition, a lymphatic vessel formation assay was performed to assess tube formation of human dermal lymphatic endothelial cells (HDLECs), and GBC-SD and NOZ cells. The results demonstrated that circMTO1 knockdown significantly attenuated the viability and migration of GBC cells and tube formation of HDLECs, and promoted apoptosis, indicating a tumor-promoting role of circMTO1. In addition, transfection with microRNA (miRNA/miR)-219a-5p inhibitor rescued short hairpin RNA-circMTO1-inhibited tumorigenesis of GBC cells, suggesting that miR-219a-5p acts as a downstream effector for circMTO1. Mechanistically, transfection with miR-219a-5p mimic suppressed the expression levels of Smad2/4 and epidermal growth factor receptor. Analysis of The Cancer Genome Atlas datasets revealed that circMTO1 expression was associated with overall survival and the stage of patients with GBC. Taken together, the results of the present study provide novel insight for the role of circMTO1-induced GBC tumorigenesis via regulation of miR-219a-5p expression.	NA	Oncol Lett. 2021 Jul;22(1):563. doi: 10.3892/ol.2021.12824. Epub 2021 May 27.
3905	Circular RNA	CircLDB2	miR-346	LIMCH1	NSCLC cell	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34096174	Circular RNA circLDB2 functions as a competing endogenous RNA to suppress development and promote cisplatin sensitivity in non-squamous non-small cell lung cancer.	BACKGROUND: Circular RNAs (circRNAs) are covalently closed RNAs and are implicated in the development of non-small cell lung cancer (NSCLC). Here, we identified the precise actions of circRNA LIM domain binding 2 (circLDB2, hsa_circ_0069244) in non-squamous NSCLC development and drug sensitivity. METHODS: CircLDB2, microRNA (miR)-346, and LIM and calponin-homology domains 1 (LIMCH1) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Ribonuclease R (RNase R), actinomycin D, and subcellular localization assays were used to characterize circLDB2. Cell proliferation and viability, colony formation, apoptosis, migration, and invasion were gauged by Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, wound-healing, and transwell assays, respectively. RNA immunoprecipitation (RIP), RNA pull-down, and dual-luciferase reporter assays were used to verify the direct relationship between miR-346 and circLDB2 or LIMCH1. Animal studies were performed to evaluate the impact of circLDB2 in vivo. RESULTS: CircLDB2 was underexpressed in non-squamous NSCLC and was identified as a bona fide circular transcript. Overexpression of circLDB2 impeded cell proliferation, migration, invasion, and enhanced apoptosis and cisplatin sensitivity in vitro, as well as promoted the antitumor effect of cisplatin in vivo. CircLDB2 regulated cell functional behaviors and cisplatin sensitivity by sponging miR-346. LIMCH1 was a direct and functional target of miR-346. Furthermore, circLDB2 acted as a competing endogenous RNA (ceRNA) for miR-346 to induce LIMCH1 expression. CONCLUSION: Our findings demonstrated that circLDB2 impeded non-squamous NSCLC development and enhanced cisplatin sensitivity partially by acting as a ceRNA, highlighting circLDB2 as a promising candidate for the development of novel antitumor therapies.	NA	Thorac Cancer. 2021 Jun 6. doi: 10.1111/1759-7714.13993.
3906	Circular RNA	Circ-KEL	miR-335-5p	LRG1	leukemic cells,bone marrow mononuclear cells	Acute Myeloid Leukemia	Homo sapiens (human)	Flow Cytometry assay;luciferase assay;	33910309	[Expression of circ-KEL in acute myeloid leukemia and its regulatory mechanisms in leukemic cells].	Objective: To explore the expression of circ-KEL in patients with acute myeloid leukemia (AML) and the effect and mechanism of circ-KEL on leukemic cells. Methods: The expression of circ-KEL was detected by quantitative real-time polymerase chain reaction in bone marrow mononuclear cells collected from 116 patients with AML and 40 healthy donors. The correlation of circ-KEL expression with the clinical characteristics of patients with AML was further systematically analyzed. The modulations among circ-KEL, miR-335-5p, and LRG1 were predicted through bioinformatics analysis and validated by dual luciferase assay. Cell proliferation and apoptosis were detected using CCK8 and flow cytometry. Results: The expression of circ-KEL was significantly elevated in patients with AML compared with the healthy controls (Relative expression level, -Δct, AML: -7.117±1.831; control: -8.669±1.771, P<0.001) . Moreover, patients with high circ-KEL expression have significantly worse overall survival. The level of circ-KEL in patients with AML was downregulated after chemo-treatment. In addition, circ-KEL could serve as the sponge of miR-335-5p and regulate LRG1. Bioinformatics analysis showed that miR-335-5p correlates with good prognosis and was negatively associated with LRG1. LRG1 could promote cell proliferation and inhibit cell apoptosis. Our results also exhibited the higher expression of LRG1 in patients with AML. Moreover, circ-KEL exerted functional effects via sponging miR-335-5p and regulating LRG1. Conclusion: circ-KEL expresses highly in patients with AML and correlates with poor prognosis, suggesting its important role in the genesis and progress of AML.	NA	Zhonghua Xue Ye Xue Za Zhi. 2021 Mar 14;42(3):230-237. doi: 10.3760/cma.j.issn.0253-2727.2021.03.009.
3907	Circular RNA	CircHIPK3	miR-124-3p	MRP4	hepatocellular carcinoma (HCC) tissues	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP;Luciferase reporter assay;	33946595	Regulation of MRP4 Expression by circHIPK3 via Sponging miR-124-3p/miR-4524-5p in Hepatocellular Carcinoma.	Multidrug resistance-associated protein 4 (MRP4), a member of the adenosine triphosphate (ATP) binding cassette transporter family, pumps various molecules out of the cell and is involved in cell communication and drug distribution. Several studies have reported the role of miRNAs in downregulating the expression of MRP4. However, regulation of MRP4 by circular RNA (circRNA) is yet to be elucidated. In this study, MRP4 was significantly upregulated in hepatocellular carcinoma (HCC) tissues compared to the adjacent noncancerous tissues. Computational prediction, luciferase reporter assay and miRNA transfection were used to investigate the interaction between miRNAs and MRP4. miR-124-3p and miR-4524-5p reduced the expression of MRP4 at the protein but not mRNA level. Circular RNA in vivo precipitation and luciferase reporter assays demonstrated that circHIPK3, as a competitive endogenous RNA, binds with miR-124-3p and miR-4524-5p. Further, knockdown of circHIPK3 resulted in downregulation of MRP4 protein, whereas cotransfection of circHIPK3-siRNA and miR-124-3p or miR-4524-5p inhibitors restored its expression. In conclusion, we report that miR-4524-5p downregulates the expression of MRP4 and circHIPK3 regulates MRP4 expression by sponging miR-124-3p and miR-4524-5p for the first time. Our results may provide novel insights into the prevention of MRP4-related proliferation and multiple drug resistance in HCC.	NA	Biomedicines. 2021 Apr 30;9(5):497. doi: 10.3390/biomedicines9050497.
3908	Circular RNA	CircHIPK3	miR-4524-5p	MRP4	hepatocellular carcinoma (HCC) tissues	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP;Luciferase reporter assay;	33946595	Regulation of MRP4 Expression by circHIPK3 via Sponging miR-124-3p/miR-4524-5p in Hepatocellular Carcinoma.	Multidrug resistance-associated protein 4 (MRP4), a member of the adenosine triphosphate (ATP) binding cassette transporter family, pumps various molecules out of the cell and is involved in cell communication and drug distribution. Several studies have reported the role of miRNAs in downregulating the expression of MRP4. However, regulation of MRP4 by circular RNA (circRNA) is yet to be elucidated. In this study, MRP4 was significantly upregulated in hepatocellular carcinoma (HCC) tissues compared to the adjacent noncancerous tissues. Computational prediction, luciferase reporter assay and miRNA transfection were used to investigate the interaction between miRNAs and MRP4. miR-124-3p and miR-4524-5p reduced the expression of MRP4 at the protein but not mRNA level. Circular RNA in vivo precipitation and luciferase reporter assays demonstrated that circHIPK3, as a competitive endogenous RNA, binds with miR-124-3p and miR-4524-5p. Further, knockdown of circHIPK3 resulted in downregulation of MRP4 protein, whereas cotransfection of circHIPK3-siRNA and miR-124-3p or miR-4524-5p inhibitors restored its expression. In conclusion, we report that miR-4524-5p downregulates the expression of MRP4 and circHIPK3 regulates MRP4 expression by sponging miR-124-3p and miR-4524-5p for the first time. Our results may provide novel insights into the prevention of MRP4-related proliferation and multiple drug resistance in HCC.	NA	Biomedicines. 2021 Apr 30;9(5):497. doi: 10.3390/biomedicines9050497.
3909	Circular RNA	Circ-HACE1	miR-485-3p	TLR4	16HBE cells	Cigarette Smoke Extract-Induced Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34103911	Circ-HACE1 Aggravates Cigarette Smoke Extract-Induced Injury in Human Bronchial Epithelial Cells via Regulating Toll-Like Receptor 4 by Sponging miR-485-3p.	BACKGROUND: Smoking is the most common cause of chronic obstructive pulmonary disease (COPD), and the early diagnosis for COPD remains poor. Exploring the molecular mechanism and finding feasible biomarkers will be beneficial for clinical management of COPD. Circular RNAs (circRNAs) are noncoding RNAs that act as miRNA sponges to regulate the expression levels of genes, leading to the changes of cellular phenotypes and disease progression. CircRNA HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (circ-HACE1) was abnormally expressed after the induction of cigarette smoke extract (CSE) in cell model. This study was performed to explore its function and mechanism in COPD. METHODS: Circ-HACE1, microRNA-485-3p (miR-485-3p) and toll-like receptor 4 (TLR4) detection was performed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis/cell cycle were respectively examined using cell counting kit-8 (CCK-8) and flow cytometry. Inflammatory cytokines were determined by enzyme-linked immunosorbent assay (ELISA). Oxidative stress was evaluated through the measurement of malondialdehyde (MDA) and superoxide dismutase (SOD). The target binding analysis was conducted via dual-luciferase reporter assay. Western blot was employed for protein expression detection of TLR4. RESULTS: Circ-HACE1 was overexpressed in smokers or smokers with COPD and CSE upregulated circ-HACE1 expression in 16HBE cells. Knockdown of circ-HACE1 attenuated CSE-stimulated cell viability and cell cycle repression, as well as the enhancement of cell apoptosis, inflammatory response and oxidative stress. MiR-485-3p was a target of circ-HACE1. Circ-HACE1 regulated CSE-induced cell injury via targeting miR-485-3p. TLR4 was a downstream target of miR-485-3p, and miR-485-3p inhibited the CSE-induced cell damages by directly downregulating the level of TLR4. Circ-HACE1/miR-485-3p regulated TLR4 expression in CSE-treated 16HBE cells, and TLR4 overexpression also reversed all effects of si-circ-HACE1 on CSE-treated 16HBE cells. CONCLUSION: These findings elucidated that circ-HACE1 contributed to the CSE-induced cell damages in COPD cell models via regulating TLR4 by acting as the sponge of miR-485-3p.	NA	Int J Chron Obstruct Pulmon Dis. 2021 Jun 1;16:1535-1547. doi: 10.2147/COPD.S304859. eCollection 2021.
3910	Circular RNA	CircFBXW7	miR-942-5p	BARX2	A549 and HCC2279 cell lines	Lung Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;RNA pull-down;	33889522	circFBXW7 attenuates malignant progression in lung adenocarcinoma by sponging miR-942-5p.	BACKGROUND: As a type of non-coding RNA, circular RNAs (circRNAs) are considered to be functional molecules associated with human cancers. An increasing number of circRNAs have been verified in malignant progression in a number of cancers. The circRNA, circFBXW7, has been proven to play an important role in tumor proliferation and metastasis. However, whether circFBXW7 influences progression in lung adenocarcinoma (LUAD) remains unclear. METHODS: Quantitative real-time reverse transcriptase PCR (qRT-PCR) was used to verify circFBXW7 in LUAD cell lines and LUAD tissues. Kaplan-Meier analysis was then used to compare the disease-free survival (DFS) and overall survival (OS) of these LUAD patients. The biological function of circFBXW7 was examined by overexpression and knockdown of circFBXW7 using MTT assay, EdU assay, wound-healing assay, and Transwell in vitro assays. To explore the mechanism of the circFBXW7, RNA pull-down assay, dual luciferase reporter assay, and RNA immunoprecipitation (RIP) assay were employed to examine the interaction between circFBXW7 and miR-942-5p. Western blot was used to study the fundamental proteins associated with the epithelial-mesenchymal transition (EMT) pathway. In vivo studies with BALB/c nude mice subcutaneously injected with cells stably overexpressing circFBXW7 were performed to further validate the in vitro results. RESULTS: circFBXW7 was downregulated in LUAD cell lines and tissues, and LUAD patients with lower levels had shorter DFS and OS. The in vitro study showed that circFBXW7 overexpression inhibited proliferation and migration of A549 and HCC2279 cell lines. These results were confirmed by circFBXW7 knockdown, which showed the reverse effect. The in vivo model showed that the circRNA levels influenced the tumor growth. Finally, we determined that circFBXW7 target miRNA-942-5p which regulates the EMT gene BARX2. The modulation of circFBXW7 levels produced significant changes in EMT genes in vitro and in vivo. CONCLUSIONS: Our findings showed that circFBXW7 inhibits proliferation and migration by controlling the miR-942-5p/BARX2 axis in LUAD cell lines and its levels correlates with patient survival suggesting that regulating circFBXW7 could have therapeutic value in treating LUAD patients.	NA	Transl Lung Cancer Res. 2021 Mar;10(3):1457-1473. doi: 10.21037/tlcr-21-230.
3911	Circular RNA	CircBFAR	miR-513a-3p	HK2	GC cells	Gastric Cancer	Homo sapiens (human)	RACE;	33979737	Knockdown of circBFAR inhibits proliferation and glycolysis in gastric cancer by sponging miR-513a-3p/hexokinase 2 axis.	The relationship between circular RNAs (circRNAs) and many types of cancer has been of great interest. A novel circRNA, circBFAR, has been identified, but the functions of circBFAR and its underlying mechanism in gastric cancer (GC) have not been reported. This study was designed to investigate the role of circBFAR in GC and its downstream miRNA targets. Quantitative real-time polymerase reaction was used to detect the expression of circBFAR and miRNAs. Cell counting kit-8 and EdU were used to detect the proliferation of GC cells. Measurement of the extracellular acidification rate, oxygen consumption rate and lactate acid production were performed to assess the glycolysis levels. The results showed that circBFAR exhibited higher expression in GC tissues and cell lines. circBFAR was proven to promote GC proliferation by targeting the miR-513a-3p/hexokinase 2 (HK2) axis. Inhibition of circBFAR also led to a significant decrease in the glycolysis levels. In this study, we found a circBFAR/miR-513a-3p/HK2 axis in GC and revealed the relationship between circBFAR and glycolysis for the first time. circBFAR may serve as a novel target of GC individualized therapy.	NA	Biochem Biophys Res Commun. 2021 Jun 30;560:80-86. doi: 10.1016/j.bbrc.2021.04.131. Epub 2021 May 9.
3912	Circular RNA	CircASXL1	miR-1205	GRIK3	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	34127015	CircASXL1 knockdown represses the progression of colorectal cancer by downregulating GRIK3 expression by sponging miR-1205.	BACKGROUND: Colorectal cancer (CRC) is a common aggressive tumor that poses a heavy burden to human health. An increasing number of studies have reported that circular RNA (circRNA) is involved in the progression of CRC. In this study, the special profiles of circASXL1 (circ_0001136) in CRC progression were revealed. METHODS: The expression of circASXL1, microRNA-1205 (miR-1205), and glutamate ionotropic receptor kainate type subunit 3 (GRIK3) mRNA was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression was determined by Western blot or immunohistochemistry. Cell colony-forming ability was investigated by colony formation assay. Cell cycle and apoptosis were demonstrated using cell-cycle and cell-apoptosis analysis assays, respectively. Cell migration and invasion were detected by wound-healing and transwell migration and invasion assays, respectively. The binding sites between miR-1205 and circASXL1 or GRIK3 were predicted by circBank or miRDB online database, and identified by dual-luciferase reporter assay. The impact of circASXL1 on tumor formation in vivo was investigated by in vivo tumor formation assay. RESULTS: CircASXL1 and GRIK3 expression were apparently upregulated, and miR-1205 expression was downregulated in CRC tissues and cells relative to control groups. CircASXL1 knockdown inhibited cell colony-forming ability, migration and invasion, whereas induced cell arrest at G0/G1 phase and cell apoptosis in CRC cells; however, these effects were attenuated by miR-1205 inhibitor. Additionally, circASXL1 acted as a sponge for miR-1205, and miR-1205 was associated with GRIK3. Furthermore, circASXL1 silencing hindered tumor formation by upregulating miR-1205 and downregulating GRIK3 expression. CONCLUSION: CircASXL1 acted an oncogenic role in CRC malignant progression via inducing GRIK3 through sponging miR-1205. Our findings provide a theoretical basis for studying circASXL1-directed therapy for CRC.	NA	World J Surg Oncol. 2021 Jun 14;19(1):176. doi: 10.1186/s12957-021-02275-6.
3913	Circular RNA	Circ-140	miR-8516	STC1	Goat Mammary Epithelial Cells	Mammary Gland Development	Homo sapiens (human)	qRT-PCR	33946970	Circ-140/chi-miR-8516/STC1-MMP1 Regulates αs1-/β-Casein Secretion and Lipid Formation in Goat Mammary Epithelial Cells.	MicroRNAs play an essential role in mammary gland development, and involution is a factor that limits lactation. Chi-miR-8516 is one of the validated microRNAs that regulates the expression of STC1 and MMP1, which surge during the involution of the mammary gland. This study aims to explore the direct or indirect regulation of STC1 and MMP1 by chi-miR-8516 and the regulation of chi-miR-8516 by circ-140. In goat mammary epithelial cells, we found that chi-miR-8516 takes circ-140 as a sponge and regulates MMP1 expression by targeting STC1 and promoting the phosphorylation of MAPK. The examination of αs1-/β-casein and lipid showed the modulation of the circ-140/chi-miR-8516/STC1-MMP1 axis in casein secretion and lipid formation, which was regulated by the phosphorylation of mTOR and STAT5. This study illustrates an axis that regulates the synthesis of milk components, and explores the pathways in which the axis participates.	NA	Genes (Basel). 2021 Apr 29;12(5):671. doi: 10.3390/genes12050671.
3914	Circular RNA	Circ-140	miR-8516	MMP1	Goat Mammary Epithelial Cells	Mammary Gland Development	Homo sapiens (human)	qRT-PCR	33946970	Circ-140/chi-miR-8516/STC1-MMP1 Regulates αs1-/β-Casein Secretion and Lipid Formation in Goat Mammary Epithelial Cells.	MicroRNAs play an essential role in mammary gland development, and involution is a factor that limits lactation. Chi-miR-8516 is one of the validated microRNAs that regulates the expression of STC1 and MMP1, which surge during the involution of the mammary gland. This study aims to explore the direct or indirect regulation of STC1 and MMP1 by chi-miR-8516 and the regulation of chi-miR-8516 by circ-140. In goat mammary epithelial cells, we found that chi-miR-8516 takes circ-140 as a sponge and regulates MMP1 expression by targeting STC1 and promoting the phosphorylation of MAPK. The examination of αs1-/β-casein and lipid showed the modulation of the circ-140/chi-miR-8516/STC1-MMP1 axis in casein secretion and lipid formation, which was regulated by the phosphorylation of mTOR and STAT5. This study illustrates an axis that regulates the synthesis of milk components, and explores the pathways in which the axis participates.	NA	Genes (Basel). 2021 Apr 29;12(5):671. doi: 10.3390/genes12050671.
3915	Circular RNA	Circ-140	miR-8516	STC1	Capra hircus (goat)	Mammary Gland Development	Homo sapiens (human)	qRT-PCR	33946970	Circ-140/chi-miR-8516/STC1-MMP1 Regulates αs1-/β-Casein Secretion and Lipid Formation in Goat Mammary Epithelial Cells.	MicroRNAs play an essential role in mammary gland development, and involution is a factor that limits lactation. Chi-miR-8516 is one of the validated microRNAs that regulates the expression of STC1 and MMP1, which surge during the involution of the mammary gland. This study aims to explore the direct or indirect regulation of STC1 and MMP1 by chi-miR-8516 and the regulation of chi-miR-8516 by circ-140. In goat mammary epithelial cells, we found that chi-miR-8516 takes circ-140 as a sponge and regulates MMP1 expression by targeting STC1 and promoting the phosphorylation of MAPK. The examination of αs1-/β-casein and lipid showed the modulation of the circ-140/chi-miR-8516/STC1-MMP1 axis in casein secretion and lipid formation, which was regulated by the phosphorylation of mTOR and STAT5. This study illustrates an axis that regulates the synthesis of milk components, and explores the pathways in which the axis participates.	NA	Genes (Basel). 2021 Apr 29;12(5):671. doi: 10.3390/genes12050671.
3916	Circular RNA	Circ-140	miR-8516	MMP1	Capra hircus (goat)	Mammary Gland Development	Homo sapiens (human)	qRT-PCR	33946970	Circ-140/chi-miR-8516/STC1-MMP1 Regulates αs1-/β-Casein Secretion and Lipid Formation in Goat Mammary Epithelial Cells.	MicroRNAs play an essential role in mammary gland development, and involution is a factor that limits lactation. Chi-miR-8516 is one of the validated microRNAs that regulates the expression of STC1 and MMP1, which surge during the involution of the mammary gland. This study aims to explore the direct or indirect regulation of STC1 and MMP1 by chi-miR-8516 and the regulation of chi-miR-8516 by circ-140. In goat mammary epithelial cells, we found that chi-miR-8516 takes circ-140 as a sponge and regulates MMP1 expression by targeting STC1 and promoting the phosphorylation of MAPK. The examination of αs1-/β-casein and lipid showed the modulation of the circ-140/chi-miR-8516/STC1-MMP1 axis in casein secretion and lipid formation, which was regulated by the phosphorylation of mTOR and STAT5. This study illustrates an axis that regulates the synthesis of milk components, and explores the pathways in which the axis participates.	NA	Genes (Basel). 2021 Apr 29;12(5):671. doi: 10.3390/genes12050671.
3917	Circular RNA	Circ_0072088	miR-375	JAK2	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34148288	Circ_0072088 promotes progression of hepatocellular carcinoma by activating JAK2/STAT3 signaling pathway via miR-375.	BACKGROUND: Circular RNAs feature prominently in cancer development. Nonetheless, the role of circ_0072088 in hepatocellular carcinoma (HCC) remains unclear. METHODS: GEO databases (GSE97332, GSE108724, GSE36915, and GSE33006) were used to screen out the differentially expressed circRNAs, miRNAs, and mRNA in HCC. The expressions of circ_0072088, miR-375, and Janus Kinase 2 (JAK2) mRNA in HCC tissue and cell lines were determined with quantitative real-time polymerase chain reaction (qRT-PCR). RNase R treatment assay was used to measure the stability of circ_0072088, and subcellular fraction assay was used to detect the localization of circ_0072088. Cell counting kit-8 (CCK-8) assay, flow cytometry, and Transwell assay were used to measure proliferation, apoptosis, migration, and invasion of HCC cells. RNA immunoprecipitation and dual-luciferase reporter gene assay were employed for investigating the binding sequence between circ_0072088 and miR-375, as well as miR-375 and JAK2 3'UTR. Western blot assay was used to detect the expression of JAK2 and p-STAT3 after circ_0072088 and miR-375 were selectively regulated. RESULTS: Circ_0072088 and JAK2 mRNA expressions were highly expressed in HCC tissues and cell lines while miR-375 expression was remarkably downregulated. Circ_0072088 was resistance to RNase R treatment and mainly located in the cytoplasm of HCC cells. The transfection of circ_0072088 overexpression plasmid or miR-375 inhibitors promoted the proliferation, migration, and invasion, and inhibited the apoptosis of HCC cells whereas transfection of circ_0072088 siRNA or miR-375 mimics exerted opposite effects. Besides, miR-375 was confirmed as a target of circ_0072088 and miR-375 could further downregulate the expression of JAK2. MiR-375 mimics could reverse the upregulation of JAK2 and p-STAT3 protein induced by circ_0072088 overexpression. CONCLUSION: Circ_0072088 can enhance the proliferation, migration, and invasion, and impede apoptosis of HCC cells. Mechanistically, circ_0072088 activates JAK2/STAT3 signaling pathway by serving as a molecular sponge of miR-375.	NA	IUBMB Life. 2021 Jun 20. doi: 10.1002/iub.2520.
3918	Circular RNA	Circ_0072088	miR-375	STAT3	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34148288	Circ_0072088 promotes progression of hepatocellular carcinoma by activating JAK2/STAT3 signaling pathway via miR-375.	BACKGROUND: Circular RNAs feature prominently in cancer development. Nonetheless, the role of circ_0072088 in hepatocellular carcinoma (HCC) remains unclear. METHODS: GEO databases (GSE97332, GSE108724, GSE36915, and GSE33006) were used to screen out the differentially expressed circRNAs, miRNAs, and mRNA in HCC. The expressions of circ_0072088, miR-375, and Janus Kinase 2 (JAK2) mRNA in HCC tissue and cell lines were determined with quantitative real-time polymerase chain reaction (qRT-PCR). RNase R treatment assay was used to measure the stability of circ_0072088, and subcellular fraction assay was used to detect the localization of circ_0072088. Cell counting kit-8 (CCK-8) assay, flow cytometry, and Transwell assay were used to measure proliferation, apoptosis, migration, and invasion of HCC cells. RNA immunoprecipitation and dual-luciferase reporter gene assay were employed for investigating the binding sequence between circ_0072088 and miR-375, as well as miR-375 and JAK2 3'UTR. Western blot assay was used to detect the expression of JAK2 and p-STAT3 after circ_0072088 and miR-375 were selectively regulated. RESULTS: Circ_0072088 and JAK2 mRNA expressions were highly expressed in HCC tissues and cell lines while miR-375 expression was remarkably downregulated. Circ_0072088 was resistance to RNase R treatment and mainly located in the cytoplasm of HCC cells. The transfection of circ_0072088 overexpression plasmid or miR-375 inhibitors promoted the proliferation, migration, and invasion, and inhibited the apoptosis of HCC cells whereas transfection of circ_0072088 siRNA or miR-375 mimics exerted opposite effects. Besides, miR-375 was confirmed as a target of circ_0072088 and miR-375 could further downregulate the expression of JAK2. MiR-375 mimics could reverse the upregulation of JAK2 and p-STAT3 protein induced by circ_0072088 overexpression. CONCLUSION: Circ_0072088 can enhance the proliferation, migration, and invasion, and impede apoptosis of HCC cells. Mechanistically, circ_0072088 activates JAK2/STAT3 signaling pathway by serving as a molecular sponge of miR-375.	NA	IUBMB Life. 2021 Jun 20. doi: 10.1002/iub.2520.
3919	Circular RNA	Circ_0049447	miR-324-5p	PTPRD	MGC-803	Gastric Cancer	Mus musculus (mouse)	Western blot;Luciferase report assay;Luciferase reporter assay;	33883408	Circ_0049447 acts as a tumor suppressor in gastric cancer through reducing proliferation, migration, invasion, and epithelial-mesenchymal transition.	BACKGROUND: Although increasing abnormal expression of circular RNAs (circRNAs) has been revealed in various cancers, there were a small number of studies about circRNAs in gastric cancer (GC). Here, we explored the expression and function of a novel circRNA, circ_0049447, in GC. METHODS: A total of 80 GC tissues and non-tumorous tissues were collected from the First Affiliated Hospital of China Medical University. And all cells were cultured with 10% fetal bovine serum and incubated at 37°C and 5% CO2. The expression of circ_0049447 was quantified by real-time polymerase chain reaction. The biological function of circ_0049447 on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) was evaluated by cell counting kit-8 (CCK-8), colony formation assay, transwell migration and invasion assay, and Western blotting. Luciferase report assay was used to verify the direct binding between circ_0049447 and predicted microRNA (miRNA). Furthermore, a xenograft mouse model was used to validate the function of circ_0049447 in vivo. RESULTS: We demonstrated that circ_0049447 was downregulated in GC (P < 0.001). The area under the receiver operating characteristic curve reached 0.838, while sensitivity was 82.3% and specificity was 77.2%. CCK-8 and colony formation assay showed that overexpression of circ_0049447 could inhibit the proliferation (P < 0.05). Transwell migration and invasion assay showed upregulated circ_0049447 could impede migration in GC cells (P < 0.05). In addition, overexpression of circ_0049447 could impede GC cell EMT. Upregulation of miR-324-5p in GC specimens and direct binding between miR-324-5p with circ_0049447 proven by luciferase reporter assay indicated that circ_0049447 may inhibit GC by sponging certain miRNA. CONCLUSION: Circ_0049447 acts as a tumor suppressor in GC through reducing proliferation, migration, invasion, and EMT, and it is a promising biomarker for diagnosis.	NA	Chin Med J (Engl). 2021 Apr 20;134(11):1345-1355. doi: 10.1097/CM9.0000000000001494.
3920	Circular RNA	Circ_0049447	miR-324-5p	PTPRD	MGC-803	Gastric Cancer	Homo sapiens (human)	Western blot;Luciferase report assay;Luciferase reporter assay;	33883408	Circ_0049447 acts as a tumor suppressor in gastric cancer through reducing proliferation, migration, invasion, and epithelial-mesenchymal transition.	BACKGROUND: Although increasing abnormal expression of circular RNAs (circRNAs) has been revealed in various cancers, there were a small number of studies about circRNAs in gastric cancer (GC). Here, we explored the expression and function of a novel circRNA, circ_0049447, in GC. METHODS: A total of 80 GC tissues and non-tumorous tissues were collected from the First Affiliated Hospital of China Medical University. And all cells were cultured with 10% fetal bovine serum and incubated at 37°C and 5% CO2. The expression of circ_0049447 was quantified by real-time polymerase chain reaction. The biological function of circ_0049447 on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) was evaluated by cell counting kit-8 (CCK-8), colony formation assay, transwell migration and invasion assay, and Western blotting. Luciferase report assay was used to verify the direct binding between circ_0049447 and predicted microRNA (miRNA). Furthermore, a xenograft mouse model was used to validate the function of circ_0049447 in vivo. RESULTS: We demonstrated that circ_0049447 was downregulated in GC (P < 0.001). The area under the receiver operating characteristic curve reached 0.838, while sensitivity was 82.3% and specificity was 77.2%. CCK-8 and colony formation assay showed that overexpression of circ_0049447 could inhibit the proliferation (P < 0.05). Transwell migration and invasion assay showed upregulated circ_0049447 could impede migration in GC cells (P < 0.05). In addition, overexpression of circ_0049447 could impede GC cell EMT. Upregulation of miR-324-5p in GC specimens and direct binding between miR-324-5p with circ_0049447 proven by luciferase reporter assay indicated that circ_0049447 may inhibit GC by sponging certain miRNA. CONCLUSION: Circ_0049447 acts as a tumor suppressor in GC through reducing proliferation, migration, invasion, and EMT, and it is a promising biomarker for diagnosis.	NA	Chin Med J (Engl). 2021 Apr 20;134(11):1345-1355. doi: 10.1097/CM9.0000000000001494.
3921	Circular RNA	Circ_0015885	miR-23b	SESN3	porcine skeletal muscle	Skeletal Muscle Growth	Homo sapiens (human)	qRT-PCR;	33932987	Comprehensive analysis of differentially expressed circRNAs and ceRNA regulatory network in porcine skeletal muscle.	BACKGROUND: Circular RNA (circRNA), a novel class of non-coding RNA, has a closed-loop structure with important functions in skeletal muscle growth. The purpose of this study was to investigate the role of differentially expressed circRNAs (DEcircRNAs), as well as the DEcircRNA-miRNA-mRNA regulatory network, at different stages of porcine skeletal muscle development. Here, we present a panoramic view of circRNA expression in porcine skeletal muscle from Large White and Mashen pigs at 1, 90, and 180 days of age. RESULTS: We identified a total of 5819 circRNAs. DEcircRNA analysis at different stages showed 327 DEcircRNAs present in both breeds. DEcircRNA host genes were concentrated predominately in TGF-β, MAPK, FoxO, and other signaling pathways related to skeletal muscle growth and fat deposition. Further prediction showed that 128 DEcircRNAs could bind to 253 miRNAs, while miRNAs could target 945 mRNAs. The constructed ceRNA network plays a vital role in skeletal muscle growth and development, and fat deposition. Circ_0015885/miR-23b/SESN3 in the ceRNA network attracted our attention. miR-23b and SESN3 were found to participate in skeletal muscle growth regulation, also playing an important role in fat deposition. Using convergent and divergent primer amplification, RNase R digestion, and qRT-PCR, circ_0015885, an exonic circRNA derived from Homer Scaffold Protein 1 (HOMER1), was confirmed to be differentially expressed during skeletal muscle growth. In summary, circ_0015885 may further regulate SESN3 expression by interacting with miR-23b to function in skeletal muscle. CONCLUSIONS: This study not only enriched the circRNA library in pigs, but also laid a solid foundation for the screening of key circRNAs during skeletal muscle growth and intramural fat deposition. In addition, circ_0015885/miR-23b/SESN3, a new network regulating skeletal muscle growth and fat deposition, was identified as important for increasing the growth rate of pigs and improving meat quality.	NA	BMC Genomics. 2021 May 1;22(1):320. doi: 10.1186/s12864-021-07645-8.
3922	Circular RNA	Circ_0008542	miR-185-5p	RANK	MC3T3-E1 cells	Osteoclast-Induced Bone Resorption	Homo sapiens (human)	qRT-PCR	34145224	Circ_0008542 in osteoblast exosomes promotes osteoclast-induced bone resorption through m6A methylation.	With an increasing aging society, China is the world's fastest growing markets for oral implants. Compared with traditional oral implants, immediate implants cause marginal bone resorption and increase the failure rate of osseointegration, but the mechanism is still unknown. Therefore, it is important to further study mechanisms of tension stimulus on osteoblasts and osteoclasts at the early stage of osseointegration to promote rapid osseointegration around oral implants. The results showed that exosomes containing circ_0008542 from MC3T3-E1 cells with prolonged tensile stimulation promoted osteoclast differentiation and bone resorption. Circ_0008542 upregulated Tnfrsf11a (RANK) gene expression by acting as a miR-185-5p sponge. Meanwhile, the circ_0008542 1916-1992 bp segment exhibited increased m6A methylation levels. Inhibiting the RNA methyltransferase METTL3 or overexpressing the RNA demethylase ALKBH5 reversed osteoclast differentiation and bone resorption induced by circ_0008542. Injection of circ_0008542 + ALKBH5 into the tail vein of mice reversed the same effects in vivo. Site-directed mutagenesis study demonstrated that 1956 bp on circ_0008542 is the m6A functional site with the abovementioned biological functions. In conclusion, the RNA methylase METTL3 acts on the m6A functional site of 1956 bp in circ_0008542, promoting competitive binding of miRNA-185-5p by circ_0008542, and leading to an increase in the target gene RANK and the initiation of osteoclast bone absorption. In contrast, the RNA demethylase ALKBH5 inhibits the binding of circ_0008542 with miRNA-185-5p to correct the bone resorption process. The potential value of this study provides methods to enhance the resistance of immediate implants through use of exosomes releasing ALKBH5.	NA	Cell Death Dis. 2021 Jun 18;12(7):628. doi: 10.1038/s41419-021-03915-1.
3923	Circular RNA	Circ_0002951	miR-548k	HAS2	laryngeal carcinoma tissue	Laryngeal Carcinoma	Homo sapiens (human)	qRT-PCR	34093817	An integrative microenvironment approach for laryngeal carcinoma: the role of immune/methylation/autophagy signatures on disease clinical prognosis and single-cell genotypes.	The effects of methylation/autophagy-related genes (MARGs) and immune infiltration in the tumor microenvironment on the prognosis of laryngeal cancer were comprehensively explored in this study. Survival analysis screened out 126 MARGs and 10 immune cells potentially associated with the prognosis of laryngeal carcinoma. Cox and lasso regression analyses were then used to select 8 MARGs (CAPN10, DAPK2, MBTPS2, ST13, CFLAR, FADD, PEX14 and TSC2) and 2 immune cells (Eosinophil and Mast cell) to obtain the prognostic risk scoring system (pRS). The pRS was used to establish a risk prediction model for the prognosis of laryngeal cancer. The predictive ability of the prediction model was evaluated by GEO datasets and our clinical samples. Further analysis revealed that pRS is highly associated with single nucleotide polymorphism (SNP), copy number variation (CNV), immune checkpoint blockade (ICB) therapy and tumor microenvironment. Moreover, the screened pRS-related ceRNA network and circ_0002951/miR-548k/HAS2 pathway provide potential therapeutic targets and biomarkers of laryngocarcinoma. Based on the clustering results of pRS-related genes, single cells were then genotyped and revealed by integrated scRNA-seq in laryngeal cancer samples. Fibroblasts were found enriched in high risk cell clusters at the scRNA-seq level. Fibroblast-related ligand-receptor interactions were then exposed and a neural network-based deep learning model based on these pRS-related hub gene signatures was also established with a high accuracy in cell type prediction. In conclusion, the combination of single-cell and transcriptome laryngeal carcinoma landscape analyses can investigate the link between the tumor microenvironmental and prognostic characteristics.	NA	J Cancer. 2021 May 13;12(14):4148-4171. doi: 10.7150/jca.58076. eCollection 2021.
3924	Circular RNA	Circ_0001982	miR-1287-5p	MUC19	BC tissues and cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	34082777	Hsa_circ_0001982 promotes the progression of breast cancer through miR-1287-5p/MUC19 axis under hypoxia.	BACKGROUND: Breast cancer (BC) is the most commonly malignant tumor among women worldwide. Many studies have reported that circular RNAs (circRNAs) were participated in the regulation of multiple cancers development. However, the mechanism underlying hsa_circ_0001982 in breast cancer development is still unclear. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the levels of circ_0001982, microRNA-1287-5p (miR-1287-5p), and mucin 19 (MUC19) in BC tissues and cells under hypoxia. Moreover, glycolysis was evaluated by glucose consumption, lactic acid production, and hexokinase II (HK2) protein levels. The protein levels of cyclin D1, proliferating cell nuclear antigen (PCNA), and HK2 were determined by western blot assay. Cell proliferation, migration, and invasion were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-h-tetrazolium bromide (MTT) and transwell assays, respectively. The relationship between miR-1287-5p and circ_0001982 or MUC19 was predicted using starbase v3.0 or Targetscan, and verified by dual-luciferase reporter assay and RNA binding protein immunoprecipitation (RIP) assay. The xenograft model in nude mice was established to examine the effect of circ_0001982 in vivo. RESULTS: The levels of circ_0001982 and MUC19 were upregulated, while miR-1287-5p was downregulated in BC tissues and cells under hypoxia. Knockdown of circ_0001982 hindered glycolysis, cell viability, migration, and invasion of BC cells under hypoxia. Mechanistic studies discovered that circ_0001982 could act as a sponge for miR-1287-5p to enhance MUC19 expression in BC cells. In addition, circ_0001982 silencing reduced xenograft tumor growth by regulating miR-1287-5p/MUC19 axis. CONCLUSION: Circ_0001982 affected BC cells glycolysis, proliferation, migration, and invasion through miR-1287-5p/MUC19 axis under hypoxia.	NA	World J Surg Oncol. 2021 Jun 3;19(1):161. doi: 10.1186/s12957-021-02273-8.
3925	LncRNA	CERS6-AS1	miR-15a-5p	HMGA1	Pancreatic Cancer Cells	Pancreatic Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;RNA pull-down;	33939677	Long Noncoding RNA CERS6-AS1 Accelerates the Proliferation and Migration of Pancreatic Cancer Cells by Sequestering MicroRNA-15a-5p and MicroRNA-6838-5p and Modulating HMGA1.	OBJECTIVES: As one of the most aggressive human tumors, pancreatic cancer (PC) is accompanied by poor treatment and prognosis. Although emerging evidence has highlighted the importance of long noncoding RNAs in multiple cancers, the specific regulatory roles mostly remain obscure. Our aim was to disclose the role of CERS6 antisense RNA 1 (CERS6-AS1) in PC. METHODS: Quantitative real-time polymerase chain reaction analysis was used to examine the expression of CERS6-AS1 in PC cell lines. Western blot analysis was used to assess the protein levels of high-mobility group AT-hook 1 (HMGA1). Colony formation, 5-ethynyl-20-deoxyuridine, transwell, and wound healing assays were performed to detect the functions of CERS6-AS1 on PC development. In addition, RNA pull-down, RNA immunoprecipitation, and luciferase reporter assays were implemented to delve into the regulatory mechanism of CERS6-AS1 in PC. RESULTS: CERS6-AS1 was significantly upregulated in PC. CERS6-AS1 silence obviously inhibited cell proliferation and migration in PC. Furthermore, CERS6-AS1 sponged microRNA-15a-5p (miR-15a-5p) and microRNA-6838-5p (miR-6838-5p) to regulate HMGA1. Moreover, rescue assays verified that CERS6-AS1 was involved in cell proliferation and migration in PC via targeting miR-15a-5p/miR-6838-5p/HMGA1 axis. CONCLUSIONS: CERS6-AS1 enhanced HMGA1 expression to contribute to the progression of PC by sequestering miR-15a-5p and miR-6838-5p.	NA	Pancreas. 2021 Apr 1;50(4):617-624. doi: 10.1097/MPA.0000000000001806.
3926	LncRNA	CERS6-AS1	miR-6838-5p	HMGA1	Pancreatic Cancer Cells	Pancreatic Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;RNA pull-down;	33939677	Long Noncoding RNA CERS6-AS1 Accelerates the Proliferation and Migration of Pancreatic Cancer Cells by Sequestering MicroRNA-15a-5p and MicroRNA-6838-5p and Modulating HMGA1.	OBJECTIVES: As one of the most aggressive human tumors, pancreatic cancer (PC) is accompanied by poor treatment and prognosis. Although emerging evidence has highlighted the importance of long noncoding RNAs in multiple cancers, the specific regulatory roles mostly remain obscure. Our aim was to disclose the role of CERS6 antisense RNA 1 (CERS6-AS1) in PC. METHODS: Quantitative real-time polymerase chain reaction analysis was used to examine the expression of CERS6-AS1 in PC cell lines. Western blot analysis was used to assess the protein levels of high-mobility group AT-hook 1 (HMGA1). Colony formation, 5-ethynyl-20-deoxyuridine, transwell, and wound healing assays were performed to detect the functions of CERS6-AS1 on PC development. In addition, RNA pull-down, RNA immunoprecipitation, and luciferase reporter assays were implemented to delve into the regulatory mechanism of CERS6-AS1 in PC. RESULTS: CERS6-AS1 was significantly upregulated in PC. CERS6-AS1 silence obviously inhibited cell proliferation and migration in PC. Furthermore, CERS6-AS1 sponged microRNA-15a-5p (miR-15a-5p) and microRNA-6838-5p (miR-6838-5p) to regulate HMGA1. Moreover, rescue assays verified that CERS6-AS1 was involved in cell proliferation and migration in PC via targeting miR-15a-5p/miR-6838-5p/HMGA1 axis. CONCLUSIONS: CERS6-AS1 enhanced HMGA1 expression to contribute to the progression of PC by sequestering miR-15a-5p and miR-6838-5p.	NA	Pancreas. 2021 Apr 1;50(4):617-624. doi: 10.1097/MPA.0000000000001806.
3927	LncRNA	CEBPA-AS1	miR-24-3p	BOK	SH-SY5Y cells	Neuron Cell Damage	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34001648	CEBPA-AS1 knockdown alleviates OGD/R-induced neuron cell damage by the miR-24-3p/BOK axis.	Cerebral ischemia/reperfusion (I/R) can lead to serious brain function impairments. Long noncoding RNA (lncRNA) CCAAT enhancer binding protein α antisense RNA 1 (CEBPA-AS1) was shown to be upregulated in human ischemic stroke. This work investigated the function and mechanism of CEBPA-AS1 in I/R. An oxygen-glucose deprivation/reperfusion (OGD/R) model was used to induce I/R injury in SH-SY5Y cells in vitro. RT-qPCR examined the expression of CEBPA-AS1, microRNA-24-3p (miR-24-3p), and Bcl-2-related ovarian killer (Bok). The cell viability, apoptosis, oxidative stress in OGD/R-treated cells were detected using CCK-8, flow cytometry, western blot, ELISA assays. The relationship among genes was tested by RNA pulldown and luciferase reporter assays. We found that OGD/R upregulated CEBPA-AS1 expression in SH-SY5Y cells. Functionally, CEBPA-AS1 depletion ameliorated OGD/R-induced apoptosis and oxidative stress in SH-SY5Y cells by reducing ROS production and superoxide dismutase (SOD) and glutathione (GSH). Mechanistic investigations indicated that CEBPA-AS1 acts as a sponge for miR-24-3p, and miR-24-3p binds to the BOK. Moreover, miR-24-3p upregulation or BOK downregulation antagonized the protective role of CEBPA-AS1 depletion in SH-SY5Y cells exposed to OGD/R. Overall, downregulation of CEBPA-AS1 exerts protective functions against OGD/R-induced injury by targeting the miR-24-3p/BOK axis.	NA	Mol Cell Biol. 2021 May 17:MCB.00065-21. doi: 10.1128/MCB.00065-21.
3928	LncRNA	CDKN2B	miR-140-5p	TGFBR2	BEAS-2B cells	Lps-Induced Cell Injury	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34126975	Long non-coding RNA CDKN2B-AS1 enhances LPS-induced apoptotic and inflammatory damages in human lung epithelial cells via regulating the miR-140-5p/TGFBR2/Smad3 signal network.	BACKGROUND: Sepsis is a complicated disease with systemic inflammation or organ dysfunction, and it is the leading cause of acute lung injury (ALI). Long non-coding RNAs (lncRNAs) have played important roles in the pathogenesis of sepsis. This study was designed to explore the biological function and regulatory mechanism of cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in lipopolysaccharide (LPS)-induced lung injury. METHODS: ALI model was established after human lung epithelial cell line BEAS-2B was exposed to LPS. CDKN2B-AS1, microRNA-140-5p (miR-140-5p) and transforming Growth Factor Beta Receptor II (TGFBR2) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was measured using Cell Counting Kit-8 (CCK-8). Cell apoptosis was assessed by caspase3 activity and flow cytometry. Inflammatory cytokines were examined via enzyme-linked immunosorbent assay (ELISA). Protein analysis was performed through western blot. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays were applied to validate the interaction between targets. RESULTS: CDKN2B-AS1 and TGFBR2 were abnormally upregulated in sepsis patients. Functionally, CDKN2B-AS1 or TGFBR2 knockdown promoted cell growth but inhibited cell apoptosis and inflammatory response in LPS-treated BEAS-2B cells. Moreover, the regulation of CDKN2B-AS1 in LPS-induced cell injury was achieved by increasing the TGFBR2 expression. CDKN2B-AS1 was identified as a miR-140-5p sponge and TGFBR2 was a target of miR-140-5p. Furthermore, CDKN2B-AS1 could regulate the TGFBR2/Smad3 pathway by sponging miR-140-5p. CONCLUSIONS: These results suggested that CDKN2B-AS1 contributed to the LPS-mediated apoptosis and inflammation in BEAS-2B cells via the miR-140-5p/TGFBR2/Smad3 axis.	NA	BMC Pulm Med. 2021 Jun 14;21(1):200. doi: 10.1186/s12890-021-01561-z.
3929	LncRNA	CDKN2B	miR-140-5p	Smad3	BEAS-2B cells	Lps-Induced Cell Injury	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34126975	Long non-coding RNA CDKN2B-AS1 enhances LPS-induced apoptotic and inflammatory damages in human lung epithelial cells via regulating the miR-140-5p/TGFBR2/Smad3 signal network.	BACKGROUND: Sepsis is a complicated disease with systemic inflammation or organ dysfunction, and it is the leading cause of acute lung injury (ALI). Long non-coding RNAs (lncRNAs) have played important roles in the pathogenesis of sepsis. This study was designed to explore the biological function and regulatory mechanism of cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in lipopolysaccharide (LPS)-induced lung injury. METHODS: ALI model was established after human lung epithelial cell line BEAS-2B was exposed to LPS. CDKN2B-AS1, microRNA-140-5p (miR-140-5p) and transforming Growth Factor Beta Receptor II (TGFBR2) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was measured using Cell Counting Kit-8 (CCK-8). Cell apoptosis was assessed by caspase3 activity and flow cytometry. Inflammatory cytokines were examined via enzyme-linked immunosorbent assay (ELISA). Protein analysis was performed through western blot. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and pull-down assays were applied to validate the interaction between targets. RESULTS: CDKN2B-AS1 and TGFBR2 were abnormally upregulated in sepsis patients. Functionally, CDKN2B-AS1 or TGFBR2 knockdown promoted cell growth but inhibited cell apoptosis and inflammatory response in LPS-treated BEAS-2B cells. Moreover, the regulation of CDKN2B-AS1 in LPS-induced cell injury was achieved by increasing the TGFBR2 expression. CDKN2B-AS1 was identified as a miR-140-5p sponge and TGFBR2 was a target of miR-140-5p. Furthermore, CDKN2B-AS1 could regulate the TGFBR2/Smad3 pathway by sponging miR-140-5p. CONCLUSIONS: These results suggested that CDKN2B-AS1 contributed to the LPS-mediated apoptosis and inflammation in BEAS-2B cells via the miR-140-5p/TGFBR2/Smad3 axis.	NA	BMC Pulm Med. 2021 Jun 14;21(1):200. doi: 10.1186/s12890-021-01561-z.
3930	LncRNA	CCDC26	miR-140-5p	GLRX5	K562/ADR cells	Leukemia	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA sequencing;	34113488	Analysis of ceRNA networks and identification of potential drug targets for drug-resistant leukemia cell K562/ADR.	BACKGROUND: Drug resistance is the main obstacle in the treatment of leukemia. As a member of the competitive endogenous RNA (ceRNA) mechanism, underlying roles of lncRNA are rarely reported in drug-resistant leukemia cells. METHODS: The gene expression profiles of lncRNAs and mRNAs in doxorubicin-resistant K562/ADR and sensitive K562 cells were established by RNA sequencing (RNA-seq). Expression of differentially expressed lncRNAs (DElncRNAs) and DEmRNAs was validated by qRT-PCR. The potential biological functions of DElncRNAs targets were identified by GO and KEGG pathway enrichment analyses, and the lncRNA-miRNA-mRNA ceRNA network was further constructed. K562/ADR cells were transfected with CCDC26 and LINC01515 siRNAs to detect the mRNA levels of GLRX5 and DICER1, respectively. The cell survival rate after transfection was detected by CCK-8 assay. RESULTS: The ceRNA network was composed of 409 lncRNA-miRNA pairs and 306 miRNA-mRNA pairs based on 67 DElncRNAs, 58 DEmiRNAs and 192 DEmRNAs. Knockdown of CCDC26 and LINC01515 increased the sensitivity of K562/ADR cells to doxorubicin and significantly reduced the half-maximal inhibitory concentration (IC(50)) of doxorubicin. Furthermore, knockdown of GLRX5 and DICER1 increased the sensitivity of K562/ADR cells to doxorubicin and significantly reduced the IC(50) of doxorubicin. CONCLUSIONS: The ceRNA regulatory networks may play important roles in drug resistance of leukemia cells. CCDC26/miR-140-5p/GLRX5 and LINC01515/miR-425-5p/DICER1 may be potential targets for drug resistance in K562/ADR cells. This study provides a promising strategy to overcome drug resistance and deepens the understanding of the ceRNA regulatory mechanism related to drug resistance in CML cells.	NA	PeerJ. 2021 May 25;9:e11429. doi: 10.7717/peerj.11429. eCollection 2021.
3931	LncRNA	LINC01515	miR-425-5p	DICER1	K562/ADR cells	Leukemia	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA sequencing;	34113488	Analysis of ceRNA networks and identification of potential drug targets for drug-resistant leukemia cell K562/ADR.	BACKGROUND: Drug resistance is the main obstacle in the treatment of leukemia. As a member of the competitive endogenous RNA (ceRNA) mechanism, underlying roles of lncRNA are rarely reported in drug-resistant leukemia cells. METHODS: The gene expression profiles of lncRNAs and mRNAs in doxorubicin-resistant K562/ADR and sensitive K562 cells were established by RNA sequencing (RNA-seq). Expression of differentially expressed lncRNAs (DElncRNAs) and DEmRNAs was validated by qRT-PCR. The potential biological functions of DElncRNAs targets were identified by GO and KEGG pathway enrichment analyses, and the lncRNA-miRNA-mRNA ceRNA network was further constructed. K562/ADR cells were transfected with CCDC26 and LINC01515 siRNAs to detect the mRNA levels of GLRX5 and DICER1, respectively. The cell survival rate after transfection was detected by CCK-8 assay. RESULTS: The ceRNA network was composed of 409 lncRNA-miRNA pairs and 306 miRNA-mRNA pairs based on 67 DElncRNAs, 58 DEmiRNAs and 192 DEmRNAs. Knockdown of CCDC26 and LINC01515 increased the sensitivity of K562/ADR cells to doxorubicin and significantly reduced the half-maximal inhibitory concentration (IC(50)) of doxorubicin. Furthermore, knockdown of GLRX5 and DICER1 increased the sensitivity of K562/ADR cells to doxorubicin and significantly reduced the IC(50) of doxorubicin. CONCLUSIONS: The ceRNA regulatory networks may play important roles in drug resistance of leukemia cells. CCDC26/miR-140-5p/GLRX5 and LINC01515/miR-425-5p/DICER1 may be potential targets for drug resistance in K562/ADR cells. This study provides a promising strategy to overcome drug resistance and deepens the understanding of the ceRNA regulatory mechanism related to drug resistance in CML cells.	NA	PeerJ. 2021 May 25;9:e11429. doi: 10.7717/peerj.11429. eCollection 2021.
3932	LncRNA	BVES-AS1	miR-522-3p	BVES	COAD cells	Colon Adenocarcinoma	Homo sapiens (human)	Western blot;RNA pull-down;	34003551	BVES-AS1 inhibits the malignant behaviors of colon adenocarcinoma cells via regulating BVES.	The underexpression of the long noncoding RNA blood vessel epicardial substance antisense RNA 1 (BVES-AS1) has been shown in colon adenocarcinoma (COAD) patients. However, its role in COAD remains to be explored. This study aimed to investigate the function and potential mechanism of BVES-AS1 in COAD. Colony formation, Cell Counting Kit-8, JC-1 mitochondrial membrane potential assay, wound healing, transwell, and western blot analyses were used to measure cell proliferation, apoptosis, migration, invasion, and epithelial-mesenchymal transition (EMT) in COAD cells. RNA pull-down, luciferase reporter, and RNA binding protein immunoprecipitation assays were used to detect the interaction of BVES-AS1 and downstream genes. BVES-AS1 was expressed at low levels in COAD cells. Overexpressed BVES-AS1 inhibited COAD cell proliferation, migration, invasion, and EMT while elevating cell apoptosis. Mechanistically, BVES-AS1 functioned as a competing endogenous RNA sponging miR-522-3p to regulate the expression of nearby gene blood vessel epicardial substance (BVES). Besides this, BVES-AS1 recruited TATA-box binding protein associated factor 15 (TAF15) to promote BVES messenger RNA stability. Taken together, our study confirmed that BVES-AS1 inhibited COAD progression via interacting with miR-522-3p and TAF15 to regulate BVES expression, which might offer a perspective for COAD treatment.	NA	Cell Biol Int. 2021 May 18. doi: 10.1002/cbin.11634.
3933	LncRNA	Bmp1	miR-128-3p	Phf6	IEC-6 or HIEC-6 cells	Intestinal Mucosal Lesions	Homo sapiens (human)	qRT-PCR	34108447	LncRNA Bmp1 promotes the healing of intestinal mucosal lesions via the miR-128-3p/PHF6/PI3K/AKT pathway.	Intestinal mucosal injuries are directly or indirectly related to many common acute and chronic diseases. Long non-coding RNAs (lncRNAs) are expressed in many diseases, including intestinal mucosal injury. However, the relationship between lncRNAs and intestinal mucosal injury has not been determined. Here, we investigated the functions and mechanisms of action of lncRNA Bmp1 on damaged intestinal mucosa. We found that Bmp1 was increased in damaged intestinal mucosal tissue and Bmp1 overexpression was able to alleviate intestinal mucosal injury. Bmp1 overexpression was found to influence cell proliferation, colony formation, and migration in IEC-6 or HIEC-6 cells. Moreover, miR-128-3p was downregulated after Bmp1 overexpression, and upregulation of miR-128-3p reversed the effects of Bmp1 overexpression in IEC-6 cells. Phf6 was observed to be a target of miR-128-3p. Furthermore, PHF6 overexpression affected IEC-6 cells by activating PI3K/AKT signaling which was mediated by the miR-128-3p/PHF6 axis. In conclusion, Bmp1 was found to promote the expression of PHF6 through the sponge miR-128-3p, activating the PI3K/AKT signaling pathway to promote cell migration and proliferation.	NA	Cell Death Dis. 2021 Jun 9;12(6):595. doi: 10.1038/s41419-021-03879-2.
3934	LncRNA	ASMTL-AS1	miR-1228-3p	SOX17	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	34006305	A novel tumor suppressor ASMTL-AS1 regulates the miR-1228-3p/SOX17/β-catenin axis in triple-negative breast cancer.	BACKGROUND: Triple-negative breast cancer (TNBC) is a special type of breast cancer that lacks effective therapeutic targets. There is a significant need to clarify its pathogenesis, so as to bring new targeted approaches for TNBC management. Here, we identified a long-non coding RNA (lncRNA) ASMTL-AS1 that linked to TNBC development and progression. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assays were used to test gene and protein levels, respectively. The regulatory axis of miR-1228-3p/SOX17/β-catenin was determined by luciferase reporter and RNA pull-down assays. In vivo assay was conducted by using the nude mice model via subcutaneous transplantation of tumor cells. RESULTS: ASMTL-AS1 was significantly downregulated in TNBC tissues compared to normal tissues, which was closely associated with aggressive clinical features and unfavorable prognosis. Lentivirus-mediated ASMTL-AS1 overexpression evidently reduced the ability of TNBC cell colony formation, activity and invasion by more than 2.5 times. RNA pull-down and luciferase reporter assays revealed that miR-1228-3p directly bound to ASMTL-AS1, ASMTL-AS1 increased SOX17 expression via sponging and repressing miR-1228-3p. Subsequently, the upregulated SOX17 trans-suppressed β-catenin expression, resulting in the inactivation of carcinogenic Wnt/β-catenin signaling, thereby restraining TNBC cell growth and dissemination. Importantly, the xenograft tumor model showed that the ASMTL-AS1 overexpression significantly retarded tumor growth, and negatively regulated Wnt/β-catenin pathway. CONCLUSIONS: Our data characterize a novel tumor suppressor in TNBC, restoration of ASMTL-AS1 may be a candidate therapeutic intervention for TNBC patients.	NA	Diagn Pathol. 2021 May 18;16(1):45. doi: 10.1186/s13000-021-01105-3.
3935	LncRNA	AL139002.1	miR-490-3p	HAV	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34002670	Long non-coding RNA AL139002.1 promotes gastric cancer development by sponging microRNA-490-3p to regulate Hepatitis A Virus Cellular Receptor 1 expression.	Mounting evidence suggests that lncRNA regulates many important diseases. However, the biological role of most lncRNAs in gastric cancer (GC) remain unclear. In this paper, we determined differential expression of lncRNAs and predicted ceRNA networks in the GC database by bioinformatics analysis and validated in GC cells. The effect of lncRNA AL139002.1 on GC cells biological function was assessed by flow cytometry, CCK-8, colony formation, wound healing assay, transwell, western blot, and qRT-PCR. And the relationship of lncRNA AL139002.1 or HAVCR1 with miR-490-3p was verified by luciferase reporter assay. The results showed that lncRNA AL139002.1 was highly expressed in GC cells and lncRNA AL139002.1 knockdown induced apoptosis, while suppressed cell proliferation, migration, invasion, and EMT. Functional examining indicated that lncRNA AL139002.1 regulated HAVCR1 expression by competitively binding miR-490-3p. In addition, lncRNA AL139002.1/miR-490-3p/HAVCR1 regulated EMT and metastasis through MEK/ERK signaling. In conclusion, lncRNA AL139002.1 was highly expressed in GC cells, and lncRNA AL139002.1/miR-490-3p/HAVCR1 functioned critically in GC by regulating MEK/ERK signaling. Our findings demonstrated that lncRNA AL139002.1 served as a potential therapeutic and anti-metastatic biotarget for GC.	NA	Bioengineered. 2021 Dec;12(1):1927-1938. doi: 10.1080/21655979.2021.1922329.
3936	LncRNA	AK087124	miR-224-5p	PTEN	atherosclerosis-related endothelial cells	Atherosclerosis	Homo sapiens (human)	luciferase assay;	33974917	LncRNA AK087124/miR-224-5p/PTEN axis modulates endothelial cell injury in atherosclerosis through apoptosis and AKT signaling pathway.	Noncoding RNAs (ncRNAs) have been shown to play important roles in atherosclerosis-related endothelial cells dysfunction during atherosclerosis processes. In the study, our purpose was to discover new long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) via competitively interacting each other to regulate the pathogenesis process of atherosclerosis. We investigated the roles of lncRNA AK087124 and miR-224-5p in atherosclerotic pathogenesis and found that AK087124 was up-regulated while miR-224-5p was down-regulated in in the plasma and plaque from atherosclerotic mice compared with normal mice. Ox-LDL was used to establish the mouse aorta endothelial cell (MAEC) injury model. The function study indicated that knockdown of AK087124 inhibited ox-LDL induced endothelial apoptosis and inflammatory response. Bioinformatic prediction combining with luciferase assays indicated that AK087124 could sponge miR-224-5p and enhance the PTEN expression which is a target of miR-224-5p. RNA pull down assays also showed that biotin-miR-224-5p probe could interacted directly with AK087124 and PTEN. Pearson correlation analysis further demonstrated that AK087124 and PTEN expression are negatively correlated with miR-224-5p. Rescue study revealed that miR-224-5p silencing and PTEN overexpression both can reverse the effect of AK087124 on the ox-LDL induced endothelial injury. These data indicated that AK087124 and miR-224-5p could be potential biomarkers and target molecules to treatment and diagnosis for atherosclerosis.	NA	Arch Biochem Biophys. 2021 Jul 15;705:108916. doi: 10.1016/j.abb.2021.108916. Epub 2021 May 8.
3937	LncRNA	AK087124	miR-224-5p	PTEN	atherosclerosis-related endothelial cells	Atherosclerosis	Mus musculus (mouse)	luciferase assay;	33974917	LncRNA AK087124/miR-224-5p/PTEN axis modulates endothelial cell injury in atherosclerosis through apoptosis and AKT signaling pathway.	Noncoding RNAs (ncRNAs) have been shown to play important roles in atherosclerosis-related endothelial cells dysfunction during atherosclerosis processes. In the study, our purpose was to discover new long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) via competitively interacting each other to regulate the pathogenesis process of atherosclerosis. We investigated the roles of lncRNA AK087124 and miR-224-5p in atherosclerotic pathogenesis and found that AK087124 was up-regulated while miR-224-5p was down-regulated in in the plasma and plaque from atherosclerotic mice compared with normal mice. Ox-LDL was used to establish the mouse aorta endothelial cell (MAEC) injury model. The function study indicated that knockdown of AK087124 inhibited ox-LDL induced endothelial apoptosis and inflammatory response. Bioinformatic prediction combining with luciferase assays indicated that AK087124 could sponge miR-224-5p and enhance the PTEN expression which is a target of miR-224-5p. RNA pull down assays also showed that biotin-miR-224-5p probe could interacted directly with AK087124 and PTEN. Pearson correlation analysis further demonstrated that AK087124 and PTEN expression are negatively correlated with miR-224-5p. Rescue study revealed that miR-224-5p silencing and PTEN overexpression both can reverse the effect of AK087124 on the ox-LDL induced endothelial injury. These data indicated that AK087124 and miR-224-5p could be potential biomarkers and target molecules to treatment and diagnosis for atherosclerosis.	NA	Arch Biochem Biophys. 2021 Jul 15;705:108916. doi: 10.1016/j.abb.2021.108916. Epub 2021 May 8.
3938	Circular RNA	AFF4	miR-135a-5p	FNDC5	Bone marrow-derived mesenchymal stem cells	Osteogenic Differentiation	Homo sapiens (human)	qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;RNA pull-down;	34145212	Circular RNA AFF4 modulates osteogenic differentiation in BM-MSCs by activating SMAD1/5 pathway through miR-135a-5p/FNDC5/Irisin axis.	Bone marrow-derived mesenchymal stem cells (BM-MSCs), the common progenitor cells of adipocytes and osteoblasts, have been recognized as the key mediator during bone formation. Herein, our study aim to investigate molecular mechanisms underlying circular RNA (circRNA) AFF4 (circ_AFF4)-regulated BM-MSCs osteogenesis. BM-MSCs were characterized by FACS, ARS, and ALP staining. Expression patterns of circ_AFF4, miR-135a-5p, FNDC5/Irisin, SMAD1/5, and osteogenesis markers, including ALP, BMP4, RUNX2, Spp1, and Colla1 were detected by qRT-PCR, western blot, or immunofluorescence staining, respectively. Interactions between circ_AFF4 and miR-135a-5p, FNDC5, and miR-135a-5p were analyzed using web tools including TargetScan, miRanda, and miRDB, and further confirmed by luciferase reporter assay and RNA pull-down. Complex formation between Irisin and Integrin αV was verified by Co-immunoprecipitation. To further verify the functional role of circ_AFF4 in vivo during bone formation, we conducted animal experiments harboring circ_AFF4 knockdown, and born samples were evaluated by immunohistochemistry, hematoxylin and eosin, and Masson staining. Circ_AFF4 was upregulated upon osteogenic differentiation induction in BM-MSCs, and miR-135a-5p expression declined as differentiation proceeds. Circ_AFF4 knockdown significantly inhibited osteogenesis potential in BM-MSCs. Circ_AFF4 stimulated FNDC5/Irisin expression through complementary binding to its downstream target molecule miR-135a-5p. Irisin formed an intermolecular complex with Integrin αV and activated the SMAD1/5 pathway during osteogenic differentiation. Our work revealed that circ_AFF4, acting as a sponge of miR-135a-5p, triggers the promotion of FNDC5/Irisin via activating the SMAD1/5 pathway to induce osteogenic differentiation in BM-MSCs. These findings gained a deeper insight into the circRNA-miRNA regulatory system in the bone marrow microenvironment and may improve our understanding of bone formation-related diseases at physiological and pathological levels.	NA	Cell Death Dis. 2021 Jun 18;12(7):631. doi: 10.1038/s41419-021-03877-4.
3939	Circular RNA	AFF4	miR-135a-5p	Irisin	Bone marrow-derived mesenchymal stem cells	Osteogenic Differentiation	Homo sapiens (human)	qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;RNA pull-down;	34145212	Circular RNA AFF4 modulates osteogenic differentiation in BM-MSCs by activating SMAD1/5 pathway through miR-135a-5p/FNDC5/Irisin axis.	Bone marrow-derived mesenchymal stem cells (BM-MSCs), the common progenitor cells of adipocytes and osteoblasts, have been recognized as the key mediator during bone formation. Herein, our study aim to investigate molecular mechanisms underlying circular RNA (circRNA) AFF4 (circ_AFF4)-regulated BM-MSCs osteogenesis. BM-MSCs were characterized by FACS, ARS, and ALP staining. Expression patterns of circ_AFF4, miR-135a-5p, FNDC5/Irisin, SMAD1/5, and osteogenesis markers, including ALP, BMP4, RUNX2, Spp1, and Colla1 were detected by qRT-PCR, western blot, or immunofluorescence staining, respectively. Interactions between circ_AFF4 and miR-135a-5p, FNDC5, and miR-135a-5p were analyzed using web tools including TargetScan, miRanda, and miRDB, and further confirmed by luciferase reporter assay and RNA pull-down. Complex formation between Irisin and Integrin αV was verified by Co-immunoprecipitation. To further verify the functional role of circ_AFF4 in vivo during bone formation, we conducted animal experiments harboring circ_AFF4 knockdown, and born samples were evaluated by immunohistochemistry, hematoxylin and eosin, and Masson staining. Circ_AFF4 was upregulated upon osteogenic differentiation induction in BM-MSCs, and miR-135a-5p expression declined as differentiation proceeds. Circ_AFF4 knockdown significantly inhibited osteogenesis potential in BM-MSCs. Circ_AFF4 stimulated FNDC5/Irisin expression through complementary binding to its downstream target molecule miR-135a-5p. Irisin formed an intermolecular complex with Integrin αV and activated the SMAD1/5 pathway during osteogenic differentiation. Our work revealed that circ_AFF4, acting as a sponge of miR-135a-5p, triggers the promotion of FNDC5/Irisin via activating the SMAD1/5 pathway to induce osteogenic differentiation in BM-MSCs. These findings gained a deeper insight into the circRNA-miRNA regulatory system in the bone marrow microenvironment and may improve our understanding of bone formation-related diseases at physiological and pathological levels.	NA	Cell Death Dis. 2021 Jun 18;12(7):631. doi: 10.1038/s41419-021-03877-4.
3940	LncRNA	AFAP-AS1	miR-155-5p	ETS1	ATC cells	Anaplastic Thyroid Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33999777	LncRNA AFAP-AS1 promotes anaplastic thyroid cancer progression by sponging miR-155-5p through ETS1/ERK pathway.	Anaplastic thyroid cancer (ATC) is the most common malignant endocrine tumors which resist to majority treatment. Thus, there is impelling need to figure out the mechanism of progress of ATC. In this study, we explored the function and mechanism of lncRNA actin filamentin-1 antisense RNA (AFAP-AS1) which provided a new biomarker for ATC. Viabilities and apoptosis were tested by CCK-8, colony formation and flow cytometry. The interactions between miR-155-5p and AFAP-AS1 or ETS1 was detected by luciferase reporter assays. ETS proto-oncogene1/mitogen-activated protein kinase1 (ETS1/ERK) pathway was assessed by Western blot. Xenograft models were built to confirm the function of AFAP-AS1 in vivo. Firstly, we showed that relative RNA expression of AFAP-AS1 in ATC cells was higher than in immortalized thyroid cells. Next, AFAP-AS1 was verified as an oncogene in ATC since knock-down of AFAP-AS1 inhibited cell proliferation and accelerated apoptosis. In addition, miR-155-5p was negatively regulated by AFAP-AS1. Moreover, AFAP-AS1 regulated ETS1/ERK pathway by sponging miR-155-5p. Finally, we confirmed knock-down of AFAP-AS1 significantly suppressed tumor proliferation in vivo. Our research proved that AFAP-AS1 could facilitate progression of thyroid cancer sponging miR-155-5p through ETS1/ERK pathway.	NA	Bioengineered. 2021 Dec;12(1):1543-1554. doi: 10.1080/21655979.2021.1918537.
3941	LncRNA	AFAP1-AS1	miR-2110	Sp1	MDA-MB-231 and MDA-MB-468 cells	Triple Negative Breast Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34145213	Long noncoding RNA AFAP1-AS1 promotes tumor progression and invasion by regulating the miR-2110/Sp1 axis in triple-negative breast cancer.	Long noncoding ribonucleic acids (LncRNAs) have been found to be involved in the proliferation, apoptosis, invasion, migration, and other pathological processes of triple-negative breast cancer (TNBC). Expression of the lncRNA actin filament-associated protein 1 antisense RNA1 (AFAP1-AS1) has been found to be significantly higher in TNBC than in other subtypes or in normal tissue samples, but the specific mechanism by which AFAP1-AS1 affects the occurrence and development of TNBC is yet to be revealed. In this study, we used Cell Counting Kit-8 (CCK-8), colony formation, wound healing migration, Transwell invasion, and nude mouse xenograft assays to confirm the role of AFAP1-AS1 in the proliferation, migration of TNBC cells in vitro and in vivo. In addition, we performed bioinformatics analyses, reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), western blot (WB), and dual-luciferase reporter assays (dual-LRA) to confirm interaction among AFAP1-AS1, micro-RNA 2110 (miR-2110), and Sp1 transcription factor (Sp1). We found that silencing AFAP1-AS1 and Sp1 or upregulating miR-2110 suppressed the proliferation, migration, and invasion of MDA-MB-231 and MDA-MB-468 cells in vitro as well as tumor growth in vivo. Mechanistically, the dual-LRA highlighted that miR-2110 was an inhibitory target of AFAP1-AS1, and that AFAP1-AS1 functioned as a miR-2110 sponge to increase Sp1 expression. AFAP1-AS1 silencing led to a reduction in Sp1 mRNA and protein levels, which could be reversed by joint transfection with miR-2110 inhibitor. Our findings demonstrated that AFAP1-AS1 could modulate the progression of breast cancer cells and affect tumorigenesis in mice by acting as a miR-2110 sponge, resulting in regulation of Sp1 expression. Therefore, AFAP1-AS1 could play a pivotal role in the treatment of TNBC.	NA	Cell Death Dis. 2021 Jun 18;12(7):627. doi: 10.1038/s41419-021-03917-z.
3942	LncRNA	AFAP1-AS1	miR-2110	Sp1	MDA-MB-231 and MDA-MB-468 cells	Triple Negative Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34145213	Long noncoding RNA AFAP1-AS1 promotes tumor progression and invasion by regulating the miR-2110/Sp1 axis in triple-negative breast cancer.	Long noncoding ribonucleic acids (LncRNAs) have been found to be involved in the proliferation, apoptosis, invasion, migration, and other pathological processes of triple-negative breast cancer (TNBC). Expression of the lncRNA actin filament-associated protein 1 antisense RNA1 (AFAP1-AS1) has been found to be significantly higher in TNBC than in other subtypes or in normal tissue samples, but the specific mechanism by which AFAP1-AS1 affects the occurrence and development of TNBC is yet to be revealed. In this study, we used Cell Counting Kit-8 (CCK-8), colony formation, wound healing migration, Transwell invasion, and nude mouse xenograft assays to confirm the role of AFAP1-AS1 in the proliferation, migration of TNBC cells in vitro and in vivo. In addition, we performed bioinformatics analyses, reverse transcriptase quantitative polymerase chain reaction (RT-qPCR), western blot (WB), and dual-luciferase reporter assays (dual-LRA) to confirm interaction among AFAP1-AS1, micro-RNA 2110 (miR-2110), and Sp1 transcription factor (Sp1). We found that silencing AFAP1-AS1 and Sp1 or upregulating miR-2110 suppressed the proliferation, migration, and invasion of MDA-MB-231 and MDA-MB-468 cells in vitro as well as tumor growth in vivo. Mechanistically, the dual-LRA highlighted that miR-2110 was an inhibitory target of AFAP1-AS1, and that AFAP1-AS1 functioned as a miR-2110 sponge to increase Sp1 expression. AFAP1-AS1 silencing led to a reduction in Sp1 mRNA and protein levels, which could be reversed by joint transfection with miR-2110 inhibitor. Our findings demonstrated that AFAP1-AS1 could modulate the progression of breast cancer cells and affect tumorigenesis in mice by acting as a miR-2110 sponge, resulting in regulation of Sp1 expression. Therefore, AFAP1-AS1 could play a pivotal role in the treatment of TNBC.	NA	Cell Death Dis. 2021 Jun 18;12(7):627. doi: 10.1038/s41419-021-03917-z.
3943	LncRNA	A1BG-AS1	miR-485-5p	FLOT1	breast cancer cells	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34115333	Long non-coding RNA A1BG-AS1 promotes tumorigenesis in breast cancer by sponging microRNA-485-5p and consequently increasing expression of FLOT1 expression.	The dysregulated long non-coding RNA A1BG antisense RNA 1 (A1BG-AS1) has been implicated in the oncogenicity of hepatocellular carcinoma. Using reverse transcription quantitative polymerase chain reaction in this study, we detected A1BG-AS1 expression in breast cancer and elucidated the regulatory functions and exact mechanisms of A1BG-AS1 in breast cancer cells. The regulatory functions of A1BG-AS1 were examined in vitro using the Cell Counting Kit-8 assay, flow cytometric, and Transwell migration and invasion assays and in vivo through tumor xenograft experiments. In addition, we performed bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation, and rescue experiments to verify the interaction among A1BG-AS1, microRNA-485-5p (miR-485-5p), and flotillin-1 (FLOT1) in breast cancer. We found A1BG-AS1 to be highly expressed in breast cancer tissues and cell lines. In terms of function, depleted A1BG-AS1 markedly suppressed cell proliferation, accelerated cell apoptosis, and hindered cell migration and invasion in breast cancer. Furthermore, A1BG-AS1 interference reduced tumor growth in vivo. Mechanistic investigations confirmed that A1BG-AS1 directly interacted with miR-485-5p as a molecular sponge. We demonstrated that FLOT1 is a direct target of miR-485-5p, which could be positively regulated by A1BG-AS1 by competing for miR-485-5p. Rescue experiments clearly showed that the downregulation of miR-485-5p and upregulation of FLOT1 were capable of reversing the anticancer activities of A1BG-AS1 deficiency in terms of breast cancer cell malignancy. A1BG-AS1 acts as a miR-485-5p sponge and subsequently increases FLOT1 expression in breast cancer cells, ultimately facilitating cancer progression. Hence, the A1BG-AS1/miR-485-5p/FLOT1 pathway might offer a novel therapeutic perspective for breast cancer.	NA	Hum Cell. 2021 Jun 11. doi: 10.1007/s13577-021-00554-8.
3944	LncRNA	4930556M19Rik	miR-27a-3p	TIMP3	DN cell	Diabetic Nephropathy	Homo sapiens (human)	RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	32896839	Overexpression of Linc 4930556M19Rik Suppresses High Glucose-Triggered Podocyte Apoptosis, Fibrosis and Inflammation via the miR-27a-3p/Metalloproteinase 3 (TIMP3) Axis in Diabetic Nephropathy.	BACKGROUND Long non-coding RNAs (lncRNAs) play vital roles in development of diabetic nephropathy (DN). The goal of our study was to investigate the functional roles of long intergenic noncoding RNA (lincRNA) 4930556M19Rik in DN. MATERIAL AND METHODS A DN cell model was constructed by exposing podocytes to high glucose (HG). A subcellular fraction assay was used to determine the level of 4930556M19Rik in the nucleus and cytoplasm of podocytes. Quantitative real-time polymerase chain reaction was used to evaluate expression of 4930556M19Rik and miR-27a-3p. Western blot assay was used to assessed levels of fibrosis-related proteins, podocin, and tissue inhibitor of metalloproteinase 3 (TIMP3). Flow cytometry analysis was performed to analyze cell apoptosis. Enzyme linked immunosorbent assay was used to examine secretion of inflammatory cytokines. Dual-luciferase reporter, RIP, and RNA pull-down assays were used to verify the relationship between miR-27a-3p and 4930556M19Rik or TIMP3. RESULTS 4930556M19Rik was significantly decreased in HG-stimulated podocytes and mainly enriched in the cytoplasm of podocytes. Elevation of 4930556M19Rik hampered HG-induced cell apoptosis, fibrosis, and inflammatory in podocytes. 4930556M19Rik sponged miR-27a-3p to negatively modulate miR-27a-3p expression. MiR-27a-3p overexpression reversed the impact of 4930556M19Rik mediated cell progression in HG-induced podocytes. Moreover, TIMP3 was the target for miR-27a-3p and miR-27a-3p inhibition slowed podocyte injury by targeting TIMP3. CONCLUSIONS 4930556M19Rik overexpression slowed HG-induced podocyte injury by downregulating miR-27a-3p and upregulating TIMP3.	NA	Med Sci Monit. 2020 Sep 8;26:e925361. doi: 10.12659/MSM.925361.
3945	LncRNA	A2M-AS1	miR-146b	MUC19	BC cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33273850	Long Non-Coding RNA A2M-AS1 Promotes Breast Cancer Progression by Sponging microRNA-146b to Upregulate MUC19.	BACKGROUND: Long non-coding RNA (lncRNA) A2M-AS1 has been indicated to be augmented in breast cancer (BC), with its specific function undetermined. Therefore, this study is designed to investigate the mechanism of lncRNA A2M-AS1 in BC. METHODS: The expression of A2M-AS1, microRNA (miR)-146b, and MUC19 in BC tissues and cells was measured. Then, the interaction among A2M-AS1, miR-146b, and MUC19 was detected. After A2M-AS1, miR-146b, and MUC19 expression were altered in BC cells, cell proliferation, invasion, and apoptosis were detected, and the protein levels of Hippo-related proteins (YAP and p-YAP) were evaluated. Tumor growth assay was also performed to validate the effects of A2M-AS1 and miR-146b in vivo. RESULTS: A2M-AS1 and MUC19 were highly expressed in BC, while miR-146b was poorly expressed. A2M-AS1 acts as a molecular sponge for miR-146b, which targeted and negatively modulated MUC19. A2M-AS1 accelerated BC cell proliferation, invasion, and colony formation and suppressed apoptosis via the miR-146b/MUC19/Hippo axis, which was confirmed in vivo. CONCLUSION: Taken above together, an oncogenic role for A2M-AS1 in BC was elicited by acting as a miR-146b sponge to promote MUC19 expression. The findings will present some cues for a further approach to BC.	NA	Int J Gen Med. 2020 Nov 27;13:1305-1316. doi: 10.2147/IJGM.S278564. eCollection 2020.
3946	LncRNA	AC007271.3	miR-125b-2-3p	Slug	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	33311454	NF-κB-mediated lncRNA AC007271.3 promotes carcinogenesis of oral squamous cell carcinoma by regulating miR-125b-2-3p/Slug.	Oral squamous cell carcinoma (OSCC) is the most common oral cancer. The molecular mechanisms of this disease are not fully understood. Our previous studies confirmed that dysregulated function of long non-coding RNA (lncRNA) AC007271.3 was associated with a poor prognosis and overexpression of AC007271.3 promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. However, the underlying mechanisms of AC007271.3 dysregulation remained obscure. In this study, our investigation showed that AC007271.3 functioned as competing endogenous RNA by binding to miR-125b-2-3p and by destabilizing primary miR-125b-2, resulted in the upregulating expression of Slug, which is a direct target of miR-125b-2-3p. Slug also inhibited the expression of E-cadherin but N-cadherin, vimentin, and β-catenin had no obvious change. The expression of AC007271.3 was promoted by the canonical nuclear factor-κB (NF-κB) pathway. Taken together, these results suggested that the classical NF-κB pathway-activated AC007271.3 regulates EMT by miR-125b-2-3p/Slug/E-cadherin axis to promote the development of OSCC, implicating it as a novel potential target for therapeutic intervention in this disease.	NA	Cell Death Dis. 2020 Dec 12;11(12):1055. doi: 10.1038/s41419-020-03257-4.
3947	LncRNA	AC010789.1	miR-432-3p	ZEB1	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33178684	LncRNA AC010789.1 Promotes Colorectal Cancer Progression by Targeting MicroRNA-432-3p/ZEB1 Axis and the Wnt/β-Catenin Signaling Pathway.	Accumulating literatures have indicated that long non-coding RNAs (lncRNAs) are crucial molecules in tumor progression in various human cancers, including colorectal cancer (CRC). However, the clinical significance and regulatory mechanism of a vast majority of lncRNAs in CRC remain to be determined. The current study aimed to explore the function and molecular mechanism of lncRNA AC010789.1 in CRC progression. AC010789.1 found to be overexpressed in CRC tissues and cells. High expression of AC010789.1 was associated with lymph node metastasis and poor prognosis. Moreover, AC010789.1 silencing inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro as well as tumorigenesis and metastasis in vivo. Mechanistically, we demonstrated that repression of AC010789.1 promoted miR-432-3p expression, and miR-432-3p directly binds to ZEB1. We then proved the anti-tumor role of miR-432-3p in CRC, showing that the inhibitory effect of AC010789.1 knockdown on CRC cells was achieved by the upregulation of miR-432-3p but downregulation of ZEB1. We also established that silencing AC010789.1 suppressed the Wnt/β-catenin signaling pathway. However, this inhibitory effect was partially counteracted by inhibition of miR-432-3p. In summary, these results reveal that silencing AC010789.1 suppresses CRC progression via miR-432-3p-mediated ZEB1 downregulation and suppression of the Wnt/β-catenin signaling pathway, highlighting a potentially promising strategy for CRC treatment.	NA	Front Cell Dev Biol. 2020 Oct 15;8:565355. doi: 10.3389/fcell.2020.565355. eCollection 2020.
3948	LncRNA	AC068039.4	miR-26a-5p	TRPC6	pulmonary artery smooth muscle cells	Hypoxic Pulmonary Arterial Hypertension	Homo sapiens (human)	microarray;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33026218	Overexpressed lncRNA AC068039.4 Contributes to Proliferation and Cell Cycle Progression of Pulmonary Artery Smooth Muscle Cells Via Sponging miR-26a-5p/TRPC6 in Hypoxic Pulmonary Arterial Hypertension.	BACKGROUND: Hypoxic pulmonary hypertension (HPH) is a devastating and incurable disease characterized by pulmonary vascular remodeling, resulting in right heart failure and even death. Accumulated evidence has confirmed long coding RNAs (lncRNAs) are involved in hypoxia-induced pulmonary vascular remodeling in HPH. The exact mechanism of lncRNA in hypoxic pulmonary hypertension remains unclear. METHODS: Microarray analysis was applied to investigate the profiles of lncRNA expression in pulmonary artery smooth muscle cells (PASMCs) cultured under hypoxia and normoxia condition. qRT-PCR was performed for the expression of lncRNAs, miRNA, and mRNAs, western blot analysis was employed for the detection of the expression of proteins. CCK-8 and transwell chamber assay were applied for the assessment of PASMC proliferation and migration, respectively. Besides, flow cytometry was performed for assessments of cell cycle progression. The binding between AC068039.4 and miR-26a-5p, miR-26a-5p, and TRPC6 3'UTR was detected by dual luciferase reporter assay. RESULTS: A total of 1,211 lncRNAs (698 up-regulated and 513 down-regulated) were differently expressed in hypoxia-induced PASMCs. Consistent with microarray analysis, quantitative PCR verified that AC068039.4 was obviously up-regulated in hypoxia-induced PASMCs. Knocking down AC068039.4 alleviated proliferation and migration of PASMCs and regulated cell cycle progression through inhibiting cells entering the G0/G1 cell cycle phase. Further experiment indicated AC068039.4 promoted hypoxic PASMCs proliferation via sponging miR-26-5p. In addition, transient receptor potential canonical 6 (TRPC6) was confirmed to be a target gene of miR-26a-5p. CONCLUSION: In conclusion, downregulation of lncRNA AC068039.4 inhibited pulmonary vascular remodeling through AC068039.4/miR-26a-5p/TRPC6 axis, providing new therapeutic insights for the treatment of HPH.	NA	Shock. 2021 Feb 1;55(2):244-255. doi: 10.1097/SHK.0000000000001606.
3949	LncRNA	AC245100.4	miR-145-5p	RBBP5	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33416179	Long non-coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA-145-5p/RBBP5 axis.	Long non-coding RNAs (lncRNAs) are markedly involved in cancer progression. Thus, identification of these lncRNAs can aid in the treatment of cancer. The present study focused on investigating the overall biological function, mechanism of action and clinical importance of lncRNA AC245100.4 in prostate cancer (PCa). The present study identified that AC245100.4 expression was significantly upregulated in PCa tissues and cell lines. Knockdown of AC245100.4 impaired tumor growth in an animal model. Biological function analysis indicated that AC245100.4 overexpression notably promoted cell proliferation and migration, while knockdown of AC245100.4 suppressed cell proliferation and migration. Mechanism studies focused on the competing endogenous RNA (ceRNA) network of AC245100.4. Bioinformatics predictions indicated that both AC245100.4 and retinoblastoma binding protein 5 (RBBP5) had microRNA (miR) response elements for miR-145-5p. This was further verified using a dual luciferase and RNA immunoprecipitation assays. AC245100.4 could positively regulate RBBP5 expression, but negatively regulated miR-145-5p expression. In addition, AC245100.4 knockdown-mediated inhibitory effects on cell proliferation and migration could be reversed by miR-145-5p silencing. Overall, the present study proposed a novel model in which the AC245100.4/miR-145-5p/RBBP5 ceRNA network induced the development of PCa, providing novel insights for PCa treatment.	NA	Oncol Rep. 2021 Feb;45(2):619-629. doi: 10.3892/or.2020.7894. Epub 2020 Dec 10.
3950	LncRNA	ACTA2-AS1	miR-532-5p	CXCL2	ovarian epithelial cells	Ovarian Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Flow Cytometry assay;	34093945	Mechanism underlying the regulation of lncRNA ACTA2-AS1 on CXCL2 by absorbing miRNA-532-5p as ceRNA in the development of ovarian cancer.	OBJECTIVE: To explore the mechanism underlying the regulation of long non-coding RNA (LncRNA) ACTA2-AS1 on CXCL2 as a ceRNA of miR-532-5p in the progression of ovarian cancer (OC). METHODS: A qRT-PCR assay was carried out for analyzing the expression changes of ACTA2-AS1, miR-532-5p, as well as CXCL2 in OC tissues and corresponding healthy paracancerous tissues HOSEpiC (human ovarian epithelial cells), and OC cells. OC cells were grouped and transfected, and the fluorescent in situ hybridization was adopted for evaluating ACTA2-AS1 in the cells. Additionally, a dual luciferase reporter (DLR) assay was carried out for verifying the correlation of ACTA2-AS1 with miR-532-5p and of miR-532-5p with CXCL2. Cells were transfected with si-ACTA2-AS1, miR-532-5p, or CXCL2 overexpression plasmids, and then the cell proliferation, invasion, and apoptosis were determined using MTT, Transwell, and flow cytometry assays, respectively. RESULTS: Compared with paracancerous tissues and HOSEpiC cells, OC tissues and cells showed increased ACTA2-AS1 and CXCL2 expression and decreased miR-532-5p expression (all P<0.05). ACTA2-AS1 acted as ceRNA in OC by negatively regulating miR-532-5p. Additionally, upregulating ACTA2-AS1 intensified the proliferation and invasion of cancer cells and suppressed their apoptosis (all P<0.05), and inhibition of it resulted in opposite results. In contrast, overexpressing miR-532-5p suppressed the proliferation, invasion, and clone formation of the cells and promoted their apoptosis (all P<0.05). The effect of ACTA2-AS1 on OC cells can be partially reversed by overexpressing miR-532-5p. Moreover, CXCL2, positively correlated with ACTA2-AS1 in expression (P<0.0001, r=0.7385), was the target of miR-532-5p, and its overexpression could partially offset the influence of miR-532-5p on OC cells. CONCLUSION: LncRNA ACTA2-AS1 can act as a tumor promoter in OC by absorbing miR-532-5p as ceRNA and regulating CXCL2, and ACTA2-AS1 inhibitor is expected to play a role in targeted therapy of OC.	NA	Int J Clin Exp Pathol. 2021 May 15;14(5):596-607. eCollection 2021.
3951	LncRNA	ADAMTS9-AS1	miR-513a-5p	ZFP36	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	33149676	LncRNA ADAMTS9-AS1 Restrains the Aggressive Traits of Breast Carcinoma Cells via Sponging miR-513a-5p.	PURPOSE: Long noncoding RNAs (lncRNAs) exert important functions in the progression of cancers. Currently, we aim to investigate the potential roles of lncRNA ADAM Metallopeptidase with Thrombospondin Type 1 Motif 9 Antisense RNA 1 (ADAMTS9-AS1) in breast carcinoma. MATERIALS AND METHODS: The expressions of ADAMTS9-AS1 and miR-513a-5p in breast carcinoma tissues and cell lines were detected using qRT-PCR. Cell Counting Kit-8 (CCK-8) and transwell assays were used to assess the viability and invasive ability of breast cancer cells. The direct interaction between ADAMTS9-AS1 and miR-513a-5p was predicted using bioinformatics tools. The target of miR-513a-5p, ZFP36 Ring Finger Protein (ZFP36) was validated by luciferase assay. The expression of ZFP36 was measured using Western blot assay. Breast cancer MDA-MB-231 cells growth in vivo was evaluated using xenograft tumor assay. RESULTS: ADAMTS9-AS1 was downregulated in breast cancer tissues as well as cell lines. Upregulation of ADAMTS9-AS1 suppressed the growth and invasiveness of breast carcinoma cells in vitro as well as inhibiting cellgrowth in vivo. Furthermore, ZFP36 was manifested as the target gene of miR-513a-5p and negatively modulated by ADAMTS9-AS1. In addition, overexpression of ADAMTS9-AS1 neutralized the promoting impact of miR-513a-5p on the aggressiveness of breast cancer cells. CONCLUSION: In conclusion, lncRNA ADAMTS9-AS1 inhibited the aggressive phenotypes of breast carcinoma cells via sponging miR-513a-5p and regulating ZFP36.	NA	Cancer Manag Res. 2020 Oct 28;12:10693-10703. doi: 10.2147/CMAR.S266575. eCollection 2020.
3952	LncRNA	ADNCR	miR-204-5p	TCF3	neurons and astrocyte induction cells	Alzheimers Disease	Homo sapiens (human)	qRT-PCR	32953727	ADNCR modulates neural stem cell differentiation and proliferation through the regulation of TCF3 expression.	BACKGROUND: Neural stem cells (NSCs) are undifferentiated precursor cells that have the ability to self-renew and proliferate and have the capacity to become either glia (oligodendrocytes and astrocytes) or neurons. NSCs can act as beneficial adjuncts for many neurological disorders, such as cerebral infarction, spinal cord injuries, Alzheimer's disease, and Parkinson's disease. Long noncoding RNAs (lncRNAs) play essential roles during cell differentiation, proliferation, and metabolism. This study aimed to explore the role played by adipocyte differentiation-associated long noncoding RNA (ADNCR) in the self-renewal and multipotency of NSCs. METHODS: In this study, we identified NSCs and verified that these cells were able to regenerate and differentiate into both astrocytes and neurons. Then we studied the relation between expression of ADNCR and transcription factor 3 (TCF3) and proliferation of NSCs. RESULTS: ADNCR and TCF3 expression have been shown to decrease during the differentiation of NSCs into both neurons and astrocyte induction cells. However, the expression of the microRNA miR-204-5p increased over time during the differentiation of NSCs into both neurons and astrocyte induction cells. ADNCR acts as a competing endogenous RNA (ceRNA) for miR-204-5p, and the overexpression of ADNCR suppressed miR-204-5p expression and enhanced TCF3 expression in NSCs, which resulted in enhanced proliferation and suppressed neural differentiation. CONCLUSIONS: These data suggested that the use of ADNCR may represent a new strategy for expanding the interventions used to treat neurological disorders.	NA	Ann Transl Med. 2020 Aug;8(15):927. doi: 10.21037/atm-20-1068.
3953	LncRNA	AFAP1-AS1	miR-145	HOXA1	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	RNA pull-down assay;RNA pull-down;	33650645	Long non-coding RNA AFAP1-AS1 facilitates the growth and invasiveness of oral squamous cell carcinoma by regulating the miR-145/HOXA1 axis.	Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) has been reported to serve important roles in multiple types of cancer. However, the biological function and underlying mechanism of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) remain largely unknown. The present study aimed to investigate the biological roles and clarify the potential mechanism of AFAP1-AS1 in OSCC. The expression levels of AFAP1-AS1 in OSCC tissues and cells were determined using reverse transcription-quantitative PCR. Cell proliferation, colony formation, migration and invasion were analyzed using Cell Counting Kit-8, colony formation, wound healing and Transwell invasion assays, respectively. The potential binding between AFAP1-AS1 and microRNA (miR)-145 was validated using dual luciferase reporter and RNA pull-down assays. A xenograft tumor model was established to evaluate the effect of AFAP1-AS1 in vivo. The results revealed that AFAP1-AS1 expression levels were markedly upregulated in OSCC tissues and cells. In addition, patients with OSCC with high expression levels of AFAP1-AS1 had a poor prognosis. Functionally, the knockdown of AFAP1-AS1 in OSCC cells significantly inhibited cell proliferation, migration and invasion in vitro. Similarly, in vivo AFAP1-AS1 knockdown prevented tumor growth and reduced tumor size and weight. Mechanistically, AFAP1-AS1 was discovered to regulate the expression levels of Homeobox A1 (HOXA1) by competing with miR-145. The inhibition of miR-145 partially attenuated the inhibitory effects of AFAP1-AS1 knockdown on OSCC cells. In conclusion, the findings of the present study suggested that AFAP1-AS1 may promote the progression of OSCC by regulating the miR-145/HOXA1 axis.	NA	Oncol Rep. 2021 Mar;45(3):1094-1104. doi: 10.3892/or.2020.7908. Epub 2020 Dec 24.
3954	LncRNA	AFAP1-AS1	miR-195-5p	FKBP1A	PCa cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33138677	LncRNA AFAP1-AS1 modulates the sensitivity of paclitaxel-resistant prostate cancer cells to paclitaxel via miR-195-5p/FKBP1A axis.	LncRNA AFAP1-AS1 has been corroborated to function in diverse cancers. Our aim was to investigate the molecular mechanism of AFAP1-AS1 in PTX resistance in PCa. The levels of AFAP1-AS1, miR-195-5p, and FKBP1A were checked by qRT-PCR. 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-Diphenyltetrazolium Bromide (MTT) assay was employed to assess the resistance of PTX-resistant PCa cells to PTX. Flow cytometry was introduced to evaluate cell apoptosis. The protein levels of C-caspase 3 were determined by western blot. The starBase was used to predict the interaction between miR-195-5p and AFAP1-AS1. Xenograft tumor model was established to investigate the biological role of AFAP1-AS1 in PTX resistance in vivo. The levels of AFAP1-AS1 and FKBP1A were upregulated in PCa tissues and cells, as well as PTX-resistant PCa cells, while the expression of miR-195-5p was declined. Knockdown of AFAP1-AS1 promoted the sensitivity of PTX-resistant PCa cells to PTX, induced apoptosis of PTX-resistant PCa cells, whereas the impacts could be reversed by reducing the expression of miR-195-5p. FKBP1A overexpression could rescue the effects of miR-195-5p-mediated enhancement on the sensitivity of PTX-resistant PCa cells to PTX, promotion on apoptosis of PTX-resistant PCa cells. AFAP1-AS1 interacted with miR-195-5p and miR-195-5p could bind to the 3'UTR of FKBP1A. AFAP1-AS1 silencing inhibited the tumor growth in mice implanted with PC3-TXR cell. The protein level of PCNA was decreased in PC3-TXR cells transfected with sh-AFAP1-AS1, while the expression of C-caspase 3 was upregulated. AFAP1-AS1 silencing attenuated the resistance of PTX-resistant PCa cells to PTX by downregulating FKBP1A via sponging miR-195-5p.	NA	Cancer Biol Ther. 2020 Nov 1;21(11):1072-1080. doi: 10.1080/15384047.2020.1829266. Epub 2020 Nov 3.
3955	LncRNA	AFAP1-AS1	miR-497-5p	SEPT2	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32955920	LncRNA AFAP1-AS1 Knockdown Represses Cell Proliferation, Migration, and Induced Apoptosis in Breast Cancer by Downregulating SEPT2 Via Sponging miR-497-5p.	Background: Long non-coding RNA actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) was confirmed to be associated with tumorigenesis. However, the role of AFAP1-AS1 in breast cancer was little known. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the levels of AFAP1-AS1, microRNA-497-5p (miR-497-5p), and Septin 2 (SEPT2) in breast cancer tissues and cells. The cell proliferation, migration, and apoptosis were tested by Methylthiazolyldiphenyl-tetrazolium bromide (MTT), Transwell and Flow cytometry assays, respectively. The targeting relationship between genes was predicted by StarBase v.3.0 and confirmed by dual-luciferase reporter assay. Pearson's correlation coefficient was applied to examine the correlation between the two groups. SEPT2 protein expression was evaluated by western blot. Xenograft models were established to investigate the role of AFAP1-AS1 knockdown in vivo. Results: AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. MiR-497-5p, which was downregulated in breast cancer, was verified to be a target of AFAP1-AS1 and inversely correlated with AFAP1-AS1 expression. SEPT2, as a target gene of miR-497-5p, was negatively regulated by miR-497-5p and positively correlated with AFAP1-AS1 expression. Importantly, AFAP1-AS1 could upregulate SEPT2 expression by sponging miR-497-5p, and modulate cell progression by regulation of the miR-497-5p/SEPT2 axis in breast cancer. Conclusion: AFAP1-AS1 knockdown repressed the progression of breast cancer cells by sponging miR-497-5p and downregulating SEPT2.	NA	Cancer Biother Radiopharm. 2020 Sep 21. doi: 10.1089/cbr.2020.3688.
3956	LncRNA	AFAP1-AS1	miR-195-5p	E2F3	enteric neural crest stem cells	Hirschsprungs Disease	Homo sapiens (human)	microarray;Flow Cytometry assay;	32959905	Involvement of the lncRNA AFAP1-AS1/microRNA-195/E2F3 axis in proliferation and migration of enteric neural crest stem cells of Hirschsprung's disease.	NEW FINDINGS: What is the central question of this study Long non-coding RNAs (lncRNAs) are widely involved in the progression of Hirschsprung's disease (HSCR), but the role of actin filament associated protein 1 antisense RNA1 (AFAP1-AS1), an lncRNA, in HSCR has not been explored before. What is the main finding and its importance Downregulation of AFAP1-AS1 blocks enteric neural crest stem cell proliferation, differentiation, migration and invasion and promotes the occurrence of HSCR via the miR-195/E2F3 axis, indicating thatAFAP1-AS might be a potential biomarker for HSCR patients. ABSTRACT: Long non-coding RNAs (lncRNAs) are involved in several human disorders. Nevertheless, it remains unclear whether they are implicated in the phenotypes of enteric neural crest stem cells (ENCSCs) in Hirschsprung's disease (HSCR). Therefore, we designed this study to explore the pathogenicity of AFAP1-AS1 for HSCR. Microarray analysis and bioinformatic tools were used to screen out the differentially lncRNAs and microRNAs (miRNAs) in patients with HSCR. Small interference RNA transfection was applied to carry out functional experiments in ENCSCs. Cellular activities were detected by cell counting kit-8, 5-ethynyl-2'-deoxyuridine, Transwell assays and flow cytometry. Finally, rescue experiments were performed to examine the cofunction of AFAP1-AS1 and miR-195 and of miR-195 and E2F transcription factor 3 (E2F3). AFAP1-AS1 was reduced in HSCR patients. Meanwhile, knockdown of AFAP1-AS1 reduced the cell migratory and proliferative capacities and facilitated cell apoptosis along with G0/G1 phase arrest. E2F3 was diminished when miR-195 was upregulated, and AFAP1-AS1 inhibition reduced its ability to bind to miR-195. Altogether, AFAP1-AS1 silencing acts as an endogenous RNA by interacting with miR-195 to alter E2F3 expression, thus conferring repressive effects on ENCSC activity and promoting HSCR progression.	NA	Exp Physiol. 2020 Sep 22. doi: 10.1113/EP088780.
3957	LncRNA	AGAP2-AS1	miR-15a-5p	CPT1	breast cancer cells	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33273726	MSC-induced lncRNA AGAP2-AS1 promotes stemness and trastuzumab resistance through regulating CPT1 expression and fatty acid oxidation in breast cancer.	Trastuzumab resistance has been becoming a major obstacle for treatment of HER-2-positive breast cancer patients. Increasing evidence suggests that mesenchymal stem cells (MSCs) play critical roles during the formation of drug resistance, however, the underlying mechanism is not well known. In this study, mass spectrometry, RNA pulldown and RNA immunoprecipitation assays were performed to verify the direct interactions among AGAP2-AS1 and other associated targets, such as human antigen R (HuR), miR-15a-5p, and carnitine palmitoyl transferase 1 (CPT1). In vitro and in vivo experimental assays were done to clarify the functional role of AGAP2-AS1 in trastuzumab resistance, stemness, and fatty acid oxidation (FAO). The results showed that MSC co-culture induced trastuzumab resistance. AGAP2-AS1 was upregulated in MSC-cultured cells, and knockdown of AGAP2-AS1 reversed the MSC-mediated trastuzumab resistance. Furthermore, MSC culture-induced AGAP2-AS1 regulates stemness and trastuzumab resistance via activating FAO. Mechanistically, AGAP2-AS1 is associated with HuR, and the AGAP2-AS1-HuR complex could directly bind to the CPT1, increasing its expression via improving RNA stability. In addition, AGAP2-AS1 could serve as ceRNA via sponging miR-15a-5p and releasing CPT1 mRNA. Clinically, increased expression of serum AGAP2-AS1 predicts poor response to trastuzumab treatment in breast cancer patients. In conclusion, MSC culture-induced AGAP2-AS1 caused stemness and trastuzumab resistance via promoting CPT1 expression and inducing FAO. Our results provide new insight of the role of MSCs in trastuzumab resistance and AGAP2-AS1 could be promising predictive biomarker and therapeutic target for HER-2+ breast cancer patients.	NA	Oncogene. 2021 Jan;40(4):833-847. doi: 10.1038/s41388-020-01574-8. Epub 2020 Dec 3.
3958	LncRNA	ANRIL	miR-324-5p	Ran	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase activity assay;MTT assay;RNA pull-down;	33500630	LncRNA ANRIL Regulates Ovarian Cancer Progression and Tumor Stem Cell-Like Characteristics via miR-324-5p/Ran Axis.	OBJECTIVE: Long non-coding RNA (lncRNA) ANRIL is emerging as a crucial role in ovarian cancer progression and prognosis. However, the precise molecular mechanism of ANRIL on ovarian cancer is not known. Thus, we aim to study the underlying mechanism of ANRIL on the action. METHODS: The MTT assay assessed cell viability. Cell migration and invasion were determined using the wound healing assay, Transwell migration, and invasion assay. The relationships of ANRIL, miR-324-5p, and RAN were evaluated using luciferase activity assay and RNA pull-down assay. Cancer stem cell was identified by flow cytometry. Sphere formation assay was conducted to determine the stem-like properties. Xenograft tumor was established to assess tumor growth in vivo. qRT-PCR and Western blot were used to detect gene expression. RESULTS: ANRIL was elevated while miR-324-5p was decreased in ovarian cancer tissues and cells. Besides, downregulated ANRIL enhanced miR-324-5p expression, and the luciferase reporting experiment and RNA pull-down assay showed the binding interaction between ANRIL and miR-324-5p. miR-324-5p directly targeted Ran and negatively modulated the expression of Ran. Besides, Ran was promoted by overexpressed ANRIL, which was reversed by overexpression of miR-324-5p. Furthermore, decreased ANRIL and increased miR-324-5p suppressed tumor growth, migration capacity, drug resistance, and alleviated stem-like characteristics in vitro and in vivo. Ran mediated the regulation of ANRIL on cell viability, stem-like properties, and drug resistance of ovarian cancer cells. CONCLUSION: The ANRIL/miR-324-5p/Ran axis regulated ovarian cancer development, making the axis meaningful targets for ovarian cancer therapy.	NA	Onco Targets Ther. 2021 Jan 19;14:565-576. doi: 10.2147/OTT.S273614. eCollection 2021.
3959	LncRNA	ANRIL	miR-15a-5p	JAK2	Human nasal epithelial cells	Allergic Rhinitis	Homo sapiens (human)	ELISA;Western blot;Luciferase reporter assay;	33325534	Knockdown of lncRNA ANRIL suppresses the production of inflammatory cytokines and mucin 5AC in nasal epithelial cells via the miR-15a-5p/JAK2 axis.	The incidence of allergic rhinitis (AR) is increasing worldwide. Human nasal epithelial cells (HNECs) are the key cells in the occurrence of AR. Antisense non-coding RNA in the INK4 locus (ANRIL) was discovered to be involved in the progression of AR. However, the mechanism by which ANRIL mediates the progression of AR remains to be determined. The present study aimed to further explore the mechanism by which ANRIL regulates AR. Thereby, HNECs were treated with IL-13 to mimic AR in vitro. The mRNA expression levels of ANRIL, microRNA (miR)-15a-5p, JAK2, mucin 5AC (MUC5AC), granulocyte-macrophage colony-stimulating factor (GM-CSF) and eotaxin-1, and protein expression levels of JAK2, STAT3 and phosphorylated-STAT3 in HNECs were analyzed using reverse transcription-quantitative PCR and western blotting, respectively. ELISAs were used to detect the secretory levels of inflammatory cytokines and mucin in cell supernatants. In addition, a dual luciferase reporter assay was used to confirm the downstream target of ANRIL and the target gene of miR-15a-5p. The results revealed that the secretory levels of eotaxin-1, GM-CSF and MUC5AC were significantly upregulated by IL-13 in the supernatant of HNECs. The expression levels of ANRIL and JAK2 were also upregulated in IL-13-induced HNECs, while the expression levels of miR-15a-5p were downregulated. In addition, ANRIL was identified to bind to miR-15a-5p. The IL-13-induced upregulation of eotaxin-1, GM-CSF and MUC5AC mRNA expression and secretory levels was significantly inhibited by the genetic knockdown of ANRIL, while the miR-15a-5p inhibitor effectively reversed this effect. JAK2 was also discovered to be directly targeted by miR-15a-5p. The overexpression of JAK2 significantly suppressed the therapeutic effect of miR-15a-5p mimics on IL-13-induced inflammation in vitro. In conclusion, the findings of the present study suggested that the genetic knockdown of ANRIL may suppress the production of inflammatory cytokines and mucin in IL-13-treated HNECs via regulation of the miR-15a-5p/JAK2 axis. Thus, ANRIL may serve as a novel target for AR treatment.	NA	Mol Med Rep. 2021 Feb;23(2):145. doi: 10.3892/mmr.2020.11784. Epub 2020 Dec 16.
3960	LncRNA	ANRIL	miR-411-3p	HIF-1	multiple myeloma cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR	32961145	Dysregulation of LncRNA ANRIL mediated by miR-411-3p inhibits the malignant proliferation and tumor stem cell like property of multiple myeloma via hypoxia-inducible factor 1α.	Long non-coding RNA (lncRNA) ANRIL has been reported to be closely related to the relapse of multiple myeloma patients. However, the functional role and underlying mechanism of lncRNA ANRIL in multiple myeloma are not known. This study aims to investigate the biological function of lncRNA ANRIL in multiple myeloma. In this study, compared with normal tissues from healthy donors, lncRNA ANRIL and HIF-1α expressions were up-regulated in tumor tissues from multiple myeloma patients. miR-411-3p expression was down-regulated in tumor tissues from multiple myeloma patients. Besides, lncRNA ANRIL can interact with miR-411-3p. HIF-1α was confirmed to be a target of miR-411-3p. Correlation analysis showed that lncRNA ANRIL expression was negatively correlated with miR-411-3p expression. HIF-1α expression was negatively correlated with miR-411-3p expression. Further transfection experiments showed that knockdown of ANRIL or overexpression of miR-411-3p significantly inhibited cell proliferation, tumor formation ability and tumor stem cell like property, promoted cell apoptosis in vitro. Finally, miR-411-3p mimic reduced tumor volume, improved survival rate, suppressed malignant proliferation and tumor stem cell like property in U266 xenograft model. Our results demonstrate that lncRNA ANRIL mediated by miR-411-3p promotes the malignant proliferation and tumor stem cell like property of multiple myeloma through regulating HIF-1α.	NA	Exp Cell Res. 2020 Nov 1;396(1):112280. doi: 10.1016/j.yexcr.2020.112280. Epub 2020 Sep 19.
3961	LncRNA	ARFRP1	miR-15a-5p	TLR4	OA cells	Osteoarthritis	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32931797	LncRNA ARFRP1 knockdown inhibits LPS-induced the injury of chondrocytes by regulation of NF-κB pathway through modulating miR-15a-5p/TLR4 axis.	AIMS: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been reported as the important regulators in osteoarthritis (OA). However, the detailed mechanism is implicated. The aim of this study is to reveal the functional mechanism of lncRNA ARFRP1 and miR-15a-5p in osteoarthritis. MATERIALS AND METHODS: The expression level of genes was detected by quantitative real time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit-8 (CCK-8) was used to assess cell viability. Cell apoptosis rate was analyzed by flow cytometry analysis. Furthermore, Enzyme-linked immunosorbent assay (ELISA) was performed to measure tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1β contents. The interaction between miR-15a-5p and ARFRP1 or Toll-like receptor 4 (TLR4) was predicted by miRcode or PITA, and then confirmed by the dual luciferase reporter assay or pull down assay. Besides, NF-κB-driven luciferase activity was determined using NF-κB luciferase reporter assay. KEY FINDINGS: ARFRP1 and TLR4 levels were increased and miR-15a-5p level was decreased in OA cartilage tissues and lipopolysaccharides (LPS)-induced chondrocytes. ARFRP1 knockdown inhibited LPS-induced the injury of chondrocytes. Interestingly, miR-15a-5p downregulated by ARFRP1 negatively modulated TLR4 expression through interaction. ARFRP1 mediated LPS-induced the injury of chondrocytes via regulating miR-15a-5p/TLR4 axis. Furthermore, ARFRP1 exerted function by modulation of NF-κB pathway. SIGNIFICANCE: Our findings confirmed that ARFRP1 mediated LPS-induced the injury of chondrocytes through regulating NF-κB pathway by modulation of miR-15a-5p/TLR4 axis, providing theoretical basis for the treatment of OA patients.	NA	Life Sci. 2020 Nov 15;261:118429. doi: 10.1016/j.lfs.2020.118429. Epub 2020 Sep 12.
3962	LncRNA	ARRDC1-AS1	miR-432-5p	PRMT5	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR	33220929	Long noncoding RNA ARRDC1-AS1 is activated by STAT1 and exerts oncogenic properties by sponging miR-432-5p/PRMT5 axis in glioma.	Dysfunction of long noncoding RNA (lncRNA) is associated with tumorigenesis of various malignancies, including glioma. Previously, lncRNA ARRDC1 antisense RNA 1(ARRDC1-AS1) has been reported to be dysregulated in several tumors. However, the roles of ARRDC1-AS1 in glioma have not been investigated. In this study, we firstly reported that ARRDC1-AS1 expression was distinctly increased in both glioma specimens and cell lines, and high ARRDC1-AS1 expression was associated with advanced clinical progression and poor prognosis of glioma patients. Additionally, STAT1 could activate the transcription of ARRDC1-AS1. Functional studies revealed that knockdown of ARRDC1-AS1 suppressed the proliferation, migration and invasion of glioma cells. Mechanisms exploration indicated ARRDC1-AS1 served as a sponge of miR-432-5p to upregulate PRMT5 expressions. Rescue experiments indicated that knockdown of miR-432-5p reversed the inhibiting effects of ARRDC1-AS1 knockdown on glioma cells. Overall, our findings highlighted the importance of STAT1/ARRDC1-AS1/miR-432-5p/PRMT5 axis in glioma progression and offered novel strategies for glioma treatments.	NA	Biochem Biophys Res Commun. 2021 Jan 1;534:511-518. doi: 10.1016/j.bbrc.2020.11.051. Epub 2020 Nov 19.
3963	LncRNA	BACE1-AS	miR-214-3p	ATG5	alleviated neuronal injury	Alzheimers Disease	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33197504	LncRNA BACE1-AS Promotes Autophagy-Mediated Neuronal Damage Through The miR-214-3p/ATG5 Signalling Axis In Alzheimer's Disease.	Alzheimer's disease (AD) is the most common neurodegenerative disease and is characterized by progressive memory loss and cognitive dysfunction. Long non-coding RNAs (lncRNAs) have been shown to be among the most promising biomarkers and therapeutic targets of AD. Here, we aimed to investigate whether lncRNA BACE1-AS plays a role in the potential mechanisms of AD. The expression of BACE1-AS, miR-214-3p and ATG5 mRNA was detected using qRT-PCR. The expression of the LC3, P62, ATG5, Bcl-2, p-Tau and cleaved-caspase 3 proteins was examined using western blot analysis. Cell apoptosis, cytotoxicity and ROS levels were estimated using flow cytometry, an LDH kit and a DCFH-DA assay, respectively. The interaction between BACE1-AS or ATG5 and miR-214-3p was validated using a dual-luciferase reporter assay. HE staining and a TUNEL assay were employed to evaluate hippocampal neuronal injury. The BACE1-AS level was found to be upregulated in serum samples of AD patients, brain tissues of AD transgenic (Tg) mice and Aβ(1-42)-treated SH-SY5Y cells. Autophagy activity was increased in both Tg mice and Aβ(1-42)-treated cells. BACE1-AS knockdown alleviated Aβ(1-42)-induced cell injury. Rapamycin abolished the protective effects of sh BACE1-AS against Aβ(1-42) induced cell injury. BACE1-AS indirectly regulated ATG5 expression by binding miR-214-3p. The miR-214-3p inhibitor reversed the protective effects of sh BACE1-AS and sh ATG5 against Aβ(1-42)-induced cell injury. Knockdown of BACE1-AS alleviated neuronal injury by repressing autophagy in vivo. Our findings demonstrate that silencing of BACE1-AS alleviated neuronal injury by regulating autophagy through the miR-214-3p/ATG5 signalling axis in AD.	NA	Neuroscience. 2021 Feb 10;455:52-64. doi: 10.1016/j.neuroscience.2020.10.028. Epub 2020 Nov 13.
3964	LncRNA	BANCR	miR-34c	NA	Human Aortic Smooth Muscle Cells	Atherosclerosis	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33151462	LncRNA BANCR induced vascular smooth muscle cell proliferation by downregulating miR-34c methylation in atherosclerosis.	Aberrant vascular smooth muscle cell (VSMCs) proliferation involves in the development of atherosclerosis. It reported that Long noncoding BRAF-activated noncoding RNA (BANCR) and miR-34c played opposite roles in the regulation of the proliferation of VSMCs, indicating that there might be a potential interaction between them. This study was to investigate the relationship between BANCR and miR-34c in atherosclerosis. Blood (5 ml) was obtained from 56 patients with atherosclerosis and 56 healthy volunteers after they were fasted overnight, and plasma was extracted from the blood. Human Aortic Smooth Muscle Cells (HASMCs) were used to perform in vitro cell experiments. RT-qPCR was performed to measure the expression of BANCR and miR-34c in plasma and HASMCs. Dual luciferase reporter assay detected the interaction between BANCR and miR-34c. CCK-8 assay was used to assess the effects of BANCR and miR-34c overexpression on the proliferation of HASMCs. Western blotting was used to assess the effects of BANCR and miR-34c overexpression on the protein expression of HMGB1, TNF-ɑ and Bcl-2. In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis. Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation. In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-ɑ and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. Therefore given BANCR upregulation in atherosclerosis, its expression may be considered as a novel and useful biomarker for atherosclerosis prevention and prognosis. However considering the possible effects of other underlying diseases on both BANCR expression and miR-34c in atherosclerosis, further investigation is suggested for future research.	NA	J Thromb Thrombolysis. 2021 May;51(4):924-932. doi: 10.1007/s11239-020-02314-1. Epub 2020 Nov 5.
3965	LncRNA	BBOX1-AS1	miR-125a-5p	CDKN2A	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33678324	A ceRNA network of BBOX1-AS1-hsa-miR-125b-5p/hsa-miR-125a-5p-CDKN2A shows prognostic value in cervical cancer.	OBJECTIVE: Cervical cancer (CC) ranks fourth most diagnosed cancer and cancer mortality in women. Long non-coding RNAs (lncRNAs) take important roles in CC development. This study aimed to identify more and novel competing endogenous RNA (ceRNA) mechanisms of lncRNAs in CC. MATERIALS AND METHODS: The miRNA expression dataset GSE20592 and lncRNA/mRNA expression dataset GSE63514 were downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs), differentially expressed lncRNAs (DElncRNAs), and differentially expressed miRNAs (DEmiRNAs) between CC tumor and normal samples were identified with the criteria of adj.P.Value < 0.05 (Benjamini & Hochberg) and |log(2)(fold change)|>2. Functional enrichment analysis was performed for DEGs. The interaction pairs among lncRNAs, miRNAs and mRNAs were predicted and the ceRNA network was then constructed. Survival analysis was performed based on the TCGA dataset. RESULTS: Totally, 42 DEmiRNAs, 25 DElncRNAs, and 518 DEGs were identified in CC tumor samples versus normal tissues. The DEGs were associated with 'GO:0006260: DNA replication', 'GO:0051301: cell division', and 'hsa01100:Metabolic pathways'. The ceRNA network consisted of 878 lncRNA-miRNA-mRNA pairs. Of the miRNAs, lncRNAs, and genes with the top 10 interaction degrees in the ceRNA network, the upregulated cyclin dependent kinase inhibitor 2A gene (CDKN2A) was targeted by the downregulated DEmiRNAs including hsa-miR-125b-5p and hsa-miR-125a-5p, which were targeted by the upregulated DElncRNA BBOX1-AS1. The high expression level of CDKN2A contributed to the poor overall survival of patients with CC. CONCLUSIONS: The BBOX1-AS1-hsa-miR-125b-5p/hsa-miR-125a-5p-CDKN2A ceRNA network is of great value in CC development.	NA	Taiwan J Obstet Gynecol. 2021 Mar;60(2):253-261. doi: 10.1016/j.tjog.2020.12.006.
3966	LncRNA	BBOX1-AS1	miR-125b-5p	CDKN2A	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33678324	A ceRNA network of BBOX1-AS1-hsa-miR-125b-5p/hsa-miR-125a-5p-CDKN2A shows prognostic value in cervical cancer.	OBJECTIVE: Cervical cancer (CC) ranks fourth most diagnosed cancer and cancer mortality in women. Long non-coding RNAs (lncRNAs) take important roles in CC development. This study aimed to identify more and novel competing endogenous RNA (ceRNA) mechanisms of lncRNAs in CC. MATERIALS AND METHODS: The miRNA expression dataset GSE20592 and lncRNA/mRNA expression dataset GSE63514 were downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs), differentially expressed lncRNAs (DElncRNAs), and differentially expressed miRNAs (DEmiRNAs) between CC tumor and normal samples were identified with the criteria of adj.P.Value < 0.05 (Benjamini & Hochberg) and |log(2)(fold change)|>2. Functional enrichment analysis was performed for DEGs. The interaction pairs among lncRNAs, miRNAs and mRNAs were predicted and the ceRNA network was then constructed. Survival analysis was performed based on the TCGA dataset. RESULTS: Totally, 42 DEmiRNAs, 25 DElncRNAs, and 518 DEGs were identified in CC tumor samples versus normal tissues. The DEGs were associated with 'GO:0006260: DNA replication', 'GO:0051301: cell division', and 'hsa01100:Metabolic pathways'. The ceRNA network consisted of 878 lncRNA-miRNA-mRNA pairs. Of the miRNAs, lncRNAs, and genes with the top 10 interaction degrees in the ceRNA network, the upregulated cyclin dependent kinase inhibitor 2A gene (CDKN2A) was targeted by the downregulated DEmiRNAs including hsa-miR-125b-5p and hsa-miR-125a-5p, which were targeted by the upregulated DElncRNA BBOX1-AS1. The high expression level of CDKN2A contributed to the poor overall survival of patients with CC. CONCLUSIONS: The BBOX1-AS1-hsa-miR-125b-5p/hsa-miR-125a-5p-CDKN2A ceRNA network is of great value in CC development.	NA	Taiwan J Obstet Gynecol. 2021 Mar;60(2):253-261. doi: 10.1016/j.tjog.2020.12.006.
3967	LncRNA	BCYRN1	miR-619-5p	CUEDC2	glioma cells	Glioma	Homo sapiens (human)	Cell migration assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;Flow Cytometry assay;Luciferase reporter assay;RNA sequencing;	32978519	LncRNA BCYRN1 inhibits glioma tumorigenesis by competitively binding with miR-619-5p to regulate CUEDC2 expression and the PTEN/AKT/p21 pathway.	Glioma is the most common malignant tumor in the central nervous system. Altered long noncoding RNAs (lncRNAs) are playing regulatory roles in physiological and pathogenic processes in cancer. Here, we uncovered a differentially expressed lncRNA called brain cytoplasmic RNA 1 (BCYRN1), and elucidated its function and molecular mechanism in the progression and development of glioma. Three fresh tumor tissues from glioma patients and three normal brain tissues from craniocerebral trauma patients were prepared for high-throughput RNA sequencing. Differential RNA transcripts and BCYRN1 were identified by RT-qPCR in glioma samples and controls. CCK-8, colony formation assays, flow cytometry, TUNEL assays, cell migration assays, wound-healing assays, and xenograft model were established to investigate the biological function of BCYRN1 both in vitro and in vivo. Various bioinformatics analysis, dual-luciferase reporter assays, biotinylated RNA pulldown assays, and rescue experiments were conducted to reveal the underlying mechanisms of competitive endogenous RNAs (ceRNAs). 183 lncRNAs were identified with significant dysregulation in glioma and randomly selected differential RNAs were further confirmed by RT-qPCR. Among them, BCYRN1 was the most downregulated lncRNA, and its low expression positively correlated with glioma progression. Functionally, BCYRN1 overexpression inhibited cell proliferation, migration in glioma cell lines, whereas BCYRN1 depletion resulted in the opposite way. MiR-619-5p was further confirmed as the direct target of BCYRN1. Mechanistically, miR-619-5p specifically targeted the CUE domain containing protein 2 (CUEDC2), and BCYRN1/miR-619-5p suppressed glioma tumorigenesis by inactivating PTEN/AKT/p21 pathway in a CUEDC2-dependent manner. Overall, our data presented that the reduced expression of BCYRN1 was associated with poor patient outcome in glioma. BCYRN1 functioned as a ceRNA to inhibit glioma progression by sponging miR-619-5p to regulate CUEDC2 expression and PTEN/AKT/p21 pathway. Our results indicated that BCYRN1 exerted tumor suppressor potential and might be a candidate in the diagnosis and treatment of glioma.	NA	Oncogene. 2020 Nov;39(45):6879-6892. doi: 10.1038/s41388-020-01466-x. Epub 2020 Sep 25.
3968	LncRNA	BCYRN1	miR-204-3p	KRAS	CRC cells	Colorectal Cancer	Homo sapiens (human)	RT-PCR;Flow Cytometry assay;Luciferase reporter assay;	32944001	Long non-coding RNA BCYRN1 exerts an oncogenic role in colorectal cancer by regulating the miR-204-3p/KRAS axis.	BACKGROUND: It has been well documented that long non-coding RNAs (lncRNAs) regulate numerous characteristics of cancer, including proliferation, migration, metastasis, apoptosis, and even metabolism. LncRNA BCYRN1 (BCYRN1) is a newly identified brain cytoplasmic lncRNA with 200 nucleotides that was discovered to be highly expressed in tumour tissues, including those of hepatocellular carcinoma, gastric cancer and lung cancer. However, the roles of BCYRN1 in colorectal cancer (CRC) remain obscure. This study was designed to reveal the role of BCYRN1 in the occurrence and progression of CRC. METHODS: RT-PCR was used to detect the expression level of BCYRN1 in tumour tissues and CRC cell lines. BCYRN1 was knocked down in CRC cells, and cell proliferation changes were evaluated by cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and Ki-67 and proliferating cell nuclear antigen (PCNA) expression assays. Cell migration and invasion changes were evaluated by wound healing, Transwell and invasion-related protein expression assays. Flow cytometry analysis was used to assess whether BCYRN1 regulates the apoptosis of CRC cells. The dual luciferase reporter gene detects the competitive binding of BCYRN1 to miR-204-3p. In vivo experiments were performed to evaluate the effect of BCYRN1 on tumour development. TargetScan analysis and dual luciferase reporter gene assays were applied to detect the target gene of miR-204-3p. Rescue experiments verified that BCYRN1 affects CRC by regulating the effect of miR-204-3p on KRAS. RESULTS: We found that compared with normal tissues and human intestinal epithelial cells (HIECs), CRC tumour tissues and cell lines had significantly increased BCYRN1 levels. We further determined that knockdown of BCYRN1 inhibited the proliferation, migration, and invasion and promoted the apoptosis of CRC cells. In addition, bioinformatics analysis and dual luciferase reporter assay showed that BCYRN1 served as a competitive endogenous RNA (ceRNA) to regulate the development of CRC through competitively binding to miR-204-3p. Further studies proved that overexpression of miR-204-3p reversed the effects of BCYRN1 on CRC. Next, TargetScan analysis and dual luciferase reporter assay indicated that KRAS is a target gene of miR-204-3p and is negatively regulated by miR-204-3p. A series of rescue experiments showed that BCYRN1 affected the occurrence and development of CRC by regulating the effects of miR-204-3p on KRAS. In addition, tumorigenesis experiments in a CRC mouse model confirmed that BCYRN1 downregulation effectively inhibited tumour growth. CONCLUSIONS: Our findings suggest that BCYRN1 plays a carcinogenic role in CRC by regulating the miR-204-3p/KRAS axis.	NA	Cancer Cell Int. 2020 Sep 14;20:453. doi: 10.1186/s12935-020-01543-x. eCollection 2020.
3969	LncRNA	BCYRN1	miR-204-3p	KRAS	CRC cells	Colorectal Cancer	Mus musculus (mouse)	RT-PCR;Flow Cytometry assay;Luciferase reporter assay;	32944001	Long non-coding RNA BCYRN1 exerts an oncogenic role in colorectal cancer by regulating the miR-204-3p/KRAS axis.	BACKGROUND: It has been well documented that long non-coding RNAs (lncRNAs) regulate numerous characteristics of cancer, including proliferation, migration, metastasis, apoptosis, and even metabolism. LncRNA BCYRN1 (BCYRN1) is a newly identified brain cytoplasmic lncRNA with 200 nucleotides that was discovered to be highly expressed in tumour tissues, including those of hepatocellular carcinoma, gastric cancer and lung cancer. However, the roles of BCYRN1 in colorectal cancer (CRC) remain obscure. This study was designed to reveal the role of BCYRN1 in the occurrence and progression of CRC. METHODS: RT-PCR was used to detect the expression level of BCYRN1 in tumour tissues and CRC cell lines. BCYRN1 was knocked down in CRC cells, and cell proliferation changes were evaluated by cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), and Ki-67 and proliferating cell nuclear antigen (PCNA) expression assays. Cell migration and invasion changes were evaluated by wound healing, Transwell and invasion-related protein expression assays. Flow cytometry analysis was used to assess whether BCYRN1 regulates the apoptosis of CRC cells. The dual luciferase reporter gene detects the competitive binding of BCYRN1 to miR-204-3p. In vivo experiments were performed to evaluate the effect of BCYRN1 on tumour development. TargetScan analysis and dual luciferase reporter gene assays were applied to detect the target gene of miR-204-3p. Rescue experiments verified that BCYRN1 affects CRC by regulating the effect of miR-204-3p on KRAS. RESULTS: We found that compared with normal tissues and human intestinal epithelial cells (HIECs), CRC tumour tissues and cell lines had significantly increased BCYRN1 levels. We further determined that knockdown of BCYRN1 inhibited the proliferation, migration, and invasion and promoted the apoptosis of CRC cells. In addition, bioinformatics analysis and dual luciferase reporter assay showed that BCYRN1 served as a competitive endogenous RNA (ceRNA) to regulate the development of CRC through competitively binding to miR-204-3p. Further studies proved that overexpression of miR-204-3p reversed the effects of BCYRN1 on CRC. Next, TargetScan analysis and dual luciferase reporter assay indicated that KRAS is a target gene of miR-204-3p and is negatively regulated by miR-204-3p. A series of rescue experiments showed that BCYRN1 affected the occurrence and development of CRC by regulating the effects of miR-204-3p on KRAS. In addition, tumorigenesis experiments in a CRC mouse model confirmed that BCYRN1 downregulation effectively inhibited tumour growth. CONCLUSIONS: Our findings suggest that BCYRN1 plays a carcinogenic role in CRC by regulating the miR-204-3p/KRAS axis.	NA	Cancer Cell Int. 2020 Sep 14;20:453. doi: 10.1186/s12935-020-01543-x. eCollection 2020.
3970	LncRNA	C1QTNF1-AS1	miR-484	HK2	CRC cells	Colorectal Cancer	Homo sapiens (human)	Cell migration and invasion assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33262654	Long Non-Coding RNA C1QTNF1 Antisense RNA 1 Upregulates Hexokinase 2 by Sponging microRNA-484 to Promote the Malignancy of Colorectal Cancer.	PURPOSE: The long noncoding RNA C1QTNF1 antisense RNA 1 (C1QTNF1-AS1) contributes to hepatocellular carcinoma development. However, its expression and roles in colorectal cancer (CRC) have not been fully explored. Therefore, this study determined the expression and roles of C1QTNF1-AS1 in CRC and elucidated its detailed mechanism of action. METHODS: C1QTNF1-AS1 expression in CRC tissues and cell lines was assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). We used Cell Counting Kit-8, flow cytometry, cell migration and invasion assays, and a xenograft tumor model to test the effects of C1QTNF1-AS1 on CRC malignancy. The associations among C1QTNF1-AS1, microRNA-484 (miR-484), and hexokinase 2 (HK2) were explored using luciferase reporter assay, RNA immunoprecipitation, RT-qPCR, and Western blotting. RESULTS: C1QTNF1-AS1 was overexpressed in CRC and related to poor prognosis. C1QTNF1-AS1 interference inhibited CRC cell proliferation, migration, and invasion but induced apoptosis. Furthermore, C1QTNF1-AS1 deficiency impaired tumor growth in vivo. Mechanistically, C1QTNF1-AS1 adsorbed miR-484, thereby increasing the expression of its target HK2. Rescue experiments revealed that the effects of C1QTNF1-AS1 deficiency in CRC cells were reversed by inhibiting miR-484 or upregulating HK2. CONCLUSION: C1QTNF1-AS1 drives CRC progression by sponging miR-484 and consequently upregulating HK2. The C1QTNF1-AS1/miR-484/HK2 pathway may serve as a diagnostic and therapeutic target for CRC.	NA	Cancer Manag Res. 2020 Nov 24;12:12053-12066. doi: 10.2147/CMAR.S262096. eCollection 2020.
3971	LncRNA	C3orf35	miR-142-3p	HMGB1	Osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	microarray;	33015161	Comprehensive Analysis of a ceRNA Network Identifies lncR-C3orf35 Associated with Poor Prognosis in Osteosarcoma.	Osteosarcoma is a highly malignant bone cancer which primarily occurs in children and young adults. Increasing evidence indicates that long noncoding RNAs (lncRNAs), which function as competing endogenous RNAs (ceRNAs) that sponge microRNAs (miRNAs) and messenger RNAs (mRNAs), play a pivotal role in the pathogenesis and progression of cancers. The regulatory mechanisms of lncRNA-mediated ceRNAs in osteosarcoma have not been fully elucidated. In this study, we identified differentially expressed lncRNAs, miRNAs, and mRNAs in osteosarcoma based on RNA microarray profiles in the Gene Expression Omnibus (GEO) database. A ceRNA network was constructed utilizing bioinformatic tools. Kaplan-Meier survival analysis showed that lncR-C3orf35 and HMGB1 were associated with poor prognosis of osteosarcoma patients. Furthermore, results of Gene Set Enrichment Analysis (GSEA) suggested that lncR-C3orf35 may be involved in cellular invasion, the Toll-like receptor signaling pathway, and immune cell infiltration in the tumor microenvironment. Further analysis showed that patients with osteosarcoma metastasis expressed higher levels of lncR-C3orf35 and HMGB1 compared to metastasis-free patients. Moreover, the metastasis-free survival rate of the high lncR-C3orf35/HMGB1 expression group was significantly lower than that of the low expression group. The ESTIMATE algorithm was used to calculate the immune score and stromal scores for each sample. High lncR-C3orf35 and HMGB1 levels were correlated with low immune scores. ImmuCellAI analysis revealed that a low proportion of macrophage infiltration was associated with high lncR-C3orf35 and HMGB1 expression. The differential expression of lncR-C3orf35, miR-142-3p, and HMGB1 was further verified by quantitative real-time PCR. This study indicates that lncR-C3orf35 could be considered as a novel potential biomarker and therapeutic target of osteosarcoma, which may contribute to a better understanding of ceRNA regulatory mechanisms.	NA	Biomed Res Int. 2020 Sep 21;2020:3178037. doi: 10.1155/2020/3178037. eCollection 2020.
3972	LncRNA	C9orf139	miR-663a	Sox12	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	33250960	LncRNA C9orf139 can regulate the growth of pancreatic cancer by mediating the miR-663a/Sox12 axis.	BACKGROUND: Recent studies have proved the important role of many oncogenic long non-coding RNAs (lncRNAs) in the progression of pancreatic cancer, but little is known about the mechanisms of tumor suppression in pancreatic cancer. AIM: To evaluate the function of tumor suppressor lncRNA C9orf139 in pancreatic cancer progression and to study the underlying mechanism. METHODS: We assigned 54 patients with pancreatic ductal adenocarcinoma treated at our hospital to the patient group and 30 normal subjects undergoing physical examination to the control group. RT-qPCR was used to measure the relative expression of C9orf139 in the tissue and serum of patients, in an attempt to investigate the prognostic value of C9orf139 in pancreatic cancer patients. The luciferase reporter gene assay was performed to determine the interaction between C9orf139 and miR-663a. The biological function of C9orf139 was assessed by in vitro assays and in vivo subcutaneous tumor formation tests in animal models. To figure out the molecular mechanism of C9orf139 to act on miR-663a/Sox12, RNA pull-down, Western blot assay, RNA immunoprecipitation assay, and co-immunoprecipitation assay were performed. RESULTS: C9orf139 level significantly increased in the tissue and serum of patients, which had clinical diagnostic value for pancreatic cancer. Patients with high C9orf139 expression had a higher risk of progressing to stage III + IV, lymph node metastasis, and poor differentiation. Cox regression analysis suggested that C9orf139, tumor-node-metastasis stage, and lymph node metastasis were independent prognostic factors in patients. The underlying mechanism of C9orf139 was that it promoted the growth of pancreatic cancer cells by modulating the miR-663a/Sox12 axis. CONCLUSION: C9orf139 is highly expressed in pancreatic cancer, qualified to be used as a potential diagnostic and prognostic marker for pancreatic cancer. Its promotion of pancreatic cancer cell growth is achieved by mediating the miR-663a/Sox12 axis.	NA	World J Gastrointest Oncol. 2020 Nov 15;12(11):1272-1287. doi: 10.4251/wjgo.v12.i11.1272.
3973	LncRNA	CA3-AS1	miR-93-5p	BTG3	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	FISH;qPCR;FISH;Luciferase reporter assay;	33051589	Long noncoding RNA CA3-AS1 suppresses gastric cancer migration and invasion by sponging miR-93-5p and targeting BTG3.	The long noncoding RNAs (lncRNAs) are a class of noncoding RNAs that are broadly expressed in various biological cells and function in regulating gene expression. However, the function of lncRNAs and the role of lncRNAs in gastric cancer remain to be determined. Herein, the function of lncRNA CA3-AS1 was investigated in gastric cancer. Firstly, we found that the expression level of CA3-AS1 was decreased in gastric cancer cell lines and tissues. Then, CA3-AS1 overexpression inhibited the gastric cancer cells migration and invasion and knockdown of CA3-AS1 enhanced the gastric cancer cells migration and invasion. Moreover, FISH assays and qPCR results revealed that CA3-AS1 was mainly expressed in the cytoplasm of gastric cancer cells. Then, the relationship between CA3-AS1 and miR-93-5p was explored. Luciferase reporter assays results showed that miR-93-5p was a direct target of CA3-AS1 in SGC-7901 and BCG-823. Furthermore, BTG3 was identified as a direct target gene of miR-93-5p. Restore experiments showed that CA3-AS1 upregulated the expression level of BTG3 and inhibited the gastric cancer cells invasion by sponging miR-93-5p. Finally, we found that CA3-AS1 inhibited the metastasis ability of gastric cancer cells in vivo. Above results suggested that CA3-AS1 acted as anti-oncogene in gastric cancer and might become a vital target for clinical treatment.	NA	Gene Ther. 2020 Oct 13. doi: 10.1038/s41434-020-00201-1.
3974	LncRNA	CASC15	miR-338-3p	RAB14	OS cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qRT-PCR;Western blot;Luciferase reporter assay;	33262606	LncRNA CASC15 is Upregulated in Osteosarcoma Plasma Exosomes and CASC15 Knockdown Inhibits Osteosarcoma Progression by Regulating miR-338-3p/RAB14 Axis.	BACKGROUND: Currently, plenty of studies have demonstrated that lncRNAs can act as crucial roles during the progression of various tumors, including osteosarcoma (OS), and emerging evidences indicated that lncRNAs are abundant and stable in exosomes. The objective of this study is to reveal the dysregulated lncRNAs in OS plasma exosomes and explore their functions in OS. MATERIALS AND METHODS: Microarray was performed to analyze dysregulated exosomal lncRNAs. Western blot, qRT-PCR assays, and Dual-luciferase reporter assay were used to verify the interaction among cancer susceptibility 15 (CASC15), miR-338-3p, and RAB14. Cck-8, colony formation assay, and transwell assay were performed to explore and characterize the effects of CASC15 on OS cells. Animal experiments were used to verify the effects of CASC15 in vivo. RESULTS: Upregulated CASC15 was observed in OS plasma exosomes compared with control, and the same expression was observed in the OS tissues and cell lines. Further assays indicated that CASC15 knockdown could restrain the proliferation, migration, and invasion of OS cells, and inhibit the growth of OS in xenograft models. Furthermore, our results demonstrated CASC15 regulated OS progression via acting as miR-338-3p sponge, and RAB14 was a direct downstream target of miR-338-3p. Rescue experiments verified CASC15 promotes OS cell growth and metastasis by upregulating RAB14 expression. CONCLUSION: Overall, our findings indicate that CASC15 plays a key role in OS progression by targeting the miR-338-3p/RAB14 axis and can serve as a possible therapeutic target for OS patients.	NA	Onco Targets Ther. 2020 Nov 23;13:12055-12066. doi: 10.2147/OTT.S282053. eCollection 2020.
3975	LncRNA	CASC19	miR-148b	E2F7	pancreatic cancer	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Luciferase reporter assay;	33155202	LncRNA CASC19 contributed to the progression of pancreatic cancer through modulating miR-148b/E2F7 axis.	OBJECTIVE: Cancer susceptibility 19 (CASC19), a crucial lncRNA associated with multiple cancers, has been reported to play a vital role in the progression of human malignant tumors. However, the underlying mechanism of CASC19 in pancreatic cancer (PC) was still unknown. The purpose of this study was to explore the biological and clinical significance of CASC19 in PC. PATIENTS AND METHODS: RT-qPCR assay was adopted to analyze CASC19 expression in PC tissues and cell lines. Furthermore, the correlation between the CASC19 level and the survival rate of PC patients was assessed by Kaplan-Meier analysis. Bioinformatics analysis and Luciferase reporter assay were utilized to confirm the interaction between miR-148b and CASC19 or E2F7. Cell viability, migration, invasion, and apoptosis were analyzed using MTT, transwell, and TUNEL assays. RESULTS: The results elucidated that CASC19 expression was markedly increased in PC tissues and cell lines. Patients with high expression of CASC19 had a short survival time. Silencing of CASC19 attenuated PC cell proliferation, migration, and invasion. Moreover, we identified that miR-148b was a target of CASC19. CASC19 was negatively correlated with miR-148b and positively correlated with E2F7. The inhibitory effect of CASC19 knockdown on the progression of PC was reversed by the down-regulation of miR-148b or up-regulation of E2F7. CONCLUSIONS: These results demonstrated that CASC19 participated in the development of PC. The CASC19/miR-148b/E2F7 axis might be a new study direction for PC treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10462-10471. doi: 10.26355/eurrev_202010_23399.
3976	LncRNA	CASC2	miR-194-5p	CAV1	BEAS-2B cells	Neonatal Lung Injury	Homo sapiens (human)	microarray;luciferase assay;	33212124	LncRNA CASC2 targets CAV1 by competitively binding with microRNA-194-5p to inhibit neonatal lung injury.	Long non-coding RNAs (lncRNAs) are vital regulators of different biological processes during bronchopulmonary dysplasia (BPD). This study was conducted to probe the biological roles of lncRNA CASC2 in the pathogenesis of BPD and neonatal lung injury. Firstly, a hyperoxia-induced mouse model with BPD was established. LncRNAs with differential expression in lung tissues of normal and BPD mice were analyzed by microarray. An adenovirus vector overexpressing CASC2 was constructed and its functions on BPD symptoms in model mice were analyzed. Gain- and loss-of function studies of CASC2 were performed in a bronchial epithelial cell line BEAS-2B to determine its role in cell apoptosis and proliferation under normoxic and hyperoxic conditions. The downstream mechanical molecules of lncRNA CASC2 were predicted on bioinformatics systems and confirmed by luciferase assays. The functional interactions among lncRNA CASC2, miR-194-5p, and CAV1 in BPD were determined by rescue experiments. Consequently, lncRNA CASC2 was found to be poorly expressed in BPD mice. Besides, overexpressed CASC2 was found to relieve the symptoms of BPD in neonatal mice and suppress apoptosis as well as promote proliferation in hyperoxia-induced BEAS-2B cells. Importantly, CASC2 was found to regulate CAV1 expression by competitively binding to miR-194-5p and downregulate the activity of the TGF-β1 signaling pathway, thereby suppressing lung injury. Either miR-194-5p upregulation or CAV1 downregulation blocked the roles of CASC2. To sum up, this study evidenced that CASC2 alleviates hyperoxia-induced lung injury in mouse and cell models with the involvement of a miR-194-5p-CAV1 crosstalk and the TGF-β1 inactivation.	NA	Exp Mol Pathol. 2021 Feb;118:104575. doi: 10.1016/j.yexmp.2020.104575. Epub 2020 Nov 17.
3977	LncRNA	CASC2	miR-194-5p	CAV1	BEAS-2B cells	Neonatal Lung Injury	Mus musculus (mouse)	microarray;luciferase assay;	33212124	LncRNA CASC2 targets CAV1 by competitively binding with microRNA-194-5p to inhibit neonatal lung injury.	Long non-coding RNAs (lncRNAs) are vital regulators of different biological processes during bronchopulmonary dysplasia (BPD). This study was conducted to probe the biological roles of lncRNA CASC2 in the pathogenesis of BPD and neonatal lung injury. Firstly, a hyperoxia-induced mouse model with BPD was established. LncRNAs with differential expression in lung tissues of normal and BPD mice were analyzed by microarray. An adenovirus vector overexpressing CASC2 was constructed and its functions on BPD symptoms in model mice were analyzed. Gain- and loss-of function studies of CASC2 were performed in a bronchial epithelial cell line BEAS-2B to determine its role in cell apoptosis and proliferation under normoxic and hyperoxic conditions. The downstream mechanical molecules of lncRNA CASC2 were predicted on bioinformatics systems and confirmed by luciferase assays. The functional interactions among lncRNA CASC2, miR-194-5p, and CAV1 in BPD were determined by rescue experiments. Consequently, lncRNA CASC2 was found to be poorly expressed in BPD mice. Besides, overexpressed CASC2 was found to relieve the symptoms of BPD in neonatal mice and suppress apoptosis as well as promote proliferation in hyperoxia-induced BEAS-2B cells. Importantly, CASC2 was found to regulate CAV1 expression by competitively binding to miR-194-5p and downregulate the activity of the TGF-β1 signaling pathway, thereby suppressing lung injury. Either miR-194-5p upregulation or CAV1 downregulation blocked the roles of CASC2. To sum up, this study evidenced that CASC2 alleviates hyperoxia-induced lung injury in mouse and cell models with the involvement of a miR-194-5p-CAV1 crosstalk and the TGF-β1 inactivation.	NA	Exp Mol Pathol. 2021 Feb;118:104575. doi: 10.1016/j.yexmp.2020.104575. Epub 2020 Nov 17.
3978	LncRNA	CASC2	miR-18a-5p	FIH1	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	Luciferase reporter assay;	33336500	CASC2 inhibits the growth, migration, and invasion of thyroid cancer cells through sponging miR-18a-5p/FIH1 axis.	Long noncoding RNA (lncRNA) Cancer Susceptibility 2 (CASC2) has been proved to contribute to the development of cancers. However, the mechanism behind the action of CASC2 in thyroid cancer is not quite clear. We demonstrated that CASC2 was downregulated in thyroid cancer. We noted that CASC2 overexpression restrained the growth, migration, and invasion of thyroid cancer cells, whereas CASC2 depletion caused opposite trends. Bioinformatics analysis predicted that hypoxia inducible factor 1 subunit alpha inhibitor (FIH-1) was potentially targeted by miR-18a-5p, which was confirmed by luciferase reporter assay. Upregulation of FIH-1 abrogated the promotive effect of miR-18a-5p on the growth and invasion of thyroid cancer cells. In addition, CASC2 serves as a competing endogenous RNA (ceRNA) and a ''sponge'' for miR-18a-5p, thereby regulating the expression of FIH-1. These data elucidated the CASC2/miR-18a-5p ceRNA network in thyroid cancer pathogenesis.	NA	Kaohsiung J Med Sci. 2021 Apr;37(4):268-275. doi: 10.1002/kjm2.12331. Epub 2020 Dec 17.
3979	LncRNA	CASC2	miR-21	NA	IDH1 wild type glioma cell	Idh1 Wild Type Glioma	Homo sapiens (human)	qPCR;RT-qPCR;	33120918	The Role of CASC2 and miR-21 Interplay in Glioma Malignancy and Patient Outcome.	Recently long non-coding RNAs (lncRNAs) were highlighted for their regulatory role in tumor biology. The novel human lncRNA cancer susceptibility candidate 2 (CASC2) has been characterized as a potential tumor suppressor in several tumor types. However, the roles of CASC2 and its interplay with miR-21 in different malignancy grade patient gliomas remain unexplored. Here we screened 99 different malignancy grade astrocytomas for CASC2, and miR-21 gene expression by real-time quantitative polymerase chain reaction (RT-qPCR) in isocitrate dehydrogenase 1 (IDH1) and O-6-methylguanine methyltransferase (MGMT) assessed gliomas. CASC2 expression was significantly downregulated in glioblastomas (p = 0.0003). Gliomas with low CASC2 expression exhibited a high level of miR-21, which was highly associated with the higher glioma grade (p = 0.0001), IDH1 wild type gliomas (p < 0.0001), and poor patient survival (p < 0.001). Taken together, these observations suggest that CASC2 acts as a tumor suppressor and potentially as a competing endogenous RNA (ceRNA) for miR-21, plays important role in IDH1 wild type glioma pathogenesis and patients' outcomes.	NA	Int J Mol Sci. 2020 Oct 27;21(21):7962. doi: 10.3390/ijms21217962.
3980	LncRNA	CASC2	miR-18a	NA	T98 and A172 cells	Glioblastoma	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	32975234	Long non-coding RNA CASC2 targeting miR-18a suppresses glioblastoma cell growth, metastasis and EMT in vitro and in vivo.	Long non-coding RNAs (lncRNAs) cancer susceptibility candidate 2 (CASC2) has been characterized as a tumor suppressor in glioma. Although CASC2 may predict the prognosis of glioma patients, the role and mechanism of CASC2 in human glioblastoma remain to be fully illuminated. Expression of CASC2 and miR- 18a was detected using RT-qPCR. Cell growth was evaluated by MTT assay, colony formation assay, and flow cytometry; metastasis and epithelial-mesenchymal transition (EMT) were determined with transwell assay and Western blot, respectively. The target binding between CASC2 and miR-18a was predicted on Starbase software, and confirmed by luciferase reporter assay and RNA immunoprecipitation. Xenograft experiment measured tumor growth. As a result, CASC2 was downregulated and miR-18a was upregulated in glioblastoma tumor tissues and cells (T98 and A172). Overexpression of CASC2 promoted apoptosis rate and E-cadherin expression, but suppressed cell viability, colony-forming ability, migration, invasion, and expression of N-cadherin and Vimentin in T98 and A172 cells, accompanied with tumor growth inhibition in vivo; whereas, silencing of CASC2 exerted the opposite effect on cell growth, metastasis and EMT of T98 and A172 cells in vitro. However, reintroduction of miR-18a could reverse CASC2 upregulation-mediated suppression on above cell behaviors in vitro. More importantly, miR-18a was a downstream target for CASC2, and was negatively regulated by CASC2. Collectively, this study demonstrated that CASC2 served as tumor suppressor in glioblastoma by inhibiting cell growth, metastasis and EMT both in vitro and in vivo partially via CASC2- miR-18a axis.	NA	J Biosci. 2020;45:107.
3981	LncRNA	CASC2	miR-27b-3p	TAB2	A549 cells	Acute Lung Injury	Homo sapiens (human)	Western blot;Flow Cytometry assay;	33174006	lncRNA CASC2 inhibits Lps-Induced Acute Lung Injury via miR-27b/TAB2 axis.	Long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) has been reported to exert an important role in acute lung injury (ALI). The present study aimed to investigate the potential underlying mechanism of CASC2 in ALI progression. Reverse transcription-quantitative PCR was conducted to examine the expression of CASC2, microRNA (miR/miRNA)-27b and TGF-β activated kinase 1 and MAP3K7-binding protein 2 (TAB2) in A549 cells. Cell viability and apoptosis were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry. Enzyme-linked immunosorbent assay was used to measure the levels of inflammatory-related cytokines to assess the inflammatory response, including interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α). The binding sites of miR-27b in CASC2 or TAB2 were predicted using LncBase or microT-CDS software, following which dual-luciferase reporter and RNA binding protein immunoprecipitation assays were performed to confirm the target relationship between miR-27b and CASC2 or TAB2. The protein expression of TAB2 was detected by western blotting. The decreased viability, and increased apoptosis and inflammatory responses were attenuated by the accumulation of CASC2 in lipopolysaccharide (LPS)-stimulated A549 cells. CASC2 could directly bind to miR-27b in A549 cells. CASC2 protected A549 cells from LPS-triggered injury by downregulating miR-27b. TAB2 was a target of miR-27b in A549 cells. The influence of miR-27b depletion was reversed by the silencing of TAB2 in an ALI cell model. CASC2 could increase the expression of TAB2 by serving as a competing endogenous RNA of miR-27b in A549 cells. Collectively, the results suggested that CASC2 attenuated LPS-induced injury in the ALI cell model by modulating the miR-27b/TAB2 axis.	NA	Mol Med Rep. 2020 Dec;22(6):5181-5190. doi: 10.3892/mmr.2020.11606. Epub 2020 Oct 16.
3982	LncRNA	CASC2	miR-18a	SOCS5	CCA tissues and cells	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	32894543	LncRNA CASC2 inhibits cell proliferation, metastasis and EMT through miR-18a/SOCS5 axis in cholangiocarcinoma.	OBJECTIVE: Cholangiocarcinoma (CCA) is one of the tumors with high malignancy of the liver and bile system, whose development and prognosis mechanisms are still not clear. Here, a preliminary illustration was made on the expression and function of long non-coding RNA (lncRNA) CASC2 and the relevant mechanism of its function. PATIENTS AND METHODS: Expression of CASC2 in CCA tissues and cells were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation ability was detected using colony formation and Cell Counting Kit-8 (CCK-8) assays while cell invasion and migration abilities were measured using transwell and Matrigel assays. Using bioinformatic analysis, underlying downstream molecules of CASC2 were predicted and by Dual-Luciferase assay and Western blot. RESULTS: It was found that CASC2 was expressed at a significantly lower level in CCA tissues and cell lines. The overexpression of CASC2 inhibited QBC939 cell proliferation, invasion and migration when the knockdown of CASC2 accelerated HUCCT1 cell growth and metastasis. Besides, miR-18a was identified as a direct target for CASC2, and SOCS5 as target for miR-18a. Moreover, CASC2 functioned as a sponge of miR-18a to promote the SOCS5 expression, then, slowed down the epithelial-to-mesenchymal transition (EMT) progression. CONCLUSIONS: CASC2 was downregulated in CCA tissues and cells. It could inhibit cell proliferation, invasion, migration and EMT via sponging miR-18a/SOCS5 axis. This might provide a novel target for CCA diagnosis and treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Aug;24(16):8367-8376. doi: 10.26355/eurrev_202008_22633.
3983	LncRNA	CASC8	miR-34a	NA	Rb cells	Retinoblastoma	Homo sapiens (human)	qPCR;RT-qPCR;	33408518	CASC8 lncRNA Promotes the Proliferation of Retinoblastoma Cells Through Downregulating miR34a Methylation.	BACKGROUND: CASC8 lncRNA has been proven to be oncogenic in a variety of cancers, but its role in other types of cancer remains unclear. This study was to investigate the role of CASC8 in retinoblastoma (Rb). METHODS: RT-qPCR was performed to determine the expression of CASC8 and miR34a in paired Rb and nontumor tissue. Overexpression of CASC8 and miR34a in Rb cells was achieved to evaluate the interaction between them. Methylation-specific PCR was used to analyze the effect of CASC8 overexpression on MIR34 A gene methylation. CCK8 assays were used to analyze cell proliferation. RESULTS: The results showed that CASC8 expression was upregulated and miR34a expression downregulated in Rb tissue. Moreover, miR34a expression was negatively correlated with the of CASC8 expression in Rb tissue. Overexpression of CASC8 decreased expression of miR34a and increased methylation of MIR 34A in Rb cells. In addition, overexpression of CASC8 reduced the inhibitory effects of miR34a on Rb-cell proliferation. CONCLUSION: CASC8 may promote Rb cell proliferation by downregulating miR34a methylation.	NA	Cancer Manag Res. 2020 Dec 30;12:13461-13467. doi: 10.2147/CMAR.S268380. eCollection 2020.
3984	LncRNA	CASC9	miR-383-5p	NA	PC12 cells	Spinal Cord Injury	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33438067	LncRNA CASC9 attenuates lactate dehydrogenase-mediated oxidative stress and inflammation in spinal cord injury via sponging miR-383-5p.	Long non-coding RNAs (lncRNAs) play important roles in various diseases, but the effect of lncRNA CASC9 on spinal cord injury (SCI) remains unclear. Therefore, the present study was conducted to explore the role of this lncRNA in SCI. SCI model was established by laminectomy in rats in vivo or induced by LPS in PC12 cells in vitro. Methylprednisolone (MP) was used for treatment in vivo. Spinal cord tissues were stained with H&E, and the oxidative stress- and inflammation-related factors were detected using their commercial kits. Cell apoptosis was determined using flow cytometry assay. Relative expression of corresponding genes was measured using qRT-PCR and western blotting. Luciferase reporter assay was used to verify binding site between CASC9 and miR-383-5p, as well as miR-383-5p and LDHA. The results showed that lncRNA CASC9 was downregulated and miR-383-5p was upregulated in SCI rats and LPS-induced PC12 cells. Severe histological injury and increased water content were also found in SCI rats. Increased levels of LDH, MDA, lactic acid, TNF-α, and IL-1β were found in SCI rats and LPS-induced PC12 cells. These changes could be reversed by MP treatment in vivo or overexpression of CASC9 in vitro. Besides, overexpression of CASC9 decreased cell apoptosis and protein expression of LDHA and increased protein expression of Nrf2 and HO-1 in LPS-induced PC12 cells. Furthermore, miR-383-5p was a direct target of CASC9 and was negatively regulated by CASC9. LDHA was a direct target of miR-383-5p and was negatively regulated by CASC9. In conclusion, lncRNA CASC9 exerted a protective role against oxidative stress, inflammation, and cell apoptosis in SCI, providing a novel therapeutic target or prognostic factor for SCI.	NA	Inflammation. 2021 Jun;44(3):923-933. doi: 10.1007/s10753-020-01387-7. Epub 2021 Jan 12.
3985	LncRNA	CASC9	miR-758-3p	TGF-b2	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	FISH;qPCR;RT-qPCR;Western blot;FISH;Luciferase reporter assay;	33200222	lncRNA CASC9 sponges miR-758-3p to promote proliferation and EMT in bladder cancer by upregulating TGF-β2.	The long noncoding RNA cancer susceptibility candidate 9 (CASC9) has been revealed to be an oncogenic gene in several types of cancer, and high CASC9 expression is related to tumorigenesis and cancer progression. However, the role of CASC9 in bladder cancer (BC), particularly during epithelial-mesenchymal transition (EMT), has not been characterized. RT-qPCR, EdU, CCK-8, wound scratch, Transwell and flow cytometric assays were performed to detect CASC9 expression, miR-758-3p expression and their functions in BC. RNA FISH was used to detect CASC9 subcellular localization. Luciferase reporter assay, RT-qPCR assay and western blotting were used to explore the relationship of CASC9, miR-758-3p and TGF-β2. In the present study, it was revealed that CASC9 regulated EMT in BC. CASC9 expression was significantly upregulated in BC cell lines and specimens compared to that in adjacent normal bladder tissues. Upregulated CASC9 was associated with increased invasion ability and poor prognosis of BC. CASC9 knockdown inhibited BC cell proliferation, migration and invasion. Furthermore, a bioinformatics study and luciferase reporter assays revealed that CASC9 functioned as a ceRNA for miR-758-3p. CASC9 inhibited microRNA (miR)-758-3p activity and resulted in the de-suppression of its target transforming growth factor (TGF)-β2. TGF-β signaling driven by TGF-β2 was crucial for CASC9 to promote EMT in BC. Collectively, these results indicated that CASC9 sponged miR-758-3p to regulate the expression of TGF-β2, which activated the TGF-β signaling pathway and promoted proliferation and EMT in BC.	NA	Oncol Rep. 2021 Jan;45(1):265-277. doi: 10.3892/or.2020.7852. Epub 2020 Nov 13.
3986	LncRNA	CASC9	miR-576-5p	AKT3	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33298846	Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3.	Increasing studies have shown that long non-coding RNAs (lncRNAs) are regarded as important regulators in the occurrence and development of colorectal cancer (CRC). Although lncRNA CASC9 has been studied in CRC, the detailed regulatory mechanism of CASC9 in CRC is still unclear. In this study, we found that CASC9 was significantly upregulated in CRC tissues and cell lines compared to normal controls and that aberrant expression was associated with the tumor-node-metastasis (TNM) stage of CRC. Functionally, CASC9 depletion efficiently inhibited the proliferation of CRC cells and induced cell apoptosis in vitro. Mechanistically, CASC9 was mainly enriched in the cytoplasm of CRC cells and interacted directly with miR-576-5p. Downregulation of miR-576-5p reversed the inhibitory effect of CASC9 siRNA on CRC cell progression. Furthermore, AKT3 has been identified as a downstream target of miR-576-5p. Spearman's correlation analysis revealed that AKT3 was negatively correlated with miR-576-5p but positively correlated with CASC9. Downregulation of miR-576-5p restored the effect of CASC9 silencing on AKT3 expression. Therefore, silencing CASC9 could downregulate the expression of AKT3 by reducing the competitive binding of CASC9 to miR-576-5p, thus suppressing CRC cell proliferation and promoting cell apoptosis. In summary, we identified CASC9 as an oncogenic lncRNA in CRC and defined the CASC9/miR-576-5p/AKT3 axis, which might be considered a potential therapeutic target for CRC patients, as a novel molecular mechanism implicated in the proliferation and apoptosis of CRC.	NA	Cell Death Discov. 2020 Oct 31;6(1):115. doi: 10.1038/s41420-020-00352-5.
3987	Circular RNA	CBFB	miR-185-5p	p66Shc	APAP and AML12 cells	Apap-Induced Liver Injury	Homo sapiens (human)	microarray;RNA immunoprecipitation;RNA immunoprecipitation;	33159035	circ-CBFB upregulates p66Shc to perturb mitochondrial dynamics in APAP-induced liver injury.	p66Shc, a master regulator of mitochondrial reactive oxygen species (mtROS), is a crucial mediator of hepatocyte oxidative stress. However, its functional contribution to acetaminophen (APAP)-induced liver injury and the mechanism by which it is modulated remain unknown. Here, we aimed to assess the effect of p66Shc on APAP-induced liver injury and to evaluate if circular RNA (circRNA) functions as a competitive endogenous RNA (ceRNA) to mediate p66Shc in APAP-induced liver injury. p66Shc-, miR-185-5p-, and circ-CBFB-silenced mice were injected with APAP. AML12 cells were transfected with p66Shc, miR-185-5p, and circ-CBFB silencing or overexpression plasmids or siRNAs prior to APAP stimulation. p66Shc was upregulated in liver tissues in response to APAP, and p66Shc silencing in vivo protected mice from APAP-induced mitochondrial dynamics perturbation and liver injury. p66Shc knockdown in vitro attenuated mitochondrial dynamics and APAP-induced hepatocyte injury. Mechanically, p66Shc perturbs mitochondrial dynamics partially by inhibiting OMA1 ubiquitination. miR-185-5p, which directly suppressed p66Shc translation, was identified by microarray and bioinformatics analyses, and its overexpression attenuated mitochondrial dynamics and hepatocyte injury in vitro. Furthermore, luciferase, pull-down and RNA immunoprecipitation assays demonstrated that circ-CBFB acts as a miRNA sponge of miR-185-5p to mediate p66Shc in APAP-induced liver injury. circ-CBFB knockdown also alleviated APAP-induced mitochondrial dynamics perturbation and hepatocyte injury. More importantly, we found that the protective effects of circ-CBFB knockdown on p66Shc, mitochondrial dynamics and liver injury were abolished by miR-185-5p inhibition both in vivo and in vitro. In conclusion, p66Shc is a key regulator of APAP-induced liver injury that acts by triggering mitochondrial dynamics perturbation. circ-CBFB functions as a ceRNA to regulate p66Shc during APAP-induced liver injury, which may provide a potential therapeutic target.	NA	Cell Death Dis. 2020 Nov 6;11(11):953. doi: 10.1038/s41419-020-03160-y.
3988	Circular RNA	CCAC1	miR-514a-5p	C22orf46	ACC cells	Adrenocortical Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;Rescue assay;	33195693	Circular RNA circ-CCAC1 Facilitates Adrenocortical Carcinoma Cell Proliferation, Migration, and Invasion through Regulating the miR-514a-5p/C22orf46 Axis.	Adrenocortical carcinoma (ACC) is a rare but clinically aggressive endocrine malignancy. Circular RNAs (circRNAs) were found to play key roles in tumorigenesis. In the current study, we aimed to investigate the functions and mechanisms of a novel circRNA, circ-CCAC1, in ACC cells. circ-CCAC1 expression levels in ACC tissue specimens and cell lines were evaluated by RT-qPCR. Kaplan-Meier analysis was applied to explore the relationship between circ-CCAC1 and patients' prognosis. Cell counting kit-8 (CCK-8), colony formation, acridine orange/ethidium bromide (AO/EB) double fluorescence staining, and Transwell assays were performed to evaluate the functions of circ-CCAC1 in ACC cells. Bioinformatics analysis and a dual-luciferase reporter assay were utilized to explore the mechanisms of circ-CCAC1. As a result, circ-CCAC1 was overexpressed in ACC tissue samples and cell lines and correlated with poor prognosis. Gain- and loss-of-function tests demonstrated that circ-CCAC1 acted as an oncogene in ACC. What is more, circ-CCAC1 enhanced C22orf46 expression by sponging miR-514a-5p in ACC cells. A rescue assay illustrated that circ-CCAC1 facilitated ACC progression through miR-514a-5p/C22orf46 signaling. To sum up, we identified a novel circRNA, circ-CCAC1, which may be used as a potential therapeutic target for ACC.	NA	Biomed Res Int. 2020 Oct 26;2020:3501451. doi: 10.1155/2020/3501451. eCollection 2020.
3989	LncRNA	CCAL	miR-29b	ANGPTL4	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33122950	LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma.	PURPOSE: The objective of this study was to detect the expression of the long noncoding RNA (lncRNA) colorectal cancer-associated lncRNA (CCAL) in osteosarcoma tissues and to investigate its role in angiogenesis and the potential molecular mechanisms associated with this effect in osteosarcoma. MATERIALS AND METHODS: CCAL expression in 40 osteosarcoma tissues and 40 noncancerous tissues was measured by qRT-PCR (quantitative real-time polymerase chain reaction). Tube formation assays were performed to explore the role of CCAL in angiogenesis in osteosarcoma. In addition, the regulatory interaction between CCAL, miR-29b, and ANGPTL4 was investigated via luciferase reporter assay and bioinformatics predictive analysis. RESULTS: Compared with noncancerous tissues, the expression of CCAL was markedly upregulated in osteosarcoma tissues. Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma. Additionally, functional analysis indicated that CCAL could facilitate tumour angiogenesis in vitro and in vivo in osteosarcoma. Mechanistically, CCAL upregulated ANGPTL4 expression in osteosarcoma cells, and ANGPTL4 mediated angiogenic induction by CCAL in osteosarcoma. Moreover, CCAL directly targeted miR-29b in osteosarcoma. More importantly, we demonstrated that CCAL upregulated the expression of ANGPTL4 by sponging miR-29b, which promoted angiogenesis in osteosarcoma. CONCLUSION: Our results show that CCAL promotes angiogenesis by regulating the miR-29b/ANGPTL4 axis in osteosarcoma.	NA	Cancer Manag Res. 2020 Oct 23;12:10521-10530. doi: 10.2147/CMAR.S272230. eCollection 2020.
3990	LncRNA	CCAT1	miR-185-3p	FOXP3	HeLa cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33394184	SOX2 Regulates lncRNA CCAT1/MicroRNA-185-3p/FOXP3 Axis to Affect the Proliferation and Self-Renewal of Cervical Cancer Stem Cells.	It has been presented the role of long non-coding RNAs (lncRNAs) in cervical cancer (CC). We aim to discuss the effect of sex-determining region Y-box 2 (SOX2)/lncRNA colon cancer-associated transcript-1 (CCAT1)/microRNA-185-3p (miR-185-3p)/forkhead box protein 3 (FOXP3) on the proliferation and self-renewal ability of CC stem cells. MiR-185-3p, SOX2, CCAT1 and FOXP3 expressions were tested in CC tissues and cells. The relationship between SOX2/CCAT1 expression and clinicopathological features in CC patients was verified. Loss- and gain-of-function investigations were conducted in CD44(+)HeLa cells to discuss biological functions and self-renewal capacity. Finally, the relationships among SOX2, CCAT1, FOXP3 and miR-185-3p were verified. miR-185-3p expression was decreased, while SOX2, CCAT1 and FOXP3 expressions were increased in CC tissues and cells. SOX2 and CCAT1 expressions were linked to tumor size, lymph node metastasis and international federation of gynecology and obstetrics stage of CC. Down-regulating SOX2 or CCAT1 and up-regulating miR-185-3p resulted in inhibition of proliferation, invasion, migration and cell sphere number as well as apoptosis acceleration of CD44(+)HeLa cells. SOX2 could bind to CCAT1 which affected miR-185-3p expression, and FOXP3 was targeted by miR-185-3p.	NA	Nanoscale Res Lett. 2021 Jan 4;16(1):2. doi: 10.1186/s11671-020-03449-z.
3991	LncRNA	CCAT1	miR-490	NA	H1299 and A549 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33325119	Long non-coding RNA CCAT1 sponges miR-490 to enhance cell proliferation and migration of non-small cell lung cancer.	BACKGROUND: Non-small cell lung cancer (NSCLC) accounts for 85% of lung cancer which is the most frequently diagnosed malignancy in China. Colon cancer associated transcript 1 (CCAT1) acts as an oncogene in enhancing tumor progression. However, the effects of CCAT1 in NSCLC remain unclear. The purpose of this study was to explore the role of CCAT1 in NSCLC. METHODS: Wound healing and transwell assays were performed to measure cell migration. RT-qPCR was employed to calculate the mRNA level of CCAT1 and miR-490. RESULTS: High expression of CCAT1 was observed in NSCLC tissues and cells, with low expression of miR-490. CCAT1 promoted the proliferation and metastasis of H1299 and A549 cells, while miR-490 had the opposite effect. CCAT1 could specifically bind to miR-490 and regulate its expression. MiR-490 partially reversed the inhibitory effect of CCAT1 on cell proliferation and metastasis. CONCLUSIONS: The CCAT1/miR-490 molecular axis has been shown to be important for the treatment of NSCLC.	NA	Thorac Cancer. 2021 Feb;12(3):364-371. doi: 10.1111/1759-7714.13758. Epub 2020 Dec 15.
3992	LncRNA	CCAT1	miR-216a-5p	RAP2B	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33023331	Long non-coding RNA CCAT1 promotes non-small cell lung cancer progression by regulating the miR-216a-5p/RAP2B axis.	The long non-coding RNA colon cancer-associated transcript 1 (CCAT1) has been investigated to involve in the progression of non-small cell lung cancer (NSCLC). Thus, this study aims to explore the detailed molecular mechanisms of CCAT1 in NSCLC. The expression of CCAT1, miR-216a-5p, RAP2B, Bax, Bcl-2, and cleaved caspase 3 was detected by qRT-PCR or Western blot. Cell proliferation, apoptosis, migration, and invasion were analyzed using cell counting kit-8, flow cytometry or Transwell assays, respectively. The interaction between miR-216a-5p and CCAT1 or RAP2B was analyzed by luciferase reporter, RNA immunoprecipitation, and pull-down assays. The expression of CCAT1 was elevated in NSCLC, and CCAT1 deletion could inhibit NSCLC cell proliferation, migration, and invasion but induce apoptosis in vitro as well as imped tumor growth in vivo. MiR-216a-5p was confirmed to be a target of CCAT1, and silencing miR-216a-5p could reverse CCAT1 depletion-mediated inhibitory effects on cell tumorigenesis in NSCLC. Besides that, miR-216a-5p was decreased in NSCLC, and miR-216a-5p restoration inhibited cell tumorigenesis by regulating RAP2B, which was verified to be a target of miR-216a-5p. Additionally, co-expression analysis suggested that CCAT1 indirectly regulated RAP2B level by targeting miR-216a-5p in NSCLC cells. Taken together, CCAT1 deletion could inhibit cell progression in NSCLC through miR-216a-5p/RAP2B axis, indicating a novel pathway underlying NSCLC cell progression and providing new potential targets for NSCLC treatment.	NA	Exp Biol Med (Maywood). 2021 Jan;246(2):142-152. doi: 10.1177/1535370220961013. Epub 2020 Oct 6.
3993	LncRNA	CCMAlnc	miR-5001-5p	HES6	CRC cells	Colorectal Cancer	Homo sapiens (human)	Western blot;luciferase assay;	33681178	CCMAlnc Promotes the Malignance of Colorectal Cancer by Modulating the Interaction Between miR-5001-5p and Its Target mRNA.	OBJECTIVE: Colorectal cancer (CRC) is highly malignant and cancer metastasis remains the predominant cause of CRC death. The potential molecular mechanism of long non-coding RNA (lncRNAs) in CRC malignance is still poorly elucidated. METHODS: CCMAlnc expression was analyzed by using the Sequence ReadArchive (SRA) database. Target gene expression was examined by real-time PCR and Western blotting. The biological function of CCMAlnc and miR-5001-5p was detected by cell invasion, CCK8 proliferation, and colony formation assays in loss of function and gain of function experiments in vitro. A luciferase assay was performed to validate the target site of miR-5001-5p on the 3'-UTR of HES6 mRNA. RESULTS: CCMAlnc was identified as a novel functional lncRNA in CRC. Elevated CCMAlnc was detected in CRC cells as well as in clinical CRC tissue samples, and the expression of this lncRNA positively correlated with the poor prognosis of CRC patients. Functional validation assays revealed that downregulation of CCMAlnc impaired CRC cell proliferation and invasion in vitro, but upregulation of CCMAlnc reversed this effect. Moreover, CCMAlnc was validated to act as a competing endogenous RNA (ceRNA) that stabilizes the expression of HES6 by downregulating miR-5001-5p. CONCLUSION: CCMAlnc/miR-5001-5p/HES6 signaling is strongly activated to promote CRC malignance. CCMAlnc is defined as a potential candidate biomarker for metastasis prediction in CRC patients and as a potential therapeutic target for CRC treatment.	NA	Front Cell Dev Biol. 2020 Dec 16;8:566932. doi: 10.3389/fcell.2020.566932. eCollection 2020.
3994	LncRNA	CDKN2B-AS1	miR-320d	STAT3	aortic vascular smooth muscle cells	Cardiovascular Disease	Homo sapiens (human)	RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	33165136	CDKN2B-AS1 Aggravates the Pathogenesis of Human Thoracic Aortic Dissection by Sponge to miR-320d.	In the present study, the role and molecular mechanism of long noncoding RNA CDKN2B-AS1 in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. The expression of CDKN2B-AS1 in human TAD and normal aortic tissues of donors were examined by quantitative real-time polymerase chain reaction. RNA pull-down assay and a series of luciferase reporter assays were performed to predict the relationships between CDKN2B-AS1, miR-320d, and STAT3. Cell counting kit 8 (CCK-8), TUNEL, and western blot assays were applied to validate the biological functions of CDKN2B-AS1 in rat aortic vascular smooth muscle cells. Results showed that CDKN2B-AS1 was expressed at a higher level in human TAD than in normal aortic tissues. CDKN2B-AS1 overexpression significantly promoted apoptosis and suppressed the proliferation of vascular smooth muscle cells. CDKN2B-AS1 silence exhibited the opposite effects. Mechanistically, CDKN2B-AS1 was identified as a molecular sponge for miR-320d and positively modulated STAT3 expression via repressing miR-320d. In conclusion, our study revealed that CDKN2B-AS1 was dysregulated and displayed multiple potential functions in human TAD. These findings suggested that CDKN2B-AS1 was a novel potential therapeutic target for human TAD.	NA	J Cardiovasc Pharmacol. 2020 Nov;76(5):592-601. doi: 10.1097/FJC.0000000000000907.
3995	LncRNA	CDKN2B-AS1	miR-320d	STAT3	aortic vascular smooth muscle cells	Cardiovascular Disease	Rattus (rat)	RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	33165136	CDKN2B-AS1 Aggravates the Pathogenesis of Human Thoracic Aortic Dissection by Sponge to miR-320d.	In the present study, the role and molecular mechanism of long noncoding RNA CDKN2B-AS1 in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. The expression of CDKN2B-AS1 in human TAD and normal aortic tissues of donors were examined by quantitative real-time polymerase chain reaction. RNA pull-down assay and a series of luciferase reporter assays were performed to predict the relationships between CDKN2B-AS1, miR-320d, and STAT3. Cell counting kit 8 (CCK-8), TUNEL, and western blot assays were applied to validate the biological functions of CDKN2B-AS1 in rat aortic vascular smooth muscle cells. Results showed that CDKN2B-AS1 was expressed at a higher level in human TAD than in normal aortic tissues. CDKN2B-AS1 overexpression significantly promoted apoptosis and suppressed the proliferation of vascular smooth muscle cells. CDKN2B-AS1 silence exhibited the opposite effects. Mechanistically, CDKN2B-AS1 was identified as a molecular sponge for miR-320d and positively modulated STAT3 expression via repressing miR-320d. In conclusion, our study revealed that CDKN2B-AS1 was dysregulated and displayed multiple potential functions in human TAD. These findings suggested that CDKN2B-AS1 was a novel potential therapeutic target for human TAD.	NA	J Cardiovasc Pharmacol. 2020 Nov;76(5):592-601. doi: 10.1097/FJC.0000000000000907.
3996	LncRNA	CDKN2B-AS1	miR-335-3p	TRAF5	pediatric T-ALL peripheral blood mononuclear cells	Pediatric T Cell Acute Lymphoblastic Leukemia	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	32976214	LncRNA CDKN2B-AS1 contributes to tumorigenesis and chemoresistance in pediatric T-cell acute lymphoblastic leukemia through miR-335-3p/TRAF5 axis.	T-cell acute lymphoblastic leukemia (T-ALL) is the most prevalent malignancy in children. Long non-coding RNAs are being found to have relevance to the pathogenesis of pediatric T-ALL. However, the function of cyclin-dependent kinase inhibitor 2B anti-sense RNA 1 (CDKN2B-AS1) in pediatric T-ALL progression and chemoresistance has not been illuminated. The levels of CDKN2B-AS1, miR-335-3p and tumor necrosis factor receptor-associated factor 5 (TRAF5) were assessed by quantitative real-time PCR. Cell proliferation and the 50% inhibitory concentration (IC50) value were detected using the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetr-azolium assay. Cell cycle and apoptosis were evaluated by flow cytometry. Western blot analysis was performed to measure protein expression. Targeted interactions among CDKN2B-AS1, miR-335-3p and TRAF5 were determined by the dual-luciferase reporter and RNA immunoprecipitation assays. Animal studies were conducted to observe the function of CDKN2B-AS1 in vivo. Our data indicated that CDKN2B-AS1 was highly expressed in pediatric T-ALL peripheral blood mononuclear cells and cells, and high CDKN2B-AS1 level was associated with adriamycin (ADR) resistance. CDKN2B-AS1 depletion hindered T-ALL/ADR cell proliferation and cell cycle progression, and promoted cell apoptosis and ADR sensitivity in vitro. Moreover, CDKN2B-AS1 knockdown repressed tumor growth and enhanced ADR sensitivity in vivo. CDKN2B-AS1 sequestered miR-335-3p, and CDKN2B-AS1 depletion exerted regulatory effect in T-ALL/ADR cell progression by up-regulating miR-335-3p. TRAF5 was a direct target of miR-335-3p, and TRAF5 mediated the regulation of miR-335-3p in T-ALL cell behaviors. Furthermore, CDKN2B-AS1 positively modulated TRAF5 expression through sponging miR-335-3p. The current work suggested that CDKN2B-AS1 knockdown repressed the progression and enhanced ADR sensitivity of pediatric T-ALL at least partly through targeting miR-335-3p/TRAF5 axis, highlighting a promising therapeutic target for the treatment of pediatric T-ALL patients.	NA	Anticancer Drugs. 2020 Sep 25. doi: 10.1097/CAD.0000000000001001.
3997	LncRNA	CDKN2B-AS1	miR-378b	NR2C2	lung cancer cells	Lung Cancer	Homo sapiens (human)	Western blot;	33116641	Long Noncoding RNA CDKN2B-AS1 Facilitates Lung Cancer Development Through Regulating miR-378b/NR2C2.	AIM: Long noncoding RNA (lncRNA) have proved to be important regulators in various diseases. CDKN2B-AS1 was a newly identified tumor-related lncRNA, and previous studies have reported its function in laryngeal squamous cancer and osteosarcoma. However, the function and mechanism of lncRNA CDKN2B-AS1 in lung cancer are still unknown. METHODS: Cell proliferation, invasion, migration and apoptosis were detected via CCK-8, transwell assay and Western blot. Bioinformatics analysis was used to predict the potential target of CDKN2B-AS1. A rescue experiment was performed to identify the relationship between CDKN2B-AS1 and miR-378b. RESULTS: The expression of lncRNA CDKN2B-AS1 was significantly upregulated in lung cancer tissues and cell lines. Overexpression of CDKN2B-AS1 promoted cell proliferation, invasion and reduced cell apoptosis. Knockdown of CDKN2B-AS1 inhibited cell proliferation, invasion and increased cell apoptosis. Bioinformatics analysis predicted that miR-378b was the direct target. We also provided evidence that NR2C2 was the target of miR-378b. The expression of NR2C2 was significantly upregulated in lung cancer tissues and cell lines. The rescue experiment further confirmed the relationship between CDKN2B-AS1 and miR-378b. Overexpression of miR-378b completely reversed the function of CDKN2B-AS1. CONCLUSION: Taken together, our results comprehensively analyzed the function of CDKN2B-AS1 in lung cancer and provided a possible mechanism that CDKN2B-AS1 facilitates lung cancer development by regulating miR-378b and NR2C2. Thus, our study offers a potential therapeutic target for treating lung cancer.	NA	Onco Targets Ther. 2020 Oct 20;13:10641-10649. doi: 10.2147/OTT.S261973. eCollection 2020.
3998	Circular RNA	Circ_ 0115744	miR-144	EZH2	CRC cells	Colorectal Cancer	Homo sapiens (human)	microarray;	33591945	Circ_ 0115744 acts as miR-144 sponge to promote and predict the metastasis of colorectal cancer.	Colorectal cancer (CRC) is one of the most common human malignant tumors in recent years. Although multiple approaches have been developed for the diagnosis and therapy of CRC, the overall survival rates of patients with metastatic and recurrent CRC remain poor. In the present study, we used the high-throughput microarray technology to screen circular RNAs (circRNAs) as a potential fingerprint for CRC. We mainly aimed to screen potential biomarkers for liver metastasis by performing risk score analysis. We detected the upregulated expression of circ_0115744 in patients with CRC with liver metastasis (CRLM). Further investigation using a validation set indicated that circ_0115744 might be considered as a fingerprint for CRLM. Functionally, the overexpression of circ_0115744 significantly promoted the invasion of CRC cell lines, while decreased expression of circ_0115744 suppressed cell invasion in vitro. Mechanistic analysis showed that circ_0115744 acted as a competing endogenous RNA of miR-144 to diminish the repressive effect of miR-144 on its target EZH2. In conclusion, we found that increased expression of circ_0115744 could differentiate CRLM from CRC and that the newly identified circ_0115744/miR-144/EZH2 axis was involved in the progression of CRC, which might be used as a potential diagnostic and therapeutic target for patients with CRC.	NA	Aging (Albany NY). 2021 Feb 11;13(4):5892-5905. doi: 10.18632/aging.202513. Epub 2021 Feb 11.
3999	Circular RNA	Circ_0000043	miR-1271-5p	CTNND1	EC cells	Endometrial Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33128584	Circular RNA circ_0000043 promotes endometrial carcinoma progression by regulating miR-1271-5p/CTNND1 axis.	BACKGROUND: Circular RNAs (circRNAs) are involved in a variety of biological processes, including tumorigenesis. However, the exact role and molecular mechanisms of circ_0000043 in endometrial carcinoma (EC) remain largely unknown. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to determine the expression levels of circ_0000043, microRNA-1271-5p (miR-1271-5p) and catenin delta 1 (CTNND1). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry were used to measure cell proliferation, cell apoptosis and cell cycle distribution, respectively. Cell migration and invasion were assessed by transwell assay. Western blot assay was performed to examine the protein expression of matrix metalloproteinase 2 (MMP2), MMP9 and CTNND1. The interaction between miR-1271-5p and circ_0000043 or CTNND1 was predicted by starBase and confirmed by dual-luciferase reporter assay. The mice xenograft model was established to investigate the role of circ_0000043 in vivo. RESULTS: Circ_0000043 and CTNND1 were highly expressed and miR-1271-5p was lowly expressed in EC tissues and cells. Knockdown of circ_0000043 inhibited the progression of EC by inhibiting cell proliferation, migration, invasion and tumor growth (in vivo) and promoting apoptosis. MiR-1271-5p was a direct target of circ_0000043 and its inhibition reversed the inhibitory effect of circ_0000043 knockdown on the progression of EC cells. In addition, CTNND1 was a downstream target of miR-1271-5p, and miR-1271-5p overexpression inhibited EC cell proliferation, migration and invasion and induced apoptosis by targeting CTNND1. Moreover, circ_0000043 positively regulated CTNND1 expression by sponging miR-1271-5p. CONCLUSION: Circ_0000043 knockdown inhibited the progression of EC by regulating miR-1271-5p/CTNND1 axis, which might provide a promising circRNA-targeted therapy for EC.	NA	Arch Gynecol Obstet. 2021 Apr;303(4):1075-1087. doi: 10.1007/s00404-020-05849-z. Epub 2020 Oct 31.
4000	Circular RNA	Circ_0000735	miR-502-5p	NA	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33425100	Cyclic RNA Circ_0000735 sponges miR-502-5p to promote bladder cancer cell proliferation and invasion and inhibit apoptosis.	OBJECTIVE: The objective of this study was to investigate the effect on the proliferation, invasion, and apoptosis of bladder cancer cells through miR-502-5p of the Circ_0000735 circular RNA. METHODS: Circ_0000735 and miR-502-5p expression of bladder cancer patients in malignant and paracancerous tissues was identified using qRT-PCR. Nucleoplasm isolation assay and RNase R enzymatic assay were used to classify Circ_0000735 subcellular origin and stability. Dual luciferase reporter assay and RIP assay were used to confirm Circ_0000735 and miR-502-5p targeting relationships. Cell proliferation, apoptosis, and invasion capacity were identified using CCK8, flow cytometry, and transwell assays. To confirm the effect of Circ_0000735 on tumorigenesis in nude mice, in vivo experiments were conducted. RESULTS: Circ_0000735 expression was increased in bladder cancer tissues and cells compared with paraneoplastic tissues and normal cells, and miR-502-5p expression was reduced (both P<0.05). In the cytoplasm, Circ_0000735 was largely clustered and could not be digested by the RNase R enzyme, and ceRNA may play a role in bladder cancer cells. Circ_0000735 silencing prevented cell proliferation and invasion and facilitated apoptosis (all P<0.05). The incorporation of miR-502-5p inhibitor rescued the effect on bladder cancer cells of Circ_0000735 silencing. In vitro experiments showed that inhibition of Circ_0000735 expression was beneficial in suppressing tumorigenic ability in nude mice. CONCLUSION: Circ_0000735 can adsorb miR-502-5p to promote bladder cancer cell proliferation and invasion and inhibit apoptosis. Circ_0000735 may be an effective molecular target for bladder cancer therapy.	NA	Int J Clin Exp Pathol. 2020 Dec 1;13(12):2994-3003. eCollection 2020.
4001	Circular RNA	Circ_0002232	miR-92a-3p	PTEN	acute myeloid leukemia cells	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR	33239917	Circ_0002232 Acts as a Potential Biomarker for AML and Reveals a Potential ceRNA Network of Circ_0002232/miR-92a-3p/PTEN.	PURPOSE: Our research aimed to investigate the expression level of circ_0002232, which is transcribed from PTEN, and find out the association of circ_0002232/miR-92a-3p/PTEN network in acute myeloid leukemia (AML). METHODS: Circ_0002232 expression in 115 AML patients and 48 controls was detected by using real-time quantitative PCR. The diagnostic value of circ_0002232 expression was evaluated by receiver operating characteristic curve. Kaplan-Meier curves were used to analyse the impact of circ_0002232 for overall survival. Associated network of circ_0002232 was predicted by using interaction prediction websites. RESULTS: Compared with controls, circ_0002232 was notably low-expressed in AML (P<0.001). According to the result of receiver operating characteristic curve, circ_0002232 expression could distinguish AML patients from controls (P<0.001). There were significant differences in patients' age (P=0.004), FAB classifications (P=0.036), white blood cell count (P=0.041) and platelet count (P=0.021) between low-expressed circ_0002232 group and high-expressed circ_0002232 group. Moreover, there was a positive correlation between circ_0002232 expression and patients' age (Pearson r=0.256, P=0.0057). Interestingly, we found that patients in low-expressed circ_0002232 group had better overall survival both in whole AML (P=0.030) and non-APL AML (P=0.014). Remarkably, the expression of circ_0002232 was positively correlated with PTEN (Spearman r=0.678, P<0.001). Furthermore, there was a negative correlation in AML between circ_0002232 and miR-92a-3p (Spearman r=-0.301, P=0.016), miR-92a-3p and PTEN (Spearman r=-0.324, P=0.034). Interaction prediction websites revealed that circ_0002232 might affect the expression of PTEN and the process of AML through sponging miR-92a-3p. CONCLUSION: Circ_0002232, one of the circRNAs transcribed from PTEN, was remarkably down-regulated in AML and could act as a promising biomarker for the diagnosis of AML. In addition, there might be a potential association network of circ_0002232/miR-92a-3p/PTEN in AML.	NA	Cancer Manag Res. 2020 Nov 19;12:11871-11881. doi: 10.2147/CMAR.S278499. eCollection 2020.
4002	Circular RNA	Circ_0004913	miR-184	HAMP	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;RNA immunoprecipitation;RNA pull-down;	33021399	Circ_0004913 Inhibits Cell Growth, Metastasis, and Glycolysis by Absorbing miR-184 to Regulate HAMP in Hepatocellular Carcinoma.	Background: Circular RNA (circRNA) can regulate the progression of hepatocellular carcinoma (HCC). However, the role and potential mechanism of circ_0004913 in HCC are not explored. Methods: Circ_0004913 was identified from two GSE datasets (GSE94508 and GSE97322) as a differentially expressed circRNA between HCC and normal tissues. Levels of circ_0004913, microRNA-184 (miR-184), and hepcidin (HAMP) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, migration, and invasion were estimated by methyl thiazolyl tetrazolium, colony formation, and Transwell assays, respectively. Levels of all proteins were examined by Western blot. Glucose consumption and lactate and ATP production were analyzed by the glucose, lactate, and ATP assay kits. Dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to verify the interactions among miR-184 and circ_0004913 or HAMP. The mice xenograft models were established to assess the effect of circ_0004913 on tumor growth in vivo. Results: Circ_0004913 was downregulated in HCC, and its expression impeded cell proliferation, migration, and invasion, EMT, and glycolysis in HCC cells. miR-184 was identified as a target miRNA of circ_0004913, and their expression levels were negatively correlated. miR-184 overexpression could reverse the inhibitory effect of circ_0004913 on HCC cell progression. Moreover, as a target gene of miR-184, HAMP expression was positively correlated with circ_0004913 expression in HCC tissues, and repression of miR-184 could inhibit the progression of HCC cells by increasing HAMP expression. Circ_0004913 could inhibit JAK2/STAT3/AKT signaling pathway and tumor growth in vivo by regulating the miR-184/HAMP axis. Conclusion: Circ_0004913 inhibited the tumorigenesis of HCC by sponging miR-184 to regulate HAMP expression in vitro and in vivo.	NA	Cancer Biother Radiopharm. 2020 Oct 6. doi: 10.1089/cbr.2020.3779.
4003	Circular RNA	Circ_0005198	miR-198	TRIM14	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR	33316781	Circ_0005198 enhances temozolomide resistance of glioma cells through miR-198/TRIM14 axis.	Circular RNAs (circRNAs) are associated with chemoresistance in many cancers. However, the function of circ_0005198 in the temozolomide (TMZ) resistance of glioma has not been well elucidated. Here, we demonstrated that circ_0005198 was considerably up-regulated in glioma tissues, serum samples and TMZ-resistant glioma cells. Silencing of circ_0005198 restrained TMZ resistance, restricted the proliferation and facilitated the apoptosis of TMZ-resistant glioma cells. MiR-198 could be sponged by circ_0005198, and we demonstrated that the effect of circ_0005198 on the progression of TMZ-resistant glioma cells was attributed to the inhibition of miR-198 activity. Moreover, TRIM14 was a target of miR-198 and silencing of TRIM14 hindered TMZ resistance and suppressed the progression of TMZ-resistant glioma cells, while TRIM14 over-expression rescued the inhibiting effect of miR-198 over-expression. We conclude that circ_0005198-miR-198-TRIM14 regulatory pathway is critical to TMZ resistance of glioma.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2198-2211. doi: 10.18632/aging.202234. Epub 2020 Dec 9.
4004	Circular RNA	Circ_001504	miR-149	NUCB2	RCC cells	Renal Cancer	Mus musculus (mouse)	qPCR;RT-qPCR;	33110207	circ_001504 promotes the development of renal cell carcinoma by sponging microRNA-149 to increase NUCB2.	Renal cancer (RCC) accounts for over 90% of primary renal tumors in adults. Although treatment approaches have steadily improved over the years, the prognosis outcome remains poor. With the aim of developing novel targets for RCC treatment, we explored the role of the circular RNA (circRNA) circ_001504 in the progression of RCC. We initially detected the expression of circ_001504 and microRNA (miRNA)-149 in RCC tissues and cells. RT-qPCR results showed that circ_001504 was highly expressed in RCC tissues, whereas miR-149 was poorly expressed. Interestingly, downregulation of circ_001504 suppressed malignant phenotypes in RCC cells, and upregulation of miR-149 exerted a similar effect. Bioinformatics analysis suggested potential binding sites between circ_001504 and miR-149, verified by a dual-luciferase reporter gene assay. Next, we identified nucleobindin 2 (NUCB2), a calcium-binding protein, as a target gene of miR-149. Furthermore, our data suggested that circ_001504 might serve as a competing endogenous RNA of miR-149, serving to elevate the expression of NUCB2. The silencing of circ_001504 resulted in decreased NUCB2 expression, which could be reversed by miR-149 inhibition. In addition, in vivo experiments demonstrated that circ_001504 depletion could suppress tumor growth in an established mouse RCC model. Collectively, reduced expression of circ_001504 lowered NUCB2 expression by sponging miR-149, thereby attenuating RCC progression, providing insight into circ_001504/miR-149/NUCB2 feedback loop into RCC treatment.	NA	Cancer Gene Ther. 2021 Jun;28(6):667-678. doi: 10.1038/s41417-020-00247-8. Epub 2020 Oct 27.
4005	Circular RNA	Circ_001504	miR-149	NUCB2	RCC cells	Renal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33110207	circ_001504 promotes the development of renal cell carcinoma by sponging microRNA-149 to increase NUCB2.	Renal cancer (RCC) accounts for over 90% of primary renal tumors in adults. Although treatment approaches have steadily improved over the years, the prognosis outcome remains poor. With the aim of developing novel targets for RCC treatment, we explored the role of the circular RNA (circRNA) circ_001504 in the progression of RCC. We initially detected the expression of circ_001504 and microRNA (miRNA)-149 in RCC tissues and cells. RT-qPCR results showed that circ_001504 was highly expressed in RCC tissues, whereas miR-149 was poorly expressed. Interestingly, downregulation of circ_001504 suppressed malignant phenotypes in RCC cells, and upregulation of miR-149 exerted a similar effect. Bioinformatics analysis suggested potential binding sites between circ_001504 and miR-149, verified by a dual-luciferase reporter gene assay. Next, we identified nucleobindin 2 (NUCB2), a calcium-binding protein, as a target gene of miR-149. Furthermore, our data suggested that circ_001504 might serve as a competing endogenous RNA of miR-149, serving to elevate the expression of NUCB2. The silencing of circ_001504 resulted in decreased NUCB2 expression, which could be reversed by miR-149 inhibition. In addition, in vivo experiments demonstrated that circ_001504 depletion could suppress tumor growth in an established mouse RCC model. Collectively, reduced expression of circ_001504 lowered NUCB2 expression by sponging miR-149, thereby attenuating RCC progression, providing insight into circ_001504/miR-149/NUCB2 feedback loop into RCC treatment.	NA	Cancer Gene Ther. 2021 Jun;28(6):667-678. doi: 10.1038/s41417-020-00247-8. Epub 2020 Oct 27.
4006	Circular RNA	Circ_0020394	miR-328-3p	NRBP1	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33016781	Puerarin Inhibits the Progression of Bladder Cancer by Regulating circ_0020394/miR-328-3p/NRBP1 Axis.	Background: Previous studies have shown puerarin to be a potential therapeutic drug for treatment of bladder cancer. But the role and possible molecular mechanism of puerarin remain unknown. Methods: Cell viability, apoptosis, migration, and invasion were assessed by Cell Counting Kit-8 (CCK-8), flow cytometry, and transwell assays, respectively. Western blot was used to measure the levels of all protein. Glucose consumption and lactate production were detected using a glucose and lactate assay kit. Circular RNA_0020394 (circ_0020394), microRNA-328-3p (miR-328-3p), and nuclear receptor binding protein 1 (NRBP1) levels were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The interaction between miRNA and circRNA or mRNA was confirmed using dual-luciferase reporter assay. In vivo experiments were performed to examine the effect of puerarin on tumor growth. Results: Puerarin suppressed cell viability, migration, invasion, and glycolysis, and induced apoptosis in bladder cancer. circ_0020394 was downregulated in puerarin-treated bladder cancer cells, and circ_0020394 overexpression attenuated the inhibitory effect of puerarin on cell progression. Moreover, circ_0020394 could bind to miR-328-3p, and miR-328-3p directly targeted NRBP1. Functionally, miR-328-3p could reverse the promotion effect of circ_0020394 overexpression on the progression of puerarin-treated cells, and silencing NRBP1 counteracted the effects of anti-miR-328-3p on puerarin-treated cells. Mechanically, circ_0020394 could increase NRBP1 expression by acting as miR-328-3p sponge in puerarin-treated bladder cancer cells. Besides, puerarin inhibited tumorigenesis in vivo by increasing miR-328-3p and decreasing the levels of circ_0020394 and NRBP1. Conclusions: Puerarin impedes cell viability, migration, invasion, and glycolysis, and promoted apoptosis in bladder cancer by regulating circ_0020394/miR-328-3p/NRBP1 axis.	NA	Cancer Biother Radiopharm. 2020 Oct 5. doi: 10.1089/cbr.2019.3382.
4007	Circular RNA	Circ_0025033	miR-184	LSM4	OC cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33285422	Circ_0025033 promotes the progression of ovarian cancer by activating the expression of LSM4 via targeting miR-184.	BACKGROUND: Ovarian cancer (OC) is the leading disorder to threaten women's lives. Numerous circular RNAs (circRNAs) were identified in cancers with dysregulation and involved in the pathogenesis of cancer. This study investigated the function and regulatory mechanism of circ_0025033 in OC development, aiming to provide a potential strategy for OC treatment. METHODS: For expression analysis, the expression levels of circ_0025033, LSM4 mRNA and miR-184 were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and the protein level of LSM4 expression was detected by western blot. For functional analysis, the capacities of colony formation, migration/invasion and glycolysis metabolism were assessed by colony formation assay, transwell assay and the levels of glucose consumption and lactate production. The interaction between miR-184 and circ_0025033 or LSM4 was predicted by the bioinformatics tool and validated by dual-luciferase reporter assay. Xenograft models were established to determine the role of circ_0025033 in vivo. RESULTS: The expression of circ_0025033 and LSM4 was promoted in OC tissues and cells. Circ_0025033 knockdown or LSM4 knockdown blocked the ability of colony formation, migration/invasion and glycolysis metabolism in OC cells. In mechanism, circ_0025033 functioned as a "competing endogenous RNA (ceRNA)" to modulate LSM4 expression by targeting miR-184. LSM4 overexpression recovered the inhibitory effects on colony formation, migration/invasion and glycolysis metabolism caused by circ_0025033 knockdown. Moreover, circ_0025033 knockdown also inhibited tumor growth in vivo by regulating LSM4 and targeting miR-184. CONCLUSION: Circ_0025033 promotes the progression of OC by regulating LSM4 expression via targeting miR-184, which provided a new strategy to treat OC.	NA	Pathol Res Pract. 2021 Jan;217:153275. doi: 10.1016/j.prp.2020.153275. Epub 2020 Nov 17.
4008	Circular RNA	Circ_0067835	miR-324-5p	HMGA1	endometrial carcinoma cells	Endometrial Cancer	Homo sapiens (human)	RNA pull-down assay;RNA pull-down;	33169939	Circ_0067835 sponges miR-324-5p to induce HMGA1 expression in endometrial carcinoma cells.	Endometrial cancer is a common gynaecological malignant tumour among women across the world. Circular RNAs (circRNAs) are a novel kind of non-coding RNAs, and they can play a crucial role in multiple cancers. Nevertheless, the mechanisms of circRNAs in regulating gene expression in endometrial cancer are still unclear. Here, our work sought to focus on the role that circ_0067835 exert in progression and development of endometrial cancer cells. We observed circ_0067835 was markedly elevated in endometrial cancer. Then, changes in endometrial cancer cell (RL95-2 and HEC-1B) function were determined after circ_0067835 knockdown. Loss-of-functional assays revealed that circ_0067835 down-regulation significantly repressed RL95-1 and HEC-1B cell proliferation, migration and invasion. Bioinformatics analysis, luciferase reporter experiment and RNA pull-down assay were employed to predict and validate circ_0067835 can bind to miR-324-5p. Increase in miR-324-5p remarkably depressed the proliferation, migration and invasion of endometrial cancer cells via inhibiting high mobility group A1 (HMGA1). HMGA1 is identified as a vital prognostic biomarker in endometrial cancer. Currently, we reported circ_0067835 was positively correlated with HMGA1 in endometrial cancer. We implied that circ_0067835 was capable of sponging miR-324-5p and inducing its downstream target HMGA1 in vitro and in vivo. In conclusion, circ_0067835 can compete with miR-324-5p, resulting in HMGA1 up-regulation, and therefore induce the development of endometrial cancer.	NA	J Cell Mol Med. 2020 Dec;24(23):13927-13937. doi: 10.1111/jcmm.15996. Epub 2020 Nov 10.
4009	Circular RNA	Circ_0075829	miR-1287-5p	LAMTOR3	SW1990 and BxPC-3 cells	Pancreatic Cancer	Homo sapiens (human)	FISH;FISH;luciferase assay;	33184989	Circ_0075829 facilitates the progression of pancreatic carcinoma by sponging miR-1287-5p and activating LAMTOR3 signalling.	Pancreatic cancer (PC) is a leading cause of cancer-related mortality globally. Though increasing evidence has demonstrated that circular RNAs (circRNAs) are linked to the development and progression of cancers, the biological functions of circRNAs in PC remain largely unexplored so far. Based on previous studies, Hsc_circ_0075829 (circ_0075829) was screened out and then further identified in PC clinical specimens and cell lines by real-time PCR. After the stability tests, a series of in vitro and in vivo functional experiments were performed to investigate the role of circ_0075829 in PC development. Furthermore, fluorescent in situ hybridization (FISH), bioinformatics tools, dual-luciferase assays and rescue experiments were conducted to clarify the regulatory mechanisms of circ_0075829 in SW1990 and BxPC-3 cells. Compared with paracancerous tissues, the expression of circ_0075829 was increased in PC tissues, which was positively correlated with the clinical features of PC. Knockdown of circ_0075829 significantly suppressed the proliferative, migratory and invasive rates of SW1990 and BxPC-3 cells both in vitro and in vivo. Bioinformatics analysis and dual-luciferase reporter gene assay indicated that circ_0075829 could bind to miR-1287-5p. Mechanism research and rescue experiments demonstrated that circ_0075829 could regulate the LAMTOR3/p-ERK signalling pathway via sponging miR-1287-5p in PC cell lines. Our data reveal that the circ_0075829 could facilitate the proliferation and metastasis of PC through circ_0075829/miR-1287-5p/LAMTOR3 axis.	NA	J Cell Mol Med. 2020 Dec;24(24):14596-14607. doi: 10.1111/jcmm.16089. Epub 2020 Nov 13.
4010	Circular RNA	Circ_C16orf62	miR-421	TUBB2A	GC cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33006960	Circular RNA circ_C16orf62 Suppresses Cell Growth in Gastric Cancer by miR-421/Tubulin beta-2A Chain (TUBB2A) Axis.	BACKGROUND Gastric cancer (GC) is the third leading cause of cancer-associated mortality in the world. Expression of circular RNA circ_C16orf62 is reported to be low in GC. The role and mechanism of circ_C16orf62 remain unclear. MATERIAL AND METHODS Expression levels of circ_C16orf62 and tubulin beta-2A chain (TUBB2A) in GC tissues and cells, and microRNA-421 (miR-421) level in GC cells were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The predominant cytoplasmic localization of circ_C16orf62 was identified by subcellular fractionation. The protein level of TUBB2A was detected by western blot assay. Cell proliferative ability, migration, and invasion were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, and several transwell assaysy. The binding relationship between miR-421 and circ_C16orf62 or TUBB2A was predicted by starBase3.0 or Targetscan, and then verified by the dual-luciferase reporter assay. The biological role ofcirc_C16orf62 was examined by xenograft tumor model in vivo. RESULTS Circ_C16orf62 andTUBB2A were downregulated in GC tissues and cells. Circ_C16orf62 was predominantly located in the cytoplasm of GC cells, and repressed proliferation, migration, and invasion of GC cells. Mechanistically, circ_C16orf62 worked as the miR-421 sponge to upregulate TUBB2A in GC, thereby hindering GC growth. Circ_C16orf62 repressed GC tumor growth in vivo. CONCLUSIONS These findings demonstrate that circ_C16orf62 impeded proliferation, migration, and invasion in vitro and retarded tumor growth in vivo by the miR-421/TUBB2A axis in GC, providing a potential therapeutic strategy for patients with GC.	NA	Med Sci Monit. 2020 Oct 2;26:e924343. doi: 10.12659/MSM.924343.
4011	Circular RNA	Circ0005875	miR-145-5p	ZEB2	renal carcinoma cells	Clear Cell Renal Cancer	Homo sapiens (human)	microarray;qPCR;Luciferase reporter assay;	33193877	Circular RNA microarray expression profile and potential function of circ0005875 in clear cell renal cell carcinoma.	Background: Circular RNAs (circRNAs), a novel class of endogenous noncoding RNAs, are involved in a variety of diseases, including several types of cancers. We hypothesized that circRNAs are involved in the tumorigenesis and development of clear cell renal cell carcinoma (ccRCC). Methods: To verify our hypothesis, we explored the circRNA expression profiles in 4 pairs of ccRCC tissues and their adjacent non-carcinoma tissues via microarray analysis. Selected circRNAs were further validated by qPCR. Moreover, hsa_circ_0005875 was selected for further study and the potential clinical values of hsa_circ_0005875 were investigated in 60 pairs of ccRCC tissues and adjacent normal controls. In addition, the role of hsa_circ_0005875 in ccRCC progression were performed using colony formation assay, Transwell assay and Martrigel-Transwell assay respectively. Finally, interactions between the circRNAs and miRNAs were predicted using Arraystar's miRNA target prediction software. Luciferase reporter assays were performed to evaluate the interaction between hsa_circ_0005875 and hsa_miR-145-5p. Results: The microarray data showed 1988 circRNAs were significantly dysregulated circRNAs, including 1033 upregulated and 955 downregulated ones in the ccRCC tissues. Hsa_circ_0005875 was confirmed to be significantly upregulated in the ccRCC tumor tissues and renal carcinoma cells. Further analysis revealed that hsa_circ_0005875 expression was associated with tumor size, pathological TNM stage, histological differentiation, and lymphatic metastasis. Functional experiments demonstrated that overexpression of hsa_circ_0005875 increased proliferation, migration and invasion abilities. Moreover, bioinformatics analysis and luciferase reporter assays suggest that hsa_circ_0005875 may serve as a ceRNA (competing endogenous RNA) of miR-145-5p to relieve the repressive effect of miR-145-5p on target ZEB2. Conclusions: These data indicate that hsa_circ_0005875 might play a role in promoting tumor growth and metastasis and be a potential biomarker of ccRCC.	NA	J Cancer. 2020 Oct 18;11(24):7146-7156. doi: 10.7150/jca.48770. eCollection 2020.
4012	Circular RNA	CircABCC4	miR-154-5p	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33023375	Circular RNA circABCC4 acts as a ceRNA of miR-154-5p to improve cell viability, migration and invasion of breast cancer cells in vitro.	Breast cancer is one of the dominant cancers of women-related death universal. This inquiry aims to disclose the probable role of circABCC4 in breast cancer. The level of circABCC4 was discovered through qRT-PCR. The reactions of circABCC4 and miR-154-5p on the cell viability, apoptosis, migration as well as invasion were, respectively, inspected by CCK-8, flow cytometry, and transwell assays. The association betwixt circABCC4 and miR-154-5p was investigated. The accumulation of NF-κB and Wnt/β-catenin pathway proteins was discovered through Western blot. The expression of circABCC4 was far great in tumor tissues than in normal tissues. Knockdown of circABCC4 could subdue cell viability, migration, invasion, and enhance apoptosis in breast cancer cell lines. CircABCC4 negatively regulated the manifestation of miR-154-5p and shared binding sites with the latter. Suppression of miR-154-5p expression partially conversed the repressive effect of circABCC4 knockdown on breast cancer cell viability, migration, invasion, and NF-κB and Wnt/β-catenin pathways. CircABCC4 knockdown repressed breast cancer cells viability, migration, and invasion by up-regulating miR-154-5p via inhibiting NF-κB and Wnt/β-catenin signal pathways.	NA	Cell Cycle. 2020 Oct;19(20):2653-2661. doi: 10.1080/15384101.2020.1815147. Epub 2020 Oct 6.
4013	Circular RNA	CircAMOTL1	miR-526b	SIK2	cervical carcinomas cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33344445	CircAMOTL1 Promotes Tumorigenesis Through miR-526b/SIK2 Axis in Cervical Cancer.	BACKGROUND: Cervical cancer is one of the most common malignancies in women, leading to major health problems for its high morbidity and mortality. Numerous studies have demonstrated that circular RNAs (circRNAs) could be participated in the progression of multifarious diseases, especially plentiful carcinomas. CircAMOTL1 (angiomotin-like1, ID: hsa_circ_0004214), which is located on human chromosome 11:9 4532555-94533477, is involved in the occurrence of breast cancer, etc. However, the intrinsic and concrete molecular mechanism of circAMOTL1 in cervical carcinomas remained thoroughly unclear, which was also the bottleneck of circRNAs studies in cancer. METHODS: The relative expression levels of circAMOTL1 and miR-526b in cervical carcinoma patients' specimens and cervical carcinoma cell lines were detected by RT-qPCR. Through experiments including loss-function and overexpression, the biological effects of circAMOTL1 and miR-526b on the proliferation, migration, apoptosis, and tumorigenicity were explored in cervical carcinomas. Dual luciferase reporter gene analysis, western blot, and other methods were adopted to explore the circAMOTL1 potential mechanism in cervical carcinomas. RESULTS: In our experiments, our researches displayed that circAMOTL1 was significantly higher expression in cervical carcinomas specimens and cell lines. Further experiments illustrated that the knockdown of circAMOTL1 could restrain the malignant phenotype, AKT signaling, and epithelial-mesenchymal transition (EMT) of in cervical carcinomas cells. Meanwhile miR-526b was downregulated in cervical carcinomas and even miR-526b could partially reverse circAMOTL1 function in malignant cervical tumor cells. CircAMOTL1 acts as a microRNA (miRNA) sponge that actively regulates the expression of salt-inducible kinase 2 (SIK2) to sponge miR-526b and subsequently increases malignant phenotypes of cervical carcinomas cells. In a word, circAMOTL1 acts a carcinogenic role and miR-526b serves as the opposite function of antioncogene in the cervical carcinoma pathogenesis. CONCLUSION: CircAMOTL1-miR-526b-SIK2 axis referred to the malignant progression and development of cervical carcinomas. CircAMOTL1 expression was inversely correlated with miR-526b and positively correlated with SIK2 mRNA in cervical cancer tissues. Thus, circAMOTL1 exerted an oncogenic role in cervical cancer progression through sponging miR-526b. Taken together, our study revealed that circAMOTL1 acted as an oncogene and probably was a potential therapeutic target for the cervical cancer.	NA	Front Cell Dev Biol. 2020 Dec 3;8:568190. doi: 10.3389/fcell.2020.568190. eCollection 2020.
4014	Circular RNA	CircArhgap12	miR-135a-5p	ADCY1	mouse heart tissue	Mouse Cardiomyocytes During Doxorubicin (Dox)-Induced Cardiotoxicity	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33245966	Circular RNA Arhgap12 modulates doxorubicin-induced cardiotoxicity by sponging miR-135a-5p.	AIM: This study aimed to investigate the regulatory role of differentially-expressed circular RNAs (circRNAs) in mouse cardiomyocytes during doxorubicin (DOX)-induced cardiotoxicity. MAIN METHODS: Two groups of mice were injected with equal volumes (0.1 mL) of normal saline and DOX. Mouse heart tissue was isolated and digested for total RNA extraction and then subjected to next-generation RNA-sequencing. Expression profiles of circRNAs and circRNA-miRNA-mRNA networks were also constructed. Overall, 48 upregulated and 16 downregulated circRNAs were found to be statistically significant (p < 0.05) in the DOX-injected group. Bioinformatics analysis revealed several potential biological pathways that might be related to apoptosis caused by DOX-induced cardiotoxicity. In addition, using qRT-PCR, we found that a circRNA coded by the Arhgap12 gene, termed circArhgap12, was upregulated in the mouse heart tissue upon DOX intervention. CircArhgap12 enhanced apoptotic cell rate, as assessed using terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay, and increased reactive oxygen species and malondialdehyde release as well as superoxide dismutase and caspase-3 activation. Using a luciferase reporter assay, we found that circArhgap12 could sponge miR-135a-5p. In rat primary cardiomyocytes, we found that si-circArhgap12 promoted apoptosis and oxidative stress by sponging the miR-135a-5p inhibitor. Using bioinformatics analysis and luciferase reporter assay, we found that miR-135a-5p might have a potential target site for ADCY1 mRNA. KEY FINDINGS: Our research demonstrated that the expression profile of circRNAs was modified significantly and that circArhgap12 might play a competitive role among endogenous RNAs in mouse cardiomyocytes during DOX-induced cardiotoxicity. SIGNIFICANCE: Our study may provide a preliminary understanding of DOX-induced cardiotoxicity modulated by circRNA and its competing endogenous RNAs network.	NA	Life Sci. 2021 Jan 15;265:118788. doi: 10.1016/j.lfs.2020.118788. Epub 2020 Nov 24.
4015	Circular RNA	CircArhgap12	miR-135a-5p	ADCY1	mouse heart tissue	Mouse Cardiomyocytes During Doxorubicin (Dox)-Induced Cardiotoxicity	Rattus (rat)	qRT-PCR;Luciferase reporter assay;	33245966	Circular RNA Arhgap12 modulates doxorubicin-induced cardiotoxicity by sponging miR-135a-5p.	AIM: This study aimed to investigate the regulatory role of differentially-expressed circular RNAs (circRNAs) in mouse cardiomyocytes during doxorubicin (DOX)-induced cardiotoxicity. MAIN METHODS: Two groups of mice were injected with equal volumes (0.1 mL) of normal saline and DOX. Mouse heart tissue was isolated and digested for total RNA extraction and then subjected to next-generation RNA-sequencing. Expression profiles of circRNAs and circRNA-miRNA-mRNA networks were also constructed. Overall, 48 upregulated and 16 downregulated circRNAs were found to be statistically significant (p < 0.05) in the DOX-injected group. Bioinformatics analysis revealed several potential biological pathways that might be related to apoptosis caused by DOX-induced cardiotoxicity. In addition, using qRT-PCR, we found that a circRNA coded by the Arhgap12 gene, termed circArhgap12, was upregulated in the mouse heart tissue upon DOX intervention. CircArhgap12 enhanced apoptotic cell rate, as assessed using terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay, and increased reactive oxygen species and malondialdehyde release as well as superoxide dismutase and caspase-3 activation. Using a luciferase reporter assay, we found that circArhgap12 could sponge miR-135a-5p. In rat primary cardiomyocytes, we found that si-circArhgap12 promoted apoptosis and oxidative stress by sponging the miR-135a-5p inhibitor. Using bioinformatics analysis and luciferase reporter assay, we found that miR-135a-5p might have a potential target site for ADCY1 mRNA. KEY FINDINGS: Our research demonstrated that the expression profile of circRNAs was modified significantly and that circArhgap12 might play a competitive role among endogenous RNAs in mouse cardiomyocytes during DOX-induced cardiotoxicity. SIGNIFICANCE: Our study may provide a preliminary understanding of DOX-induced cardiotoxicity modulated by circRNA and its competing endogenous RNAs network.	NA	Life Sci. 2021 Jan 15;265:118788. doi: 10.1016/j.lfs.2020.118788. Epub 2020 Nov 24.
4016	Circular RNA	CircArhgap12	miR-135a-5p	ADCY1	mouse heart tissue	Mouse Cardiomyocytes During Doxorubicin (Dox)-Induced Cardiotoxicity	Mus musculus (mouse)	qRT-PCR;Luciferase reporter assay;	33245966	Circular RNA Arhgap12 modulates doxorubicin-induced cardiotoxicity by sponging miR-135a-5p.	AIM: This study aimed to investigate the regulatory role of differentially-expressed circular RNAs (circRNAs) in mouse cardiomyocytes during doxorubicin (DOX)-induced cardiotoxicity. MAIN METHODS: Two groups of mice were injected with equal volumes (0.1 mL) of normal saline and DOX. Mouse heart tissue was isolated and digested for total RNA extraction and then subjected to next-generation RNA-sequencing. Expression profiles of circRNAs and circRNA-miRNA-mRNA networks were also constructed. Overall, 48 upregulated and 16 downregulated circRNAs were found to be statistically significant (p < 0.05) in the DOX-injected group. Bioinformatics analysis revealed several potential biological pathways that might be related to apoptosis caused by DOX-induced cardiotoxicity. In addition, using qRT-PCR, we found that a circRNA coded by the Arhgap12 gene, termed circArhgap12, was upregulated in the mouse heart tissue upon DOX intervention. CircArhgap12 enhanced apoptotic cell rate, as assessed using terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay, and increased reactive oxygen species and malondialdehyde release as well as superoxide dismutase and caspase-3 activation. Using a luciferase reporter assay, we found that circArhgap12 could sponge miR-135a-5p. In rat primary cardiomyocytes, we found that si-circArhgap12 promoted apoptosis and oxidative stress by sponging the miR-135a-5p inhibitor. Using bioinformatics analysis and luciferase reporter assay, we found that miR-135a-5p might have a potential target site for ADCY1 mRNA. KEY FINDINGS: Our research demonstrated that the expression profile of circRNAs was modified significantly and that circArhgap12 might play a competitive role among endogenous RNAs in mouse cardiomyocytes during DOX-induced cardiotoxicity. SIGNIFICANCE: Our study may provide a preliminary understanding of DOX-induced cardiotoxicity modulated by circRNA and its competing endogenous RNAs network.	NA	Life Sci. 2021 Jan 15;265:118788. doi: 10.1016/j.lfs.2020.118788. Epub 2020 Nov 24.
4017	Circular RNA	CircASH2L	miR-665	VEGFA	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33330483	CircASH2L Promotes Ovarian Cancer Tumorigenesis, Angiogenesis, and Lymphangiogenesis by Regulating the miR-665/VEGFA Axis as a Competing Endogenous RNA.	Ovarian cancer is the leading cause of gynecologic cancer-related deaths. Emerging research has revealed a close relationship between circular RNAs (circRNAs) and ovarian cancer development, metastasis, and prognosis. The objective of our research was to further explore the relationship between circASH2L and ovarian cancer. Quantitative real-time polymerase chain reaction was used to detect the differential expression of circRNAs between normal ovaries and ovarian cancer tissues. The impact of circASH2L on the proliferation, invasion, and tumorigenicity of ovarian cancer cells was evaluated using gain- and loss-of-function experiments. The molecular mechanisms of circASH2L function were investigated using bioinformatics analysis, RNA fluorescence in situ hybridization, western blots, and dual-luciferase reporter assays. The results showed that circASH2L was remarkably upregulated in ovarian cancer. The invasion and growth of ovarian cancer cells were suppressed by circASH2L knockdown in vitro, and downregulation of circASH2L restrained both angiogenesis and lymphangiogenesis of tumor xenografts in vivo. Furthermore, circASH2L was mostly distributed in the cytoplasm, where it competes with vascular endothelial growth factor A (VEGFA) for binding to miR-665. These findings indicate that circASH2L has an oncogenic function in ovarian cancer. In conclusion, circASH2L plays a critical role in regulating ovarian cancer cell tumorigenesis, angiogenesis, and lymphangiogenesis through the miR-665/VEGFA axis and, therefore, is a possible candidate target for ovarian cancer treatment.	NA	Front Cell Dev Biol. 2020 Nov 19;8:595585. doi: 10.3389/fcell.2020.595585. eCollection 2020.
4018	Circular RNA	Circ-BIRC6	miR-4491	NA	NCI-H460 and A549 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;	33177288	Depletion of circ-BIRC6, a circular RNA, suppresses non-small cell lung cancer progression by targeting miR-4491.	Circular RNAs (circRNAs) are non-coding RNAs molecules consisting of a covalently closed continuous loop which have no 5'-3' polarity and contain no polyA tail. Accumulating evidence demonstrates that circRNAs are involved in the initiation and progression of human malignancies. In this study, we explored the expression profile and regulatory role of circ-baculoviral IAP repeat-containing 6 (circ-BIRC6), a circular RNA, in malignant behaviors in non-small cell lung cancer (NSCLC). Expression levels of circ-BIRC6 and miR-4491 were examined in NSCLC patient samples and cell lines using quantitative real time PCR (qRT-PCR). In vitro roles of circ-BIRC6 knockdown on cell viability, colony formation, and apoptosis were assessed using the CCK-8, colony formation assay, and flow cytometry, respectively. The interactions between circ-BIRC6 and miR-449 were assessed using luciferase reporter and qRT-PCR assays. The in vivo role of circ-BIRC6 knockdown on tumor growth and apoptosis was evaluated in a xenograft mouse model of NSCLC. We found that expression levels of circ-BIRC6 in NSCLC patient samples and cell lines were elevated. Small interfering RNA (siRNA)-mediated circ-BIRC6 knockdown suppressed cell proliferation, colony formation, migration and invasion, and promoted apoptosis in NCI-H460 and A549 cells. In addition, miR-4491 was identified as a tumor-suppressor miRNA in NSCLC and circ-BIRC6 functions as a molecular sponge for miR-4491. Furthermore, circ-BIRC6 knockdown suppressed Wnt2B/β-catenin pathway. In vivo assay showed that depletion of circ-BIRC6 suppressed tumor growth, enhanced apoptosis, and decreased miR-4491 levels in a mouse xenograft model. These findings demonstrate that circ-BIRC6 functions as a critical regulator of proliferation and apoptosis via binding to and negatively regulating miR-4491, suggesting that circ-BIRC6 might be a potential target for treatment of NSCLC.	NA	Biosci Trends. 2021 Jan 23;14(6):399-407. doi: 10.5582/bst.2020.03310. Epub 2020 Nov 10.
4019	Circular RNA	Circ-BIRC6	miR-4491	NA	NCI-H460 and A549 cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	qRT-PCR;Flow Cytometry assay;	33177288	Depletion of circ-BIRC6, a circular RNA, suppresses non-small cell lung cancer progression by targeting miR-4491.	Circular RNAs (circRNAs) are non-coding RNAs molecules consisting of a covalently closed continuous loop which have no 5'-3' polarity and contain no polyA tail. Accumulating evidence demonstrates that circRNAs are involved in the initiation and progression of human malignancies. In this study, we explored the expression profile and regulatory role of circ-baculoviral IAP repeat-containing 6 (circ-BIRC6), a circular RNA, in malignant behaviors in non-small cell lung cancer (NSCLC). Expression levels of circ-BIRC6 and miR-4491 were examined in NSCLC patient samples and cell lines using quantitative real time PCR (qRT-PCR). In vitro roles of circ-BIRC6 knockdown on cell viability, colony formation, and apoptosis were assessed using the CCK-8, colony formation assay, and flow cytometry, respectively. The interactions between circ-BIRC6 and miR-449 were assessed using luciferase reporter and qRT-PCR assays. The in vivo role of circ-BIRC6 knockdown on tumor growth and apoptosis was evaluated in a xenograft mouse model of NSCLC. We found that expression levels of circ-BIRC6 in NSCLC patient samples and cell lines were elevated. Small interfering RNA (siRNA)-mediated circ-BIRC6 knockdown suppressed cell proliferation, colony formation, migration and invasion, and promoted apoptosis in NCI-H460 and A549 cells. In addition, miR-4491 was identified as a tumor-suppressor miRNA in NSCLC and circ-BIRC6 functions as a molecular sponge for miR-4491. Furthermore, circ-BIRC6 knockdown suppressed Wnt2B/β-catenin pathway. In vivo assay showed that depletion of circ-BIRC6 suppressed tumor growth, enhanced apoptosis, and decreased miR-4491 levels in a mouse xenograft model. These findings demonstrate that circ-BIRC6 functions as a critical regulator of proliferation and apoptosis via binding to and negatively regulating miR-4491, suggesting that circ-BIRC6 might be a potential target for treatment of NSCLC.	NA	Biosci Trends. 2021 Jan 23;14(6):399-407. doi: 10.5582/bst.2020.03310. Epub 2020 Nov 10.
4020	Circular RNA	CircCSNK1G3	miR-143-3p	HOXA10	LUAD cells	Lung Cancer	Homo sapiens (human)	FISH;microarray;qRT-PCR;Western blot;FISH;Immunohistochemistry;	33118120	Circular RNA circCSNK1G3 induces HOXA10 signaling and promotes the growth and metastasis of lung adenocarcinoma cells through hsa-miR-143-3p sponging.	BACKGROUND: In the last decade, a relatively novel, ubiquitous and highly stable subclass of non-coding RNAs, called circular (circ)-RNAs, has increasingly been implicated in cancer development, and several of them have been shown to act as microRNA sponges. As yet, however, the role of circRNAs in lung adenocarcinoma (LUAD) development has largely remained unexplored. METHODS: Bioinformatics, microarray-based and qRT-PCR expression assays were used to assess circRNA, miRNA and mRNA expression in LUAD patient samples and cell lines. siRNA-mediated silencing was used to assess the effect of circCSNK1G3 on various LUAD-associated characteristics such as proliferation, migration, invasion and tumorigenesis, both in vitro and in vivo. Western blotting, immunohistochemistry, fluorescence in situ hybridization (FISH) and luciferase reporter activity assays were used to characterize relationships between circCSNK1G3, miR-143-3p and HOXA10 in LUAD cells. RESULTS: By screening for differentially expressed circRNAs, we found that circCSNK1G3 was aberrantly expressed in primary LUAD tissues and cell lines. An oncogenic role of circCSNK1G3 was deduced from its aberrant expression and associated enhancement of LUAD A549 and H1299 cell proliferation, migration and invasion. We also found that circCSNK1G3 can directly interact with and suppress miR-143-3p expression by serving as a 'miR-143-3p sponge'. In addition, we found that circCSNK1G3 can modulate homeobox (HOX) A10 expression through miR-143-3p signaling and, thereby, affect LUAD tumorigenesis. CONCLUSIONS: Our data indicate that circCSNK1G3 can induce HOXA10 expression and, thereby, promote the growth and metastasis of LUAD cells through hsa-miR-143-3p sponging. As such, our data highlight the targetability of the circCSNK1G3/miR-143-3p/HOXA10 signaling axis in patients with LUAD. Graphical abstract.	NA	Cell Oncol (Dordr). 2021 Apr;44(2):297-310. doi: 10.1007/s13402-020-00565-x. Epub 2020 Oct 29.
4021	Circular RNA	CircFAT1	miR-30a-5p	REEP3	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33179443	CircFAT1 promotes hepatocellular carcinoma progression via miR-30a-5p/REEP3 pathway.	As newly found non-coding RNAs, circular RNAs (circRNAs) are involved in multiple biological processes. Emerging evidence has illustrated the pivotal roles of circRNAs in various human cancers. However, the function of circFAT1 in hepatocellular carcinoma (HCC) remains largely unclear. In the present study, we found that circFAT1 expression is up-regulated in HCC tissues and cells. In addition, circFAT1 level is positively correlated with TNM stage and tumour size. To further explore the function of circFAT1 in HCC, in vitro and in vivo experiments were performed. The results show that circFAT1 inhibition reduces the proliferation and invasion of HCC cells and tumorigenesis in vivo, whereas REEP3 overexpression reverses these processes. In conclusion, circFAT1 sponges miR-30a-5p to regulate the expression of REEP3, thus promoting hepatocarcinogenesis. New HCC diagnosis or treatment strategies may be developed from circFAT1 as a target.	NA	J Cell Mol Med. 2020 Dec;24(24):14561-14570. doi: 10.1111/jcmm.16085. Epub 2020 Nov 11.
4022	Circular RNA	CircGLIS3	miR-644a	PTBP1	NSCLC tissues and cell lines	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33520363	A circGLIS3/miR-644a/PTBP1 positive feedback loop promotes the malignant biological progressions of non-small cell lung cancer.	Non-small cell lung cancer (NSCLC) is a severe cancer which critically threatens human health in the world. Circular RNAs (circRNAs) are non-coding RNAs that involve in cancer progression. We want to explore the roles of circRNAs in NSCLC in this study. In current study, circGLIS3 was found to be highly expressed in NSCLC tissues and cell lines and high circGLIS3 level was correlated to malignant characteristics and poor prognosis of NSCLC. Functional experiments suggested that circGLIS3 promoted proliferation, migration and invasion and arrested apoptosis of NSCLC cells in vitro. CircGLIS3 also participated in the in vivo process by accelerate NSCLC tumor growth and metastasis. Mechanistically, circGLIS3 could sponging multiple anti-cancer miRNAs including miR-526b, miR-198, miR-498 and miR-664a. Here, we for the first time confirmed that miR-644a was downregulated and functioned as a tumor suppression gene in NSCLC. In addition, we found PTBP1 as a novel target of miR-644a and circGLIS3 could raise the expression of PTBP1 via miR-644a. And PTBP1 could bind to the flanking introns of circGLIS3 and thereby promoting looping of circGLIS3. In conclusion, CircGLIS3 functions as an oncogene via sponging multiple tumor-suppressive miRNAs in NSCLC. A circGLIS3/miR-644a/PTBP1 positive feedback loop exists in the tumorigenesis and development of NSCLC.	NA	Am J Cancer Res. 2021 Jan 1;11(1):108-122. eCollection 2021.
4023	Circular RNA	CircHBEGF	miR-646	EGFR	trabecular meshwork cells	Primary Open-Angle Glaucoma	Homo sapiens (human)	RACE;	33335643	Oxidative Stress-Induced circHBEGF Promotes Extracellular Matrix Production via Regulating miR-646/EGFR in Human Trabecular Meshwork Cells.	Primary open-angle glaucoma (POAG), a leading cause of irreversible vision loss, presents with increased prevalence and a higher degree of clinical severity in the world. Growing evidence has shown that ncRNAs are involved in the fibrotic process, which is thought to be the proegumenal cause of POAG. Here, we screened out a differentially expressed circRNA (named circHBEGF) in human trabecular meshwork cells (HTMCs) under oxidative stress, which is spliced from pre-HBEGF. circHBEGF promotes the expression of extracellular matrix (ECM) genes (fibronectin and collagen I). Further studies revealed that circHBEGF could competitively bind to miR-646 as a miRNA sponge to regulate EGFR expression in HTMCs. Importantly, HBEGF can also activate EGF signaling pathways, through which can transcriptionally activate ECM genes in HTMCs. In summary, this study investigates the functions and molecular mechanisms of oxidative stress-induced circHBEGF in the regulation of ECM production in HTMCs through the miR646/EGFR pathway. These findings further elucidate the pathogenic mechanism and may identify novel targets for the molecular therapy of POAG.	NA	Oxid Med Cell Longev. 2020 Nov 24;2020:4692034. doi: 10.1155/2020/4692034. eCollection 2020.
4024	Circular RNA	Circ-HIPK2	miR-485-5p	ATG101	H2O2-injured mouse neonatal cardiomyocytes	Heart Diseases Including Myocarditis	Mus musculus (mouse)	qRT-PCR	33027196	Circ-HIPK2 Accelerates Cell Apoptosis and Autophagy in Myocardial Oxidative Injury by Sponging miR-485-5p and Targeting ATG101.	Myocardial injury has been deemed as a major cause of heart diseases including myocarditis and coronary heart disease, which have brought multiple mortalities globally. Long non-coding RNAs (lncRNAs) are widely recognized in diverse diseases. However, the role of circular RNA HIPK2 (circ-HIPK2) remains unclear in myocardial injury induced by H2O2. We attempted to investigate the probable role of circ-HIPK2 in myocardial injury induced by H2O2. This study discovered that the treatment of H2O2 inhibited cell proliferation but boosted cell apoptosis and autophagy. ATG101 was upregulated in primary mouse neonatal cardiomyocytes under H2O2 treatment. ATG101 knockdown promoted proliferation and limited apoptosis by attenuating autophagy in H2O2-injured mouse neonatal cardiomyocytes. Furthermore, miR-485-5p was validated to combine with ATG101 and circ-HIPK2, and circ-HIPK2 positively regulated ATG101 expression by sponging miR-485-5p. At last, silenced circ-HIPK2 mediated the promotion of cell proliferation, and repression of cell apoptosis was restored by ATG101 amplification. In a word, circ-HIPK2 facilitates autophagy to accelerate cell apoptosis and cell death in H2O2-caused myocardial oxidative injury through the miR-485-5p/ATG101 pathway, indicating a novel therapeutic target point for patients with myocardial injury.	NA	J Cardiovasc Pharmacol. 2020 Oct;76(4):427-436. doi: 10.1097/FJC.0000000000000879.
4025	Circular RNA	Circ-HIPK2	miR-485-5p	ATG101	H2O2-injured mouse neonatal cardiomyocytes	Coronary Heart Disease	Mus musculus (mouse)	qRT-PCR	33027196	Circ-HIPK2 Accelerates Cell Apoptosis and Autophagy in Myocardial Oxidative Injury by Sponging miR-485-5p and Targeting ATG101.	Myocardial injury has been deemed as a major cause of heart diseases including myocarditis and coronary heart disease, which have brought multiple mortalities globally. Long non-coding RNAs (lncRNAs) are widely recognized in diverse diseases. However, the role of circular RNA HIPK2 (circ-HIPK2) remains unclear in myocardial injury induced by H2O2. We attempted to investigate the probable role of circ-HIPK2 in myocardial injury induced by H2O2. This study discovered that the treatment of H2O2 inhibited cell proliferation but boosted cell apoptosis and autophagy. ATG101 was upregulated in primary mouse neonatal cardiomyocytes under H2O2 treatment. ATG101 knockdown promoted proliferation and limited apoptosis by attenuating autophagy in H2O2-injured mouse neonatal cardiomyocytes. Furthermore, miR-485-5p was validated to combine with ATG101 and circ-HIPK2, and circ-HIPK2 positively regulated ATG101 expression by sponging miR-485-5p. At last, silenced circ-HIPK2 mediated the promotion of cell proliferation, and repression of cell apoptosis was restored by ATG101 amplification. In a word, circ-HIPK2 facilitates autophagy to accelerate cell apoptosis and cell death in H2O2-caused myocardial oxidative injury through the miR-485-5p/ATG101 pathway, indicating a novel therapeutic target point for patients with myocardial injury.	NA	J Cardiovasc Pharmacol. 2020 Oct;76(4):427-436. doi: 10.1097/FJC.0000000000000879.
4026	Circular RNA	CircHIPK3	miR-338-3p	RAB23	thyroid cancer cell lines (K1, CAL-62, TPC1)	Thyroid Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33105143	CircHIPK3 Promotes Thyroid Cancer Tumorigenesis and Invasion through the Mirna-338-3p/RAB23 Axis.	Objective：Thyroid cancer is a common type of endocrine malignancy, and its incidence has been steadily increasing in many regions of the world. Numerous studies have found that the circRNAs in various cancer types are aberrantly expressed, which could be potential biological diagnostic markers and therapeutic targets. The purpose of this study was to investigate the role of circHIPK3 in the development and progression of thyroid cancer and its mechanism. Subject and Methods：qRT-PCR was used to detect the relative expression levels of circHIPK3 in thyroid cancer cell lines (K1, CAL-62, TPC1), human thyroid normal cells (Nthy-ori 3-1), 10 pairs of thyroid cancer tissues and corresponding adjacent normal tissues. CCK-8 and Transwell assays were used to detect the proliferation and metastasis ability of cells. The targeted relationships between circHIPK3-miR-338-3p and miR-338-3p-RAB23 were predicted by bioinformatics analysis and verified by dual-luciferase reporter assays. Results and Conclusion: The downregulation of circHIPK3 significantly reduced the migration, invasion and proliferation of thyroid carcinoma. Then, we demonstrated that circHIPK3 up-regulated the expression of its target gene RAB23 by sponging miR-338-3p to promote the tumorigenesis and invasiveness of thyroid cancer. This study is the first to find that circHIPK3 plays the role of oncogenetic circRNA in thyroid cancer, which may provide new insights into how circRNA affects the progression of thyroid cancer. Our study also showed that circHIPK3 could be a novel biomarker for thyroid cancer.	NA	Med Princ Pract. 2020 Oct 26. doi: 10.1159/000512548.
4027	Circular RNA	CircMCTP2	miR-99a-5p	MTMR3	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;RNA sequencing;	33198772	Circular RNA MCTP2 inhibits cisplatin resistance in gastric cancer by miR-99a-5p-mediated induction of MTMR3 expression.	BACKGROUND: Cisplatin (CDDP) is the first-line chemotherapy for gastric cancer (GC). The poor prognosis of GC patients is partially due to the development of CDDP resistance. Circular RNAs (circRNAs) are a subclass of noncoding RNAs that function as microRNA (miRNA) sponges. The role of circRNAs in CDDP resistance in GC has not been evaluated. METHODS: RNA sequencing was used to identify the differentially expressed circRNAs between CDDP-resistant and CDDP-sensitive GC cells. qRT-PCR was used to detect the expression of circMCTP2 in GC tissues. The effects of circMCTP2 on CDDP resistance were investigated in vitro and in vivo. Pull-down assays and luciferase reporter assays were performed to confirm the interactions among circMCTP2, miR-99a-5p, and myotubularin-related protein 3 (MTMR3). The protein expression levels of MTMR3 were detected by western blotting. Autophagy was evaluated by confocal microscopy and transmission electron microscopy (TEM). RESULTS: CircMCTP2 was downregulated in CDDP-resistant GC cells and tissues compared to CDDP-sensitive GC cells and tissues. A high level of circMCTP2 was found to be a favorable factor for the prognosis of patients with GC. CircMCTP2 inhibited proliferation while promoting apoptosis of CDDP-resistant GC cells in response to CDDP treatment. CircMCTP2 was also found to reduce autophagy in CDDP-resistant GC cells. MiR-99a-5p was verified to be sponged by circMCTP2. Inhibition of miR-99a-5p could sensitize GC cells to CDDP. MTMR3 was confirmed to be a direct target of miR-99a-5p. Knockdown of MTMR3 reversed the effects of circMCTP2 on the proliferation, apoptosis and autophagy of CDDP-resistant GC cells. CircMCTP2 was also confirmed to inhibit CDDP resistance in vivo in a nude mouse xenograft model. CONCLUSIONS: CircMCTP2 sensitizes GC to CDDP through the upregulation of MTMR3 by sponging miR-99a-5p. Overexpression of CircMCTP2 could be a new therapeutic strategy for counteracting CDDP resistance in GC.	NA	J Exp Clin Cancer Res. 2020 Nov 17;39(1):246. doi: 10.1186/s13046-020-01758-w.
4028	Circular RNA	CircMCTP2	miR-99a-5p	MTMR3	GC cells	Gastric Cancer	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;RNA sequencing;	33198772	Circular RNA MCTP2 inhibits cisplatin resistance in gastric cancer by miR-99a-5p-mediated induction of MTMR3 expression.	BACKGROUND: Cisplatin (CDDP) is the first-line chemotherapy for gastric cancer (GC). The poor prognosis of GC patients is partially due to the development of CDDP resistance. Circular RNAs (circRNAs) are a subclass of noncoding RNAs that function as microRNA (miRNA) sponges. The role of circRNAs in CDDP resistance in GC has not been evaluated. METHODS: RNA sequencing was used to identify the differentially expressed circRNAs between CDDP-resistant and CDDP-sensitive GC cells. qRT-PCR was used to detect the expression of circMCTP2 in GC tissues. The effects of circMCTP2 on CDDP resistance were investigated in vitro and in vivo. Pull-down assays and luciferase reporter assays were performed to confirm the interactions among circMCTP2, miR-99a-5p, and myotubularin-related protein 3 (MTMR3). The protein expression levels of MTMR3 were detected by western blotting. Autophagy was evaluated by confocal microscopy and transmission electron microscopy (TEM). RESULTS: CircMCTP2 was downregulated in CDDP-resistant GC cells and tissues compared to CDDP-sensitive GC cells and tissues. A high level of circMCTP2 was found to be a favorable factor for the prognosis of patients with GC. CircMCTP2 inhibited proliferation while promoting apoptosis of CDDP-resistant GC cells in response to CDDP treatment. CircMCTP2 was also found to reduce autophagy in CDDP-resistant GC cells. MiR-99a-5p was verified to be sponged by circMCTP2. Inhibition of miR-99a-5p could sensitize GC cells to CDDP. MTMR3 was confirmed to be a direct target of miR-99a-5p. Knockdown of MTMR3 reversed the effects of circMCTP2 on the proliferation, apoptosis and autophagy of CDDP-resistant GC cells. CircMCTP2 was also confirmed to inhibit CDDP resistance in vivo in a nude mouse xenograft model. CONCLUSIONS: CircMCTP2 sensitizes GC to CDDP through the upregulation of MTMR3 by sponging miR-99a-5p. Overexpression of CircMCTP2 could be a new therapeutic strategy for counteracting CDDP resistance in GC.	NA	J Exp Clin Cancer Res. 2020 Nov 17;39(1):246. doi: 10.1186/s13046-020-01758-w.
4029	Circular RNA	CircPTK2	miR-92a	E-cadherin	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	33015774	The circular RNA circPTK2 inhibits EMT in hepatocellular carcinoma by acting as a ceRNA and sponging miR-92a to upregulate E-cadherin.	OBJECTIVE: Hepatocellular carcinoma (HCC) is a common malignant tumor. Increasing evidence has demonstrated that microRNAs (miRNAs) play an important role in a wide variety of cellular processes. However, there are few reports about the role and underlying molecular mechanisms of miRNAs in HCC. PATIENTS AND METHODS: qRT-PCR and Western blots were performed to quantify the expression of miR-92a, E-cadherin, and circPTK2. Proliferation and invasion assays were performed to explore the function of miR-92a and circPTK2. A Luciferase assay was used to test the relationship between miR-92a, E-cadherin, and circPTK2. RESULTS: In this study, we found that miR-92a was upregulated in HCC tissues and HCC cell lines. Overexpression of miR-92a enhanced cell proliferation and invasion by targeting the E-cadherin 3'UTR in HCC cells. Furthermore, we found that circPTK2 inhibited EMT by inhibiting miR-92a, preventing its ability to downregulate E-cadherin in HCC cells. CONCLUSIONS: We identified a regulatory axis comprising circPTK2/miR-92a/E-cadherin in HCC cells that may serve as a valuable biomarker and therapeutic target for patients with HCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9333-9342. doi: 10.26355/eurrev_202009_23015.
4030	Circular RNA	CircRNA_001306	miR-584-5p	CDK16	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33135290	circRNA 001306 enhances hepatocellular carcinoma growth by up-regulating CDK16 expression via sponging miR-584-5p.	Circular RNAs (circRNAs) have been demonstrated to play important roles in cancer progress. However, the roles in hepatocellular carcinoma (HCC) are still unclear. Here, we found has_circRNA_001306 (circ_1306) was up-regulated in HCC tissues and cell lines. Knockdown the expression circ_1306 significantly suppressed HCC cell proliferation and induced the cell apoptosis in vitro and in vivo. Furthermore, we identified circ_1306 could up-regulate the expression of CDK16 by sponging miR-584-5p. The expression of miR-584-5p was decreased, and the expression of CDK16 was increased in HCC tissues and cell lines. Meanwhile, either knockdown of miR-584-5p or overexpression of CDK16 could suppress the HCC cell proliferation. In vivo, overexpression of miR-584-5p or knockdown of circ_1306 could inhibit the expression of CDK16, and suppress tumour growth. Altogether, our findings suggested that circ_1306 could promoter HCC progress by miR-584-5p/CDK16 axis, which provided a novel marker for HCC diagnosis and treatment.	NA	J Cell Mol Med. 2020 Dec;24(24):14306-14315. doi: 10.1111/jcmm.16047. Epub 2020 Nov 1.
4031	Circular RNA	CircRNA_010383	miR-135a	TRPC1	diabetic kidneys, mesangial cells	Renal Fibrosis	Homo sapiens (human)	microarray;RACE;	33472945	circRNA_010383 Acts as a Sponge for miR-135a and Its Downregulated Expression Contributes to Renal Fibrosis in Diabetic Nephropathy.	Diabetic nephropathy (DN), a vascular complication of diabetes, is the leading cause of death in patients with diabetes. The contribution of aberrantly expressed circular RNAs (circRNAs) to DN in vivo is poorly understood. Integrated comparative circRNA microarray profiling was used to examine the expression of circRNAs in diabetic kidney of db/db mice. We found that circRNA_010383 expression was markedly downregulated in diabetic kidneys, mesangial cells, and tubular epithelial cells cultured in high-glucose conditions. circRNA_010383 colocalized with miRNA-135a (miR-135a) and inhibited miR-135a function by directly binding to miR-135a. In vitro, the knockdown of circRNA_010383 promoted the accumulation of extracellular matrix (ECM) proteins and downregulated the expression of transient receptor potential cation channel, subfamily C, member 1 (TRPC1), which is a target protein of miR-135a. Furthermore, circRNA_010383 overexpression effectively inhibited the high-glucose-induced accumulation of ECM and increased TRPC1 levels in vitro. More importantly, the kidney target of circRNA_010383 overexpression inhibited proteinuria and renal fibrosis in db/db mice. Mechanistically, we identified that a loss of circRNA_010383 promoted proteinuria and renal fibrosis in DN by acting as a sponge for miR-135a. This study reveals that circRNA_010383 may be a novel therapeutic target for DN in the future.	NA	Diabetes. 2021 Feb;70(2):603-615. doi: 10.2337/db20-0203.
4032	Circular RNA	CircRNA_010383	miR-135a	TRPC1	diabetic kidneys, mesangial cells and tubular epithelial cells	Diabetic Nephropathy	Homo sapiens (human)	microarray;RACE;	33203695	circRNA_010383 Acts as a Sponge for miR-135a and its Downregulated Expression Contributes to Renal Fibrosis in Diabetic Nephropathy.	Diabetic nephropathy (DN), a vascular complication of diabetes mellitus, is the leading cause of death in diabetic patients. The contribution of aberrantly expressed circRNAs to diabetic nephropathy in vivo is poorly understood. Integrated comparative circRNA microarray profiling was used to examine the expression of circRNAs in diabetic kidney of db/db mice. We found that circRNA_010383 expression was markedly downregulated in diabetic kidneys, mesangial cells and tubular epithelial cells cultured in high-glucose conditions. circRNA_010383 colocalized with microRNA-135a (miR-135a) and inhibited miR-135a function by directly binding to miR-135a. In vitro, the knockdown of circRNA_010383 promoted the accumulation of extracellular matrix (ECM) proteins and downregulated the expression of transient receptor potential cation channel, subfamily C, member (TRPC1), which is a target protein of miR-135a. Furthermore, circRNA_010383 overexpression effectively inhibited the high-glucose-induced accumulation of ECM and increased TRPC1 levels in vitro More importantly, the kidney-target of circRNA_010383 overexpression inhibited proteinuria and renal fibrosis in db/db mice. Mechanistically, we identified that a loss of circRNA_010383 promoted proteinuria and renal fibrosis in DN by acting as a sponge for miRNA-135a. This study reveals that circRNA_010383 may be a novel therapeutic target for DN in the future.	NA	Diabetes. 2020 Nov 17:db200203. doi: 10.2337/db200203.
4033	Circular RNA	CircRNA_ACAP2	miR-21-5p	STAT3	HNSCC cells	Head And Neck Squamous  Carcinoma 	Homo sapiens (human)	qRT-PCR	33363013	CircRNA_ACAP2 Suppresses EMT in Head and Neck Squamous Cell Carcinoma by Targeting the miR-21-5p/STAT3 Signaling Axis.	Circular RNAs (circRNAs) contain microRNA (miRNA)-specific binding sites and can function as miRNA sponges to regulate gene expression by suppressing the inhibitory effect of miRNAs on their target genes. MiR-21-5p has been reported to be involved in the development of head and neck squamous cell carcinoma (HNSCC) and plays an important role in the activation of epithelial-mesenchymal transition (EMT). However, the upstream regulatory mechanism and downstream targets of miR-21-5p in tumor cells remain unknown. CircRNA_ACAP2 inhibits the function of miR-21-5p by binding to its specific binding sites in HNSCC cells. Overexpression of CircRNA_ACAP2 inhibits the proliferation and migration of HNSCC cells, while downregulation of CircRNA_ACAP2 has the opposite effect. STAT3 is a direct target gene of miR-21-5p and a transcription factor of ZEB1. We demonstrate that CircRNA_ACAP2 functions as a tumor suppressor gene in HNSCC and that its function is regulated via the miR-21-5p/STAT3 signaling axis.	NA	Front Oncol. 2020 Dec 11;10:583682. doi: 10.3389/fonc.2020.583682. eCollection 2020.
4034	Circular RNA	CircRNA-0006896	miR-1264	DNMT1	endothelial cells	Atherosclerosis	Homo sapiens (human)	Western blot;	33649864	circRNA-0006896-miR1264-DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells in atherosclerosis.	Atherosclerosis (AS) is a chronic inflammatory disease of the vascular wall with multiple causes. AS is the primary pathological basis of cardiovascular disease and stroke. Moreover, carotid plaque rupture and thrombus formation are the main causes of ischemic stroke. Therefore, understanding the formation of carotid plaques may help improve the prediction and prevention of cardiovascular and cerebrovascular events. Endothelial cell dysfunction results in re-endothelialization and angiogenesis in atherosclerotic plaques, thus promoting plaque destabilization. The aim of the present study was to evaluate the effect of circular RNA (circRNA) molecules in serum exosomes (serum-Exos) from patients with stable plaque atherosclerosis (SA) and unstable/vulnerable plaque atherosclerosis (UA). Specifically, the effect of circRNA on human umbilical vein endothelial cell (HUVEC) behavior and the mechanisms underlying plaque destabilization in AS were evaluated. Serum-Exos were isolated, then identified using transmission electron microscopy, nanoparticle tracking analysis and western blotting. The serum-Exo-circRNA expression profile of patients with SA or UA was investigated using a circRNA array. The relationship between circRNA-006896 in serum-Exos and biochemical parameters of patients with SA and UA were analyzed using Spearman's correlation. In addition, HUVECs were incubated with serum-Exos for in vitro functional assays. The present study demonstrated that circRNAs expression profiles in SA and UA serum-Exos were significantly different, indicating a potential role for circRNAs in carotid plaque destabilization. The expression of circRNA-0006896 was positively correlated with triglyceride, low-density lipoprotein cholesterol (LDL-C) and C-reactive protein levels, and negatively correlated with albumin levels in patients with UA. However, circRNA-0006896 expression was positively correlated with LDL-C in patients with SA. Using bioinformatic analysis, a competing endogenous RNA (ceRNA) network was selected to study the regulatory roles of circRNA-0006896 in serum-Exos. Additionally, in HUVECs treated with serum-Exos derived from patients with UA, the expression of circRNA-0006896 in HUVECs was upregulated. This was accompanied by decreased expression of microRNA-1264 and SOCS3, increased levels of DNMT1 and phosphorylated STAT3. HUVEC proliferation and migration were significantly increased in the UA group, compared with the mock and SA groups. This finding indicates that the circRNA-0006896-miR-1264-DNMT1 axis plays an important role in carotid plaque destabilization by regulating the behavior of endothelial cells. Moreover, it suggests that circRNA-0006896 may represent a therapeutic target for controlling JNK/STAT3 signaling in HUVECs. Thus, this study may provide insight on potential interventions against vulnerable plaque formation in patients with AS.	NA	Mol Med Rep. 2021 May;23(5):311. doi: 10.3892/mmr.2021.11950. Epub 2021 Mar 2.
4035	Circular RNA	CircRNA-1806	miR-126	NA	experimental murine cryptococcosis model	Fatal Cryptococcal Meningitis	Homo sapiens (human)	microarray;	33281794	CircRNA-1806 Decreases T Cell Apoptosis and Prolongs Survival of Mice After Cryptococcal Infection by Sponging miRNA-126.	CircRNAs are a recently well-known regulator that mediates a variety of biological processes. Cryptococcus neoformans is an environmental fungal pathogen that can cause fatal cryptococcal meningitis in immunocompromised individuals. However, the involvement of circRNA in cryptococcal infection remains unclear. In this study, high-throughput microarray was performed to identify the circRNA expression profile in cryptococcal meningitis patients. Circ_0001806 was significantly decreased in cryptococcal meningitis individuals. Then the effects of circ_0001806 and its interaction with miRNAs were explored in vivo and in vitro. The knock-down of circ_0001806 led to higher fungal infection and shorter survival in an experimental murine cryptococcosis model. Transcriptome analysis showed that decreased circ_0001806 regulated pathways related to the host antimicrobe response in T cells. Furthermore, in vitro experiments showed that circ_0001806 positively modulates ADM level, decreasing cell apoptosis and G1S arrest in T cells. Finally, we found circ_0001806 exerted its effects by sponging miRNA-126 in T cells. Taken together, our results reveal the role of circRNA-1806/miRNA-126 in the regulation of cell cycle and apoptosis in cryptococcal infection and can provide a new insights of the pathogenesis of cryptococcal infection.	NA	Front Microbiol. 2020 Nov 13;11:596440. doi: 10.3389/fmicb.2020.596440. eCollection 2020.
4036	Circular RNA	CircRPPH1	miR-556-5p	YAP1	breast cancer cells	Triple Negative Breast Cancer	Homo sapiens (human)	RT-PCR;RNA immunoprecipitation;RNA immunoprecipitation;	33194025	Circular RNA circRPPH1 promotes triple-negative breast cancer progression via the miR-556-5p/YAP1 axis.	Circular RNAs (circRNAs), which are considered to be important functional regulators in cancer, have provided a new perspective regarding our understanding of tumor biology, including that of breast cancer. To investigate the regulatory effect of circRPPH1 on cellular behaviors of breast cancer and the potential mechanism, the expression of circRPPH1 and miR-556-5p in breast cancer tissues and cell lines were examined by quantitative RT-PCR. The regulatory effects of the circRPPH1/miR-556-5p/YAP1 axis on cellular behaviors of breast cancer cells were evaluated through functional experiments in vitro and tumor growth in vivo. The relationship between circRPPH1 and miR-556-5p/YAP1 was assessed using dual-luciferase reporter and RNA immunoprecipitation assays. PCR results showed that circRPPH1 levels were significantly upregulated in tumor tissues and breast cancer cells. Functionally, circRPPH1 promoted the proliferation, migration, invasion, and angiogenesis of breast cancer cell lines and tumor growth in vivo. Regarding the mechanism, dual-luciferase reporter and RNA immunoprecipitation assays showed that circRPPH1 was capable of sponging miR-556-5p to increase expression of the oncogene YAP1. Our data reveal that circRPPH1 plays a vital regulatory role in breast cancer via the miR-556-5p/YAP1 axis and may serve as a promising therapeutic target for breast cancer treatment.	NA	Am J Transl Res. 2020 Oct 15;12(10):6220-6234. eCollection 2020.
4037	Circular RNA	CircSMYD4	miR-584-5p	AFP	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA pull-down assay;Western blot;Flow Cytometry assay;Immunohistochemistry;luciferase assay;RNA pull-down;	33292243	CircSMYD4 regulates proliferation, migration and apoptosis of hepatocellular carcinoma cells by sponging miR-584-5p.	BACKGROUND: There is evidence that circSMYD4 is differentially expressed in hepatocellular carcinoma (HCC), but its mechanism of action remains unclear. Therefore, this study aimed to explore the role of circSMYD4 in the occurrence and development of HCC and its specific molecular mechanism. METHODS: The expressions of related genes and proteins in the development of HCC were detected by real-time quantitative-PCR and Western blot. HCC cells treated with RNase R and Actinomycin D were used to examine the stability of circSMYD4. Bioinformatics analysis, RNA pull-down assay, luciferase assay and Spearman correlation analysis were performed to evaluate the interaction between circSMYD4 and miRNA. Cell Counting Kit-8, clone formation assay, wound healing assay, Transwell, flow cytometry, nude tumor formation experiment, and immunohistochemistry were employed to analyze the function of circSMYD4 in HCC. A rescue experiment was conducted to analyze the effect of miR-584-5p on the physiological functions of cells. RESULTS: CircSMYD4 was down-regulated in HCC tissues and cells, and was not easily affected by RNase R and Actinomycin D. The abundances of circSMYD4 and SMYD4 in the cytoplasm were significantly higher than in the nucleus. Up-regulation of circSMYD4 inhibited the proliferation, invasion and migration and promoted the apoptosis of HCC cells in vitro, while it inhibited tumor growth, promoted apoptosis-related proteins, and suppressed alpha-fetoprotein (AFP) levels in vivo. CircSMYD4 could be used as a miRNA sponge to target miR-584-5p. In addition, miR-584-5p overexpression partially reversed the regulatory effect of circSMYD4 on HCC. CONCLUSION: CircSMYD4 prevents the development of HCC through regulating multiple signaling pathways such as metastasis and apoptosis by sponging miR-584-5p.	NA	Cancer Cell Int. 2020 Nov 19;20(1):556. doi: 10.1186/s12935-020-01648-3.
4038	Circular RNA	CircTGFBR2	miR-107	TGFBR2	NPC cells	Nasopharyngeal Cancer	Homo sapiens (human)	microarray;	33160003	Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107.	Circular RNAs (circRNAs) act as competing endogenous RNAs, which are involved in the regulation of many types of cancers. They primarily function by sponging microRNAs (miRNAs) and influencing the expression of miRNA by target messenger RNA. However, the role of circRNAs in the progression of nasopharyngeal carcinoma (NPC) remains largely unclear. In this study, differentially expressed miRNAs associated with NPC were screened using microarray analyses, from which miR-107 was identified. Increased miR-107 expression was associated with poor prognosis in NPC, and miR-107 promoted the proliferation and migration of NPC cells. TGFBR2 was identified as the direct target of miR-107, which could reverse its effect on NPC cells. Furthermore, the expression of circTGFBR2 was downregulated in NPC tissue samples, while circTGFBR2 overexpression correlated with favorable prognosis in NPC. Functionally, circTGFBR2 overexpression inhibited the proliferation and migration of NPC cells both in vitro and in vivo. Further analysis showed that circTGFBR2 sponged miR-107, leading to the upregulation of TGFBR2 expression and suppression of NPC progression. Therefore, circTGFBR2 may serve as a novel tumor suppressive factor and potential target for new therapies in NPC patients.	NA	Cancer Lett. 2021 Feb 28;499:301-313. doi: 10.1016/j.canlet.2020.11.001. Epub 2020 Nov 4.
4039	LncRNA	CR594175	miR-142-3p	CTNNB1	HepG2 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	32983253	A study of the mechanism of lncRNA-CR594175 in regulating proliferation and invasion of hepatocellular carcinoma cells in vivo and in vitro.	BACKGROUND: Hepatocellular carcinoma (HCC) is one of the cancers of highest incidence and mortality worldwide. The proliferation and invasion of tumor cells are the main reason for poor prognosis after HCC surgery. Long non-coding RNA (lncRNA) has been shown to play a key role in the progression of HCC. LncRNA-CR594175 is one of the highly expressed lncRNAs in HCC tumors and their metastatic tumors that we have obtained by the High-throughput screening method. METHODS: To elucidate the role of lncRNA-CR594175 in regulating the proliferation and invasion of human hepatoma cell line, HepG2, we operated through lncRNA-CR594175 silencing to inhibit the progression of HCC, either through in vitro or in vivo experiments. RESULTS: We found that lncRNA-CR594175 was lower in adjacent non-cancerous tissues than in primary HCC, and was lower in primary HCC than in its metastasis. Silencing of lncRNA-CR594175 inhibited the proliferation and invasion of HepG2 cells and growth of subcutaneous tumors. The results revealed that lncRNA-CR594175, as a RNA sponge, broke the negative regulation of hsa-miR-142-3p on Catenin, beta-1 (CTNNB1), and once lncRNA-CR594175 was silenced, the hsa-miR142-3p regained its negative regulation on CTNNB1 which can promote HCC progression by activating the wnt pathway. CONCLUSIONS: Our present study demonstrated for the first time that lncRNA-CR594175 silencing suppressed proliferation and invasion of HCC cells in vivo and in vitro by restoring the negative regulation of hsa-miR-142-3p on CTNNB1, laying a solid theoretical base for using lncRNA-CR594175 as genetic target therapy for HCC and offering a reasonable explanation for inactivation of miRNA in different tumors or in the tumor at different stages.	NA	Infect Agent Cancer. 2020 Sep 22;15:55. doi: 10.1186/s13027-020-00321-8. eCollection 2020.
4040	LncRNA	CRNDE	miR-4262	ZEB1	cervical cancer tumors and cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33469312	CRNDE Contributes Cervical Cancer Progression by Regulating miR-4262/ZEB1 Axis.	BACKGROUND: Cervical cancer is a lethal gynecologic cancer in women. Long non-coding RNA colorectal neoplasia differentially expressed (LncRNA CRNDE) was recognized as a significant oncogene in multiple cancers. However, the functional role of CRNDE in cervical cancer remains poorly explored. METHODS: The expression of CRNDE, microRNA-4262 (miR-4262) and zinc-finger E-box binding homeobox 1 (ZEB1) in cervical cancer tumors and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Colony formation and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) were performed to detect cell viability. Flow cytometry and caspase-3 activity assay were conducted to evaluate cell apoptosis. The interaction between miR-4262 and CRNDE or ZEB1 was verified by dual-luciferase reporter system. Transwell assay was employed to evaluate cell migration and invasion. The relative protein expression was assessed by Western blot. RESULTS: CRNDE and ZEB1 were up-regulated, while miR-4262 was down-regulated in cervical cancer tissues and cells. We found that CRNDE sponged miR-4262 and ZEB1 was a target of miR-4262. In addition, miR-4262 inhibitor abolished CRNDE silencing-induced repression on cell proliferation, EMT, migration, invasion and promotion on cell apoptosis. Furthermore, ZEB1 rescued the effects of miR-4262 overexpression or CRNDE deletion on cervical cancer progression. Our data showed that CRNDE targeted miR-4262 to regulate ZEB1 expression in cervical cancer cells. Besides, CRNDE expedited cervical cancer progression through wnt/β-catenin pathway via sponging miR-4262 and altering ZEB1 expression. CONCLUSION: Our findings demonstrated that CRNDE facilitated the progression of cervical cancer through activation of wnt/β-catenin pathway by regulating miR-4262/ZEB1 axis, representing a prospective targeted therapy for cervical cancer.	NA	Onco Targets Ther. 2021 Jan 13;14:355-366. doi: 10.2147/OTT.S263505. eCollection 2021.
4041	LncRNA	CTBP1-AS2	miR-370-3p	Wnt7a	U87-MG and LN229 cells	Glioma	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	33150795	lncRNA CTBP1-AS2 promotes proliferation and migration of glioma by modulating miR-370-3p-Wnt7a-mediated epithelial-mesenchymal transition.	Glioma is one of the most common and aggressive malignant primary brain tumors, with a poor 5-year survival rate. The long noncoding RNA (lncRNA) CTBP1-AS2 has been shown to be correlated with the prognosis of cancer, but the role of CTBP1-AS2 in glioma and its concrete mechanism is fully unknown. The clinical data and tissues of glioma patients were analyzed. Cell viability and migration assays were performed. Western blotting and qRT-PCR were adopted for investigation of target protein expressions. Double luciferase assay was used to investigate the interaction between different elements. The lncRNA CTBP1-AS2 had increased expression profiles in tumor tissues, which is associated with poor prognosis. In detail, CTBP1-AS2 knockdown decreased proliferation and migration phenotypes in both U87-MG and LN229 cells. Moreover, CTBP1-AS2 knockdown suppressed the key epithelial-mesenchymal transition (EMT) markers by downregulating Wnt7a-mediated signaling. Furthermore, miR-370-3p functioned as a link that could be absorbed by CTBP1-AS2, thus regulating Wnt7a expression. Lastly, the CTBP1-AS2-miR-370-3p-Wnt7a axis modulated EMT in glioma cells in vitro and in vivo. This study provides new insights that a novel lncRNA, CTBP1-AS2, regulates EMT of glioma by modulating the miR-370-3p-Wnt7a axis.	NA	Biochem Cell Biol. 2020 Dec;98(6):661-668. doi: 10.1139/bcb-2020-0065. Epub 2020 Nov 5.
4042	LncRNA	CTBP1-AS2	miR-139-3p	MMP11	GC cells	Gastric Cancer	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase report assay;RNA pull-down;	33204108	LncRNA CTBP1-AS2 Facilitates Gastric Cancer Progression via Regulating the miR-139-3p/MMP11 Axis.	BACKGROUND: This study aimed at probing into the effect of long non-coding RNA (lncRNA) C-terminal binding protein 1 antisense RNA 2 (CTBP1-AS2) on gastric cancer (GC) cell proliferation and apoptosis, and its regulatory function on miR-139-3p and MMP11. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to examine the expressions of CTBP1-AS2, miR-139-3p and MMP11 mRNA in GC cell lines and clinical specimens. Cell counting kit-8 (CCK-8) assay, flow cytometry and EdU assay were conducted to examine the effects of CTBP1-AS2 and miR-139-3p on GC cell proliferation and apoptosis. Western blot was applied for detecting the expressions of Bax, Bcl-2 and MMP11. A lung metastasis mouse model was used to evaluate metastasis of GC cells in vivo. Bioinformatics, dual-luciferase report assay, RIP and RNA pull-down assays were utilized to validate the targeted relationship between CTBP1-AS2 and miR-139-3p as well as the targeting relationship between miR-139-3p and MMP11. RESULTS: CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues. Meanwhile, CTBP1-AS2 promoted GC cell proliferation, metastasis and suppressed apoptosis, while miR-139-3p could weaken these effects. In addition, CTBP1-AS2 was identified as a molecular sponge for miR-139-3p, and MMP11 was verified as a target gene of CTBP1-AS2. CTBP1-AS2 could increase the expression of MMP11 via repressing miR-139-3p. CONCLUSION: CTBP1-AS2 promotes GC cells and inhibits apoptosis by regulating the miR-139-3p/MMP11 molecular axis.	NA	Onco Targets Ther. 2020 Nov 10;13:11537-11547. doi: 10.2147/OTT.S264394. eCollection 2020.
4043	LncRNA	CTBP1-AS2	miR-139-3p	MMP11	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase report assay;RNA pull-down;	33204108	LncRNA CTBP1-AS2 Facilitates Gastric Cancer Progression via Regulating the miR-139-3p/MMP11 Axis.	BACKGROUND: This study aimed at probing into the effect of long non-coding RNA (lncRNA) C-terminal binding protein 1 antisense RNA 2 (CTBP1-AS2) on gastric cancer (GC) cell proliferation and apoptosis, and its regulatory function on miR-139-3p and MMP11. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to examine the expressions of CTBP1-AS2, miR-139-3p and MMP11 mRNA in GC cell lines and clinical specimens. Cell counting kit-8 (CCK-8) assay, flow cytometry and EdU assay were conducted to examine the effects of CTBP1-AS2 and miR-139-3p on GC cell proliferation and apoptosis. Western blot was applied for detecting the expressions of Bax, Bcl-2 and MMP11. A lung metastasis mouse model was used to evaluate metastasis of GC cells in vivo. Bioinformatics, dual-luciferase report assay, RIP and RNA pull-down assays were utilized to validate the targeted relationship between CTBP1-AS2 and miR-139-3p as well as the targeting relationship between miR-139-3p and MMP11. RESULTS: CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues. Meanwhile, CTBP1-AS2 promoted GC cell proliferation, metastasis and suppressed apoptosis, while miR-139-3p could weaken these effects. In addition, CTBP1-AS2 was identified as a molecular sponge for miR-139-3p, and MMP11 was verified as a target gene of CTBP1-AS2. CTBP1-AS2 could increase the expression of MMP11 via repressing miR-139-3p. CONCLUSION: CTBP1-AS2 promotes GC cells and inhibits apoptosis by regulating the miR-139-3p/MMP11 molecular axis.	NA	Onco Targets Ther. 2020 Nov 10;13:11537-11547. doi: 10.2147/OTT.S264394. eCollection 2020.
4044	LncRNA	CTBP1-AS2	miR-195-5p	CEP55	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	32988587	SP1-induced upregulation of lncRNA CTBP1-AS2 accelerates the hepatocellular carcinoma tumorigenesis through targeting CEP55 via sponging miR-195-5p.	As reported in many research, LncRNA CTBP1 divergent transcript (CTBP1-AS2) remarkably affects the progression of several tumors. However, the precise role and function of CTBP1-AS2 in hepatocellular carcinoma (HCC) remained unknown. We found that CTBP1-AS2 expressions were increased in HCC samples and cells. After treatment with microwave ablation (MWA), CTBP1-AS2 was distinctly up-regulated in residual HCC tissues compared with HCC samples. CTBP1-AS2 was upregulated under the induction of the nuclear transcription factor SP1. As revealed by the clinical assays, high CTBP1-AS2 expression usually related to lymph node metastasis, clinical stage and weaker prognosis specific to HCC patients. Functionally, CTBP1-AS2 knockdown suppressed HCC cells in terms of the proliferation, migration, invasion, chemotherapy resistance as well as EMT progress, but promoted apoptosis. Mechanistically, CTBP1-AS2 was a sponge of miR-195-5p for elevating CEP55 expression, a target of miR-195-5p, and thereby exhibited its oncogenic roles in HCC progression. Overall, an emerging regulatory mechanism of SP1/CTBP1-AS2/miR-195-5p/CEP55 axis was reported in the paper, which possibly served as a new therapeutic HCC treatment target.	NA	Biochem Biophys Res Commun. 2020 Dec 17;533(4):779-785. doi: 10.1016/j.bbrc.2020.09.080. Epub 2020 Sep 26.
4045	Circular RNA	CUL2	miR-142-3p	ROCK2	GC cells	Gastric Cancer	Homo sapiens (human)	FISH;microarray;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;FISH;luciferase assay;RNA immunoprecipitation;RNA pull-down;	33153478	circCUL2 regulates gastric cancer malignant transformation and cisplatin resistance by modulating autophagy activation via miR-142-3p/ROCK2.	BACKGROUND: Circular RNAs (circRNAs) are a class of noncoding RNAs (ncRNAs) and can modulate gene expression by binding to miRNAs; further, circRNAs have been shown to participate in several pathological processes. However, the expression and biological function of circCUL2 in gastric cancer (GC) remains largely unknown. METHODS: circRNA microarrays and quantitative real-time PCR (qRT-PCR) were used to identify differentially expressed circRNAs in GC tissues and cell lines. circCUL2 knockdown and overexpression were performed to indicate the functional role of circCUL2 in vitro and in vivo. The expression and regulation of circCUL2, miR-142-3p and ROCK2 were evaluated using fluorescence in situ hybridization (FISH), dual-luciferase assays, RNA pull-down assays, RNA immunoprecipitation (RIP) and rescue experiments. Furthermore, the regulation of cisplatin sensitivity and autophagy by circCUL2/miR-142-3p/ROCK2 was demonstrated by cellular apoptosis assays, western blot, immunofluorescence and transmission electron microscopy analyses. RESULTS: The level of circCUL2, which is stable and cytoplasmically localized, was significantly reduced in GC tissues and cells. Overexpressed circCUL2 inhibited malignant transformation in vitro and tumorigenicity in vivo. In the AGS and SGC-7901 cell lines, circCUL2 sponged miR-142-3p to regulate ROCK2, thus modulating tumor progression. Furthermore, in the AGS/DDP and SGC-7901/DDP cell lines, circCUL2 regulated cisplatin sensitivity through miR-142-3p/ROCK2-mediated autophagy activation. CONCLUSION: circCUL2 may function as a tumor suppressor and regulator of cisplatin sensitivity through miR-142-3p/ROCK2-mediated autophagy activation, which could be a key mechanism and therapeutic target for GC.	NA	Mol Cancer. 2020 Nov 5;19(1):156. doi: 10.1186/s12943-020-01270-x.
4046	LncRNA	CYTOR	miR-125b-5p	KIAA1522	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Immunohistochemistry;	33318318	LncRNA CYTOR affects the proliferation, cell cycle and apoptosis of hepatocellular carcinoma cells by regulating the miR-125b-5p/KIAA1522 axis.	We aimed to investigate whether lncRNA CYTOR could sponge miR-125b-5p to affect hepatocellular carcinoma (HCC) cells through targeting KIAA1522. The expression of CYTOR, miR-125b-5p and KIAA1522 in HCC cells was detected by Real-time quantitative polymerase chain reaction (RT-qPCR) analysis. KIAA1522 expression in HCC tissues was detected by immunohistochemistry. The proliferation, cell cycle and apoptosis of HCC cells after transfection were respectively detected by Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis, and related protein expression was determined by Western blot analysis. As a result, The Cancer Genome Atlas (TCGA) database indicated that expression of CYTOR and KIAA1522 was increased in HCC tissues and high expression of CYTOR and KIAA1522 was related to worse overall survival. MiR-125b-5p expression was decreased in HCC tissues, which was negatively correlated with the expression of CYTOR and KIAA1522. The proliferation and cell cycle of HCC cells were suppressed by CYTOR interference while promoted by miR-125b-5p interference and KIAA1522 overexpression. The apoptosis of HCC cells was promoted by CYTOR interference while inhibited by miR-125b-5p interference and KIAA1522 overexpression. In conclusion, CYTOR interference suppressed the proliferation and cell cycle, and promoted the apoptosis of HCC cells by regulating the miR-125b-5p/KIAA1522 axis.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2626-2639. doi: 10.18632/aging.202306. Epub 2020 Dec 9.
4047	LncRNA	Dancr	miR-6324	NA	H9C2 cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33300079	Overexpression of lncRNA Dancr inhibits apoptosis and enhances autophagy to protect cardiomyocytes from endoplasmic reticulum stress injury via sponging microRNA-6324.	Endoplasmic reticulum stress (ERS) contributes to the pathogenesis of myocardial ischemia/reperfusion injury and myocardial infarction (MI). Long non-coding RNAs (lncRNAs) serve an important role in cardiovascular diseases, and lncRNA discrimination antagonizing non-protein coding RNA (Dancr) alleviates cardiomyocyte damage. microRNA (miR)-6324 was upregulated in MI model rats and was predicted to bind to Dancr. The present study aimed to investigate the role of Dancr in ERS-induced cardiomyocytes and the potential underlying mechanisms. Tunicamycin (Tm) was used to induce ERS. Cell viability, apoptosis and levels of associated proteins, ERS and autophagy in Dancr-overexpression H9C2 cells and miR-6234 mimic-transfected H9C2 cells were assessed using Cell Counting Kit-8, TUNEL staining and western blot assay, respectively. The results suggested that Dancr expression levels and cell viability were downregulated by Tm in a concentration-dependent manner compared with the control group. Tm induced apoptosis, ERS and autophagy, as indicated by an increased ratio of apoptotic cells, increased expression levels of Bax, cleaved (c)-caspase-3/9, glucose-regulated protein 78 kDa (GRP78), phosphorylated (p)-inositol-requiring enzyme-1α (IRE1α), spliced X-box-binding protein 1 (Xbp1s), IRE1α, activating transcription factor (ATF)6, ATF4, Beclin 1 and microtubule associated protein 1 light chain 3α (LC3)II/I, and decreased expression levels of Bcl-2, unspliced Xbp1 (Xbp1u) and p62 in the Tm group compared with the control group. Moreover, the results indicated that compared with the Tm + overexpression (Oe)-negative control (NC) group, the Tm + Oe-Dancr group displayed decreased apoptosis, but enhanced ERS and autophagy to restore cellular homeostasis. Compared with the Tm + Oe-NC group, the Tm + Oe-Dancr group decreased the ratio of apoptotic cells, decreased expression levels of Bax, c-caspase-3/9 and Xbp1u, and increased expression levels of Bcl-2, p-IRE1α, Xbp1s, Beclin 1 and LC3II/I. Dancr overexpression also significantly downregulated miR-6324 expression compared with Oe-NC. The dual-luciferase reporter assay further indicated an interaction between Dancr and miR-6324. In addition, miR-6324 mimic partially reversed the effects of Dancr overexpression on Tm-induced apoptosis, ERS and autophagy. In conclusion, lncRNA Dancr overexpression protected cardiomyocytes against ERS injury via sponging miR-6324, thus inhibiting apoptosis, enhancing autophagy and restoring ER homeostasis.	NA	Mol Med Rep. 2021 Feb;23(2):116. doi: 10.3892/mmr.2020.11755. Epub 2020 Dec 10.
4048	LncRNA	DANCR	miR-874-3p	SOX2	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;	33058834	LncRNA DANCR upregulation induced by TUFT1 promotes malignant progression in triple negative breast cancer via miR-874-3p-SOX2 axis.	Triple negative breast cancer (TNBC) is a subtype of breast cancer with poorest survival outcome and is prone to metastasis. TUFT1 and the long non-coding RNA (lncRNA), DANCR, play vital roles in metastasis and progression of various cancers. However, the correlation between TUFT1 and DANCR in TNBC and their downstream molecular mechanisms are still undetermined. We demonstrated that upregulation of TUFT1 in TNBC was related to a worse survival in TNBC patients. The TNBC cells invasiveness was augmented by TUFT1 in a dose-dependent manner, while inhibiting TUFT1 repressed the invasiveness. Particularly, the expression of TUFT1 was positively correlated with the expression of DANCR in TNBC tissues. In addition, TUFT1 increased DANCR expression, while silencing DANCR ameliorated the invasiveness of TNBC cells induced by TUFT1. As demonstrated, TUFT1 interacted with miR-874-3p. Subsequently, qRT-PCR together with luciferase reporter further demonstrated that DANCR acted as competing endogenous (ceRNA) for miR-874-3p, thereby regulating the de-repression of SOX2 and advancing epithelial-mesenchymal transition (EMT) in TNBC. The present research shows that TUFT1 promotes the malignant development in TNBC via enhancing the expression of DANCR. The upregulation of DANCR may contribute to the progression and tumor invasiveness of TNBC, considering that DANCR functions as a miR-874-3p sponge, thus modulating SOX2 positively. Collectively, the present study explored the molecular mechanism underlying TUFT1 in TNBC, raising a TUFT1-mediated therapy for the treatment of patients with TNBC.	NA	Exp Cell Res. 2020 Nov 15;396(2):112331. doi: 10.1016/j.yexcr.2020.112331. Epub 2020 Oct 13.
4049	LncRNA	DANCR	miR-222-3p	ATG7	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RACE;Western blot;	32964966	LncRNA DANCR promotes ATG7 expression to accelerate hepatocellular carcinoma cell proliferation and autophagy by sponging miR-222-3p.	OBJECTIVE: LncRNA differentiation antagonizing non-protein coding RNA (DANCR) is an oncogene in various malignant cancers, including hepatocellular carcinoma (HCC). Autophagy is an intracellular self-digestion mechanism that accelerates the progression of HCC via promoting cell survival. However, the role of lncRNA DANCR in HCC, and the mechanism of lncRNA DANCR in the regulation of autophagy in HCC remains unknown. Therefore, the aims of this study are the investigation of the role of lncRNA DANCR in HCC, and the exploration of the molecular mechanism of lncRNA DANCR in regulating autophagy of HCC cells. PATIENTS AND METHODS: In this study, the expression of lncRNA DANCR, miR-222-3p, and autophagy-related gene 7 (ATG7) was detected by qRT-PCR. The cell proliferation and colony formation were measured by Cell Counting Kit-8 (CCK-8) assay and colony formation assay. And the autophagic flux was evaluated by mRFP-GFP-LC3B reporter. The autophagy related proteins were analyzed by Western blotting. Besides, the relationship between lncRNA DANCR and miR-222-3p, as well as between miR-222-3p and ATG7, was determined by Dual-Luciferase reporter system. RESULTS: We found high expression of lncRNA DANCR and ATG7, and low expression of miR-222-3p in HCC tissues and cell lines. And lncRNA DANCR positively correlated with poor survival of HCC patients. Moreover, the knockdown of lncRNA DANCR inhibited cell proliferation and autophagy of HCC cells. And we predicted and proved that lncRNA DANCR induced cell proliferation, colony formation and autophagy by increasing ATG7 and suppressing miR-222-3p. CONCLUSIONS: Our study demonstrates the promoting role of lncRNA DANCR in HCC, and indicates the regulatory effects of lncRNA DANCR on regulating autophagy of HCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8778-8787. doi: 10.26355/eurrev_202009_22816.
4050	LncRNA	DARS-AS1	miR-188-5p	HMGB1	SiHa and HeLa cells	Cervical Cancer	Homo sapiens (human)	Flow Cytometry assay;Luciferase reporter assay;	33176595	DARS-AS1 Knockdown Inhibits the Growth of Cervical Cancer Cells via Downregulating HMGB1 via Sponging miR-188-5p.	BACKGROUND: Evidence has been shown that long noncoding RNAs (lncRNAs) play an important role in the development of cervical cancer. Recently, lncRNA DARS-AS1 was shown to be dysregulated in several cancer types, but the role of DARS-AS1 in cervical cancer remains unclear. METHODS: Immunofluorescence staining, flow cytometry and transwell invasion assays were used to determine proliferation, apoptosis and invasion in cervical cancer cells, respectively. The dual luciferase reporter system assay was performed to assess the interaction between DARS-AS1, miR-188-5p, and high mobility group box 1 (HMGB1) in cervical cancer cells. RESULTS: Downregulation of DARS-AS1 markedly inhibited the proliferation and invasion of cervical cancer cells. Moreover, DARS-AS1 knockdown obviously induced the apoptosis of SiHa and HeLa cells. Meanwhile, luciferase reporter assay identified that miR-188-5p was the potential miRNA binding of DARS-AS1, and HMGB1 was the potential binding target of miR-188-5p. Mechanistic analysis indicated that downregulation of DARS-AS1 decreased the expression of HMGB1 by acting as a competitive "sponge" of miR-188-5p. CONCLUSION: In this study, we found that DARS-AS1 knockdown suppressed the growth of cervical cancer cells via downregulating HMGB1 via sponging miR-188-5p. Therefore, DARS-AS1 might serve as a potential target for the treatment of cervical cancer.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820971669. doi: 10.1177/1533033820971669.
4051	LncRNA	DARS-AS1	miR-628-5p	JAG1	CC cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33292218	DARS-AS1 accelerates the proliferation of cervical cancer cells via miR-628-5p/JAG1 axis to activate Notch pathway.	BACKGROUND: Growing evidence has indicated the vital parts of long non-coding RNAs (lncRNAs) in modulating the progression of assorted human cancers, including cervical cancer (CC). Nevertheless, the role and mechanism of aspartyl-tRNA synthetase antisense RNA 1 (DARS-AS1) have been not comprehensively illustrated in CC yet. METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) was exploited for assessing RNA expression while western blot for protein expression in CC cells. The cell counting kit-8 (CCK-8), colony formation and TdT-mediated dUTP Nick-End Labeling (TUNEL) assays, as well as flow cytometry analysis, were employed to evaluate the modulation of DARS-AS1 on the proliferation and apoptosis of CC cells. In addition, RNA immunoprecipitation (RIP), RNA pull down assay and luciferase reporter assay confirmed the interactivity among DARS-AS1, miR-628-5p and jagged canonical Notch ligand 1 (JAG1). RBP-JK luciferase reporter assay determined the activity of Notch pathway. RESULTS: DARS-AS1 level was significantly increased in CC cells. Moreover, down-regulation of DARS-AS1 hampered cell the proliferation and accelerated the apoptosis of CC cells. Importantly, DARS-AS1 was a competing endogenous RNA (ceRNA) to elevate JAG1 level through sequestering miR-628-5p, leading to activated Notch pathway to aggravate CC tumorigenesis. CONCLUSIONS: DARS-AS1/miR-628-5p/JAG1/Notch signaling accelerates CC progression, indicating DARS-AS1 as a novel therapeutic target for patients with CC.	NA	Cancer Cell Int. 2020 Nov 3;20(1):535. doi: 10.1186/s12935-020-01592-2.
4052	LncRNA	DCST1-AS1	miR-21	PLAP-1	periodontal ligament cells	Periodontitis	Homo sapiens (human)	CCK-8 assay;qPCR;Western blot;	33533513	LncRNA DCST1-AS1 inhibits PDLCs' proliferation in periodontitis and may bind with miR-21 precursor to upregulate PLAP-1.	OBJECTIVE: This study aimed to investigate the potential interactions among long noncoding RNA domain containing 1-antisense (lncRNA DCST1-AS1), miR-21, and periodontal ligament-associated protein-1 (PLAP-1) in periodontitis. BACKGROUND DATA DISCUSSING THE PRESENT STATE OF THE FIELD: It has been verified that miR-21 can target PLAP-1 to regulate the osteogenic differentiation of periodontal ligament cells (PDLCs). METHODS: Differential expression of DCST1-AS1 and miR-21 in PDLCs derived from periodontitis patients and healthy controls was determined by qPCR and unpaired t test. QPCR and Western blots were conducted to evaluate the effects of overexpression of DCST1-AS1 and miR-21 on the expression of PLAP-1. CCK-8 assay was applied to evaluate the effect of DCST1-ASI, miR-21, or PLAP-1 on PDLCs' proliferation. Western blotting was conducted to detect the expression levels of CKD family (CDK4, CDK6, and CCND1). RESULTS: DCST1-AS1 was downregulated in PDLCs derived from periodontitis patients, and its expression was inversely correlated with the expression of miR-2 but positively correlated with PLAP-1. Bioinformatics analysis showed that DCST1-AS1 might bind with miR-21 precursor but not mature miR-21. Transfection experiments showed that overexpression of DCST1-AS1 led to decreased expression levels of miR-21 and significantly increased the expression levels of PLAP-1 at both mRNA and protein levels, while overexpression of miR-21 resulted in a dramatic lower level of PLAP-1. CCK-8 assay indicated that overexpression of DCST1-AS1 or PLAP-1 prohibited PDLCs' proliferation. However, elevation of miR-21 had a contrary effect on the proliferation of PDLCs. And increased expression levels of DCST1-AS1 could significantly inhibit the expression of CDK4, CDK6, and CCND-1, while overexpression of miR-21 inversed the effects of DCST1-AS1. CONCLUSION: Therefore, the expression levels of DCST1-AS1 are much lower in periodontitis patients compared to that in healthy controls, and overexpression of DCST1-AS1 can significantly elevate the expression of PLAP-1 by inhibiting miR-21 in PDLCs.	NA	J Periodontal Res. 2021 Apr;56(2):256-264. doi: 10.1111/jre.12809. Epub 2021 Feb 3.
4053	LncRNA	DCST1-AS1	miR-874-3p	NA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33025624	Inhibition of lncRNA DCST1-AS1 suppresses proliferation, migration and invasion of cervical cancer cells by increasing miR-874-3p expression.	BACKGROUND: Cervical cancer seriously threatens both the health and life of women. We aimed to investigate whether RNA interference of long non-coding RNA (lncRNA) DCST1-AS1 could promote miR-874-3p expression to affect the proliferation, migration and invasion of cervical cancer cells. METHODS: DCST1-AS1 expression levels in cervical cancer cells and transfection effects were detected by quantitative reverse transcriptase-polymerase chain reaction analysis. Proliferation, invasion and migration of cells were separately shown by cell-counting kit-8, wound healing and transwell assays, and relative protein expression was determined by western blot analysis. Dual-luciferase reporter and RNA immunoprecipitation assays verified the interaction of DCST1-AS1 and miR-874-3p. RESULTS: DCST1-AS1 expression was increased in cervical cancer tissues and cells. The DCST1-AS1 expression in Hela and SiHa cells was the highest, and so the cells were selected for the next experiment. Inhibition of DCST1-AS1 suppressed the proliferation, invasion and migration of cervical cancer cells and decreased the expression of KI67, proliferating cell nuclear antigen, matrix metalloproteinase (MMP)-2 and MMP-9. miR-874-3p expression was increased when cells were transfected with miR-874-3p mimic or shRNA-DCST1-AS1-1, and DCST1-AS1 expression was down-regulated when cells were transfected with miR-874-3p mimic. DCST1-AS1 can directly target miR-874-3p. Furthermore, inhibition of miR-874-3p could effectively alleviate the effect of inhibition of DCST1-AS1 with respect to the proliferation, invasion and migration of cervical cancer cells. CONCLUSIONS: Inhibition of DCST1-AS1 suppressed the proliferation, migration and invasion of cervical cancer cells by increasing miR-874-3p expression, which could be alleviated by the inhibition of miR-874-3p.	NA	J Gene Med. 2021 Jan;23(1):e3281. doi: 10.1002/jgm.3281. Epub 2020 Nov 20.
4054	LncRNA	DDX11-AS1	miR-195-5p	MACC1	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	32961346	LncRNA DDX11-AS1 accelerates hepatocellular carcinoma progression via the miR-195-5p/MACC1 pathway.	INTRODUCTION AND AIM: Long non-coding RNA (lncRNA) has been shown to be a vital regulator of cancer progression, including hepatocellular carcinoma (HCC). However, the role of DEAD/H box protein 11 antisense RNA 1 (DDX11-AS1) in HCC remains to be further studied. MATERIAL AND METHODS: The expression levels of DDX11-AS1, miR-195-5p and metastasis-associated in colon cancer-1 (MACC1) were determined by quantitative real-time PCR (qRT-PCR). Cell counting kit-8 (CCK-8), transwell and apoptosis determination assays were used to evaluate cell proliferation, migration, invasion and apoptosis, respectively. Mice xenograft models were constructed to verify the effect of DDX11-AS1 on HCC tumor growth in vivo. Furthermore, lactate production, glucose consumption, ATP level and glucose uptake were detected to assess cell glucose metabolism. The interactions among DDX11-AS1, miR-195-5p and MACC1 were verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Moreover, western blot (WB) analysis was performed to evaluate the protein levels. RESULTS: DDX11-AS1 was upregulated in HCC tissues and cells, and its silencing could inhibit HCC cell proliferation, migration, invasion and glucose metabolism, and promote apoptosis in vitro. Also, DDX11-AS1 knockdown reduced HCC tumor growth in vivo. Besides, DDX11-AS1 could interact with miR-195-5p, and miR-195-5p inhibitor reversed the inhibitory effect of silenced DDX11-AS1 on HCC cell progression. In addition, MACC1 was a target of miR-195-5p, and its overexpression reversed the suppression effect of miR-195-5p on HCC cell progression. CONCLUSION: Our data revealed that DDX11-AS1 could act as an oncogenic regulator in HCC, providing a potential therapeutic target for HCC treatment.	NA	Ann Hepatol. 2021 Jan-Feb;20:100258. doi: 10.1016/j.aohep.2020.09.003. Epub 2020 Sep 19.
4055	LncRNA	DGCR5	miR-218-5p	NA	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33155263	LncRNA DGCR5 promotes non-small cell lung cancer progression via sponging miR-218-5p.	Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "LncRNA DGCR5 promotes non-small cell lung cancer progression via sponging miR-218-5p, by J. Wang, H.-Z. Shu, C.-Y. Xu, S.-G. Guo, published in Eur Rev Med Pharmacol Sci 2019; 23 (22): 9947-9954-DOI: 10.26355/eurrev_201911_19561-PMID: 31799664" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19561.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10303. doi: 10.26355/eurrev_202010_23355.
4056	LncRNA	DLEU1	miR-429	TFAP2A	OC cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33170430	Silencing of lncRNA DLEU1 inhibits tumorigenesis of ovarian cancer via regulating miR-429/TFAP2A axis.	Long non-coding RNAs (lncRNAs) are known as crucial regulators in the development of OC. In the current study, we aim to explore the function and molecular mechanism of lncRNA DLEU1 in OC. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to determine the expression of DLEU1, miR-429, and TFAP2A in OC cells and tissues. The relationship among DLEU1, miR-429, and TFAP2A was tested by dual-luciferase reporter (DLR) assay. Besides, the proliferative, migratory and invasive abilities of OC cells were analyzed by MTT, wound healing, and transwell assays, respectively. Western blot was performed to determine the protein expression of TFAP2A. The expression of lncRNA DLEU1 and TFAP2A were upregulated, and miR-429 was downregulated in OC tissues. Silencing of DLEU1 inhibited the proliferation, migration, and invasion of OC cells. Bioinformation and DLR assay showed that DLEU1 acted as the sponge for miR-429. Moreover, miR-429 could directly target TFAP2A and inhibit the proliferation, migration, and invasion of OC cells. Moreover, we observed a negative correlation between miR-429 and DLEU1, and between miR-429 and TFAP2A in OC tissues. The transfection of miR-429 inhibitor or pcDNA-TFAP2A reversed the inhibitory effects of si-DLEU1 on the proliferation, migration, and invasion of OC cells. Silencing of DLEU1 inhibited the proliferation, migration, and invasion of OC cells by regulating miR-429/TFAP2A axis, indicating a potential therapeutic target for OC.	NA	Mol Cell Biochem. 2021 Feb;476(2):1051-1061. doi: 10.1007/s11010-020-03971-9. Epub 2020 Nov 10.
4057	LncRNA	DLEU1	miR-133a-3p	SRPK1	CCI rats	Chronic Constrictive Injury 	Rattus (rat)	ELISA;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;Rescue assay;	33167866	Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.	BACKGROUND: Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. METHODS: We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and IL-1β. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. RESULTS: Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1β and TNF-α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. CONCLUSION: DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.	NA	Mol Med. 2020 Nov 10;26(1):104. doi: 10.1186/s10020-020-00235-6.
4058	LncRNA	DLG1-AS1	miR-497	YAP1	PTC cells	Papillary Thyroid Cancer	Mus musculus (mouse)	qRT-PCR	33197895	The DLG1-AS1/miR-497/YAP1 axis regulates papillary thyroid cancer progression.	The long non-coding RNA (lncRNA), DLG1-AS1, is upregulated in papillary thyroid cancer (PTC) tissues and cell lines. Here, we found that increased expression of DLG1-AS1 caused lymph node metastasis and advanced tumor-node-metastasis (TNM) stage. DLG1-AS1 knockdown inhibited proliferation, invasion, and migration of PTC cells, and impaired tumorigenesis in vivo in mouse xenografts. DLG1-AS1 functions as a competing endogenous RNA (ceRNA) for miR-497. Further investigation revealed that DLG1-AS1 regulated yes-associated protein 1 (YAP1; a known target of miR-497) by competitively binding to miR-497. Moreover, inhibition of miR-497 abrogated the inhibitory effects of DLG1-AS1 depletion on PTC cells. These findings demonstrate that the DLG1-AS1-miR-497-YAP1 axis promotes the growth and metastasis of PTC by forming a ceRNA network.	NA	Aging (Albany NY). 2020 Nov 16;12(22):23326-23336. doi: 10.18632/aging.104121. Epub 2020 Nov 16.
4059	LncRNA	DLEU1	miR-133a-3p	SRPK1	CCI rats	Chronic Constrictive Injury 	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;Rescue assay;	33167866	Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.	BACKGROUND: Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. METHODS: We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and IL-1β. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. RESULTS: Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1β and TNF-α in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. CONCLUSION: DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.	NA	Mol Med. 2020 Nov 10;26(1):104. doi: 10.1186/s10020-020-00235-6.
4060	LncRNA	DLG1-AS1	miR-497	YAP1	PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	qRT-PCR	33197895	The DLG1-AS1/miR-497/YAP1 axis regulates papillary thyroid cancer progression.	The long non-coding RNA (lncRNA), DLG1-AS1, is upregulated in papillary thyroid cancer (PTC) tissues and cell lines. Here, we found that increased expression of DLG1-AS1 caused lymph node metastasis and advanced tumor-node-metastasis (TNM) stage. DLG1-AS1 knockdown inhibited proliferation, invasion, and migration of PTC cells, and impaired tumorigenesis in vivo in mouse xenografts. DLG1-AS1 functions as a competing endogenous RNA (ceRNA) for miR-497. Further investigation revealed that DLG1-AS1 regulated yes-associated protein 1 (YAP1; a known target of miR-497) by competitively binding to miR-497. Moreover, inhibition of miR-497 abrogated the inhibitory effects of DLG1-AS1 depletion on PTC cells. These findings demonstrate that the DLG1-AS1-miR-497-YAP1 axis promotes the growth and metastasis of PTC by forming a ceRNA network.	NA	Aging (Albany NY). 2020 Nov 16;12(22):23326-23336. doi: 10.18632/aging.104121. Epub 2020 Nov 16.
4061	LncRNA	DLX6-AS1	miR-497-5p	SNCG	PCa tissues and cells	Prostate Cancer	Homo sapiens (human)	Rescue assay;	33035382	DLX6-AS1 accelerates cell proliferation through regulating miR-497-5p/SNCG pathway in prostate cancer.	Prostate cancer (PCa) has become the second leading cause of cancer-related mortality in males worldwide. Although the long noncoding RNA DLX6-AS1 has been recognized to be an oncogene in multiple cancers, the biological function and regulatory mechanism of DLX6-AS1 in prostate cancer are still obscure. In the present study, we observed that DLX6-AS1 was significantly upregulated in PCa tissues and cells. Knockdown of DLX6-AS1 inhibited PCa progression by suppressing cell proliferation and accelerating cell apoptosis. Molecular mechanism exploration indicated that DLX6-AS1 acted as a sponge for miR-497-5p and synuclein gamma (SNCG) was a downstream target gene of miR-497-5p. In addition, there was a negative correlation between DLX6-AS1 and miR-497-5p in PCa tissues. Rescue assays showed that SNCG overexpression could partially recover DLX6-AS1 knockdown-mediated inhibition of progression in PCa. Furthermore, xenograft tumor model was established to determine the role of DLX6-AS1 in PCa tumor growth and the results suggested that DLX6-AS1 could facilitate tumor growth by regulating SNCG in vivo. In conclusion, our study investigated the biological function and underlying mechanism of DLX6-AS1 in PCa and validated that DLX6-AS1 functioned as an oncogene through miR-497-5p/SNCG axis.	NA	Environ Toxicol. 2021 Mar;36(3):308-319. doi: 10.1002/tox.23036. Epub 2020 Oct 9.
4062	LncRNA	DLX6-AS1	miR-513c	Cul4A	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33277615	Upregulated lncRNA DLX6-AS1 underpins hepatocellular carcinoma progression via the miR-513c/Cul4A/ANXA10 axis.	Recent studies have illustrated the role of aberrant regulatory interactions in the mediation of malignant phenotypes of cancer cells, which could potentially provide novel therapeutic targets to limit the destructive recurrence and metastasis of hepatocellular carcinoma (HCC). Herein, we clarify the oncogenic role of the long noncoding RNA (lncRNA) distal-less homeobox 6 antisense 1 (DLX6-AS1) in HCC in vivo and in vitro. To this end, we knocked down lncRNA DLX6-AS1 and manipulated the expression of miR-513c to characterize their effects in HCC cell viability, migration, invasion, and apoptosis. Furthermore, we probed the interactions with miR-513c's target gene Cullin4A (Cul4A) and the degradation of Annexin A10 (ANXA10) protein. Our data show that lncRNA DLX6-AS1 and Cul4A were highly expressed, while miR-513c and ANXA10 were poorly expressed in HCC tissues and cells. Moreover, the silencing of lncRNA DLX6-AS1 impeded the viability, invasion, and migration of HCC cells, while stimulating cell apoptosis. Further data indicated that lncRNA DLX6-AS1 targeted and repressed miR-513c expression, where the tumor-inhibiting effects of lncRNA DLX6-AS1 silencing was achieved by elevating miR-513c expression. Importantly, the lncRNA DLX6-AS1 upregulated the expression of Cul4A through sponging of miR-513c. The silencing of Cul4A restricted the malignant phenotypes of HCC cells by repressing the ubiquitination-mediated degradation of ANXA10. In vivo experiments verified that lncRNA DLX6-AS1 promoted the progression of HCC through the miR-513c/Cul4A/ANXA10 axis. Thus, the silencing of lncRNA DLX6-AS1 impaired miR-513c-dependent Cul4A inhibition and subsequently elevated ubiquitination-mediated degradation of ANXA10, thereby preventing the occurrence and development of HCC.	NA	Cancer Gene Ther. 2021 May;28(5):486-501. doi: 10.1038/s41417-020-00233-0. Epub 2020 Dec 4.
4063	LncRNA	DLX6-AS1	miR-513c-5p	PLK4	NB tissues and cells	Neuroblastoma	Homo sapiens (human)	qRT-PCR	33031637	Silencing of long non-coding RNA DLX6-AS1 weakens neuroblastoma progression by the miR-513c-5p/PLK4 axis.	Emerging evidence has demonstrated the crucial roles of long noncoding RNAs in human cancers, including neuroblastoma (NB). DLX6 antisense RNA 1 (DLX6-AS1) has been identified as an oncogenic driver in NB. However, the mechanisms of DLX6-AS1 in NB progression are not fully understood. Our data showed that DLX6-AS1 was significantly overexpressed in NB tissues and cells. Moreover, DLX6-AS1 silencing repressed NB cell viability, colony formation, migration, and invasion, and promoted cell cycle arrest and apoptosis in vitro, as well as decreased tumor growth in vivo. Mechanistically, DLX6-AS1 operated as a miR-513c-5p sponge. MiR-513c-5p mediated the regulation of DLX6-AS1 on NB cell malignant progression in vitro. PLK4 was a target of miR-513c-5p- and DLX6-AS1-controlled PLK4 expression via sponging miR-513c-5p. Furthermore, the suppressive effect of miR-513c-5p overexpression on NB cell malignant progression in vitro was reversed by PLK4 upregulation. Our findings identified a novel regulatory mechanism, the DLX6-AS1/miR-513c-5p/PLK4 axis, in NB progression, highlighting a strong rationale for developing DLX6-AS1 as a new target for NB management.	NA	IUBMB Life. 2020 Dec;72(12):2627-2636. doi: 10.1002/iub.2392. Epub 2020 Oct 8.
4064	LncRNA	DNAH17-AS1	miR-877-5p	CCNA2	H1299 and 95D cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	32981678	Long noncoding RNA DNAH17-AS1 promotes tumorigenesis and metastasis of non-small cell lung cancer via regulating miR-877-5p/CCNA2 pathway.	A growing number of studies have revealed that long noncoding RNAs (lncRNAs) can function as important oncogenes or tumor suppressors. This study aimed to investigate the regulatory role of lncRNA DNAH17 antisense RNA 1 (DNAH17-AS1) on non-small cell lung cancer (NSCLC) and the underlying molecular mechanisms. We observed that the expression of DNAH17-AS1 and CCNA2 mRNA was distinctly upregulated in NSCLC specimens and cell lines, while miR-877-5p expression was significantly decreased. DNAH17-AS1 could be used to distinguish NSCLC specimens from adjacent non-tumor tissues. Clinical assays revealed that high DNAH17-AS1 was associated with TNM stage, distant metastasis and shorter overall survival and disease-free survival. Functional assays indicated that knockdown of DNAH17-AS1 suppressed the proliferation, migration and invasion of H1299 and 95D cells, and promoted apoptosis. Mechanically, DNAH17-AS1 served as competing endogenous RNA (ceRNA) for miR-877-5p to positively recover CCNA2. Overall, we identified a novel NSCLC-related lncRNA, DNAH17-AS1 which may exert an oncogenic function via serving as a sponge for miR-877-5p to upregulate CCNA2. Our study presents novel insights into NSCLC progression and provided a prospective therapeutic target for NSCLC.	NA	Biochem Biophys Res Commun. 2020 Dec 10;533(3):565-572. doi: 10.1016/j.bbrc.2020.09.047. Epub 2020 Sep 25.
4065	LncRNA	DSCAM-AS1	miR-186-5p	GPRC5A	OS cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	32865178	DSCAM-AS1 accelerates cell proliferation and migration in osteosarcoma through miR-186-5p/GPRC5A signaling.	Osteosarcoma (OS) is one of the most primary bone malignancies, often occurring in adolescents or children. Numerous scientific findings have introduced that long noncoding RNAs (lncRNAs) can be involved in tumor occurrence and development. Although DSCAM-AS1 has been studied in several cancers, its role and mechanism in OS are poorly understood. In this work, high level of DSCAM-AS1 was validated in OS cell lines. Depleting DSCAM-AS1 inhibited cell proliferation, migration and EMT process in OS. Subsequently, we disclosed that DSCAM-AS1 was mainly observed in the cytoplasm of OS cells and could bind with miR-186-5p in OS. Moreover, inhibiting miR-186-5p rescued the impact of silenced DSCAM-AS1 on OS progression. Additionally, GPRC5A was verified as the target downstream of miR-186-5p, and it was negatively modulated by miR-186-5p but positively regulated by DSCAM-AS1. More importantly, DSCAM-AS1 enhanced GPRC5A level in OS by sequestering miR-186-5p. Finally, up-regulating GPRC5A reversed the influences of DSCAM-AS1 repression on the oncogenic behaviors of OS cells. Knockdown of DSCAM-AS1 suppressed NPC tumor growth in vivo. All findings uncovered that DSCAM-AS1 aggravated OS progression through sponging miR-186-5p to up-regulate GPRC5A expression. Thus, we proposed DSCAM-AS1 as a probable target for OS treatment.	NA	Cancer Biomark. 2021;30(1):29-39. doi: 10.3233/CBM-190703.
4066	LncRNA	DUXAP8	miR-485-5p	FOXM1	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;RNA pull-down;	33313387	lncRNA DUXAP8 Facilitates Multiple Malignant Phenotypes and Resistance to PARP Inhibitor in HCC via Upregulating FOXM1.	In this study, we examined the clinical significance and molecular mechanisms of a long non-coding RNA (lncRNA), double homeobox A pseudogene 8 (DUXAP8) in hepatocellular carcinoma (HCC). DUXAP8 expression was compared using quantitative real-time PCR in HCC versus adjacent tissues and in HCC cell lines versus normal hepatic epithelial cells. The correlations between DUXAP8 level and clinicopathological features were analyzed. Assays including MTT, colony-forming analysis, Transwell assay, western blot, xenograft formation, experimental metastasis, luciferase assay, RNA pull-down, and RNA immunoprecipitation were used to examine DUXAP8-induced malignant phenotypes, its regulation on forkhead box protein M1 (FOXM1), and the importance of FOXM1 in mediating DUXAP8 phenotypes. Our results showed that DUXAP8 was significantly upregulated in HCC tissues or cell lines associated with tumors of advanced grades, tumors that were positive for lymph node metastasis, and patients with poor overall survival. DUAXP8 was essential in maintaining multiple malignant phenotypes (including resistance to olaparib) both in vitro and in vivo. Mechanistically, DUXAP8 upregulated FOXM1 expression by sponging miR-485-5p and interacting with the RNA-binding protein Fused in Sarcoma (FUS). Functionally, FOXM1 essentially mediated the oncogenic phenotypes of DUXAP8. Collectively, DUXAP8 acts through two distinct mechanisms to upregulate FOXM1 and becomes a pleotropic oncogenic lncRNA in HCC.	NA	Mol Ther Oncolytics. 2020 Oct 22;19:308-322. doi: 10.1016/j.omto.2020.10.010. eCollection 2020 Dec 16.
4067	LncRNA	DUXAP8	miR-26b-5p	NA	H1975 and A549 cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33269379	Silencing lncRNA DUXAP8 inhibits lung adenocarcinoma progression by targeting miR-26b-5p.	Lung adenocarcinoma (LUAD), a common type of lung cancer, has become a popularly aggressive cancer. Long noncoding RNAs (lncRNAs) play a critical role in the pathogenesis of human cancers, while the function of double homeobox A pseudogene 8 (DUXAP8) in LUAD remains to be fully inquired. Therefore, our study was conducted to elucidate the DUXAP8 expression in LUAD and its mechanism on the biological features of LUAD cells. Loss-of-function experiments were performed to assess the function of DUXAP8 proliferation and apoptosis of H1975 and A549 cells. Functionally, silencing DUXAP8 inhibited proliferation and induced apoptosis of LUAD cells. Mechanistically, further correlation assay indicated a negative association between miR-26b-5p and DUXAP8 expression. Subsequently, we testified that DUXAP8 exerted its role in the progression and development of LUAD through targeting miR-26b-5p. In summary, our results elucidated that that DUXAP8 promoted tumor progression in LUAD by targeting miR-26b-5p, which provide a novel therapeutic target for diagnosis and therapy of LUAD.	NA	Biosci Rep. 2021 Jan 29;41(1):BSR20200884. doi: 10.1042/BSR20200884.
4068	LncRNA	Eif4g2	miR-3074-5p	Nrf2	mouse tail-cells,INS-1E cells	Type 2 Diabetes Mellitus	Mus musculus (mouse)	qRT-PCR;RACE;	32956705	lncRNA Eif4g2 improves palmitate-induced dysfunction of mouse β-cells via modulation of Nrf2 activation.	Chronic oxidative stress resulting from hyperlipidemia is thought to be a key pathogenic driver of pancreatic β-cell dysfunction in leading to the onset of type 2 diabetes mellitus (T2DM). Long non-coding RNAs (lncRNAs) have been increasingly recognized to regulate dysfunction within pancreatic β-cells in the context of T2DM. In the present study, we sought to comprehensively analyze the roles of lncRNAs in dysfunctional β-cells and mouse islets. Analyses of INS-1E cells were performed by RNA-seq and qRT-PCR after treating with or without 0.5 mM palmitate for 4 days, leading us to identify the novel lncRNA Eif4g2 (lncEif4g2) as a functional regulator within these cells. When we overexpressed lncEif4g2 in INS-1E β-cells and mouse islets, this was sufficient for the reversal of palmitate-mediated reductions in cell viability, insulin production, ATP production by mitochondria, and creation of intracellular reactive oxygen species (ROS) and the dysfunction of mouse islets, with nuclear factor erythroid 2 related factor 2 (Nrf2) activation also being observed. In contrast, when lncEif4g2 was knocked down this led INS-1E cells and mouse islets to become more sensitive to palmitate-induced dysfunction, with reduced Nrf2 nuclear translocation also being detected. When antioxidants were used to treat INS-1E cells and mouse islets, however, these negative effects were reversed. Additional functional analyses revealed lncEif4g2 to be capable of directly binding to miR-3074-5p in β-cells, with the expression of lncEif4g2 and miR-3074-5p being negatively correlated with one another. We further found that cAMP-responsive element binding-protein (CREB) was a miR-3074-5p target gene in these cells, thus at least in part serving as a functional mediator of the lncEif4g2/miR-3074-5p axis within dysfunctional β-cells. In summary, our results thus reveal that lncEif4g2 is able to indirectly regulate the expression of CREB via targeting miR-3074-5p in INS-1E cells and mouse islets, thereby leading to enhanced Nrf2 activation.	NA	Exp Cell Res. 2020 Nov 15;396(2):112291. doi: 10.1016/j.yexcr.2020.112291. Epub 2020 Sep 19.
4069	LncRNA	Eif4g2	miR-3074-5p	Nrf2	mouse tail-cells,INS-1E cells	Type 2 Diabetes Mellitus	Homo sapiens (human)	qRT-PCR;RACE;	32956705	lncRNA Eif4g2 improves palmitate-induced dysfunction of mouse β-cells via modulation of Nrf2 activation.	Chronic oxidative stress resulting from hyperlipidemia is thought to be a key pathogenic driver of pancreatic β-cell dysfunction in leading to the onset of type 2 diabetes mellitus (T2DM). Long non-coding RNAs (lncRNAs) have been increasingly recognized to regulate dysfunction within pancreatic β-cells in the context of T2DM. In the present study, we sought to comprehensively analyze the roles of lncRNAs in dysfunctional β-cells and mouse islets. Analyses of INS-1E cells were performed by RNA-seq and qRT-PCR after treating with or without 0.5 mM palmitate for 4 days, leading us to identify the novel lncRNA Eif4g2 (lncEif4g2) as a functional regulator within these cells. When we overexpressed lncEif4g2 in INS-1E β-cells and mouse islets, this was sufficient for the reversal of palmitate-mediated reductions in cell viability, insulin production, ATP production by mitochondria, and creation of intracellular reactive oxygen species (ROS) and the dysfunction of mouse islets, with nuclear factor erythroid 2 related factor 2 (Nrf2) activation also being observed. In contrast, when lncEif4g2 was knocked down this led INS-1E cells and mouse islets to become more sensitive to palmitate-induced dysfunction, with reduced Nrf2 nuclear translocation also being detected. When antioxidants were used to treat INS-1E cells and mouse islets, however, these negative effects were reversed. Additional functional analyses revealed lncEif4g2 to be capable of directly binding to miR-3074-5p in β-cells, with the expression of lncEif4g2 and miR-3074-5p being negatively correlated with one another. We further found that cAMP-responsive element binding-protein (CREB) was a miR-3074-5p target gene in these cells, thus at least in part serving as a functional mediator of the lncEif4g2/miR-3074-5p axis within dysfunctional β-cells. In summary, our results thus reveal that lncEif4g2 is able to indirectly regulate the expression of CREB via targeting miR-3074-5p in INS-1E cells and mouse islets, thereby leading to enhanced Nrf2 activation.	NA	Exp Cell Res. 2020 Nov 15;396(2):112291. doi: 10.1016/j.yexcr.2020.112291. Epub 2020 Sep 19.
4070	LncRNA	ELFN1-AS1	miR-191-5p	SATB1	colon cancer cells	Colon Cancer	Homo sapiens (human)	qRT-PCR;	33634016	Long Non-Coding RNA ELFN1-AS1 Promoted Colon Cancer Cell Growth and Migration via the miR-191-5p/Special AT-Rich Sequence-Binding Protein 1 Axis.	Long non-coding RNAs (lncRNAs) are reported to participate in tumor development. It has been manifested in previous researches that lncRNA ELFN1-AS1 is involved in early-stage colon adenocarcinoma with potential diagnostic value. However, no studies have revealed the specific mechanism of ELFN1-AS1 in colon cancer, and there are no other studies on whether ELFN1-AS1 is associated with tumorigenesis. In our study, ELFN1-AS1 with high expression in colon cancer was selected by TCGA analysis, and the survival analysis was carried out to verify it. Subsequently, qRT-PCR was adopted for validating the results in tissues and cell lines. Cell counting kit-8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU), cell colon, cell apoptosis, cell cycle, cell migration, and invasion assays were utilized to assess the role of ELFN1-AS1 in colon cancer. Results uncovered that ELFN1-AS1 expression was prominently raised in colon cancer cells and tissues. ELFN1-AS1 decrement restrained cells to grow through interfering with distribution of cell cycle and promoting apoptosis. Meanwhile, ELFN1-AS1 decrement weakened the capacity of cells to migrate and invade. What's more, ELFN1-AS1 was uncovered to act as a competing endogenous RNA (ceRNA) to decrease miR-191-5p expression, thus raising special AT-rich sequence-binding protein 1 (SATB1), a downstream target of ceRNA. To sum up, ELFN1-AS1 drives colon cancer cells to proliferate and invade through adjusting the miR-191-5p/SATB1 axis. The above results disclose that lncRNA ELFN1-AS1 is possibly a novel treatment target for colon cancer cases.	NA	Front Oncol. 2021 Feb 9;10:588360. doi: 10.3389/fonc.2020.588360. eCollection 2020.
4071	Circular RNA	ERBIN	miR-125a-5p	HIF-1a	CRC cells	Colorectal Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;	33225938	The circular RNA circ-ERBIN promotes growth and metastasis of colorectal cancer by miR-125a-5p and miR-138-5p/4EBP-1 mediated cap-independent HIF-1α translation.	BACKGROUND: Circular RNA (circRNAs) and hypoxia have been found to play the key roles in the pathogenesis and progression of cancer including colorectal cancer (CRC). However, the expressions and functions of the specific circRNAs in regulating hypoxia-involved CRC metastasis, and the circRNAs that are relevant to regulate HIF-1α levels in CRC remain elusive. METHODS: qRT-PCR was used to detect the expression of circRNAs and mRNA in CRC cells and tissues. Fluorescence in situ hybridization (FISH) was used to analyze the location of circ-ERBIN. Function-based experiments were performed using circ-ERBIN overexpression and knockdown cell lines in vitro and in vivo, including CCK8, colony formation, EdU assay, transwell, tumor growth and metastasis models. Mechanistically, luciferase reporter assay, western blots and immunohistochemical stainings were performed. RESULTS: Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo. Notably, circ-Erbin overexpression significantly promoted angiogenesis by increasing the expression of hypoxia induced factor (HIF-1α) in CRC. Mechanistically, circ-Erbin accelerated a cap-independent protein translation of HIF-1α in CRC cells as the sponges of miR-125a-5p and miR-138-5p, which synergistically targeted eukaryotic translation initiation factor 4E binding protein 1(4EBP-1). CONCLUSIONS: Our findings uncover a key mechanism for circ-Erbin mediated HIF-1α activation by miR-125a-5p-5p/miR-138-5p/4EBP-1 axis and circ-ERBIN is a potential target for CRC treatment.	NA	Mol Cancer. 2020 Nov 23;19(1):164. doi: 10.1186/s12943-020-01272-9.
4072	Circular RNA	ERBIN	miR-138-5p	HIF-1a	CRC cells	Colorectal Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;	33225938	The circular RNA circ-ERBIN promotes growth and metastasis of colorectal cancer by miR-125a-5p and miR-138-5p/4EBP-1 mediated cap-independent HIF-1α translation.	BACKGROUND: Circular RNA (circRNAs) and hypoxia have been found to play the key roles in the pathogenesis and progression of cancer including colorectal cancer (CRC). However, the expressions and functions of the specific circRNAs in regulating hypoxia-involved CRC metastasis, and the circRNAs that are relevant to regulate HIF-1α levels in CRC remain elusive. METHODS: qRT-PCR was used to detect the expression of circRNAs and mRNA in CRC cells and tissues. Fluorescence in situ hybridization (FISH) was used to analyze the location of circ-ERBIN. Function-based experiments were performed using circ-ERBIN overexpression and knockdown cell lines in vitro and in vivo, including CCK8, colony formation, EdU assay, transwell, tumor growth and metastasis models. Mechanistically, luciferase reporter assay, western blots and immunohistochemical stainings were performed. RESULTS: Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo. Notably, circ-Erbin overexpression significantly promoted angiogenesis by increasing the expression of hypoxia induced factor (HIF-1α) in CRC. Mechanistically, circ-Erbin accelerated a cap-independent protein translation of HIF-1α in CRC cells as the sponges of miR-125a-5p and miR-138-5p, which synergistically targeted eukaryotic translation initiation factor 4E binding protein 1(4EBP-1). CONCLUSIONS: Our findings uncover a key mechanism for circ-Erbin mediated HIF-1α activation by miR-125a-5p-5p/miR-138-5p/4EBP-1 axis and circ-ERBIN is a potential target for CRC treatment.	NA	Mol Cancer. 2020 Nov 23;19(1):164. doi: 10.1186/s12943-020-01272-9.
4073	Circular RNA	ERBIN	miR-125a-5p	4EBP-1	CRC cells	Colorectal Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;	33225938	The circular RNA circ-ERBIN promotes growth and metastasis of colorectal cancer by miR-125a-5p and miR-138-5p/4EBP-1 mediated cap-independent HIF-1α translation.	BACKGROUND: Circular RNA (circRNAs) and hypoxia have been found to play the key roles in the pathogenesis and progression of cancer including colorectal cancer (CRC). However, the expressions and functions of the specific circRNAs in regulating hypoxia-involved CRC metastasis, and the circRNAs that are relevant to regulate HIF-1α levels in CRC remain elusive. METHODS: qRT-PCR was used to detect the expression of circRNAs and mRNA in CRC cells and tissues. Fluorescence in situ hybridization (FISH) was used to analyze the location of circ-ERBIN. Function-based experiments were performed using circ-ERBIN overexpression and knockdown cell lines in vitro and in vivo, including CCK8, colony formation, EdU assay, transwell, tumor growth and metastasis models. Mechanistically, luciferase reporter assay, western blots and immunohistochemical stainings were performed. RESULTS: Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo. Notably, circ-Erbin overexpression significantly promoted angiogenesis by increasing the expression of hypoxia induced factor (HIF-1α) in CRC. Mechanistically, circ-Erbin accelerated a cap-independent protein translation of HIF-1α in CRC cells as the sponges of miR-125a-5p and miR-138-5p, which synergistically targeted eukaryotic translation initiation factor 4E binding protein 1(4EBP-1). CONCLUSIONS: Our findings uncover a key mechanism for circ-Erbin mediated HIF-1α activation by miR-125a-5p-5p/miR-138-5p/4EBP-1 axis and circ-ERBIN is a potential target for CRC treatment.	NA	Mol Cancer. 2020 Nov 23;19(1):164. doi: 10.1186/s12943-020-01272-9.
4074	Circular RNA	ERBIN	miR-138-5p	4EBP-1	CRC cells	Colorectal Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;	33225938	The circular RNA circ-ERBIN promotes growth and metastasis of colorectal cancer by miR-125a-5p and miR-138-5p/4EBP-1 mediated cap-independent HIF-1α translation.	BACKGROUND: Circular RNA (circRNAs) and hypoxia have been found to play the key roles in the pathogenesis and progression of cancer including colorectal cancer (CRC). However, the expressions and functions of the specific circRNAs in regulating hypoxia-involved CRC metastasis, and the circRNAs that are relevant to regulate HIF-1α levels in CRC remain elusive. METHODS: qRT-PCR was used to detect the expression of circRNAs and mRNA in CRC cells and tissues. Fluorescence in situ hybridization (FISH) was used to analyze the location of circ-ERBIN. Function-based experiments were performed using circ-ERBIN overexpression and knockdown cell lines in vitro and in vivo, including CCK8, colony formation, EdU assay, transwell, tumor growth and metastasis models. Mechanistically, luciferase reporter assay, western blots and immunohistochemical stainings were performed. RESULTS: Circ-Erbin was highly expressed in the CRC cells and Circ-Erbin overexpression facilitated the proliferation, migration and metastasis of CRC in vitro and in vivo. Notably, circ-Erbin overexpression significantly promoted angiogenesis by increasing the expression of hypoxia induced factor (HIF-1α) in CRC. Mechanistically, circ-Erbin accelerated a cap-independent protein translation of HIF-1α in CRC cells as the sponges of miR-125a-5p and miR-138-5p, which synergistically targeted eukaryotic translation initiation factor 4E binding protein 1(4EBP-1). CONCLUSIONS: Our findings uncover a key mechanism for circ-Erbin mediated HIF-1α activation by miR-125a-5p-5p/miR-138-5p/4EBP-1 axis and circ-ERBIN is a potential target for CRC treatment.	NA	Mol Cancer. 2020 Nov 23;19(1):164. doi: 10.1186/s12943-020-01272-9.
4075	LncRNA	ESCCAL-1	miR-590-3p	APOBEC3G	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	32905814	Long non-coding RNA ESCCAL-1 promotes esophageal squamous cell carcinoma by down regulating the negative regulator of APOBEC3G.	The expression of lncRNA ESCCAL-1 is upregulated in esophageal squamous cell carcinoma (ESCC). However, the molecular pathways regulated by ESCCAL-1 in esophageal cancer remain obscure. We found that high expression of the lncRNA ESCCAL-1 in human ESCC tumors correlated with worse clinicopathologic features. Furthermore, depletion of ESCCAL-1 in ESCC models inhibited the cellular processes associated with malignancy, including proliferation, migration and invasion, resistance to apoptosis, and impaired tumor growth in mice. Using a combinatorial approach, we discovered that ESCCAL-1 regulates malignant phenotypes in ESCC by acting as a molecular sponge for miR-590-3p. This interaction prevents miR-590-3p from suppressing APOBEC3G expression. Increased APOBEC3G was also a biomarker of worse clinicopathologic features in human ESCC tumors. Depletion of ESSCAL-1 or APOBEC3G, or overexpression of miR-590-3p resulted in increased apoptosis due to downregulation of the PI3K/Akt signaling. This study demonstrates that the lncRNA ESCCAL-1 promotes malignant features of ESCC by relieving the inhibitory effect of miR-590-3p on APOBEC3G expression and identifies potential biomarkers or therapeutic targets to improve ESCC treatment outcomes.	NA	Cancer Lett. 2020 Nov 28;493:217-227. doi: 10.1016/j.canlet.2020.09.001. Epub 2020 Sep 6.
4076	LncRNA	EWSAT1	miR-24-3p	ROCK1	MNNG/HOS and 143B cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33225581	Long non-coding RNA EWSAT1 promoted metastasis and actin cytoskeleton changes via miR-24-3p sponging in osteosarcoma.	Non-coding RNAs are closely associated with tumorigenesis in multiple malignant tumours, including osteosarcoma (OS). Long non-coding RNA Ewing sarcoma-associated transcript 1 (EWSAT1) plays a role in metastasis, and actin cytoskeletal changes in OS remain unclear. In the current study, we showed that EWSAT1 expression was up-regulated in OS and that an elevation in the EWSAT1 expression level was correlated with poor prognosis in patients with OS. Functionally, we showed that knockdown of EWSAT1 suppressed migration and induced actin stress fibre degradation in MNNG/HOS and 143B cells. Moreover, we found that ROCK1 was a key downstream effector in EWSAT1-mediated cell migration and actin stress fibre changes. Furthermore, we demonstrated that ROCK1 and EWSAT1 shared a similar microRNA response element of microRNA-24-3p (miR-24-3p). Moreover, we verified that miR-24-3p suppressed ROCK1 and its mediated migration and actin stress fibres change by direct targeting. EWSAT1 promoted ROCK1-mediated migration and actin stress fibre formation through miR-24-3p sponging. Lastly, through an in vivo study, we demonstrated that EWSAT1 promoted lung metastasis in OS. According to the above-mentioned results, we suggest that EWSAT1 acts as an oncogene and that EWSAT1/miR-24-3p/ROCK1 axial could be a new target in the treatment of OS.	NA	J Cell Mol Med. 2021 Jan;25(2):716-728. doi: 10.1111/jcmm.16121. Epub 2020 Nov 22.
4077	LncRNA	EWSAT1	miR-326	FBXL20	Colorectal Cancer cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33469313	LncRNA EWSAT1 Promotes Colorectal Cancer Progression Through Sponging miR-326 to Modulate FBXL20 Expression.	BACKGROUND: Ewing sarcoma-associated transcript 1 (EWSAT1) has been reported to be a pivotal modulator in a series of cancers. However, the function of EWSAT1 in colorectal cancer (CRC) has not been elaborated. This study aimed to explore the role of EWSAT1 in CRC progression and the underlying mechanisms. METHODS: The expression patterns of EWSAT1, miR-326 and FBXL20 were examined by qCRCR. Si-EWSAT1 was transfected to study the effects of EWSAT1 on cell proliferation and metastasis. Rescue experiments were performed to investigate the underlying mechanisms in vitro. Xenograft models were used to evaluate the role of EWSAT1 in vivo. RESULTS: We found that EWSAT1 was highly expressed in CRC tissues and cell lines and associated with poor overall survival. In vitro, knockdown of EWSAT1 suppressed the cell proliferation, migration and invasion. Moreover, miR-326 was found to be a target of EWSAT1, and miR-326 inhibitor could partially reverse the effects on CRC cell progression induced by si-EWSAT1. Subsequently, we validated FBXL20 as a vital downstream target for miR-326, and EWSAT1 positively regulated FBXL20 via miR-326 in vitro. In addition, these findings were confirmed by in vivo experiments. CONCLUSION: Taken together, the data showed that EWSAT1 promoted CRC progression via targeting miR-326/FBXL20 pathway, which might provide a novel therapeutic target for CRC treatment.	NA	Onco Targets Ther. 2021 Jan 13;14:367-378. doi: 10.2147/OTT.S272895. eCollection 2021.
4078	Circular RNA	EYA1	miR-582-3p	CXCL14	cervical adenocarcinoma cells	Cervical Cancer	Homo sapiens (human)	RNA sequencing;	33312754	circEYA1 Functions as a Sponge of miR-582-3p to Suppress Cervical Adenocarcinoma Tumorigenesis via Upregulating CXCL14.	Circular RNAs (circRNAs) function as efficient microRNA (miRNA) sponges that regulate gene expression in the pathogenesis of many human malignancies. However, their roles in cervical adenocarcinoma remain largely unknown. In this study, we aimed to seek novel circRNAs that regulate cervical adenocarcinoma carcinogenesis and to explore their regulatory mechanisms as well as clinical significance. We identified that 24 circRNAs were differentially expressed in cervical adenocarcinoma tissues by RNA sequencing. Among them, circEYA1 was the most significantly downregulated circRNA in cervical adenocarcinoma. In cervical adenocarcinoma cells, circEYA1 overexpression led to suppression of cell viability and colony formation, promotion of apoptosis, and a decrease of the xenograft tumor growth. The mechanism underlying these observations is that circEYA1 functioned as a sponge of miR-582-3p and abrogated its suppression of CXCL14 expression. Consistently, miR-582-3p inhibition phenocopied the biological effects of circEYA1 overexpression in cervical adenocarcinoma cells. Moreover, miR-582-3p overexpression reversed the suppressive behaviors of circEYA1 in vitro and in vivo. In addition, the expression, correlation, and clinical diagnostic value of circEYA1/miR-582-3p/CXCL14 were confirmed in 198 clinical cervical tissue samples. In summary, our findings highlight a novel tumor suppressive role of circEYA1 in cervical adenocarcinoma tumorigenesis and may provide a potential diagnostic marker and therapeutic target for patients with cervical adenocarcinoma.	NA	Mol Ther Nucleic Acids. 2020 Oct 22;22:1176-1190. doi: 10.1016/j.omtn.2020.10.026. eCollection 2020 Dec 4.
4079	LncRNA	FALEC	miR-2116-3p	PIWIL1	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33073675	Long non-coding RNA FALEC promotes colorectal cancer progression via regulating miR-2116-3p-targeted PIWIL1.	BACKGROUND: Colorectal cancer (CRC) is one of the most common digestive malignant tumors globally. Focally amplified lncRNA on chromosome 1 (FALEC) is a novel lncRNA that has been reported to be involved in many biological processes during carcinogenesis. However, its role in CRC remains poorly understood. METHODS: Gene expression at mRNA or protein level was measured by qRT-PCR or western blot, respectively. In vitro experiments including EdU, colony formation, flow cytometry, wound-healing and transwell assays, as well as in vivo xenograft experiment, were utilized to determine the functional role of FALEC in CRC. Relevant mechanical assays were performed to investigate the underlying molecular mechanism. RESULTS: FALEC was aberrantly up-regulated in CRC. FALEC knockdown could impair CRC cell proliferation, migration and invasion, whereas facilitate cell apoptosis. MiR-2116-3p was revealed to be sponged by FALEC. PIWIL1 was identified as the target of miR-2116-3p. Mechanically, FALEC restored the expression of PIWIL1 via absorbing miR-2116-3p. MiR-2116-3p inhibition and PIWIL1 enrichment could counteract the anti-tumor impact induced by silenced FALEC on the oncogenic behaviors of CRC cells. CONCLUSION: Our study revealed that FALEC promoted CRC progression via restoring the expression of miR-2116-3p-targeted PIWIL1, suggesting the potential application of targeting FALEC in the treatment of CRC.	NA	Cancer Biol Ther. 2020 Nov 1;21(11):1025-1032. doi: 10.1080/15384047.2020.1824514. Epub 2020 Oct 19.
4080	LncRNA	FAM201A	miR-186-5p	TNKS1BP1	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33011533	TCF3-activated FAM201A enhances cell proliferation and invasion via miR-186-5p/TNKS1BP1 axis in triple-negative breast cancer.	Increasing evidence shows that long non-coding RNAs (lncRNAs) are closely associated with the development of cancers, including triple-negative breast cancer (TNBC). LncRNA FAM201A has been identified as a key regulator in some cancers. However, its role has not been explored in TNBC. In this work, we investigated the biological role and regulatory mechanism of FAM201A in TNBC. The expression pattern of FAM201A was determined by RT-qPCR analysis. The biological effect of FAM201A on cellular process of TNBC was tested using colony formation, EdU, caspase-3 activity detection, flow cytometry, wound healing, and Transwell assays. ChIP and luciferase reporter assays were performed to verify the interaction between transcription factor 3 (TCF3) and FAM201A. The interaction among FAM201A, microRNA-186-5p (miR-186-5p), and tankyrase 1 binding protein 1 (TNKS1BP1) was evaluated by luciferase reporter and RIP assays. The results showed that FAM201A expression was significantly upregulated in TNBC tissues and cells. Functionally, FAM201A knockdown inhibited TNBC cell proliferation, migration and invasion, and accelerated cell apoptosis. In mechanism, it was confirmed that FAM201A was transcriptionally activated by TCF3 and served as a sponge for miR-186-5p to upregulate TNKS1BP1 expression in TNBC cells. Collectively, our study revealed that TCF3-activated FAM201A promoted aggressive phenotypes of TNBC cells by upregulating TNKS1BP1 expression.	NA	Bioorg Chem. 2020 Nov;104:104301. doi: 10.1016/j.bioorg.2020.104301. Epub 2020 Sep 22.
4081	LncRNA	FAM225A	miR-197-5p	NONO	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	33442405	Long Noncoding RNA FAM225A Promotes Esophageal Squamous Cell Carcinoma Development and Progression via Sponging MicroRNA-197-5p and Upregulating NONO.	Esophageal squamous cell carcinoma (ESCC) is the major subclass of esophageal cancer and one of the most life-threatening malignancies with high morbidity and mortality. Long noncoding RNAs (lncRNAs) participate in tumorigenesis and metastasis of various tumors. Here, we investigated the function of a newly identified lncRNA FAM225A in ESCC. LncRNA FAM225A expression was significantly higher in ESCC and predicted poor prognosis of ESCC patients. We confirmed that upregulation of FAM225A in ESCC and overexpression of FAM225A was associated with poor outcome in ESCC patients using TCGA ESCC cohort. Knockdown of FAM225A significantly inhibited cell growth, migration and invasion of ESCC cells in vitro and inhibited ESCC xenograft development in vivo. Mechanistically, we demonstrated that lncRNA FAM225A functioned as a competing endogenous RNA (ceRNA) via sponging miR-197-5p. LncRNA FAM225A exerted its regulatory function on ESCC proliferation and metastasis via modulating expression of miR-197-5p. MiR-197-5p overexpression antagonized the function of FAM225A, with decreased cell growth and invasion. Moreover, we identified that RNA binding protein NONO was a direct target of miR-197-5p and miR-197-5p negatively regulated NONO expression and TGF-β signaling in ESCC cells. In summary, our findings suggest that lncRNA FAM225A promotes ESCC development and progression via sponging miR-197-5p and upregulating NONO expression. These results suggest that lncRNA FAM225A could be explored as a new therapy target in ESCC treatment.	NA	J Cancer. 2021 Jan 1;12(4):1073-1084. doi: 10.7150/jca.51292. eCollection 2021.
4082	LncRNA	FAM83A-AS1	miR-495-3p	NA	OE19 and OE33 cells	Esophageal Cancer	Homo sapiens (human)	luciferase assay;	33015782	LncRNA FAM83A-AS1 aggravates the malignant development of esophageal cancer by binding to miR-495-3p.	OBJECTIVE: It is of significance to screen out differentially expressed long non-coding RNAs (lncRNAs) that can be utilized as tumor biomarkers in esophageal cancer. This study aims to uncover the effect of lncRNA FAM83A-AS1 on regulating migratory potential in esophageal cancer and the underlying mechanism. PATIENTS AND METHODS: Tumor tissues and adjacent normal ones were collected from 62 esophageal cancer patients for detecting FAM83A-AS1 levels. Correlations of FAM83A-AS1 with clinical indexes and overall survival of esophageal cancer patients were analyzed. Thereafter, regulatory effects of FAM83A-AS1 on migratory potential in OE19 and OE33 cells were examined by transwell and wound healing assay. Then, the target genes of FAM83A-AS1 were predicted and functionally analyzed, and a protein interaction network was constructed. Finally, the mechanism of FAM83A-AS1 in regulating the downstream gene miR-495-3p was analyzed through Luciferase assay and rescue experiments. RESULTS: It was found that FAM83A-AS1 was upregulated in esophageal cancer tissues and cell lines. Higher rates of lymphatic and distant metastasis and worse survival were observed in esophageal cancer patients expressing higher level of FAM83A-AS1. Besides, the knockdown of FAM83A-AS1 suppressed migratory potential in OE19 cells, while the overexpression of FAM83A-AS1 yielded the opposite trend in OE33 cells. Moreover, miR-495-3p was indicated to be the target gene binding FAM83A-AS1, and it was lowly expressed in esophageal cancer and negatively regulated by FAM83A-AS1. Furthermore, the overexpression of miR-495-3p partially abolished the regulatory effect of FAM83A-AS1 on migratory potential in esophageal cancer. CONCLUSIONS: FAM83A-AS1 is upregulated in esophageal cancer, and it stimulates migratory potential in esophageal cancer by negatively regulating miR-495-3p.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9408-9415. doi: 10.26355/eurrev_202009_23024.
4083	LncRNA	FBXL19-AS1	miR-431	ZEB1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33168132	Long non-coding RNA FBXL19-AS1 serves as a competing endogenous RNA to regulate ZEB1 expression by sponging miR-431 in gastric cancer.	unknown	NA	J Biol Regul Homeost Agents. 2020 Sep-Oct;34(5):1847-1855. doi: 10.23812/20-311-L.
4084	LncRNA	FEZF1-AS1	miR-516b-5p	ITGA11	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	microarray;Luciferase reporter assay;	33174014	Long non-coding RNA FEZF1-AS1 facilitates non-small cell lung cancer progression via the ITGA11/miR-516b-5p axis.	Long non-coding RNAs (lncRNAs) have emerged as key players in the development and progression of cancer. FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) is a novel lncRNA that is involved in the development of cancer and acts as a potential biomarker for cancer. However, the clinical significance and molecular mechanism of FEZF1-AS1 in non-small cell lung cancer (NSCLC) remains uncertain. In the present study, FEZF1-AS1 was selected using Arraystar Human lncRNA microarray and was identified to be upregulated in NSCLC tissues and negatively associated with the overall survival of patients with NSCLC. Loss-of-function assays revealed that FEZF1-AS1 inhibition decreased cell proliferation and migration, and arrested cells at the G2/M cell cycle phase. Mechanistically, FEZF1-AS1 expression was influenced by N6-methyladenosine (m6A) modification. Since FEZF1-AS1 was mainly located in the cytoplasmic fraction of NSCLC cells, it was hypothesized that it may be involved in competing endogenous RNA regulatory network to impact the prognosis of NSCLC. Via integrating Arraystar Human mRNA microarray data and miRNA bioinformatics analysis, it was revealed that ITGA11 expression was decreased with loss of FEZF1-AS1 and increased with gain of FEZF1-AS1 expression, and microRNA (miR)-516b-5p inhibited the expression levels of both FEZF1-AS and ITGA11. RNA-binding protein immunoprecipitation and RNA pulldown assays further demonstrated that FEZF1-AS1 could bind to miR-516b-5p and that ITGA11 was a direct target of miR-516b-5p by luciferase reporter assay. Overall, the present findings demonstrated that FEZF1-AS1 was upregulated and acted as an oncogene in NSCLC by regulating the ITGA11/miR-516b-5p axis, suggesting that FEZF1-AS1 may be a potential prognostic biomarker and therapeutic target for NSCLC.	NA	Int J Oncol. 2020 Dec;57(6):1333-1347. doi: 10.3892/ijo.2020.5142. Epub 2020 Oct 29.
4085	LncRNA	FGD5-AS1	miR-142-5p	PD-L1	A549/DDP cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33416094	FGD5-AS1 promotes cisplatin resistance of human lung adenocarcinoma cell via the miR-142-5p/PD-L1 axis.	Previous studies have reported that long non-coding (lnc) RNA FGD5-antisense 1 (FGD5-AS1) promotes tumor proliferation, migration and invasion. Therefore, the present study aimed to elucidate the biological role and underlying molecular mechanisms of FGD5-AS1 in cisplatin (DDP) resistance of lung adenocarcinoma (LAD) cells. The results demonstrated that FGD5-AS1 was highly expressed in DDP-resistant LAD tissues and cells. Knockdown of FGD5-AS1 decreased the proliferative, migratory and invasive abilities of DDP-resistant LAD cells. Moreover, it was identified that FGD5-AS1 acted as a molecular sponge for microRNA (miR)-142, and FGD5-AS1 enhanced the resistance of A549/DDP cells to DDP by directly interacting with miR-142. Programmed cell death 1 ligand 1 (PD-L1) was also found to be a key effector of the FGD5-AS1/miR-142 axis to regulate the chemoresistance of DDP-resistant LAD cells. In conclusion, the present study demonstrated that FGD5-AS1 increased DDP resistance of LAD via the miR-142/PD-L1 axis, which may offer a novel treatment strategy for patients with DDP-resistant LAD.	NA	Int J Mol Med. 2021 Feb;47(2):523-532. doi: 10.3892/ijmm.2020.4816. Epub 2020 Dec 14.
4086	LncRNA	FGD5-AS1	miR-5590-3p	NA	renal cancer cells	Renal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;luciferase assay;RNA pull-down;	32964964	LncRNA FGD5-AS1/miR-5590-3p axis facilitates the proliferation and metastasis of renal cell carcinoma through ERK/AKT signalling.	OBJECTIVE: Amongst noncoding RNAs, competing endogenous RNAs (ceRNAs) are popular and interesting regulatory mechanisms involved in oncogenesis and tumour progression. LncRNA FGD5-AS1, also known as miR-5590-3p, is involved in the regulatory role of ceRNA in many cancers. However, the roles of lncRNA FGD5-AS1 or miR-5590-3p in renal cell carcinoma (RCC) remain unclear. We investigated how FGD5-AS1 and miR-5590-3p regulated clear cell proliferation and metastasis in RCC. PATIENTS AND METHODS: Real Time-quantitative PCR (RT-qPCR) was used to detect the expression of FGD5-AS1 in tumour issues and renal cancer cell lines. MTT, scratch test and transwell assay were performed to confirm the effect of FGD5-AS1 on the proliferation, migration or invasion of the above cell lines. RNA pull-down and Luciferase assays were used to detect the target site between FGD5-AS1 and miR-5590-3p. In addition, we examined the proteins related to ERK/AKT signalling related via Western blot analysis. Finally, we used the RT-qPCR method to detect the mRNA levels of E-cadherin and vimentin. RESULTS: LncRNA FGD5-AS1 was highly expressed in renal cancer tissues, especially in patients with metastasis. This effect facilitated the proliferation, migration, epithelial-mesenchymal transition and invasion of renal cancer cells. Silencing the expression of FGD5-AS1 with FGD5-AS1 siRNA significantly inhibited the malignancy of tumour cells. RNA pull-down and Luciferase assays demonstrated that FGD5-AS1 targeted miR-5590-3p to interact with miR-5590-3p negatively. Furthermore, miR-5590-3p inhibitors could eliminate the FGD5-AS1 siRNA-induced upregulation of E-cadherin and downregulation of vimentin. CONCLUSIONS: Mechanistically, lncRNA FGD5-AS1 can competitively interact with miR-5590-3p and regulate the downstream signalling of ErkAKT to enhance the malignancy of tumours. This lncRNA could become a potential target molecule for treating and diagnosing RCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8756-8766. doi: 10.26355/eurrev_202009_22814.
4087	LncRNA	FGF14-AS2	miR-370-3p	FGF14	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33083023	Long noncoding RNA FGF14-AS2 inhibits breast cancer metastasis by regulating the miR-370-3p/FGF14 axis.	Long noncoding RNAs (lncRNAs) have emerged as important regulators in cancers, including breast cancer. However, the overall biological roles and clinical significance of most lncRNAs are not fully understood. This study aimed to elucidate the potential role of a novel lncRNA FGF14-AS2 and the mechanisms underlying metastasis in breast cancer. The lncRNA FGF14-AS2 was significantly downregulated in breast cancer tissues; patients with lower FGF14-AS2 expression had advanced clinical stage. In vitro and in vivo assays of FGF14-AS2 alterations revealed a complex integrated phenotype affecting breast cancer cell migration, invasion, and tumor metastasis. Mechanistically, FGF14-AS2 functioned as a competing endogenous RNA of miR-370-3p, thereby leading to the activation of its coding counterpart, FGF14. Clinically, we observed increased miR-370-3p expression in breast cancer tissues, whereas FGF14 expression was decreased in breast cancer tissues compared to the adjacent normal breast tissues. FGF14-AS2 expression was significantly negatively correlated with miR-370-3p expression, and correlated positively to FGF14 expression. Collectively, our findings support a model in which the FGF14-AS2/miR-370-3p/FGF14 axis is a critical regulator in breast cancer metastasis, suggesting a new therapeutic direction in breast cancer.	NA	Cell Death Discov. 2020 Oct 12;6:103. doi: 10.1038/s41420-020-00334-7. eCollection 2020.
4088	LncRNA	FLVCR1-AS1	miR-381	RAP2A	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33313944	lncRNA FLVCR1-AS1 drives colorectal cancer progression via modulation of the miR-381/RAP2A axis.	Colorectal cancer (CRC) is one of the most prevalent types of cancer globally. Long non-coding RNAs (lncRNAs) have been suggested to serve as vital regulators in CRC. lncRNA feline leukemia virus subgroup C receptor 1 antisense RNA 1 (FLVCR1-AS1) is closely associated with the tumorigenesis of various types of cancer. The aim of the present study was to investigate the molecular mechanisms of lncRNA FLVCR1-AS1 in CRC progression. The expression levels of FLVCR1-AS1, microRNA (miR)-381 and Ras-related protein 2a (RAP2A) were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A Kaplan-Meier analysis was performed to determine the overall survival rate of patients with CRC. Furthermore, cell viability, migration and invasion were assessed using Cell Counting Kit-8 (CCK-8) and Transwell assays. The interaction between genes was confirmed using dual-luciferase reporter and pull-down assays. The results demonstrated that FLVCR1-AS1 was upregulated in CRC tissues and cells, and increased FLVCR1-AS1 expression levels in patients with CRC were associated with poor prognosis. FLVCR1-AS1 knockdown significantly attenuated the viability, migration and invasion ability of CRC cells. In addition, the results confirmed that FLVCR1-AS1 directly binds with miR-381-3p, and that RAP2A is a direct target of miR-381-3p. The overexpression of FLVCR1-AS1 increased RAP2A expression levels. Functional assays revealed that miR-381 inhibitor or RAP2A overexpression attenuated the suppressive effects of FLVCR1-AS1 silencing on CRC cell viability, migration and invasion. Overall, the findings of the current study suggest that FLVCR1-AS1 promotes CRC progression via the miR-381/RAP2A pathway. These findings may provide a novel approach for CRC treatment.	NA	Mol Med Rep. 2021 Feb;23(2):139. doi: 10.3892/mmr.2020.11778. Epub 2020 Dec 14.
4089	LncRNA	FOXD2-AS1	miR-205-5p	VEGF-A	HPF-R cell line	Recurrent Pterygium	Homo sapiens (human)	ChIP;qRT-PCR;RIP assay;RNA pull-down assay;RNA pull-down;	33098266	Activation of LncRNA FOXD2-AS1 by H3K27 acetylation regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium.	LncRNA FOXD2-AS1 is abnormally expressed in many diseases. However, the molecular mechanisms whereby FOXD2-AS1 is involved in recurrent pterygium remain unknown. Here, qRT-PCR was performed to quantify FOXD2-AS1 expression, while CCK-8, flow cytometer and neoplasm xenograft assays were used to investigate its function. Dual-luciferase reporter, RIP and RNA pull-down assays were conducted to address the relationship between FOXD2-AS1, miR-205-5p and VEGF-A, while ChIP assays were used to detect H3K27 acetylation at the FOXD2-AS1 promoter. FOXD2-AS1 expression was up-regulated in recurrent pterygium tissues. Moreover, a high FOXD2-AS1 expression was associated with advanced stages, increased microvessel density and shorter recurrent-free survival. In addition, ROC analysis showed that FOXD2-AS1 is a valid predictor of recurrent pterygium. Furthermore, we show that FOXD2-AS1 induced proliferation and inhibited apoptosis in a cell line derived from recurrent pterygia (HPF-R) at least partially through the regulation of the miR-205-VEGF pathway. In addition, the up-regulation of FOXD2-AS1 was attributed to the H3K27 acetylation at the promoter region. In conclusion, FOXD2-AS1 is activated via its H3K27 acetylation and regulates VEGF-A expression by sponging miR-205-5p in recurrent pterygium. Our results may provide a basis for the development of new therapeutic targets and biomarkers for recurrent pterygium.	NA	J Cell Mol Med. 2020 Dec;24(24):14139-14151. doi: 10.1111/jcmm.16024. Epub 2020 Oct 23.
4090	LncRNA	FOXD3-AS1	miR-296-5p	ZCCHC3	OS cells	Osteosarcoma	Homo sapiens (human)	Rescue assay;	33204608	ELF1-activated FOXD3-AS1 promotes the migration, invasion and EMT of osteosarcoma cells via sponging miR-296-5p to upregulate ZCCHC3.	Osteosarcoma (OS) is a malignant carcinoma often occurring in adolescents. The critical function of long non-coding RNAs (lncRNAs) in cancer arouses increasing attention. Nevertheless, the specific function of FOXD3 Antisense RNA 1 (FOXD3-AS1) in OS has not been understood yet. In this research, FOXD3-AS1 showed strengthened level in OS specimens and cell lines, and its deficiency restrained cell migration, invasion and epithelial-to-mesenchymal transition (EMT) in OS. Then, we confirmed the interaction of FOXD3-AS1 with microRNA-296-5p (miR-296-5p) and that miR-296-5p overexpression blocked OS cell migration, invasion and EMT. Besides, miR-296-5p targeted zinc finger CCHC-type containing 3 (ZCCHC3), and FOXD3-AS1 released ZCCHC3 via sequestering miR-296-5p. Moreover, rescue assays delineated that ZCCHC3 upregulation neutralized the inhibitory effect of FOXD3-AS1 depletion on in vitro behaviors and in vivo tumorigenesis in OS. In addition, E74 like ETS transcription factor 1 (ELF1) stimulated FOXD3-AS1 transcription, and ELF1 silence-suppressed malignant phenotypes of OS cells were offset by FOXD3-AS1 upregulation. Overall, present work elucidated that ELF1-activated FOXD3-AS1 aggravated cell migration, invasion and EMT in OS via absorbing miR-296-5p to augment ZCCHC3 expression, which might provide potential guidance for researchers to find effective targets for OS treatment.	NA	J Bone Oncol. 2020 Oct 22;26:100335. doi: 10.1016/j.jbo.2020.100335. eCollection 2021 Feb.
4091	LncRNA	FOXD3-AS1	miR-765	BCL2L13	neuroblastoma cells	Neuroblastoma	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33068927	LncRNA FOXD3-AS1 knockdown protects against cerebral ischemia/reperfusion injury via miR-765/BCL2L13 axis.	AIMS: Long non-coding RNAs (lncRNAs) FOXD3-AS1 was reported to be increased in cardiomyocyte ischemic injury. However, its role and underlying molecular mechanism in ischemic stroke remain unknown. This study was to investigate the role of FOXD3-AS1 in cerebral ischemia/reperfusion injury. METHODS: The expression of FOXD3-AS1 and miR-765 were measured with qRT-PCR. The shared putative miR-765 binding sites both in BCL2L13 and FOXD3-AS1 were identified with bioinformatics, luciferase reporter assay and RNA immunoprecipitation. Apoptosis and its related proteins were detected by TUNEL assay, Hoechst 33,258 staining, flow cytometry and western blot. Infarct volume and the neurological status were evaluated with TTC staining and neurologic deficit score, respectively. RESULTS: The up-regulation of FOXD3-AS1 and down-regulation of miR-765 were found in both mouse brains after cerebral ischemia/reperfusion (I/R) and neuroblastoma cells of neuro-2A (N2a) after oxygen-glucose deprivation/reoxygenation (OGD/R). Moreover, the overexpression of miR-765 reduced N2a cell apoptosis caused by OGD/R. MiR-765 could target BCL2L13 directly. In addition, we found that FOXD3-AS1 bound to miR-765 directly, acting as a ceRNA to modulate the expression of BCL2L13. Overexpression of FOXD3-AS1 antagonized the inhibitory impact of miR-765 on the expression of BCL2L13 and the apoptosis of N2a cells treated with OGD/R, while FOXD3-AS1 knockdown promoted the inhibitory impact of miR-765 on the expression of BCL2L13 and the apoptosis of N2a cells treated with OGD/R. Furthermore, we found that neurological deficits and brain injury induced by I/R in vivo were attenuated by FOXD3-AS1 knockdown. CONCLUSIONS: We verified a critical signaling pathway of FOXD3-AS1/miR-765/BCL2L13 in regulating cerebral ischemia/reperfusion injury.	NA	Biomed Pharmacother. 2020 Dec;132:110778. doi: 10.1016/j.biopha.2020.110778. Epub 2020 Oct 14.
4092	LncRNA	FOXD3-AS1	miR-765	BCL2L13	neuroblastoma cells	Neuroblastoma	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33068927	LncRNA FOXD3-AS1 knockdown protects against cerebral ischemia/reperfusion injury via miR-765/BCL2L13 axis.	AIMS: Long non-coding RNAs (lncRNAs) FOXD3-AS1 was reported to be increased in cardiomyocyte ischemic injury. However, its role and underlying molecular mechanism in ischemic stroke remain unknown. This study was to investigate the role of FOXD3-AS1 in cerebral ischemia/reperfusion injury. METHODS: The expression of FOXD3-AS1 and miR-765 were measured with qRT-PCR. The shared putative miR-765 binding sites both in BCL2L13 and FOXD3-AS1 were identified with bioinformatics, luciferase reporter assay and RNA immunoprecipitation. Apoptosis and its related proteins were detected by TUNEL assay, Hoechst 33,258 staining, flow cytometry and western blot. Infarct volume and the neurological status were evaluated with TTC staining and neurologic deficit score, respectively. RESULTS: The up-regulation of FOXD3-AS1 and down-regulation of miR-765 were found in both mouse brains after cerebral ischemia/reperfusion (I/R) and neuroblastoma cells of neuro-2A (N2a) after oxygen-glucose deprivation/reoxygenation (OGD/R). Moreover, the overexpression of miR-765 reduced N2a cell apoptosis caused by OGD/R. MiR-765 could target BCL2L13 directly. In addition, we found that FOXD3-AS1 bound to miR-765 directly, acting as a ceRNA to modulate the expression of BCL2L13. Overexpression of FOXD3-AS1 antagonized the inhibitory impact of miR-765 on the expression of BCL2L13 and the apoptosis of N2a cells treated with OGD/R, while FOXD3-AS1 knockdown promoted the inhibitory impact of miR-765 on the expression of BCL2L13 and the apoptosis of N2a cells treated with OGD/R. Furthermore, we found that neurological deficits and brain injury induced by I/R in vivo were attenuated by FOXD3-AS1 knockdown. CONCLUSIONS: We verified a critical signaling pathway of FOXD3-AS1/miR-765/BCL2L13 in regulating cerebral ischemia/reperfusion injury.	NA	Biomed Pharmacother. 2020 Dec;132:110778. doi: 10.1016/j.biopha.2020.110778. Epub 2020 Oct 14.
4093	LncRNA	FOXP4-AS1	miR-423-5p	NACC1	MCL cells	Mantle Cell Lymphoma	Homo sapiens (human)	luciferase assay;Rescue assay;	33416160	lncRNA FOXP4-AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR-423-5p/NACC1 pathway.	Long non-coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4-AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4-AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4-AS1 were explored in MCL clinical samples. The effects of FOXP4-AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK-8, crystal violet and Transwell assays. The downstream molecules of FOXP4-AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4-AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4-AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4-AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4-AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4-AS1 was found to act as a competing endogenous (ce)RNA for miR-423-5p to regulate the expression of nucleus accumbens-associated 1 (NACC1). The negative regulation of FOXP4-AS1 on miR-423-5p compared to that of miR-423-5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4-AS1 and miR-423-5p, and that between miR-423-5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR-423-5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4-AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4-AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR-423-5p. FOXP4-AS1 may serve as a novel therapeutic target for patients with MCL.	NA	Oncol Rep. 2021 Feb;45(2):469-480. doi: 10.3892/or.2020.7897. Epub 2020 Dec 11.
4094	LncRNA	GABPB1-IT1	miR-93	PEDF	SNU-398 cells	Hepatocellular Carcinoma	Homo sapiens (human)	Luciferase activity assay;	33664823	lncRNA GABPB1 intronic transcript 1 upregulates pigment epithelium-derived factor via miR-93 to suppress cell proliferation in hepatocellular carcinoma.	Liver cancer ranks in the top 10 most common malignancies for both mortality rate and incidence worldwide. Hepatocellular carcinoma (HCC) is the most common subtype of liver cancer. It has been reported that long non-coding RNA GABPB1 intronic transcript 1 (IT1) is downregulated in lung cancer and predicts poor survival. However, its role in live cancer remains unclear. Therefore, the present study aimed to investigate the role of GABPB1-IT1 in HCC. A total of 64 patients with HCC (40 males and 24 females; range, 43-67 years old; mean age=55.1±5.1 years) were enrolled at the 96604 Military Hospital of the Chinese People's Liberation Army between May 2012 and May 2014. The expression levels of GABPB1-IT1 and microRNA (miR)-93 in tumor and adjacent normal tissues were measured using quantitative PCR. A dual luciferase activity assay was performed to analyze the interaction between miR-93 and GABPB1-IT1. A Cell Counting Kit-8 assay was used to analyze the effect of miR transfection on the proliferation of SNU-398 cells. It was demonstrated that GABPB1-IT1 can interact with miR-93 in HCC cells, while overexpression of GABPB1-IT1 and miR-93 in HCC cells did not affect the expression of each other. GABPB1-IT1 was downregulated in HCC tissues compared with paired non-tumor tissues and predicted poor survival. Notably, overexpression of GABPB1-IT1 in HCC cells led to upregulation of pigment epithelium-derived factor (PEDF), a target of miR-93. In addition, overexpression of GABPB1-IT1 reduced the enhancing effects of miR-93 on HCC cell proliferation. Therefore, GABPB1-IT1 may upregulate PEDF through miR-93 to suppress cell proliferation in HCC.	NA	Oncol Lett. 2021 Apr;21(4):260. doi: 10.3892/ol.2021.12521. Epub 2021 Feb 4.
4095	LncRNA	GACAT1	miR-422a	YY1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33416153	Downregulation of long non-coding RNA GACAT1 suppresses proliferation and induces apoptosis of NSCLC cells by sponging microRNA-422a.	Increasing evidence has demonstrated the important roles of long non-coding (lnc) RNA in non-small cell lung cancer (NSCLC). lncRNA gastric cancer-associated transcript 1 (GACAT1) has been reported to play an oncogenic role in different types of cancer; however, the function of GACAT1 in NSCLC remains unclear. The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)-422a mechanically and negatively regulated miR-422a expression. Reduced expression of miR-422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR-422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR-422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. Taken together, these results revealed the novel role of the GACAT1/miR-422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment.	NA	Int J Mol Med. 2021 Feb;47(2):659-667. doi: 10.3892/ijmm.2020.4826. Epub 2020 Dec 22.
4096	LncRNA	GAS5	miR-382-3p	CYP2C8	liver cancer cells	Liver Cancer	Homo sapiens (human)	Rescue assay;	33180658	CYP2C8 regulated by GAS5/miR-382-3p exerts anti-cancerous properties in liver cancer.	A cornucopia of literatures has characterized the involvement of a host of functional molecules in liver cancer. Herein, according to online datasets, we found that cytochrome P450 family 2 subfamily C member 8 (CYP2C8) was downregulated in liver cancer, and high CYP2C8 expression was associated with favorable overall survival. Lower levels of CYP2C8 were confirmed in liver cancer cells. CYP2C8 overexpression efficiently attenuated liver cancer cell proliferation and promoted apoptosis. We then discovered that miR-382-3p directly targeted CYP2C8 to inhibit its expression in liver cancer cells based on bioinformatic prediction and experimental confirmation. Moreover, a cytoplasmic long noncoding RNA (lncRNA), growth arrest-specific 5 (GAS5), sponged and down-regulated miR-382-3p, thus positively modulating CYP2C8 expression. Rescue assays indicated that GAS5 overexpression gave rise to decreased proliferation and increased apoptosis of liver cancer cells, while CYP2C8 knockdown counteracted GAS5-mediated anti-carcinogenic effects. In summary, our work offered a solid experimental foundation for understanding the functional role of CYP2C8 and the mechanism of GAS5/miR-382-3p/CYP2C8 axis in cell proliferation and apoptosis of liver cancer.	NA	Cancer Biol Ther. 2020 Dec 1;21(12):1145-1153. doi: 10.1080/15384047.2020.1840886. Epub 2020 Nov 12.
4097	LncRNA	GAS5	miR-217	LHPP	NSCLC/DDP cell	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33418541	The long intergenic noncoding RNA GAS5 reduces cisplatin-resistance in non-small cell lung cancer through the miR-217/LHPP axis.	Long noncoding RNAs (lncRNAs) are known to exert their effects to tumor progression. In this study, the role of the lncRNA GAS5 (growth arrest specific 5) was confirmed in reducing non-small cell lung cancer (NSCLC) cisplatin (DDP) resistance. In NSCLC tissue samples, GAS5 expression decreased significantly. Low GAS5 levels were positively correlated with NSCLC characteristics including TNM, tumor size and lymphatic metastasis. Functionally, GAS5 significantly reduced NSCLC/DDP cell migration, invasion and epithelial-mesenchymal transition (EMT) progression in vitro. In vivo, GAS5 upregulation inhibited remarkably NSCLC/DDP cell tumor growth. Mechanism analysis suggested that GAS5 was a molecular sponge of miR-217, inhibiting the expression of phospholysine phosphohistidine inorganic pyrophosphate phosphatase (LHPP). In conclusion, this study reveals that the GAS5/miR-217/LHPP pathway reduces NSCLC cisplatin resistance and that LHPP may serve as a potential therapeutic target for NSCLC cisplatin resistance.	NA	Aging (Albany NY). 2021 Jan 8;13(2):2864-2884. doi: 10.18632/aging.202352. Epub 2021 Jan 8.
4098	LncRNA	GAS5	miR-23a-3p	PTEN	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4099	LncRNA	GAS5	miR-23a-3p	PI3K	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4100	LncRNA	GAS5	miR-23a-3p	AKT	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4101	LncRNA	GAS5	miR-34b-3p	AHR	HL-1 cells	Diabetic Cardiomyopathy	Homo sapiens (human)	qRT-PCR	33092444	LncRNA GAS5 inhibits NLRP3 inflammasome activation-mediated pyroptosis in diabetic cardiomyopathy by targeting miR-34b-3p/AHR.	Long noncoding RNA GAS5 is down-regulated in cardiomyocytes in diabetic cardiomyopathy (DCM). Here, we studied the involvement of GAS5 in DCM by analyzing its expression in DCM mouse model and cardiac muscle cell line (HL-1 cells). Compared with normal mice, GAS5 was severely down-regulated in heart tissues of DCM mice. GAS5 overexpression improved cardiac function and myocardial hypertrophy in DCM mice. In addition, the expression of NLRP3, caspase-1, Pro-caspase-1, IL-1β and IL-18 were increased in heart tissues of DCM mice and high glucose-treated HL-1 cells, which was repressed by GAS5 up-regulation. GAS5 overexpression suppressed caspase-1 activity, LDH release and the levels of IL-1β, IL-18 in the high glucose-treated HL-1 cells. Moreover, GAS5 regulated AHR expression by sponging miR-34b-3p. Furthermore, GAS5 overexpression suppressed NLRP3 inflammasome activation-mediated pyroptosis by regulating miR-34b-3p/AHR axis. In summary, our study demonstrates that GAS5 acts as a competing endogenous RNA to enhance AHR expression by sponging miR-34b-3p, which consequently represses NLRP3 inflammasome activation-mediated pyroptosis to improve DCM. Thus, our data provide a novel lncRNA GAS5 that could be a valuable target for DCM treatment.	NA	Cell Cycle. 2020 Nov;19(22):3054-3065. doi: 10.1080/15384101.2020.1831245. Epub 2020 Oct 23.
4102	LncRNA	GAS5	miR-23a-3p	PTEN	osteosarcoma cells	Osteosarcoma	Mus musculus (mouse)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4103	LncRNA	GAS5	miR-23a-3p	PI3K	osteosarcoma cells	Osteosarcoma	Mus musculus (mouse)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4104	LncRNA	GAS5	miR-23a-3p	AKT	osteosarcoma cells	Osteosarcoma	Mus musculus (mouse)	RNA immunoprecipitation;RNA immunoprecipitation;	33121268	LncRNA GAS5 Suppresses the Proliferation and Invasion of Osteosarcoma Cells via the miR-23a-3p/PTEN/PI3K/AKT Pathway.	Accumulating evidence has shown that long noncoding RNA GAS5 is a well-known tumor suppressor in the pathogenesis of a variety of human cancers. However, the detailed role of GAS5 in osteosarcoma is still largely unclear. In this study, we found that GAS5 was downregulated in human osteosarcoma tissues and cell lines compared with matched adjacent tissues and normal osteoblast cells. Overexpression of GAS5 could significantly suppress the growth and invasion of osteosarcoma cells, while downregulation of GAS5 promoted cell proliferation and invasion. We confirmed that GAS5 could directly bind with miR-23a-3p by using luciferase reporter gene and RNA immunoprecipitation and pull-down assay. Downregulation of miR-23a-3p repressed cell proliferation and invasion. Overexpression of miR-23a-3p counterbalanced the inhibition effect of GAS5 on cell proliferation and invasion. Further studies indicated that overexpression of GAS5 inhibited cell proliferation and metastasis by regulating phosphatase and tensin homolog (PTEN). PTEN was authenticated as a target of miR-23a-3p. Upregulation of GAS5 or silence of miR-23a-3p increased the level of PTEN, while downregulation of GAS5 or overexpression of miR-23a-3p suppressed the expression of PTEN. In addition, overexpression of GAS5 could neutralize the effect of downregulating PTEN on osteosarcoma cell functions. We proved that GAS5 regulated the viability and invasion of osteosarcoma cells through the PI3K/AKT pathway. Moreover, overexpression of GAS5 could inhibit tumor growth in a xenograft nude mouse model in vivo. In summary, GAS5 functions as a competing endogenous RNA, sponging miR-23a-3p, to promote PTEN expression and suppress cell growth and invasion in osteosarcoma by regulating the PI3K/AKT pathway.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720953093. doi: 10.1177/0963689720953093.
4105	LncRNA	GAS5	miR-34b-3p	AHR	HL-1 cells	Diabetic Cardiomyopathy	Mus musculus (mouse)	qRT-PCR	33092444	LncRNA GAS5 inhibits NLRP3 inflammasome activation-mediated pyroptosis in diabetic cardiomyopathy by targeting miR-34b-3p/AHR.	Long noncoding RNA GAS5 is down-regulated in cardiomyocytes in diabetic cardiomyopathy (DCM). Here, we studied the involvement of GAS5 in DCM by analyzing its expression in DCM mouse model and cardiac muscle cell line (HL-1 cells). Compared with normal mice, GAS5 was severely down-regulated in heart tissues of DCM mice. GAS5 overexpression improved cardiac function and myocardial hypertrophy in DCM mice. In addition, the expression of NLRP3, caspase-1, Pro-caspase-1, IL-1β and IL-18 were increased in heart tissues of DCM mice and high glucose-treated HL-1 cells, which was repressed by GAS5 up-regulation. GAS5 overexpression suppressed caspase-1 activity, LDH release and the levels of IL-1β, IL-18 in the high glucose-treated HL-1 cells. Moreover, GAS5 regulated AHR expression by sponging miR-34b-3p. Furthermore, GAS5 overexpression suppressed NLRP3 inflammasome activation-mediated pyroptosis by regulating miR-34b-3p/AHR axis. In summary, our study demonstrates that GAS5 acts as a competing endogenous RNA to enhance AHR expression by sponging miR-34b-3p, which consequently represses NLRP3 inflammasome activation-mediated pyroptosis to improve DCM. Thus, our data provide a novel lncRNA GAS5 that could be a valuable target for DCM treatment.	NA	Cell Cycle. 2020 Nov;19(22):3054-3065. doi: 10.1080/15384101.2020.1831245. Epub 2020 Oct 23.
4106	LncRNA	GAS5	miR-34b-3p	AHR	HL-1 cells	Diabetic Cardiomyopathy	Mus musculus (mouse)	qRT-PCR	33092444	LncRNA GAS5 inhibits NLRP3 inflammasome activation-mediated pyroptosis in diabetic cardiomyopathy by targeting miR-34b-3p/AHR.	Long noncoding RNA GAS5 is down-regulated in cardiomyocytes in diabetic cardiomyopathy (DCM). Here, we studied the involvement of GAS5 in DCM by analyzing its expression in DCM mouse model and cardiac muscle cell line (HL-1 cells). Compared with normal mice, GAS5 was severely down-regulated in heart tissues of DCM mice. GAS5 overexpression improved cardiac function and myocardial hypertrophy in DCM mice. In addition, the expression of NLRP3, caspase-1, Pro-caspase-1, IL-1β and IL-18 were increased in heart tissues of DCM mice and high glucose-treated HL-1 cells, which was repressed by GAS5 up-regulation. GAS5 overexpression suppressed caspase-1 activity, LDH release and the levels of IL-1β, IL-18 in the high glucose-treated HL-1 cells. Moreover, GAS5 regulated AHR expression by sponging miR-34b-3p. Furthermore, GAS5 overexpression suppressed NLRP3 inflammasome activation-mediated pyroptosis by regulating miR-34b-3p/AHR axis. In summary, our study demonstrates that GAS5 acts as a competing endogenous RNA to enhance AHR expression by sponging miR-34b-3p, which consequently represses NLRP3 inflammasome activation-mediated pyroptosis to improve DCM. Thus, our data provide a novel lncRNA GAS5 that could be a valuable target for DCM treatment.	NA	Cell Cycle. 2020 Nov;19(22):3054-3065. doi: 10.1080/15384101.2020.1831245. Epub 2020 Oct 23.
4107	LncRNA	GAS5	miR-4465	COX2	nasopharyngeal carcinoma tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR	33092435	LncRNA GAS5/miR-4465 axis regulates the malignant potential of nasopharyngeal carcinoma by targeting COX2.	Nasopharyngeal carcinoma is a malignant tumor that not only negatively affects the physical and mental health but also the quality of life of the patients. Growth arrest-specific transcript 5 (GAS5) is a common long-chain non-coding RNA (lncRNA) that has been reported to participate in the development of various cancers. However, the biological functions of lncRNA GAS5 in the occurrence and development of nasopharyngeal carcinoma are elusive. The expression of lncRNA GAS5 in nasopharyngeal carcinoma and normal samples were analyzed. Bioinformatic tool was utilized to predict the potential function of lncRNA in nasopharyngeal carcinoma. Transplanted mice were used for in vivo experiments. We observed that the expression of lncRNA GAS5 was upregulated in nasopharyngeal carcinoma tissues and cells. Down-regulation of lncRNA GAS5 inhibited the proliferation and promoted apoptosis of nasopharyngeal carcinoma cells. The expression of miR-4465 was down regulated in nasopharyngeal carcinoma tissues and cells. LncRNA GAS5 could directly bind to miR-4465 and regulated the expression of miR-4465. It was further confirmed that miR-4465 could directly bind with COX2 and inhibit the expression of COX2. Down-regulation of lncRNA GAS5 suppressed tumor growth, promoted the expression levels of miR-18a-5p and suppressed the expression of COX2 in vivo. LncRNA GAS5 regulated nasopharyngeal carcinoma malignancy through targeting miR-4465 and modulating COX2. The GAS5/miR-4465/COX2 axis in nasopharyngeal carcinoma pathogenesis was confirmed, which would provide a new therapeutic target for nasopharyngeal carcinoma.	NA	Cell Cycle. 2020 Nov;19(22):3004-3017. doi: 10.1080/15384101.2020.1816280. Epub 2020 Oct 23.
4108	LncRNA	GAS5	miR-135a	NA	THP-1 cells	Atherosclerosis	Homo sapiens (human)	Rescue assay;	33128668	GAS5 knockdown suppresses inflammation and oxidative stress induced by oxidized low-density lipoprotein in macrophages by sponging miR-135a.	A large number of long non-coding RNAs have been confirmed to play vital roles in regulating various biological processes. Abnormal expression of growth arrest-specific transcript 5 (GAS5) is reported to be involved in the development of atherosclerosis (AS). This work is to explore the detailed mechanism underling how GAS5 regulates AS progression. We found that the abundance of GAS5 was markedly increased, and miR-135a was decreased in AS patient serums and ox-LDL-induced human THP-1 cells dose and time dependently. Interference of GAS5 suppressed inflammation and oxidative stress induced by ox-LDL in THP-1 cells. Mechanistically, GAS5 acted as a molecular sponge of microRNA-135a (miR-135a). Rescue assays indicated that knockdown of miR-135a partially rescued small interference RNA for GAS5-inhibited inflammatory cytokines release and oxidative stress in ox-LDL-triggered THP-1 cells. In conclusion, the absence of GAS5-inhibited inflammatory response and oxidative stress induced by ox-LDL in THP-1 cells via sponging miR-135a, providing a deep insight into the molecular target for AS treatment.	NA	Mol Cell Biochem. 2021 Feb;476(2):949-957. doi: 10.1007/s11010-020-03962-w. Epub 2020 Oct 31.
4109	LncRNA	GAS5	miR-128-3p	FBLN2	ox-LDL-induced THP-1 cells	Atherosclerosis	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33074219	Long non-coding RNA GAS5 knockdown facilitates proliferation and impedes apoptosis by regulating miR-128-3p/FBLN2 axis in ox-LDL-induced THP-1 cells.	BACKGROUND: Long non-coding RNAs (lncRNAs) are found to involve in modulating the development of atherosclerosis (AS). But the molecular mechanism of lncRNA growth-arrest specific transcript 5 (GAS5) in AS is not fully understood. METHODS: QRT-PCR was performed to measure the abundances of GAS5, miR-128-3p and fibulin 2 (FBLN2). Oxidized low-density lipoprotein (ox-LDL)-treated THP-1 cells were employed as cell models of AS. The cell proliferation and apoptosis were analyzed using CCK-8 and Flow cytometry assays, respectively. Levels of all protein were examined by western blot. The interaction among GAS5, miR-128-3p and FBLN2 was confirmed via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. RESULTS: GAS5 was elevated and miR-128-3p was decreased in the serum of patients with AS and ox-LDL-stimulated THP-1 cells. Ox-LDL stimulation inhibited proliferation and induced apoptosis of THP-1 cells. Meanwhile, GAS5 directly targeted miR-128-3p and inversely modulated its expression. Importantly, GAS5 depletion facilitated cell proliferation and impaired apoptosis in ox-LDL-induced THP-1 cells. Additionally, GAS5 augmented FBLN2 expression through sponging miR-128-3p, and miR-128-3p facilitated proliferation and retarded apoptosis of ox-LDL-induced THP-1 cells by targeting FBLN2. CONCLUSION: GAS5 knockdown promoted the growth of ox-LDL-induced THP-1 cells through down-modulating FBLN2 and increasing miR-128-3p, suggesting the potential value of GAS5 for treatment of AS.	NA	Clin Hemorheol Microcirc. 2021;77(2):153-164. doi: 10.3233/CH-200897.
4110	LncRNA	GAS5	miR-34a	SIRT1	CRC cells	Colorectal Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;luciferase assay;	33416133	lncRNA GAS5 inhibits malignant progression by regulating macroautophagy and forms a negative feedback regulatory loop with the miR-34a/mTOR/SIRT1 pathway in colorectal cancer.	Long non-coding RNA growth arrest specific 5 (GAS5) exerts inhibitory effects through the modulation of several target microRNAs (miRs) in cancer. However, its potential roles and underlying relationship during colorectal cancer (CRC) progression are unclear. Therefore, we explored the role of the negative feedback loop formed by the GAS5/miR-34a axis and mammalian target of rapamycin/sirtuin 1 (mTOR/SIRT1) pathway on macroautophagy and apoptosis in CRC. Expression of GAS5, miR-34a, SIRT1 and mTOR in CRC patients and cell lines was detected by quantitative reverse transcription polymerase chain reaction. Online bioinformatic analysis was used to predict the downstream miRs of GAS5. Luciferase assay and western blotting were performed to demonstrate miR-34a as a downstream target gene of GAS5 in CRC cells. The effects of the GAS5/miR-34a axis on apoptosis, macroautophagy, and the mTOR/SIRT1 pathway were assessed by flow cytometry, transmission electron microscopy and western blotting, respectively. Our results suggested that GAS5 was downregulated and acted as a molecular sponge of miR-34a during CRC progression. miR-34a participated in regulating GAS5-suppressed CRC cell macroautophagy and induced apoptosis through the mTOR/SIRT1 pathway. GAS5-mediated macroautophagy was maintained in an equilibrium state that might have a protective effect on CRC cell apoptosis. The mTOR signaling pathway suppressed GAS5 expression and formed a negative regulation feedback loop with miR-34a in CRC cells. Our results suggested that the GAS5/miR-34a/SIRT1/mTOR negative regulatory feedback loop mediated CRC cell macroautophagy, and maintained the cells in an autonomous equilibrium state, but not excessive activation state, which functions as a strong antiapoptotic phenotype during human CRC progression.	NA	Oncol Rep. 2021 Jan;45(1):202-216. doi: 10.3892/or.2020.7825. Epub 2020 Oct 26.
4111	LncRNA	Gas5	miR-23b-3p	KCNK3	pulmonary artery smooth muscular cells	Pulmonary Hypertension	Rattus (rat)	qRT-PCR;	33010302	Down-regulation of lncRNA Gas5 promotes hypoxia-induced pulmonary arterial smooth muscle cell proliferation by regulating KCNK3 expression.	Pulmonary hypertension (PH) is a progressive and potentially serious lung disease, defined by an abnormal elevation of pulmonary arterial pressure. PH occurs for many reasons, and hypoxia is considered as an important stimulus for the disease. Proliferation and migration of pulmonary artery smooth muscular cells (PASMCs) in the small peripheral pulmonary arteries are common characteristic features in hypoxia-induced PH (HPH). However, the mechanisms involved in the hypoxia-induced cell proliferation and migration are not clear. The aim of the present study was to investigate the role of lncRNA Gas5 in the hypoxia-stimulated proliferation and migration of human PASMCs (hPASMCs). We found that the expression of Gas5 was down-regulated in a rat model with hypoxia and in cultured hypoxic hPASMCs, and silence of Gas5 significantly promoted hPASMCs proliferation and migration in both normal and hypoxia condition. Subsequent studies revealed that miR-23b-3p interacted with Gas5 by directly targeting the miRNA-binding site in the Gas5 sequence, and qRT-PCR results showed miR-23b-3p and Gas5 could affect each other's expression, respectively. Further study demonstrated that Gas5 acted as a competing endogenous RNA (ceRNA) for miR-23b-3p to modulate the KCNK3 expression, and these interactions led to promotion of hPASMCs proliferation and migration. This study identified that Gas5/miR-23b-3p/KCNK3 axis may be a mechanism that hypoxia-induced PASMCs proliferation and migration, providing a strategy for clinical treatment of HPH in the future.	NA	Eur J Pharmacol. 2020 Dec 15;889:173618. doi: 10.1016/j.ejphar.2020.173618. Epub 2020 Sep 30.
4112	LncRNA	Gas5	miR-23b-3p	KCNK3	pulmonary artery smooth muscular cells	Pulmonary Hypertension	Homo sapiens (human)	qRT-PCR;	33010302	Down-regulation of lncRNA Gas5 promotes hypoxia-induced pulmonary arterial smooth muscle cell proliferation by regulating KCNK3 expression.	Pulmonary hypertension (PH) is a progressive and potentially serious lung disease, defined by an abnormal elevation of pulmonary arterial pressure. PH occurs for many reasons, and hypoxia is considered as an important stimulus for the disease. Proliferation and migration of pulmonary artery smooth muscular cells (PASMCs) in the small peripheral pulmonary arteries are common characteristic features in hypoxia-induced PH (HPH). However, the mechanisms involved in the hypoxia-induced cell proliferation and migration are not clear. The aim of the present study was to investigate the role of lncRNA Gas5 in the hypoxia-stimulated proliferation and migration of human PASMCs (hPASMCs). We found that the expression of Gas5 was down-regulated in a rat model with hypoxia and in cultured hypoxic hPASMCs, and silence of Gas5 significantly promoted hPASMCs proliferation and migration in both normal and hypoxia condition. Subsequent studies revealed that miR-23b-3p interacted with Gas5 by directly targeting the miRNA-binding site in the Gas5 sequence, and qRT-PCR results showed miR-23b-3p and Gas5 could affect each other's expression, respectively. Further study demonstrated that Gas5 acted as a competing endogenous RNA (ceRNA) for miR-23b-3p to modulate the KCNK3 expression, and these interactions led to promotion of hPASMCs proliferation and migration. This study identified that Gas5/miR-23b-3p/KCNK3 axis may be a mechanism that hypoxia-induced PASMCs proliferation and migration, providing a strategy for clinical treatment of HPH in the future.	NA	Eur J Pharmacol. 2020 Dec 15;889:173618. doi: 10.1016/j.ejphar.2020.173618. Epub 2020 Sep 30.
4113	LncRNA	GAS6-AS1	miR-324-3p	SETD1A	breast cancer cells	Breast Cancer	Homo sapiens (human)	Rescue assay;	33223203	LncRNA GAS6-AS1 facilitates the progression of breast cancer by targeting the miR-324-3p/SETD1A axis to activate the PI3K/AKT pathway.	Breast cancer is one of the most prevalent cancers in women with a high incidence and mortality worldwide. A great number of studies have indicated that long non-coding RNAs (lncRNAs) play significant roles in the initiation and development of human cancers. Although it has been revealed that lncRNA GAS6-AS1 is involved in the regulation of several cancer types, the role and regulatory mechanism of GAS6-AS1 in breast cancer remain unclear. In this paper, our findings showed that GAS6-AS1 expression was significantly elevated in breast cancer tissues and cell lines, and the high level of GAS6-AS1 reflected a poor prognosis of patients with breast cancer. Moreover, GAS6-AS1 knockdown suppressed cell proliferation, migration and invasion as well as facilitated cell apoptosis. We further found that the depletion of GAS6-AS1 suppressed the PI3K/AKT signaling pathway through inhibiting the levels of pathway-related proteins. Mechanically, GAS6-AS1 acted as a competing endogenous RNA (ceRNA) to sponge miR-324-3p and upregulate SETD1A expression. Besides, GAS6-AS1 activated the PI3K/AKT pathway by targeting the miR-324-3p/SETD1A axis. Rescue assays showed that SETD1A overexpression or 740Y-P treatment reversed the inhibitory effect of silenced GAS6-AS1 on cellular progresses of breast cancer. In summary, this work first explored the molecular regulatory mechanism of GAS6-AS1 in breast cancer cells and revealed that GAS6-AS1 facilitated the malignant behaviors of breast cancer cells by the miR-324-3p/SETD1A axis to activate the PI3K/AKT pathway.	NA	Eur J Cell Biol. 2020 Nov;99(8):151124. doi: 10.1016/j.ejcb.2020.151124. Epub 2020 Sep 16.
4114	LncRNA	GAS8-AS1	miR-1343-3p	ATG7	PTC cells	Thyroid Cancer	Homo sapiens (human)	Immunohistochemistry;Luciferase reporter assay;	33230459	ATF2-Induced lncRNA GAS8-AS1 Promotes Autophagy of Thyroid Cancer Cells by Targeting the miR-187-3p/ATG5 and miR-1343-3p/ATG7 Axes.	Long non-coding RNAs (lncRNAs) play an essential regulatory role in multiple cancers. However, the role of lncRNAs in papillary thyroid carcinoma (PTC) is still unknown. Here, GAS8-AS1, a novel lncRNA that is significantly downregulated in PTC, was selected for further investigation. The roles of GAS8-AS1 in PTC cells were verified by gain- and loss-of-function experiments. The functional mechanism of GAS8-AS1 on the microRNA (miR)-187-3p/ATG5 axis and miR-1343-3p/ATG7 axis in PTC cells was evaluated using bioinformatics analysis, luciferase reporter assay, Cell Counting Kit-8 (CCK-8) assay, immunohistochemistry analysis, transmission electron microscopy, and immunofluorescence. We found that GAS8-AS1 was downregulated in PTC tissues and cell lines. In patients with PTC, low GAS8-AS1 expression was associated with higher tumor-node-metastasis (TNM) stage and lymph node metastasis (LNM). Functionally, GAS8-AS1 significantly promoted autophagy and inhibited PTC cell proliferation in vitro and promoted tumorigenesis in vivo. Mechanistically, GAS8-AS1 acted as a sponge of miR-187-3p and miR-1343-3p and upregulated ATG5 and ATG7 expression, respectively. The transcription factor ATF2 regulated GAS8-AS1 by binding to the GAS8-AS1 promoter. In conclusion, upregulation of ATF2 activated GAS8-AS1-promoted autophagy of PTC cells by sponging oncogenic miR-187-3p and miR-1343-3p and upregulating the expression of ATG5 and ATG7, respectively, making GAS8-AS1 a potential prognostic biomarker and therapeutic target for PTC.	NA	Mol Ther Nucleic Acids. 2020 Sep 23;22:584-600. doi: 10.1016/j.omtn.2020.09.022. eCollection 2020 Dec 4.
4115	LncRNA	GASL1	miR-106a	NA	GC cells	Gastric Cancer	Homo sapiens (human)	Cell transfection;Cell transfection;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	32897806	Long non-coding RNA GASL1 restrains gastric carcinoma cell proliferation and metastasis by sponging microRNA-106a.	Background: Gastric carcinoma (GC) is a common malignant tumor. Recently, it has been found that long non-coding RNAs (lncRNAs) play important role in cancer. In this paper, we investigated the effects and mechanism of lncRNA GASL1 in GC cells. Methods: GASL1 level in GC cells was up-regulated via cell transfection. Cell proliferation, migration, invasion were detected by CCK-8, BrdU, Transwell assays and western blot. In addition, the regulation of GASL1 on microRNA (miR)-106a level was detected using RT-qPCR and the binding between GASL1 and miR-106a was confirmed by bioinformatic prediction and luciferase reporter assay. The effects of overexpressing miR-106a on GASL1-regulated GC cell behaviors were further explored. Moreover, western blot also was used to detect the pathway-related proteins. Results: Overexpression of GASL1 decreased the viability and BrdU levels. Meanwhile, CyclinD1 level was decreased while p53 and p21 levels were strengthened by overexpression of GASL1. On cell metastasis, up-regulation of GASL1 decreased cell migration, invasion and related proteins matrix metalloproteinase (MMP)-9 and Vimentin levels. Meanwhile, silencing GASL1 exerted opposite effects on GC cells. Moreover, GASL1 negatively regulated and targeted miR-106a. Up-regulation of miR-106a weakened the functions of GASL1 in cell proliferation and metastasis. Besides, GASL1 decreased the relate-protein levels of PI3K/AKT and ras/raf/MEK/ERK pathways while miR-106a weakened these changes. ConclusionGASL1 restrained GC cell proliferation and metastasis and blocked PI3K/AKT and ras/raf/MEK/ERK pathways by sponging miR-106a.	NA	Cell Cycle. 2020 Oct;19(20):2611-2621. doi: 10.1080/15384101.2020.1812918. Epub 2020 Sep 8.
4116	LncRNA	GATA6-AS	miR-205	NA	CSCC cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33167959	LncRNA GATA6-AS inhibits cancer cell proliferation and promotes cancer cell apoptosis in cervical cancer by down-regulating miR-205.	BACKGROUND: Dysregulated endothelial cell growth is involved in many types of human cancer, including cervical cancer. LncRNA GATA6-AS was reported to regulate endothelial cell growth, suggesting it might involve in cervical cancer. Our study was carried out to explore the involvement of GATA6-AS in cervical squamous cell carcinoma (CSCC), a subtype of cervical cancer. METHODS: To explore the expression of GATA6-AS, RT-qPCR was performed to detect GATA6-AS in plasma of 65 CSCC patients and 58 healthy females. To detect the expression of GATA6-AS, total RNAs were extracted. RESULTS: We found that plasma GATA6-AS expression was down-regulated in CSCC patients than that in healthy females, and HPV infection did not significantly affect the plasma expression of GATA6-AS. Moreover, we found that plasma GATA6-AS showed diagnostic values for CSCC by performing ROC curve analysis. The expression of miR-205 in plasma was also found to be up-regulated in CSCC patients than that in healthy females and inversely correlated with the expression of GATA6-AS in CSCC patients. Furthermore, over-expression of miR-205 did not significantly affect the expression of GATA6-AS in CSCC cells, while over-expression of GATA6-AS down-regulated miR-205 expression. In addition, GATA6-AS over-expression inhibited CSCC cell proliferation and promoted CSCC cell apoptosis, while miR-205 over-expression played opposite roles and attenuated the effects of GATA6-AS over-expression on CSCC cells. CONCLUSION: Taken together, these results suggest that GATA6-AS may inhibit cell proliferation and promote cell apoptosis in CSCC by down-regulating miR-205.	NA	BMC Womens Health. 2020 Nov 9;20(1):247. doi: 10.1186/s12905-020-01082-7.
4117	LncRNA	GCMA	miR-124	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	32913198	Correction: SP1-activated long noncoding RNA lncRNA GCMA functions as a competing endogenous RNA to promote tumor metastasis by sponging miR-124 and miR-34a in gastric cancer.	An amendment to this paper has been published and can be accessed via a link at the top of the paper.	NA	Oncogene. 2020 Oct;39(42):6621. doi: 10.1038/s41388-020-1377-2.
4118	LncRNA	GCMA	miR-34a	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	32913198	Correction: SP1-activated long noncoding RNA lncRNA GCMA functions as a competing endogenous RNA to promote tumor metastasis by sponging miR-124 and miR-34a in gastric cancer.	An amendment to this paper has been published and can be accessed via a link at the top of the paper.	NA	Oncogene. 2020 Oct;39(42):6621. doi: 10.1038/s41388-020-1377-2.
4119	LncRNA	GHET1	miR-105	RAP2B	AML cell lines	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33123297	Long non-coding RNA GHET1/miR-105/RAP2B axis regulates the progression of acute myeloid leukemia.	Background: To explore the biological effects and potential molecular mechanisms of long non-coding RNA (lncRNA) gastric carcinoma proliferation enhancing transcript 1 (GHET1) in acute myeloid leukemia (AML). Methods: Fluorescence in situ hybridization was performed to determine the location of GHET1. Quantitative polymerase chain reaction (qPCR) was performed to verify RNA expression. GHET1 overexpression and knockdown were achieved by transfection of the expression vector or short hairpin RNA. Western blotting, qPCR, Cell Counting Kit-8 assay, JC-1 staining, and flow cytometry were performed to measure GHET1 function. The dual luciferase reporter assay was performed to confirm the relationship between microRNA 105 (mir-105) and Ras-related protein Rap-2B (RAP2B). Results: GHET1 was localized in the nucleus of NB4 cell lines. GHET1 expression was elevated in AML cell lines compared with normal bone marrow mononuclear cells. GHET1 knockdown led to inhibition of proliferation and promoted the differentiation and apoptosis of AML cell lines. Furthermore, GHET1 directly bound to miR-105 and downregulated miR-105 expression. MiR-105 overexpression suppressed proliferation and induced the differentiation and apoptosis of AML cell lines. In addition, RAP2B was confirmed to be a target gene of miR-105 and an inverse correlation was shown between their expression levels in AML cell lines; when miR-105 increased, Rap-2B level decreased and vice versa. Conclusion: This study demonstrated that the GHET1/miR-105/Rap2B axis may be a critical signaling pathway involved in AML progression.	NA	J Cancer. 2020 Oct 17;11(23):7081-7090. doi: 10.7150/jca.47294. eCollection 2020.
4120	LncRNA	Gm15834	miR-30b-3p	ULK1	cardiac hypertrophy	Transverse Aortic Constriction	Homo sapiens (human)	qRT-PCR	33130312	Inhibition of lncRNA Gm15834 Attenuates Autophagy-Mediated Myocardial Hypertrophy via the miR-30b-3p/ULK1 Axis in Mice.	Emerging evidence reveals that autophagy plays crucial roles in cardiac hypertrophy. Long noncoding RNAs (lncRNAs) are novel transcripts that function as gene regulators. However, it is unclear whether lncRNAs regulate autophagy in cardiac hypertrophy. Here, we identified a novel transcript named lncRNA Gm15834, which was upregulated in the transverse aortic constriction (TAC) model in vivo and the angiotensin-II (Ang-II)-induced cardiac hypertrophy model in vitro and was regulated by nuclear factor kappa B (NF-κB). Importantly, forced expression of lncRNA Gm15834 enhanced autophagic activity of cardiomyocytes and promoted myocardial hypertrophy, whereas silencing of lncRNA Gm15834 attenuated autophagy-induced myocardial hypertrophy. Mechanistically, we found that lncRNA Gm15834 could function as an endogenous sponge RNA of microRNA (miR)-30b-3p, which was downregulated in cardiac hypertrophy. Inhibition of miR-30b-3p enhanced cardiomyocyte autophagic activity and aggravated myocardial hypertrophy, whereas overexpression of miR-30b-3p suppressed autophagy-induced myocardial hypertrophy by targeting the downstream autophagy factor of unc-51-like kinase 1 (ULK1). Moreover, inhibition of lncRNA Gm15834 by adeno-associated virus carrying short hairpin RNA (shRNA) suppressed cardiomyocyte autophagic activity, improved cardiac function, and mitigated cardiac hypertrophy. Taken together, our study identified a novel regulatory axis encompassing lncRNA Gm15834/miR-30b-3p/ULK1/autophagy in cardiac hypertrophy, which may provide a potential therapy target for cardiac hypertrophy.	NA	Mol Ther. 2021 Mar 3;29(3):1120-1137. doi: 10.1016/j.ymthe.2020.10.024. Epub 2020 Oct 31.
4121	LncRNA	Gm28309	miR-3068-5p	NF-kB	THP-1 cells, RAW264.7 cells	Brucellosis	Homo sapiens (human)	ELISA;microarray;qPCR;RT-qPCR;RACE;Western blot;Immunohistochemistry;Luciferase reporter assay;	33414782	Brucella-Induced Downregulation of lncRNA Gm28309 Triggers Macrophages Inflammatory Response Through the miR-3068-5p/NF-κB Pathway.	OBJECTIVES: The underlying mechanism of the inflammatory response against Brucellosis caused by Brucella remains poorly understood. This study aimed to determine the role of long non-coding RNAs (lncRNAs) in regulating of inflammatory and anti-Brucella responses. MATERIALS AND METHODS: Microarray analysis was performed to detect differentially expressed lncRNAs in THP-1 cells infected with an S2308 Brucella strain. The candidate lncRNAs were screened using bioinformatic analysis and siRNAs; bioinformatic prediction and luciferase reporter assay were also conducted, while inflammatory responses was assessed using RT-qPCR, western blot, immunofluorescence, ELISA, HE, and immunohistochemistry. RESULTS: The lncRNA Gm28309 was identified to be involved in regulating inflammation induced by Brucella. Gm28309, localized in the cytoplasm, was down-expressed in RAW264.7 cells infected with S2308. Overexpression of Gm28309 or inhibition of miR-3068-5p repressed p65 phosphorylation and reduced NLRP3 inflammasome and IL-1β and IL-18 secretion. Mechanistically, Gm28309 acted as a ceRNA of miR-3068-5p to activate NF-κB pathway by targeting κB-Ras2, an inhibitor of NF-κB signaling. Moreover, the number of intracellular Brucella was higher when Gm28309 was overexpressed or when miR-3068-5p or p65 was inhibited. However, these effects were reversed by the miR-3068-5p mimic. CONCLUSIONS: Our study demonstrates, for the first time, that LncRNAs are involved in regulating immune responses during Brucella infection, and Gm28309, an lncRNA, plays a crucial role in activating NF-κB/NLRP3 inflammasome signaling pathway.	NA	Front Immunol. 2020 Dec 22;11:581517. doi: 10.3389/fimmu.2020.581517. eCollection 2020.
4122	LncRNA	Gm7237	miR-142a	MRF	central nervous	Central Nervous System (Cns) Demyelination	Homo sapiens (human)	qRT-PCR	33151124	Gastrodin promotes CNS myelination via a lncRNA Gm7237/miR-142a/MRF pathway.	Treatment of central nervous system (CNS) demyelination is greatly hindered by lack of the knowledge regarding to underlying molecular mechanisms as well as therapeutic agents. Here, we report a novel small molecule agent, gastrodin (GAS), which can significantly promote CNS myelination in in vivo mice models. By using high-throughput sequencing analysis, we discover a key long non-coding RNA Gm7237 that can enhance CNS myelination and is up-regulated by GAS. Through using bioinformatic analysis and experimental validations, we further unravel that microRNA-142a (miR-142a) and its target myelin gene regulatory factor (MRF) is under the direct regulation by Gm7237. Finally, we demonstrate that Gm7237/miR-142a/MRF axis is the key pathway involved in CNS myelination mediated by GAS. Overall, our results provide not only a novel agent for therapeutic treatment of CNS demyelination but also a molecular basis responsible for GAS-promoted CNS myelination.	NA	RNA Biol. 2020 Nov 5:1-12. doi: 10.1080/15476286.2020.1841976.
4123	LncRNA	Gpr137b-ps	miR-200a-3p	CXCL14	hepatic stellate cells	Hepatic Fibrosis	Homo sapiens (human)	RACE;	33069761	A lncRNA Gpr137b-ps/miR-200a-3p/CXCL14 axis modulates hepatic stellate cell (HSC) activation.	Hepatic fibrosis is the wound healing response upon the liver tissue damage caused by multiple stimuli. Targeting activated hepatic stellate cells (HSCs), the major extracellular matrix (ECM)-producing cells within the damaged liver, has been regarded as one of the main treatments for hepatic fibrosis. In the present study, we performed preliminary bioinformatics analysis attempting to identify possible factors related to hepatic fibrosis and found that lncRNA G protein-coupled receptor 137B (Gpr137b-ps) and C-X-C motif chemokine ligand 14 (CXCL14) showed to be markedly upregulated within carbon tetrachloride (CCl4)-caused hepatic fibrotic mice tissue samples and activated HSCs. CXCL14 The silencing of lncRNA Gpr137b-ps or CXCL14 alone could significantly improve CCl4-induced fibrotic changes in mice liver in vivo and collagen I and III release by HSCs and HSC proliferation in vitro. miR-200a-3p directly targeted lncRNA Gpr137b-ps and CXCL14, respectively. LncRNA Gpr137b-ps relieved miR-200a-3p-induced inhibition on CXCL14 expression via acting as a ceRNA. In HSCs, the effects of lncRNA Gpr137b-ps silencing on collagen I and III release by HSCs and HSC proliferation were significantly reversed by miR-200a-3p inhibition, and the effects of miR-200a-3p inhibition were reversed by CXCL14 silencing. In conclusion, we demonstrated a lncRNA Gpr137b-ps/miR-200a-3p/CXCL14 axis that modulates HSC activation and might exert an effect on the pathogenesis of liver fibrosis.	NA	Toxicol Lett. 2021 Jan 1;336:21-31. doi: 10.1016/j.toxlet.2020.10.001. Epub 2020 Oct 15.
4124	LncRNA	H19	miR-22-3p	MMP14	DLD1, HCT116, SW480 and SW620	Colorectal Cancer	Homo sapiens (human)	microarray;RT-PCR;Western blot;Chromatin immunoprecipitation;	33267897	HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer.	BACKGROUND: Emerging evidence suggests that epithelial mesenchymal transition (EMT) and epigenetic mechanisms promote metastasis. Histone deacetylases (HDACs) and noncoding RNAs (ncRNAs) are important epigenetic regulators. Here, we elucidated a novel role of histone deacetylase 2 (HDAC2) in regulating EMT and CRC metastasis via ncRNA. METHODS: The expression of HDACs in CRC was analyzed using the public databases and matched primary and metastatic tissues, and CRC cells with different metastatic potentials (DLD1, HCT116, SW480 and SW620). Microarray analysis was used to identify differential genes in parental and HDAC2 knockout CRC cells. EMT and histone modifications were determined using western blot and immunofluorescence. Migration ability was assessed by transwell assay, and metastasis was assessed in vivo using a tail vain injection. Gene expression and regulation was assessed by RT-PCR, chromatin immunoprecipitation and reporter assays. Protein interaction was assessed by immunoprecipitation. Specific siRNAs targeting H19, SP1 and MMP14 were used to validate their role in HDAC2 loss induced EMT and metastasis. RESULTS: Reduced HDAC2 expression was associated with poor prognosis in CRC patients and found in CRC metastasis. HDAC2 deletion or knockdown induced EMT and metastasis by upregulating the long noncoding RNA H19 (LncRNA H19). HDAC2 inhibited LncRNA H19 expression by histone H3K27 deacetylation in its promoter via binding with SP1. LncRNA H19 functioned as a miR-22-3P sponge to increase the expression of MMP14. HDAC2 loss strongly promoted CRC lung metastasis, which was suppressed LncRNA H19 knockdown. CONCLUSION: Our study supports HDAC2 as a CRC metastasis suppressor through the inhibition of EMT and the expression of H19 and MMP14.	NA	J Exp Clin Cancer Res. 2020 Dec 2;39(1):270. doi: 10.1186/s13046-020-01783-9.
4125	LncRNA	H19	miR-200b-3p	PPP1CA	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33615520	H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen-Activated Protein Kinase-Dependent Manner and Sponging microRNA 200b-3p.	BACKGROUND AND AIMS: Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. APPROACH AND RESULTS: The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p. CONCLUSIONS: H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA-induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR-200b-3p.	NA	Hepatology. 2020 Dec 6. doi: 10.1002/hep.31673.
4126	LncRNA	H19	miR-200b-3p	PPP1CA	HCC cell line	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR	33615520	H19 Promotes HCC Bone Metastasis Through Reducing Osteoprotegerin Expression in a Protein Phosphatase 1 Catalytic Subunit Alpha/p38 Mitogen-Activated Protein Kinase-Dependent Manner and Sponging microRNA 200b-3p.	BACKGROUND AND AIMS: Bone is the second most frequent site of metastasis for HCC, which leads to an extremely poor prognosis. HCC bone metastasis is typically osteolytic, involving the activation of osteoclasts. Long noncoding RNA H19 plays an important role in the pathogenesis of human cancers. Nonetheless, the mechanism underlying the participation of H19 in HCC bone metastasis remains unclear. APPROACH AND RESULTS: The current study established a mouse HCC bone metastasis model by using serial intracardiac injection and cell isolation to obtain cells with distinct bone metastasis ability. H19 was highly expressed in these cells and in clinical HCC bone metastasis specimens. Both osteoclastogenesis in vitro and HCC bone metastasis in vivo were promoted by H19 overexpression, whereas these processes were suppressed by H19 knockdown. H19 overexpression attenuated p38 phosphorylation and further down-regulated the expression of osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor. However, up-regulated OPG expression as well as suppressed osteoclastogenesis caused by H19 knockdown were recovered by p38 interference, indicating that p38 mitogen-activated protein kinase (MAPK)-OPG contributed to H19-promoted HCC bone metastasis. Furthermore, we demonstrated that H19 inhibited the expression of OPG by binding with protein phosphatase 1 catalytic subunit alpha (PPP1CA), which dephosphorylates p38. SB-203580-mediated inactivation of p38MAPK reversed the down-regulation of HCC bone metastasis caused by H19 knockdown in vivo. Additionally, H19 enhanced cell migration and invasion by up-regulating zinc finger E-box binding homeobox 1 through the sequestration of microRNA (miR) 200b-3p. CONCLUSIONS: H19 plays a critical role in HCC bone metastasis by reducing OPG expression, which is mediated by the PPP1CA-induced inactivation of the p38MAPK pathway; and H19 also functions as a sponge for miR-200b-3p.	NA	Hepatology. 2020 Dec 6. doi: 10.1002/hep.31673.
4127	LncRNA	H19	miR-599	PAPPA	Ox-LDL-induced Vascular Smooth Muscle Cell	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33235026	Knockdown of H19 Attenuates Ox-LDL-induced Vascular Smooth Muscle Cell Proliferation, Migration, and Invasion by Regulating miR-599/PAPPA Axis.	Long noncoding RNAs could participate in the development of atherosclerosis (AS). However, the underlying mechanism by which long noncoding RNA H19 is implicated in AS remains largely unknown. In this study, we investigated the function of H19 on cell proliferation, migration, and invasion in oxidized low-density lipoprotein (ox-LDL)-treated human aortic vascular smooth muscle cells (HA-VSMCs), and on hyperlipidemia response in high-fat diet (HFD)-treated ApoE-/- mice. Moreover, we explored the target interaction among H19, microRNA (miR)-599, and pappalysin 1 (PAPPA). Our results showed that H19 expression was elevated in serum samples of patients with AS and ox-LDL-treated HA-VSMC. H19 silence mitigated ox-LDL-induced proliferation, migration, and invasion of HA-VSMCs. H19 acted as a sponge for miR-599, and miR-599 knockdown reversed the suppressive effect of H19 silence on proliferation, migration, and invasion of HA-VSMCs. PAPPA was a target of miR-599 and attenuated the inhibitive role of miR-599 in HA-VSMC processes. H19 knockdown repressed PAPPA expression by increasing miR-599. Moreover, H19 interference alleviated hyperlipidemia response in HFD-treated ApoE-/- mice. Collectively, knockdown of H19 inhibited proliferation, migration, and invasion of ox-LDL-treated HA-VSMCs and hyperlipidemia response in HFD-treated ApoE-/- mice by regulating miR-599/PAPPA axis, indicating H19 might act as a potential target for the treatment of AS.	NA	J Cardiovasc Pharmacol. 2021 Mar 1;77(3):386-396. doi: 10.1097/FJC.0000000000000959.
4128	LncRNA	H19	miR-29b	SIRT1	HT22 cells	Middle Cerebral Artery Occlusion	Mus musculus (mouse)	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	33313940	Long non-coding RNA H19 inhibition ameliorates oxygen-glucose deprivation-induced cell apoptosis and inflammatory cytokine expression by regulating the microRNA-29b/SIRT1/PGC-1α axis.	As one of the earliest discovered long non-coding (lnc)RNAs, lncRNA H19 imprinted maternally expressed transcript (H19) participates in regulating ischemic stroke. The present study aimed to investigate the combined roles of lncRNA H19, microRNA (miR)-29b, silent mating-type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor-g co-activator-1α (PGC-1α) following ischemic stroke. lncRNA H19 expression levels in the middle cerebral artery occlusion (MCAO) mouse model and HT22 cells subjected to oxygen-glucose deprivation (OGD) were detected via reverse transcription-quantitative PCR (RT-qPCR). H19 small interfering RNA was used to knockdown H19 expression. Following OGD treatment, MTT, flow cytometry, ELISA, RT-qPCR and western blotting assays were performed to assess cell proliferation, cell apoptosis, inflammatory cytokine concentrations, and lncRNA H19, miR-29b, SIRT1, PGC-1α expression levels, respectively. In the present study, MCAO model mice and OGD-treated cells displayed significantly increased lncRNA H19 expression levels compared with sham mice and control cells, respectively. lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations. Furthermore, lncRNA H19 knockdown also attenuated OGD-mediated downregulation of miR-29b, SIRT1 and PGC-1α expression levels. Collectively, the results of the present study demonstrated that lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations by regulating miR-29b, SIRT1 and PGC-1α expression levels, which suggested the potential role of lncRNA H19 in ischemic stroke.	NA	Mol Med Rep. 2021 Feb;23(2):131. doi: 10.3892/mmr.2020.11770. Epub 2020 Dec 14.
4129	LncRNA	H19	miR-29b	SIRT1	HT22 cells	Middle Cerebral Artery Occlusion	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	33313940	Long non-coding RNA H19 inhibition ameliorates oxygen-glucose deprivation-induced cell apoptosis and inflammatory cytokine expression by regulating the microRNA-29b/SIRT1/PGC-1α axis.	As one of the earliest discovered long non-coding (lnc)RNAs, lncRNA H19 imprinted maternally expressed transcript (H19) participates in regulating ischemic stroke. The present study aimed to investigate the combined roles of lncRNA H19, microRNA (miR)-29b, silent mating-type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptor-g co-activator-1α (PGC-1α) following ischemic stroke. lncRNA H19 expression levels in the middle cerebral artery occlusion (MCAO) mouse model and HT22 cells subjected to oxygen-glucose deprivation (OGD) were detected via reverse transcription-quantitative PCR (RT-qPCR). H19 small interfering RNA was used to knockdown H19 expression. Following OGD treatment, MTT, flow cytometry, ELISA, RT-qPCR and western blotting assays were performed to assess cell proliferation, cell apoptosis, inflammatory cytokine concentrations, and lncRNA H19, miR-29b, SIRT1, PGC-1α expression levels, respectively. In the present study, MCAO model mice and OGD-treated cells displayed significantly increased lncRNA H19 expression levels compared with sham mice and control cells, respectively. lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations. Furthermore, lncRNA H19 knockdown also attenuated OGD-mediated downregulation of miR-29b, SIRT1 and PGC-1α expression levels. Collectively, the results of the present study demonstrated that lncRNA H19 knockdown ameliorated OGD-induced cell apoptosis and increases in inflammatory cytokine concentrations by regulating miR-29b, SIRT1 and PGC-1α expression levels, which suggested the potential role of lncRNA H19 in ischemic stroke.	NA	Mol Med Rep. 2021 Feb;23(2):131. doi: 10.3892/mmr.2020.11770. Epub 2020 Dec 14.
4130	LncRNA	H19	miR-342	Wnt5a	glioma tissues and cells	Glioma	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33161527	LncRNA H19 Promotes Cell Proliferation, Migration, and Angiogenesis of Glioma by Regulating Wnt5a/β-Catenin Pathway via Targeting miR-342.	Glioma is the most common malignant brain tumor and long non-coding RNAs (lncRNAs) have been reported to play an important role in the growth and angiogenesis of glioma. However, the potential mechanisms of lncRNA H19 in glioma remain unclear. In the present study, the effects of lncRNA H19 on glioma cell proliferation, migration, and angiogenesis were evaluated. The expression levels of H19, miR-342, and Wnt5a in glioma tissues and cells were detected by RT-qPCR or Western blotting. Dual luciferase reporter assay confirmed the interaction between H19, miR-342, and Wnt5a. Cell proliferation, migration, and angiogenesis were analyzed by colony formation, transwell, and tube formation assays, respectively. IHC was performed to test the angiogenesis-related factor CD31. H19 and Wnt5a expression were remarkably upregulated in glioma tissues and cells, whereas miR-342 expression was downregulated. Moreover, functional analysis confirmed that knockdown of H19 or overexpression of miR-342 suppressed glioma cell proliferation, migration, and angiogenesis in vitro. Besides, H19 was found to directly target miR-342 to promote Wnt5a expression and activate β-catenin pathway in glioma cells. Moreover, suppression of miR-342 or overexpression of Wnt5a reversed the inhibitory effect of sh-H19 on glioma growth and metastasis. Additionally, we verified that H19 promoted glioma cell proliferation, migration, and angiogenesis via miR-342/Wnt5a/β-catenin axis in vivo. H19 regulates glioma cell growth and metastasis through miR-342 to mediate Wnt5a/β-catenin signaling pathway, which provides new therapeutic targets for glioma treatment.	NA	Cell Mol Neurobiol. 2020 Nov 7. doi: 10.1007/s10571-020-00995-z.
4131	LncRNA	H19	miR-29b	Akt3	brain tissue	Hypoxic-Ischemic (Hi)-Related Brain Injury	Rattus (rat)	microarray;	33111281	Mechanisms Underlying Abnormal Expression of lncRNA H19 in Neonatal Hypoxic-Ischemic Encephalopathy.	OBJECTIVE: Hypoxic-ischemic (HI)-related brain injury, especially HI encephalopathy (HIE) is a leading cause of morbidity and disability in newborns. Long noncoding RNAs (lncRNAs) are implicated in the progress of HI brain damage. However, the mechanisms underlying the regulatory effects of lncRNA H19 on autophagy in HIE remain unknown. This study was designed to identify the potential mechanisms involving lncRNA H19 in HIE. STUDY DESIGN: We selected three HIE newborns and three healthy newborns for neonatal behavioral neurological assessment and screened the differentially expressed lncRNAs by microarray analysis and detected H19 expression in serum. After that, neonatal HIE rats were established and injected with H19 overexpression lentivirus vector or autophagy activator Rapa. The structure and apoptotic levels of brain tissue were observed, and righting reflex and geotaxis reflex were utilized to evaluate the short-term neurological function of HIE rats. The Morris water maze was performed to measure the long-term neurological functions of HIE rats. The binding relationships among H19/miR-19b/protein kinase B3 (Akt3) were verified. Levels of Akt3- and autophagy-related proteins were measured. RESULTS: H19 was upregulated in HIE newborns and rat models. The areas of cerebral infarction and apoptosis in neonatal HIE rats were increased, and the nerve functions were compromised. The overexpression of H19 alleviated nerve damage of neonatal HIE rats, and reduced autophagy of brain tissue. H19 upregulated Akt3 as a miR-29b sponge. The protective effects of overexpression of H19 on brain tissue and nerve functions of neonatal HIE rats were partially reversed by autophagy activator. CONCLUSION: H19 improved the brain tissue and alleviated nerve damage of neonatal HIE rats by upregulating the Akt3/mTOR pathway as a miR-29b sponge. KEY POINTS: · H19 overexpression reduces the nerve damage in neonatal HIE rats.. · H19 reduces autophagy in neonatal HIE rats by the miR-29b/Akt3/mTOR axis.. · Autophagy activator reverses the protection of H19 in neonatal HIE..	NA	Am J Perinatol. 2020 Oct 27. doi: 10.1055/s-0040-1718947.
4132	LncRNA	H19	miR-29b	Akt3	brain tissue	Hypoxic-Ischemic (Hi)-Related Brain Injury	Homo sapiens (human)	microarray;	33111281	Mechanisms Underlying Abnormal Expression of lncRNA H19 in Neonatal Hypoxic-Ischemic Encephalopathy.	OBJECTIVE: Hypoxic-ischemic (HI)-related brain injury, especially HI encephalopathy (HIE) is a leading cause of morbidity and disability in newborns. Long noncoding RNAs (lncRNAs) are implicated in the progress of HI brain damage. However, the mechanisms underlying the regulatory effects of lncRNA H19 on autophagy in HIE remain unknown. This study was designed to identify the potential mechanisms involving lncRNA H19 in HIE. STUDY DESIGN: We selected three HIE newborns and three healthy newborns for neonatal behavioral neurological assessment and screened the differentially expressed lncRNAs by microarray analysis and detected H19 expression in serum. After that, neonatal HIE rats were established and injected with H19 overexpression lentivirus vector or autophagy activator Rapa. The structure and apoptotic levels of brain tissue were observed, and righting reflex and geotaxis reflex were utilized to evaluate the short-term neurological function of HIE rats. The Morris water maze was performed to measure the long-term neurological functions of HIE rats. The binding relationships among H19/miR-19b/protein kinase B3 (Akt3) were verified. Levels of Akt3- and autophagy-related proteins were measured. RESULTS: H19 was upregulated in HIE newborns and rat models. The areas of cerebral infarction and apoptosis in neonatal HIE rats were increased, and the nerve functions were compromised. The overexpression of H19 alleviated nerve damage of neonatal HIE rats, and reduced autophagy of brain tissue. H19 upregulated Akt3 as a miR-29b sponge. The protective effects of overexpression of H19 on brain tissue and nerve functions of neonatal HIE rats were partially reversed by autophagy activator. CONCLUSION: H19 improved the brain tissue and alleviated nerve damage of neonatal HIE rats by upregulating the Akt3/mTOR pathway as a miR-29b sponge. KEY POINTS: · H19 overexpression reduces the nerve damage in neonatal HIE rats.. · H19 reduces autophagy in neonatal HIE rats by the miR-29b/Akt3/mTOR axis.. · Autophagy activator reverses the protection of H19 in neonatal HIE..	NA	Am J Perinatol. 2020 Oct 27. doi: 10.1055/s-0040-1718947.
4133	LncRNA	H19	miR-30a-5p	AAV2	hypoxic endothelial cells (ECs) and tubular epithelial cells (TECs)	Renal Ischemia Reperfusion Injury	Homo sapiens (human)	qRT-PCR	33478972	Renal AAV2-Mediated Overexpression of Long Non-Coding RNA H19 Attenuates Ischemic Acute Kidney Injury Through Sponging of microRNA-30a-5p.	BACKGROUND: Renal ischemia-reperfusion (I/R) injury is a major cause of AKI. Noncoding RNAs are intricately involved in the pathophysiology of this form of AKI. Transcription of hypoxia-induced, long noncoding RNA H19, which shows high embryonic expression and is silenced in adults, is upregulated in renal I/R injury. METHODS: Lentivirus-mediated overexpression, as well as antisense oligonucleotide-based silencing, modulated H19 in vitro. In vivo analyses used constitutive H19 knockout mice. In addition, renal vein injection of adeno-associated virus 2 (AAV2) carrying H19 caused overexpression in the kidney. Expression of H19 in kidney transplant patients with I/R injury was investigated. RESULTS: H19 is upregulated in kidney biopsies of patients with AKI, in murine ischemic kidney tissue, and in cultured and ex vivo sorted hypoxic endothelial cells (ECs) and tubular epithelial cells (TECs). Transcription factors hypoxia-inducible factor 1-α, LHX8, and SPI1 activate H19 in ECs and TECs. H19 overexpression promotes angiogenesis in vitro and in vivo. In vivo, transient AAV2-mediated H19 overexpression significantly improved kidney function, reduced apoptosis, and reduced inflammation, as well as preserving capillary density and tubular epithelial integrity. Sponging of miR-30a-5p mediated the effects, which, in turn, led to target regulation of Dll4, ATG5, and Snai1. CONCLUSIONS: H19 overexpression confers protection against renal injury by stimulating proangiogenic signaling. H19 overexpression may be a promising future therapeutic option in the treatment of patients with ischemic AKI.	NA	J Am Soc Nephrol. 2021 Feb;32(2):323-341. doi: 10.1681/ASN.2020060775. Epub 2021 Jan 21.
4134	LncRNA	H19	miR-29a	SMAD3	human dermal microvascular endothelial cells	Kidney Fibrosis	Homo sapiens (human)	qRT-PCR	33324218	Knockdown of LncRNA-H19 Ameliorates Kidney Fibrosis in Diabetic Mice by Suppressing miR-29a-Mediated EndMT.	Diabetic nephropathy is the leading cause of kidney fibrosis. Recently, altered expressed or dysfunction of some long non-coding RNAs (lncRNAs) has been linked to kidney fibrosis; however, the mechanisms of lncRNAs in kidney fibrosis remain unclear. We have shown that the DPP-4 inhibitor linagliptin can inhibit endothelial-mesenchymal transition (EndMT) and ameliorate diabetic kidney fibrosis associated with DPP-4 protein levels via the induction of miR-29. Here, we found that expression of the lncRNA H19 was significantly up-regulated in TGF-β2-induced fibrosis in human dermal microvascular endothelial cells (HMVECs) in vitro, and in kidney fibrosis of streptozotocin-induced diabetic CD-1 mice. We also detected up-regulated H19 expression and down-regulated miR-29a expression in the early and advanced mouse models of diabetic kidney fibrosis. H19 knockdown significantly attenuated kidney fibrosis in vitro and in vivo, which was associated with the inhibition of the EndMT-associated gene FSP-1. We also found that the up-regulation of H19 observed in fibrotic kidneys associated with the suppression of miR-29a in diabetic mice. H19, miR-29a, and EndMT contribute to a regulatory network involved in kidney fibrosis, and are associated with regulation of the TGF-β/SMAD3 singling pathway. This study indicates that inhibition of LncRNA H19 represents a novel anti-fibrotic treatment for diabetic kidney diseases.	NA	Front Pharmacol. 2020 Nov 26;11:586895. doi: 10.3389/fphar.2020.586895. eCollection 2020.
4135	LncRNA	H19	miR-29a	SMAD3	human dermal microvascular endothelial cells	Kidney Fibrosis	Mus musculus (mouse)	qRT-PCR	33324218	Knockdown of LncRNA-H19 Ameliorates Kidney Fibrosis in Diabetic Mice by Suppressing miR-29a-Mediated EndMT.	Diabetic nephropathy is the leading cause of kidney fibrosis. Recently, altered expressed or dysfunction of some long non-coding RNAs (lncRNAs) has been linked to kidney fibrosis; however, the mechanisms of lncRNAs in kidney fibrosis remain unclear. We have shown that the DPP-4 inhibitor linagliptin can inhibit endothelial-mesenchymal transition (EndMT) and ameliorate diabetic kidney fibrosis associated with DPP-4 protein levels via the induction of miR-29. Here, we found that expression of the lncRNA H19 was significantly up-regulated in TGF-β2-induced fibrosis in human dermal microvascular endothelial cells (HMVECs) in vitro, and in kidney fibrosis of streptozotocin-induced diabetic CD-1 mice. We also detected up-regulated H19 expression and down-regulated miR-29a expression in the early and advanced mouse models of diabetic kidney fibrosis. H19 knockdown significantly attenuated kidney fibrosis in vitro and in vivo, which was associated with the inhibition of the EndMT-associated gene FSP-1. We also found that the up-regulation of H19 observed in fibrotic kidneys associated with the suppression of miR-29a in diabetic mice. H19, miR-29a, and EndMT contribute to a regulatory network involved in kidney fibrosis, and are associated with regulation of the TGF-β/SMAD3 singling pathway. This study indicates that inhibition of LncRNA H19 represents a novel anti-fibrotic treatment for diabetic kidney diseases.	NA	Front Pharmacol. 2020 Nov 26;11:586895. doi: 10.3389/fphar.2020.586895. eCollection 2020.
4136	LncRNA	H19	miR-29b-3p	SOX9	human umbilical cord-derived mesenchymal stem cells	Chondrogenic Differentiation	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33058414	Platelet lysate induces chondrogenic differentiation of umbilical cord-derived mesenchymal stem cells by regulating the lncRNA H19/miR-29b-3p/SOX9 axis.	Platelet lysate (PL) has been shown to induce chondrogenic differentiation of human umbilical cord-derived mesenchymal stem cells (hUCMSCs). However, the underlying mechanism is still not clear. The aim of this study was to investigate whether long noncoding RNA H19 is involved in this process. hUCMSCs were isolated, identified and cultured in 5% PL-supplemented chondrogenic differentiation medium. Chondrogenic differentiation was assessed by Alcian blue staining. The expressions of H19, miR-29b-3p, SRY-related high-mobility-group box 9 (SOX9), collagen II and aggrecan were determined by quantitative real-time PCR and western blot. The interaction between miR-29b-3p and H19 or SOX9 was analyzed by luciferase reporter assay. During PL-induced chondrogenic differentiation of hUCMSCs, expressions of H19 and SOX9 were increased, whereas miR-29b-3p expression was decreased. H19 overexpression promoted, whereas H19 silencing attenuated the PL-induced chondrogenic differentiation of hUCMSCs. SOX9 was identified as a direct target of miR-29b-3p, and H19 was observed to act as a sponge of miR-29b-3p to up-regulate SOX9 expression. The chondrogenic differentiation-promoting effect of H19 overexpression was negated when miR-29b-3p expression was up-regulated by Lenti-miR-29b-3p infection. In conclusion, PL induced chondrogenic differentiation of hUCMSCs by regulating the H19/miR-29b-3p/SOX9 axis.	NA	FEBS Open Bio. 2020 Dec;10(12):2656-2665. doi: 10.1002/2211-5463.13002. Epub 2020 Nov 6.
4137	LncRNA	H19	miR-29a-3p	NA	osteoporosis cells	Osteoporosis	Homo sapiens (human)	qRT-PCR	33207859	An emerging potential therapeutic target for osteoporosis: LncRNA H19/miR-29a-3p axis.	Osteoporosis (OP) is a complex systemic disease characterized by a loss of bone density, leading to bone fragility and an increase risk of fractures of the hip, spine and wrist. The clinical therapeutic effect is still far from satisfactory. Thus, further studies are urgently needed to explore the pathogenesis of OP. In this study, our aim is to explore the underlying molecular mechanism of lncRNA H19/miR-29a-3p axis for regulating of inflammation, proliferation and apoptosis in OP. The expression of lncRNA H19 was significantly upregulated in OP samples compared with the health control. Subsequently, we found that miR-29a-3p is the target of lncRNA H19 in OP. Furthermore, the knockdown of lncRNA H19 was validated to promote the expression of pro-inflammatory mediators, repress cell proliferation and inhibit cell apoptosis in vitro. Moreover, the modulating effects of lncRNA-H19 on the expressions of pro-inflammatory mediators, cell proliferation and apoptosis in vitro were diminished after co-transfecting with miR-29a-3p inhibitor and siRNA-H19. Thus, we concluded that lncRNA H19/miR-29a-3p axis was involved in the development of OP. This study might provide a better understanding of OP development and a potential therapeutic target for OP intervention.	NA	Eur J Histochem. 2020 Nov 6;64(4):3155. doi: 10.4081/ejh.2020.3155.
4138	LncRNA	H19	miR-138-5p	PTK2	mesenchymal stem cells	Acute Pancreatitis	Homo sapiens (human)	qRT-PCR	32977843	Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p.	BACKGROUND: Patients with severe acute pancreatitis (SAP), which is characterized by high morbidity and mortality, account for an increasing medical burden worldwide. We previously found that mesenchymal stem cells (MSCs) could attenuate SAP and that expression of long noncoding RNA H19 (LncRNA H19) was upregulated in rats receiving MSCs. In the present study, we investigated the mechanisms of LncRNA H19 regulating the therapeutic efficacy of MSCs in the alleviation of SAP. METHODS: MSCs transfected with LncRNA H19 overexpression and knockdown plasmids were intravenously injected into rats 12 h after sodium taurocholate (NaT) administration to induce SAP. RESULTS: Overexpressing LncRNA H19 in MSCs significantly enhanced the anti-inflammatory capacity of the MSCs, inhibited autophagy via promotion of focal adhesion kinase (FAK)-associated pathways, and facilitated cell proliferation by increasing the level of β-catenin in rats with SAP. LncRNA H19 functioned as a competing endogenous RNA by sponging miR-138-5p and miR-141-3p. Knocking down miR-138-5p in MSCs increased the expression of protein tyrosine kinase 2 (PTK2, encoding FAK) to suppress autophagy, while downregulating miR-141-3p enhanced the level of β-catenin to promote cell proliferation. CONCLUSIONS: In conclusion, LncRNA H19 effectively increased the therapeutic efficacy of MSCs in rats with SAP via the miR-138-5p/PTK2/FAK and miR-141-3p/β-catenin pathways.	NA	Stem Cell Res Ther. 2020 Sep 25;11(1):420. doi: 10.1186/s13287-020-01940-z.
4139	LncRNA	H19	miR-141-3p	PTK2	mesenchymal stem cells	Acute Pancreatitis	Homo sapiens (human)	qRT-PCR	32977843	Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p.	BACKGROUND: Patients with severe acute pancreatitis (SAP), which is characterized by high morbidity and mortality, account for an increasing medical burden worldwide. We previously found that mesenchymal stem cells (MSCs) could attenuate SAP and that expression of long noncoding RNA H19 (LncRNA H19) was upregulated in rats receiving MSCs. In the present study, we investigated the mechanisms of LncRNA H19 regulating the therapeutic efficacy of MSCs in the alleviation of SAP. METHODS: MSCs transfected with LncRNA H19 overexpression and knockdown plasmids were intravenously injected into rats 12 h after sodium taurocholate (NaT) administration to induce SAP. RESULTS: Overexpressing LncRNA H19 in MSCs significantly enhanced the anti-inflammatory capacity of the MSCs, inhibited autophagy via promotion of focal adhesion kinase (FAK)-associated pathways, and facilitated cell proliferation by increasing the level of β-catenin in rats with SAP. LncRNA H19 functioned as a competing endogenous RNA by sponging miR-138-5p and miR-141-3p. Knocking down miR-138-5p in MSCs increased the expression of protein tyrosine kinase 2 (PTK2, encoding FAK) to suppress autophagy, while downregulating miR-141-3p enhanced the level of β-catenin to promote cell proliferation. CONCLUSIONS: In conclusion, LncRNA H19 effectively increased the therapeutic efficacy of MSCs in rats with SAP via the miR-138-5p/PTK2/FAK and miR-141-3p/β-catenin pathways.	NA	Stem Cell Res Ther. 2020 Sep 25;11(1):420. doi: 10.1186/s13287-020-01940-z.
4140	LncRNA	H19	miR-93-5p	SORBS2	H9C2 cells	Myocardial Injury	Homo sapiens (human)	ELISA;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	32996061	LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis.	Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury in vitro. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury via regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury in vitro via modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.	NA	Inflammation. 2021 Feb;44(1):344-357. doi: 10.1007/s10753-020-01340-8. Epub 2020 Sep 29.
4141	LncRNA	HAGLR	miR-6785-5p	NA	Bel-7402 and Hub7 cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33015776	LncRNA HAGLR exacerbates hepatocellular carcinoma through negatively regulating miR-6785-5p.	OBJECTIVE: The purpose of this study was to explore the role of long non-coding RNA (lncRNA) HAGLR in exacerbating the development of hepatocellular carcinoma (HCC) by targeting microRNA-6785-5p (miR-6785-5p). PATIENTS AND METHODS: HAGLR levels in 46 HCC tissues and paracancerous tissues were detected. The relationship between HAGLR level and clinical features of HCC patients was analyzed. After knockdown of HAGLR, proliferative, and metastatic potential changes in Bel-7402 and Hub7 cells were assessed. Thereafter, the interaction between HAGLR and miR-6785-5p, as well as the involvement of miR-6785-5p in HAGLR-regulated HCC phenotypes were finally determined. RESULTS: It was found that HAGLR level was higher in HCC tissues than paracancerous ones and correlated with rates of lymphatic metastasis and distant metastasis but not with age, gender, and tumor staging in HCC patients. Survival analysis uncovered that HAGLR level was negatively linked to overall survival in HCC. After knockdown of HAGLR, proliferative, and metastatic potentials in Bel-7402 and Hub7 cells were attenuated. MiR-6785-5p was proven as the target gene binding to HAGLR. It was lowly expressed in HCC species, and negatively correlated with HAGLR level. Moreover, rescue experiments demonstrated that miR-6785-5p was responsible for HAGLR-regulated HCC phenotypes. CONCLUSIONS: LncRNA HAGLR stimulates proliferative and metastatic potentials in HCC via negatively regulating miR-6785-5p level, thus exacerbating the development of HCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9353-9360. doi: 10.26355/eurrev_202009_23018.
4142	LncRNA	HAS2-AS1	miR-137	EZH2	glioma cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33064966	HAS2-AS1 Acts as a Molecular Sponge for miR-137 and Promotes the Invasion and Migration of Glioma Cells by Targeting EZH2.	This study aims to explore the molecular mechanism by which HAS2-AS1 acts as a ceRNA to promote the invasion and migration of glioma cells, which will provide a novel potential target for the targeted therapy of glioma. Gene expression profiles and corresponding clinical data were accessed from the TCGA_LGG and TCGA_GBM databases and then differential analysis was conducted using the "edgeR" package. miRDB, miRTarBase and TargetScan databases were employed to predict target genes and sequentially a ceRNA network was constructed. Quantitative real-time PCR was performed to detect gene expression in glioma cells. Transwell assay was operated to assess cell migratory and invasive abilities. Western blot was conducted to evaluate the protein expression. Dual-luciferase reporter assay and RNA immunoprecipitation experiment were performed to validate the targeting relationship between genes. HAS2-AS1 was markedly upregulated in glioma, and the overall survival time of patients with high HAS2-AS1 expression was significantly shorter than that of patients with low one. Silencing HAS2-AS1 inhibited the migration and invasion of glioma cells, while overexpressing HAS2-AS1 produced opposite results. miR-137 was validated as a direct target of and negatively regulated by HAS2-AS1. Further exploration of the downstream target gene indicated that EZH2 competed with HAS2-AS1 to interact with miR-137. Suppressing miR-137 or up-regulating EZH2 reversed the impact of HAS2-AS1 knockdown on glioma cell invasion and migration. HAS2-AS1 regulates EZH2 by sponging miR-137 for the migratory and invasive abilities of glioma cells, which provides a new idea for exploring metastasis mechanism of glioma.	NA	Cell Cycle. 2020 Nov;19(21):2826-2835. doi: 10.1080/15384101.2020.1826237. Epub 2020 Oct 16.
4143	LncRNA	HCG11	miR-455-5p	PTPRS	OSCC cells	Oral Squamous Cell Cancer	Mus musculus (mouse)	MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33151000	Down-regulation of lncRNA HCG11 promotes cell proliferation of oral squamous cell carcinoma through sponging miR-455-5p.	BACKGROUND: As a type of head and neck squamous cell carcinoma (HNSCC), oral squamous cell carcinoma (OSCC) has a high incidence and low survival rate. Frequent deletion of protein tyrosine phosphatase receptor type sigma (PTPRS) has been found in HNSCC. Long non-coding RNA (lncRNA) HCG11 and miR-455-5p have been reported to be involved in several cancers, in which miR-455-5p was found to be up-regulated in the OSCC. However, the role of HCG11 in OSCC development is still unclear. METHODS: Several co-transfection systems were established to explore the regulation of HCG11 on OSCC cells. Cell proliferation was evaluated by the MTT assay, flow cytometry of cell cycle distribution, immunofluorescence of Ki67 and western blotting. A dual luciferase reporter assay was performed to verify the binding effects of miR-455-5p on HCG11 and PTPRS. The role of HCG11 knockdown in OSCC cell growth was also confirmed by nude mouse tumorigenicity assay in vivo. RESULTS: Knockdown of HCG11 increased OSCC cell proliferation, as indicated by enhanced cell vitalities over time, increased G1/S transition and Ki67 levels. Furthermore, lncRNA HCG11 was shown to negatively regulate miR-455-5p and miR-455-5p targeted PTPRS directly to affect its downstream indicators, which can further modulate OSCC cell proliferation and growth. The results obtained in vivo confirmed that HCG11 knockdown promoted OSCC cell growth. CONCLUSIONS: The lncRNA HCG11/miR-R-455-5p axis can be considered as an upstream signalling circuit of PTPRS with respect to regulating its activity and downstream pathways to further influence the progression of OSCC. This finding may provide a novel RNA-based therapeutic target for OSCC treatment.	NA	J Gene Med. 2021 Mar;23(3):e3293. doi: 10.1002/jgm.3293. Epub 2021 Jan 27.
4144	LncRNA	HCG11	miR-455-5p	PTPRS	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33151000	Down-regulation of lncRNA HCG11 promotes cell proliferation of oral squamous cell carcinoma through sponging miR-455-5p.	BACKGROUND: As a type of head and neck squamous cell carcinoma (HNSCC), oral squamous cell carcinoma (OSCC) has a high incidence and low survival rate. Frequent deletion of protein tyrosine phosphatase receptor type sigma (PTPRS) has been found in HNSCC. Long non-coding RNA (lncRNA) HCG11 and miR-455-5p have been reported to be involved in several cancers, in which miR-455-5p was found to be up-regulated in the OSCC. However, the role of HCG11 in OSCC development is still unclear. METHODS: Several co-transfection systems were established to explore the regulation of HCG11 on OSCC cells. Cell proliferation was evaluated by the MTT assay, flow cytometry of cell cycle distribution, immunofluorescence of Ki67 and western blotting. A dual luciferase reporter assay was performed to verify the binding effects of miR-455-5p on HCG11 and PTPRS. The role of HCG11 knockdown in OSCC cell growth was also confirmed by nude mouse tumorigenicity assay in vivo. RESULTS: Knockdown of HCG11 increased OSCC cell proliferation, as indicated by enhanced cell vitalities over time, increased G1/S transition and Ki67 levels. Furthermore, lncRNA HCG11 was shown to negatively regulate miR-455-5p and miR-455-5p targeted PTPRS directly to affect its downstream indicators, which can further modulate OSCC cell proliferation and growth. The results obtained in vivo confirmed that HCG11 knockdown promoted OSCC cell growth. CONCLUSIONS: The lncRNA HCG11/miR-R-455-5p axis can be considered as an upstream signalling circuit of PTPRS with respect to regulating its activity and downstream pathways to further influence the progression of OSCC. This finding may provide a novel RNA-based therapeutic target for OSCC treatment.	NA	J Gene Med. 2021 Mar;23(3):e3293. doi: 10.1002/jgm.3293. Epub 2021 Jan 27.
4145	LncRNA	HCG11	miR-204-5p	SIRT1	adipose-derived mesenchymal stem cells	Adipogenesis	Homo sapiens (human)	Western blot;RNA pull-down;	33086891	LncRNA HCG11 Inhibits Adipocyte Differentiation in Human Adipose-Derived Mesenchymal Stem Cells by Sponging miR-204-5p to Upregulate SIRT1.	Long noncoding RNAs (lncRNAs) have been discovered to play a key role in adipogenesis, while the role of lncRNA human leukocyte antigen complex group 11 (HCG11) in adipocyte differentiation has not been studied clearly. We used human adipose-derived mesenchymal stem cells (hAdMSCs) to establish a model of cell differentiation in vitro and found that expression of lncRNA HCG11 was decreased during adipogenesis through real-time quantitative polymerase chain reaction analysis. Then, hAdMSCs were transfected with pcDNA-HCG11 or HCG11-shRNA (sh-HCG11); the adipogenic marker proteins were detected by Western blot, and the activity of lipogenesis enzymes was detected by spectrophotometry. The expression of CCAAT-enhancer-binding protein α, fatty acid-binding protein, peroxisome proliferator-activated receptor gamma 2 and the levels of acetyl coenzyme A carboxylase and fatty acid synthase FAS were significantly downregulated in hAdMSCs at different stages transfected with pcDNA-HCG11, while knockdown of lncRNA HCG11 promoted adipocyte differentiation. Bioinformatic analysis indicated that miR-204-5p was a potential target gene of HCG11, which was confirmed by luciferase reporter gene analysis and RNA pull-down analysis. In addition, miR-204-5p directly targeting the 3'-untranslated region of SIRT1 was also predicted by StarBase and verified by luciferase reporter gene analysis. Enforced expression of miR-204-5p negatively regulated the SIRT1 protein level. Furthermore, SIRT1 overexpression significantly inhibited adipogenic marker protein, levels of lipogenesis enzymes, and the proliferation of hAdMSCs. When pcDNA-HCG11 and miR-204-5p mimic were co-transfected into hAdMSCs, we found that the miR-204-5p mimic reversed the suppressor effect of pcDNA-HCG11. Taken together, we found that HCG11 negatively regulated cell proliferation and adipogenesis by the miR-204-5p/SIRT1 axis. Our findings might provide a new target for the study of adipogenesis in hAdMSCs and obesity.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720968090. doi: 10.1177/0963689720968090.
4146	LncRNA	HCG11	miR-26b-5p	QKI5	vascular endothelial cells	Acute Coronary Syndrome	Homo sapiens (human)	RIP assay;Luciferase reporter assay;	33128346	LncRNA HCG11/miR-26b-5p/QKI5 feedback loop reversed high glucose-induced proliferation and angiogenesis inhibition of HUVECs.	Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non-coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose-induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular-related RNA-binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA-binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR-26b-5p, and QKI5 was speculated as the target of miR-26b-5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR-26b-5p/QKI-5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.	NA	J Cell Mol Med. 2020 Dec;24(24):14231-14246. doi: 10.1111/jcmm.16040. Epub 2020 Oct 30.
4147	LncRNA	HCG11	miR-144-3p	FOXF1	human vascular smooth muscle cells	Atherosclerosis	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;	33008472	LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis in atherosclerosis.	BACKGROUND: Atherosclerosis (AS) is the main pathological basis of coronary heart disease, cerebral infarction and peripheral vascular disease, which seriously endanger people's life and health. In recent years, long non-coding RNA (lncRNA) has been found to be involved in gene expression regulation, but the research on AS is still in the initial stage. In this study, we mainly studied the role of HCG11 in patients with AS. Quantitative Real-time Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of HCG11 and miR-144 in the serum of AS patients and healthy volunteers. Oxidation Low Lipoprotein (Ox-LDL), interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) radiation were used to establish human vascular smooth muscle cells (VSMCs) in vitro model. Cell proliferation was determined by Cell Counting Kit-8 (CCK-8) assay. The apoptosis rate was determined by flow cytometry (FACS) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. The expression levels of Forkhead box protein F1 (FOXF1), B cell lymphoma-2 (Bcl-2) and BCL2-Associated X (Bax) were detected by qRT-PCR. Luciferase gene reporter and RNA pull down experiments confirmed the relationship between HCG11 and miR-144, miR-144 and FOXF1. RESULTS: This study showed that HCG11 was significantly upregulated in patients with AS, while miR-144 was down-regulated in patients with AS. Ox-LDL and IL-6 in VSMCs induced up-regulation of HCG11 and down-regulation of miR-144. Overexpression of HCG11 promoted the proliferation and inhibited apoptosis of VSMCs. Luciferase gene reporter gene assay showed that HCG11 could bind to miR-144, and miR-144 could bind to FOXF1. Overexpression of miR-144 reversed the effect of HCG11 on VSMCs. CONCLUSIONS: LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis.	NA	Biol Res. 2020 Oct 2;53(1):44. doi: 10.1186/s40659-020-00306-2.
4148	LncRNA	HCG18	miR-197-3p	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	ChIP;Chromatin immunoprecipitation;luciferase assay;	33090399	E2F1-induced upregulation of lncRNA HCG18 stimulates proliferation and migration in gastric cancer by binding to miR-197-3p.	OBJECTIVE: LncRNA HCG18 is considered to be an oncogene in many types of tumors. The aim of this study was to explore the role of lncRNA HCG18 in gastric cancer (GC). PATIENTS AND METHODS: HCG18 levels in GC tissues were detected. Potential biological influences of HCG18 on GC cell phenotypes were examined by Cell Counting Kit-8 (CCK-8), wound healing and transwell assay. Subsequently, bioinformatics analysis, Chromatin immunoprecipitation (ChIP), Luciferase assay and rescue experiments were conducted to identify the regulatory network of HCG18 in GC. RESULTS: It was found that HCG18 was upregulated in GC samples, and the knockdown of HCG18 inhibited proliferative and migratory abilities in GC. The transcription factor E2F1 could directly bind to the promoter region of HCG18 and thus activate its transcription. In addition, HCG18 sponged miR-197-3p to stimulate the malignant development of GC. CONCLUSIONS: HCG18 is upregulated in GC samples by E2F1 induction, which stimulates proliferative and migratory abilities in GC by binding to miR-197-3p.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(19):9949-9956. doi: 10.26355/eurrev_202010_23207.
4149	LncRNA	HCG18	miR-146a	TRAF6	DPN tissue	Diabetic Peripheral Neuropathy	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32996080	Long non-coding RNA HCG18 promotes M1 macrophage polarization through regulating the miR-146a/TRAF6 axis, facilitating the progression of diabetic peripheral neuropathy.	Diabetic peripheral neuropathy (DPN) is one of the most important complications in diabetes mellitus (DM), which has been reported to be modulated by long non-coding RNAs (lncRNAs). The purpose of the current study is to explore the regulatory mechanism of lncRNA HCG18 on DPN in vitro. The expression of lncRNA HCG18, miR-146a, TRAF6, CD11c, and iNOS was detected by qRT-PCR. Through Enzyme-linked immunosorbent assay, the levels of inflammatory factors (TNF-α, IL-1β, and IL-6) were determined. M1 macrophage polarization was measured by flow cytometry analysis. The interactions between miR-146a and HCG18/TRAF6 were predicted by Starbase/Targetscan software and verified by the dual luciferase reporter assay. Western blot assay was performed to determine the protein expression of TRAF6. LncRNA HCG18 was highly expressed in DPN model and HG-induced macrophages. The levels of inflammatory factors (TNF-α, IL-1β, and IL-6) were elevated in DPN model. The expression of M1 markers (CD11c and iNOS) was visibly up-regulated in DPN model and was positively correlated with HCG18 expression. LncRNA HCG18 facilitated M1 macrophage polarization. In addition, miR-146a was identified as a target of lncRNA HCG18. Overexpression of miR-146a reversed the promoting effect of HCG18 on M1 macrophage polarization. Simultaneously, TRAF6 was a target gene of miR-146a TRAF6 expression was positively modulated by HCG18 and was negatively modulated by miR-146a. Down-regulation of TRAF6 reversed the promoting effect of HCG18 on M1 macrophage polarization. LncRNA HCG18 promotes M1 macrophage polarization via regulating the miR-146a/TRAF6 axis, facilitating the progression of DPN. This study provides a possible therapeutic strategy for DPN.	NA	Mol Cell Biochem. 2021 Jan;476(1):471-482. doi: 10.1007/s11010-020-03923-3. Epub 2020 Sep 29.
4150	LncRNA	HCG18	miR-30a-5p	NOTCH1	bone marrow mesenchymal stem cells	Osteoporosis	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;luciferase assay;	33176682	Long noncoding RNA HCG18 inhibits the differentiation of human bone marrow-derived mesenchymal stem cells in osteoporosis by targeting miR-30a-5p/NOTCH1 axis.	BACKGROUND: Recent studies have demonstrated that long non-coding RNAs (LncRNAs) can influence bone cell differentiation and formation. However, it is unclear whether lncRNA HCG18 is involved in osteoporosis (OP). This study was conducted to investigate the regulation of HCG18 in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). METHODS: BMSCs were isolated and cultured from mouse pathological models and osteoporosis patients. RT-qPCR was performed to detect the expression of HCG18 and miR-30a-5p in BMSCs. The interaction between HCG18 and miR-30a-5p was analyzed by dual luciferase assay and RNA pulldown assay. The interaction between miR-30a-5p and NOTCH1 3'-UTR was analyzed by dual luciferase assay. RT-qPCR and Western blotting were used to detect the expression of osteogenic genes Runx2, OCN and OPN. Hindlimb-unloaded (HU) mice model was established, and HCG18 was knocked down on bone-formation surfaces by using lentivirus mediated shRNA transfection. RESULTS: The expression of HCG18 was increased in BMSCs of OP patients, while the expression of miR-30a-5p was decreased. The expression of HCG18 and miR-30a-5p was negatively correlated in BMSCs. During the differentiation from BMSCs to osteoblasts, the expression of HCG18 was significantly downregulated, and the expression of miR-30a-5p was significantly upregulated. Overexpression of HCG18 was able to reverse the osteogenic-induced upregulation of miR-30a-5p expression, and knockdown of HCG18 further promoted the expression of miR-30a-5p. In addition, miR-30a-5p partially abolished the effect of HCG18 on osteogenic differentiation of BMSCs. NOTCH1 was a target protein of miR-30a-5p, and upregulation of NOTCH1 reversed the effect of miR-30a-5p on osteogenic differentiation of BMSCs. Furthermore, this study found that lentivirus mediated HCG18 knockdown on the bone-formation surfaces of hindlimb-unloaded (HU) mice partially alleviated unloading-induced bone loss CONCLUSIONS: HCG18 inhibited osteogenic differentiation of BMSCs induced by OP via the miR-30a-5p/NOTCH1 axis. HCG18 can be identified as a regulator of osteogenic differentiation of BMSCs.	NA	Mol Med. 2020 Nov 11;26(1):106. doi: 10.1186/s10020-020-00219-6.
4151	LncRNA	HCG18	miR-30a-5p	NOTCH1	bone marrow mesenchymal stem cells	Osteoporosis	Mus musculus (mouse)	qPCR;RT-qPCR;Western blot;luciferase assay;	33176682	Long noncoding RNA HCG18 inhibits the differentiation of human bone marrow-derived mesenchymal stem cells in osteoporosis by targeting miR-30a-5p/NOTCH1 axis.	BACKGROUND: Recent studies have demonstrated that long non-coding RNAs (LncRNAs) can influence bone cell differentiation and formation. However, it is unclear whether lncRNA HCG18 is involved in osteoporosis (OP). This study was conducted to investigate the regulation of HCG18 in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). METHODS: BMSCs were isolated and cultured from mouse pathological models and osteoporosis patients. RT-qPCR was performed to detect the expression of HCG18 and miR-30a-5p in BMSCs. The interaction between HCG18 and miR-30a-5p was analyzed by dual luciferase assay and RNA pulldown assay. The interaction between miR-30a-5p and NOTCH1 3'-UTR was analyzed by dual luciferase assay. RT-qPCR and Western blotting were used to detect the expression of osteogenic genes Runx2, OCN and OPN. Hindlimb-unloaded (HU) mice model was established, and HCG18 was knocked down on bone-formation surfaces by using lentivirus mediated shRNA transfection. RESULTS: The expression of HCG18 was increased in BMSCs of OP patients, while the expression of miR-30a-5p was decreased. The expression of HCG18 and miR-30a-5p was negatively correlated in BMSCs. During the differentiation from BMSCs to osteoblasts, the expression of HCG18 was significantly downregulated, and the expression of miR-30a-5p was significantly upregulated. Overexpression of HCG18 was able to reverse the osteogenic-induced upregulation of miR-30a-5p expression, and knockdown of HCG18 further promoted the expression of miR-30a-5p. In addition, miR-30a-5p partially abolished the effect of HCG18 on osteogenic differentiation of BMSCs. NOTCH1 was a target protein of miR-30a-5p, and upregulation of NOTCH1 reversed the effect of miR-30a-5p on osteogenic differentiation of BMSCs. Furthermore, this study found that lentivirus mediated HCG18 knockdown on the bone-formation surfaces of hindlimb-unloaded (HU) mice partially alleviated unloading-induced bone loss CONCLUSIONS: HCG18 inhibited osteogenic differentiation of BMSCs induced by OP via the miR-30a-5p/NOTCH1 axis. HCG18 can be identified as a regulator of osteogenic differentiation of BMSCs.	NA	Mol Med. 2020 Nov 11;26(1):106. doi: 10.1186/s10020-020-00219-6.
4152	LncRNA	HCP5	miR-186-5p	MAP3K2	NB cells	Neuroblastoma	Homo sapiens (human)	qRT-PCR	33189302	LncRNA HCP5 promotes neuroblastoma proliferation by regulating miR-186-5p/MAP3K2 signal axis.	INTRODUCTION: Neuroblastoma (NB) is the most common solid tumor in children. Studies showed that long-chain noncoding RNA (lncRNA) HCP5 played an important role in tumorigenesis, but its role in NB remained unclear. This study aims to determine the role of HCP5 in NB and its possible molecular mechanism. METHODS: We analyzed the expression levels of miRNA-186-5p and HCP5 in neuroblastoma and neuroblastoma cell lines SHSY-5Y, Kelly, NBL-S and SK-N-AS, and explored their roles. RESULTS: We found that the HCP5 expression was up-regulated in NB tissues and cells. The higher the HCP5 expression in NB cells, the stronger the ability of clone formation. Down regulation of the HCP5 expression inhibited the proliferation of NB cells and the growth of subcutaneous transplanted tumor in nude mice. HCP5 could competitively bind miR-186-5p, while miR-186-5p could target the 3'-UTR of MAP3K2. The expression level of miR-186-5p was down regulated while the expression level of MAP3K2 was up-regulated in NB tissues. The expression level of HCP5 and miR-186-5p, the expression level of miR-186-5p and MAP3K2 were negatively correlated. The decreased proliferation of NB cells induced by down-regulation of HCP5 expression can be counteracted by miR-186-5p inhibitor or MAP3K2, and vice versa. CONCLUSION: This study showed that lncRNA HCP5, as ceRNA, regulated MAP3K2 to promote NB progression through competitive binding of miR-186-5p. We revealed a new signaling pathway that mediates NB, which provided a new target for the diagnosis and treatment of NB.	NA	J Pediatr Surg. 2021 Apr;56(4):778-787. doi: 10.1016/j.jpedsurg.2020.10.011. Epub 2020 Oct 17.
4153	LncRNA	HCP5	miR-29b-3p	HMGB1	RT4 cells	Bladder Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33235469	LncRNA HCP5 Promotes Cell Invasion and Migration by Sponging miR-29b-3p in Human Bladder Cancer.	BACKGROUND: Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. In this study, the roles of lncRNA HCP5 (human major histocompatibility complex p5) and miR-29b-3p in human BC were investigated. Their regulations involved in cell invasion and migration were also evaluated. METHODS: Luciferase reporter assay was performed to detect the binding between miR-29b-3p and HCP5 or high-mobility group box 1 (HMGB1). Cell viability, migration, invasion and apoptosis were assessed by CCK-8, colony formation, transwell assay and flow cytometry, respectively. Expression levels of HMGB1/toll-like receptor 4 (TLR4) proteins were measured by Western blot. Xenograft model was built, and tumor volumes and weights were calculated. RESULTS: The results revealed dysregulation of HCP5 and miR-29b-3p in BC samples and cells. HCP5 negatively regulated the expression of miR-29b-3p and enhanced cell viability, migration and invasion. MiR-29b-3p mediated the effect of HCP5 on cell viability, proliferation, migration and invasion in RT4 cells. In addition, miR-29b-3p could regulate the expression of HMGB1 through interaction with HMGB1. CONCLUSION: The findings in this study supported that lncRNA HCP5 could promote cell invasion and migration by sponging miR-29b-3p in human BC.	NA	Onco Targets Ther. 2020 Nov 17;13:11827-11838. doi: 10.2147/OTT.S249770. eCollection 2020.
4154	LncRNA	HCP5	miR-27b-3p	MET	DLBCL cells	Gastric Cancer	Homo sapiens (human)	Luciferase reporter assay;	33162801	Geniposide inhibits proliferation and induces apoptosis of diffuse large B-cell lymphoma cells by inactivating the HCP5/miR-27b-3p/MET axis.	Diffuse large B-cell lymphoma (DLBCL) is commonly treated with R-CHOP, but ~30 to 50% of the patients are poorly responsive to this strategy. Geniposide, an extract from the Gardenia jasminoides Ellis, plays antitumor roles in human gastric cancer, hepatocellular carcinoma, and oral squamous carcinoma. However, the effects of geniposide treatment on DLBCL cells, as well as its underlying mechanism, are still unknown. Here, we found that geniposide inhibited the proliferation of OCI-LY7 and OCI-LY3 cells in a dose-dependent manner. Furthermore, geniposide increased the percentage of apoptotic cells and upregulated the levels of cleaved PARP and cleaved caspase-3 in DLBCL cells. Interestingly, geniposide treatment significantly reduced the expression of the long noncoding RNA HLA complex P5 (lncRNA HCP5) in DLBCL cells. HCP5 expression was revealed to be upregulated in DLBCL tissues and cell lines. Moreover, HCP5 knockdown resulted in proliferation inhibition and apoptosis in OCI-LY7 and OCI-LY3 cells. miR-27b-3p was predicted as a potential target of HCP5 using the lnCAR web tool. Both HCP5 silencing and geniposide treatment increased the level of miR-27b-3p in DLBCL cells. Accordingly, a luciferase reporter assay identified miR-27b-3p as a direct target of HCP5. The expression of miR-27b-3p was upregulated and inversely correlated with the HCP5 level in DLBCL tissues. HCP5 knockdown reduced MET protein expression, which was subsequently rescued by miR-27b-3p silencing in DLBCL cells. Importantly, the restoration of MET partially reversed the geniposide-induced proliferation inhibition and apoptosis of DLBCL cells. In conclusion, geniposide inhibits the proliferation and induces the apoptosis of DLBCL cells at least partially by regulating the HCP5/miR-27b-3p/MET axis, indicating a potential strategy for DLBCL treatment.	NA	Int J Med Sci. 2020 Sep 23;17(17):2735-2743. doi: 10.7150/ijms.51329. eCollection 2020.
4155	LncRNA	HEIH	miR-3619-5p	CTTNBP2	OC cells	Ovarian Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;Rescue assay;	33110047	lncRNA HEIH accelerates cell proliferation and inhibits cell senescence by targeting miR-3619-5p/CTTNBP2 axis in ovarian cancer.	OBJECTIVE: Epithelial ovarian cancer is the most lethal malignancy in gynecology. Numerous studies have confirmed that long noncoding RNAs (lncRNAs) are abnormally expressed in ovarian cancer and are closely associated with the cell proliferation and senescence in cancers. However, the role and underlying molecular mechanism of long noncoding RNA high expression in hepatocellular carcinoma (HEIH) in ovarian cancer remain unknown. METHODS: Experiments including Real-time quantitative polymerase chain reaction, RNA immunoprecipitation, luciferase reporter, Fluorescence in situ hybridization, western blot, colony formation assays, β-galactosidase senescence assay, cell apoptosis, proliferation, invasion, and migration assays were applied to investigate the role of HEIH in ovarian cancer. The data were expressed as the mean ± standard deviation. Student t test was used to compare the data between two groups. The one-way analysis of variance was applied to compare the data among multiple groups with Tukey post hoc test. All experiments were repeated three times. P < 0.05 was considered statistically significant. RESULTS: Herein, HEIH expression was found to be up-regulated in ovarian cancer tissues (n = 25; twofold higher than normal tissues, P < 0.05) and cell lines (sixfold higher than normal ovarian epithelial cell line on average, P < 0.05), and high HEIH expression predicted poor prognosis (survival rate is about 25% after 40 mo; P < 0.05). Moreover, we found that HEIH accelerated proliferation, migration, and invasion, whereas inhibited cell senescence in ovarian cancer (P < 0.05). In mechanism, HEIH was confirmed to serve as a sponge for miR-3619-5p, and miR-3619-5p counteracted HEIH-mediated regulation of ovarian cancer (P < 0.05). Besides, cortactin-binding protein 2 (CTTNBP2) was found to be the downstream target of miR-3619-5p. Rescue assays validated that CTTNBP2 up-regulation significantly reversed the inhibitory effects of HEIH knockdown on ovarian cancer progression (P < 0.05). Furthermore, we found that HEIH facilitated tumor growth in vivo by regulating CTTNBP2 expression (P < 0.05). CONCLUSIONS: In conclusion, our research revealed that HEIH accelerated cell proliferation, migration and invasion, whereas inhibited cell senescence in ovarian cancer via targeting the miR-3619-5p/CTTNBP2 axis. These findings may be valuable for finding new therapeutic targets to improve ovarian cancer treatment.	NA	Menopause. 2020 Nov;27(11):1302-1314. doi: 10.1097/GME.0000000000001655.
4156	LncRNA	HEIH	miR-3619-5p	HDGF	SCC4/S and SCC4/DDP cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR	33130420	Exosomal lncRNA HEIH promotes cisplatin resistance in tongue squamous cell carcinoma via targeting miR-3619-5p/HDGF axis.	BACKGROUND: Accumulating evidence has suggested that long noncoding RNAs (lncRNAs) are involved in the progression of types of human cancers. It has been known that exosomes can mediate cell-cell crosstalk by transferring lncRNAs in tumor progression. This study aimed to investigate the role of exosomal lncRNA HEIH on cisplatin (DDP) resistance in tongue squamous cell carcinoma (TSCC). METHODS: The expression of HEIH in human oral keratinocytes cell line (HOK), DDP-sensitive TSCC cell line (SCC4/S) and DDP-resistant TSCC cell line (SCC4/DDP) was measured. SCC4/S and SCC4/DDP cells were transfected with sh-HEIH to examine TSCC cell proliferation and apoptosis. The DDP-resistant exosomes were extracted and identified. The expression of miR-3619-5p and TDGF in DDP-sensitive recipient cells was determined. The binding capacity between HEIH and miR-3619-5p, along with miR-3619-5p and TDGF was verified. RESULTS: HEIH expression was significantly upregulated in SCC4/DDP cells. Downregulation of HEIH inhibited DDP resistance and cell proliferation and promoted cell apoptosis. HEIH acted as a competing endogenous RNA (ceRNA) for miR-3619-5p to upregulate HDGF expression. Exosomal HEIH promoted cell proliferation and drug resistance and inhibited cell apoptosis by sponging miR-3169-5p and upregulating HDGF. CONCLUSION: Exosomal HEIH acted as a ceRNA for miR-3619-5p to upregulate HDGF, thereby promoting DDP resistance in TSCC cells.	NA	Acta Histochem. 2020 Dec;122(8):151647. doi: 10.1016/j.acthis.2020.151647. Epub 2020 Oct 30.
4157	LncRNA	HEIH	miR-194-5p	WEE1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33262604	Long Noncoding RNA HEIH Promotes Proliferation, Migration and Invasion of Retinoblastoma Cells Through miR-194-5p/WEE1 Axis.	BACKGROUND: Abnormally expressed long noncoding RNA (lncRNA) high expression in hepatocellular carcinoma (HEIH) has been implicated in many types of human cancer, and plays crucial roles in tumor development and progression. However, little is known about its function in retinoblastoma. METHODS: qRT-PCR was used to determine the expression levels of HEIH, miR-194-5p and WEE1 in retinoblastoma tissues and cell lines. The trypan blue exclusion method, colony formation assay, wound-healing assay and transwell invasion assay were performed to evaluate the effects of HEIH, miR-194-5p and WEE1 on cell proliferation, migration and invasion. Bioinformatics analysis, dual-luciferase reporter assay and Western blot were employed to investigate the regulatory relationship among HEIH, miR-194-5p and WEE1. RESULTS: We found that HEIH was up-regulated in retinoblastoma tissues and cell lines. Furthermore, high level of HEIH was associated with TNM stage, optic nerve invasion and choroidal invasion of patients with retinoblastoma. Functional studies showed that HEIH knockdown significantly suppressed retinoblastoma cell proliferation, migration and invasion. Mechanistically, HEIH promoted retinoblastoma progression by serving as a sponge of miR-194-5p to regulate WEE1 expression. CONCLUSION: Our work suggests that HEIH acts as an oncogenic lncRNA to promote retinoblastoma proliferation and metastasis, providing a new insight into the retinoblastoma treatment.	NA	Onco Targets Ther. 2020 Nov 23;13:12033-12041. doi: 10.2147/OTT.S268942. eCollection 2020.
4158	Circular RNA	HIPK3	miR-185-3p	CASR	cardiac hypertrophy cells	Cardiac Hypertrophy	Homo sapiens (human)	ChIP;FISH;qRT-PCR;RNA immunoprecipitation;FISH;Luciferase reporter assay;RNA immunoprecipitation;	33402817	Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p.	BACKGROUND: Cardiac hypertrophy is induced by diverse patho-physiological stimuli and indicates an increase in cardiomyocyte size. Circular RNAs (circRNAs) and microRNAs (miRNAs), members of noncoding RNAs, are involved in several biological processes and cardiovascular diseases (CVD). Here, we investigated the potential role of circHIPK3, which is produced by the third exon of the HIPK3 gene in cardiac hypertrophy. METHODS: qRT-PCR and Sanger sequencing were conducted to identify the expression and characteristics (head-to-tail structure, stability, and location) of circHIPK3 in cardiac hypertrophy; Immunostaining of α-SMA was performed to evaluate the size of the cardiomyocytes; Transverse aortic constriction (TAC) induced hypertrophy models of mice were established to investigate the effect of circHIPK3 in vivo. Bioinformatics analysis and luciferase reporter assays, RNA immunoprecipitation, and fluorescence in situ hybridization (FISH) experiments were conducted to investigate the mechanism of circHIPK3-mediated cardiac hypertrophy. RESULTS: circHIPK3 is circular, more stable, and mainly located in the cytoplasm. Silencing of circHIPK3 inhibited the TAC induced cardiac hypertrophy, and reversed the effect of TAC on the echocardiograph parameters, such as left ventricular end-diastolic pressure (LVEDPS), left ventricular fraction shortening (LVFS), left ventricular ejection fraction (LVEF), and left ventricular systolic dysfunction (LVSD), and also the heart weight to tibial length (HW/TL). Angiotensin II (Ang II) Ang II-treated cardiomyocytes showed larger size of cardiomyocyte and upregulation of fetal genes, biomarkers of cardiac hypertrophy, peptide hormones, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), and myofilament protein, β-myosin heavy chain (β-MHC). These effects were reversed by circHIPK3 knockdown. Mechanically, circHIPK3 sponges miR-185-3p. In addition, miR-185-3p targets CASR. The rescue experiments confirmed the interaction between circHIPK3 and miR-185-3p as well as miR-185-3p and CASR. DISCUSSION: Our data suggested that circHIPK3 serve as a miR-185-3p sponge to regulate cardiac hypertrophy revealing a potential new target for the prevention of TAC- and Ang-II induced cardiac hypertrophy.	NA	Drug Des Devel Ther. 2020 Dec 29;14:5699-5710. doi: 10.2147/DDDT.S245199. eCollection 2020.
4159	LncRNA	HOTAIR	miR-218	PDE7A	Glioma cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;Flow Cytometry assay;Luciferase reporter assay;	33425098	Adsorption of miR-218 by lncRNA HOTAIR regulates PDE7A and affects glioma cell proliferation, invasion, and apoptosis.	OBJECTIVE: To evaluate the role of targeted adsorption of miR-218 by long-chain non-coding RNAHOTAIR to regulate PDE7A on glioma cell proliferation, invasion, and apoptosis. METHODS: The expressions of lncRNA HOTAIR, miR-218, and PDE7A in glioma tissues and normal parcancer tissues, NHA and glioma cell lines were determined, and correlations among the three genes were analyzed. The subcellular localization of lncRNA HOTAIR was determined by fluorescent in situ hybridization. Dual-luciferase reporter assay was used to validate the targeted relationship between lncRNA HOTAIR/miR-218/PDE7A. Glioma cells were grouped to receive intervention of lncRNA HOTAIR or miR-218. MTT, transwell, and flow cytometry were performed to determine the proliferation, invasion, and apoptosis of cells. RESULTS: Compared with the normal tissues and cells, the expression of lncRNA HOTAIR was increased while miR-218 was suppressed in glioma tissues samples and cells (all P<0.05). Inhibition of lncRNA HOTAIR expression, was able to induce apoptosis and suppress the proliferation and invasion of cells (all P<0.05). LncRNA HOTAIR is mainly localized in the cytoplasm, and is able to adsorb miR-218 as ceRNA. The effect of knockdown of HOTAIR on glioma cells could be partially rescued by miR-218 inhibitor. The expression of PDE7A was enhanced in glioma tissues and cells compared to normal tissues and cells (all P<0.05), which positively correlated with the expression of HOTAIR (r=0.546, P<0.05) and negatively correlated with the expression of miR-218 (r=0.363, P<0.05). The targeted relationship between miR-218 and PDE7A was validated: Overexpression of miR-218 was able to suppress the proliferation and invasion of glioma cells and restrain apoptosis compared to the miR-NC group (all P<0.05). The effect of miR-218 on glioma cells could be partially rescued by PDE7A. CONCLUSION: lncRNA HOTAIR can adsorb miR-218 to regulate expression of PDE7A and promote the malignant biologic behavior of glioma cells.	NA	Int J Clin Exp Pathol. 2020 Dec 1;13(12):2973-2983. eCollection 2020.
4160	LncRNA	HOTAIR	miR-130a-3p	MDM4	H9c2 (rat cardiomyocyte line) cells	Apoptosis Induced By Ischemia-Reperfusion Injury	Homo sapiens (human)	Cell transfection;Cell transfection;microarray;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33398378	Investigating the effect of lncRNA HOTAIR on apoptosis induced by myocardial ischemia-reperfusion injury.	The present study aimed to investigate the effect of the long non-coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on apoptosis induced by ischemia-reperfusion injury. Differential lncRNAs in myocardial ischemia rats were screened by a lncRNA microarray and the expression levels of lncRNA HOTAIR and microRNA (miR)-130a-3p were analyzed using reverse transcription-quantitative polymerase chain reaction in hypoxia-induced cardiomyocytes. The mechanism of lncRNA HOTAIR in cardiotoxicity was investigated using cell transfection, lncRNA knockdown, Cell Counting Kit-8, flow cytometry, western blotting, dual luciferase reporter assays and RNA immunoprecipitation. The expression level of lncRNA HOTAIR was significantly downregulated in the ischemic myocardium of rats. Overexpression of HOTAIR in H9c2 (rat cardiomyocyte line) cells could inhibit the apoptosis induced by H2O2. A direct interaction was found between HOTAIR and miR-130a-3p, and mouse double minute 4 (MDM4) was also found to be a potential target of miR-130a-3p. The overexpression of MDM4 in H9c2 cells transfected with miR-130a-3p mimics increased apoptosis, and miR-130a-3p targeted inhibition of MDM4 promoted H2O2-induced apoptosis of H9c2 cells. Overall, HOTAIR was found to inhibit the apoptosis of H9c2 cells induced by H2O2 through the miR-130a-3p/MDM4 axis.	NA	Mol Med Rep. 2021 Mar;23(3):169. doi: 10.3892/mmr.2020.11808. Epub 2021 Jan 5.
4161	LncRNA	HOTAIR	miR-130a-3p	MDM4	H9c2 (rat cardiomyocyte line) cells	Apoptosis Induced By Ischemia-Reperfusion Injury	Rattus (rat)	Cell transfection;Cell transfection;microarray;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33398378	Investigating the effect of lncRNA HOTAIR on apoptosis induced by myocardial ischemia-reperfusion injury.	The present study aimed to investigate the effect of the long non-coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on apoptosis induced by ischemia-reperfusion injury. Differential lncRNAs in myocardial ischemia rats were screened by a lncRNA microarray and the expression levels of lncRNA HOTAIR and microRNA (miR)-130a-3p were analyzed using reverse transcription-quantitative polymerase chain reaction in hypoxia-induced cardiomyocytes. The mechanism of lncRNA HOTAIR in cardiotoxicity was investigated using cell transfection, lncRNA knockdown, Cell Counting Kit-8, flow cytometry, western blotting, dual luciferase reporter assays and RNA immunoprecipitation. The expression level of lncRNA HOTAIR was significantly downregulated in the ischemic myocardium of rats. Overexpression of HOTAIR in H9c2 (rat cardiomyocyte line) cells could inhibit the apoptosis induced by H2O2. A direct interaction was found between HOTAIR and miR-130a-3p, and mouse double minute 4 (MDM4) was also found to be a potential target of miR-130a-3p. The overexpression of MDM4 in H9c2 cells transfected with miR-130a-3p mimics increased apoptosis, and miR-130a-3p targeted inhibition of MDM4 promoted H2O2-induced apoptosis of H9c2 cells. Overall, HOTAIR was found to inhibit the apoptosis of H9c2 cells induced by H2O2 through the miR-130a-3p/MDM4 axis.	NA	Mol Med Rep. 2021 Mar;23(3):169. doi: 10.3892/mmr.2020.11808. Epub 2021 Jan 5.
4162	LncRNA	HOTAIR	miR-130a-3p	MDM4	H9c2 (rat cardiomyocyte line) cells	Apoptosis Induced By Ischemia-Reperfusion Injury	Mus musculus (mouse)	Cell transfection;Cell transfection;microarray;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33398378	Investigating the effect of lncRNA HOTAIR on apoptosis induced by myocardial ischemia-reperfusion injury.	The present study aimed to investigate the effect of the long non-coding ribonucleic acid (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) on apoptosis induced by ischemia-reperfusion injury. Differential lncRNAs in myocardial ischemia rats were screened by a lncRNA microarray and the expression levels of lncRNA HOTAIR and microRNA (miR)-130a-3p were analyzed using reverse transcription-quantitative polymerase chain reaction in hypoxia-induced cardiomyocytes. The mechanism of lncRNA HOTAIR in cardiotoxicity was investigated using cell transfection, lncRNA knockdown, Cell Counting Kit-8, flow cytometry, western blotting, dual luciferase reporter assays and RNA immunoprecipitation. The expression level of lncRNA HOTAIR was significantly downregulated in the ischemic myocardium of rats. Overexpression of HOTAIR in H9c2 (rat cardiomyocyte line) cells could inhibit the apoptosis induced by H2O2. A direct interaction was found between HOTAIR and miR-130a-3p, and mouse double minute 4 (MDM4) was also found to be a potential target of miR-130a-3p. The overexpression of MDM4 in H9c2 cells transfected with miR-130a-3p mimics increased apoptosis, and miR-130a-3p targeted inhibition of MDM4 promoted H2O2-induced apoptosis of H9c2 cells. Overall, HOTAIR was found to inhibit the apoptosis of H9c2 cells induced by H2O2 through the miR-130a-3p/MDM4 axis.	NA	Mol Med Rep. 2021 Mar;23(3):169. doi: 10.3892/mmr.2020.11808. Epub 2021 Jan 5.
4163	LncRNA	HOTAIR	miR-129-5p	FZD7	breast cancer tissues and SKBR3 and MCF7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33104019	LncRNA HOTAIR promotes breast cancer progression through regulating the miR-129-5p/FZD7 axis.	Breast cancer is the most common malignancies worldwide. LncRNA HOX transcript antisense intergenic RNA (HOTAIR) has been shown to promote progression and metastasis of various cancers, including breast cancer. This reasearch aimed to investigate the downstream regulatory pathways of HOTAIR in breast cancer. The levels of HOTAIR and miR-129-5p were examined in breast cancer tissues and SKBR3 and MCF7 cells by quantitative real-time PCR (qRT-PCR). Cell proliferation was examined by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were estimated by transwell assay. Epithelial-to-mesenchymal transition (EMT)-related markers (E-cadherin, N-cadherin and Vimentin) were measured by Western blot assay. The expression of Frizzled 7 (FZD7) was detected using qRT-PCR or Western blot assay. Bioinformatics analysis, luciferase reporter assay or RNA Immunoprecipitation (RIP) assay was performed to explore the molecular mechanism of HOTAIR in breast cancer. Xenograft analysis was utilized to evaluate the tumor growth in vivo. HOTAIR and FZD7 were upregulated, while miR-129-5p was down-regulated in breast cancer tissues and cells. Knockdown of miR-129-5p reversed the effect of HOTAIR knockdown on cell proliferation, migration, invasion and EMT. FZD7 restored the inhibition of miR-129-5p on breast cancer progression. Furthermore, HOTAIR was a sponge of miR-129-5p and FZD7 was a target of miR-129-5p. Knockdown of HOTAIR inhibited the tumor growth in vivo. HOTAIR facilitated breast cancer progression by regulating the miR-129-5p/FZD7 axis, indicating that HOTAIR may be a potential biomarker and therapeutic target for breast cancer.	NA	Cancer Biomark. 2021;30(2):203-212. doi: 10.3233/CBM-190913.
4164	LncRNA	HOTAIR	miR-613	Cx43	HL-1 cells	Cardiovascular Disease	Homo sapiens (human)	luciferase assay;	33294032	Long Noncoding RNA HOTAIR Functions as a Competitive Endogenous RNA to Regulate Connexin43 Remodeling in Atrial Fibrillation by Sponging MicroRNA-613.	Several studies have indicated that long noncoding RNAs (lncRNAs)-HOX transcript antisense RNA (HOTAIR) is involved in some cardiovascular diseases by regulating gene expression as a competitive endogenous RNA (ceRNA). GJA1 encoding Cx43 is one potential target gene of microRNA-613 (miR-613). Meanwhile, there is a potential target regulatory relationship between HOTAIR and miR-613. The present study is aimed at investigating whether HOTAIR functions as a ceRNA to regulate the Cx43 expression in atrial fibrillation (AF) by sponging miR-613. The expressions of HOTAIR, miR-613, and Cx43 were detected in the right atrial appendages of 45 patients with heart valve disease, including 23 patients with chronic AF. The HOTAIR overexpressed and underexpressed HL-1 cell model were constructed to confirm the effect of HOTAIR on Cx43. Then, the Cx43 expression was detected to testify the interplay between HOTAIR and miR-613 after cotransfecting HOTAIR and miR-613. Furthermore, luciferase assays were performed to verify that HOTAIR could regulate Cx43 remolding as a ceRNA by sponging miR-613. The expression of HOTAIR and Cx43 was significantly downregulated in chronic AF group. HOTAIR regulated positively the Cx43 expression in HL-1 cells. The upregulated effect of HOTAIR on the Cx43 expression could be remarkably attenuated by miR-613. Moreover, the inhibitory effect of miR-613 on the Cx43 expression could be obviously mitigated by HOTAIR. At last, luciferase assays confirmed HOTAIR functioned as a ceRNA in the Cx43 expression by sponging miR-613. Our study suggests that HOTAIR, functioning as a ceRNA by sponging miR-613, is an important contributor to Cx43 remolding in AF.	NA	Cardiovasc Ther. 2020 Nov 17;2020:5925342. doi: 10.1155/2020/5925342. eCollection 2020.
4165	LncRNA	HOTAIR	miR-126	NA	HaCaT cells	Psoriasis	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33747185	Role of the long non-coding RNA HOTAIR/miR-126 axis in an in vitro psoriasis model.	Psoriasis is a T-cell-mediated inflammatory skin disease that is characterized by excessive keratinocyte proliferation and persistent skin inflammation. Accumulating evidence suggests that long non-coding RNAs (lncRNAs) are dysregulated in a number of inflammatory conditions. In the present study, an in vitro psoriasis cell model was established. Human HaCaT keratinocytes were activated using the inflammatory factor IL-22. Briefly, HaCaT cells were starved in serum-free DMEM for 24 h and then stimulated with 100 ng/ml IL-22 in serum-free DMEM for 24 h. Previous research indicated that HOX transcript antisense RNA (HOTAIR) may participate in the development of psoriasis. First, reverse transcription-quantitative PCR (RT-qPCR) analysis was performed to detect HOTAIR expression. The results indicated that HOTAIR expression was reduced in IL-22-stimulated HaCaT cells. Subsequently, a dual-luciferase reporter assay was performed to verify the binding site between HOTAIR and microRNA (miR)-126. The RT-qPCR results indicated that miR-126 expression was increased in IL-22-stimulated HaCaT cells. Moreover, the effects of HOTAIR and miR-126 on IL-22-stimulated HaCaT cell proliferation and apoptosis were assessed. HaCaT cells were transfected with control-plasmid, HOTAIR-plasmid, HOTAIR-plasmid + mimic control or HOTAIR-plasmid + miR-126 mimic for 24 h. At 24 h post-transfection, the cells were stimulated with 100 ng/ml IL-22 for 24 h and experiments were conducted. IL-22 induced cell proliferation and suppressed apoptosis. However, HOTAIR-plasmid inhibited cell viability and induced apoptosis in IL-22-stimulated HaCaT cells. In addition, the western blotting results indicated that HOTAIR-plasmid increased cleaved caspase-3 expression and the cleaved caspase-3/caspase-3 ratio, whereas the HOTAIR-plasmid-mediated effects were reversed by miR-126 mimic. Collectively, the results of the present study demonstrated that the lncRNA-HOTAIR/miR-126 axis may be implicated in the regulation of psoriasis progression and may serve as a potential therapeutic target for psoriasis.	NA	Exp Ther Med. 2021 May;21(5):450. doi: 10.3892/etm.2021.9878. Epub 2021 Mar 1.
4166	LncRNA	HOTAIR	miR-126	SRSF1	H9c2 cells	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;Luciferase reporter assay;	32964995	LncRNA HOTAIR aggravates myocardial ischemia-reperfusion injury by sponging microRNA-126 to upregulate SRSF1.	OBJECTIVE: Acute myocardial infarction (AMI) is a severe fatal disease throughout the world. Myocardial IR limits the recovery of impaired cardiac function in AMI patients. This study aims to elucidate the role of long non-coding RNA (lncRNA) HOTAIR in myocardial ischemia-reperfusion (IR) and the underlying mechanism, thus providing a novel therapy for AMI. MATERIALS AND METHODS: Myocardial IR model in mice was firstly constructed by LAD. Plasma levels of LDH, CK-MB, HOTAIR, and microRNA-126 in mice were detected. Subsequently, in vitro HR model was constructed in H9c2 cells. Regulatory effects of HOTAIR on proliferative ability, LDH release, and Caspase-3 activity in H2O2-induced H9c2 cells were determined. Relative levels of inflammatory factors in in vitro HR model were measured by enzyme-linked immunosorbent assay (ELISA). The regulatory loop HOTAIR/microRNA-126/SRSF1 was finally verified by Dual-Luciferase reporter assay. RESULTS: LDH and CK-MB were significantly released in mice with myocardial IR. HOTAIR was upregulated, while microRNA-126 was downregulated in IR mice and H2O2-induced H9c2 cells. Overexpression of HOTAIR stimulated proliferative ability, LDH release, and Caspase-3 activity in H2O2-induced H9c2 cells. Besides, overexpression of microRNA-126 inhibited the release of inflammatory factors in H9c2 cells undergoing HR induction. The regulatory loop HOTAIR/microRNA-126/SRSF1 was identified to influence IR development. CONCLUSIONS: HOTAIR aggravates myocardial IR by competitively binding SRSF1 with microRNA-126.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):9046-9054. doi: 10.26355/eurrev_202009_22850.
4167	LncRNA	HOTAIRM1	miR-433-5p	PIK3CD	PCOS tissues	Polycystic Ovary Syndrome	Homo sapiens (human)	Flow cytometry assay;qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33485372	LncRNA HOTAIRM1, miR-433-5p and PIK3CD function as a ceRNA network to exacerbate the development of PCOS.	BACKGROUND: Currently, several non-coding RNAs (ncRNAs) were distinguished in polycystic ovarian syndrome (PCOS). This present study aims to explore the potential function of lncRNA HOTAIRM1/miR-433-5p/PIK3CD in ovarian granulosa cells. METHODS: We analyzed the expression profiles of HOTAIRM1, miR-433-5p and PIK3CD in PCOS samples by enquiring GEO database. GSEA was applied to enrich the pathways related to PCOS. The target association between HOTAIRM1 and miR-433-5p or the binding association between miR-433-5p and PIK3CD were assessed by online prediction tools and a dual luciferase reporter assay. qPCR and western blotting assays were used to detect PIK3CD expression after HOTAIRM1 and miR-433-5p treatment. The proliferation and apoptosis of ovarian granulosa cells were estimated by cell counting kit-8 and flow cytometry assays, respectively. RESULTS: The expression profiles of HOTAIRM1 and PIK3CD were increased, whereas miR-433-5p was decreased in PCOS tissues. PIK3CD expression was positively regulated by HOTAIRM1 and negatively modulated by miR-433-5p. Overexpression of HOTAIRM1 reduced the proliferative ability and increased the apoptotic ability of granulosa cells, whereas upregulation of miR-433-5p or downregulation of PIK3CD reversed the effects of HOTAIRM1 on granulosa cells. Moreover, overexpression of miR-433-5 displayed a results with increasing proliferative ability and decreasing apoptotic ability, but upregulation of PIK3CD eliminated the function of miR-433-5p on granulosa cells. CONCLUSIONS: Our findings illustrated that HOTAIRM1 could sponge miR-433-5p to promote PIK3CD expression, thereby regulating the growth and apoptosis of granulose cells in PCOS.	NA	J Ovarian Res. 2021 Jan 23;14(1):19. doi: 10.1186/s13048-020-00742-4.
4168	LncRNA	HOTAIRM1	miR-148a	Wnt10b	BCPAP cells	Thyroid Cancer	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;Western blot;luciferase assay;MTT assay;	33650656	lncRNA HOTAIRM1 regulates cell proliferation and the metastasis of thyroid cancer by targeting Wnt10b.	Long non-coding RNAs play a role in a variety of malignancies, such as thyroid cancer (TC). However, the effects and function of lincRNA HOTAIRM1 (LINC HOTAIRM1) in TC remains obscure. In the present study, the expression of HOTAIRM1 was evaluated in TC tissues and cells by RT-qPCR and the association between the lncRNA and disease progression was assessed. In vitro, the biological function of HOTAIRM1 was assessed in TC. Moreover, changes in the expression of Wnt10b were measured by western blot analysis. In addition, MTT assay, bioinformatics analysis and luciferase assays were performed to determine the target binding effect between LINC HOTAIRM1 and miR-148a, as well as that between Wnt10b and miR-148a. The changes in the metastatic ability of TPC-1 and BCPAP cells were evaluated by Transwell assay. The pronounced upregulated expression of HOTAIRM1 was evident in TC cells and tissues, and was associated with TNM stage and lymph node metastasis. When HOTAIRM1 was knocked down, this inhibited the proliferative and invasive abilities of TPC-1 and BCPAP cells in vitro. The knockdown of this lncRNA also increased the expression of microRNA-148a (miR-148a) and decreased Wnt10b expression in these cells, whereas transfection with miR-148a inhibitor was sufficient to overcome this Wnt10b downregulation. In line with these results, the overexpression of miR-148a markedly suppressed Wnt10b expression, whereas miR-148a inhibition resulted in the opposite effects. The overexpression of Wnt10b was also sufficient to overcome the effects of miR-148a mimics on TPC-1 and BCPAP cells. Taken together, these results suggest that miR-148a and Wnt10b are downstream effectors of the HOTAIRM1 signaling pathway in TC. This HOTAIRM1/miR-148a/Wnt10 axis may thus be amenable to therapeutic targeting in order to improve disease outcomes in patients with TC.	NA	Oncol Rep. 2021 Mar;45(3):1083-1093. doi: 10.3892/or.2020.7919. Epub 2020 Dec 31.
4169	LncRNA	HOTAIRM1	miR-125b-2-3p	RIZ1	liver cancer cells	Liver Cancer	Homo sapiens (human)	CCK-8 assay;ChIP;qRT-PCR;luciferase assay;Luciferase reporter assay;	32964965	Inactivation of lncRNA HOTAIRM1 caused by histone methyltransferase RIZ1 accelerated the proliferation and invasion of liver cancer.	OBJECTIVE: Liver cancer is the second most common cause of cancer death, causing more than 700,000 deaths every year. It has been demonstrated that Long non-coding RNA (LncRNA) plays an important regulatory role in a series of diseases. However, the regulatory mechanism of LncRNAs in liver cancer has not been fully elucidated. The purpose of this study was to explore the interaction of lncRNA HOTAIRM1 and aberrant histone modification in liver cancer. MATERIALS AND METHODS: qRT-PCR was used to detect the expression levels of RIZ1 and miR-125b in liver cancer cells. Cell proliferation was measured using the CCK8 assay. ChIP-Real-time PCR confirmed the binding site of the promoter of HOTAIRM1 by H3K9me1. The direct target of HOTAIRM1 and miR-125b in liver cancer cells was measured by a luciferase reporter assay. Cell proliferation was detected by Cell Counting Kit-8 (CCK8). Cell invasion was measured by transwell assays and cell migration was detected by wound healing assay. RESULTS: The expression level of RIZ1 and miR-125b was upregulated, and HOTAIRM1 was downregulated in liver cancer cells. Transwell and CCK-8 assay showed that RIZ1 expression is associated with the proliferation, invasion and migration of liver cancer cells, silencing of RIZ1 inhibited cell proliferation, migration, and invasion in HEPG2 and HCC-LM3 cells. RIZ1 interference could significantly inhibit H3K9me1 expression. H3K9me1 protein can bind to HOTAIRM1 promoter directly. Furthermore, the bioinformatics prediction and luciferase assay demonstrated that miR-125b can interact with HOTAIRM1 by direct binding. HOTAIRM1 down-expression promoted HEPG2 cell growth and metastasis, which was further strengthened following the co-transfection of miR-125b. Furthermore, overexpressed HOTAIRM1 inhibited HCC-LM3 cell growth and metastasis and a complete reversal of the results seen when transfected with miR-125b. CONCLUSIONS: For the first time, we found that RIZ1 was upregulated in liver cancer cells and RIZ1-mediated H3K9me1 enrichment on the HOTAIRM1 promoter regulated the growth and metastasis of liver cancer cells by targeting miR-125b, which could further accelerate tumor proliferation, migration and invasion. It may serve as a therapeutic marker for liver cancer treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8767-8777. doi: 10.26355/eurrev_202009_22815.
4170	LncRNA	HOTAIRM1	miR-153-5p	SNAI2	GBM cells	Glioblastoma	Homo sapiens (human)	ChIP;RIP assay;Luciferase reporter assay;	33323548	Upregulation of HOTAIRM1 increases migration and invasion by glioblastoma cells.	Long noncoding RNAs (lncRNAs) promote invasion and migration by glioblastoma (GBM) cells. In this study, quantitative real-time polymerase chain reaction was used to detect expression levels of the lncRNA HOTAIRM1 in GBM tissue samples and cells. The function of HOTAIRM1 was examined using wound healing assays, transwell assays, and in vivo experiments after GBM cells were transfected with either sh-ctrl or sh-HOTAIRM1. Luciferase reporter assays and RIP assays were performed to determine the interactions between HOTAIRM1 and miR-153-5p and between miR-153-5p and SNAI2. We also used luciferase reporter assays and ChIP assays to assess the transcriptional regulation of HOTAIRM1 by SNAI2 and CDH1. HOTAIRM1 was significantly overexpressed in GBM tissues and cells. HOTAIRM1 knockdown significantly weakened the migration and invasion by GBM cells. HOTAIRM1 was found to sponge miR-153-5p, and SNAI2 is a direct target of miR-153-5p. In addition, SNAI2 was shown to force HOTAIRM1 expression through directly promoting transcription and suppressing the negative regulation of CDH1 on transcription. Our results indicate a positive feedback loop between HOTAIRM1 and SNAI2, and suggest that the lncRNA HOTAIRM1 is a potential biomarker and therapeutic target in GBM.	NA	Aging (Albany NY). 2020 Dec 11;13(2):2348-2364. doi: 10.18632/aging.202263. Epub 2020 Dec 11.
4171	LncRNA	HOTTIP	miR-214	KPNA3	CRC cells	Colorectal Cancer	Homo sapiens (human)	RACE;RNA pull-down assay;RNA pull-down;	33585440	Exosomal Long Non-coding RNA HOTTIP Increases Resistance of Colorectal Cancer Cells to Mitomycin via Impairing MiR-214-Mediated Degradation of KPNA3.	It has been reported that long non-coding RNA HOXA distal transcript antisense RNA (lncRNA HOTTIP) functions as a tumor promoter in colorectal cancer (CRC). Hence, we paid attention to exploring whether exosomes could carry lncRNA HOTTIP to affect the mitomycin resistance in CRC and to identify the underlying mechanisms. High expression of HOTTIP was detected in mitomycin-resistant CRC cells. Inhibition of HOTTIP reduced the mitomycin resistance. In the co-culture system of mitomycin-resistant cells or their derived exosomes with CRC cells, the HOTTIP was found to be transferred into the parental cells via extracellular vesicles (EVs) secreted from mitomycin-resistant cells and to contribute to the mitomycin resistance. Based on the bioinformatics databases, possible interaction network of HOTTIP, microRNA-214 (miR-214) and Karyopherin subunit alpha 3 (KPNA3) in CRC was predicted, which was further analyzed by dual-luciferase reporter, RNA binding protein immunoprecipitation and RNA pull-down assays. As HOTTIP down-regulated miR-214 to elevate the KPNA3 expression, HOTTIP enhanced the mitomycin resistance through impairing miR-214-dependent inhibition of KPNA3. Finally, HOTTIP was suggested as an independent factor predicting mitomycin response in patients with CRC. Those data together confirmed the promotive effects of EV-carried HOTTIP on the mitomycin resistance, while targeting HOTTIP might be a promising strategy overcoming drug resistance in CRC.	NA	Front Cell Dev Biol. 2021 Jan 28;8:582723. doi: 10.3389/fcell.2020.582723. eCollection 2020.
4172	LncRNA	HOXB-AS1	miR-149-3p	Wnt10b	endometrial carcinoma cells	Endometrial Cancer	Homo sapiens (human)	qRT-PCR	33073693	Long Noncoding RNA HOXB-AS1 Is Upregulated in Endometrial Carcinoma and Sponged miR-149-3p to Upregulate Wnt10b.	The functions of Long noncoding RNA (lncRNA) HOXB-AS1 have been investigated in glioblastoma and multiple myeloma. However, the role of lncRNA HOXB-AS1 in endometrial carcinoma (EC) remains largely unknown. This study investigated the underlying mechanisms of the lncRNA HOXB-AS1 on the progression of EC. In this study, We found that HOXB-AS1 expression was significantly upregulated in EC tissue samples and was associated with shorter survival time. Furthermore, upregulation of HOXB-AS1 promoted proliferation, invasion, and migration of EC cell. HOXB-AS1 and Wnt10b directly bound to miR-149-3p. HOXB-AS1 increased the expression of Wnt10b by binding to miR-149-3p. We further verified the upregulation of β-catenin, cyclin D1, and c-myc induced by HOXB-AS1. In conclusion, our results indicated that HOXB-AS1 exerted oncogenic function as competing endogenous RNA (ceRNA) of miR-149-3p to release Wnt10b and activated Wnt/β-catenin pathway.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820967462. doi: 10.1177/1533033820967462.
4173	LncRNA	HOXB-AS3	miR-378a-3p	LDHA	EOC cells	Ovarian Cancer	Homo sapiens (human)	RACE;Western blot;Luciferase reporter assay;	33148416	LncRNA HOXB-AS3 promotes growth, invasion and migration of epithelial ovarian cancer by altering glycolysis.	HEADING AIMS: LncRNA HOXB-AS3 is proved as an oncogene in tumors. Herein, we determine the function and mechanism of HOXB-AS3 in epithelial ovarian cancer (EOC) cells. MATERIALS AND METHODS: Chi-square test, Kaplan-Meier (KM) analysis and Cox regression analysis were used to analyze the clinicopathological features of HOXB-AS3 in EOC patients. CCK8, transwell and wound healing assay were used to test the function of HOXB-AS3. Luciferase reporter assay, western blot and glycolysis rate assay were used for further mechanistic studies. KEY FINDINGS: HOXB-AS3 was abundantly expressed in EOC tissues, and higher levels of HOXB-AS3 in EOC patients were significantly associated with disease status and overall survival status. EOC patients with high levels of HOXB-AS3 had strikingly shorter disease-free survival (DFS) and overall survival (OS) times than those with low levels. HOXB-AS3 also might as an independent prognostic factor. Further study revealed knockdown of HOXB-AS3 significantly inhibited the proliferation, invasion and migration of EOC cells. Mechanistic investigations suggested that knockdown of HOXB-AS3 could decrease lactate dehydrogenase A (LDHA) expression and the extracellular acidification rate (ECAR) by sponging miR-378a-3p. SIGNIFICANCE: To our knowledge, this is the first study to suggest that HOXB-AS3 could crosstalk with miRNA in the cytoplasm and alter glycolysis in cancer cells. Our results improve our understanding of the mechanism of HOXB-AS3 and suggest that HOXB-AS3 can act as a predictor of OS and a target for EOC therapies.	NA	Life Sci. 2021 Jan 1;264:118636. doi: 10.1016/j.lfs.2020.118636. Epub 2020 Oct 24.
4174	LncRNA	HOXD-AS1	miR-877-3p	FGF2	CC tissues and cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	32977766	HOXD-AS1 facilitates cell migration and invasion as an oncogenic lncRNA by competitively binding to miR-877-3p and upregulating FGF2 in human cervical cancer.	BACKGROUND: Long non-coding RNAs (LncRNAs) are dysregulated in multiple human cancers and they are highly involved in tumor progression. Previous studies have identified the oncogenic lncRNA HOXD cluster antisense RNA 1 (HOXD-AS1) in human cancers, while its roles in cervical cancer (CC) remain unclear. Herein we intended to characterize the implication of HOXD-AS1 in CC. METHODS: qRT-PCR was applied to examine the relative expression of HOXD-AS1 in CC tissues, cell lines and transfected cells. Wound healing and transwell assays were applied to detect cell migration and invasion alteration. The targeting relationship between miRNA and mRNA/lncRNA was determined by dual luciferase reporter, qRT-PCR and western blot assays. RESULTS: HOXD-AS1 was overexpressed in CC tissues and cell lines. Its higher level predicted worse prognosis of CC patients. SiRNA mediated knockdown of HOXD-AS1 repressed CC cell migration and invasion, and its overexpression did the opposite. Mechanistically, HOXD-AS1 acted as a competing endogenous RNA (ceRNA) to sponge miR-877-3p and led to upregulation of FGF2, a target of miR-877-3p. Importantly, either miR-877-3p overexpression or FGF2 inhibition could abolish the migration and invasion promotion induced by HOXD-AS1. CONCLUSION: HOXD-AS1 functions as a tumor-promoting lncRNA via the miR-877-3p/FGF2 axis in CC. HOXD-AS1 might be a promising therapeutic target as well as a novel prognostic biomarker for CC.	NA	BMC Cancer. 2020 Sep 25;20(1):924. doi: 10.1186/s12885-020-07441-9.
4175	Circular RNA	hsa_circ_0000199	miR-206	NA	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR	33495420	Hsa_circ_0000199 facilitates chemo-tolerance of triple-negative breast cancer by interfering with miR-206/613-led PI3K/Akt/mTOR signaling.	Increasing attentions have been paid to the role of circRNAs in the etiology of triple-negative breast cancer (TNBC), and we strived to figure out the association of circRNA AKT3/miRNA axis with TNBC chemo-resistance. Altogether 207 BC patients were divided into TNBC group (n=83) and non-TNBC group (n=124), and MCF-10A, MDA-MB-231, MDA-MB-468, SK-BR-3 and MCF-7 cell lines were prepared in advance. Expressions of AKT3-derived circRNAs and relevant miRNAs in the TNBC tissues and cell lines were determined by employing real-time polymerase chain reaction (PCR). It was indicated that hsa_circ_0000199 expression was higher in TNBC tissues than in non-TNBC tissues, and high hsa_circ_0000199 expression was predictive of large tumor size, advanced TNM grade, high Ki-67 level and poor 3-year survival of TNBC patients (all P<0.05). Furthermore, miR-613 and miR-206 were sponged and negatively regulated by hsa_circ_0000199 (P<0.001), and PI3K/Akt/mTOR signaling was depressed by si-hsa_circ_0000199 in TNBC cell lines (P<0.01). Ultimately, miR-206/miR-613 inhibitor reversed impacts of si-hsa_circ_0000199 on PI3K/Akt/mTOR signaling, proliferation, migration, invasion, chemo-sensitivity and autophagy of TNBC cells (all P<0.01). Conclusively, silencing of hsa_circ_0000199 enhanced TNBC chemo-sensitivity by promoting miR-206/miR-613 expression and deactivating PI3K/Akt/mTOR signaling, which was conducive to improving chemotherapeutic efficacy of TNBC patients.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4522-4551. doi: 10.18632/aging.202415. Epub 2021 Jan 20.
4176	Circular RNA	hsa_circ_0000199	miR-613	NA	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR	33495420	Hsa_circ_0000199 facilitates chemo-tolerance of triple-negative breast cancer by interfering with miR-206/613-led PI3K/Akt/mTOR signaling.	Increasing attentions have been paid to the role of circRNAs in the etiology of triple-negative breast cancer (TNBC), and we strived to figure out the association of circRNA AKT3/miRNA axis with TNBC chemo-resistance. Altogether 207 BC patients were divided into TNBC group (n=83) and non-TNBC group (n=124), and MCF-10A, MDA-MB-231, MDA-MB-468, SK-BR-3 and MCF-7 cell lines were prepared in advance. Expressions of AKT3-derived circRNAs and relevant miRNAs in the TNBC tissues and cell lines were determined by employing real-time polymerase chain reaction (PCR). It was indicated that hsa_circ_0000199 expression was higher in TNBC tissues than in non-TNBC tissues, and high hsa_circ_0000199 expression was predictive of large tumor size, advanced TNM grade, high Ki-67 level and poor 3-year survival of TNBC patients (all P<0.05). Furthermore, miR-613 and miR-206 were sponged and negatively regulated by hsa_circ_0000199 (P<0.001), and PI3K/Akt/mTOR signaling was depressed by si-hsa_circ_0000199 in TNBC cell lines (P<0.01). Ultimately, miR-206/miR-613 inhibitor reversed impacts of si-hsa_circ_0000199 on PI3K/Akt/mTOR signaling, proliferation, migration, invasion, chemo-sensitivity and autophagy of TNBC cells (all P<0.01). Conclusively, silencing of hsa_circ_0000199 enhanced TNBC chemo-sensitivity by promoting miR-206/miR-613 expression and deactivating PI3K/Akt/mTOR signaling, which was conducive to improving chemotherapeutic efficacy of TNBC patients.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4522-4551. doi: 10.18632/aging.202415. Epub 2021 Jan 20.
4177	Circular RNA	hsa_circ_0001785	miR-942	SOCS3	BC cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33054543	Circular RNA hsa_circ_0001785 inhibits the proliferation, migration and invasion of breast cancer cells in vitro and in vivo by sponging miR-942 to upregulate SOCS3.	Circular RNAs (circRNAs) are a class of widely expressed noncoding RNA with significant regulatory potential discovered in recent years. The purpose of this study was to investigate the effects of hsa_circ_0001785 on the proliferation, migration and invasion of breast cancer (BC) cells in vivo and in vitro and the potential underlying molecular mechanism. In the present study, the expressions of hsa_circ_0001785 in five BC cells (T47D, MCF-7, MDA-MB-453, MDA-MB-231 and BT-549) and one normal breast cell (MCF-10A) were the first to examined by qRT-PCR. Then, we studied the biological function of hsa_circ_0001785 in BC by in vivo and in vitro experiments. CCK-8, clone formation, wound-healing and Transwell assays were performed to analyze the cellular proliferation, migration and invasion in vitro. The subcutaneous tumor model of nude mice was used for in vivo experiment. In addition, we determined that hsa_circ_0001785 acted as competing endogenous RNAs (ceRNAs) in BC by RNA immunoprecipitation (RIP) and dual-luciferase reporter assays. Results showed that the expressions of hsa_circ_0001785 were decreased in BC cells. Hsa_circ_0001785 overexpression inhibited the proliferation, migration, invasion of BC cells and tumor growth in nude mice. RIP and dual-luciferase reporter assay demonstrated that hsa_circ_0001785 could regulate the SOCS3 by sponging miR-942. In general, circular RNA hsa_circ_0001785 inhibits the proliferation, migration and invasion of BC cells by modulating the miR-942/SOCS3 signaling axis.	NA	Cell Cycle. 2020 Nov;19(21):2811-2825. doi: 10.1080/15384101.2020.1824717. Epub 2020 Oct 15.
4178	Circular RNA	hsa_circ_0004872	miR-224	Smad4	GC cells	Gastric Cancer	Homo sapiens (human)	ChIP;FISH;qRT-PCR;RIP assay;Western blot;FISH;Luciferase reporter assay;	33172486	Circular RNA hsa_circ_0004872 inhibits gastric cancer progression via the miR-224/Smad4/ADAR1 successive regulatory circuit.	BACKGROUND: Emerging evidence has shown that circular RNAs (circRNAs) play a crucial regulatory role in the occurrence and development of cancer. Exploring the roles and mechanisms of circRNAs in tumorigenesis and progression may help to identify new diagnostic markers and therapeutic targets. In the present study, we investigated the role and regulatory mechanism of hsa_circ_0004872 in gastric cancer (GC). METHODS: qRT-PCR was used to determine the expression of hsa_circ_0004872 in GC tissues and cells. EdU, CCK-8, transwell and scratch wound healing assays were used to assess the role of hsa_circ_0004872 in GC cell proliferation, invasion and migration, respectively. Subcutaneous and tail vein tumor injections in nude mice were used to assess the role of hsa_circ_0004872 in vivo. RIP assay, biotin-coupled probe pull-down assay, FISH and luciferase reporter assay were performed to confirm the relationship between hsa_circ_0004872 and the identified miRNA. ChIP assay, luciferase reporter assay and western blot were used to determine the direct binding of Smad4 to the promoter of the ADAR1 gene. RESULTS: In this study, we found that hsa_circ_0004872 was dramatically downregulated in GC tissues compared with adjacent noncancerous tissues. The expression level of hsa_circ_0004872 was associated with tumor size and local lymph node metastasis. Enforced expression of hsa_circ_0004872 inhibited the proliferation, invasion and migration of GC cells, whereas knockdown of hsa_circ_0004872 had the opposite effects. Nude mice experiments showed that ectopic expression of hsa_circ_0004872 dramatically inhibited tumor growth and metastasis in vivo. Moreover, we demonstrated that hsa_circ_0004872 acted as a "molecular sponge" for miR-224 to upregulate the expression of the miR-224 downstream targets p21 and Smad4. Importantly, we found that the RNA-editing enzyme ADAR1 inhibited hsa_circ_0004872 expression and further led to the upregulation of miR-224. Smad4, the downstream target of miR-224, could further affect hsa_circ_0004872 levels by directly binding to the promoter region of ADAR1 to inhibit ADAR1 expression. CONCLUSIONS: Our findings showed that hsa_circ_0004872 acted as a tumor suppressor in GC by forming a negative regulatory loop consisting of hsa_circ_0004872/miR-224/Smad4/ADAR1. Thus, hsa_circ_0004872 may serve as a potential biomarker and therapeutic target for GC.	NA	Mol Cancer. 2020 Nov 10;19(1):157. doi: 10.1186/s12943-020-01268-5.
4179	Circular RNA	hsa_circ_0005114	miR-142-3p	APC	glioma cells	Glioma	Homo sapiens (human)	microarray;	33281969	Circular RNA hsa_circ_0005114-miR-142-3p/miR-590-5p-adenomatous polyposis coli protein axis as a potential target for treatment of glioma.	Glioma is the most common type of brain tumor and is associated with a high mortality rate. Despite recent advances in treatment options, the overall prognosis in patients with glioma remains poor. Studies have suggested that circular (circ)RNAs serve important roles in the development and progression of glioma and may have potential as therapeutic targets. However, the expression profiles of circRNAs and their functions in glioma have rarely been studied. The present study aimed to screen differentially expressed circRNAs (DECs) between glioma and normal brain tissues using sequencing data collected from the Gene Expression Omnibus database (GSE86202 and GSE92322 datasets) and explain their mechanisms based on the competing endogenous (ce)RNA regulatory hypothesis. In total, 424 commonly downregulated DECs (with the Gene_symbol annotated in the circBase database) in these two datasets were identified. Using the CircInteractome and Starbase databases, 18 micro (mi)RNAs (miRs) were predicted to interact with DECs, while 22 glioma-related genes obtained from the Comparative Toxicogenomics Database were predicted to be regulated by 15 miRNAs via the miRwalk 2.0 database. A ceRNA network was established based on 115 DECs, 15 miRNAs and 22 mRNAs. LinkedOmics online analysis using The Cancer Genome Atlas (TCGA) data showed that hsa-miR-142-3p/hsa-miR-590-5p and their target gene adenomatous polyposis coli protein (APC) were all significantly associated with overall survival rate and their prognosis trend was opposite, revealing that high expression levels of hsa-miR-142-3p/hsa-miR-590-5 were associated with a poor overall survival rate, while high APC expression with a good overall survival rate. UALCAN analysis using TCGA data of glioblastoma multiforme and the GSE25632 and GSE103229 microarray datasets showed that hsa-miR-142-3p/hsa-miR-590-5p was upregulated and APC was downregulated. Thus, hsa-miR-142-3p/hsa-miR-590-5p-APC-related circ/ceRNA axes may be important in glioma, and hsa_circ_0005114 interacted with both of these miRNAs. Functional analysis showed that hsa_circ_0005114 was involved in insulin secretion, while APC was associated with the Wnt signaling pathway. In conclusion, hsa_circ_0005114-miR-142-3p/miR-590-5p-APC ceRNA axes may be potential targets for the treatment of glioma.	NA	Oncol Lett. 2021 Jan;21(1):58. doi: 10.3892/ol.2020.12320. Epub 2020 Nov 19.
4180	Circular RNA	hsa_circ_0005114	miR-590-5p	APC	glioma cells	Glioma	Homo sapiens (human)	microarray;	33281969	Circular RNA hsa_circ_0005114-miR-142-3p/miR-590-5p-adenomatous polyposis coli protein axis as a potential target for treatment of glioma.	Glioma is the most common type of brain tumor and is associated with a high mortality rate. Despite recent advances in treatment options, the overall prognosis in patients with glioma remains poor. Studies have suggested that circular (circ)RNAs serve important roles in the development and progression of glioma and may have potential as therapeutic targets. However, the expression profiles of circRNAs and their functions in glioma have rarely been studied. The present study aimed to screen differentially expressed circRNAs (DECs) between glioma and normal brain tissues using sequencing data collected from the Gene Expression Omnibus database (GSE86202 and GSE92322 datasets) and explain their mechanisms based on the competing endogenous (ce)RNA regulatory hypothesis. In total, 424 commonly downregulated DECs (with the Gene_symbol annotated in the circBase database) in these two datasets were identified. Using the CircInteractome and Starbase databases, 18 micro (mi)RNAs (miRs) were predicted to interact with DECs, while 22 glioma-related genes obtained from the Comparative Toxicogenomics Database were predicted to be regulated by 15 miRNAs via the miRwalk 2.0 database. A ceRNA network was established based on 115 DECs, 15 miRNAs and 22 mRNAs. LinkedOmics online analysis using The Cancer Genome Atlas (TCGA) data showed that hsa-miR-142-3p/hsa-miR-590-5p and their target gene adenomatous polyposis coli protein (APC) were all significantly associated with overall survival rate and their prognosis trend was opposite, revealing that high expression levels of hsa-miR-142-3p/hsa-miR-590-5 were associated with a poor overall survival rate, while high APC expression with a good overall survival rate. UALCAN analysis using TCGA data of glioblastoma multiforme and the GSE25632 and GSE103229 microarray datasets showed that hsa-miR-142-3p/hsa-miR-590-5p was upregulated and APC was downregulated. Thus, hsa-miR-142-3p/hsa-miR-590-5p-APC-related circ/ceRNA axes may be important in glioma, and hsa_circ_0005114 interacted with both of these miRNAs. Functional analysis showed that hsa_circ_0005114 was involved in insulin secretion, while APC was associated with the Wnt signaling pathway. In conclusion, hsa_circ_0005114-miR-142-3p/miR-590-5p-APC ceRNA axes may be potential targets for the treatment of glioma.	NA	Oncol Lett. 2021 Jan;21(1):58. doi: 10.3892/ol.2020.12320. Epub 2020 Nov 19.
4181	Circular RNA	hsa_circ_0008003	miR-488	ZNF281	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	microarray;qRT-PCR;	33320427	Circular RNA hsa_circ_0008003 facilitates tumorigenesis and development of non-small cell lung carcinoma via modulating miR-488/ZNF281 axis.	As one of the most aggressive malignancies, non-small cell lung carcinoma (NSCLC) has high risks of death. It has been demonstrated that circRNAs accelerate NSCLC progression, but the underlying molecular mechanisms of circRNAs in NSCLC were still obscure. In the first place, the circRNA microarray of NSCLC was investigated in this study, and hsa_circ_0008003 (circ-0008003) was chosen as the research object. Then, it was unveiled that the expression of circ-0008003 examined via qRT-PCR was elevated in tumour tissues relative to the non-tumour tissues, which was associated with TNM stage and lymphatic metastasis in NSCLC. Additionally, the prognosis of NSCLC patients with high circ-0008003 level was poor. Besides, circ-0008003 silencing dampened the invasion and proliferation of NSCLC cells. Next, according to the mechanistic studies, circ-0008003 functioned as a ceRNA of ZNF281 in NSCLC by acting as the endogenous sponge for miR-488, which was proved to be a tumour suppressor in NSCLC. Additionally, ZNF281 overexpression and miR-488 suppression recovered the influences of repressed circ-0008003 on NSCLC cellular processes. It was validated in this research that circ-0008003 triggered tumour formation in NSCLC, which was adjusted via miR-488/ZNF281 axis, casting a novel light on the resultful target for treating NSCLC and predicting the prognosis.	NA	J Cell Mol Med. 2020 Dec 15. doi: 10.1111/jcmm.15987.
4182	Circular RNA	hsa_circ_0026416	miR-346	NFIB	Colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33061846	Hsa_circ_0026416 promotes proliferation and migration in colorectal cancer via miR-346/NFIB axis.	BACKGROUND: Colorectal cancer (CRC) is one of the most common cancers worldwide. Circular RNAs (circRNAs), a novel class of non-coding RNAs, have been confirmed to be key regulators of many diseases. With many scholars devoted to studying the biological function and mechanism of circRNAs, their mysterious veil is gradually being revealed. In our research, we explored a new circRNA, hsa_circ_0026416, which was identified as upregulated in CRC with the largest fold change (logFC = 3.70) of the evaluated circRNAs via analysing expression profiling data by high throughput sequencing of members of the GEO dataset (GSE77661) to explore the molecular mechanisms of CRC. METHODS: qRT-PCR and western blot analysis were utilized to assess the expression of hsa_circ_0026416, miR-346 and Nuclear Factor I/B (NFIB). CCK-8 and transwell assays were utilized to examine cell proliferation, migration and invasion in vitro, respectively. A luciferase reporter assay was used to verify the combination of hsa_circ_0026416, miR-346 and NFIB. A nude mouse xenograft model was also utilized to determine the role of hsa_circ_0026416 in CRC cell growth in vivo. RESULTS: Hsa_circ_0026416 was markedly upregulated in CRC patient tissues and plasma and was a poor prognosis in CRC patients. In addition, the area under the curve (AUC) of hsa_circ_0026416 (0.767) was greater than the AUC of CEA (0.670), CA19-9 (0.592) and CA72-4 (0.575). Functionally, hsa_circ_0026416 promotes cell proliferation, migration and invasion both in vitro and in vivo. Mechanistically, hsa_circ_0026416 may function as a ceRNA via competitively absorbing miR-346 to upregulate the expression of NFIB. CONCLUSIONS: In summary, our findings demonstrate that hsa_circ_0026416 is an oncogene in CRC. Hsa_circ_0026416 promotes the progression of CRC via the miR-346/NFIB axis and may represent a potential biomarker for diagnosis and therapy in CRC.	NA	Cancer Cell Int. 2020 Oct 12;20:494. doi: 10.1186/s12935-020-01593-1. eCollection 2020.
4183	Circular RNA	hsa_circ_0026416	miR-346	NFIB	Colorectal cancer cells	Colorectal Cancer	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;	33061846	Hsa_circ_0026416 promotes proliferation and migration in colorectal cancer via miR-346/NFIB axis.	BACKGROUND: Colorectal cancer (CRC) is one of the most common cancers worldwide. Circular RNAs (circRNAs), a novel class of non-coding RNAs, have been confirmed to be key regulators of many diseases. With many scholars devoted to studying the biological function and mechanism of circRNAs, their mysterious veil is gradually being revealed. In our research, we explored a new circRNA, hsa_circ_0026416, which was identified as upregulated in CRC with the largest fold change (logFC = 3.70) of the evaluated circRNAs via analysing expression profiling data by high throughput sequencing of members of the GEO dataset (GSE77661) to explore the molecular mechanisms of CRC. METHODS: qRT-PCR and western blot analysis were utilized to assess the expression of hsa_circ_0026416, miR-346 and Nuclear Factor I/B (NFIB). CCK-8 and transwell assays were utilized to examine cell proliferation, migration and invasion in vitro, respectively. A luciferase reporter assay was used to verify the combination of hsa_circ_0026416, miR-346 and NFIB. A nude mouse xenograft model was also utilized to determine the role of hsa_circ_0026416 in CRC cell growth in vivo. RESULTS: Hsa_circ_0026416 was markedly upregulated in CRC patient tissues and plasma and was a poor prognosis in CRC patients. In addition, the area under the curve (AUC) of hsa_circ_0026416 (0.767) was greater than the AUC of CEA (0.670), CA19-9 (0.592) and CA72-4 (0.575). Functionally, hsa_circ_0026416 promotes cell proliferation, migration and invasion both in vitro and in vivo. Mechanistically, hsa_circ_0026416 may function as a ceRNA via competitively absorbing miR-346 to upregulate the expression of NFIB. CONCLUSIONS: In summary, our findings demonstrate that hsa_circ_0026416 is an oncogene in CRC. Hsa_circ_0026416 promotes the progression of CRC via the miR-346/NFIB axis and may represent a potential biomarker for diagnosis and therapy in CRC.	NA	Cancer Cell Int. 2020 Oct 12;20:494. doi: 10.1186/s12935-020-01593-1. eCollection 2020.
4184	Circular RNA	hsa_circ_0069767	miR-636	KRAS	Multiple Myeloma Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR;RT-PCR;Western blot;Flow Cytometry assay;	33192092	Effect of the Up-Regulation of Circular RNA Hsa_circ_0069767 Derived from C-KIT on the Biological Behavior of Multiple Myeloma Cells.	PURPOSE: Multiple myeloma (MM) is an incurable disease. This study focused on the expression of circular RNA circ_0069767 in MM and its influence on prognosis, in order to provide a potential target. PATIENTS AND METHODS: Totally 66 MM patients participated in this research. Using RT-PCR method to determine the expression level of circ_0069767 in 66 sorted samples from multiple myeloma patients and 21 normal control bone marrow samples, Kaplan-Meier was applied for survival analysis. We constructed stable over-expressing circ_0069767 and silenced circ_0069767 cell lines and used MTS experiment to detect cell viability, transwell experiment to detect cell migration and invasion ability and flow cytometry to detect cell apoptosis. Dual luciferase experiment, qRT-PCR experiment and Western blot were used to explore miRNA and downstream genes. RESULTS: The expression of circ_0069767 in MM was significantly higher than that of the normal control group. Patients with high expression of circ_0069767 had longer PFS and OS. Cell function experiments showed that overexpression of circ_0069767 in MM cells led to decreased proliferation, migration and invasion, but increased apoptosis; meanwhile, knockdown of circ_0069767 caused opposite biological behaviors. Circ_0069767 by sponging miR-636 in MM cells regulates the expression of K-RAS while the K-RAS gene remained unmutated. CONCLUSION: Circ_0069767 plays an antitumor role and its expression can be used as a reliable prognostic indicator for MM patients.	NA	Cancer Manag Res. 2020 Nov 6;12:11321-11331. doi: 10.2147/CMAR.S259393. eCollection 2020.
4185	Circular RNA	hsa_circ_0079480	miR-654-3p	HDGF	AML cells	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR	33290265	Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis.	Circular RNAs (circRNAs) are newly-discovered endogenous non-coding RNAs that have vital functions in regulating gene expression in tumorigenesis. Nonetheless, the function of circRNAs in acute myeloid leukemia (AML) are not yet clarified. In this analysis, hsa_circ_0079480, a novel circRNA, has been identified as being highly expressed in AML. Loss-of-function assays showed that reduction of hsa_circ_0079480 decreased the growth and stimulated apoptosis of AML cells in vitro. Furthermore, miR-654-3p was sponged by hsa_circ_0079480, and hepatoma-derived growth factor (HDGF) was targeted by miR-654-3p with respect to the fundamental mechanism. Moreover, the influence on growth and apoptosis of AML cells stimulated by hsa_circ_0079480 inhibition can be rescued by miR-654-3p inhibitor or HDGF overexpression. In summary, hsa_circ_0079480 is highly expressed in AML and drives by tumor progression via regulation of hsa_circ_0079480/miR-654-3p/HDGF axis, indicating that hsa_circ_0079480 may function as a new treatment target for AML therapy.	NA	Aging (Albany NY). 2020 Dec 3;13(1):1120-1131. doi: 10.18632/aging.202240. Epub 2020 Dec 3.
4186	Circular RNA	hsa_circ_104566	miR-338-3p	FOXP1	Hepatocellular Carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33028110	circRNA hsa_circ_104566 Sponged miR-338-3p to Promote Hepatocellular Carcinoma Progression.	Circular RNAs (circRNAs) could sponge micro-RNAs (miRNAs) to regulate tumor progression of hepatocellular carcinoma (HCC). Hsa_circ_104566 contributes to papillary thyroid carcinoma progression. However, the tumorigenic mechanism of hsa_circ_104566 on HCC remains enigmatic. The role of hsa_circ_104566 on HCC was therefore evaluated in this study. First, the high expression of hsa_circ_104566 was found in HCC tissues, which was significantly associated with poor prognosis in HCC patients. Second, Hsa_circ_104566 promoted HCC progression by decreasing apoptosis and E-cadherin, while increasing cell viability, proliferation, migration, invasion, and N-cadherin. On the other hand, HCC progression was suppressed by knockdown of hsa_circ_104566. Hsa_circ_104566 could target miR-338-3p, and its expression was negatively correlated with miR-338-3p in HCC patients. Moreover, miR-338-3p suppressed protein expression of Forkhead box protein 1 (FOXP1) and had a negative correlation with FOXP1 in HCC patients. Functional assay further indicated that the promotion of HCC progression by hsa_circ_104566 was reversed by miR-338-3p, and miR-338-3p inhibitor could counteract the effect of hsa_circ_104566 knockdown on the suppression of HCC progression. In vivo assay indicated that hsa_circ_104566 knockdown suppressed HCC tumor growth and metastasis. In conclusion, hsa_circ_104566 sponged miR-338-3p to promote HCC progression, providing a potential therapeutic target for cancer intervention.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720963948. doi: 10.1177/0963689720963948.
4187	LncRNA	ILF3-AS1	miR-320a	NA	nasopharyngeal carcinoma tissues and adjacent normal nasopharyngeal tissues	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;	32962500	Up-regulated long non-coding RNA ILF3-AS1 indicates poor prognosis of nasopharyngeal carcinoma and promoted cell metastasis.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been confirmed to participate in the regulation of nasopharyngeal carcinoma. Here, we endeavored to explore the character of lncRNA ILF3-AS1 in the nasopharyngeal carcinoma and its function. METHODS: A total of 68 nasopharyngeal carcinoma tissues and adjacent normal nasopharyngeal tissues were collected. Expressions of lncRNA ILF3-AS1 in these tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between the expression level of lncRNA ILF3-AS1 and clinical pathological characteristics was analyzed. Inhibition of lncRNA ILF3-AS1 was done using small interference RNA. RESULTS: lncRNA ILF3-AS1 expression was significantly up-regulated in the 68 nasopharyngeal carcinoma tissue samples compared to their adjacent normal tissue samples. Increased lncRNA ILF3-AS1 level was related to the advanced tumor node metastasis stage and the metastasis of nasopharyngeal carcinoma. Also, increased lncRNA ILF3-AS1 indicated poor prognosis of nasopharyngeal carcinoma patients. Inhibition of lncRNA ILF3-AS1 reduced proliferation, invasion and migration of nasopharyngeal carcinoma cells. MicroRNA-320a (miR-320a) was determined as a direct target for lncRNA ILF3-AS1 in nasopharyngeal carcinoma. Furthermore, lncRNA ILF3-AS1 could sponge miR-320a to promote BMI1 expression. The expression of BMI1 was significantly inhibited by the down-regulation of lncRNA ILF3-AS1. CONCLUSIONS: For the first time, we demonstrated that lncRNA ILF3-AS1 was markedly over-expressed in nasopharyngeal carcinoma tissues and cells. Elevated lncRNA ILF3-AS1 expression was correlated with severe cancer stage and poor prognosis. lncRNA ILF3-AS1 could promote proliferation, invasion, and migration of cells, which might indicate a novel target site for the future diagnosis and therapy of nasopharyngeal carcinoma.	NA	Int J Biol Markers. 2020 Dec;35(4):61-70. doi: 10.1177/1724600820955199. Epub 2020 Sep 22.
4188	LncRNA	IMFlnc1	miR-199a-5p	CAV-1	Muscle cell	Intramuscular-Fat (Imf) Content	Homo sapiens (human)	qRT-PCR	33148167	LncRNA IMFlnc1 promotes porcine intramuscular adipocyte adipogenesis by sponging miR-199a-5p to up-regulate CAV-1.	BACKGROUND: Local Chinese local pig breeds have thinner muscle fiber and higher intramuscular-fat (IMF) content. But its regulation mechanism has not been discussed in-depth. Studies indicated that long non coding RNAs (lncRNAs) play important role in muscle and fat development. RESULTS: The lncRNAs expressional differences in the longissimus dorsi (LD) muscle were identified between Huainan pigs (local Chinese pigs, fat-type, HN) and Large White pigs (lean-type, LW) at 38, 58, and 78 days post conception (dpc). In total, 2131 novel lncRNAs were identified in 18 samples, and 291, 305, and 683 differentially expressed lncRNAs (DELs) were found between these two breeds at three stages, respectively. The mRNAs that co-expressed with these DELs were used for GO and KEGG analysis, and the results showed that muscle development and energy metabolism were more active at 58 dpc in HN, but at 78 dpc in LW pigs. Muscle cell differentiation and myofibril assembly might associated with earlier myogenesis and primary-muscle-fiber assembly in HN, and cell proliferation, insulin, and the MAPK pathway might be contribute to longer proliferation and elevated energy metabolism in LW pigs at 78 dpc. The PI3K/Akt and cAMP pathways were associated with higher IMF deposition in HN. Intramuscular fat deposition-associated long noncoding RNA 1 (IMFlnc1) was selected for functional verification, and results indicated that it regulated the expressional level of caveolin-1 (CAV-1) by acting as competing endogenous RNA (ceRNA) to sponge miR-199a-5p. CONCLUSIONS: Our data contributed to understanding the role of lncRNAs in porcine-muscle development and IMF deposition, and provided valuable information for improving pig-meat quality.	NA	BMC Mol Cell Biol. 2020 Nov 4;21(1):77. doi: 10.1186/s12860-020-00324-8.
4189	LncRNA	INHBA-AS1	miR-422a	AKT1	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33090398	LncRNA INHBA-AS1 promotes colorectal cancer cell proliferation by sponging miR-422a to increase AKT1 axis.	OBJECTIVE: In recent years, long non-coding RNAs (lncRNAs) have emerged for regulating the development, as well as progression in colorectal cancer (CRC), which assists in finding new targets for CRC treatment. A previous study indicated that INHBA-AS1 promotes oral squamous cell progression by sponging miR-143-3p. However, the exact function possessed by lncRNA INHBA-AS1 in CRC development remains unclear. PATIENTS AND METHODS: The expression level of INHBA-AS1 in CRC tissues and cell lines was determined by qRT-PCR. The functional role of INHBA-AS1 in CRC was investigated by a series of in vitro assays. RNA immunoprecipitation (RIP), bioinformatics analysis was utilized to explore the potential mechanisms of INHBA-AS1. RESULTS: The present study identified INHBA-AS1 as a kind of lncRNA with high expression in CRC tissues and cells. Functionally, NHBA-AS1 downregulation in CRC cells suppressed CRC cell proliferation as well as colony formability. Mechanistically, INHBA-AS1/miR-422a/AKT1 established the ceRNA network to regulate MMP-2, -7, -9 expressions that participated the modulation of CRC progression. CONCLUSIONS: In summary, LncRNA INHBA-AS1 contributes to CRC progression through AKT1 pathway, and provides a new mechanism to regulate CRC development, as well as a potential target for treating CRC.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(19):9940-9948. doi: 10.26355/eurrev_202010_23206.
4190	LncRNA	INHBA-AS1	miR-143-3p	NA	oral squamous cell carcinoma cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	33015761	LncRNA INHBA-AS1 promotes cell growth, migration, and invasion of oral squamous cell carcinoma by sponging miR-143-3p.	Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "LncRNA INHBA-AS1 promotes cell growth, migration, and invasion of oral squamous cell carcinoma by sponging miR-143-3p, by W.-Q. Ma, J. Chen, W. Fang, X.-Q. Yang, A. Zhu, D. Zhang, H.-L. Zhong, B. Yang, Z. Luo, published in Eur Rev Med Pharmacol Sci 2020; 24 (4): 1821-1828-DOI: 10.26355/eurrev_202002_20360-PMID: 32141551" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20360.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9240. doi: 10.26355/eurrev_202009_23000.
4191	LncRNA	IUR	miR-2467	P53	LSCC cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	Cell proliferation assay;qPCR;RT-qPCR;	33235495	LncRNA-IUR Sponges miR-24 to Upregulate P53 in Laryngeal Squamous Cell Carcinoma.	OBJECTIVE: The functions of lncRNA-IUR in laryngeal squamous cell carcinoma (LSCC) were investigated in this study. METHODS: RT-qPCR and paired t-test were used to measure and compare expression levels of IUR, miR-24 and p53 in LSCC and non-tumor tissues. Human LSCC cell line UM-SCC-17A was used and transfected by pcDNA3.1 vector to overexpress IUR and miR-24. The transwell assay and wound healing assay illustrated the effect of overexpression of IUR or miR-24 in the cell invasion and migration of LSCC. Subcutaneous tumor model in nude mice was carried out to demonstrate the mechanism between IUR and miR-24 in regulating tumor growth. RESULTS: We found that IUR was downregulated in LSCC. Low expression levels of IUR were correlated with the poor survival of LSCC patients. Overexpression experiments showed that overexpression of IUR led to increased, while overexpression of miR-24 led to decreased expression levels of p53 in LSCC cells. And bioinformatics analysis showed that IUR may sponge miR-24. Cell proliferation assay showed that overexpression of IUR and p53 led to decreased proliferation rate of LSCC cells, while overexpression of miR-24 led to increased proliferation rate of LSCC cells. We also illustrated that overexpression of IUR promoted cell migration and invasion while miR-24 had opposite effects. In addition, subcutaneous tumor model in nude mice showed that overexpression of miR-24 attenuated the effects of overexpression of IUR on the expression of p53 and cancer cell proliferation. CONCLUSION: IUR sponges miR-24 to upregulate p53 in LSCC, thereby inhibiting cancer cell proliferation.	NA	Cancer Manag Res. 2020 Nov 16;12:11639-11647. doi: 10.2147/CMAR.S236188. eCollection 2020.
4192	LncRNA	JHDM1D-AS1	miR-450a-2-3p	PRAF2	GC tissues and cell lines	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;Western blot;Luciferase reporter assay;	33245963	JHDM1D-AS1 aggravates the development of gastric cancer through miR-450a-2-3p-PRAF2 axis.	AIMS: To investigate the molecular function and mechanisms of JHDM1D antisense 1 (JHDM1D-AS1) during gastric cancer (GC) progression. MATERIALS AND METHODS: The qPCR assay was used to detect the JHDM1D-AS1 and miR-450a-2-3p expression levels in GC tissues and cell lines. Bioinformatics analysis was used for exploring the lncRNA-microRNA-mRNA interaction network. We performed dual-luciferase reporter assay and qPCR assay in order to validate the direct interactions. We explored the JHDM1D-AS1 and miR-450a-2-3p on GC progression by using JHDM1D-AS1 siRNA and miR-450a-2-3p inhibitor; in vitro CCK-8 assay, colony formation assay, and invasion assay were conducted. Further, in vivo animal experiments were performed, and the expression levels of miR-450a-2-3p and PRAF2 in the tumor tissues were detected using qPCR and western blot analysis. KEY FINDINGS: The expression levels of JHDM1D-AS1 and miR-450a-2-3p in GC tissues and cell lines were higher and lower as compared to those in the corresponding normal controls, respectively. Moreover, high levels of JHDM1D-AS1 were closely related with metastasis and the GC TNM stage. Functionally, JHDM1D-AS1 depletion caused an obvious reduction in cell proliferation and invasion both in vitro and in vivo, while the addition of miR-450a-2-3p inhibitor could nullify these effects. Mechanically, JHDM1D-AS1 promoted GC progression via the sponging of miR-450a-2-3p in order to increase PRAF2 expression. SIGNIFICANCE: The present results showed that the increased expression of JHDM1D-AS1 was closely associated with tumor progression of GC. JHDM1D-AS1/miR-450a-2-3p/PRAF2 axis may be a promising target for GC treatment.	NA	Life Sci. 2021 Jan 15;265:118805. doi: 10.1016/j.lfs.2020.118805. Epub 2020 Nov 24.
4193	LncRNA	KCNMB2-AS1	miR-374a-3p	ROCK1	NSCLC tissues and cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33335424	Long Noncoding RNA KCNMB2-AS1 Increases ROCK1 Expression by Sponging microRNA-374a-3p to Facilitate the Progression of Non-Small-Cell Lung Cancer.	PURPOSE: The expression and roles of most long noncoding RNAs (lncRNAs) in non-small-cell lung cancer (NSCLC) remain poorly understood. Thus, this study investigated KCNMB2 antisense RNA 1 (KCNMB2-AS1) expression in NSCLC and determined the roles and mechanisms of KCNMB2-AS1 in regulating NSCLC progression. METHODS: KCNMB2-AS1 expression in NSCLC tissues and cells was detected using reverse transcription-quantitative polymerase chain reaction. Cell proliferation, apoptosis, migration, and invasion were evaluated using Cell Counting Kit-8, flow cytometry, Transwell migration, and Transwell invasion assays, respectively. In vivo tumor xenograft models were constructed to assess tumorigenicity. Bioinformatics predictions were performed to identify microRNAs targeting KCNMB2-AS1. Interactions between KCNMB2-AS1 and miR-374a-3p were analyzed using RNA immunoprecipitation, luciferase reporter, and rescue experiments. RESULTS: KCNMB2-AS1 levels were increased in NSCLC tissues and cells. KCNMB2-AS1 silencing hindered NSCLC cell proliferation, migration, and invasion and promoted apoptosis in vitro. Additionally, KCNMB2-AS1 knockdown decreased tumor growth in vivo. Mechanistically, KCNMB2-AS1 functioned as an endogenous miR-374a-3p sponge and increased ρ-associated coiled-coil-containing protein kinase 1 (ROCK1) expression. Furthermore, increased miR-374a-3p/ROCK1 output attenuated KCNMB2-AS1 silencing-induced inhibition of NSCLC progression. CONCLUSION: The KCNMB2-AS1/miR-374a-3p/ROCK1 pathway drives NSCLC progression, suggesting that this pathway can be targeted to reduce NSCLC progression.	NA	Cancer Manag Res. 2020 Dec 11;12:12679-12695. doi: 10.2147/CMAR.S270646. eCollection 2020.
4194	LncRNA	KCNMB2-AS1	miR-130b-5p	IGF2BP3	Cervical Cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33028109	Long Noncoding RNA KCNMB2-AS1 Stabilized by N(6)-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA.	Long noncoding RNA (lncRNA) is emerging as an essential regulator in the development and progression of cancer, including cervical cancer (CC). In this study, we found a CC-related lncRNA, KCNMB2-AS1, which was significantly overexpressed in CC and linked to poor outcomes. Depletion of KCNMB2-AS1 remarkably inhibited CC cell proliferation and induced apoptosis. In vivo xenograft models revealed that knockdown of KCNMB2-AS1 evidently delayed tumor growth. Mechanistically, KCNMB2-AS1 was predominantly located in the cytoplasm and served as a competing endogenous RNA to abundantly sponge miR-130b-5p and miR-4294, resulting in the upregulation of IGF2BP3, a well-documented oncogene in CC. Moreover, IGF2BP3 was able to bind KCNMB2-AS1 by three N(6)-methyladenosine (m(6)A) modification sites on KCNMB2-AS1, in which IGF2BP3 acted as an m(6)A "reader" and stabilized KCNMB2-AS1. Thus, KCNMB2-AS1 and IGF2BP3 formed a positive regulatory circuit that enlarged the tumorigenic effect of KCNMB2-AS1 in CC. Together, our data clearly suggest that KCNMB2-AS1 is a novel oncogenic m(6)A-modified lncRNA in CC, targeting KCNMB2-AS1 and its related molecules implicate the therapeutic possibility for CC patients.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720964382. doi: 10.1177/0963689720964382.
4195	LncRNA	KCNMB2-AS1	miR-4294	IGF2BP3	Cervical Cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33028109	Long Noncoding RNA KCNMB2-AS1 Stabilized by N(6)-Methyladenosine Modification Promotes Cervical Cancer Growth Through Acting as a Competing Endogenous RNA.	Long noncoding RNA (lncRNA) is emerging as an essential regulator in the development and progression of cancer, including cervical cancer (CC). In this study, we found a CC-related lncRNA, KCNMB2-AS1, which was significantly overexpressed in CC and linked to poor outcomes. Depletion of KCNMB2-AS1 remarkably inhibited CC cell proliferation and induced apoptosis. In vivo xenograft models revealed that knockdown of KCNMB2-AS1 evidently delayed tumor growth. Mechanistically, KCNMB2-AS1 was predominantly located in the cytoplasm and served as a competing endogenous RNA to abundantly sponge miR-130b-5p and miR-4294, resulting in the upregulation of IGF2BP3, a well-documented oncogene in CC. Moreover, IGF2BP3 was able to bind KCNMB2-AS1 by three N(6)-methyladenosine (m(6)A) modification sites on KCNMB2-AS1, in which IGF2BP3 acted as an m(6)A "reader" and stabilized KCNMB2-AS1. Thus, KCNMB2-AS1 and IGF2BP3 formed a positive regulatory circuit that enlarged the tumorigenic effect of KCNMB2-AS1 in CC. Together, our data clearly suggest that KCNMB2-AS1 is a novel oncogenic m(6)A-modified lncRNA in CC, targeting KCNMB2-AS1 and its related molecules implicate the therapeutic possibility for CC patients.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720964382. doi: 10.1177/0963689720964382.
4196	LncRNA	KCNQ1OT1	miR-2054	AKT3	transverse aortic constriction (TAC) mice	Cardiac Diseases	Homo sapiens (human)	qRT-PCR;	33145050	Knockdown of KCNQ1OT1 attenuates cardiac hypertrophy through modulation of the miR-2054/AKT3 axis.	BACKGROUND: Persistent cardiac hypertrophy threatens health worldwide. Long non-coding RNAs (lncRNAs) attracted lots of attention in cardiac diseases such as cardiac hypertrophy. In this study, we aimed to study the function of KCNQ1OT1 in cardiac hypertrophy. METHODS: We first used qRT-PCR to detect the expression of KCNQ1OT1 in Ang-II-induced cardiomyocytes and mouse cardiac hypertrophy models. The function of KCNQ1OT1 was investigated by a loss-of-function test. Analysis of the luciferase reporter gene and RNA pulldown confirmed the interaction between KCNQ1OT1 and miR-2054. The target gene of miR-2054 was predicted by bioinformatics analysis and confirmed by luciferase reporter gene detection. Rescue experiments were performed to evaluate the role of miR-2054/AKT3 in the function of KCNQ1OT1. RESULTS: Our results suggested that KCNQ1OT1 was up-regulated in Ang-II-induced cardiomyocytes and transverse aortic constriction (TAC) mice. Knocking down of KCNQ1OT1 can reduce cell size and downregulate the expression of ANF, BNP and α-MHC in response to Ang-II. KCNQ1OT1 has been shown to compete competitively with miR-2054 and has a negative correlation with its expression. The combination of miR-2054 can reverse the effect of the KCNQ1OT1 combination in Ang-II-induced cardiomyocytes. In addition, AKT3 is a target of miR-2054 and mediates its effect on Ang-II-induced cardiomyocytes. CONCLUSIONS: Knockdown of KCNQ1OT1 could attenuate cardiac hypertrophy through modulation of the miR-2054/AKT3 axis.	NA	J Thorac Dis. 2020 Sep;12(9):4771-4780. doi: 10.21037/jtd-20-203.
4197	LncRNA	KCNQ1OT1	miR-2054	AKT3	transverse aortic constriction (TAC) mice	Cardiac Diseases	Mus musculus (mouse)	qRT-PCR;	33145050	Knockdown of KCNQ1OT1 attenuates cardiac hypertrophy through modulation of the miR-2054/AKT3 axis.	BACKGROUND: Persistent cardiac hypertrophy threatens health worldwide. Long non-coding RNAs (lncRNAs) attracted lots of attention in cardiac diseases such as cardiac hypertrophy. In this study, we aimed to study the function of KCNQ1OT1 in cardiac hypertrophy. METHODS: We first used qRT-PCR to detect the expression of KCNQ1OT1 in Ang-II-induced cardiomyocytes and mouse cardiac hypertrophy models. The function of KCNQ1OT1 was investigated by a loss-of-function test. Analysis of the luciferase reporter gene and RNA pulldown confirmed the interaction between KCNQ1OT1 and miR-2054. The target gene of miR-2054 was predicted by bioinformatics analysis and confirmed by luciferase reporter gene detection. Rescue experiments were performed to evaluate the role of miR-2054/AKT3 in the function of KCNQ1OT1. RESULTS: Our results suggested that KCNQ1OT1 was up-regulated in Ang-II-induced cardiomyocytes and transverse aortic constriction (TAC) mice. Knocking down of KCNQ1OT1 can reduce cell size and downregulate the expression of ANF, BNP and α-MHC in response to Ang-II. KCNQ1OT1 has been shown to compete competitively with miR-2054 and has a negative correlation with its expression. The combination of miR-2054 can reverse the effect of the KCNQ1OT1 combination in Ang-II-induced cardiomyocytes. In addition, AKT3 is a target of miR-2054 and mediates its effect on Ang-II-induced cardiomyocytes. CONCLUSIONS: Knockdown of KCNQ1OT1 could attenuate cardiac hypertrophy through modulation of the miR-2054/AKT3 axis.	NA	J Thorac Dis. 2020 Sep;12(9):4771-4780. doi: 10.21037/jtd-20-203.
4198	LncRNA	KCNQ1OT1	miR-4319	DRAM2	GC cells	Gastric Cancer	Homo sapiens (human)	Flow cytometry assay;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33100093	KCNQ1OT1 accelerates gastric cancer progression via miR-4319/DRAM2 axis.	INTRODUCTION: This work was to explore the connection of KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) and microRNA-4319 (miR-4319), and to investigate the associated underlying mechanisms in gastric cancer (GC) progression. METHODS: Quantitative real-time PCR was performed to measure KCNQ1OT1, miR-4319 and DNA-damage regulated autophagy modulator 2 (DRAM2) expression levels in GC cells. Moreover, expression level of KCNQ1OT1 and DRAM2 in GC tissues was analyzed at ENCORI website (http://starbase.sysu.edu.cn/index.php). Cell proliferation, colony formation assay and flow cytometry assays were performed to analyze effects of KCNQ1OT1, miR-4319 and DRAM2 on cell growth and death. Dual-luciferase activity reporter assay and RNA immunoprecipitation assay was conducted to verify the interactions of KCNQ1OT1 or DRAM2 and miR-4319. RESULTS AND CONCLUSION: We found KCNQ1OT1 level was increased in tumor tissues and cells. Force the expression of KCNQ1OT1 promotes, while knockdown KCNQ1OT1 inhibits GC cell growth. Further studies indicated miR-4319 functioned as a bridge between KCNQ1OT1 and DRAM2. Finally, we showed KCNQ1OT1/miR-4319/DRAM2 axis regulates GC cell growth in vitro and in vivo. lncRNA KCNQ1OT1 promotes GC progression by sponging miR-4319 to upregulate DRAM2, indicating KCNQ1OT1 might be a promising target for GC treatment.	NA	Int J Immunopathol Pharmacol. 2020 Jan-Dec;34:2058738420954598. doi: 10.1177/2058738420954598.
4199	LncRNA	KCNQ1OT1	miR-146b-5p	STC1	A172 and U251 cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	32996777	Sevoflurane Suppresses Glioma Cell Proliferation, Migration, and Invasion Both In Vitro and In Vivo Partially Via Regulating KCNQ1OT1/miR-146b-5p/STC1 Axis.	Background: Sevoflurane (Sev), a volatile anesthetic agent, is widely used in neurosurgery for anesthesia maintenance, accompanied with antitumor activity postanesthesia in multiple human cancers, including glioma. However, the molecular mechanism hidden in Sev in glioma is largely unclear, including associated informative noncoding RNAs, such as long noncoding RNAs (lncRNA) and microRNAs (miRNAs). Methods: Expression of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), miRNA (miR)-146b-5p, and stanniocalcin-1 (STC1) was measured by real-time quantitative polymerase chain reaction and western blotting. Cell proliferation, apoptosis, migration, and invasion in vitro were examined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay, fluorescence-activated cell sorting method, and transwell assays, respectively. Tumor growth in vivo was determined by xenograft models. The direct interaction between genes was confirmed by dual-luciferase reporter assay. Results: Sev enhanced apoptotic rate, but inhibited cell viability, migration, and invasion abilities of human glioma A172 and U251 cells in vitro, as well as tumor growth inhibition in vivo. The tumor-suppressive role of Sev in glioma was accompanied with downregulated KCNQ1OT1 and STC1, and upregulated miR-146b-5p. Overexpression of KCNQ1OT1 through transfection reversed, while KCNQ1OT1 silencing aggravated the antitumor role of Sev in A172 and U251 cells. Moreover, KCNQ1OT1-mediated tumor-promoting activity in A172 and U251 cells under Sev treatment was abrogated by miR-146b-5p restoration or STC1 deletion. Essentially, KCNQ1OT1 could positively regulate STC1 by acting as miR-146b-5p decoy. Conclusion: KCNQ1OT1 knockdown mediated the role of Sev in glioma cell proliferation, apoptosis, migration, and invasion both in vitro and in vivo through miR-146b-5p/STC1 pathway.	NA	Cancer Biother Radiopharm. 2020 Sep 30. doi: 10.1089/cbr.2020.3762.
4200	LncRNA	KCNQ1OT1	miR-206	BDNF	PC-12 cells	Neural Injury	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33204065	LncRNA KCNQ1OT1 Sponges miR-206 to Ameliorate Neural Injury Induced by Anesthesia via Up-Regulating BDNF.	OBJECTIVE: Widely used in anesthesia, ketamine is reported to induce neurotoxicity in patients. This study aimed to investigate the molecular regulatory mechanism of long non-coding RNA (lncRNA) KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in ameliorating ketamine-induced neural injury. MATERIALS AND METHODS: Sprague-Dawley rats were intraperitoneally injected with ketamine to induce neuronal injury. PC-12 cells treated with ketamine were used as the cell model. Ketamine-induced aberrant expression of KCNQ1OT1, miR-206 and brain-derived neurotrophic factor (BDNF) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of KCNQ1OT1 and miR-206 on ketamine-induced neural injury in PC-12 cells were then examined by MTT and LDH assay. The regulatory relationships between KCNQ1OT1 and miR-206, and miR-206 and BDNF were detected by dual-luciferase reporter assay. RESULTS: Ketamine induced the apoptosis of neurons of the hippocampus in rats, and the apoptosis of PC-12 cells, accompanied by down-regulation of KCNQ1OT1 and BDNF expressions, and up-regulation of miR-206 expression. Overexpression of KCNQ1OT1 enhanced the resistance to apoptosis of PC-12 cells and significantly ameliorated ketamine-induced nerve injury, while transfection of miR-206 had opposite effects. Mechanistically, KCNQ1OT1 could target miR-206 and reduce its expression level, in turn indirectly increase the expression level of BDNF, and play a protective role in neural injury. CONCLUSION: KCNQ1OT1/miR-206/BDNF axis is demonstrated to be an important regulatory mechanism in regulating ketamine-induced neural injury. Our study helps to clarify the mechanism by which ketamine exerts its toxicological effects and provides clues for the neuroprotection during anesthesia.	NA	Drug Des Devel Ther. 2020 Nov 9;14:4789-4800. doi: 10.2147/DDDT.S256319. eCollection 2020.
4201	LncRNA	KCNQ1OT1	miR-146a-5p	ACER3	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32936716	LncRNA KCNQ1OT1 inhibits the radiosensitivity and promotes the tumorigenesis of hepatocellular carcinoma via the miR-146a-5p/ACER3 axis.	Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death, and radiotherapy is currently one of the main treatments. Long non-coding RNAs (lncRNAs) are associated with the radiosensitivity and tumorigenesis of HCC. However, the role and molecular mechanism of potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) in HCC are still unclear. The relative expression of KCNQ1OT1, microRNA-146a-5p (miR-146a-5p) and alkaline ceramidase 3 (ACER3) was quantified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was measured by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. Clonogenic assay was used to assess the radiosensitivity of cells. Cell apoptosis and metastasis were evaluated by flow cytometry and transwell assays, respectively. The protein levels of apoptosis markers, metastasis markers and ACER3 were detected by western blot (WB) analysis. The relationship between miR-146a-5p and KCNQ1OT1 or ACER3 was determined by dual-luciferase reporter assay. Additionally, animal experiments were carried out to explore the effect of KCNQ1OT1 silencing on HCC tumor growth in vivo. KCNQ1OT1 was highly expressed in HCC, and its knockdown hindered the proliferation and metastasis, while increased the radiosensitivity and apoptosis of HCC cells. MiR-146a-5p could interact with KCNQ1OT1, and its inhibition reversed the effects of silenced-KCNQ1OT1 on the radiosensitivity and tumorigenesis of HCC cells. Besides, ACER3 was a target of miR-146a-5p, and its overexpression inversed the effects of miR-146a-5p mimic on the radiosensitivity and tumorigenesis of HCC cells. The expression of ACER3 was regulated by KCNQ1OT1 and miR-146a-5p. Furthermore, KCNQ1OT1 also could reduce the growth of HCC by regulating the miR-146a-5p/ACER3 axis in vivo. Our study suggested that KCNQ1OT1 improved ACER3 expression to regulate the radiosensitivity and tumorigenesis of HCC through sponging miR-146a-5p, indicating that KCNQ1OT1 might be a new therapeutic target for HCC.	NA	Cell Cycle. 2020 Oct;19(19):2519-2529. doi: 10.1080/15384101.2020.1809259. Epub 2020 Sep 16.
4202	Pseudogene	KRT17P3	miR-497-5p	mTOR	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33179318	Pseudogene KRT17P3 drives cisplatin resistance of human NSCLC cells by modulating miR-497-5p/mTOR.	Chemoresistance is a major obstacle in non-small cell lung cancer (NSCLC) treatment. The pseudogene keratin 17 pseudogene 3 (KRT17P3) has been previously shown to be upregulated in lung cancer tissues of patients with cisplatin resistance. In the present study, RT-qPCR was performed to evaluate KRT17P3 levels in plasma samples collected from 30 cisplatin-resistant and 32 cisplatin-sensitive patients. We found that the plasma level of KRT17P3 is upregulated in cisplatin-resistant patients, and the increased expression of plasma KRT17P3 is associated with poor chemotherapy response. Functional studies demonstrated that KRT17P3 overexpression in cultured NSCLC cells increases cell viability and decreases apoptosis upon cisplatin treatment in vitro and in vivo, while KRT17P3 knockdown has the opposite effect. Mechanistically, bioinformatics analysis, RNA immunoprecipitation, and dual luciferase reporter assay indicated that KRT17P3 acts as a molecular sponge for miR-497-5p and relieves the binding of miR-497-5p to its target gene mTOR. Rescue experiments validated the functional interaction between KRT17P3, miR-497-5p, and mTOR. Taken together, our findings indicate that KRT17P3/miR-497-5p/mTOR regulates the chemosensitivity of NSCLC, suggesting a potential therapeutic target for cisplatin-resistant NSCLC patients. KRT17P3 may be a potential peripheral blood marker of NSCLC patients resistant to cisplatin.	NA	Cancer Sci. 2021 Jan;112(1):275-286. doi: 10.1111/cas.14733. Epub 2020 Nov 28.
4203	LncRNA	LBX2-AS1	miR-455-5p	E2F2	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33342041	LBX2-AS1 promotes ovarian cancer progression by facilitating E2F2 gene expression via miR-455-5p and miR-491-5p sponging.	LBX2-AS1 is a long non-coding RNA that facilitates the development of gastrointestinal cancers and lung cancer, but its participation in ovarian cancer development remained uninvestigated. Clinical data retrieved from TCGA ovarian cancer database and the clinography of 60 ovarian cancer patients who received anti-cancer treatment in our facility were analysed. The overall cell growth, colony formation, migration, invasion, apoptosis and tumour formation on nude mice of ovarian cancer cells were evaluated before and after lentiviral-based LBX2-AS1 knockdown. ENCORI platform was used to explore LBX2-AS1-interacting microRNAs and target genes of the candidate microRNAs. Luciferase reporter gene assay and RNA pulldown assay were used to verify the putative miRNA-RNA interactions. Ovarian cancer tissue specimens showed significant higher LBX2-AS1 expression levels that non-cancerous counterparts. High expression level of LBX2-AS1 was significantly associated with reduced overall survival of patients. LBX2-AS1 knockdown significantly down-regulated the cell growth, colony formation, migration, invasion and tumour formation capacity of ovarian cancer cells and increased their apoptosis in vitro. LBX2-AS1 interacts with and thus inhibits the function of miR-455-5p and miR-491-5p, both of which restrained the expression of E2F2 gene in ovarian cancer cells via mRNA targeting. Transfection of miRNA inhibitors of these two miRNAs or forced expression of E2F2 counteracted the effect of LBX2-AS1 knockdown on ovarian cancer cells. LBX2-AS1 was a novel cancer-promoting lncRNA in ovarian cancer. This lncRNA increased the cell growth, survival, migration, invasion and tumour formation of ovarian cancer cells by inhibiting miR-455-5p and miR-491-5p, thus liberating the expression of E2F2 cancer-promoting gene.	NA	J Cell Mol Med. 2021 Jan;25(2):1178-1189. doi: 10.1111/jcmm.16185. Epub 2020 Dec 20.
4204	LncRNA	LBX2-AS1	miR-491-5p	E2F2	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33342041	LBX2-AS1 promotes ovarian cancer progression by facilitating E2F2 gene expression via miR-455-5p and miR-491-5p sponging.	LBX2-AS1 is a long non-coding RNA that facilitates the development of gastrointestinal cancers and lung cancer, but its participation in ovarian cancer development remained uninvestigated. Clinical data retrieved from TCGA ovarian cancer database and the clinography of 60 ovarian cancer patients who received anti-cancer treatment in our facility were analysed. The overall cell growth, colony formation, migration, invasion, apoptosis and tumour formation on nude mice of ovarian cancer cells were evaluated before and after lentiviral-based LBX2-AS1 knockdown. ENCORI platform was used to explore LBX2-AS1-interacting microRNAs and target genes of the candidate microRNAs. Luciferase reporter gene assay and RNA pulldown assay were used to verify the putative miRNA-RNA interactions. Ovarian cancer tissue specimens showed significant higher LBX2-AS1 expression levels that non-cancerous counterparts. High expression level of LBX2-AS1 was significantly associated with reduced overall survival of patients. LBX2-AS1 knockdown significantly down-regulated the cell growth, colony formation, migration, invasion and tumour formation capacity of ovarian cancer cells and increased their apoptosis in vitro. LBX2-AS1 interacts with and thus inhibits the function of miR-455-5p and miR-491-5p, both of which restrained the expression of E2F2 gene in ovarian cancer cells via mRNA targeting. Transfection of miRNA inhibitors of these two miRNAs or forced expression of E2F2 counteracted the effect of LBX2-AS1 knockdown on ovarian cancer cells. LBX2-AS1 was a novel cancer-promoting lncRNA in ovarian cancer. This lncRNA increased the cell growth, survival, migration, invasion and tumour formation of ovarian cancer cells by inhibiting miR-455-5p and miR-491-5p, thus liberating the expression of E2F2 cancer-promoting gene.	NA	J Cell Mol Med. 2021 Jan;25(2):1178-1189. doi: 10.1111/jcmm.16185. Epub 2020 Dec 20.
4205	LncRNA	LBX2-AS1	miR-4784	KDM5C	OC cells	Ovarian Cancer	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Western blot;	33099720	ELK1 activated-long noncoding RNA LBX2-AS1 aggravates the progression of ovarian cancer through targeting miR-4784/KDM5C axis.	As one of the most common cancers in female, ovarian cancer (OC) has become a serious public burden now. Mounting researches have indicated long noncoding RNAs (lncRNAs) can affect many biological processes including cancer development. LncRNA LBX2-AS1 was identified to be an oncogene in some cancers, but the role of LBX2-AS1 in OC remains to be elucidated. Bioinformatics analysis and experiments including ChIP, RT-qPCR, RIP, luciferase reporter, western blot and CCK-8 were performed to explore the role of LBX2-AS1 in OC. LBX2-AS1 expression was markedly increased in OC tissues and cell lines. Functionally, LBX2-AS1 silencing inhibited cell proliferation, migration and stemness but facilitated cell apoptosis in OC. Moreover, depletion of LBX2-AS1 suppressed tumor growth of OC in vivo. Mechanically, LBX2-AS1 was activated by transcriptional factor ELK1. ELK1 enhanced the expression of LBX2-AS1 in OC cells. In addition, miR-4784 was confirmed to be sponged by LBX2-AS1. There was a negative expression correlation between LBX2-AS1 and miR-4784 in OC tissues. Subsequently, KDM5C was identified to be a direct target of miR-4784 in OC cells. KDM5C was negatively regulated by miR-4784 and positively regulated by LBX2-AS1 in terms of expression level. Upregulation of KDM5C reversed the inhibitory effect of LBX2-AS1 depletion on the progression of OC. This study proved that ELK1 activated-LBX2-AS1 aggravated the progression of OC by targeting the miR-4784/KDM5C axis, suggesting that LBX2-AS2 may be a promising diagnostic biomarker of OC.	NA	J Mol Histol. 2021 Feb;52(1):31-44. doi: 10.1007/s10735-020-09921-5. Epub 2020 Oct 24.
4206	LncRNA	LBX2-AS1	miR-4766-5p	CXCL5	BGC-823 and SGC-7901 cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33061849	Long noncoding RNA LBX2-AS1-modulated miR-4766-5p regulates gastric cancer development through targeting CXCL5.	BACKGROUND: Long noncoding RNAs (LncRNAs) have been reported to critically regulate gastric cancer (GC). Recently, it was reported that LBX2 antisense RNA 1 (LBX2-AS1) is abnormally expressed in GC. However, the role of LBX2-AS1 in the malignancy of GC is worth further discussion. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the LBX2-AS1, miR-4766-5p and C-X-C motif chemokine (CXCL5) expression in GC tissues and cells. Dual-luciferase reporter assay was applied to examine the target relationship between LBX2-AS1 and miR-4766-5p or miR-4766-5p and CXCL5. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect cell proliferation, migration and invasion rates. The protein expression of CXCL5 was confirmed using western blot. The RNA pull down experiment was used to verify the specificity of LBX2-AS1 and miR-4766-5p on BGC-823 and SGC-7901 cells. RESULTS: LBX2-AS1 was up-regulated in GC tissues and cells, and its knockdown suppressed proliferation, migration and invasion of GC cells. While, overexpression of LBX2-AS1 increased proliferation and increased CXCL5 mRNA level. CXCL5 improved cell proliferation, migration and invasion of GC cells. LBX2-AS1 could bind to miR-4766-5p to regulate CXCL5 expression. Overexpression of CXCL5 overturned those effects of miR-4766-5p in GC cells. RNA Pull down shown that BGC-823 and SGC-7901 cells, miR-4766-5p specifically binds to LBX2-AS1. CONCLUSIONS: In short, this study demonstrated that LBX2-AS1 promoted proliferation, migration and invasion through up-regulation CXCL5 mediated by miR-4766-5p in GC. The LBX2-AS1/miR-4766-5p/CXCL5 regulatory axis provides a theoretical basis for the research on lncRNA-directed therapeutics in GC.	NA	Cancer Cell Int. 2020 Oct 12;20:497. doi: 10.1186/s12935-020-01579-z. eCollection 2020.
4207	LncRNA	LEF1-AS1	miR-222-5p	RAMP3	microglia cells	Spinal Cord Injury	Homo sapiens (human)	ELISA;Western blot;Flow Cytometry assay;	33407665	Knockdown of long non-coding RNA LEF1-AS1 attenuates apoptosis and inflammatory injury of microglia cells following spinal cord injury.	BACKGROUND: Spinal cord injury (SCI) is associated with health burden both at personal and societal levels. Recent assessments on the role of lncRNAs in SCI regulation have matured. Therefore, to comprehensively explore the function of lncRNA LEF1-AS1 in SCI, there is an urgent need to understand its occurrence and development. METHODS: Using in vitro experiments, we used lipopolysaccharide (LPS) to treat and establish the SCI model primarily on microglial cells. Gain- and loss of function assays of LEF1-AS1 and miR-222-5p were conducted. Cell viability and apoptosis of microglial cells were assessed via CCK8 assay and flow cytometry, respectively. Adult Sprague-Dawley (SD) rats were randomly divided into four groups: Control, SCI, sh-NC, and sh-LEF-AS1 groups. ELISA test was used to determine the expression of TNF-α and IL-6, whereas the protein level of apoptotic-related markers (Bcl-2, Bax, and cleaved caspase-3) was assessed using Western blot technique. RESULTS: We revealed that LncRNA LEF1-AS1 was distinctly upregulated, whereas miR-222-5p was significantly downregulated in LPS-treated SCI and microglial cells. However, LEF1-AS1 knockdown enhanced cell viability, inhibited apoptosis, as well as inflammation of LPS-mediated microglial cells. On the contrary, miR-222-5p upregulation decreased cell viability, promoted apoptosis, and inflammation of microglial cells. Mechanistically, LEF1-AS1 served as a competitive endogenous RNA (ceRNA) by sponging miR-222-5p, targeting RAMP3. RAMP3 overexpression attenuated LEF1-AS1-mediated protective effects on LPS-mediated microglial cells from apoptosis and inflammation. CONCLUSION: In summary, these findings ascertain that knockdown of LEF1-AS1 impedes SCI progression via the miR-222-5p/RAMP3 axis.	NA	J Orthop Surg Res. 2021 Jan 6;16(1):6. doi: 10.1186/s13018-020-02041-6.
4208	LncRNA	LEF1-AS1	miR-328	CD44	AIPC cells	Prostate Cancer	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Chromatin immunoprecipitation;	33292271	LncRNA LEF1-AS1 promotes metastasis of prostatic carcinoma via the Wnt/β-catenin pathway.	BACKGROUND: Long noncoding RNAs (lncRNAs) are important functional regulators of many biological processes of cancers. However, the mechanisms by which lncRNAs modulate androgen-independent prostate cancer (AIPC) development remain largely unknown. METHODS: Next-generation sequencing technology and RT-qPCR were used to assess LEF1-AS1 expression level in AIPC tissues and adjacent normal tissues. Functional in vitro experiments, including colony formation, EDU and transwell assays were performed to assess the role of LEF1-AS1 in AIPC. Xenograft assays were conducted to assess the effect of LEF1-AS1 on cell proliferation in vivo. Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) assays were performed to elucidate the regulatory network of LEF1-AS1. RESULTS: The next-generation sequencing results showed that LEF1-AS1 is significantly overexpressed in AIPC. Furthermore, our RT-qPCR assay data showed that LEF1-AS1 is overexpressed in AIPC tissues. Functional experiments showed that LEF1-AS1 promotes the proliferation, migration, invasion and angiogenic ability of AIPC cells in vitro and tumour growth in vivo by recruiting the transcription factor C-myb to the promoter of FZD2, inducing its transcription. Furthermore, LEF1-AS1 was shown to function as a competing endogenous RNA (ceRNA) that sponges miR-328 to activate CD44. CONCLUSION: In summary, the results of our present study revealed that LEF1-AS1 acts as a tumour promoter in the progression of AIPC. Furthermore, the results revealed that LEF1-AS1 functions as a ceRNA and regulates Wnt/β-catenin pathway activity via FZD2 and CD44. Our results provide new insights into the mechanism that links the function of LEF1-AS1 with AIPC and suggests that LEF1-AS1 may serve as a novel potential target for the improvement of AIPC therapy.	NA	Cancer Cell Int. 2020 Nov 10;20(1):543. doi: 10.1186/s12935-020-01624-x.
4209	LncRNA	LHFPL3-AS1	miR-181a-5p	BCL2	melanoma stem cells	Melanoma	Homo sapiens (human)	qRT-PCR	33149126	LncRNA LHFPL3-AS1 contributes to tumorigenesis of melanoma stem cells via the miR-181a-5p/BCL2 pathway.	Long noncoding RNAs (lncRNAs) are recognized as a new area for cancer therapy. B-cell lymphoma-2 (Bcl-2)-mediated suppression of apoptosis is an important molecular hallmark of cancer. However, the influence of lncRNA on the regulation of oncogenic Bcl-2 in cancer stem cells has not been explored. In this study, our findings revealed that the lncRNA LHFPL3-AS1-long, generated from the polypyrimidine tract binding protein 1 (PTBP1)-mediated splicing of the LHFPL3-AS1 precursor, upregulated BCL2 protein to contribute to tumorigenesis of melanoma stem cells. The in vitro and in vivo results showed that LHFPL3-AS1-long directly interacted with miR-181a-5p to inhibit the mRNA degradation of Bcl-2 (the target of miR-181), thus suppressing apoptosis of melanoma stem cells. The splicing factor PTBP1 regulated the alternative splicing of LHFPL3-AS1 transcript by preferentially binding to the motifs located in exon3 of LHFPL3-AS1 precursor, leading to the biogenesis of LHFPL3-AS1-long in melanoma stem cells. In patients with melanoma, the expressions of PTBP1 and LHFPL3-AS1 were significantly upregulated compared with the healthy donors. Therefore, our study revealed a mechanistic crosstalk among an onco-splicing factor, lncRNA and tumorigenesis of melanoma stem cells, enabling PTBP1 and LHFPL3-AS1 to serve as the attractive therapeutic targets for melanoma.	NA	Cell Death Dis. 2020 Nov 4;11(11):950. doi: 10.1038/s41419-020-03141-1.
4210	LncRNA	LIFR-AS1	miR-29a-3p	COL1A2	gastric tumor tissues and cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33407453	LncRNA LIFR-AS1 promotes proliferation and invasion of gastric cancer cell via miR-29a-3p/COL1A2 axis.	BACKGROUND: LncRNA was known to be closely associated with the progression of human tumors. The role of lncRNA LIFR-AS1 in the pathogenesis and progression of gastric tumor is still unclear. The aim of this study was to investigate the function of LIFR-AS1 and the underlying mechanism in the pathogenesis and progression of gastric cancer. METHODS: QRT-PCR was used to evaluate the expression of LIFR-AS1, miR-29a-3p and COL1A2 in gastric tumor tissues and cells. Western blotting was used to evaluate the protein expression of COL1A2 in gastric tumor cells. CCK-8 assay, transwell assay and flow cytometry were used to evaluate the roles of LIFR-AS1, miR-29a-3p and COL1A2 in cell proliferation, invasion, migration and apoptosis. The relationship among LIFR-AS1, miR-29a-3p and COL1A2 was assessed by bioinformatics analyses and luciferase reporter assay. RESULTS: The expression levels of LIFR-AS1 were significantly increased in gastric tumor tissues and cells, while the expression levels of miR-29a-3p were decreased. The expression of miR-29a-3p was negatively correlated with the expression of LIFR-AS1 in gastric cancer tumor tissues. Knocking down of LIFR-AS1 inhibited proliferation, invasion and migration of gastric tumor cells, and induced apoptosis of gastric tumor cells. Bioinformatics analyses and integrated experiments revealed that LIFR-AS1 elevated the expression of COL1A2 through sponging miR-29a-3p, which further resulted in the progression of gastric tumor. CONCLUSION: LIFR-AS1 plays an important role as a competing endogenous RNA in gastric tumor pathogenesis and may be a potential target for the diagnosis and treatment of gastric tumor.	NA	Cancer Cell Int. 2021 Jan 6;21(1):7. doi: 10.1186/s12935-020-01644-7.
4211	LncRNA	LINC00173	miR-338-3p	Rab25	PCa cells	Prostate Cancer	Homo sapiens (human)	Flow cytometry assay;RT-PCR;RNA pull-down assay;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33015770	Long non-coding RNA LINC00173 serves as sponge for miR-338-3p to promote prostate cancer progression via regulating Rab25.	OBJECTIVE: Long non-coding RNA LINC00173 (LINC00173) has been shown to facilitate the progression of a number of malignancies. In this study, we aimed to investigate the function of LINC00173 on prostate cancer (PCa) and discover the potential regulatory mechanism. PATIENTS AND METHODS: RT-PCR was used to determine the levels of LINC00173, miR-338-3p and Rab25 in PCa patients and cell lines. The clinical significance of LINC00173 was statistically analyzed in 124 PCa patients. CCK-8, colony formation, transwell, scratch wound, Ethynyldeoxyuridine (EdU) assays and flow cytometry assays were used to detect the proliferation, apoptosis, invasion and migration of PCa cells. The mechanism of LINC00173 action was explored through bioinformatics, RNA pull-down assays and Luciferase reporter assays. RESULTS: We observed that the expression of LINC00173 and Rab25 was distinctly upregulated in both PCa specimens and cell lines, while miR-338-3p expression was significantly down-regulated. High LINC00173 expression was associated with Gleason score, preoperative PSA level and reduced patient survivals. Functional assays revealed that knockdown of LINC00173 suppressed the proliferation, migration and invasion of PCa cells, and promoted apoptosis. Mechanistically, LINC00173 acted as a competitive endogenous RNA in PCa and increased Rab25 expressions via sponging miR-338-3p. Moreover, LINC00173 promoted PCa progression by interacting with miR-338-3p and Rab25. CONCLUSIONS: Our findings, for the first time, identified a novel PCa-related lncRNA, LINC00173 which might serve as an oncogene in PCa. The discovery of the LINC00173/miR-338-3p/Rab25 pathways provided new thinking for the treatments of PCa.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9290-9302. doi: 10.26355/eurrev_202009_23011.
4212	LncRNA	LINC00174	miR-145-5p	SCD5	TET cells	Thymic Cancer	Homo sapiens (human)	microarray;	33161413	LINC00174 is a novel prognostic factor in thymic epithelial tumors involved in cell migration and lipid metabolism.	Long non-coding RNAs are emerging as new molecular players involved in many biological processes, such as proliferation, apoptosis, cell cycle, migration, and differentiation. Their aberrant expression has been reported in variety of diseases. The aim of this study is the identification and functional characterization of clinically relevant lncRNAs responsible for the inhibition of miR-145-5p, a key tumor suppressor in thymic epithelial tumors (TETs). Starting from gene expression analysis by microarray in a cohort of fresh frozen thymic tumors and normal tissues, we identified LINC00174 as upregulated in TET. Interestingly, LINC00174 expression is positively correlated with a 5-genes signature in TETs. Survival analyses, performed on the TCGA dataset, showed that LINC00174 and its associated 5-genes signature are prognostic in TETs. Specifically, we show that LINC00174 favors the expression of SYBU, FEM1B, and SCD5 genes by sponging miR-145-5p, a well-known tumor suppressor microRNA downregulated in a variety of tumors, included TETs. Functionally, LINC00174 impacts on cell migration and lipid metabolism. Specifically, SCD5, one of the LINC00174-associated genes, is implicated in the control of lipid metabolism and promotes thymic cancer cells migration. Our study highlights that LINC00174 and its associated gene signature are relevant prognostic indicators in TETs. Of note, we here show that a key controller of lipid metabolism, SCD5, augments the migration ability of TET cells, creating a link between lipids and motility, and highlighting these pathways as relevant targets for the development of novel therapeutic approaches for TET.	NA	Cell Death Dis. 2020 Nov 7;11(11):959. doi: 10.1038/s41419-020-03171-9.
4213	LncRNA	LINC00200	miR-143-3p	SERPINE1	Gastric Cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;Rescue assay;	33141390	Knockdown of Long Non-coding RNA LINC00200 Inhibits Gastric Cancer Progression by Regulating miR-143-3p/SERPINE1 Axis.	BACKGROUND: An increasing number of studies have found that long non-coding RNAs (lncRNAs) play an important role in carcinogenesis and tumor progression, whereas their molecular mechanisms of function remain largely unknown. AIMS: This study was aimed to explore the biological function and underlying mechanism of a new lncRNA LINC00200 in gastric cancer (GC). METHODS: qRT-PCR analysis was conducted to examine the LINC00200 expression level in both GC tissues and cell lines. Functional assays were carried out to detect the effect of LINC00200 on GC cell proliferation, invasion and migration. The interaction between LINC00200 and miR-143-3p was confirmed by luciferase reporter assays. Rescue assays were performed to confirm the influence of LINC00200-miR-143-3p-SERPINE1 axis on GC development. RESULTS: LINC00200 was found to be upregulated in GC tissues and cell lines. Moreover, knockdown of LINC00200 suppressed GC cell proliferation, invasion and migration in vitro and inhibited tumorigenesis in mouse xenografts. Finally, mechanism research indicated that LINC00200 functioned as a ceRNA to sponge for miR-143-3p, thus leading to the disinhibition of its target gene SERPINE1. CONCLUSIONS: LINC00200 is significantly overexpressed in GC and accelerates GC progression through regulating miR-143-3p/SERPINE1 axis. Our results may provide a potential diagnostic biomarker and therapeutic target for the management of GC patients.	NA	Dig Dis Sci. 2020 Nov 3. doi: 10.1007/s10620-020-06691-8.
4214	LncRNA	LINC00200	miR-143-3p	SERPINE1	Gastric Cancer cells	Gastric Cancer	Mus musculus (mouse)	qRT-PCR;Luciferase reporter assay;Rescue assay;	33141390	Knockdown of Long Non-coding RNA LINC00200 Inhibits Gastric Cancer Progression by Regulating miR-143-3p/SERPINE1 Axis.	BACKGROUND: An increasing number of studies have found that long non-coding RNAs (lncRNAs) play an important role in carcinogenesis and tumor progression, whereas their molecular mechanisms of function remain largely unknown. AIMS: This study was aimed to explore the biological function and underlying mechanism of a new lncRNA LINC00200 in gastric cancer (GC). METHODS: qRT-PCR analysis was conducted to examine the LINC00200 expression level in both GC tissues and cell lines. Functional assays were carried out to detect the effect of LINC00200 on GC cell proliferation, invasion and migration. The interaction between LINC00200 and miR-143-3p was confirmed by luciferase reporter assays. Rescue assays were performed to confirm the influence of LINC00200-miR-143-3p-SERPINE1 axis on GC development. RESULTS: LINC00200 was found to be upregulated in GC tissues and cell lines. Moreover, knockdown of LINC00200 suppressed GC cell proliferation, invasion and migration in vitro and inhibited tumorigenesis in mouse xenografts. Finally, mechanism research indicated that LINC00200 functioned as a ceRNA to sponge for miR-143-3p, thus leading to the disinhibition of its target gene SERPINE1. CONCLUSIONS: LINC00200 is significantly overexpressed in GC and accelerates GC progression through regulating miR-143-3p/SERPINE1 axis. Our results may provide a potential diagnostic biomarker and therapeutic target for the management of GC patients.	NA	Dig Dis Sci. 2020 Nov 3. doi: 10.1007/s10620-020-06691-8.
4215	LncRNA	Linc00210	miR-16-5p	PTK2	NSCLC cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	33015786	Long noncoding RNA Linc00210 promotes non-small cell lung cancer progression via sponging miR-16-5p/PTK2 axis.	OBJECTIVE: Long noncoding RNAs (lncRNAs) are important regulators involved in a variety of cancer development. However, the role of Linc00210 in non-small cell lung cancer (NSCLC) remains unknown. This study aims to investigate the clinical value of Linc00210 in NSCLC patients and the biological functions of Linc00210 in NSCLC. PATIENTS AND METHODS: Gene expression in NSCLC tissues and cell lines was detected using qRT-PCR or Western blot. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and colony formation assays were conducted to evaluate the effect of Linc00210 on NSCLC cell proliferation. Transwell assay and annexin V-Fluorescein 5-isothiocyanate (FITC)/Propidium Iodide (PI) were done to analyze the effect of Linc00210 on cancer cell invasion and apoptosis, respectively. Luciferase reporter assay and RIP assay were performed to determine the target of Linc00210 and miR-16-5p. Besides, these assays were used to determine reciprocally inhibition of each other-controlled NSCLC cell behaviors. In vivo tumorigenesis experiments were applied to exhibit subcutaneous tumor growth. RESULTS: Linc0021 was highly expressed in NSCLC tissues and cell lines. Knockdown of Linc00210 inhibited cancer cell proliferation and invasion, and increased cell apoptosis, and regulated the expression of Cyclin A1, proliferating cell nuclear antigen (PCNA), E-cadherin, N-cadherin, Bax, and Bcl-2 in NSCLC cells. Further data showed Linc00210 bound to and directly modulated the miR-16-5p levels. Impressively, overexpression of miR-16-5p suppressed NSCLC cell proliferation and invasion, but increased cell apoptosis, and these behaviors could be overturned by overexpression of Linc00210 in vitro and in vivo. Finally, Linc00210 and miR-16-5p cooperatively controlled expression of protein tyrosine kinase 2 (PTK2), a miR-16-5p target. CONCLUSIONS: Linc00210/miR-16-5p/PTK2 signaling suggests a promising novel strategy for anti-NSCLC therapy.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9438-9452. doi: 10.26355/eurrev_202009_23029.
4216	LncRNA	LINC00239	miR-484	KLF12	Colorectal Cancer cells	Colorectal Cancer	Homo sapiens (human)	Cell migration and invasion assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33262607	Long Non-Coding RNA LINC00239 Functions as a Competitive Endogenous RNA by Sponging microRNA-484 and Enhancing KLF12 Expression to Promote the Oncogenicity of Colorectal Cancer.	BACKGROUND: Long intergenic non-protein coding RNA 239 (LINC00239) is an oncogenic long non-coding RNA in acute myeloid leukemia. We aimed to determine LINC00239 expression in colorectal cancer (CRC) and examine the influences of LINC00239 on tumor behaviors of CRC cells. Furthermore, the mechanism underlying the actions of LINC00239 in CRC was unveiled in detail. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction was used to detect LINC00239 expression in CRC tissues and cell lines. CRC cell proliferation, apoptosis, migration, and invasion were investigated by cell counting kit-8 assays, flow cytometry, and cell migration and invasion assays, respectively. Tumor xenograft experiments were performed to evaluate the tumor growth of CRC cells in vivo. The interactions among LINC00239, microRNA-484 (miR-484), and kruppel-like factor 12 (KLF12) were analyzed by bioinformatics prediction, RNA immunoprecipitation and luciferase reporter assay. RESULTS: LINC00239 was upregulated in CRC tissues and cell lines. LINC00239 knockdown impaired CRC cell proliferation, migration, and invasion and promoted apoptosis in vitro. Additionally, LINC00239 deficiency inhibited CRC growth in vivo. Mechanistically, LINC00239 functioned as a competing endogenous RNA by directly sponging miR-484, thereby enhancing KLF12 expression. Rescue experiments further corroborated that miR-484 inhibition or KLF12 overexpression reversed the inhibitory actions of LINC00239 knockdown in CRC cells. CONCLUSION: The LINC00239/miR-484/KLF12 pathway executed critical roles in CRC oncogenicity and may provide potential targets for CRC treatments.	NA	Onco Targets Ther. 2020 Nov 23;13:12067-12081. doi: 10.2147/OTT.S278582. eCollection 2020.
4217	LncRNA	LINC00240	miR-4465	HGF	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;	33155201	LINC00240 sponges miR-4465 to promote proliferation, migration, and invasion of hepatocellular carcinoma cells via HGF/c-MET signaling pathway.	OBJECTIVE: LINC00240, as a novel long non-coding RNAs (lncRNAs), has never been studied in hepatocellular carcinoma (HCC). This research reported the expression and function of LINC00240 in HCC. PATIENTS AND METHODS: LINC00240 expression in 180 HCC patients was downloaded from the Cancer Genome Atlas (TCGA) database. HCC patients' survival was analyzed via Kaplan-Meier analysis. The expression of LINC00240, miR-4465 and HGF in Hep3B and Huh7 cells were regulated by transfection. Cell viability was determined by MTT assay. Transwell experiment was used for the detection of cells migration and invasion abilities. The interaction between LINC00240, miR-4465 and HGF was reflected by Luciferase reporter assay. LINC00240, miR-4465, HGF and p-c-MET expression in HCC cells were researched by real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. RESULTS: TCGA data showed that high LINC00240 expression was markedly associated with lower survival of HCC patients (p = 0.036). LINC00240 expression was aberrantly upregulated in HCC cells. Silencing of LINC00240 significantly reduced HCC cells viability, migration and invasion. miR-4465 was a target gene of LINC00240. Silencing of LINC00240 reduced HCC cells viability, migration and invasion via directly promoting miR-4465 expression. HGF was target gene of miR-4465. miR-4465 up-regulation obviously suppressed HGF and p-c-MET expression. According to rescue experiment, LINC00240 silencing inhibited HCC cells viability, migration and invasion by suppressing HGF/c-MET signaling pathway via targeting miR-4465. CONCLUSIONS: LINC00240 sponges miR-4465 to promote HCC cells proliferation, migration and invasion via HGF/c-MET signaling pathway.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10452-10461. doi: 10.26355/eurrev_202010_23397.
4218	LncRNA	LINC00261	miR-550a-3p	SDPR	MCF-7 cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33274565	LINC00261/microRNA-550a-3p/SDPR axis affects the biological characteristics of breast cancer stem cells.	Long non-coding RNAs (lncRNAs) have been shown to play key roles in the pathogenesis of breast cancer (BC). The study was to explore the effect of long non-coding RNA LINC00261/microRNA (miR)-550a-3p/serum deprivation response (SDPR) axis on the biological characteristics of BC stem cells (BCSCs). BC and adjacent normal tissues of patients were collected. LINC00261, miR-550a-3p and SDPR expression in BC tissues and cell lines and CD24 and CD44 expression in BC tissues was detected. CD44(+) /CD24(-/low) BCSCs were sorted. CD44(+) /CD24(-/low) MDA-MB-231 and MCF-7 cells were screened and transfected with altered expression of LINC00261 or miR-550a-3p to explore their roles in cell viability, microsphere (MS) formation ability, migration and invasion of CD44(+) /CD24(-/low) BCSCs. The targeting relationships of LINC00261, miR-550a-3p and SDPR were detected. Reduced LINC00261, decreased SDPR and elevated miR-550a-3p exhibited in BC tissues of patients and cell lines. Elevated CD44(+/) CD24(-) were present in BC tissues. LINC00261 up-regulated SDPR expression as a sponge of miR-550a-3p. Elevated LINC00261 suppressed BC cell viability, MS formation ability, migration and invasion of CD44(+) /CD24(-/low) BCSCs. Moreover, up-regulated miR-550a-3p reversed the inhibitive effect of elevated LINC00261 on BCSCs, and reduced SDPR reversed the promotive effect of decreased miR-550a-3p on BCSCs. The study highlights that LINC00261 can adsorb miR-550a-3p to modulate SDPR, thus inhibiting the viability and MS formation of BC cells, reducing migration and invasion of CD44(+) /CD24(-/low) BCSCs, exerting a potential effect on therapy.	NA	IUBMB Life. 2021 Jan;73(1):188-201. doi: 10.1002/iub.2416. Epub 2020 Dec 3.
4219	LncRNA	LINC00261	miR-222-3p	HIPK2	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33122827	Epigenetic silencing of LncRNA LINC00261 promotes c-myc-mediated aerobic glycolysis by regulating miR-222-3p/HIPK2/ERK axis and sequestering IGF2BP1.	Long noncoding RNAs have been identified as key regulators in the progression of various cancers. LINC00261 has been reported as a tumor suppressor in multiple cancers. However, its function and underlying mechanisms in pancreatic cancer remain largely unclear. Quantitative real-time PCR was performed to detect RNA expression. In situ hybridization was used to discover the subcellular location. The direct binding of LINC00261 to miR-222-3p was verified using a dual-luciferase reporter assay and RNA immunoprecipitation. LINC00261-binding proteins were detected using an RNA pulldown assay. LINC00261 was downregulated in pancreatic cancer tissues and cell lines. Its reduced expression was correlated with advanced pathological stage and poor prognosis. Forced expression of LINC00261 suppressed pancreatic cancer glycolysis and proliferation and induced cell cycle arrest and apoptosis. Mechanistically, downregulation of LINC00261 was caused by hypermethylation of the CpG island in the promoter region and EZH2-mediated histone H3 lysine 27 trimethylation. Moreover, LINC00261 exerted its biological function by binding to miR-222-3p to activate the HIPK2/ERK/c-myc pathway. In addition, LINC00261 could also reduce c-myc expression by sequestering IGF2BP1. Our study suggests that LINC00261 functions as a tumor suppressor in pancreatic cancer and identifies novel epigenetic and posttranscriptional regulatory mechanisms of LINC00261, which contribute to the targeted therapy of pancreatic cancer.	NA	Oncogene. 2021 Jan;40(2):277-291. doi: 10.1038/s41388-020-01525-3. Epub 2020 Oct 29.
4220	LncRNA	LINC00324	miR-195-5p	TRIM29	PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	qRT-PCR	33318312	Suppression of long noncoding RNA LINC00324 restricts cell proliferation and invasion of papillary thyroid carcinoma through downregulation of TRIM29 via upregulating microRNA-195-5p.	Long noncoding RNAs (lncRNAs) are identified as novel regulators of carcinogenesis. To date, the precise functions of lncRNAs in papillary thyroid carcinoma (PTC) remains poorly understood. The purposes of this work were to explore the potential relevance of lncRNA 00324 (LINC00324) in PTC. Levels of LINC00324 were markedly up-regulated in PTC. Silencing of LINC00324 significantly repressed the proliferation and invasion of PTC cells. LINC00324 was documented as a sponge of microRNA-195-5p (miR-195-5p). Decreased levels of miR-195-5p were detected in PTC. The up-regulation of miR-195-5p suppressed PTC cellular proliferation and invasion. Suppression of miR-195-5p partially reversed the LINC00324-knockdown-mediated effects in PTC cells. We identified tripartite motif-containing 29 (TRIM29) as a target gene of miR-195-5p. TRIM29 overexpression partially reversed the LINC00324-knockdown- or miR-195-5p-overexpression-mediated effects in PTC cells. In short, this work demonstrates that LINC00324 knockdown inhibits the proliferation and invasion of PTC cells by decreasing TRIM29 expression via up-regulating miR-195-5p expression.	NA	Aging (Albany NY). 2020 Dec 14;12(24):26000-26011. doi: 10.18632/aging.202219. Epub 2020 Dec 14.
4221	LncRNA	LINC00339	miR-378a-3p	MED19	CRC cells	Colorectal Cancer	Homo sapiens (human)	RNA pull-down assay;Western blot;Flow Cytometry assay;luciferase assay;RNA pull-down;	33235461	The SP1-Induced Long Noncoding RNA, LINC00339, Promotes Tumorigenesis in Colorectal Cancer via the miR-378a-3p/MED19 Axis.	INTRODUCTION: Accumulating evidence has indicated that long noncoding RNAs (lncRNAs) are pivotal regulators involved in the pathogenesis of cancer; however, the molecular mechanism of LINC00339 in colorectal cancer (CRC) remains unclear. METHODS: The quantitative real-time polymerase chain reaction for the expression of LINC00339 and miR-378a-3p and Western blots for MED19 were performed. A dual-luciferase assay was used to investigate the interaction between LIN00339 and miR-378a-3p, as well as between miR-378a-3p and MED19. Cell proliferation was determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) assay. The cell cycle was analyzed by propidium iodide staining followed by flow cytometry analysis. The wound-healing and transwell invasion assays were used to evaluate cell migration and invasion. RESULTS: The expression of LINC00339 was significantly upregulated in CRC cells and tissues, and high LINC00339 expression indicated an advanced tumor stage. Further experiments demonstrated that SP1 activated LINC00339 expression by binding to its promoter region. Luciferase activity and RNA pull-down assays demonstrated a direct interaction between LINC00339 and miR-378a-3p. miR-378a-3p expression was decreased in CRC samples and negatively correlated with LINC00339 expression in tumors. Gain- and loss-of-function assays indicated that LINC00339 contributed to cell proliferation, cell cycle progression, migration, and invasion, while miR-378a-3p reversed these effects. Furthermore, cotransfection of wild-type MED19 3'-UTR reporters and miR-378a-3p significantly reduced luciferase activity. MED19 mRNA and protein expression was inhibited and enhanced by miR-378a-3p and LINC00339, respectively. MED19 overexpression reversed the effect of miR-378a-3p on cellular processes. Moreover, LINC00339 promoted tumor growth in vivo and induced epithelial-mesenchymal transition (EMT) and activated the Wnt/β-catenin signaling pathway in cells. CONCLUSION: Our findings demonstrate the regulatory role of the SP1/LINC00339/miR-378a-3p/MED19 axis in CRC tumorigenesis and provide novel insight into the molecular mechanism underlying CRC.	NA	Onco Targets Ther. 2020 Nov 16;13:11711-11724. doi: 10.2147/OTT.S277254. eCollection 2020.
4222	LncRNA	LINC00346	miR-128-3p	SZRD1	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	33015801	Long non-coding RNA LINC00346 regulates proliferation and apoptosis by targeting miR-128-3p/SZRD1 axis in glioma.	OBJECTIVE: Long non-coding RNAs (lncRNAs) participate in multiple processes of malignant tumors, including glioma. In this study, we aimed to explore the effect of LINC00346 on glioma and its underlying mechanism. MATERIALS AND METHODS: The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases were used to analyze the expression patterns and survival risk of LINC00346, miR-128-3p and SUZ RNA binding domain containing 1 (SZRD1) in glioma tissues. The binding sites were predicted by bioinformatic databases, and then, validated by Dual-Luciferase assay and RNA immunoprecipitation (RIP). qRT-PCR and Western blot were performed to evaluate the gene expression levels. CellTiter-Glo® and colony formation assays were used to detect the proliferation of glioma cells. Flow cytometric analysis was used to evaluate the apoptosis of glioma cells. The xenograft models were established to investigate the impact of LINC00346 on tumor growth in vivo. RESULTS: We found that both LINC00346 and SZRD1 expression were negatively related to the poor overall survival rate in glioma patients. However, miR-128-3p showed the opposite effect of survival outcomes. LINC00346 knockdown remarkably restrained cell proliferation both in vitro and in vivo, as well as inducing apoptosis by acting as a molecular sponge of miR-128-3p. Moreover, miR-128-3p bound to SZRD1 3'-UTR in a sequence-specific manner. In addition, LINC00346 knockdown significantly inhibited the expression of SZRD1 and the inhibition could be reversed by miR-128-3p mimics. Furthermore, cell proliferation and apoptosis affected by LINC00346 were partially rescued by modulating miR-128-3p or SZRD1 expression. CONCLUSIONS: LINC00346/miR-128-3p/SZRD1 axis played a crucial role in modulating the malignant progression of glioma, which may serve as a prognostic indicator and a probable therapeutic target for glioma.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9581-9590. doi: 10.26355/eurrev_202009_23046.
4223	LncRNA	LINC00346	miR-340-5p	ROCK1	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR	32996285	Long noncoding RNA LINC00346 promotes glioma cell migration, invasion and proliferation by up-regulating ROCK1.	Long noncoding RNAs have key roles in glioma progression. However, the function and mechanisms of action of the long noncoding RNA, LINC00346, in glioma remain unclear. In our study, we observed that LINC00346 levels were increased in glioma tissue samples, and according to Gene Expression Profiling Interactive Analysis, its levels were related to disease-free survival and overall survival rates, suggesting that a high level of LINC00346 expression corresponds to a poor prognosis. We next confirmed the high levels of LINC00346 expression in glioma tissues and cell lines and showed that LINC00346 knockdown suppressed glioma cell proliferation, migration and invasion; promoted apoptosis; and delayed tumour growth. Moreover, the oncogenic function of LINC00346 may be explained, in part, by the down-regulation of miR-340-5p and the de-repression of ROCK1. We showed that LINC00346 may function as a competing endogenous RNA of miR-340-5p, thereby de-repressing ROCK1. This study revealed a new regulatory network in glioma and identified potential therapeutic targets for this cancer.	NA	J Cell Mol Med. 2020 Nov;24(22):13010-13019. doi: 10.1111/jcmm.15899. Epub 2020 Sep 29.
4224	LncRNA	Linc00426	miR-455-5p	UBE2V1	LUAD tissues and cells	Lung Cancer	Homo sapiens (human)	microarray;	33311443	Linc00426 accelerates lung adenocarcinoma progression by regulating miR-455-5p as a molecular sponge.	Increasing lines of evidence indicate the role of long non-coding RNAs (LncRNAs) in gene regulation and tumor development. Hence, it is important to elucidate the mechanisms of LncRNAs underlying the proliferation, metastasis, and invasion of lung adenocarcinoma (LUAD). We employed microarrays to screen LncRNAs in LUAD tissues with and without lymph node metastasis and revealed their effects on LUAD. Among them, Linc00426 was selected for further exploration in its expression, the biological significance, and the underlying molecular mechanisms. Linc00426 exhibits ectopic expression in LUAD tissues and cells. The ectopic expression has been clinically linked to tumor size, lymphatic metastasis, and tumor differentiation of patients with LUAD. The deregulation of Linc00426 contributes to a notable impairment in proliferation, invasion, metastasis, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Mechanistically, the deregulation of Linc00426 could reduce cytoskeleton rearrangement and matrix metalloproteinase expression. Meanwhile, decreasing the level of Linc00426 or increasing miR-455-5p could down-regulate the level of UBE2V1. Thus, Linc00426 may act as a competing endogenous RNA (ceRNA) to abate miR-455-5p-dependent UBE2V1 reduction. We conclude that Linc00426 accelerates LUAD progression by acting as a molecular sponge to regulate miR-455-5p, and may be a potential novel tumor marker for LUAD.	NA	Cell Death Dis. 2020 Dec 11;11(12):1051. doi: 10.1038/s41419-020-03259-2.
4225	LncRNA	LINC00460	miR-320b	PBX3	AML cells	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR	33846790	Long non-coding RNA LINC00460 serves as a potential biomarker and oncogene via regulation of the miR-320b/PBX3 axis in acute myeloid leukemia.	Long non-coding RNA 00460 (LINC00460) has been reported to be involved in the tumorigenesis of various cancer types. However, the function of LINC00460 in acute myeloid leukemia (AML) remains elusive. Therefore, the present study aimed to investigate the role of LINC00460 in AML. The expression of LINC00460 in the serum of 80 diagnosed patients with AML and 67 healthy controls was measured via reverse transcription-quantitative polymerase chain reaction, and the results were compared with clinical features and patient outcomes. The expression of LINC00460 in 45 patients with cytogenetically normal-AML (CN-AML) was also assayed. Receiver operating characteristic (ROC) curves were generated to evaluate the sensitivity and specificity of serum LINC00460. In addition, the effects of LINC00460 on the viability, cell cycle distribution and apoptosis of AML cells were investigated. Bioinformatics tools were used to identify the possible mechanisms of how LINC00460 affects AML cells. It was found that the expression of LINC00460 was significantly upregulated in the serum of patients with AML and those with CN-AML. Higher expression of serum LINC00460 was positively associated with French-American-British classification and cytogenetics. Furthermore, ROC curve analyses demonstrated that serum LINC00460 could differentiate patients with AML from healthy individuals with an area under the curve of 0.8488 (95% CI, 0.7697-0.9279). The serum LINC00460 expression was also significantly decreased when the patients achieved complete remission. Kaplan-Meier analysis indicated that patients with high serum LINC00460 expression had a shorter overall survival time compared with the low serum LINC00460 expression group. Knockdown of LINC00460 inhibited viability, while inducing cell cycle arrest and apoptosis in AML cells. LINC00460 was also a decoy of microRNA (miR)-320b, which can further inhibit the expression of PBX homeobox 3 (PBX3). Collectively, the results suggested that LINC00460 may be applied as a potential diagnostic and prognostic biomarker for patients with AML. It was identified that LINC00460 may exert its effects, at least partly, via the miR-320b/PBX3 axis in AML.	NA	Mol Med Rep. 2021 Jun;23(6):435. doi: 10.3892/mmr.2021.12074. Epub 2021 Apr 13.
4226	LncRNA	LINC00460	miR-149-5p	p53	SW480/OxR cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33251049	LINC00460-miR-149-5p/miR-150-5p-Mutant p53 Feedback Loop Promotes Oxaliplatin Resistance in Colorectal Cancer.	Oxaliplatin resistance is a major challenge in the clinical treatment for advanced colorectal cancer (CRC). Long non-coding RNAs (lncRNAs) are involved in tumorigenesis and progression as critical regulators, while their potential roles in chemoresistance are poorly understood. In this study, we report that the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop is responsible for oxaliplatin resistance in CRC. First, LINC00460 was found to exhibit higher expression in oxaliplatin-resistant CRC (CRC/OxR) cells compared with parental oxaliplatin-sensitive ones, and this expression pattern depends on mutant p53 (SW480/OxR), not wild-type p53 (HCT116/OxR). Oxaliplatin-induced LINC00460 in SW480/OxR cells was mainly located in the cytoplasm and was associated with AGO2 protein. LINC00460 functions as a competing endogenous RNA (ceRNA) to promote oxaliplatin resistance through sequestering miR-149-5p/miR-150-5p and upregulating the expression of the microRNA (miRNA) target p53. Knockdown of LINC00460 sensitized SW480/OxR cells to oxaliplatin by modulating p53 in vitro and in vivo. In turn, mutant p53 positively regulated the expression of LINC00460, thus forming a feedback loop. Clinical data showed that LINC00460 was upregulated in CRC tissues compared with paired normal tissues and was significantly correlated with clinical stage and node (N) status. Our findings uncover a mechanism for the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop in oxaliplatin resistance of CRC, and they provide potential therapeutic targets for tumor chemoresistance.	NA	Mol Ther Nucleic Acids. 2020 Oct 15;22:1004-1015. doi: 10.1016/j.omtn.2020.10.018. eCollection 2020 Dec 4.
4227	LncRNA	LINC00460	miR-150-5p	p53	SW480/OxR cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33251049	LINC00460-miR-149-5p/miR-150-5p-Mutant p53 Feedback Loop Promotes Oxaliplatin Resistance in Colorectal Cancer.	Oxaliplatin resistance is a major challenge in the clinical treatment for advanced colorectal cancer (CRC). Long non-coding RNAs (lncRNAs) are involved in tumorigenesis and progression as critical regulators, while their potential roles in chemoresistance are poorly understood. In this study, we report that the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop is responsible for oxaliplatin resistance in CRC. First, LINC00460 was found to exhibit higher expression in oxaliplatin-resistant CRC (CRC/OxR) cells compared with parental oxaliplatin-sensitive ones, and this expression pattern depends on mutant p53 (SW480/OxR), not wild-type p53 (HCT116/OxR). Oxaliplatin-induced LINC00460 in SW480/OxR cells was mainly located in the cytoplasm and was associated with AGO2 protein. LINC00460 functions as a competing endogenous RNA (ceRNA) to promote oxaliplatin resistance through sequestering miR-149-5p/miR-150-5p and upregulating the expression of the microRNA (miRNA) target p53. Knockdown of LINC00460 sensitized SW480/OxR cells to oxaliplatin by modulating p53 in vitro and in vivo. In turn, mutant p53 positively regulated the expression of LINC00460, thus forming a feedback loop. Clinical data showed that LINC00460 was upregulated in CRC tissues compared with paired normal tissues and was significantly correlated with clinical stage and node (N) status. Our findings uncover a mechanism for the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop in oxaliplatin resistance of CRC, and they provide potential therapeutic targets for tumor chemoresistance.	NA	Mol Ther Nucleic Acids. 2020 Oct 15;22:1004-1015. doi: 10.1016/j.omtn.2020.10.018. eCollection 2020 Dec 4.
4228	LncRNA	LINC00466	miR-508	CHEK1	glioma cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Flow Cytometry assay;luciferase assay;Luciferase reporter assay;	33037684	YY1-mediated up-regulation of lncRNA LINC00466 facilitates glioma progression via miR-508/CHEK1.	BACKGROUND: The abnormal expression of lncRNA LINC00466 (LINC00466) has been demonstrated in several tumor types. However, the expression pattern and functions of LINC00466 in glioma remain uninvestigated. METHODS: A reverse transcriptase-polymerase chain reaction (RT-PCR) was utilized to analyze LINC00466 in human glioma tissues and cell lines. Luciferase reporter assays were performed to explore whether YY1 could bind to the promoter region of LINC00466. Cell counting kit-8, flow cytometry, colony-formation, transwell migration and invasion assays were carried out to determine the involvement of INC00466 in glioma. Luciferase assays and pulldown assays were conducted to verify the binding sites. RESULTS: We report that LINC00466 expression is increased in glioma cells and tissues. YY1 transcription factor (YY1) can bind directly to the LINC00466 promoter region. Clinical studies revealed that the elevated expression of LINC00466 is closely correlated with an advanced World Health Organization grade (p = 0.008), Karnofsky Performance Status score (p = 0.004) and a short overall survival (p = 0.0035) of glioma patients. Functional assays revealed that LINC00466 knockdown distinctly suppresses glioma cell proliferation, migration, invasion and epithelial-mesenchymal progress, and also promotes apoptosis. Moreover, dual-luciferase reporter assays indicated that LINC00466 acts as an endogenous sponge via binding to miR-508 and decreasing its expression. Luciferase assays and RT-PCR assays demonstrated that checkpoint kinase 1 (CHEK1) is a target of miR-508, and LINC00466 modulates CHEK1 levels by competing for miR-508. LINC00466 may exhibit its anti-oncogenic roles through targeting the miR-508/CHEK1 axis. CONCLUSIONS: Our findings identified a novel glioma-related long non-coding RNA, LINC00466, which may provide a potential novel prognostic and therapeutic target for glioma.	NA	J Gene Med. 2021 Jan;23(1):e3287. doi: 10.1002/jgm.3287. Epub 2020 Nov 24.
4229	LncRNA	LINC00472	miR-373-3p	TRIM8	THLE-3 cells	Sepsis-Induced Acute Hepatic Injury	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33129786	Down-regulation of long noncoding RNA LINC00472 alleviates sepsis-induced acute hepatic injury by regulating miR-373-3p/TRIM8 axis.	BACKGROUND: The long noncoding RNAs (lncRNAs) have been confirmed to be involved in sepsis-induced organ injury. Here, we first investigated the functional role and the underlying mechanism of lncRNA LINC00472 in sepsis-induced acute hepatic injury (AHI). METHODS: Human liver THLE-3 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced AHI in vitro; intraperitoneal injection of LPS in rats were used as an in vivo model of AHI induced by sepsis. The expressions of LINC00472, miR-373-3p, and TRIM8 mRNA were detected by qRT-PCR. The effects of LINC00472 and miR-373-3p on the viability of THLE-3 cells were assessed by CCK-8 assay. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to determine the binding relationship between LINC00472 and miR-373-3p as well as between miR-373-3p and TRIM8. The expressions of apoptosis-related proteins and TRIM8 were detected by Western blot; the levels of ALT, AST, TNF-α, IL-6, and IL-10 in the serum of rats were measured using ELSA assay. RESULTS: LINC00472 and TRIM8 were significantly upregulated in liver tissues and THLE-3 cells in sepsis-induced AHI models, while miR-373-3p was downregulated. Silencing of LINC00472 promoted cell viability and suppressed cell apoptosis in LPS-treated THLE-3 cells, whereas upregulation of LINC00472 had the opposite effect. Moreover, LINC00472 served as a sponge for miR-373-3p and negatively regulated its expression. miR-373-3p mimics could promote THLE-3 cell viability and suppress cell apoptosis. Additionally, TRIM8 was a direct target of miR-373-3p, which was downregulated in LINC00472-silenced cells and upregulated by the miR-373-3p inhibitor. Further, the co-transfection of miR-373-3p inhibitor reversed the effects of LINC00472 knockdown on cell viability and apoptosis. Downregulation of LINC00472 in rats restored the levels of ALT, AST, IL-6, IL-10, and TNF-α. CONCLUSION: Downregulation of LINC00472 ameliorates sepsis-induced AHI by regulating the miR-373-3p/TRIM8 axis.	NA	Exp Mol Pathol. 2020 Dec;117:104562. doi: 10.1016/j.yexmp.2020.104562. Epub 2020 Oct 28.
4230	LncRNA	LINC00473	miR-513a-3p	NA	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;	33103510	Knockdown of LINC00473 promotes radiosensitivity of non-small cell lung cancer cells via sponging miR-513a-3p.	Non-small cell lung cancer (NSCLC) is the most common form of lung cancer. Radioresistance is a significant obstacle in NSCLC radiotherapy. Long non-coding RNA LINC00473 has been found to impact the radiotherapy in several malignant tumours. This study aimed to investigate the underlying role and mechanism of LINC00473 in regulating radiosensitivity of NSCLC cells. The levels of LINC00473 and miR-513a-3p were measured by quantitative Real-Time PCR. The relationship of LINC00473 with overall survival was tested by the Kaplan-Meier method. The effects of LINC00473 on cell viability and cell survival were assessed by cell counting kit-8 (CCK-8) and colony survival assay in NSCLC cells exposed to different doses of radiation. A luciferase reporter assay was used to investigate the correlation between LINC00473 and miR-513a-3p. The present study showed that the relative LINC00473 expression was upregulated and miR-513a-3p expression was downregulated in radioresistant NSCLC patients compared with radiosensitive patients. And upregulated LINC00473 expression was associated with poor prognosis of NSCLC patients after radiotherapy. Radiation led to an increase in LINC00473 expression in a dose- and time-dependent manner. The knockdown of LINC00473 markedly promoted radiosensitivity in NSCLC cells under different doses of radiation. LINC00473 was a sponge of miR-513a-3p and negatively regulated the miR-513a-3p expression. In conclusion, the inhibition of miR-513a-3p markedly reversed the promoted effect of LINC00473 knockdown on cell radiosensitivity. LINC00473 inhibition enhances radiosensitivity of NSCLC by sponging miR-513a-3p, providing a promising therapeutic target to increase the sensitivity of radiotherapy in NSCLC patients.	NA	Free Radic Res. 2020 Oct;54(10):756-764. doi: 10.1080/10715762.2020.1841900. Epub 2020 Nov 5.
4231	LncRNA	Linc00475	miR-141-3p	YAP1	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR;Rescue assay;	33336871	Linc00475 promotes the progression of glioma by regulating the miR-141-3p/YAP1 axis.	Glioma is the most prevalent and lethal primary brain tumour. Abundant long non-coding RNAs ( lncRNAs) are aberrant and play crucial roles in the oncogenesis of glioma. The exact functions of linc00475 in glioma remain blurred. Here, we analysed the expression levels of linc00475 by qRT-PCR and discovered that linc00475 was up-regulated in glioma and predicted a poor prognosis in patients with glioma. Besides, inhibiting linc00475 restrained the progression of glioma in vitro and in vivo. Further experiments confirmed that linc00475 regulated the progression of glioma by acting as a sponge for miR-141-3p. Moreover, we detected the binding sites of linc00475 and miR-141-3p, the YAP1- 3'UTR and miR-141-3p by luciferase reporters. The rescue assays confirmed that inhibiting linc00475 restrained the progression of glioma through the miR-141-3p/YAP1 pathway. Collectively, our research demonstrates the key roles of linc00475 in glioma, which could be a promising therapeutic target.	NA	J Cell Mol Med. 2021 Jan;25(1):463-472. doi: 10.1111/jcmm.16100. Epub 2020 Dec 18.
4232	LncRNA	LINC00519	miR-876-3p	MACC1	TSCC tumor cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	Cell migration and invasion assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33244240	Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1.	PURPOSE: Long intergenic non-protein coding RNA 519 (LINC00519) promotes the development of lung squamous cell carcinoma. In this study, we detected the expression of LINC00519 in tongue squamous cell carcinoma (TSCC) and examined its clinical significance. Additionally, the regulatory effects of LINC00519 on behaviors of TSCC tumor cells were explored through functional experiments. Finally, mechanistic studies were performed to elucidate the molecular events underlying the tumor-promoting actions of LINC00519 in TSCC. MATERIALS AND METHODS: The expression of LINC00519 in TSCC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 assay, flow cytometric analysis, cell migration and invasion assays and xenograft tumor model analyses were used to detect TSCC cell proliferation, apoptosis, migration and invasion and in vivo tumor growth, respectively. Mechanistic studies were performed using bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay and rescue experiments. RESULTS: LINC00519 was overexpressed in both TSCC tissues and cell lines. A high LINC00519 level was associated with poor overall survival in patients with TSCC. In vitro, LINC00519 played cancer-promoting roles in TSCC progression by facilitating cell proliferation, migration and invasion and restraining cell apoptosis. In vivo, LINC00519 downregulation resulted in decreased TSCC tumor growth. Mechanistically, LINC00519 acted as a competing endogenous RNA for microRNA-876-3p (miR-876-3p), which directly targets metastasis associated with colon cancer-1 (MACC1), in TSCC cells. LINC00519 upregulated the expression of MACC1 in TSCC cells by sequestering miR-876-3p. Rescue experiments further affirmed that miR-876-3p inhibition or MACC1 overexpression mitigated the inhibitory influences of LINC00519 depletion on cell proliferation, migration and invasion and neutralized the promoting actions of LINC00519 knockdown on cell apoptosis in TSCC. CONCLUSION: LINC00519 aggravated the oncogenicity of TSCC by regulating the miR-876-3p/MACC1 axis. Our findings suggest that the LINC00519/miR-876-3p/MACC1 pathway may be an underlying therapeutic target in TSCC.	NA	Onco Targets Ther. 2020 Nov 20;13:11975-11990. doi: 10.2147/OTT.S279798. eCollection 2020.
4233	LncRNA	LINC00657	miR-20a-5p	RUNX3	NK cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;	33129959	Long noncoding RNA LINC00657 inhibits cervical cancer development by sponging miR-20a-5p and targeting RUNX3.	Long noncoding RNAs act essential regulators in cervical cancer progression. Our study aimed to investigate the underlying function and molecular mechanisms of LINC00657 in cervical cancer. QRT-PCR results indicated that LINC00657 was significantly decreased in cervical cancer. Gain-and loss-of-function experiments were performed in SiHa and HeLa. Functional assays demonstrated that LINC00657 inhibited cervical cancer cell growth, migration and invasion. Moreover, miR-20a-5p was confirmed as a target of LINC00657. Furthermore, miR-20a-5p promoted the development of cervical cancer via targeting RUNX3. DR5 acts as a vital promoter in activating NK cells and is a downstream target of RUNX3. We found that LINC00657 overexpression promoted the cytotoxic activity of NK cells via regulating RUNX3/DR5 axis. Therefore, LINC00657 suppressed cervical cancer progression via inducing miR-20a-5p/RUNX3/DR5 mediated NK cell tolerance. In conclusion, LINC00657 was identified as a novel tumor-suppressor in cervical cancer and could function as a potential therapeutic target for clinical treatment.	NA	Cancer Lett. 2021 Feb 1;498:130-141. doi: 10.1016/j.canlet.2020.10.044. Epub 2020 Oct 28.
4234	LncRNA	LINC00657	miR-424-5p	PD-L1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Cell Invasion Assay;Flow Cytometry assay;	32996041	LINC00657 knockdown suppresses hepatocellular carcinoma progression by sponging miR-424 to regulate PD-L1 expression.	BACKGROUND: Hepatocellular carcinoma (HCC) is the sixth most commonly diagnosed malignant tumor and the fourth leading cause of cancer-related deaths worldwide. As a novel non-coding RNA, LINC00657 was firstly identified as an oncogenic role in breast cancer. However, few research focus on the effect of LINC00657 on the progression of HCC. OBJECTIVES: The purpose of this study was to investigate the effect of LINC00657 on HCC tissues and cells, and further explore the potential mechanism. METHODS: We first measured the expression of LINC00657 in HCC tissues and cell lines using qRT-PCR. Next we established LINC00657 knockdown in HCC cells. CCK-8 assay, cell invasion assay, flow cytometry analysis, qRT-PCR and western blotting were applied to assess the role of LINC00657 knockdown in the biological behavior of HCC cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. RESULTS: LINC00657 was remarkably overexpressed in HCC tissues and cell lines, associated with poor prognosis. LINC00657 knockdown repressed cell proliferation and invasion, promoted cell apoptosis of HCC cell lines. The bioinformatics analysis showed LINC00657 sponged miR-424 as a ceRNA. Besides, PD-L1 mimic rescued the suppression of si-LINC00657 in the biological behavior of HCC cells. CONCLUSION: In a word, we observed LINC00657 regulated PD-L1 expression by sponging miR-424, thus affecting the developments of hepatocellular carcinoma. These findings LINC00657 may provide new evidence for therapeutic application in hepatocellular carcinoma.	NA	Genes Genomics. 2020 Nov;42(11):1361-1368. doi: 10.1007/s13258-020-01001-y. Epub 2020 Sep 29.
4235	LncRNA	LINC00662	miR-320d	E2F1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33589572	Exosomal long non-coding RNA LINC00662 promotes non-small cell lung cancer progression by miR-320d/E2F1 axis.	Non-small cell lung cancer (NSCLC) is the most common tumor affecting modern people and is associated with severe morbidity and high mortality. Exosomal long non-coding RNAs as crucial regulators are involved in cancer progression. However, the role of exosomal lncRNA LINC00662 in the development of NSCLC remains unclear. Here, we aimed to explore the impact of exosomal lncRNA LINC00662 on the NSCLC progression and the underlying mechanism. Significantly, we revealed that the expression of lncRNA LINC00662 was elevated in the plasma exosome of NSCLC patients. Exosomal LINC00662 promoted proliferation, invasion, and migration, and inhibited apoptosis and cell cycle arrest of NSCLC cells. Mechanically, LINC00662 was able to serve as a miR-320d sponge in NSCLC cells. MiR-320d could target E2F1 in NSCLC cells. Exosomal LINC00662 contributed to the progression of NSCLC by miR-320d/E2F1 axis in vitro. Remarkably, exosomal LINC00662 enhanced the tumor growth of NSCLC in vivo. Thus, we conclude that exosomal lncRNA LINC00662 promotes NSCLC progression by modulating miR-320d/E2F1 axis. Our finding provides new insights into the mechanism by which exosomal lncRNA LINC00662 contributes to the development of NSCLC. LncRNA LINC00662, miR-320d, and E2F1 may serve as potential targets for NSCLC therapy.	NA	Aging (Albany NY). 2021 Feb 11;13(4):6010-6024. doi: 10.18632/aging.202522. Epub 2021 Feb 11.
4236	LncRNA	linc00662	miR-145-5p	PAFAH1B2	A549 and H460 cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33108738	Silencing linc00662 inhibits cell proliferation and colony formation of lung cancer cells via regulating the miR-145-5p-PAFAH1B2 axis.	Lung cancer is the most common cause of cancer-related death in the world. Long non-coding RNAs (lncRNAs) are longer than 200 nucleotide transcripts, and are not translated into protein. The lncRNA linc00662 is overexpressed in lung cancer; however, its role in lung cancer is still unknown. In our study, by analyzing the TCGA data, we found that linc00662 was overexpressed in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). We knocked-down the expression of linc00662 using siRNA, and found that silencing linc00662 significantly inhibited the proliferation and colony formation of the lung cancer cell lines A549 and H460. We also found that knockdown of linc00662 increased the expression of the microRNA miR-145-5p and decreased the expression of the platelet-activating factor acetylhydrolase IB subunit beta (PAFAH1B2) gene. We further show that linc00662 binds with miR-145-5p, and that miR-145-5p binds to the 3'UTR of PAFAH1B2. miR-145-5p negatively regulates PAFAH1B2 both at the mRNA and the protein level. Loss of miR-145-5p abolished the inhibitory effects of silencing linc00662 on the proliferation and colony formation of A549 and H460 cells. These findings indicate that linc00662 functions as an oncogene by acting as a competing endogenous RNA (ceRNA) and sponges and regulates miR-145-5p in lung cancer, and thus may provide a potential target for treating lung cancer.	NA	Biochem Cell Biol. 2021 Jun;99(3):330-338. doi: 10.1139/bcb-2019-0396. Epub 2020 Oct 27.
4237	LncRNA	LINC00662	miR-890	ELK3	A375 and SK-MEL-1 cells	Skin Cancer	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;Luciferase reporter assay;MTT assay;Rescue assay;	32894549	LINC00662 promotes cell proliferation, migration and invasion of melanoma by sponging miR-890 to upregulate ELK3.	OBJECTIVE: Melanoma is one of the most malignant types of skin tumors and accounts for the majority of skin cancer-related deaths. LINC00662 is a tumor promoter in multiple types of cancer, but the role of LINC00662 in melanoma has not been fully elucidated. MATERIALS AND METHODS: The expression levels of LINC00662, miR-890, and ELK3 were detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). MTT assay was performed to measure the cell proliferation ability in A375 and SK-MEL-1 cells. Cell migration and invasion abilities were measured by wound healing assay and transwell assay, respectively. Besides, Luciferase reporter assay was employed to examine the interaction between miR-890 and LINC00662 or ELK3. RESULTS: In the present study, it was demonstrated that melanoma patients with high expression levels of LINC00662 had a shorter survival time than those with low expression levels of LINC00662. LINC00662 exhibited higher expression levels in melanoma tissues and cell lines. Additionally, suppression of LINC00662 impaired cell proliferation, migration, and invasion. Furthermore, animal experiments demonstrated that LINC00662 facilitated tumor growth in vivo. LINC00662 was confirmed to bind with miR-890, and ELK3 was identified as a downstream target gene of miR-890. Furthermore, miR-890 was found to negatively regulate ELK3 expression. Through rescue assays, overexpression of ELK3 reversed the inhibitive effects of LINC00662 knockdown or miR-890 mimics on the cell proliferative, migratory, and invasive abilities. CONCLUSIONS: Our results demonstrated that LINC00662 facilitated the occurrence and development of melanoma by sponging miR-890 to upregulate ELK3. This discovery implied that LINC00662 may be a promising prognostic and therapeutic biomarker for patients with melanoma.	NA	Eur Rev Med Pharmacol Sci. 2020 Aug;24(16):8429-8438. doi: 10.26355/eurrev_202008_22640.
4238	LncRNA	LINC00662	miR-34a-5p	LMAN2L	glioma cells	Glioma	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33116598	Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma.	BACKGROUND: Numerous studies suggest that long non-coding RNAs (lncRNAs) participate in the biological process of diverse malignancies, including glioma. Although many differentially expressed lncRNAs have been identified in glioma, to our best knowledge, the role of LINC00662 and its potential underlying mechanism in glioma progression remains unclear. This study aimed to explore the function and regulatory network of LINC00662 in glioma. METHODS: Expressions of LINC00662, miR-34a-5p and lectin mannose-binding 2-like (LMAN2L) in glioma tissues were analyzed using The Cancer Genome Atlas Program (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Colony formation, Celltiter-Glo and BrdU (5-bromo-2'-deoxyuridine) incorporation assays were used to detect cell proliferation in vitro. Xenograft mouse models were established to determine cell proliferation in vivo. Transwell and wound healing assay was used to detect cell migration. In addition, epithelial-mesenchymal transition (EMT) markers were detected by Western blot. Annexin V and 7-AAD were used to stain apoptotic cells. Interactions between miR-34a-5p and LINC00662 or the 3'-UTR of LMAN2L were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) assays. RESULTS: High LINC00662 level predicted poor overall survival of glioma patients. Functional studies revealed that suppression of LINC00662 remarkably inhibited cell proliferation, clonogenicity and EMT pathway. Mechanistically, LINC00662 sponged miR-34a-5p to regulate LMAN2L expression. Furthermore, miR-34a-5p inhibitor reversed the anti-proliferation and anti-migration effect of LINC00662 knockdown, which could be rescued by downregulation of LMAN2L in glioma cells. CONCLUSION: Our study was the first to report that LINC00662 acted as a competing endogenous RNA (ceRNA) to regulate glioma progression by targeting miR-34a-5p/LMAN2L axis, providing a new therapeutic target for glioma.	NA	Onco Targets Ther. 2020 Oct 9;13:10161-10172. doi: 10.2147/OTT.S272616. eCollection 2020.
4239	LncRNA	LINC00662	miR-34a-5p	LMAN2L	glioma cells	Glioma	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33116598	Long Non-Coding RNA LINC00662 Regulated Proliferation and Migration by Targeting miR-34a-5p/LMAN2L Axis in Glioma.	BACKGROUND: Numerous studies suggest that long non-coding RNAs (lncRNAs) participate in the biological process of diverse malignancies, including glioma. Although many differentially expressed lncRNAs have been identified in glioma, to our best knowledge, the role of LINC00662 and its potential underlying mechanism in glioma progression remains unclear. This study aimed to explore the function and regulatory network of LINC00662 in glioma. METHODS: Expressions of LINC00662, miR-34a-5p and lectin mannose-binding 2-like (LMAN2L) in glioma tissues were analyzed using The Cancer Genome Atlas Program (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Colony formation, Celltiter-Glo and BrdU (5-bromo-2'-deoxyuridine) incorporation assays were used to detect cell proliferation in vitro. Xenograft mouse models were established to determine cell proliferation in vivo. Transwell and wound healing assay was used to detect cell migration. In addition, epithelial-mesenchymal transition (EMT) markers were detected by Western blot. Annexin V and 7-AAD were used to stain apoptotic cells. Interactions between miR-34a-5p and LINC00662 or the 3'-UTR of LMAN2L were predicted and determined by bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) assays. RESULTS: High LINC00662 level predicted poor overall survival of glioma patients. Functional studies revealed that suppression of LINC00662 remarkably inhibited cell proliferation, clonogenicity and EMT pathway. Mechanistically, LINC00662 sponged miR-34a-5p to regulate LMAN2L expression. Furthermore, miR-34a-5p inhibitor reversed the anti-proliferation and anti-migration effect of LINC00662 knockdown, which could be rescued by downregulation of LMAN2L in glioma cells. CONCLUSION: Our study was the first to report that LINC00662 acted as a competing endogenous RNA (ceRNA) to regulate glioma progression by targeting miR-34a-5p/LMAN2L axis, providing a new therapeutic target for glioma.	NA	Onco Targets Ther. 2020 Oct 9;13:10161-10172. doi: 10.2147/OTT.S272616. eCollection 2020.
4240	LncRNA	LINC00665	miR-224-5p	VMA21	melanoma cells	Melanoma	Homo sapiens (human)	qRT-PCR;	33247967	Long non-coding RNA LINC00665 promotes melanoma cell growth and migration via regulating the miR-224-5p/VMA21 axis.	Melanoma is an aggressive malignant skin tumor endangering the health of patients. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been increasingly reported to be implicated in the carcinogenesis of melanoma. Long intergenic non-coding RNA 00665 (LINC00665) has been found to exert important regulatory roles in some cancers, yet its function in melanoma remains to be investigated. QRT-PCR analysis was conducted to evaluate the relative expression of RNAs. Functional experiments in vitro including colony formation, EdU, wound-healing and transwell assays, as well as in vivo xenograft assays, were utilized to study the role of LINC00665 in melanoma. Mechanical experiments were implemented to probe into the molecular linkage of LINC00665, miR-224-5p and VMA21. LINC00665 was abnormally highly expressed in melanoma cells. Silencing LINC00665 could inhibit the proliferation and migration of melanoma cells. LINC00665 sponged miR-224-5p to upregulate VMA21. VMA21 knockdown exerted similarly interfering effects on above biological processes in melanoma cells. However, VMA21 overexpression abolished the in vitro and in vivo outcomes of LINC00665 silencing. LINC00665 promotes proliferative and migrating abilities of melanoma cells via targeting miR-224-5p/VMA21 axis.	NA	Exp Dermatol. 2020 Nov 28. doi: 10.1111/exd.14246.
4241	LncRNA	LINC00665	miR-3619-5p	NA	OS cells	Osteosarcoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;	33090388	LINC00665 facilitates the progression of osteosarcoma via sponging miR-3619-5p.	OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including osteosarcoma (OS). The present study aims to investigate the role of LINC00665 in OS progression. PATIENTS AND METHODS: The expression levels of LINC00665 and miR-3619 were assessed by RT-qPCR. The correlation between LINC00665 and miR-3619 expression was evaluated by Pearson's correlation analysis. The interaction between LINC00665 and miR-3619 was predicted by starBase, which was further confirmed by Luciferase reporter assay and RIP assay. The viability, invasion, and migration of OS cells were analyzed by CCK-8 and transwell assays. RESULTS: LINC00665 expression was upregulated in OS tissues and cell lines, and the high level of LINC00665 was associated with poor prognosis in OS. Moreover, LINC00665 knockdown attenuated the viability, invasion, and migration of OS cells. In addition, miR-3619 was demonstrated to be a target of LINC00665. Overexpression of miR-3619 inhibited OS progression, while this effect was abolished by the upregulation of LINC00665. CONCLUSIONS: We demonstrated that LINC 00665 accelerated OS development by targeting miR-3619. These findings might provide potential treatment strategies for patients with OS.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(19):9852-9859. doi: 10.26355/eurrev_202010_23195.
4242	LncRNA	LINC00665	miR-3619-5p	NA	BC tissues and cells	Breast Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	32983239	Knockdown of LINC00665 inhibits proliferation and invasion of breast cancer via competitive binding of miR-3619-5p and inhibition of catenin beta 1.	BACKGROUND: Long intergenic non-protein coding RNA00665 (LINC00665) plays a crucial tumorigenic role in many cancers, such as gastric cancer and lung adenocarcinoma. However, its role and mechanism of action in the progression of breast cancer (BC) are unknown. METHODS: LINC00665 expression levels were determined using quantitative polymerase chain reaction analysis with BC tissues and cell lines. BC cell proliferation was tested by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays, whereas BC cell migration and invasion capabilities were analyzed by performing transwell migration assays. Percentages of apoptotic cells were measured by flow cytometry. Interactions between LINC00665 and miR-3169-5p were examined by performing luciferase reporter assays, and the expression levels of proteins, such as β-catenin, were examined by western blot analysis. RESULTS: LINC00665 was expressed at high levels in BC tissues and cells. Upregulated LINC00665 expression correlated with tumor size and tumor, node, and metastasis stages, but not with the age of patients. LINC00665 knockdown inhibited BC cell proliferation, migration, and invasion, whereas it promoted apoptosis. Moreover, bioinformatics analysis and the luciferase reporter assay revealed that LINC00665 bound the microRNA (miR) miR-3619-5p. miR-3619-5p expression correlated negatively with LINC00665 expression in BC tissues. miR-3619-5p overexpression inhibited BC cell proliferation, migration, and invasion, but promoted apoptosis. Simultaneous knockdown of LINC00665 and miR-3619-5p led to increased cell proliferation, migration, and invasion, and inhibited apoptosis. Additionally, catenin beta 1, which encodes the β-catenin protein, was the target gene of miR-3619-5p. β-catenin expression clearly decreased after LINC00665 knockdown and miR-3619-5p overexpression, but increased after simultaneous knockdown of LINC00665 and miR-3619-5p. CONCLUSION: LINC00665 knockdown inhibited BC cell proliferation and invasion by binding miR-3619-5p and inhibiting β-catenin expression.	NA	Cell Mol Biol Lett. 2020 Sep 24;25:43. doi: 10.1186/s11658-020-00235-8. eCollection 2020.
4243	LncRNA	LINC00667	miR-200c-3p	PDK1	CCA cells	Cholangiocarcinoma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Western blot;	33040228	Yin Yang 1-induced LINC00667 up-regulates pyruvate dehydrogenase kinase 1 to promote proliferation, migration and invasion of cholangiocarcinoma cells by sponging miR-200c-3p.	Cholangiocarcinoma (CCA) is one of the most aggressive and lethal malignancies. Long noncoding RNAs (lncRNAs) are being found to play crucial roles in CCA progression. This work aims to investigate the roles of long intergenic non-protein coding RNA 667 (LINC00667) in progression of CCA. RT-qPCR and western blot were applied to detect gene expression. Clinical correlation and survival were analyzed by statistical methods. Overexpression and RNA interference approaches were used to investigate the effects of LINC00667 on CCA cells. Tumor xenograft assay was performed to detect the function of LINC00667 in vivo. Transcriptional regulation and competing endogenous RNA (ceRNA) mechanism were predicted via bioinformatics analysis. ChIP, luciferase reporter, and Ago2 RIP assays further confirmed the predicted results. Our data indicated that LINC00667 was highly expressed in CCA tissues and cells, and transcription factor Yin Yang 1 (YY1) induced LINC00667 expression in CCA cells. Up-regulated LINC00667 was significantly associated with lymph node metastasis, advanced TNM stage, and poor prognosis. Knockdown of LINC00667 suppressed the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of CCA cells, while overexpression of LINC00667 acquired opposite effects. Moreover, knockdown of LINC00667 inhibited tumor growth in vivo. In addition, LINC00667 was demonstrated to function as a ceRNA for miR-200c-3p, and then LINC00667 up-regulated pyruvate dehydrogenase kinase 1 (PDK1) to promote CCA development by inhibiting miR-200c-3p. These findings identified a pivotal role of LINC00667 in tumorigenesis and development of CCA. Targeting the YY1/LINC00667/miR-200c-3p/PDK1 axis may provide a new therapeutic strategy for CCA treatment.	NA	Hum Cell. 2021 Jan;34(1):187-200. doi: 10.1007/s13577-020-00448-1. Epub 2020 Oct 10.
4244	LncRNA	LINC00673	miR-126-5p	NA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;Luciferase activity assay;	32950808	LINC00673 exerts oncogenic function in cervical cancer by negatively regulating miR-126-5p expression and activates PTEN/PI3K/AKT signaling pathway.	BACKGROUND: Recent studies have indicated the crucial regulator roles of a long non-coding RNA (lncRNA) LINC00673 in cancer pathogenesis and development. However, the clinical significance and functional effects of LINC00673 in cervical cancer remains unknown. METHODS: LINC00673 mRNA expression in cervical cancer tissues was measured by quantitative Real-time PCR (qRT-PCR), and the association between LINC00673 expression and the overall survival (OS) time of patients was analyzed by Kaplan-Meier survival plot. Cell proliferation was assessed using CCK8 assay, Flow cytometry analysis and cell colony formation assay. The association between miR-126-5p and LINC00673 was clarified by Luciferase activity assay. Furthermore, xenografts model in mice in vivo were used to evaluate the effects of LINC00673 expression on tumor growth of cervical cancer. RESULTS: It was confirmed that the relative mRNA expression of LINC00673 was promoted in cervical cancer tissues and cancer cell lines compared with its corresponding normal tissues and cells (P < 0.05). Higher LINC00673 expression was associated with tumor size, lymph node metastasis, and International Federation of Gynecology and Obstetrics (FIGO) stage (P < 0.05). Survival analysis showed higher LINC00673 expression predicted poor OS of cervical cancer patients, and Multivariate Cox analysis demonstrated that higher LINC00673 expression was identified as an independent risk factor for OS. LINC00673 overexpression promoted cell proliferation and cell cycle progression, but LINC00673 knockdown inhibited cell proliferation and cell cycle progression significantly (P < 0.05). Besides, overexpression of LINC00673 was negatively correlated with lower miR-126-5p expression in cervical cancer tissues. In vivo xenograft tumor assay indicated that LINC00673 silencing reduced the tumor volume and weight. Bioinformatics analysis revealed that miR-126-5p targeted 3'-UTR of LINC00673, and LINC00673 promoted cell proliferation by sponging to miR-126-5p in cervical cancer cells. Additionally, it was demonstrated that LINC00673 significantly activated the PTEN/PI3K/AKT signaling pathway in cervical cancer cells. CONCLUSION: These results provide the evidence that LINC00673 overexpression promotes cervical cancer cells progression through regulating miR-126-5p and activating the PTEN/PI3K/AKT signaling pathway, indicating that LINC00673 may be a potential therapeutic target for cervical cancer treatment.	NA	Cytokine. 2020 Dec;136:155286. doi: 10.1016/j.cyto.2020.155286. Epub 2020 Sep 17.
4245	LncRNA	LINC00675	miR-942-5p	GFI1	SMCC-7721 and QGY-7703 cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	33489916	GFI1-Mediated Upregulation of LINC00675 as a ceRNA Restrains Hepatocellular Carcinoma Metastasis by Sponging miR-942-5p.	Hepatocellular carcinoma (HCC) is a common malignant liver tumor worldwide. Tumor recurrence and metastasis contribute to the bad clinical outcome of HCC patients. Substantial studies have displayed lncRNAs modulate various tumorigenic processes of many cancers. Our current work was aimed to investigate the function of LINC00675 in HCC and to recognize the potential interactions between lncRNAs and microRNAs. GFI1 can exhibit a significant role in the progression of human malignant tumors. Firstly, GFI1 was identified using real-time PCR in HCC tissues and cells. In this work, we indicated GFI1 was remarkably reduced in HCC tissues and cells. Meanwhile, GFI1 specifically interacted with the promoter of LINC00675. Up-regulation of LINC00675 obviously repressed the migration and invasion capacity of SMCC-7721 and QGY-7703 cells in vitro. Moreover, decrease of LINC00675 competitively bound to miR-942-5p that contributed to the miRNA-mediated degradation of GFI1, thus facilitated HCC metastasis. The ceRNA function of LINC00675 in HCC cells was assessed and confirmed using RNA immunoprecipitation assay and RNA pull-down assays in our work. Additionally, we proved overexpression of miR-942-5p promoted HCC progression, which was reversed by the up-regulation of GFI1. In summary, LINC00675 might act as a prognostic marker for HCC, which can inhibit HCC development via regulating miR-942-5p and GFI1.	NA	Front Oncol. 2021 Jan 8;10:607593. doi: 10.3389/fonc.2020.607593. eCollection 2020.
4246	LncRNA	LINC00689	miR-142-3p	USP6NL	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33054738	USP6NL mediated by LINC00689/miR-142-3p promotes the development of triple-negative breast cancer.	BACKGROUND: Triple-negative breast cancer (TNBC), in part because of the high metastasis rate, is one of the most prevalent causes of malignancy-related mortality globally. Ubiquitin specific peptidase 6 N-terminal like (USP6NL) has been unmasked to be implicated in some human cancers. However, the precise biological function of USP6NL in TNBC has not been defined. METHODS: RNA expression was examined by real-time quantitative PCR (RT-qPCR), while USP6NL protein level was tested through western blot. Besides, cell proliferation was assessed by using colony formation assay, whereas cell apoptosis estimated by flow cytometry analysis, JC-1 assay and TUNEL assay. Transwell assays were adopted to detect the migration and invasion of indicated TNBC cells. Immunofluorescence (IF) assay evaluated epithelial-mesenchymal transitions (EMT) progress in TNBC. Further, RNA immunoprecipitation (RIP), RNA pull down and luciferase reporter assays were implemented for measuring the mutual interplay among USP6NL, miR-142-3p and long intergenic non-protein coding RNA 689 (LINC00689). RESULTS: Elevated USP6NL level was uncovered in TNBC cells. RNA interference-mediated knockdown of USP6NL inhibited TNBC cell growth, motility and EMT. Further, USP6NL was proved as the target of a tumor-inhibitor miR-142-3p, and LINC00689 augmented USP6NL expression by absorbing miR-142-3p. Importantly, miR-142-3p deficiency or USP6NL overexpression fully abolished the inhibitory effect of LINC00689 silence on TNBC cellular behaviors. CONCLUSION: All data revealed the important role of USP6NL/LINC00689/miR-142-3p signaling in TNBC. The findings might provide a new and promising therapeutic biomarker for treating patients with TNBC.	NA	BMC Cancer. 2020 Oct 14;20(1):998. doi: 10.1186/s12885-020-07394-z.
4247	LncRNA	LINC00707	miR-613	NA	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR;	33107401	The Long Intergenic Noncoding RNA 00707 Sponges MicroRNA-613 (miR-613) to Promote Proliferation and Invasion of Gliomas.	BACKGROUND: Glioma is one of the most deadly malignant tumors in humans. Long non-coding RNA (lncRNA) plays a key role in the occurrence, development and invasion of tumors by regulating oncogenic and tumor suppressor pathways. However, the role and action mechanism of long intergenic non-coding RNA 00707 (LINC00707) in gliomas have not been elucidated. This study aimed to investigate the interaction between LINC00707 and miR-613 as well as its role in gliomas. MATERIALS AND METHODS: The expression levels of LINC00707 and miR-613 were detected by qRT-PCR. The chi-square test was used to analyze the correlation between LINC00707 expression and clinicopathological parameters. CCK-8 and colony formation assays were used to detect glioma cell proliferation; and wound healing and transwell assays were used to detect glioma cell migration and invasion. The relationship between LINC00707 and miR-613 was predicted by Starbase, and verified by qRT-PCR and dual luciferase reporter gene assay. RESULTS: LINC00707 was up-regulated in gliomas. Up-regulated LINC00707 increased the proliferation, migration and invasion of glioma cells, and silenced LINC00707 reduced these abilities. The increase of the expression level of LINC00707 down-regulated miR-613 in glioma cells, while the inhibition of the expression level of LINC00707 up-regulated miR-613 in glioma cells. The high expression of LINC00707 was related to the Karnofsky performance status (KPS) score and WHO staging. LINC00707 could offset the ability of miR-613 to inhibit glioma proliferation and invasion. CONCLUSION: LINC00707 promotes proliferation and invasion of glioma cells by sponging miR-613. The regulatory axis of LINC00707/miR-613 provides new insights into the mechanism and treatment of gliomas.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820962092. doi: 10.1177/1533033820962092.
4248	LncRNA	LINC00707	miR-223-5p	NA	MRC-5 cells	Pneumonia	Homo sapiens (human)	qRT-PCR	33604647	Knockdown of lncRNA LINC00707 alleviates LPS-induced injury in MRC-5 cells by acting as a ceRNA of miR-223-5p.	Pneumonia is a common respiratory disease worldwide. Long noncoding RNAs have been implicated in the pathogenesis of pneumonia. However, the effect and mechanism of long intergenic nonprotein-coding RNA (LINC00707) on pneumonia pathogenesis were still unclear. Lipopolysaccharide (LPS) reduced cell viability and promoted apoptosis and inflammation in MRC-5 cells. LINC00707 was increased, and miR-223-5p was decreased in LPS-treated MRC-5 cells. LINC00707 knockdown relieved LPS-triggered injury in MRC-5 cells. LINC00707 directly interacted with miR-223-5p through acting as a miR-223-5p sponge. Moreover, miR-223-5p mediated the regulation of LINC00707 silencing on LPS-stimulated cytotoxicity in MRC-5 cells. p38 mitogen-activated protein kinases and nuclear factor-κB signaling pathways were modulated by the LINC00707/miR-223-5p axis in LPS-induced MRC-5 cells. Our present study indicated that LINC00707 depletion alleviated LPS-induced injury in MRC-5 cells at least partly by acting as a sponge of miR-223-5p, highlighting a new potential therapeutic avenue for pneumonia treatment.	NA	Biosci Biotechnol Biochem. 2021 Feb 18;85(2):315-323. doi: 10.1093/bbb/zbaa069.
4249	LncRNA	LINC00858	miR-363-3p	FOXP4	BGC-823 cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Luciferase reporter assay;	33015780	Long noncoding RNA LINC00858 promotes the proliferation, migration and invasion of gastric cancer cells via the miR-363-3p/FOXP4 axis.	OBJECTIVE: Long non-coding RNA (lncRNA) LINC00858 has been found to exert oncogenic activity in several types of cancers, except gastric cancer (GC). In the present study, we aimed to explore the potential role of LINC00858 in GC and the underlying molecular mechanism. PATIENTS AND METHODS: The expression patterns of LINC00858 were determined using qRT-PCR in GC samples and cell lines. Cell proliferation was examined utilizing CCK-8 assay. Cell migration and invasion were evaluated using transwell assays. We used the bioinformatics software StarBase and TargetScan to predict lncRNA-miRNA and miRNA-mRNA interactions. RESULTS: Our findings revealed that LINC00858 expression was markedly upregulated in GC tissues and cell lines. Loss-of-function experiments demonstrated that LINC00858 silencing inhibited the proliferation, migration and invasion of GC cells. Bioinformatics analysis showed that there were several complementary binding sites between LINC00858 and microRNA (miR)-363-3p, and further Luciferase reporter assay confirmed the interaction between LINC00858 and miR-363-3p. In addition, forkhead box P4 protein (FOXP4) was found to be a target gene of miR-363-3p in GC cells. FOXP4 overexpression reversed the inhibitory effects of miR-363-3p mimics on cell proliferation, migration and invasion of BGC-823 cells. CONCLUSIONS: Collectively, LINC00858 acted as an oncogene in GC via regulating miR-363-3p/FOXP4 axis, which indicated that LINC00858 might be a novel therapeutic target for the treatment of GC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9391-9399. doi: 10.26355/eurrev_202009_23022.
4250	LncRNA	LINC00858	miR-153-3p	Rabl3	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;	33015775	Long non-coding RNA LINC00858 promotes cells proliferation and invasion through the miR-153-3p/Rabl3 axis in hepatocellular carcinoma.	OBJECTIVE: Long non-coding RNA (lncRNA) LINC00858 is a cancer-associated lncRNA frequently dysregulated in many types of human cancers. In the current study, we aimed to explore the role of LINC00858 in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: The relative expression levels of LINC00858 in HCC samples and adjacent non-tumor samples were determined by qRT-PCR. Loss-of-function assay was performed to examine the function of LINC00858 in HCC in vitro. Bioinformatic analysis and the following Luciferase activity reporter assay were utilized to explore the downstream molecules of LINC00858. CCK-8 assay was performed to detect cell proliferation of HCC cells. Transwell assay was performed to evaluate the invasive ability of HCC cells. RESULTS: Our results showed that LINC00858 was highly expressed in both HCC tissues and cell lines. Knockdown of LINC00858 inhibited the proliferation and invasion of HCC cells. Moreover, LINC00858 was found to act as a sponge of miR-153-3p, which directly bound to Rabl3 and regulated the Rabl3 expression. Furthermore, inhibition of miR-153-3p counteracted the effects of LINC00858 knockdown on proliferation and invasion of HCC cells. In addition, the overexpression of Rabl3 rescued the effects of miR-153-3p on cell proliferation and invasion of HCC cells. CONCLUSIONS: In summary, these findings showed that LINC00858 exerted an ontogenetic role in HCC via regulating miR-153-3p/Rabl3 axis. Thus, LINC00858 might be utilized as a therapeutic target for the treatment of HCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9343-9352. doi: 10.26355/eurrev_202009_23017.
4251	LncRNA	LINC00861	miR-513b-5p	PTEN	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Western blot;luciferase assay;	33179755	LINC00861 inhibits the progression of cervical cancer&nbsp;cells by functioning as a ceRNA for miR-513b-5p and&nbsp;regulating the PTEN/AKT/mTOR signaling pathway.	Long non-coding RNAs (lncRNAs) have been discovered to serve important roles in a variety of types of cancer, including cervical cancer. The low expression of lncRNA long intergenic non-protein coding RNA 861 (LINC00861) is related to poor prognosis in ovarian cancer. However, the effects and underlying mechanisms of LINC00861 in cervical cancer remain largely unknown. The present study aimed to examine the role of LINC00861 in the development and progression of ovarian cancer and its underlying mechanisms. The expression levels of LINC00861 and microRNA (miR)-513b-5p were analyzed using reverse transcription-quantitative PCR analysis. Cell proliferation, migration and invasion were measured by using Cell Counting Kit-8, colony formation, wound healing and Transwell assays, respectively. A luciferase assay was used to determine whether miR-513b-5p targeted LINC00861 and PTEN. The expression of protein was measured by using western blot assay. The results of the present study discovered that LINC00861 expression levels were significantly downregulated in cervical cancer tissues and CaSki and ME-180 cell lines. Downregulated LINC00861 expression levels were identified to be associated with an advanced-stage, lymph node metastasis and the poor survival of patients with cervical cancer. Gene Set Enrichment Analysis revealed that the PI3K/AKT/mTOR signaling pathway was significantly enriched in cervical tumors expressing low expression levels of LINC00861 compared with tumors expressing high levels of LINC00861. The overexpression of LINC00861 reduced cervical cancer cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) processes, upregulated PTEN protein expression levels and downregulated phosphorylated (p)-AKT and p-mTOR protein expression levels. The regulatory relationship between LINC00861, microRNA (miR)-513b-5p and PTEN was validated using a dual luciferase reporter gene assay. PTEN expression levels were significantly downregulated in the miR-513b-5p mimic group and significantly upregulated in the miR-513b-5p inhibitor group compared with the mimic NC and inhibitor NC in both cell lines. Furthermore, LINC00861 was suggested to serve as a competing endogenous RNA by sponging miR-513b-5p and consequently upregulating the expression levels of PTEN in cervical cancer cells. The expression of PTEN, the phosphorylation of Akt and mTOR and and the EMT phenotype were rescued following co-transfection with LINC00861 and miR-513b-5p mimics. In conclusion, the findings of the present study indicated that the LINC00861/miR-513b-5p axis may inhibit the progression of cervical cancer cells through the PTEN/AKT/mTOR signaling pathway to suppress the EMT process.	NA	Mol Med Rep. 2021 Jan;23(1):24. doi: 10.3892/mmr.2020.11662. Epub 2020 Nov 12.
4252	LncRNA	LINC00887	miR-206	NRP1	A549 and NCI-H460 cells	Lung Cancer	Homo sapiens (human)	luciferase assay;	33376520	Long non-coding RNA LINC00887 promotes progression of lung carcinoma by targeting the microRNA-206/NRP1 axis.	Long non-coding RNAs (lncRNAs) have been reported to participate in multiple biological processes, including tumorigenesis. In the current study, the function of a novel lncRNA LINC00887 was investigated in lung carcinoma. For this purpose, LINC00887 expression was assessed by reverse-transcription quantitative PCR. Cell viability was determined by the CCK-8 and EdU assays. Cell invasion, migration were assessed by the transwell and wound healing assays, respectively. A dual luciferase assay was used for analysis of the interaction between LINC00887 and miR-206, as well as the relationship of miR-206 with NRP1. A tumor xenograft study was performed to investigate the LINC00887-miR-206-NRP1 axis in vivo. The expression levels of LINC00887 were upregulated in lung carcinoma tissues and cells compared with adjacent tissues or normal cells (BEAS-2B). Knockdown LINC00887 significantly inhibited the proliferation, migration and invasion of lung carcinoma A549 and NCI-H460 cells. Furthermore, LINC00887 was identified as a competing endogenous RNA and to directly interact with miR-206. Mechanistically, miR-206 was demonstrated to regulate neuropilin-1 (NRP1) expression by targeting the NRP1 3'-untranslated region. The results of the present study suggested that the LINC00887-miR-206-NRP1 axis served a critical role in regulating lung carcinoma cell proliferation, migration and invasion. In addition, xenograft tumor model experiments revealed that silencing LINC00887 suppressed lung carcinoma tumor growth of in vivo. In summary, our results suggest that LINC00887 may serve an oncogenic role in lung carcinoma by targeting the miR-206/NRP1 axis, providing a potential therapeutic target for patients with lung carcinoma.	NA	Oncol Lett. 2021 Feb;21(2):87. doi: 10.3892/ol.2020.12348. Epub 2020 Dec 6.
4253	LncRNA	LINC00887	miR-203b-3p	NUP205	NPC tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;	32964975	LINC00887 regulates the proliferation of nasopharyngeal carcinoma via targeting miRNA-203b-3p to upregulate NUP205.	OBJECTIVE: The purpose of this study was to uncover the regulatory effect of LINC00887 on the progression of nasopharyngeal carcinoma (NPC) and the underlying mechanism. PATIENTS AND METHODS: Relative level of LINC00887 in NPC tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Thereafter, the regulatory effect of LINC00887 on proliferative ability in SUNE-1 and HK-1 cells was examined by cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay. Through Dual-Luciferase reporter gene assay and RNA-Binding Protein Immunoprecipitation (RIP) assay, the interaction in the regulatory loop LINC00887/miRNA-203b-3p/NUP205 was ascertained. At last, rescue experiments were conducted to clarify the involvement of the regulatory loop LINC00887/miRNA-203b-3p/NUP205 in the progression of NPC. RESULTS: Results showed that LINC00887 was upregulated in NPC tissues and cells, and its overexpression markedly stimulated the proliferative ability in NPC cells. In addition, a potential interaction in the regulatory loop LINC00887/miRNA-203b-3p/NUP205 was discovered, which was responsible for promoting the proliferative ability in NPC. CONCLUSIONS: LINC00887 promotes the proliferative ability in NPC via absorbing miRNA-203b-3p to upregulate NUP205.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8863-8870. doi: 10.26355/eurrev_202009_22826.
4254	LncRNA	LINC00958	miR-106a-5p	NA	HNSCC tissues and cells	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;	32894548	Silencing of long non-coding RNA LINC00958 inhibits head and neck squamous cell carcinoma progression and AKT/mTOR signaling pathway by targeting miR-106a-5p.	OBJECTIVE: The long non-coding RNA LINC00958 acts as an oncogenic regulator in many human tumors. In this study, we aimed to investigate the role and potential molecular biological mechanisms of LINC00958 in head and neck squamous cell carcinoma (HNSCC). MATERIALS AND METHODS: Aberrantly expressed LINC00958 was screened out of TCGA database. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine LINC00958 and miR-106a-5p expression. Cellular biological behaviors were investigated using CCK-8, colony formation, wound healing and transwell assays. Xenograft mouse models were established to determine the role of LINC00958 in HNSCC growth in vivo. The interaction between LINC00958 and miR-106a-5p was validated by Dual-Luciferase reporter gene assay. Additionally, the underlying pathways affected by LINC00958 were measured by Western blot. RESULTS: LINC00958 expression was upregulated in HNSCC tissues and cells. High LINC00958 level was correlated with the poor prognosis of HNSCC patients. Functional assays showed that the knockdown of LINC00958 inhibited HNSCC malignant phenotypes in vitro and in vivo. Mechanistically, miR-106a-5p was a potential target of LINC00958, and its expression was negatively regulated by LINC00958 in HNSCC. LINC00958 could activate AKT/mTOR signaling pathway, which was mediated by miR-106a-5p. CONCLUSIONS: Taken together, our results suggest that LINC00958 acts as an oncogenic role in HNSCC and activates AKT/mTOR signaling pathway by sponging miR-106a-5p. LINC00958 may serve as a potential target for HNSCC diagnosis and treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Aug;24(16):8408-8417. doi: 10.26355/eurrev_202008_22638.
4255	LncRNA	LINC00958	miR-106a-5p	NA	HNSCC tissues and cells	Head And Neck Squamous  Carcinoma	Mus musculus (mouse)	qRT-PCR;Western blot;	32894548	Silencing of long non-coding RNA LINC00958 inhibits head and neck squamous cell carcinoma progression and AKT/mTOR signaling pathway by targeting miR-106a-5p.	OBJECTIVE: The long non-coding RNA LINC00958 acts as an oncogenic regulator in many human tumors. In this study, we aimed to investigate the role and potential molecular biological mechanisms of LINC00958 in head and neck squamous cell carcinoma (HNSCC). MATERIALS AND METHODS: Aberrantly expressed LINC00958 was screened out of TCGA database. The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to determine LINC00958 and miR-106a-5p expression. Cellular biological behaviors were investigated using CCK-8, colony formation, wound healing and transwell assays. Xenograft mouse models were established to determine the role of LINC00958 in HNSCC growth in vivo. The interaction between LINC00958 and miR-106a-5p was validated by Dual-Luciferase reporter gene assay. Additionally, the underlying pathways affected by LINC00958 were measured by Western blot. RESULTS: LINC00958 expression was upregulated in HNSCC tissues and cells. High LINC00958 level was correlated with the poor prognosis of HNSCC patients. Functional assays showed that the knockdown of LINC00958 inhibited HNSCC malignant phenotypes in vitro and in vivo. Mechanistically, miR-106a-5p was a potential target of LINC00958, and its expression was negatively regulated by LINC00958 in HNSCC. LINC00958 could activate AKT/mTOR signaling pathway, which was mediated by miR-106a-5p. CONCLUSIONS: Taken together, our results suggest that LINC00958 acts as an oncogenic role in HNSCC and activates AKT/mTOR signaling pathway by sponging miR-106a-5p. LINC00958 may serve as a potential target for HNSCC diagnosis and treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Aug;24(16):8408-8417. doi: 10.26355/eurrev_202008_22638.
4256	LncRNA	LINC00998	miR-34c-5p	NA	glioblastoma tissues	Glioma	Homo sapiens (human)	luciferase assay;Rescue assay;RNA pull-down;	33268783	LncRNA LINC00998 inhibits the malignant glioma phenotype via the CBX3-mediated c-Met/Akt/mTOR axis.	Long noncoding RNAs (lncRNAs), once considered to be nonfunctional relics of evolution, are emerging as essential genes in tumor progression. However, the function and underlying mechanisms of lncRNAs in glioma remain unclear. This study aimed to investigate the role of LINC00998 in glioma progression. Through screening using TCGA database, we found that LINC00998 was downregulated in glioblastoma tissues and that low expression of LINC00998 was associated with poor prognosis. Overexpression of LINC00998 inhibited glioma cell proliferation in vitro and in vivo and blocked the G1/S cell cycle transition, which exerted a tumor-suppressive effect on glioma progression. Mechanistically, RNA pull-down and mass spectrometry results showed an interaction between LINC00998 and CBX3. IP assays demonstrated that LINC00998 could stabilize CBX3 and prevent its ubiquitination degradation. GSEA indicated that LINC00998 could regulate the c-Met/Akt/mTOR signaling pathway, which was further confirmed by a rescue assay using siRNA-mediated knockdown of CBX3 and the Akt inhibitor MK2206. In addition, dual-luciferase assays showed that miR-34c-5p could directly bind to LINC00998 and downregulate its expression. Our results identified LINC00998 as a novel tumor suppressor in glioma, and LINC00998 could be a novel prognostic biomarker, providing a strategy for precision therapy in glioma patients.	NA	Cell Death Dis. 2020 Dec 2;11(12):1032. doi: 10.1038/s41419-020-03247-6.
4257	LncRNA	LINC01006	miR-34a-5p	DAAM1	Prostate cancer cells	Prostate Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	33088221	LINC01006 facilitates cell proliferation, migration and invasion in prostate cancer through targeting miR-34a-5p to up-regulate DAAM1.	BACKGROUND: Prostate cancer (PCa) is a kind of malignancy occurring in the prostate gland. Substantial researches have proved the major role of long noncoding RNAs (lncRNAs) in PCa. However, the role of long intergenic non-protein coding RNA 1006 (LINC01006) in PCa has not been investigated yet. METHODS: RT-qPCR was used to examine the expression levels of LINC01006 and its downstream targets. The function of LINC01006 in PCa was tested by in vitro and in vivo assays. With application of RNA pull down, RNA immunoprecipitation (RIP) and luciferase reporter assays, the interaction among LINC01006, miR-34a-5p and disheveled associated activator of morphogenesis 1 (DAAM1) were verified. RESULTS: LINC01006 expression presented high in PCa cell lines. LINC01006 silencing suppressed cell proliferative, migratory, invasive capacities while accelerated apoptotic rate. Besides, LINC01006 knockdown also suppressed tumor growth and metastasis in vivo. Furthermore, miR-34a-5p, a tumor suppressor in PCa, was sponged by LINC01006. Moreover, DAAM1 was targeted by miR-34a-5p and promoted PCa progression. More intriguingly, rescue assays suggested that the inhibitory effect of LINC01006 knockdown on PCa development was offset by DAAM1 overexpression. CONCLUSIONS: LINC01006 promoted PCa progression by sponging miR-34a-5p to up-regulate DAAM1, providing a novel target for PCa therapy.	NA	Cancer Cell Int. 2020 Oct 19;20:515. doi: 10.1186/s12935-020-01577-1. eCollection 2020.
4258	LncRNA	LINC01089	miR-3187-3p	NA	A549 and SK-MES-1 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;	33269007	Long Intergenic Non-Protein Coding RNA 01089 Weakens Tumor Proliferation, Migration, and Invasion by Sponging miR-3187-3p in Non-Small Cell Lung Cancer.	BACKGROUND: Long non-coding RNAs (lncRNAs), a class of endogenous non-coding RNAs, play an important role in the development and metastasis of non-small cell lung cancer (NSCLC). However, the function and mechanism of action of long intergenic non-protein coding RNA 1089 (LINC01089) in NSCLC remains unclear. This study aimed to identify the role of LINC01089 in cell proliferation, migration, and invasion of NSCLC. METHODS: Expression of LINC01089 and the relationship between LINC01089 and overall survival (OS) in NSCLC were determined using GEPIA 2.0. Similarly, microRNAs (miRNAs) that showed increased expression in NSCLC and correlated with OS were identified using the online OncomiR cancer database. Target miRNAs of LINC01089 were predicted using starBase. Cell models of LINC01089 and miR-3187-3p overexpression were constructed using transfection. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed to analyze the expression of LINC01089 and miR-3187-3p. MTS assay was used to assess cell proliferation. Transwell was used for migration and invasion assays. RESULTS: LINC01089 expression was significantly reduced in NSCLC tissues and cells. Gain-of-function studies further demonstrated that LINC01089 overexpression inhibited proliferation, migration, and invasion of lung cancer cell lines, A549 and SK-MES-1. Based on starBase prediction and subsequent verification, we revealed that miR-3187-3p is a target miRNA of LINC01089. Additionally, miR-3187-3p expression was significantly increased in NSCLC tissues and cells. Overexpression of miR-3187-3p promoted proliferation, migration, and invasion of A549 and SK-MES-1 cells, thereby reversing the effect of LINC01089. CONCLUSION: LINC01089 attenuates tumor proliferation, migration, and invasion by sponging miR-3187-3p in NSCLC. LINC01089 acts as a tumor suppressor and represents a potential therapeutic target in NSCLC.	NA	Cancer Manag Res. 2020 Nov 25;12:12151-12162. doi: 10.2147/CMAR.S258532. eCollection 2020.
4259	LncRNA	LINC01089	miR-27a-3p	BTG2	CC cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33025678	LINC01089 inhibits the progression of cervical cancer via inhibiting miR-27a-3p and increasing BTG2.	BACKGROUND: Increasing evidence confirms that long non-coding RNA (lncRNA) has a vital impact on the procession of cervical cancer (CC). The present study aimed to investigate the clinical significance of LINC01089 in CC, as well as explore its biological functions and potential molecular mechanisms. METHODS: A quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to investigate the expression of LINC01089 and miR-27a-3p in CC cells and tissues. Analysis of the correlation between the expression level of LINC01089 and the clinical pathological parameters of CC was then conducted. The human CC cell lines HeLa and SiHa were utilized for transfection to establish a gain-of-function model and loss-of-function models. Western blotting and a qRT-PCR were performed to detect B-cell translocation gene-2 (BTG2) expression in CC cells. Cell counting kit (CCK)-8 and 5-bromo-2-deoxyuridine (BrdU) assays were performed to detect the proliferation of CC cells. The transwell method was employed to evaluate the migration and invasion of CC cells. The interactions between LINC01089 and miR-27a-3p were verified by bioinformatics, a dual luciferase reporter gene experiment and a RNA immunoprecipitation experiment, respectively. RESULTS: The expression of LINC01089 in CC was markedly down-regulated. The low expression of LINC01089 in CC was closely associated with a larger tumor size and positive lymph node metastasis. Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had the opposite biological functions. In terms of mechanism, LINC01089 could sponge miR-27a-3p and indirectly up-regulate BTG2 expression. CONCLUSIONS: LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to up-regulate BTG2 expression.	NA	J Gene Med. 2021 Jan;23(1):e3280. doi: 10.1002/jgm.3280. Epub 2020 Oct 29.
4260	LncRNA	LINC01089	miR-27a-3p	TET1	GC tissues and cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;	33088215	LINC01089 is a tumor-suppressive lncRNA in gastric cancer and it regulates miR-27a-3p/TET1 axis.	BACKGROUND: Gastric cancer (GC) is one of the most common malignancies around the world. Recently, the role of long non-coding RNA (lncRNA) in cancer biology has become a hot research topic. This work aimed to explore the biological function and underlying mechanism of LINC01089 in GC. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to investigate the expression of LINC01089 in GC tissues and cells. The relationship between the expression level of LINC01089 and the clinicopathological parameters of GC was assessed. Cell models of LINC01089 overexpression, LINC01089 knockdown, miR-27a-3p overexpression, and miR-27a-3p inhibition were established by transfection. CCK-8 assay, BrdU assay, and Transwell assay were utilized to investigate the malignant biological behaviors of GC cell lines after transfection. Dual luciferase activity reporter assay, Pearson's correlation analysis, and Western blot were utilized to the regulatory relationships among LINC01089, miR-27a-3p and tet methylcytosine dioxygenase 1 (TET1). RESULT: LINC01089 down-regulation was observed in GC tissues and cell lines. Low expression level of LINC01089 in GC tissues was markedly linked to larger tumor size, higher T stage, as well as lymphatic metastasis of the patients. Functional experiments implied that LINC01089 overexpression impeded the proliferation, migration, as well as invasion of GC cells, whereas LINC01089 knockdown promoted the above malignant phenotypes. Additionally, up-regulation of miR-27a-3p was also observed in GC tissues. Functional experiments also showed that, miR-27a-3p overexpression boosted the malignant biological behaviors of GC cells; on the contrast, these phenotypes were impeded by miR-27a-3p inhibition. Moreover, LINC01089 interacted with and repressed miR-27a-3p, and miR-27a-3p antagonized the impact of LINC01089 on GC cells. Additionally, TET1 was verified as a target gene of miR-27a-3p, and could be positively regulated by LINC01089. CONCLUSION: LINC01089 impedes the proliferation, migration, and invasion of GC cells by adsorbing miR-27a-3p and up-regulating the expression of TET1.	NA	Cancer Cell Int. 2020 Oct 16;20:507. doi: 10.1186/s12935-020-01561-9. eCollection 2020.
4261	LncRNA	LINC01089	miR-27a	SFRP1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33282723	LINC01089 Inhibits Tumorigenesis and Epithelial-Mesenchymal Transition of Non-small Cell Lung Cancer via the miR-27a/SFRP1/Wnt/β-catenin Axis.	Long noncoding RNAs (lncRNAs) have emerged as regulators of gene expression and play critical regulatory roles in diverse biological functions and diseases, including cancer. In this study, we report the downregulation of LINC01089 in non-small cell lung cancer (NSCLC) samples, relative to adjacent non-tumor tissues, and demonstrate its role in the inhibition of proliferation, migration, and epithelial-mesenchymal transition (EMT) of NSCLC cells. Mechanistic analysis indicates that LINC01089 acts as a sponge for miR-27a, regulating its expression in NSCLC. Interestingly, LINC01089 mediated the upregulation of SFRP1 expression by inhibiting the Wnt/β-catenin-EMT pathway and inhibiting the epithelial-mesenchymal transition of NSCLC via sponging miR-27a. Overall, our findings highlight LINC01089's tumorigenic role and regulatory mechanism in NSCLC, thereby suggesting its potential as a therapeutic target for managing NSCLC.	NA	Front Oncol. 2020 Nov 17;10:532581. doi: 10.3389/fonc.2020.532581. eCollection 2020.
4262	LncRNA	LINC01094	miR-577	NA	OC cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33069244	LINC01094/miR-577 axis regulates the progression of ovarian cancer.	BACKGROUND: Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, β-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. RESULTS: LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of β-catenin, c-Myc and cyclin D1 in OC cells. CONCLUSION: LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.	NA	J Ovarian Res. 2020 Oct 17;13(1):122. doi: 10.1186/s13048-020-00721-9.
4263	LncRNA	LINC01116	miR-9-5p	FOXP1	ectopic primary endometrial stromal cells	Endometriosis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;RNA sequencing;	33372387	LINC01116 promotes proliferation and migration of endometrial stromal cells by targeting FOXP1 via sponging miR-9-5p in endometriosis.	Endometriosis is a common multi-factorial gynaecological disease. Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of endometriosis. In the present study, the expression profiles of lncRNAs in 6 pairs of endometriosis ectopic endometrium (ecEM) and eutopic endometrium (euEM) tissues were analysed by RNA sequencing. From the profiles, LINC01116 was found to be up-regulated in ecEM tissues compared to euEM tissues and was verified by quantitative real-time PCR (qRT-PCR). Then, functional experiments demonstrated that LINC01116 promoted the proliferation and migration of ectopic primary endometrial stromal cells (ESCs), while miR-9-5p exerted the opposite effects. Dual-luciferase reporter assays verified that LINC01116 directly sponged miR-9-5p and relieved the suppression of its target, Forkhead box protein P1 (FOXP1). Rescue experiments further demonstrated that LINC01116 could promote proliferation and migration of ESCs by targeting FOXP1 via sponging miR-9-5p. Overall, our study illuminates that LINC01116 promotes the progression of endometriosis through the miR-9-5p/FOXP1 axis. This finding provides a novel therapeutic target for patients with endometriosis.	NA	J Cell Mol Med. 2021 Feb;25(4):2000-2012. doi: 10.1111/jcmm.16039. Epub 2020 Dec 28.
4264	LncRNA	LINC01123	miR-449b-5p	ZEB1	LUAD cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;	33191397	ZEB1-activated LINC01123 accelerates the malignancy in lung adenocarcinoma through NOTCH signaling pathway.	Growing incidence of lung adenocarcinoma (LUAD) has been detected recently. Multiple long non-coding RNAs (lncRNAs) have been proven as tumor facilitators or inhibitors by extensive works. Present study concentrated on characterizing the potential role of LINC01123 in LUAD. We explored the differential expression of LINC01123 through qRT-PCR and found the amplification of LINC01123 in LUAD cell lines. It was ascertained that LINC01123 was definitely responsible for the malignant processes of LUAD cells. Further, we validated the ceRNA network of LINC01123/miR-449b-5p/NOTCH1 in LUAD via mechanical experiments. As a transcriptional factor related to epithelial mesenchymal transition (EMT), ZEB1 was responsible for the transcriptional activation of both LINC01123 and NOTCH1. The involvement of NOTCH signaling in LUAD was interrogated through evaluating functional changes after treating with FLI-06 (NOTCH pathway suppressor). It showed that FLI-06-caused NOTCH signaling inactivation suppressed malignant functions in LUAD cells. Additionally, LINC01123 facilitated NOTCH1-dependent NOTCH signaling activation. Rescue experiments probed the modulatory function of LINC01123/miR-449b-5p/NOTCH1 in LUAD cellular processes. Altogether, ZEB1-activated LINC01123 accelerates the malignancy in LUAD through miR-449b-5p/NOTCH1 axis-mediated NOTCH signaling pathway, while NOTCH1 boosts ZEB1 in return. These observations suggest the huge potential of LINC01123 as a new target for LUAD therapy.	NA	Cell Death Dis. 2020 Nov 15;11(11):981. doi: 10.1038/s41419-020-03166-6.
4265	LncRNA	LINC01126	miR-518a-5p	HIF-1a	human periodontal ligament cells (hPDLCs)	Periodontitis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;microarray;MTT assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33231338	Long non-coding RNA 01126 promotes periodontitis pathogenesis of human periodontal ligament cells via miR-518a-5p/HIF-1α/MAPK pathway.	BACKGROUND: Periodontitis is a prevalent oral inflammatory disease, which can cause periodontal ligament to a local hypoxia environment. However, the mechanism of hypoxia associated long non-coding RNAs (lncRNAs) involved in periodontitis is still largely unknown. METHODS: Microarray was performed to detect the expression patterns of lncRNAs in 3 pairs of gingival tissues from patients with periodontitis and healthy controls. The expression of lncRNA 01126 (LINC01126), miR-518a-5p and hypoxia-inducible factor-1α (HIF-1α) in periodontal tissues and in human periodontal ligament cells (hPDLCs) under hypoxia was measured by quantitative real-time polymerase chain reaction or western blot. Fluorescence in situ hybridization and cell fraction assay were performed to determine the subcellular localization of LINC01126 and miR-518a-5p. Overexpression or knockdown of LINC01126 or HIF-1α was used to confirm their biological roles in hPDLCs. MTT assays were performed to evaluate hPDLCs proliferation ability. Flow cytometry was used to detect apoptosis. ELISA was used to measure the expression levels of interleukin (IL)-1β, IL-6, IL-8 and TNF-α. Dual-luciferase reporter assays were performed to assess the binding of miR-518a-5p to LINC01126 and HIF-1α. RNA immunoprecipitation assay was used to identify whether LINC01126 and miR-518a-5p were significantly enriched in AGO-containing micro-ribonucleoprotein complexes. RESULTS: We selected LINC01126, which was the most highly expressed lncRNA, to further verify its functions in periodontitis-induced hypoxia. The expression of LINC01126 was increased in periodontal tissues. In vitro experiment demonstrated that LINC01126 suppressed proliferation, promoted apoptosis and inflammation of hPDLCs under hypoxia via sponging miR-518a-5p. Moreover, we identified HIF-1α acted as a direct target of miR-518a-5p in hPDLCs and LINC01126 promoted periodontitis pathogenesis by regulating the miR-518a-5p/HIF-1α/MAPK pathway. CONCLUSION: LINC01126 promotes periodontitis pathogenesis of hPDLCs via miR-518a-5p/HIF-1α/MAPK pathway, providing a possible clue for LINC01126-based periodontal therapeutic approaches.	NA	Cell Prolif. 2021 Jan;54(1):e12957. doi: 10.1111/cpr.12957. Epub 2020 Nov 24.
4266	LncRNA	LINC01126	miR-518a-5p	MAPK	human periodontal ligament cells (hPDLCs)	Periodontitis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;microarray;MTT assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	33231338	Long non-coding RNA 01126 promotes periodontitis pathogenesis of human periodontal ligament cells via miR-518a-5p/HIF-1α/MAPK pathway.	BACKGROUND: Periodontitis is a prevalent oral inflammatory disease, which can cause periodontal ligament to a local hypoxia environment. However, the mechanism of hypoxia associated long non-coding RNAs (lncRNAs) involved in periodontitis is still largely unknown. METHODS: Microarray was performed to detect the expression patterns of lncRNAs in 3 pairs of gingival tissues from patients with periodontitis and healthy controls. The expression of lncRNA 01126 (LINC01126), miR-518a-5p and hypoxia-inducible factor-1α (HIF-1α) in periodontal tissues and in human periodontal ligament cells (hPDLCs) under hypoxia was measured by quantitative real-time polymerase chain reaction or western blot. Fluorescence in situ hybridization and cell fraction assay were performed to determine the subcellular localization of LINC01126 and miR-518a-5p. Overexpression or knockdown of LINC01126 or HIF-1α was used to confirm their biological roles in hPDLCs. MTT assays were performed to evaluate hPDLCs proliferation ability. Flow cytometry was used to detect apoptosis. ELISA was used to measure the expression levels of interleukin (IL)-1β, IL-6, IL-8 and TNF-α. Dual-luciferase reporter assays were performed to assess the binding of miR-518a-5p to LINC01126 and HIF-1α. RNA immunoprecipitation assay was used to identify whether LINC01126 and miR-518a-5p were significantly enriched in AGO-containing micro-ribonucleoprotein complexes. RESULTS: We selected LINC01126, which was the most highly expressed lncRNA, to further verify its functions in periodontitis-induced hypoxia. The expression of LINC01126 was increased in periodontal tissues. In vitro experiment demonstrated that LINC01126 suppressed proliferation, promoted apoptosis and inflammation of hPDLCs under hypoxia via sponging miR-518a-5p. Moreover, we identified HIF-1α acted as a direct target of miR-518a-5p in hPDLCs and LINC01126 promoted periodontitis pathogenesis by regulating the miR-518a-5p/HIF-1α/MAPK pathway. CONCLUSION: LINC01126 promotes periodontitis pathogenesis of hPDLCs via miR-518a-5p/HIF-1α/MAPK pathway, providing a possible clue for LINC01126-based periodontal therapeutic approaches.	NA	Cell Prolif. 2021 Jan;54(1):e12957. doi: 10.1111/cpr.12957. Epub 2020 Nov 24.
4267	LncRNA	LINC01128	miR-299-3p	MMP2	OS cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;Rescue assay;	33108067	LINC01128 regulates the development of osteosarcoma by sponging miR-299-3p to mediate MMP2 expression and activating Wnt/β-catenin signalling pathway.	Osteosarcoma (OS) is one of the most common metastatic bone cancers, which results in significant morbidity and mortality. The important role of long non-coding RNAs (lncRNAs) in the biological processes of OS has been demonstrated through several studies. In the current study, we evaluated the role of the lncRNA, LINC01128, in OS. We analysed the expression of LINC01128 in three OS gene expression omnibus (GEO) data sets GSE21257, GSE36001 and GSE42352. The expression of LINC01128 in OS tissues and matched non-tumour tissues obtained from 50 OS patients was detected using qRT-PCR. The association between LINC01128 expression and overall survival of OS patients was evaluated using the Kaplan-Meier method. The effects of LINC01128 knockdown and overexpression were evaluated through in vitro and in vivo assays. The LINC01128/miR-299-3p/ MMP2 axis was verified using dual-luciferase reporter assay and qRT-PCR assays. GEO data sets analysis revealed that the expression of LINC01128 was increased in OS. Elevated LINC01128 expression was accompanied by shorter overall survival in OS patients. Functional studies revealed that LINC01128 knockdown reduced the proliferation, migration and invasion of OS cells both in vitro and in vivo. Mechanistically, LINC01128 sponged miR-299-3p to increase MMP2 expression. Rescue assays determined the role of the LINC01128/miR-299-3p/MMP2 axis in the proliferation, migration and invasion of OS cells. Additionally, the Wnt/β-catenin signalling pathway was activated by LINC01128 and MMP2 in OS cell lines. In summary, this study demonstrates that LINC01128 facilitates OS by functioning as a sponge of miR-299-3p, thus promoting MMP2 expression and activating the Wnt/β-catenin signalling pathway.	NA	J Cell Mol Med. 2020 Dec;24(24):14293-14305. doi: 10.1111/jcmm.16046. Epub 2020 Oct 27.
4268	LncRNA	LINC01133	miR-30a-5p	NA	AC16 cell line	Ischemic Reperfusion Injury	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33175096	Sevoflurane protects cardiomyocytes against hypoxia/reperfusion injury via LINC01133/miR-30a-5p axis.	Previous studies failed to elucidate the detailed mechanisms of anesthetic preconditioning as a protective approach against ischemic/reperfusion (I/R) injury in cells. The present study mainly centered on discovering the mechanisms of Sevoflurane (Sev) in preventing cardiomyocytes against I/R injury. Human cardiomyocyte AC16 cell line was used to simulate I/R injury based on a hypoxia/reperfusion (H/R) model. After Sev treatment, cell viability and apoptosis were detected by MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) content was measured using an LDH Detection Kit. Relative mRNA and protein expressions of LINC01133, miR-30a-5p and apoptosis-related proteins were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. Target gene of miR-30a-5p and their potential binding sites were predicted using Starbase and confirmed by dual-luciferase reporter assay. Cell behaviors were assessed again after miR-30a-5p and LINC01133 transfection. Sev could improve cell viability, reduce LDH leakage, and down-regulate the expressions of apoptosis-related proteins (Bax, cleaved caspase-3 and cleaved caspase-9) and LINC01133 as well as up-regulate miR-30a-5p and Bcl-2 expressions in H/R cells. MiR-30a-5p was the target of LINC01133, and up-regulating miR-30a-5p enhanced the effects of Sev in H/R cells, with a suppression on H/R-induced activation of the p53 signaling pathway. However, up-regulating LINC01133 reversed the enhancing effects of miR-30a-5p on Sev pretreatment in H/R cells. Sev could protect cardiomyocytes against H/R injury through the miR-30a-5p/LINC01133 axis, which may provide a possible therapeutic method for curing cardiovascular I/R injury.	NA	Biosci Rep. 2020 Dec 23;40(12):BSR20200713. doi: 10.1042/BSR20200713.
4269	LncRNA	LINC01133	miR-30b-5p	Rab3D	RCC cells	Renal Cancer	Homo sapiens (human)	qRT-PCR	33054325	Long Noncoding RNA LINC01133 Promotes the Malignant Behaviors of Renal Cell Carcinoma by Regulating the miR-30b-5p/Rab3D Axis.	Renal cancer (RCC) is the most common type of kidney cancer with rising incidence. Long noncoding RNA (lncRNA) LINC01133 is a novel lncRNA that is involved in the development of several types of cancers. However, the role of LINC01133 in RCC has not been reported. Thus, in this study, we investigated the functions of LINC01133 in RCC. The qualitative real-time polymerase chain reaction analysis was performed to examine the levels of LINC01133 in RCC tissues and adjacent tissues, as well as RCC cell lines. The results showed that LINC01133 was highly expressed in RCC tissue specimens and cell lines. Downregulation of LINC01133 significantly inhibited the proliferation, migration, and invasion of RCC cells. Further mechanistic investigations proved that LINC01133 directly interacted with microRNA (miR)-30b-5p and regulated the miR-30b-5p expression in RCC cell lines. Moreover, miR-30b-5p exhibited tumor-suppressive activity in RCC cell lines, which was mediated by targeting Ras-related protein Rab-3D (Rab3D). In vivo study showed that LINC01133 knockdown suppressed tumor growth in the nude mice. Taken together, these findings indicated that LINC01133 might be an oncogene in RCC through regulation of the miR-30b-5p/Rab3D axis. Thus, LINC01133 might serve as a potential therapeutic target for the treatment of RCC.	NA	Cell Transplant. 2020 Jan-Dec;29:963689720964413. doi: 10.1177/0963689720964413.
4270	LncRNA	LINC01133	miR-495-3p	TPD52	epithelial ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33036757	LINC01133 contribute to epithelial ovarian cancer metastasis by regulating miR-495-3p/TPD52 axis.	Currently, there is increasing evidence that long noncoding RNAs (lncRNAs) initiate and promote the progression of epithelial ovarian cancer (EOC). In this study, we revealed the roles and the potential mechanisms of long intergenic non-protein coding RNA 1133 (LINC01133) in EOC, which remains not well understood. We found that LINC01133 was upregulated in EOC tissues and cell lines. Besides, it was associated with the clinicopathological feature of metastasis. Functional experiments demonstrated that LINC01133 could facilitate cancer cell migration and invasion in vitro and tumor metastasis in vivo. Further molecular mechanisms studies indicated that LINC01133 and miR-495-3p reciprocally repressed expression of each other. We also realized that LINC01133 shared the same binding sites for miR-495-3p with tumor protein D52 (TPD52). We confirmed that TPD52 functioned as a direct target of miR-495-3p and mediated the enhancing effect of LINC01133 on cancer metastasis. Generally, our study showed that LINC01133 interacted with miR-495-3p to promote metastasis in EOC by regulating TPD52. LINC01133 also provided a potential therapeutic perspective for future clinical treatment.	NA	Biochem Biophys Res Commun. 2020 Dec 17;533(4):1088-1094. doi: 10.1016/j.bbrc.2020.09.074. Epub 2020 Oct 6.
4271	LncRNA	LINC01152	miR-466	MAML2	GBM tissues and cells	Glioblastoma	Homo sapiens (human)	ChIP;qRT-PCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33483471	LINC01152 upregulates MAML2 expression to modulate the progression of glioblastoma multiforme via Notch signaling pathway.	Glioblastoma multiforme (GBM) brings serious physical and psychological pain to GBM patients, whose survival rate remains not optimistic. Long noncoding RNAs (lncRNAs) have been reported to participate in the progression of many cancers, including GBM. However, the mechanism and function of long intergenic non-protein coding RNA 1152 (LINC01152) in GBM are still unclear. In our study, we aimed to explore the function and mechanism of LINC01152 in GBM. Then qRT-PCR analysis was implemented to search the expression of RNAs in GBM tissues and cells. Functional assays such as EdU assay, colony formation assay, TUNEL assay and flow cytometry analysis were conducted to estimate GBM cell proliferation and apoptosis. RNA pull down assay, luciferase reporter assay, RIP and ChIP assays were implemented to search the binding between molecules. As a result, we discovered that LINC01152 was upregulated in GBM tissues and cells. LINC01152 and mastermind like transcriptional coactivator 2 (MAML2) could both play the oncogenic part in GBM. Moreover, LINC01152 positively regulated MAML2 in GBM by sponging miR-466 and recruiting SRSF1. In turn, RBPJ/MAML2 transcription complex was found to activate the transcription of LINC01152 in GBM cells. In conclusion, LINC01152 could upregulate the expression of MAML2 to promote tumorigenesis in GBM via Notch signaling pathway.	NA	Cell Death Dis. 2021 Jan 22;12(1):115. doi: 10.1038/s41419-020-03163-9.
4272	LncRNA	LINC01189	miR-155-5p	NA	HCC cells	Hcv-Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33059056	Long noncoding RNA LINC01189 is associated with HCV-hepatocellular carcinoma and regulates cancer cell proliferation and chemoresistance through hsa-miR-155-5p.	INTRODUCTION AND OBJECTIVES: Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) may be closely associated with Hepatitis C virus (HCV) infection and the development of hepatocellular carcinoma (HCC). In this study, we investigated the expression and functions of a lncRNA, LINC01189, in HCV-associated HCC. PATIENTS OR MATERIALS AND METHODS: LINC01189 expression was measured in HCC tumors, HCV-infected HCC tumors and HCV-infected HCC cells. LINC01189 was overexpressed in HCV-infected HepG2 cells to measure its function on HCV-correlated cancer proliferation. In HCC cell lines of Huh7 and Hep3B, LINC01189 was upregulated to investigate its effects on cancer cell proliferation and 5-FU chemoresistance. The competing endogenous RNA (ceRNA) target of LINC01189, human microRNA-155-5p (hsa-miR-155-5p) was probed by dual-luciferase assay and qRT-PCR. Hsa-miR-155-5p was upregulated in LINC01189-overexpessed Huh7 and Hep3B cells to investigate their epigenetic correlation on HCC development regulation. RESULTS: LINC01189 is downregulated in HCV-infected HCC tumors and cell lines. LINC01189 overexpression inhibited HCC cancer cell proliferation and 5-FU chemoresistance. Hsa-miR-155-5p was confirmed to be a ceRNA target of LINC01189 in HCC. Upregulating hsa-miR-155-5p reversed the LINC01189-mediated inhibition on HCC proliferation and 5-FU chemoresistance. CONCLUSIONS: LINC01189 downregulation is associated with HCV infection in HCC, and it has tumor-suppressing effects on HCC development through hsa-miR-155-5p.	NA	Ann Hepatol. 2021 May-Jun;22:100269. doi: 10.1016/j.aohep.2020.09.013. Epub 2020 Oct 12.
4273	LncRNA	LINC01207	miR-3125	TRIM22	SW480 and HT-29 cells	Colon Cancer	Homo sapiens (human)	Rescue assay;	33299853	Long Noncoding RNA LINC01207 Promotes Colon Cancer Cell Proliferation and Invasion by Regulating miR-3125/TRIM22 Axis.	Increasing study has validated that long noncoding RNAs (lncRNAs) are involved in the growth and metastasis of colon cancer. LINC01207 has been reported to play vital roles in certain types of cancer, while the precise function of LINC01207 in the progression of colon cancer remains unclear. The objective of this study was to investigate the effect of LINC01207 on the growth and metastasis of colon cancer cells and to explore the underlying mechanism. We found that the expression of LINC01207 was significantly upregulated in colon adenocarcinoma tissues compared with normal tissues by the GEPIA database. Notably, silencing of LINC01207 significantly suppressed the proliferation, migration, and invasion abilities of SW480 and HT-29 cells. Mechanistically, our data demonstrated that LINC01207 could sponge miR-3125 in colon cancer cells. Moreover, miR-3125 could directly target TRIM22 and negatively regulate its expression. Rescue assays revealed that miR-3125 inhibitor or TRIM22 overexpression significantly reversed the repressive role of LINC01207 knockdown in colon cancer cell proliferation and invasion. In conclusion, LINC01207 exerts an oncogenic role in the progression of colon cancer by absorbing miR-3125 to modulating TRIM22 expression.	NA	Biomed Res Int. 2020 Nov 22;2020:1216325. doi: 10.1155/2020/1216325. eCollection 2020.
4274	LncRNA	LINC01278	miR-134-5p	KDM2A	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33155208	LncRNA LINC01278 accelerates colorectal cancer progression via miR-134-5p/KDM2A axis.	OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including colorectal cancer (CRC). Nevertheless, the regulatory mechanisms of LINC01278 in CRC remain unknown. Our research aims to identify the regulatory mechanisms of LINC01278 in CRC. PATIENTS AND METHODS: The expression of LINC01278 was examined by quantitative real-time polymerase chain reaction (RT-qPCR). StarBase and TargetScan websites were used to predict the interaction between miR-134 and LINC01278 or KDM2A, which was further confirmed by Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell viability, migration, and invasion were detected by Cell Counting Kit-8 (CCK-8) and transwell assays. RESULTS: LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression. In addition, LINC01278 inhibited miR-134 expression by direct interaction, and the inhibition of miR-134 abolished the suppressive effects of LINC01278 knockdown on viability, migration, and invasion of CRC cells. Furthermore, KDM2A was confirmed to be a target gene of miR-134. Overexpression of KDM2A facilitated the tumorigenesis of CRC, while this effect was reversed by the upregulation of miR-143. Finally, it was demonstrated that miR-134 inhibitor reversed the shLINC01278-mediated inhibitory effect on KDM2A expression. CONCLUSIONS: Our study demonstrated that LINC01278 upregulated KDM2A to promote CRC progression by interacting with miR-143, suggesting that LINC01278 might be a new therapeutic target of CRC.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10526-10534. doi: 10.26355/eurrev_202010_23405.
4275	LncRNA	LINC01305	miR-129-5p	Sox4	Hela and SiHa cells	Cervical Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33312390	LINC01305 inhibits malignant progression of cervical cancer via miR-129-5p/Sox4 axis.	BACKGROUND: The association between LINC01305, a newly discovered long non-coding RNA (lncRNA), and cervical cancer (CC) has been poorly analyzed. In the present study, we revealed high expression of LINC01305 in CC by the cancer genome atlas (TCGA) and Gene Expression Omnibus (GEO), and dissected the related mechanisms. METHODS: LINC01305, microRNA (miR) -129-5p and SRY-related high-mobility group box 4 (Sox4) mRNA levels were quantitated by quantitative reverse transcription-PCRy qRT-PCR). CC tissues and cell lines and corresponding controls were enrolled for the quantification of LINC01305 expression in CC. Effects of LINC01305 and miR-129-5p on cell proliferation, metastasis, and apoptosis were evaluated by MTT, colony formation, wound healing, Transwell and flow cytometry assays. Sox4 protein levels were tested by Western blot (WB). Bioinformatics analysis, RNA immunoprecipitation (RIP), RNA pull-down and dual-luciferase reporter (DLR) assay were performed to determine molecular mechanisms of LINC01305 in CC. Xenograft models of CC were constructed to evaluate the role of LINC01305 in vivo. RESULTS: The expression of LINC01305 was evidently elevated in CC tissues and cell lines than that in controls and associated with clinicopathological features. Downregulating LINC01305 suppressed malignant phenotypes (proliferation, migration, invasion) of Hela and SiHa cells. In addition, silencing miR-129-5p by its inhibitor eliminated the inhibition of growth and metastasis induced by LINC01305 siRNA. Sox4 might serve as a direct target for miR-129-5p and was negatively regulated by miR-129-5p and LINC01305. CONCLUSION: LINC01305 acts as a competitive endogenous RNA (ceRNA) and regulates Sox4 via sponging miR-129-5p, contributing to the diagnosis and treatment of CC.	NA	Am J Transl Res. 2020 Nov 15;12(11):7581-7592. eCollection 2020.
4276	LncRNA	LINC01315	miR-205-3p	PRKAA1	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33162032	LINC01315 silencing inhibits the aggressive phenotypes of colorectal carcinoma by sponging miR-205-3p.	Long non-coding RNAs (lncRNAs) are important regulatory factors in the progression of cancers. In this study, we investigated the molecular mechanism of long intergenic non-coding 01315 (LINC01315) in inhibiting the aggressive characteristics of colorectal carcinoma (CRC) cells. We proved that LINC01315 was significantly upregulated in CRC. Knockdown of LINC01315 decreased CRC cell growth and invasion in vitro. Bioinformatics analysis and a luciferase reporter experiment showed direct binding between LINC01315 and miR-205-3p. Furthermore, LINC01315 positively modulated protein kinase AMP-activated catalytic subunit α 1 (PRKAA1) expression by serving as a "sponge" for miR-205-3p. Moreover, LINC01315 regulated the growth and invasive phenotypes of CRC cells by sponging miR-205-3p. Downregulation of LINC01315 remarkedly impaired the tumorigenicity of CRC cells in vivo in a transplanted tumour model. Altogether, our results demonstrated that downregulation of LINC01315 suppresses CRC progression by sponging miR-205-3p.	NA	Biochem Biophys Res Commun. 2021 Jan 1;534:1033-1039. doi: 10.1016/j.bbrc.2020.10.041. Epub 2020 Nov 6.
4277	LncRNA	LINC01426	miR-519d-5p	ETS1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33335425	Long Noncoding RNA LINC01426 Sequesters microRNA-519d-5p to Promote Non-Small Cell Lung Cancer Progression by Increasing ETS1 Expression.	PURPOSE: Recent studies have identified important roles for long intergenic non-protein coding RNA 1426 (LINC01426) in glioma and clear cell renal cell carcinoma. The present study evaluated the expression profile of LINC01426 in non-small cell lung cancer (NSCLC) tissues and cell lines. Furthermore, the function of LINC01426 in NSCLC and the molecular mechanisms involved were extensively studied. METHODS: The abundance of LINC01426 in NSCLC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. The cell counting kit-8 assay, flow cytometry, transwell experiments for migration and invasion, and xenograft tumor model were used to assess the function of LINC01426 in NSCLC cells. Mechanistic studies were performed using the luciferase reporter assay and RNA immunoprecipitation. RESULTS: Significant LINC01426 upregulation was observed in NSCLC tissues and cell lines. Silencing LINC01426 inhibited proliferation, migration, and invasion of NSCLC cells and facilitated cell apoptosis in vitro. Furthermore, interference of LINC01426 restricted tumor growth of NSCLC cells in vivo. In addition, LINC01426 showed the ability to directly bind to microRNA-519d-5p (miR-519d-5p) and act as a molecular sponge for miR-519d-5p in NSCLC cells. Furthermore, the ETS proto-oncogene 1 (ETS1) was identified as a direct target of miR-519d-5p and LINC01426 could indirectly upregulate ETS1 expression by sponging miR-519d-5p. Moreover, the cancer-inhibiting activities of LINC01426 knockdown in NSCLC cells were partially offset by miR-519d-5p inhibition. CONCLUSION: LINC01426 increases ETS1 expression by sequestering miR-519d-5p, thereby aggravating the malignant progression of NSCLC. The LINC01426/miR-519d-5p/ETS1 competing endogenous RNA pathway may provide a target for designing therapeutic agents for NSCLC treatment.	NA	Cancer Manag Res. 2020 Dec 10;12:12697-12708. doi: 10.2147/CMAR.S277113. eCollection 2020.
4278	LncRNA	LINC01503	miR-133a-5p	VIM	Gastric Cardia Adenocarcinoma cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Luciferase reporter assay;	33200343	Long Non-coding RNA LINC01503 Promotes Gastric Cardia Adenocarcinoma Progression via miR-133a-5p/VIM Axis and EMT Process.	BACKGROUND: LINC01503 has been reported to act as a candidate oncogenic lncRNA in several types of human cancer. However, the functions and underlying mechanisms of LINC01503 in gastric cardia adenocarcinoma (GCA) remain unclear. AIMS: To investigate the roles and underlying mechanisms of LINC01503 in GCA progression. MATERIALS AND METHODS: Gene expressions were detected by quantitative real-time PCR (qRT-PCR). Gain-of-function assays were performed to evaluate the function of LINC01503 in gastric cancer cells. Bioinformatics analysis, luciferase reporter assay, and RIP assay were performed to identify associations among LINC01503, miR-133a-5p, and VIM. RESULTS: The expression level of LINC01503 was significantly elevated in GCA tissues and cell lines. High expression of LINC01503 was correlated with lymph node metastasis, TNM stage, and poor prognosis of GCA patients. Knockdown of LINC01503 significantly reduced proliferation, migration, and invasion ability in GC cells. LINC01503 might function as a competing endogenous RNA (ceRNA) via sponging miR-133a-5p to upregulate the expression of VIM. Furthermore, overexpression of LINC01503 promoted the progression of epithelial mesenchymal transition (EMT) in vitro. CONCLUSION: LINC01503 serves as an oncogenic lncRNA to promote GCA progression via affecting LINC01503/miR-133a-5p/VIM axis and EMT process. LINC01503 not only has a critical role in GCA progression but also provide a novel potential biomarker in predicting prognosis for GCA patients.	NA	Dig Dis Sci. 2020 Nov 17. doi: 10.1007/s10620-020-06690-9.
4279	LncRNA	LINC01572	miR-497-5p	ATG14	GC cells	Gastric Cancer	Homo sapiens (human)	qPCR;	33149605	LINC01572 Regulates Cisplatin Resistance in Gastric Cancer Cells by Mediating miR-497-5p.	BACKGROUND: Chemotherapy resistance has long been recognized as a major obstacle to cancer treatment. Therefore, elucidating the underlying mechanisms of chemotherapy resistance is conducive to developing new strategies to improve patients' response to chemotherapy drugs. MATERIALS AND METHODS: Real-time quantitative PCR (QPCR) was applied to measure the expression levels of lncRNAs. LINC01572 was down-regulated or up-regulated in GC cells transfected with either LINC01572 shRNA or overexpression vectors. In vitro and in vivo experiments were conducted to investigate the role of LINC01572 in autophagy-related chemotherapy resistance. RESULTS: Compared with the parental cells, drug-resistant GC cells had a higher level of LINC01572. Silencing of LINC01572 inhibited chemotherapy-induced autophagy, while its knockout sensitized GC cells against chemotherapy drugs. As a competitive endogenous RNA of miR-497-5p, LINC01572 weakened the inhibitory effect of miR-497-5p on ATG14, leading to chemically induced autophagy and chemotherapy resistance in GC cells. CONCLUSION: A new mechanism of GC autophagy-related chemotherapy resistance regulated by lncRNA was explored in this study, providing a new perspective for understanding chemotherapy resistance.	NA	Onco Targets Ther. 2020 Oct 27;13:10877-10887. doi: 10.2147/OTT.S267915. eCollection 2020.
4280	LncRNA	LINC01667	miR-138-5p	Cyclin-E1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;	33390953	Bruceine D inhibits Cell Proliferation Through Downregulating LINC01667/MicroRNA-138-5p/Cyclin E1 Axis in Gastric Cancer.	Objective: Gastric cancer is one of the most common malignant tumors. Bruceine D (BD) is one of the extracts of Brucea javanica. In recent years, it has been reported that BD has anti-tumor activity in some human cancers through different mechanisms. Here, this study try to explore the effect of BD on gastric cancer and its regulatory mechanism. Methods: Cell proliferation ability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays, 5-bromo-2-deoxyuridine (BrdU) staining and soft agar colony formation assay, respectively. The tumor xenograft model was used to verify the effect of BD on the tumorigenicity of gastric cancer cells in vivo. Flow cytometry analysis and Western blot assay were performed to detect cell cycle and apoptosis. Gastric cancer cells were analyzed by transcriptome sequencing. The interaction between LINC01667, microRNA-138-5p (miR-138-5p) and Cyclin E1 was verified by dual luciferase experiment and RT-PCR assays. Results: We found that BD significantly inhibited cell proliferation and induced cell cycle arrest at S phase in gastric cancer cells. Transcriptome analysis found that the expression of a long non-coding RNA, LINC01667, were significantly down-regulated after BD treatment. Mechanically, it was discovered that LINC01667 upregulated the expression of Cyclin E1 by sponging miR-138-5p. Furthermore, BD enhanced the chemosensitivity of gastric cancer cells to doxorubicin, a clinically used anti-cancer agent. Conclusion: BD inhibit the growth of gastric cancer cells by downregulating the LINC01667/miR-138-5p/Cyclin E1 axis. In addition, BD enhances the chemosensitivity of gastric cancer cells to doxorubicin. This study indicates that BD may be used as a candidate drug for the treatment of patients with gastric cancer.	NA	Front Pharmacol. 2020 Nov 24;11:584960. doi: 10.3389/fphar.2020.584960. eCollection 2020.
4281	LncRNA	Linc01833	miR-519e-3p	S100A4	LC cells	Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;Rescue assay;	33173348	The Long Noncoding RNA Linc01833 Enhances Lung Adenocarcinoma Progression via MiR-519e-3p/S100A4 Axis.	INTRODUCTION: Lung cancer (LC) is among the most prevalent malignancies worldwide, with extremely high morbidity and mortality rates. Mounting evidence has suggested that the abnormally expressed long noncoding RNA (lncRNA) in lung cancer tissues may play vital roles in tumor progression. In the present research, we aimed to examine the functions and underlying mechanism of linc01833 in lung adenocarcinoma (LUAD). METHODS: qRT-PCR was employed to determine transfection efficiency. CCK-8, transwell invasion assay, Western blotting analysis and qRT-PCR were used to detect proliferation as well as migration of different LUAD cell lines, and were also applied to determine the changes during epithelial-mesenchymal transformation (EMT). Afterwards, bioinformatics and dual-luciferase reporter assay were utilized to explore and to identify the potential corresponding targets of linc01833 and miR-519e-3p. RESULTS: Linc01833 OE can significantly improve proliferation as well as invasion ability of LC cells and promote the EMT process. Dual-luciferase reporter assay demonstrated that linc01833 could directly bind to miR-519e-3p, thereby inhibiting its expression. Further experiments showed that S100A4 was a direct target of miR-519e-3p. Rescue assay demonstrated that linc01833 acted on the miR-519e-3p/S100A4 axis. CONCLUSION: We verified the mechanism of linc01833 in promoting infiltration and metastasis in LUAD. To be specific, linc01833 can function as a competitive endogenous RNA (ceRNA) to adsorb miR-519e-3p through a sponge and regulate S100A4 in lung cancer, thereby being involved in LUAD progression. Collectively, our research provides new insights towards the in-depth understanding of LC progression mechanisms.	NA	Cancer Manag Res. 2020 Nov 3;12:11157-11167. doi: 10.2147/CMAR.S279623. eCollection 2020.
4282	LncRNA	LINC02418	miR-34b-5p	BCL2	HCT116 and LoVo cells	Colorectal Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;luciferase assay;	32973404	LINC02418 promotes colon cancer progression by suppressing apoptosis via interaction with miR-34b-5p/BCL2 axis.	BACKGROUND: LncRNAs act as functional regulators in tumor progression through interacting with various signaling pathways in multiple types of cancer. However, the effect of LINC02418 on colorectal cancer (CRC) progression and the underling mechanisms remain unclear. METHODS: LncRNA expression profile in CRC tissues was investigated by the TCGA database. The expressional level of LINC02418 in CRC patients was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Kaplan-Meier analyses was used to investigate the correlation between LINC02418 and overall survival (OS) of CRC patients. Cell proliferative, migratory and invasive abilities were detected by CCK-8 assays, colony formation assays and trans-well assays in HCT116 and LoVo cells which were stably transduced with sh-LINC02418 or sh-NC. The binding between LINC02418 and miR-34b-5p, and the interaction between miR-34b-5p and BCL2 were determined by dual-luciferase assays. Western blot experiments were conducted to further explore the effect of miR-34b-5p on BCL2 signaling pathway. Rescue experiments were performed to uncover the role of LINC02418/miR-34b-5p/BCL2 axis in CRC progression. RESULTS: LINC02418 was upregulated in human colon cancer samples when compared with adjacent tissue, and its high expressional level correlated with poor prognosis of CRC patients. LINC02418 promoted cancer progression by enhancing tumor growth, cell mobility and invasiveness of colon cancer cells. Additionally, LINC02418 could physically bind to miR-34b-5p and subsequently affect BCL2 signaling pathway. Down-regulation of LINC02418 reduced cell proliferation, while transfection of miR-34b-5p inhibitor or BCL2 into LINC02418-silenced CRC cells significantly promoted CRC cells growth. CONCLUSIONS: LINC02418 was upregulated in human CRC samples and could be used as the indicator for prediction of prognosis. LINC02418 acted as a tumor driver by negatively regulating cell apoptosis through LINC02418/miR-34b-5p/BCL2 axis in CRC.	NA	Cancer Cell Int. 2020 Sep 22;20:460. doi: 10.1186/s12935-020-01530-2. eCollection 2020.
4283	LncRNA	LINC02747	miR-608	TFE3	ccRCC cells	Clear Cell Renal Cancer	Homo sapiens (human)	qRT-PCR	33425728	Long Non-Coding RNA LINC02747 Promotes the Proliferation of Clear Cell Renal Cell Carcinoma by Inhibiting miR-608 and Activating TFE3.	With the rapid development of biotechnology, long noncoding RNAs (lncRNAs) have exhibited good application prospects in the treatment of cancer, and they may become new treatment targets for cancer. This study aimed to explore lncRNAs in clear cell renal cell carcinoma (ccRCC). Differentially expressed lncRNAs in 54 pairs of ccRCC tissues and para-carcinoma tissues were analyzed in The Cancer Genome Atlas (TCGA), and the most significant lncRNAs were selected and verified in ccRCC tissues. We found that lncRNA LINC02747 was highly expressed in ccRCC (P < 0.001) and was closely related to high TNM stage (P = 0.006) and histological grade (P = 0.004) and poor prognosis of patients (P < 0.001). In vivo and in vitro experiments confirmed that LINC02747 could promote the proliferation of ccRCC cells. We also found that LINC02747 regulated the proliferation of RCC cells by adsorbing miR-608. Subsequent mechanistic research showed that miR-608 is downregulated in ccRCC (P < 0.001), and overexpression of miR-608 inbibited the proliferation of RCC cells. Moreover, we found that TFE3 is a direct target gene of miR-608. MiR-608 regulated the proliferation of RCC cells by inhibiting TFE3. In conclusion, LINC02747 upregulates the expression of TFE3 by adsorbing miR-608, ultimately promoting the proliferation of ccRCC cells. The above findings indicate that LINC02747 acts as an oncogene in ccRCC and may be developed as a molecular marker for the diagnosis and prognosis of ccRCC. The LINC02747/miR-608/TFE3 pathway may become a new therapeutic target for ccRCC.	NA	Front Oncol. 2020 Dec 23;10:573789. doi: 10.3389/fonc.2020.573789. eCollection 2020.
4284	LncRNA	linc-FAM138B	miR-765	NA	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33401249	Exosomal linc-FAM138B from cancer cells alleviates hepatocellular carcinoma progression via regulating miR-765.	Exosomes are small vesicles with a diameter of 30-150 nm secreted by cells, which can be used as signal carriers to transfer nucleic acids, proteins, lipids and other functional substances to the recipient cells and play a role in cell communication. Hepatocellular carcinoma is the fourth most common cause of cancer-related death worldwide. Studies have shown that long non-coding RNAs (lncRNAs) are involved in the development and progression of many types of tumors. Our present study found that linc-FAM138B was reduced in HCC tissues and cell lines, low expression of linc-FAM138B indicated a poor prognosis in HCC patients. Interestingly, linc-FAM138B could be packaged into cancer cells. And exo-FAM138B inhibited the proliferation, migration and invasion of HCC cells. Furthermore, linc-FAM138B sponged miR-765 levels. And exo-si-FAM138B promoted HCC progression, while deletion of miR-765 reversed the role of exo-si-FAM138B. In vivo tumorigenesis experiments showed that exo-FAM138B suppressed HCC growth via modulating miR-765. In conclusion, exo-linc-FAM138B secreted by cancer cells inhibited HCC development via targeting miR-765, which provided a new idea and perspective for in-depth understanding of the complex signal regulation in HCC process.	NA	Aging (Albany NY). 2020 Dec 26;12(24):26236-26247. doi: 10.18632/aging.202430. Epub 2020 Dec 26.
4285	LncRNA	LINC-P21	miR-766-3p	NR3C2	INS-1 cells	Type 2 Diabetes Mellitus	Homo sapiens (human)	ELISA;	33007789	Elevated Circulating LINC-P21 Serves as a Diagnostic Biomarker of Type 2 Diabetes Mellitus and Regulates Pancreatic β-cell Function by Sponging miR-766-3p to Upregulate NR3C2.	OBJECTIVE: The purpose of this study was to evaluate the clinical value and biological function of long non-coding RNA (lncRNA) LINC-P21 in type 2 diabetes mellitus (T2DM), and explore the underlying mechanisms. METHODS: The expression of LINC-P21 was estimated using quantitative real-time PCR. The functional role of LINC-P21 was explored by gain- and loss-of-function experiments. INS-1 cell proliferation was analyzed using a cell counting kit-8 (CCK-8)assay, and the glucose-stimulated insulin secretion was measured using an ELISA kit. The miRNAs that might be sponged by LINC-P21 were analyzed, and the subsequent target genes were predicted and assessed in INS-1 cells. RESULTS: Serum expression of LINC-P21 was elevated in T2DM patients, which was correlated with fasting blood glucose levels and disease diagnosis. The glucose-stimulated insulin secretion and the proliferation of INS-1 cells were enhanced by LINC-P21 knockdown, but the overexpression of LINC-P21 led to opposite effects. miR-766-3p could be directly inhibited by LINC-P21 in INS-1 cells and reverse the effects of LINC-P21 on β-cell function. Additionally, NR3C2 was determined as a target of miR-766-3p, which could be positively regulated by LINC-P21 and had same effects with LINC-P21 on INS-1 cell proliferation and insulin secretion. CONCLUSION: All the data demonstrated that serum elevated LINC-P21 and decreased miR-766-3p serve as candidate diagnostic biomarkers in T2DM patients. LINC-P21 acts as a potential regulator in insulin secretion and proliferation of pancreatic β-cells through targeting miR-766-3p to upregulate NR3C2.	NA	Exp Clin Endocrinol Diabetes. 2020 Oct 2. doi: 10.1055/a-1247-4978.
4286	LncRNA	LincRNA-p21	miR-17-5p	SIRT7	Peripheral blood	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33169349	p53-Dependent LincRNA-p21 Protects Against Proliferation and Anti-apoptosis of Vascular Smooth Muscle Cells in Atherosclerosis by Upregulating SIRT7 via MicroRNA-17-5p.	This study investigated the functional role of p53-lincRNA-p21 in atherosclerosis (AS) by mediating the microRNA-17-5p (miR-17-5p)/SIRT7 axis. Peripheral blood was collected from AS patients, and an ApoE(-/-) mouse model of AS (AS-M) was induced by high-fat diet. The relationship among p53, lincRNA-p21, miR-17-5p, and SIRT7 was validated, and their effects on AS progression and vascular smooth muscle cell (VSMC) functions were analyzed using gain- and loss-of-function experiments in AS mice and human and mouse VSMCs. p53, lincRNA-p21, and SIRT7 were downregulated, and miR-17-5p was upregulated in AS-M and peripheral blood of AS patients. p53 positively regulated lincRNA-p21, while miR-17-5p, reversely targeted by lincRNA-p21, could target SIRT7. Overexpressing p53, lincRNA-p21, or SIRT7 contributed to impaired proliferation and promoted apoptosis of VSMCs in vitro as well as reducing the vulnerable plaque and lipid accumulation in AS mice. Collectively, p53-dependent lincRNA-p21 expression downregulated miR-17-5p, which consequently protecting against AS progression via SIRT7 elevation. Graphical abstract Collectively, p53-dependent lincRNA-p21 expression downregulated miR-17-5p, whichconsequently protecting against AS progression via SIRT7 elevation.	NA	J Cardiovasc Transl Res. 2020 Nov 9. doi: 10.1007/s12265-020-10074-9.
4287	LncRNA	LincRNA-p21	miR-17-5p	SIRT7	Peripheral blood	Atherosclerosis	Mus musculus (mouse)	qRT-PCR	33169349	p53-Dependent LincRNA-p21 Protects Against Proliferation and Anti-apoptosis of Vascular Smooth Muscle Cells in Atherosclerosis by Upregulating SIRT7 via MicroRNA-17-5p.	This study investigated the functional role of p53-lincRNA-p21 in atherosclerosis (AS) by mediating the microRNA-17-5p (miR-17-5p)/SIRT7 axis. Peripheral blood was collected from AS patients, and an ApoE(-/-) mouse model of AS (AS-M) was induced by high-fat diet. The relationship among p53, lincRNA-p21, miR-17-5p, and SIRT7 was validated, and their effects on AS progression and vascular smooth muscle cell (VSMC) functions were analyzed using gain- and loss-of-function experiments in AS mice and human and mouse VSMCs. p53, lincRNA-p21, and SIRT7 were downregulated, and miR-17-5p was upregulated in AS-M and peripheral blood of AS patients. p53 positively regulated lincRNA-p21, while miR-17-5p, reversely targeted by lincRNA-p21, could target SIRT7. Overexpressing p53, lincRNA-p21, or SIRT7 contributed to impaired proliferation and promoted apoptosis of VSMCs in vitro as well as reducing the vulnerable plaque and lipid accumulation in AS mice. Collectively, p53-dependent lincRNA-p21 expression downregulated miR-17-5p, which consequently protecting against AS progression via SIRT7 elevation. Graphical abstract Collectively, p53-dependent lincRNA-p21 expression downregulated miR-17-5p, whichconsequently protecting against AS progression via SIRT7 elevation.	NA	J Cardiovasc Transl Res. 2020 Nov 9. doi: 10.1007/s12265-020-10074-9.
4288	LncRNA	Lnc712	miR-142-3p	Bach-1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	CCK-8 assay;Flow cytometry assay;Flow Cytometry assay;	33177878	LncRNA Lnc712 Promotes Tumorigenesis in Hepatocellular Carcinoma by Targeting miR-142-3p/Bach-1 Axis.	BACKGROUND: It is known that Lnc712 plays an important role in the pathogenesis of breast cancer. However, whether it is involved in hepatocellular carcinoma (HCC) remains unknown. In this study, we aimed to investigate the role and underlying mechanism of Lnc712 in HCC. METHODS: Sixty-four HCC patients were enrolled and followed up for 5 years to analyze the prognostic value of Lnc712 for HCC. HCC cells were transfected with Lnc712 expression vector, Bach-1 expression vector (or siRNA) and miR-142-3p mimic (or inhibitor) to explore the interactions among Lnc712, miR-142-3p and Bach-1. Cell proliferation, migration, invasion and cell cycle were analyzed by CCK-8 assay, transwell assay, wound healing assay and flow cytometry assay, respectively. RESULTS: The expression of Lnc712 was upregulated in HCC, and the upregulated Lnc712 expression was significantly related to poor overall survival in HCC patients. In HCC cells, Lnc712 interacted with miR-142-3p and upregulated Bach-1, a target of miR-142-3p. In addition, Lnc712 promoted HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by miR-142-3p mimic. Moreover, miR-142-3p mimic enhanced HCC cell proliferation, migration, invasion and cell cycle, while its effects were abolished by Bach-1 overexpression. miR-142-3p inhibitor repressed cell proliferation, migration, invasion and cell cycle in HCC cells, while its effects were abolished by Bach-1 knockdown. Furthermore, Lnc712 knockdown remarkably inhibited HCC tumor growth in nude mice. CONCLUSION: Lnc712 may promote the development of HCC by targeting the miR-142-3p/Bach-1 axis.	NA	Cancer Manag Res. 2020 Nov 5;12:11285-11294. doi: 10.2147/CMAR.S254950. eCollection 2020.
4289	LncRNA	lncGALM	miR-200	ZEB1	GBC cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR	33252861	Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1β-dependent liver arrest and tumor extravasation.	BACKGROUND: Long noncoding RNAs (lncRNA) represent significant factors of the mammalian transcriptome that mediates varied biological and pathological processes. The liver is the most common site for gallbladder cancer (GBC) distant metastasis and contributes to the majority of GBC-related death. How lncRNA affects GBC metastasis is not completely understood. RESULTS: A novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1β mRNA and stabilized the IL-1β gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis. lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. CONCLUSIONS: lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.	NA	Clin Transl Med. 2020 Nov;10(7):e201. doi: 10.1002/ctm2.201.
4290	LncRNA	lncGALM	miR-200	ZEB2	GBC cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR	33252861	Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1β-dependent liver arrest and tumor extravasation.	BACKGROUND: Long noncoding RNAs (lncRNA) represent significant factors of the mammalian transcriptome that mediates varied biological and pathological processes. The liver is the most common site for gallbladder cancer (GBC) distant metastasis and contributes to the majority of GBC-related death. How lncRNA affects GBC metastasis is not completely understood. RESULTS: A novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1β mRNA and stabilized the IL-1β gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis. lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. CONCLUSIONS: lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.	NA	Clin Transl Med. 2020 Nov;10(7):e201. doi: 10.1002/ctm2.201.
4291	LncRNA	LncOR13C9	miR-23a-5p	ABCA1	glomerular endothelial cells	Diabetic Nephropathy	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;microarray;qPCR;RT-qPCR;RACE;Western blot;FISH;Luciferase reporter assay;Rescue assay;	33192550	High Glucose Aggravates Cholesterol Accumulation in Glomerular Endothelial Cells Through the LXRs/LncRNAOR13C9/ABCA1 Regulatory Network.	BACKGROUND: The underlying mechanisms by which diabetes and dyslipidemia contribute to diabetic nephropathy (DN) are not fully understood. In this study, we aimed to investigate the role of high glucose (HG) on intracellular cholesterol accumulation in glomerular endothelial cells (GEnCs) and its potential mechanism. METHODS: Oil red O staining, RT-qPCR, Western blotting, and immunocytofluorescence analyses were used to determine cholesterol accumulation and the expressions of LXRs and ABCA1 in GEnCs under high cholesterol (HC) and/or HG conditions, and the effect of these treatments was compared to that of low glucose without adding cholesterol. LncRNA microarrays were used to identify a long non-coding RNA (LncRNA OR13C9), of which levels increased in cells treated with the LXR agonist, GW3965. Fluorescence in situ hybridization (FISH) was conducted to confirm subcellular localization of LncOR13C9 and a bioinformatics analysis was used to identify competing endogenous RNA (ceRNA) regulatory networks between LncOR13C9 and microRNA-23a-5p (miR-23a-5p). Gain and loss of function, rescue assay approaches, and dual-luciferase reporter assay were conducted to study interactions between LncOR13C9, miR-23a-5p, and ABCA1. RESULTS: We showed that HG could decrease the response ability of GEnCs to cholesterol load, specifically that HG could downregulate LXRs expression in GEnCs under cholesterol load and that the decrease in LXRs expression suppressed ABCA1 expression and increased cholesterol accumulation. We focused on the targets of LXRs and identified a long non-coding RNA (LncOR13C9) that was downregulated in GEnCs grown in HG and HC conditions, compared with that grown in HC conditions. We speculated that LncRNAOR13C9 was important for LXRs to increase cholesterol efflux via ABCA1 under HC. Furthermore, using gain of function, loss of function, and rescue assay approaches, we showed that LncOR13C9 could regulate ABCA1 by inhibiting the action of miR-23a-5p in the LXR pathway. Furthermore, dual-luciferase reporter assay was conducted to study the interaction of LncOR13C9 with miR-23a-5p. CONCLUSION: Overall, our study identified the LXRs/LncOR13C9/miR23A-5p/ABCA1 regulatory network in GEnCs, which may be helpful to better understand the effect of HG on cholesterol accumulation in GEnCs under cholesterol load and to explore new therapeutic tools for the management of DN patients.	NA	Front Physiol. 2020 Oct 19;11:552483. doi: 10.3389/fphys.2020.552483. eCollection 2020.
4292	LncRNA	LncRNA-RP11	miR-29a	NA	lung fibroblasts cell lines HFL-1 and WI-38 	Radiation-Induced Lung Injury	Homo sapiens (human)	microarray;RACE;	33117089	LncRNA-RP11 Modulates TGF-β1-Activated Radiation-Induced Lung Injury Through Downregulating microRNA-29a.	Radiation-induced lung injury (RILI) is one of the most serious complications of thoracic radiation and TGF-β1 is a central regulator of RILI. However, the molecular mechanism underlying the fine tuning of TGF-β1 signaling in RILI has not been fully understood. In the current study, differentially expressed long non-coding RNAs (LncRNAs) among human lung fibroblasts cell lines HFL-1 and WI-38 treated with TGF-β1, were identified by microarray and validated by real time PCR. LncRNA-RP11 was found to be the most increased LncRNA and it mediated the promotion of fibrogenic activity in human lung fibroblasts after TGF-β1 treatment. Bioinformatic analysis revealed that TGF-β1 may be associated with the component and structure of extracellular matrix in lung fibroblasts cells, and LncRNA-RP11 was predicted and confirmed to be a competing endogenous RNA by directly binding to miR-29a. Functional experiments investigating the biological role of LncRNA-RP11/miR-29a axis in RILI, were then carried out in human fibroblasts. The results showed that radiation promoted the expression of LncRNA-RP11, but regressed the expression of miR-29a. Furthermore, radiation elevated the expression of various common collagenic proteins, which could be abolished by overexpression of miR-29a.	NA	Dose Response. 2020 Oct 16;18(4):1559325820949071. doi: 10.1177/1559325820949071. eCollection 2020 Oct-Dec.
4293	LncRNA	lncRNA-SNHG7-003	miR-1306-5p	SIRT7	vascular smooth muscle cells	Atherosclerosis	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33416100	lncRNA-SNHG7-003 inhibits the proliferation, migration and invasion of vascular smooth muscle cells by targeting the miR-1306-5p/SIRT7 signaling pathway.	Long non-coding RNAs (lncRNAs) have been discovered to participate in the progression of various types of disease and may be a promising biomarker for atherosclerosis (AS). The present study aimed to investigate the regulatory mechanisms of the lncRNA, small nucleolar RNA host gene 7-003 (SNHG7-003), on the proliferation, migration and invasion of vascular smooth muscle cells (VSMCs). VSMCs were first stimulated with oxidized low-density lipoprotein (ox-LDL) to simulate AS in a high fat environment. The expression levels of SNHG7-003, microRNA (miRNA/miR)-1306-5p and sirtuin 7 (SIRT7) were analyzed by reverse transcription-quantitative PCR and the effects of each of these factors on VSMC proliferation, migration and invasion were determined by Cell Counting Kit-8, wound healing and Transwell assays, respectively. Western blot analysis was also used to analyze the protein expression levels of α-smooth muscle actin (α-SMA), matrix metalloproteinase (MMP)2 and MMP9. The interactions between SNHG7-003 or SIRT7 and miR-1306-5p were determined using dual-luciferase reporter assays. The results revealed that the SNHG7-003 expression levels were downregulated in VSMCs exposed to ox-LDL, while the overexpression (OE) of SNHG7-003 significantly inhibited the proliferation, migration and invasion of VSMCs induced by ox-LDL. Transfection with miR-1306-5p mimic abrogated the effects of the inhibitory effects induced by SNHG7-003 OE. SIRT7 was validated to be a target gene of miR-1306-5p, exhibiting similar inhibitory effects as SNHG7-003 in AS. It was also discovered to be involved in the regulatory effects of the SNHG7-003/miR-1306-5p axis in VSMCs. On the whole, the findings of the present study indicate that SNHG7-003 may inhibit the proliferation, migration and invasion of VSMCs via the miR-1306-5p/SIRT7 signaling pathway. These findings may provide a novel basis for the development of treatment strategies for AS.	NA	Int J Mol Med. 2021 Feb;47(2):741-750. doi: 10.3892/ijmm.2020.4821. Epub 2020 Dec 16.
4294	LncRNA	LOC100912373	miR-17-5p	PDK1	fibroblast-like synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33437356	LncRNA LOC100912373 modulates PDK1 expression by sponging miR-17-5p to promote the proliferation of fibroblast-like synoviocytes in rheumatoid arthritis.	Rheumatoid arthritis (RA) is a common autoimmune disease and characterized by chronic inflammation, abnormal synovial cell proliferation, and joint swelling and tenderness, and it causes patients substantial pain. To date, the pathogenesis of RA remains unclear, and specific treatment is still lacking in the clinic. Evidence from previous research indicated that the long noncoding RNA (lncRNA) LOC100912373 is a key lncRNA and involved in RA. However, our understanding of the specific mechanism of lncRNA LOC100912373 in RA development and progression is still in its infancy. In this study, fibroblast-like synoviocytes (FLSs) were cultured by enzyme-dispersed and substrate-attached explant methods. The MTT method, flow cytometry and transmission electron microscopy were used to determine the effect of lncRNA LOC100912373 on FLSs. The expression of key genes such as lncRNA LOC100912373, miR-17-5p, PDK1 and AKT in FLSs was detected by RT-qPCR, immunofluorescence and Western blot. The localization of lncRNA LOC100912373 was determined by fluorescence in situ hybridization. The specific targeting relationship between lncRNA LOC100912373 and miR-17-5p/PDK1 was verified by RNA immunoprecipitation and luciferase reporter gene analysis. The results showed that lncRNA LOC100912373 localized in the cytoplasm and was highly expressed in the synovial tissues and FLSs of AA rats. LncRNA LOC100912373 overexpression promoted the proliferation of FLSs. In addition, lncRNA LOC100912373 could bind to miR-17-5p, and the expression of lncRNA LOC100912373 was negatively correlated with miR-17-5p and positively correlated with PDK1/AKT. In conclusion, lncRNA LOC100912373 may upregulate the expression of PDK1 by sponging miR-17-5p, accelerating the phosphorylation of AKT and inducing the proliferation of FLSs, thus promoting the occurrence and development of RA.	NA	Am J Transl Res. 2020 Dec 15;12(12):7709-7723. eCollection 2020.
4295	LncRNA	LOC100912373	miR-17-5p	AKT	fibroblast-like synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33437356	LncRNA LOC100912373 modulates PDK1 expression by sponging miR-17-5p to promote the proliferation of fibroblast-like synoviocytes in rheumatoid arthritis.	Rheumatoid arthritis (RA) is a common autoimmune disease and characterized by chronic inflammation, abnormal synovial cell proliferation, and joint swelling and tenderness, and it causes patients substantial pain. To date, the pathogenesis of RA remains unclear, and specific treatment is still lacking in the clinic. Evidence from previous research indicated that the long noncoding RNA (lncRNA) LOC100912373 is a key lncRNA and involved in RA. However, our understanding of the specific mechanism of lncRNA LOC100912373 in RA development and progression is still in its infancy. In this study, fibroblast-like synoviocytes (FLSs) were cultured by enzyme-dispersed and substrate-attached explant methods. The MTT method, flow cytometry and transmission electron microscopy were used to determine the effect of lncRNA LOC100912373 on FLSs. The expression of key genes such as lncRNA LOC100912373, miR-17-5p, PDK1 and AKT in FLSs was detected by RT-qPCR, immunofluorescence and Western blot. The localization of lncRNA LOC100912373 was determined by fluorescence in situ hybridization. The specific targeting relationship between lncRNA LOC100912373 and miR-17-5p/PDK1 was verified by RNA immunoprecipitation and luciferase reporter gene analysis. The results showed that lncRNA LOC100912373 localized in the cytoplasm and was highly expressed in the synovial tissues and FLSs of AA rats. LncRNA LOC100912373 overexpression promoted the proliferation of FLSs. In addition, lncRNA LOC100912373 could bind to miR-17-5p, and the expression of lncRNA LOC100912373 was negatively correlated with miR-17-5p and positively correlated with PDK1/AKT. In conclusion, lncRNA LOC100912373 may upregulate the expression of PDK1 by sponging miR-17-5p, accelerating the phosphorylation of AKT and inducing the proliferation of FLSs, thus promoting the occurrence and development of RA.	NA	Am J Transl Res. 2020 Dec 15;12(12):7709-7723. eCollection 2020.
4296	LncRNA	LOC400043	miR-21	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	microarray;qPCR;RT-qPCR;luciferase assay;	33194632	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway.	Gastric cancer is one of the common causes of cancer mortality worldwide, with a low survival rate for the affected people. Recent studies have revealed the key role of long non-coding RNAs (lncRNAs) in the development and progression of many cancers, including gastric cancer. Looking for the potential molecular regulators of gastric cancer incidence and progression, LINC02381 was identified as a downregulated lncRNA in gastric cancer tissues by analysis of available microarray and RNA-seq data and RT-qPCR confirmed this differential expression. MiR-21, miR-590, and miR-27a miRNAs were predicted to be sponged by LINC02381, and dual luciferase assay verified LINC02381 as a competitive endogenous RNA (CeRNA), which binds to them. Furthermore, we found that increased expression of LINC02381 attenuates Wnt pathway activity. Also, functional analysis indicates that LINC02381 arrests cell cycle, increases apoptosis and caspase activity, and reduces cell survival and proliferation rate of the human gastric cancer cell lines AGS and MKN45. Moreover, EMT analysis showed that LINC02381 is involved in gastric cancer progression and inhibits metastasis. Overall, this work for the first time introduces LINC02381 as a CeRNA involved in gastric cancer and provides novel insight into the molecular pathogenesis of gastric cancer.	NA	Front Oncol. 2020 Oct 23;10:562253. doi: 10.3389/fonc.2020.562253. eCollection 2020.
4297	LncRNA	LOC400043	miR-590	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	microarray;qPCR;RT-qPCR;luciferase assay;	33194632	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway.	Gastric cancer is one of the common causes of cancer mortality worldwide, with a low survival rate for the affected people. Recent studies have revealed the key role of long non-coding RNAs (lncRNAs) in the development and progression of many cancers, including gastric cancer. Looking for the potential molecular regulators of gastric cancer incidence and progression, LINC02381 was identified as a downregulated lncRNA in gastric cancer tissues by analysis of available microarray and RNA-seq data and RT-qPCR confirmed this differential expression. MiR-21, miR-590, and miR-27a miRNAs were predicted to be sponged by LINC02381, and dual luciferase assay verified LINC02381 as a competitive endogenous RNA (CeRNA), which binds to them. Furthermore, we found that increased expression of LINC02381 attenuates Wnt pathway activity. Also, functional analysis indicates that LINC02381 arrests cell cycle, increases apoptosis and caspase activity, and reduces cell survival and proliferation rate of the human gastric cancer cell lines AGS and MKN45. Moreover, EMT analysis showed that LINC02381 is involved in gastric cancer progression and inhibits metastasis. Overall, this work for the first time introduces LINC02381 as a CeRNA involved in gastric cancer and provides novel insight into the molecular pathogenesis of gastric cancer.	NA	Front Oncol. 2020 Oct 23;10:562253. doi: 10.3389/fonc.2020.562253. eCollection 2020.
4298	LncRNA	LOC400043	miR-27a	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	microarray;qPCR;RT-qPCR;luciferase assay;	33194632	Long Noncoding RNA LOC400043 (LINC02381) Inhibits Gastric Cancer Progression Through Regulating Wnt Signaling Pathway.	Gastric cancer is one of the common causes of cancer mortality worldwide, with a low survival rate for the affected people. Recent studies have revealed the key role of long non-coding RNAs (lncRNAs) in the development and progression of many cancers, including gastric cancer. Looking for the potential molecular regulators of gastric cancer incidence and progression, LINC02381 was identified as a downregulated lncRNA in gastric cancer tissues by analysis of available microarray and RNA-seq data and RT-qPCR confirmed this differential expression. MiR-21, miR-590, and miR-27a miRNAs were predicted to be sponged by LINC02381, and dual luciferase assay verified LINC02381 as a competitive endogenous RNA (CeRNA), which binds to them. Furthermore, we found that increased expression of LINC02381 attenuates Wnt pathway activity. Also, functional analysis indicates that LINC02381 arrests cell cycle, increases apoptosis and caspase activity, and reduces cell survival and proliferation rate of the human gastric cancer cell lines AGS and MKN45. Moreover, EMT analysis showed that LINC02381 is involved in gastric cancer progression and inhibits metastasis. Overall, this work for the first time introduces LINC02381 as a CeRNA involved in gastric cancer and provides novel insight into the molecular pathogenesis of gastric cancer.	NA	Front Oncol. 2020 Oct 23;10:562253. doi: 10.3389/fonc.2020.562253. eCollection 2020.
4299	LncRNA	LOC441178	miR-182	NA	ESCC cells	Esophageal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;	33173314	LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182.	BACKGROUND: Long noncoding RNAs (lncRNAs) have been shown to play an important role in the development and progression of esophageal carcinoma (EC). Recently, lncRNA LOC441178 was shown to be dysregulated in many cancer types; however, the role of LOC441178 in EC remains unclear. MATERIALS AND METHODS: Flow cytometry, transwell and wound healing assays were used to measure the apoptosis and migration in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR was used to detect the level of miR-182 in LOC441178-overexpressed EC cells. In addition, DNA methylation status of miR-182 promoter in LOC441178-overexpressed ESCC cells was detected by methylation-specific PCR (MSP) and bisulfite sequencing PCR. RESULTS: In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells. In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. Moreover, overexpression of LOC441178 markedly inhibited the phosphorylation of Akt and phosphorylation FOXO3a and increased the expression of FOXO3a in ESCC cells via downregulation of miR-182. Mechanistically, LOC441178 overexpression epigenetically suppressed miR-182 expression via DNA methylation. In vivo experiments revealed that overexpression of LOC441178 inhibited ESCC tumor growth in mouse xenograft model. CONCLUSION: Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.	NA	Onco Targets Ther. 2020 Nov 3;13:11253-11263. doi: 10.2147/OTT.S271711. eCollection 2020.
4300	LncRNA	LOC441178	miR-182	NA	ESCC cells	Esophageal Cancer	Mus musculus (mouse)	qPCR;RT-qPCR;Flow Cytometry assay;	33173314	LOC441178 Overexpression Inhibits the Proliferation and Migration of Esophageal Carcinoma Cells via Methylation of miR-182.	BACKGROUND: Long noncoding RNAs (lncRNAs) have been shown to play an important role in the development and progression of esophageal carcinoma (EC). Recently, lncRNA LOC441178 was shown to be dysregulated in many cancer types; however, the role of LOC441178 in EC remains unclear. MATERIALS AND METHODS: Flow cytometry, transwell and wound healing assays were used to measure the apoptosis and migration in esophageal squamous cell carcinoma (ESCC) cells. RT-qPCR was used to detect the level of miR-182 in LOC441178-overexpressed EC cells. In addition, DNA methylation status of miR-182 promoter in LOC441178-overexpressed ESCC cells was detected by methylation-specific PCR (MSP) and bisulfite sequencing PCR. RESULTS: In this study, we found that LOC441178 negatively regulated miR-182 expression in ESCC cells. In addition, overexpression of LOC441178 inhibited the proliferation and migration and induced apoptosis in ESCC cells via downregulation of miR-182. Moreover, overexpression of LOC441178 markedly inhibited the phosphorylation of Akt and phosphorylation FOXO3a and increased the expression of FOXO3a in ESCC cells via downregulation of miR-182. Mechanistically, LOC441178 overexpression epigenetically suppressed miR-182 expression via DNA methylation. In vivo experiments revealed that overexpression of LOC441178 inhibited ESCC tumor growth in mouse xenograft model. CONCLUSION: Collectively, our data suggested that LOC441178 overexpression epigenetically inhibited tumorigenesis of ESCC via DNA methylation of miR-182. These data indicated that the LOC441178/miR-182 axis might represent a novel therapeutic option for the treatment of ESCC.	NA	Onco Targets Ther. 2020 Nov 3;13:11253-11263. doi: 10.2147/OTT.S271711. eCollection 2020.
4301	LncRNA	LOXL1-AS1	miR-589-5p	CBX5	RCC cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33185692	Long non-conding RNA LOXL1-AS1 sponges miR-589-5p to up-regulate CBX5 expression in renal cell carcinoma.	BACKGROUND: Renal cancer (RCC) is a common malignant tumor that seriously endangers people's health. In recent years, long non-coding RNAs (lncRNAs) have been discovered to play vital roles in diverse cancers, including RCC. LncRNA lysyl oxidase like 1 antisense RNA 1 (LOXL1-AS1) has been found to exert carcinogenic functions in several cancers, but its role and mechanism in RCC have not been investigated. METHODS: qRT-PCR was utilized for testing RNA expression and Western blot for protein expression in RCC tissues or cells. Then, we assessed cell function by conducting a series of functional experiments, such as 5-ethynyl-2'-deoxyuridine staining, colony formation, flow cytometry, JC-1, Western blot and transwell migration experiments. Following, RNA immunoprecipitation, pull down and luciferase reporter experiments were carried out to explore the regulatory mechanisms of LOXL1-AS1 in RCC. RESULTS: LOXL1-AS1 was highly expressed in RCC tissues and cells. Moreover, knockdown of LOXL1-AS1 hampered RCC cell proliferation and migration. Importantly, miR-589-5p that was lowly expressed and worked as a tumor-inhibitor in RCC was found to bind with LOXL1-AS1. Furthermore, chromobox 5 (CBX5) targeted by miR-589-5p could expedite cell proliferation and migration in RCC. Finally, overexpressed CBX5 or inhibited miR-589-5p reversed the repressive impacts of silenced LOXL1-AS1 on RCC malignant phenotypes. CONCLUSIONS: LncRNA LOXL1-AS1 sequestered miR-589-5p to augment CBX5 expression in RCC cells, opening a new way for potential development in RCC treatment.	NA	Biosci Rep. 2020 Nov 27;40(11):BSR20200212. doi: 10.1042/BSR20200212.
4302	LncRNA	LOXL1-AS1	miR-589-5p	TRAF6	laryngocarcinoma cells	Laryngocarcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;	33061856	LOXL1-AS1 contributes to the proliferation and migration of laryngocarcinoma cells through miR-589-5p/TRAF6 axis.	BACKGROUND: LOXL1-AS1 is a long non-coding RNA (lncRNA) that plays crucial roles in various cancers. However, the functional role of LOXL1-AS1 in laryngocarcinoma remains unclear. Thus we planned to probe into the function and underlying mechanism of LOXL1-AS1 in laryngocarcinoma. METHODS: Gene expression was evaluated in laryngocarcinoma cells using RT-qPCR. The ability of cell proliferation and migration was assessed by CCK8, colony formation, wound healing and transwell assays. The interaction among LOXL1-AS1, miR-589-5p and TRAF6 was detected by Ago2-RIP, RNA pull down and luciferase reporter assays. RESULTS: LOXL1-AS1 was overexpressed in laryngocarcinoma cells. Silencing of LOXL1-AS1 suppressed cell proliferation, migration and EMT in laryngocarcinoma. Moreover, miR-589-5p, the downstream of LOXL1-AS1, directly targeted TRAF6 in laryngocarcinoma. Importantly, LOXL1-AS1 augmented TRAF6 expression in laryngocarcinoma cells by sequestering miR-589-5p. Besides, miR-589-5p worked as a tumor-inhibitor while TRAF6 functioned as a tumor-facilitator in laryngocarcinoma. Of note, rescue experiments both in vitro and in vivo validated that LOXL1-AS1 aggravated the malignancy in laryngocarcinoma by targeting miR-589-5p/TRAF6 pathway. CONCLUSIONS: LOXL1-AS1 promotes the proliferation and migration of laryngocarcinoma cells through absorbing miR-589-5p to upregulate TRAF6 expression.	NA	Cancer Cell Int. 2020 Oct 13;20:504. doi: 10.1186/s12935-020-01565-5. eCollection 2020.
4303	LncRNA	LUADT1	miR-195	Pim-1	cardiac endothelial cells	Sepsis	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase activity assay;Luciferase reporter assay;	33225891	LncRNA LUADT1 sponges miR-195 to prevent cardiac endothelial cell apoptosis in sepsis.	BACKGROUND: The oncogenic role of the newly identified lncRNA LUADT1 has been revealed in lung adenocarcinoma. It was reported that LUADT1 plays a critical role in multiple human diseases. This study was carried out to investigate the role of LUADT1 in sepsis. METHODS: Sixty patients with sepsis and sixty healthy volunteers were recruited for this study. Plasma samples were collected from all participants. Human primary coronary artery endothelial cells were also used in this study. The expression of Pim-1, miR-195 and LUADT1 were detected by RT-qPCR. The interaction between miR-195 and LUADT1 was determined by overexpression experiments and luciferase activity assay. Cell apoptosis was detected by flow cytometry. The expression of apoptosis-related protein was detected by Western blotting. RESULTS: Bioinformatics analysis revealed the potential interaction between LUADT1 and miR-195, which was confirmed by dual luciferase reporter assay. LUADT1 was downregulated in patients with sepsis. Moreover, LPS treatment downregulated the expression of LUADT1 in primary cardiac endothelial cells. Overexpression of LUADT1 and miR-195 did not affect the expression of each other in primary cardiac endothelial cells. Interestingly, overexpression of LUADT1 was found to upregulate the expression of Pim-1, a target of miR-195. In addition, it was found that overexpression of LUADT1 and Pim-1 reduced the enhancement effects of miR-195 on LPS-induced cardiac endothelial cell apoptosis. CONCLUSION: In summary, LUADT1 may protect cardiac endothelial cells against apoptosis in sepsis by regulating the miR-195/Pim-1 axis.	NA	Mol Med. 2020 Nov 23;26(1):112. doi: 10.1186/s10020-020-00228-5.
4304	LncRNA	LUCAT1	miR-181c-5p	Bcl2	UM-UC-3 and T24 cell lines	Bladder Cancer	Homo sapiens (human)	Flow cytometry assay;RT-PCR;Western blot;Flow Cytometry assay;	33282949	Downregulation of Long Noncoding RNA LUCAT1 Suppresses the Migration and Invasion of Bladder Cancer by Targeting miR-181c-5p.	PURPOSE: The long noncoding RNA LUCAT1 (lung cancer-associated transcript 1) has been reported to be highly expressed in bladder cancer samples, but its role and molecular mechanisms need to be elucidated. METHODS: Bioinformatics methods show that miR-181c-5p is a target of LUCAT1. Here, we aimed to reveal whether LUCAT1 participates in the development of bladder cancer via targeting miR-181c-5p. The expression levels of LUCAT1 and miR-181c-5p were detected by RT-PCR technology in bladder cells and tissues. The effects of the LUCAT1/miR-181c-5p axis on cell proliferation, migration, invasion, and apoptosis were tested by CCK-8, wound healing, Transwell chambers, and flow cytometry assays. The expressions of apoptosis/migration-related proteins were detected by western blotting assays. RESULTS: The results demonstrated that LUCAT1 was overexpressed in bladder cancer tissue and cells, while miR-181c-5p showed a low expression pattern as compared to normal bladder cells and tissues. Cell proliferation, migration, and invasion capacities were significantly impaired, and cell apoptosis was enhanced when LUCAT1 was silenced in UM-UC-3 and T24 cell lines, but this effect was abolished by miR-181c-5p downregulation. In addition, miR-181c-5p downregulation impaired LUCAT1 downregulation which mediated the decreased expressions of Bcl2 and N-cadherin and the increased expressions of Bax and E-cadherin. Moreover, we found that KRAS was a direct target of miR-181c-5p and was under the positive regulation of LUCAT1. CONCLUSION: Collectively, this study reveals that knockdown of LUCAT1 inhibits the migration and invasion of bladder cancer cells in a miR-181c-5p-dependent manner, which may be related to KRAS downregulation.	NA	Biomed Res Int. 2020 Nov 17;2020:4817608. doi: 10.1155/2020/4817608. eCollection 2020.
4305	LncRNA	LUCAT1	miR-493-5p	ADAM10	TC cells	Thyroid Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33116777	Long Non-Coding RNA LUCAT1 Promotes Progression of Thyroid Carcinoma by Reinforcing ADAM10 Expression Through Sequestering microRNA-493.	BACKGROUND: Long non-coding RNA (lncRNA) LUCAT1 has recently been recognized as an oncogene in several malignancies. This study was launched to probe its role in thyroid carcinoma (TC) development and the implicated molecules. METHODS: LUCAT1 expression in TC cell lines and in normal thyroid follicular epithelial cell line Nthy-ori3-1 was determined by RT-qPCR. Binding relationships between LUCAT1 and microRNA (miR)-493, and between miR-493 and a disintegrin and metalloproteinase-10 (ADAM10) were predicted on a bioinformatics system and then validated through luciferase reporter gene assays. Expression of miR-493 and ADAM10 in TC cells was determined. Gain- and loss-of functions of LUCAT1, miR-493 and ADAM10 were performed to explore their influences on the behaviors of TC cells. Xenograft tumors were induced in nude mice for in vivo studies. RESULTS: LUCAT1 and ADAM10 were highly expressed, while miR-493 was poorly expressed in TC cell lines. LUCAT1 served as a miR-493 sponge to upregulate ADAM10 expression. Silencing of LUCAT1 discouraged proliferation, invasion, and migration but triggered apoptosis of TC cells. By contrast, these changes were abrogated by further miR-493 inhibition or ADAM10 upregulation. The in vitro experiment results were reproduced in vivo. In addition, miR-493 inhibition or ADAM10 overexpression was found to increase the phosphorylation of STAT3 in cells. CONCLUSION: This study evidenced that LUCAT1 increases ADAM10 expression through sequestering miR-493, leading to JAK-STAT activation and TC cell growth and metastasis. LUCAT1 and ADAM10 may serve as therapeutic targets for TC treatment.	NA	Int J Gen Med. 2020 Oct 14;13:847-860. doi: 10.2147/IJGM.S273461. eCollection 2020.
4306	LncRNA	LUNAR1	miR-495-3p	MYCBP	CRC cells	Colorectal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Luciferase reporter assay;	33300052	lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR-495-3p/MYCBP axis.	Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non-coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B-cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK-8, clone formation, wound-healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR-495-3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR-495-3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR-495-3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR-495-3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR-495-3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.	NA	Int J Oncol. 2020 Nov;57(5):1157-1168. doi: 10.3892/ijo.2020.5128. Epub 2020 Sep 25.
4307	LncRNA	MALAT1	miR-181a-5p	NA	HPMECs	Helial Cell (Hpmec) Injury	Rattus (rat)	qRT-PCR	33197806	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Med. 2020 Dec;175:106210. doi: 10.1016/j.rmed.2020.106210. Epub 2020 Nov 4.
4308	LncRNA	MALAT1	miR-181a-5p	NA	HPMECs	Helial Cell (Hpmec) Injury	Homo sapiens (human)	qRT-PCR	33197806	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Med. 2020 Dec;175:106210. doi: 10.1016/j.rmed.2020.106210. Epub 2020 Nov 4.
4309	LncRNA	MALAT1	miR-211	SIRT1	melanoma and nonmelanoma skin cancer cells	Melanoma	Homo sapiens (human)	RNA sequencing;	33152110	The long noncoding RNA MALAT1 suppresses miR-211 to confer protection from ultraviolet-mediated DNA damage in vitiligo epidermis by upregulating sirtuin 1.	BACKGROUND: The absence of melanocytes poses a challenge for long-term tissue homeostasis in vitiligo. Surprisingly, while individuals with Fitzpatrick phototypes I-II (low melanin content) have a higher incidence of melanoma and nonmelanoma skin cancer, people with vitiligo are at a decreased risk for the same. OBJECTIVES: To understand the molecular mechanisms that protect vitiligo skin from ultraviolet (UV)-induced DNA damage by (i) characterizing differentially expressed microRNAs in lesional vs. nonlesional epidermis and (ii) identifying their upstream regulators and downstream gene targets. METHODS: Genome-wide microRNA profiling of nonlesional and lesional epidermis was performed on five individuals with stable nonsegmental vitiligo using next-generation RNA sequencing. The relevance of the upstream regulator and downstream target gene of the most differentially expressed microRNA was studied. RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated microRNA in lesional epidermis. Inhibition of SIRT1 with EX-527 downregulated keratin 10 and involucrin, suggesting that SIRT1 promotes keratinocyte differentiation. Overexpression of miR-211 mimic led to a significant increase in γ-H2AX positivity and cyclobutane pyrimidine dimer (CPD) formation, hallmarks of UVB-mediated DNA damage. These effects could be ameliorated by the addition of resveratrol, a SIRT1 activator. Furthermore, a long noncoding RNA, MALAT1, was identified as a negative upstream regulator of miR-211. Overexpression of MALAT1 resulted in increased expression of SIRT1 and a concomitant removal of UVB-induced CPDs in primary keratinocytes. CONCLUSIONS: These findings establish a novel MALAT1-miR-211-SIRT1 signalling axis that potentially confers protection to the 'amelanotic' keratinocytes in vitiligo.	NA	Br J Dermatol. 2021 Jun;184(6):1132-1142. doi: 10.1111/bjd.19666. Epub 2020 Dec 30.
4310	LncRNA	MALAT1	miR-211	SIRT1	melanoma and nonmelanoma skin cancer cells	Nonmelanoma Skin Cancer	Homo sapiens (human)	RNA sequencing;	33152110	The long noncoding RNA MALAT1 suppresses miR-211 to confer protection from ultraviolet-mediated DNA damage in vitiligo epidermis by upregulating sirtuin 1.	BACKGROUND: The absence of melanocytes poses a challenge for long-term tissue homeostasis in vitiligo. Surprisingly, while individuals with Fitzpatrick phototypes I-II (low melanin content) have a higher incidence of melanoma and nonmelanoma skin cancer, people with vitiligo are at a decreased risk for the same. OBJECTIVES: To understand the molecular mechanisms that protect vitiligo skin from ultraviolet (UV)-induced DNA damage by (i) characterizing differentially expressed microRNAs in lesional vs. nonlesional epidermis and (ii) identifying their upstream regulators and downstream gene targets. METHODS: Genome-wide microRNA profiling of nonlesional and lesional epidermis was performed on five individuals with stable nonsegmental vitiligo using next-generation RNA sequencing. The relevance of the upstream regulator and downstream target gene of the most differentially expressed microRNA was studied. RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated microRNA in lesional epidermis. Inhibition of SIRT1 with EX-527 downregulated keratin 10 and involucrin, suggesting that SIRT1 promotes keratinocyte differentiation. Overexpression of miR-211 mimic led to a significant increase in γ-H2AX positivity and cyclobutane pyrimidine dimer (CPD) formation, hallmarks of UVB-mediated DNA damage. These effects could be ameliorated by the addition of resveratrol, a SIRT1 activator. Furthermore, a long noncoding RNA, MALAT1, was identified as a negative upstream regulator of miR-211. Overexpression of MALAT1 resulted in increased expression of SIRT1 and a concomitant removal of UVB-induced CPDs in primary keratinocytes. CONCLUSIONS: These findings establish a novel MALAT1-miR-211-SIRT1 signalling axis that potentially confers protection to the 'amelanotic' keratinocytes in vitiligo.	NA	Br J Dermatol. 2021 Jun;184(6):1132-1142. doi: 10.1111/bjd.19666. Epub 2020 Dec 30.
4311	LncRNA	MALAT1	miR-206	VEGFA	endothelial cells	Diabetes Mellitus-Induced Erectile Dysfunction	Homo sapiens (human)	Luciferase reporter assay;RNA pull-down;	33121336	LncRNA MALAT1 facilitates BM-MSCs differentiation into endothelial cells via targeting miR-206/VEGFA axis.	Bone marrow-derived mesenchymal stem cells (BM-MSCs) implantation shows a repair effect on erectile function in diabetes mellitus-induced erectile dysfunction (DMED) due to its differentiative capacity into endothelial cells (ECs) that contributes to endothelial repair. This study was designed to explore the functional role and mechanism of long noncoding RNA (lncRNA)-metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in BM-MSCs-mediated DMED repairing. The DMED rat model was established and the erectile function was evaluated by calculating the intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio in the DMED models with or without BM-MSCs implantation. The differentiation of BM-MSCs toward ECs was assessed by measuring the expression of EC-specific genes. RNA pull-down and luciferase reporter assay were performed to explore the interaction between miR-206 and MALAT1 or VEGFA. BM-MSCs implantation improved the erectile function of DMED rats and increased MALAT1 expression. MALAT1 was time-dependently upregulated during the VEGF-induced BM-MSCs differentiation into ECs. Mechanistically, MALAT1 acted as a sponge of miR-206 to upregulate VEGFA expression, thereby promoting the differentiation of BM-MSCs into ECs. Moreover, MALAT1 silencing in vivo impaired the repairing effect of BM-MSCs on erectile dysfunction. Collectively, MALAT1 facilitates BM-MSCs differentiation into ECs via regulating miR-206/VEGFA axis.	NA	Cell Cycle. 2020 Nov;19(22):3018-3028. doi: 10.1080/15384101.2020.1829799. Epub 2020 Oct 29.
4312	LncRNA	MALAT1	miR-206	VEGFA	endothelial cells	Diabetes Mellitus-Induced Erectile Dysfunction	Rattus (rat)	Luciferase reporter assay;RNA pull-down;	33121336	LncRNA MALAT1 facilitates BM-MSCs differentiation into endothelial cells via targeting miR-206/VEGFA axis.	Bone marrow-derived mesenchymal stem cells (BM-MSCs) implantation shows a repair effect on erectile function in diabetes mellitus-induced erectile dysfunction (DMED) due to its differentiative capacity into endothelial cells (ECs) that contributes to endothelial repair. This study was designed to explore the functional role and mechanism of long noncoding RNA (lncRNA)-metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in BM-MSCs-mediated DMED repairing. The DMED rat model was established and the erectile function was evaluated by calculating the intracavernous pressure (ICP)/mean arterial pressure (MAP) ratio in the DMED models with or without BM-MSCs implantation. The differentiation of BM-MSCs toward ECs was assessed by measuring the expression of EC-specific genes. RNA pull-down and luciferase reporter assay were performed to explore the interaction between miR-206 and MALAT1 or VEGFA. BM-MSCs implantation improved the erectile function of DMED rats and increased MALAT1 expression. MALAT1 was time-dependently upregulated during the VEGF-induced BM-MSCs differentiation into ECs. Mechanistically, MALAT1 acted as a sponge of miR-206 to upregulate VEGFA expression, thereby promoting the differentiation of BM-MSCs into ECs. Moreover, MALAT1 silencing in vivo impaired the repairing effect of BM-MSCs on erectile dysfunction. Collectively, MALAT1 facilitates BM-MSCs differentiation into ECs via regulating miR-206/VEGFA axis.	NA	Cell Cycle. 2020 Nov;19(22):3018-3028. doi: 10.1080/15384101.2020.1829799. Epub 2020 Oct 29.
4313	LncRNA	MALAT1	miR-149-5p	NA	retinal ganglion cells	Retinal Ganglion	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33108931	Long Non-coding RNA MALAT1 Alleviates the Elevated Intraocular Pressure (Eiop)-induced Glaucoma Progression via Sponging miR-149-5p.	Background: Glaucoma is an optic neuropathic disease and contributed to the irreversible blindness caused by the slow death of retinal ganglion cells (RGCs). Long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was reported to be aberrantly expressed in diverse diseases, including glaucoma. However, the mechanism of MALAT1 in glaucoma was still undefined.Methods: The levels of MALAT1, microRNA-149-5p (miR-149-5p) in RGCs cultured under elevated pressure were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The putative target of MALAT1 was predicted by starBase v2.0 online database, and dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were performed to verify this interaction. The cell viability of RGCs was measured by Cell Counting Kit-8 (CCK-8) assay. The apoptotic rate was evaluated via flow cytometry. The protein levels of apoptosis-related proteins (Bax, B-cell lymphoma 2 (Bcl-2)) and Cleaved caspase 3 were assessed by Western blot.Results: The level of MALAT1 was significantly down-regulated, and the level of miR-149-5p was distinctly up-regulated in RGCs under pressure in a dose-dependent manner. Functionally, MALAT1 overexpression or miR-149-5p inhibitor alleviated the inhibitory effect on cell viability and the promoted effect on apoptotic rate of RGCs in EIOP. The interaction between MALAT1 and miR-149-5p was predicted by starBase v2.0 online database, and dual luciferase reporter assay, RIP assay and RNA pull-down assay validated the interaction. Combined with the loss and gain experiment results, miR-149-5p was negatively interacted with MALAT1. Furthermore, miR-149-5p mimics mitigated the promoted impact on cell viability and the suppressive impact on apoptotic rate by targeting MALAT1.Conclusion: MALAT1 promoted cell proliferation and inhibited cell apoptosis of RGCs via targeting miR-149-5p in glaucoma in vitro, which might shed light on the mechanism of glaucoma pathogenesis.	NA	Curr Eye Res. 2021 Jun;46(6):903-911. doi: 10.1080/02713683.2020.1843686. Epub 2020 Nov 12.
4314	LncRNA	MALAT1	miR-144-3p	NRF2	Lens Epithelial Cells	Diabetic Cataract	Homo sapiens (human)	qRT-PCR;RACE;Western blot;	33274006	LncRNA MALAT1 Regulates miR-144-3p to Facilitate Epithelial-Mesenchymal Transition of Lens Epithelial Cells via the ROS/NRF2/Notch1/Snail Pathway.	Diabetic cataract is a common complication of diabetes. The epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs) is a key event in the development of diabetic cataracts. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been reported to be highly expressed in different tissues of diabetic patients. This study is aimed at investigating the function and mechanism of MALAT1 in the regulation of EMT in human LECs under high glucose conditions. MALAT1, α-smooth muscle actin (α-SMA), fibronectin (FN), and nuclear factor erythroid-derived 2-like 2 (NRF2) were highly expressed in the LECs of diabetic cataract patients and in the human LECs under high glucose conditions; meanwhile, the decreased expressions of E-cadherin and zonula occludens 1 (ZO-1) were detected. Knockdown of MALAT1 could significantly reduce ROS, prevent EMT, arrest S phase cell cycle, and suppress the expression of total NRF2 and its nucleus translocation in LECs. Furthermore, after NRF2 was knocked down, total NRF2, α-SMA, and FN in cells, and NRF2, Notch intracellular domain (NICD), and Snail were decreased in the nucleus. Using bioinformatics methods, we predicted that MALAT1 and NRF2 shared the same microRNA-144-3p (miR-144-3p) combining site. Luciferase reporter coupled with qRT-PCR assays revealed that miR-144-3p was a target of MALAT1, which was confirmed to downregulate miR-144-3p in the LECs. In addition, after transfection of miR-144-3p mimics or inhibitor, western blot assay demonstrated that miR-144-3p negatively regulated the expression of total NRF2, α-SMA, and FN in cells, and NRF2, NICD, and Snail in the nucleus without affecting Kelch-like ECH-associated protein 1 (KEAP1). Finally, we confirmed that transfection of shMALAT1 inhibited NRF2 expression, and its mediated EMT could be rescued by miR-144-3p inhibitor; transfection of pcDNA3.1-MALAT1 promoted NRF2 expression, and its mediated EMT could be reversed by miR-144-3p inhibitor. In summary, we demonstrate that MALAT1 regulates miR-144-3p to facilitate EMT of LECs via the ROS/NRF2/Notch1/Snail pathway.	NA	Oxid Med Cell Longev. 2020 Nov 12;2020:8184314. doi: 10.1155/2020/8184314. eCollection 2020.
4315	LncRNA	MALAT1	miR-185-5p	MDM4	NSCLC cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33146951	LncRNA MALAT1 accelerates non-small cell lung cancer progression via regulating miR-185-5p/MDM4 axis.	Non-small cell lung cancer (NSCLC) is the commonest malignancy with high death rate around the world. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is greatly overexpressed in multifarious cancers, including NSCLC. However, the precise mechanism of MALAT1 in NSCLC tumorigenesis is blurry. This paper aims to investigate the theory of MALAT1 action in NSCLC progression. The levels of MALAT1, microRNA (miR)-185-5p, and mouse double minute 4 protein (MDM4) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation and apoptosis were, respectively, determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and flow cytometry. Cell migratory and invasive abilities were inspected by transwell assay. The binding relationship between miR-185-5p and MALAT1 or MDM4 was confirmed by dual-luciferase reporter assay. The impacts of MALAT1 on tumor growth in vivo were measured by a xenograft experiment. We found MALAT1 and MDM4 were upregulated and MALAT1 positively regulated the MDM4 expression. MALAT1 and MDM4 deletion significantly hindered the proliferation, metastasis, and expedited the apoptosis of NSCLC cells. MDM4 overexpression partly overturned the influence of MALAT1 downregulation on cell development. Moreover, miR-185-5p, as a target of MALAT1, could directly target MDM4, and miR-185-5p upregulation exerted inhibitory effects on NSCLC cells. Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR-185-5p/MDM4 axis in NSCLC. Collectively, MALAT1 contributed to proliferation, migration, invasion, and impeded apoptosis by regulating the MDM4 expression mediated by miR-185-5p in NSCLC cells.	NA	Cancer Med. 2020 Dec;9(23):9138-9149. doi: 10.1002/cam4.3570. Epub 2020 Nov 4.
4316	LncRNA	MALAT1	miR-141-3p	ZNF217	human fibroblast cells	Wound Healing Process	Homo sapiens (human)	qRT-PCR;Western blot;	33426220	LncRNA MALAT1 promotes wound healing via regulating miR-141-3p/ZNF217 axis.	BACKGROUND: The process of wound healing is complex. Increasing evidences have shown that lncRNA MALAT1 is abundant in fibroblasts and may be engaged in wound healing process. Therefore, we explored the mechanism of MALAT1 affecting wound healing. METHODS: The expression levels of MALAT1, miR-141-3p as well as ZNF217 in human fibroblast cells (HFF-1) were quantified by qRT-PCR. HFF-1 proliferation was measured by MTT, while migration was detected by wound healing assay. SMAD2 activation and matrix proteins expression were detected by western blotting. The interaction between miR-141-3p and MALAT1 or ZNF217 was further confirmed using the luciferase reporter gene assay. In vivo wound healing was assessed by full-thickness wound healing model on C57BL/6 mice. RESULT: Knockdown of MALAT1 as well as overexpression miR-141-3p remarkably inhibited the proliferation, migration and matrix protein expression in HFF-1 cells. MALAT1 directly targeted and inhibited the expression of miR-141-3p. MiR-141-3p suppressed the activation of TGF-β2/SMAD2 signaling pathway by targeting ZNF217. Knockdown of MALAT1 inhibited wound healing process in mice. CONCLUSIONS: MALAT1 up-regulates ZNF217 expression by targeting miR-141-3p, thus enhances the activity of TGF-β2/SMAD2 signaling pathway and promotes wound healing process. This investigation shed new light on the understanding of the role of MALAT1 in wound healing, and may provide potential target for the diagnosis or therapy of chronic wounds.	NA	Regen Ther. 2020 Oct 16;15:202-209. doi: 10.1016/j.reth.2020.09.006. eCollection 2020 Dec.
4317	LncRNA	MALAT1	miR-370-3p	HMGB1	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	32998017	Paclitaxel alleviates the sepsis-induced acute kidney injury via lnc-MALAT1/miR-370-3p/HMGB1 axis.	AIMS: To investigate the effects of paclitaxel on lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and its related mechanisms. MAIN METHODS: The sepsis-associated AKI was induced by LPS using HK-2 cells. Then the mRNA and protein expression levels of relevant genes in the serum of sepsis patients and HK-2 cells with LPS-induced AKI were detected by qRT-PCR and western blot analyses before and after paclitaxel treatment, respectively. Subsequently, the cell counting kit-8 (CCK-8) and flow cytometry assays were performed to estimate the effects of paclitaxel, lnc-MALAT1, miR-370-3p and HMGB1 on the proliferation and apoptosis of HK-2 cells injured by LPS. KEY FINDINGS: Lnc-MALAT1 was increased both in the serum of sepsis patients and cells injured by LPS, which could inhibit the cell proliferation, promote the cell apoptosis and increase the expression of TNF-α, IL-6 and IL-1β caused by paclitaxel. Moreover, lnc-MALAT1 was sponged with miR-370-3p which had the inverse effects with lnc-MALAT1 in LPS induced HK-2 cells. What's more, miR-370-3p targeted HMGB1 which was induced in serum and cells of sepsis. Knockdown of miR-370-3p inhibited the expression of HMGB1 and suppressed the proliferation but promoted the apoptosis of HK-2 cells injured by LPS as well as the expression of TNF-α, IL-6 and IL-1β. Besides, paclitaxel restrained the expression of HMGB1 via regulating lnc-MALAT1/miR-370-3p axis. SIGNIFICANCE: Paclitaxel could protect against LPS-induced AKI via the regulation of lnc-MALAT1/miR-370-3p/HMGB1 axis and the expression of TNF-α, IL-6 and IL-1β, revealing that paclitaxel might act as a therapy drug in reducing sepsis-associated AKI.	NA	Life Sci. 2020 Dec 1;262:118505. doi: 10.1016/j.lfs.2020.118505. Epub 2020 Sep 28.
4318	LncRNA	MALAT1	miR-30	Spastin	Hippocampal Neurite cells	Hippocampal Neurite	Homo sapiens (human)	Luciferase reporter assay;	33192306	The lncRNA MALAT1/miR-30/Spastin Axis Regulates Hippocampal Neurite Outgrowth.	Spastin, a microtubule-severing enzyme, is important for neurite outgrowth. However, the mechanisms underlying the post-transcriptional regulation of spastin during microtubule-related processes are largely unknown. We demonstrated that the spastin expression level is controlled by a long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-30 (miR-30) axis during neurite outgrowth. The miR-30 expression level decreased in hippocampal neurons with increasing days in culture, and miR-30 overexpression suppressed while miR-30 inhibition promoted neurite outgrowth in hippocampal neurons. Spastin was validated as a target gene of miR-30 using the luciferase reporter assay. The protein expression, microtubule severing activity, and neurite promoting effect of spastin were suppressed by the overexpression of miR-30 mimics and increased by miR-30 inhibitors. MALAT1 expression increased during neurite outgrowth and MALAT1 silencing impaired neurite outgrowth. miR-30 was a sponge target of MALAT1 and MALAT1/miR-30 altered neurite outgrowth in hippocampal neurons. MALAT1 overexpression reversed the inhibitory effect of miR-30 on the activity of a luciferase reporter construct containing spastin, as well as spastin mRNA and protein expression, indicating that spastin was a downstream effector of MALAT1/miR-30. The MALAT1/miR-30 cascade also modulated spastin-induced microtubule severing, and the MALAT1/miR-30/spastin axis regulated neurite outgrowth in hippocampal neurons. This study suggests a new mechanism governing neurite outgrowth in hippocampal neurons involving MALAT1/miR-30-regulated spastin expression.	NA	Front Cell Neurosci. 2020 Oct 20;14:555747. doi: 10.3389/fncel.2020.555747. eCollection 2020.
4319	LncRNA	MALAT1	miR-204-5p	IGF2BP2	TC cells	Thyroid Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33312756	Oncogenic Role of Long Noncoding RNAMALAT1 in Thyroid Cancer Progression through Regulation of the miR-204/IGF2BP2/m6A-MYC Signaling.	Accumulating studies highlight the role of long noncoding RNAs (lncRNAs)/microRNAs (miRNAs)/messenger RNAs (mRNAs) as important regulatory networks in various human cancers, including thyroid cancer (TC). This study aimed to investigate a novel regulatory network dependent on lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in relation to TC development. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were initially employed to detect the expression of MALAT1, insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2), and myelocytomatosis (MYC) in TC cells. Interactions among MALAT1, miR-204, and IGF2BP2 were then identified in vitro. The biological processes of proliferation, migration, invasion, and apoptosis were evaluated in vitro via gain- and loss-of-function experiments, followed by in vivo validation using xenograft mice. Our data indicated that MALAT1 and IGF2BP2 were highly expressed, while miR-204 was poorly expressed in TC. IGF2BP2 was verified as a target of miR-204. MALAT1 was found to upregulate IGF2BP2 and enhance MYC expression via m6A modification recognition by competitively binding to miR-204, conferring a stimulatory effect on proliferation, migration, and invasion of TC cells, which was accompanied by weakened tumor growth and cell apoptosis. Altogether, the central findings of our study suggest that MALAT1 contributes to TC progression through the upregulation of IGF2BP2 by binding to miR-204.	NA	Mol Ther Nucleic Acids. 2020 Sep 26;23:1-12. doi: 10.1016/j.omtn.2020.09.023. eCollection 2021 Mar 5.
4320	LncRNA	MALAT1	miR-30b	CNR1	PC12 and C6 cells	Alzheimers Disease	Homo sapiens (human)	microarray;	32976819	Neuro-protective roles of long non-coding RNA MALAT1 in Alzheimer's disease with the involvement of the microRNA-30b/CNR1 network and the following PI3K/AKT activation.	Long non-coding RNAs (lncRNAs) have been increasingly found to fulfill key functions in neurodegenerative diseases. This study aimed to probe the function of lncRNA MALAT1 in neuronal recovery in Alzheimer's disease (AD). Aβ25-35 was used to induce AD in a rat model and neuronal injury in PC12 and C6 cells. Aberrantly expressed lncRNAs/microRNAs (miRNAs) in AD rats were screened out by microarray analyses. Altered expression of MALAT1, miR-30b and CNR1 was performed to explore their roles in neuronal recovery in rat and cell models. Consequently, LncRNA MALAT1 and CNR1 were poorly expressed while miR-30b was highly expressed in Aβ25-35-induced rat models and cells. Overexpression of MALAT1 or CNR1 reduced neuronal injury in rat hippocampus. It increased viability and decreased apoptosis in injured PC12 and C6 cells, and decreased the secretion of pro-inflammatory factor IL-6 and TNF-α but increased IL-10 production. However, overexpression of miR-30b reversed these trends. MALAT1 could served as a sponge for mR-30b to up-regulate CNR1 expression. The phosphorylation of PI3K and AKT was stimulated when MALAT1 or CNR1 was overexpressed. To sum up, we found MALAT1 could promote neuronal recovery following AD through the miR-30b/CNR1 network and the PI3K/AKT signaling activation.	NA	Exp Mol Pathol. 2020 Dec;117:104545. doi: 10.1016/j.yexmp.2020.104545. Epub 2020 Sep 22.
4321	LncRNA	MALAT1	miR-30b	CNR1	PC12 and C6 cells	Alzheimers Disease	Rattus (rat)	microarray;	32976819	Neuro-protective roles of long non-coding RNA MALAT1 in Alzheimer's disease with the involvement of the microRNA-30b/CNR1 network and the following PI3K/AKT activation.	Long non-coding RNAs (lncRNAs) have been increasingly found to fulfill key functions in neurodegenerative diseases. This study aimed to probe the function of lncRNA MALAT1 in neuronal recovery in Alzheimer's disease (AD). Aβ25-35 was used to induce AD in a rat model and neuronal injury in PC12 and C6 cells. Aberrantly expressed lncRNAs/microRNAs (miRNAs) in AD rats were screened out by microarray analyses. Altered expression of MALAT1, miR-30b and CNR1 was performed to explore their roles in neuronal recovery in rat and cell models. Consequently, LncRNA MALAT1 and CNR1 were poorly expressed while miR-30b was highly expressed in Aβ25-35-induced rat models and cells. Overexpression of MALAT1 or CNR1 reduced neuronal injury in rat hippocampus. It increased viability and decreased apoptosis in injured PC12 and C6 cells, and decreased the secretion of pro-inflammatory factor IL-6 and TNF-α but increased IL-10 production. However, overexpression of miR-30b reversed these trends. MALAT1 could served as a sponge for mR-30b to up-regulate CNR1 expression. The phosphorylation of PI3K and AKT was stimulated when MALAT1 or CNR1 was overexpressed. To sum up, we found MALAT1 could promote neuronal recovery following AD through the miR-30b/CNR1 network and the PI3K/AKT signaling activation.	NA	Exp Mol Pathol. 2020 Dec;117:104545. doi: 10.1016/j.yexmp.2020.104545. Epub 2020 Sep 22.
4322	LncRNA	MALAT1	miR-22-3p	IAPs	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33135336	Suppression of lncRNA MALAT1 by betulinic acid inhibits hepatocellular carcinoma progression by targeting IAPs via miR-22-3p.	Betulinic acid (BA) is a natural product extracted from a broad range of medicinal and edible herbal plants. Previous studies showed that BA induces cell death in tumors derived from multiple tissues; however, the underlying mechanism remains obscure. The present study aimed to study the effects of BA on autophagy and apoptosis of hepatocellular carcinoma (HCC). Human HCC cell lines and orthotopic HCC implanted mice were employed to examine the BA-induced tumor suppression; RT(2) long noncoding RNA (lncRNA) PCR array and database analysis were used to explore the possible mechanisms; validation of pathways was performed using siRNA and miRNA inhibitors. The results indicated that BA regulated autophagy and induced apoptosis in HCC. The degradation of inhibitor of apoptosis proteins (IAPs), the conversion of LC3-I to LC3-II, and p62 accumulation were enhanced by BA, thereby suggesting that the downregulation of IAPs and autophagic cell death are induced by BA. The addition of autophagy and lysosomal inhibitors indicated that BA induced autophagy-independent apoptosis via degradation of IAPs. Moreover, RT(2) lncRNA PCR array and database analysis suggested that BA downregulated the levels of lncRNA MALAT1, which is considered to be an oncogene. Further investigations demonstrated that lncRNA MALAT1 functioned as a ceRNA (competing endogenous RNA) to contribute to BA-mediated degradation of IAPs by sponging miR-22-3p. Therefore, BA could be developed as a potential anticancer agent for HCC.	NA	Clin Transl Med. 2020 Oct;10(6):e190. doi: 10.1002/ctm2.190.
4323	LncRNA	MALAT1	miR-146a	BRCA1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	MTT assay;Flow Cytometry assay;luciferase assay;MTT assay;	33030583	Targeting MALAT1 induces DNA damage and sensitize non-small cell lung cancer cells to cisplatin by repressing BRCA1.	PURPOSE: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA which has been identified to be involved in alternative non-homologous end joining (A-NHEJ) pathways by binding with PARP1 and LIG3 in myeloma cells. This study aims to explore the roles of MALAT1 in DNA repair processes in non-small cell lung cancer (NSCLC). METHODS: The interactions between MALAT1 and proteins were identified by co-immunoprecipitation and RNA pulldown. The interactions between MALAT1 and microRNAs (miRNA) were predicted by bioinformatics tools and confirmed by luciferase assay and RNA pulldown. The DNA damages were quantified by comet assay. The cell viability was examined by MTT assay and the cell apoptosis was determined by flow cytometry. RESULTS: MALAT1 is identified to be involved in A-NHEJ pathway in NSCLC cells. However, in LIG3-null cells where A-NHEJ pathway is inactivated, targeting MALAT1 still increases DNA damages, suggesting that MALAT1 participates in other DNA repair pathways. Subsequently, MALAT1 is identified to bind with miR-146a and miR-216b, which directly target the 3'UTR of BRCA1. MALAT1 is confirmed to functions as a competing endogenous RNA (ceRNA) absorbing miR-146a and miR-216b, upregulating BRCA1 expression and protecting Homologous Recombination (HR) pathway in NSCLC cells. Finally, overexpression MALAT1 protects NSCLC cells from the cytotoxic effect of cisplatin. While, targeting MALAT1 in NSCLC cells induces DNA damages by repressing HR pathway and sensitizes NSCLC cells to cisplatin which had the potential for NSCLC treatment. CONCLUSION: MALAT1 is involved in HR pathway by protecting BRCA1 and targeting MALAT1 induces DNA damages in NSCLC.	NA	Cancer Chemother Pharmacol. 2020 Nov;86(5):663-672. doi: 10.1007/s00280-020-04152-7. Epub 2020 Oct 8.
4324	LncRNA	MALAT1	miR-216b	BRCA1	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	MTT assay;Flow Cytometry assay;luciferase assay;MTT assay;	33030583	Targeting MALAT1 induces DNA damage and sensitize non-small cell lung cancer cells to cisplatin by repressing BRCA1.	PURPOSE: Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA which has been identified to be involved in alternative non-homologous end joining (A-NHEJ) pathways by binding with PARP1 and LIG3 in myeloma cells. This study aims to explore the roles of MALAT1 in DNA repair processes in non-small cell lung cancer (NSCLC). METHODS: The interactions between MALAT1 and proteins were identified by co-immunoprecipitation and RNA pulldown. The interactions between MALAT1 and microRNAs (miRNA) were predicted by bioinformatics tools and confirmed by luciferase assay and RNA pulldown. The DNA damages were quantified by comet assay. The cell viability was examined by MTT assay and the cell apoptosis was determined by flow cytometry. RESULTS: MALAT1 is identified to be involved in A-NHEJ pathway in NSCLC cells. However, in LIG3-null cells where A-NHEJ pathway is inactivated, targeting MALAT1 still increases DNA damages, suggesting that MALAT1 participates in other DNA repair pathways. Subsequently, MALAT1 is identified to bind with miR-146a and miR-216b, which directly target the 3'UTR of BRCA1. MALAT1 is confirmed to functions as a competing endogenous RNA (ceRNA) absorbing miR-146a and miR-216b, upregulating BRCA1 expression and protecting Homologous Recombination (HR) pathway in NSCLC cells. Finally, overexpression MALAT1 protects NSCLC cells from the cytotoxic effect of cisplatin. While, targeting MALAT1 in NSCLC cells induces DNA damages by repressing HR pathway and sensitizes NSCLC cells to cisplatin which had the potential for NSCLC treatment. CONCLUSION: MALAT1 is involved in HR pathway by protecting BRCA1 and targeting MALAT1 induces DNA damages in NSCLC.	NA	Cancer Chemother Pharmacol. 2020 Nov;86(5):663-672. doi: 10.1007/s00280-020-04152-7. Epub 2020 Oct 8.
4325	LncRNA	MALAT1	miR-429	ZEB1	FaDu cells	Hypopharyngeal Squamous Cell Carcinoma	Homo sapiens (human)	CCK-8 assay;Western blot;Flow Cytometry assay;	32980391	Inhibition of long non-coding RNA MALAT1 elevates microRNA-429 to suppress the progression of hypopharyngeal squamous cell carcinoma by reducing ZEB1.	OBJECTIVE: Hypopharyngeal squamous cell carcinoma (HSCC) is a common type of malignant tumor. Long non-coding RNAs (lncRNAs) are known to participate in HSCC development, while the role of lncRNA MALAT1 in HSCC remains largely unknown. We aimed to explore function of the lncRNA MALAT1/miR-429/ZEB1 axis in HSCC progression. METHODS: Levels of MALAT1, miR-429 and ZEB1 in HSCC tissues samples were assessed. The FaDu cells were respectively treated with relative sequence or plasmid of MALAT1, miR-429, or ZEB1. Then, CCK-8 assay, colony formation assay, flow cytometry and Transwell assay were used to determine the cell proliferation, apoptosis, cell cycle, migration and invasion of the cells. The PI3K/Akt/mTOR signaling pathway-related proteins, proliferation-related proteins, cell cycle-related proteins, apoptosis-related proteins, and migration-related proteins were detected using Western blot analysis. The cell growth in vivo was observed. The targeting relationships between MALAT1 and miR-429, and between miR-429 and ZEB1 were confirmed. RESULTS: MALAT1 and ZEB1 expression in HSCC was upregulated while miR-429 expression was downregulated. Reduced MALAT1 and ZEB1, and upregulated miR-429 inactivated the PI3K/Akt/mTOR signaling pathway, suppressed in vitro viability, colony formation ability, migration and invasion, as well as cell growth in vivo, and promoted the apoptosis of FaDu cells. Downregulated miR-429 reversed the role of MALAT1 inhibition in FaDu cell growth. LncRNA MALAT1 served as a sponge of miR-429, thus regulating ZEB1 expression. CONCLUSION: Inhibition of MALAT1 was able to elevate miR-429 to suppress the progression of HSCC via reducing ZEB1. Our research provided a potential therapeutic target for HSCC.	NA	Life Sci. 2020 Dec 1;262:118480. doi: 10.1016/j.lfs.2020.118480. Epub 2020 Sep 25.
4326	LncRNA	MALAT1	miR-324-3p	ADAM17	CRC tissues and cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33005106	Long non-coding RNA MALAT1 regulates oxaliplatin-resistance via miR-324-3p/ADAM17 axis in colorectal cancer cells.	BACKGROUND: Colorectal cancer (CRC) is one of the most general malignant tumors. Accumulating evidence implied that long non-coding RNA Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) participated in the tumorigenesis of CRC. However, the effect of MALAT1 in drug-resistance needed to be further illustrated. METHODS: Levels of MALAT1, microRNA (miR)-324-3p, and a disintegrin and metalloprotease metallopeptidase domain 17 (ADAM17) were detected using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell Counting Kit 8 (CCK-8) was used to assess the half maximal inhibitory concentration (IC50) of oxaliplatin (Ox). Meanwhile, cell proliferation, migration and apoptosis were detected by CCK-8, transwell assay, and flow cytometry, respectively. The interaction between miR-324-3p and MALAT1 or ADAM17 was clarified by dual-luciferase reporter assay. Also, the effect of MALAT1 on tumor growth was detected in xenograft tumor mice treated with Ox. RESULTS: Significant up regulation of MALAT1 and ADAM17, and decrease of miR-324-3p were observed in Ox-resistant CRC tissues and cells. MALAT1 deficiency enhanced the sensitivity of Ox-resistant CRC cells response to Ox, while miR-324-3p repression or ADAM17 acceleration could overturn this effect. Moreover, MALAT1 silencing repressed tumor growth in Ox-treated nude mice. Mechanically, MALAT1 exerted promotion effect on the resistance response to Ox via miR-324-3p/ADAM17 axis in Ox-resistant CRC cells. CONCLUSION: MALAT1 modulated the sensitivity of Ox through ADAM17 in Ox-resistant CRC cells by sponging miR-324-3p, thus MALAT1 might serve as a novel insight for the therapy of CRC.	NA	Cancer Cell Int. 2020 Sep 29;20:473. doi: 10.1186/s12935-020-01549-5. eCollection 2020.
4327	LncRNA	MALAT1	miR-3129-5p	Nova1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32965597	LncRNA MALAT1 mediates doxorubicin resistance of hepatocellular carcinoma by regulating miR-3129-5p/Nova1 axis.	Drug resistance is one of the major challenges for cancer therapies. In recent years, research on disease-related molecular signaling pathways has become the key ways to understand and overcome obstacles. Dysregulation of MALAT1 could regulate doxorubicin resistance of hepatocellular carcinoma (HCC), but how MALAT1 involving in managing doxorubicin resistance remains unclear yet. We aimed to elucidate the specific molecular mechanism of MALAT1 with doxorubicin resistance in HCC cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was engaged to detect the expression levels of MALAT1, miR-3129-5p and Nova1 mRNA; MTT, western blot, flow cytometry and luciferase reporter assays were executed to identify the influence of MALAT1 on doxorubicin resistance of HCC cells. Xenograft tumor model was created to confirm the biological function of MALAT1 in doxorubicin resistance of HCC cells in vivo. MALAT1 and Nova1 were upregulated, while miR-3129-5p expression was decreased in doxorubicin-resistant HCC tissues and cells. Knockdown of MALAT1 regulated doxorubicin resistance of HCC cells through inhibiting cell proliferation, migration, invasion and promoting apoptosis, but antisense miR-3129-5p released the functional effect of MALAT1 knockdown. Nova1, as a target gene of miR-3129-5p, reversed the results of miR-3129-5p expression and enhanced doxorubicin resistance of HCC cells. Xenograft tumor model suggested that dysregulation of MALAT1 regulated tumor growth and Nova1 to mediate doxorubicin resistance of HCC cells by as a sponge for miR-3129-5p in vivo. Elevation of LncRNA MALAT1 mediated doxorubicin resistance and the progression of HCC via a MALAT1/miR-3129-5p/Nova1 axis. This study would be expected to enrich the understanding of doxorubicin resistance of HCC and provide new ideas for HCC treatment strategies.	NA	Mol Cell Biochem. 2021 Jan;476(1):279-292. doi: 10.1007/s11010-020-03904-6. Epub 2020 Sep 23.
4328	LncRNA	MALAT1	miR-1271-5p	E2F5	OC tissues and cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33116856	LncRNA MALAT1 Regulates the Progression and Cisplatin Resistance of Ovarian Cancer Cells via Modulating miR-1271-5p/E2F5 Axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) were reported to be related to the development of ovarian cancer (OC). In this study, the functional mechanisms of lncRNA metastasis associated with lung adenocarcinoma transcript 1 (MALAT1) and microRNA-1271-5p (miR-1271-5p) were explored in OC. METHODS: The level of MALAT1, miR-1271-5p, or E2F transcription factor 5 (E2F5) was detected by qRT-PCR. MTT assay, flow cytometry analysis and transwell migration and invasion assays were performed to determine cell proliferation, apoptosis, migration and invasion, respectively. E2F5 protein expression was detected by Western blot. The interaction between miR-1271-5p and MALAT1 or E2F transcription factor 5 (E2F5) was confirmed by the dual-luciferase reporter assay. RESULTS: MALAT1 and E2F5 level were increased, while miR-1271-5p level was decreased in cisplatin (DDP)-resistant OC tissues and cells. MALAT1 knockdown or miR-1271-5p upregulation decreased IC(50) of cisplatin, and inhibited cell proliferation, migration, invasion, and facilitated cell apoptosis in DDP-resistant OC cells. Moreover, MALAT1 sponged miR-1271-5p to upregulate E2F5 expression. Besides, MALAT1 knockdown decreased DDP resistance, inhibited cell proliferation, migration, invasion, and promoted cell apoptosis by sponging miR-1271-5p to downregulate E2F5 expression in DDP-resistant OC cell. CONCLUSION: We demonstrated that MALAT1 mediated DDP-resistant OC development through miR-1271-5p/E2F5 axis, providing the theoretical basis for OC therapy.	NA	Cancer Manag Res. 2020 Oct 12;12:9999-10010. doi: 10.2147/CMAR.S261979. eCollection 2020.
4329	LncRNA	MALAT1	miR-22	ABCA1	tic coronary artery cells	Tic Coronary Artery Disease	Homo sapiens (human)	qRT-PCR	33097254	MALAT1-mediated recruitment of the histone methyltransferase EZH2 to the microRNA-22 promoter leads to cardiomyocyte apoptosis in diabetic cardiomyopathy.	Diabetic patients often have a heightened risk of cardiomyopathy, even in the absence of traditional risk factors such as hypertension and atherosclerotic coronary artery disease. Diabetic cardiomyopathy is characterized by a typical cardiomyopathy specific to diabetes, the pathogenesis of which has yet to be fully elucidated. As a well-documented oncogenic long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in a variety of pathological processes, including diabetic complications. This study aimed to evaluate the functional roles of MALAT1 in the pathogenesis of diabetic cardiomyopathy. Spontaneously diabetic (db/db) C57BL/Ks mice were employed to establish diabetic cardiomyopathy models in vivo and high glucose (HG)-cultured mouse cardiomyocytes for myocardial damage models in vitro. Mouse left ventricular volume and function were evaluated by echocardiography, while the myocyte cross-sectional area was calculated to evaluate the degree of myocardial hypertrophy. TUNEL staining and flow cytometric analysis were performed to evaluate myocardial damage and cardiomyocyte apoptosis. Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes. MALAT1 recruited the histone methyltransferase EZH2 to the miR-22 promoter region and inhibited its expression. EZH2 induced an increased in the expression of ATP-binding cassette transporter A1 (ABCA1), which was identified to be a target gene of miR-22. Silencing of EZH2 was found to improve cardiac function and prevent cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes in the presence of MALAT1, suggesting that MALAT1 mediated myocardial damage by recruiting EZH2 to the miR-22 promoter. Taken together, this study's findings provide evidence confirming our hypothesis, suggesting the involvement of MALAT1 in the processes of cardiac function and cardiomyocyte apoptosis via the EZH2/miR-22/ABCA1 signaling cascade, which has potential therapeutic implications for the understanding of diabetic cardiomyopathy.	NA	Sci Total Environ. 2021 Apr 20;766:142191. doi: 10.1016/j.scitotenv.2020.142191. Epub 2020 Sep 4.
4330	LncRNA	MALAT1	miR-22	EZH2	tic coronary artery cells	Tic Coronary Artery Disease	Mus musculus (mouse)	qRT-PCR	33097254	MALAT1-mediated recruitment of the histone methyltransferase EZH2 to the microRNA-22 promoter leads to cardiomyocyte apoptosis in diabetic cardiomyopathy.	Diabetic patients often have a heightened risk of cardiomyopathy, even in the absence of traditional risk factors such as hypertension and atherosclerotic coronary artery disease. Diabetic cardiomyopathy is characterized by a typical cardiomyopathy specific to diabetes, the pathogenesis of which has yet to be fully elucidated. As a well-documented oncogenic long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in a variety of pathological processes, including diabetic complications. This study aimed to evaluate the functional roles of MALAT1 in the pathogenesis of diabetic cardiomyopathy. Spontaneously diabetic (db/db) C57BL/Ks mice were employed to establish diabetic cardiomyopathy models in vivo and high glucose (HG)-cultured mouse cardiomyocytes for myocardial damage models in vitro. Mouse left ventricular volume and function were evaluated by echocardiography, while the myocyte cross-sectional area was calculated to evaluate the degree of myocardial hypertrophy. TUNEL staining and flow cytometric analysis were performed to evaluate myocardial damage and cardiomyocyte apoptosis. Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes. MALAT1 recruited the histone methyltransferase EZH2 to the miR-22 promoter region and inhibited its expression. EZH2 induced an increased in the expression of ATP-binding cassette transporter A1 (ABCA1), which was identified to be a target gene of miR-22. Silencing of EZH2 was found to improve cardiac function and prevent cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes in the presence of MALAT1, suggesting that MALAT1 mediated myocardial damage by recruiting EZH2 to the miR-22 promoter. Taken together, this study's findings provide evidence confirming our hypothesis, suggesting the involvement of MALAT1 in the processes of cardiac function and cardiomyocyte apoptosis via the EZH2/miR-22/ABCA1 signaling cascade, which has potential therapeutic implications for the understanding of diabetic cardiomyopathy.	NA	Sci Total Environ. 2021 Apr 20;766:142191. doi: 10.1016/j.scitotenv.2020.142191. Epub 2020 Sep 4.
4331	LncRNA	MALAT1	miR-22	ABCA1	tic coronary artery cells	Tic Coronary Artery Disease	Homo sapiens (human)	qRT-PCR	33097254	MALAT1-mediated recruitment of the histone methyltransferase EZH2 to the microRNA-22 promoter leads to cardiomyocyte apoptosis in diabetic cardiomyopathy.	Diabetic patients often have a heightened risk of cardiomyopathy, even in the absence of traditional risk factors such as hypertension and atherosclerotic coronary artery disease. Diabetic cardiomyopathy is characterized by a typical cardiomyopathy specific to diabetes, the pathogenesis of which has yet to be fully elucidated. As a well-documented oncogenic long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in a variety of pathological processes, including diabetic complications. This study aimed to evaluate the functional roles of MALAT1 in the pathogenesis of diabetic cardiomyopathy. Spontaneously diabetic (db/db) C57BL/Ks mice were employed to establish diabetic cardiomyopathy models in vivo and high glucose (HG)-cultured mouse cardiomyocytes for myocardial damage models in vitro. Mouse left ventricular volume and function were evaluated by echocardiography, while the myocyte cross-sectional area was calculated to evaluate the degree of myocardial hypertrophy. TUNEL staining and flow cytometric analysis were performed to evaluate myocardial damage and cardiomyocyte apoptosis. Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes. MALAT1 recruited the histone methyltransferase EZH2 to the miR-22 promoter region and inhibited its expression. EZH2 induced an increased in the expression of ATP-binding cassette transporter A1 (ABCA1), which was identified to be a target gene of miR-22. Silencing of EZH2 was found to improve cardiac function and prevent cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes in the presence of MALAT1, suggesting that MALAT1 mediated myocardial damage by recruiting EZH2 to the miR-22 promoter. Taken together, this study's findings provide evidence confirming our hypothesis, suggesting the involvement of MALAT1 in the processes of cardiac function and cardiomyocyte apoptosis via the EZH2/miR-22/ABCA1 signaling cascade, which has potential therapeutic implications for the understanding of diabetic cardiomyopathy.	NA	Sci Total Environ. 2021 Apr 20;766:142191. doi: 10.1016/j.scitotenv.2020.142191. Epub 2020 Sep 4.
4332	LncRNA	MALAT1	miR-22	EZH2	tic coronary artery cells	Tic Coronary Artery Disease	Mus musculus (mouse)	qRT-PCR	33097254	MALAT1-mediated recruitment of the histone methyltransferase EZH2 to the microRNA-22 promoter leads to cardiomyocyte apoptosis in diabetic cardiomyopathy.	Diabetic patients often have a heightened risk of cardiomyopathy, even in the absence of traditional risk factors such as hypertension and atherosclerotic coronary artery disease. Diabetic cardiomyopathy is characterized by a typical cardiomyopathy specific to diabetes, the pathogenesis of which has yet to be fully elucidated. As a well-documented oncogenic long noncoding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in a variety of pathological processes, including diabetic complications. This study aimed to evaluate the functional roles of MALAT1 in the pathogenesis of diabetic cardiomyopathy. Spontaneously diabetic (db/db) C57BL/Ks mice were employed to establish diabetic cardiomyopathy models in vivo and high glucose (HG)-cultured mouse cardiomyocytes for myocardial damage models in vitro. Mouse left ventricular volume and function were evaluated by echocardiography, while the myocyte cross-sectional area was calculated to evaluate the degree of myocardial hypertrophy. TUNEL staining and flow cytometric analysis were performed to evaluate myocardial damage and cardiomyocyte apoptosis. Silencing of MALAT1 was found to attenuate cardiac dysfunction and inhibit cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes. MALAT1 recruited the histone methyltransferase EZH2 to the miR-22 promoter region and inhibited its expression. EZH2 induced an increased in the expression of ATP-binding cassette transporter A1 (ABCA1), which was identified to be a target gene of miR-22. Silencing of EZH2 was found to improve cardiac function and prevent cardiomyocyte apoptosis in db/db mice and HG-cultured mouse cardiomyocytes in the presence of MALAT1, suggesting that MALAT1 mediated myocardial damage by recruiting EZH2 to the miR-22 promoter. Taken together, this study's findings provide evidence confirming our hypothesis, suggesting the involvement of MALAT1 in the processes of cardiac function and cardiomyocyte apoptosis via the EZH2/miR-22/ABCA1 signaling cascade, which has potential therapeutic implications for the understanding of diabetic cardiomyopathy.	NA	Sci Total Environ. 2021 Apr 20;766:142191. doi: 10.1016/j.scitotenv.2020.142191. Epub 2020 Sep 4.
4333	LncRNA	MALAT1	miR-194-5p	FOXP2	pulmonary alveolar epithelial cells	Acute Lung Injury	Homo sapiens (human)	qPCR;Western blot;Flow Cytometry assay;	33117815	Knockdown of lncRNA MALAT1 Alleviates LPS-Induced Acute Lung Injury via Inhibiting Apoptosis Through the miR-194-5p/FOXP2 Axis.	PURPOSE: We aimed to identify and verify the key genes and lncRNAs associated with acute lung injury (ALI) and explore the pathogenesis of ALI. Research showed that lower expression of the lncRNA metastasis-associated lung carcinoma transcript 1 (MALAT1) alleviates lung injury induced by lipopolysaccharide (LPS). Nevertheless, the mechanisms of MALAT1 on cellular apoptosis remain unclear in LPS-stimulated ALI. We investigated the mechanism of MALAT1 in modulating the apoptosis of LPS-induced human pulmonary alveolar epithelial cells (HPAEpiC). METHODS: Differentially expressed lncRNAs between the ALI samples and normal controls were identified using gene expression profiles. ALI-related genes were determined by the overlap of differentially expressed genes (DEGs), genes correlated with lung, genes correlated with key lncRNAs, and genes sharing significantly high proportions of microRNA targets with MALAT1. Quantitative real-time PCR (qPCR) was applied to detect the expression of MALAT1, microRNA (miR)-194-5p, and forkhead box P2 (FOXP2) mRNA in 1 μg/ml LPS-treated HPAEpiC. MALAT1 knockdown vectors, miR-194-5p inhibitors, and ov-FOXP2 were constructed and used to transfect HPAEpiC. The influence of MALAT1 knockdown on LPS-induced HPAEpiC proliferation and apoptosis via the miR-194-5p/FOXP2 axis was determined using Cell counting kit-8 (CCK-8) assay, flow cytometry, and Western blotting analysis, respectively. The interactions between MALAT1, miR-194-5p, and FOXP2 were verified using dual-luciferase reporter gene assay. RESULTS: We identified a key lncRNA (MALAT1) and three key genes (EYA1, WNT5A, and FOXP2) that are closely correlated with the pathogenesis of ALI. LPS stimulation promoted MALAT1 expression and apoptosis and also inhibited HPAEpiC viability. MALAT1 knockdown significantly improved viability and suppressed the apoptosis of LPS-stimulated HPAEpiC. Moreover, MALAT1 directly targeted miR-194-5p, a downregulated miRNA in LPS-stimulated HPAEpiC, when FOXP2 was overexpressed. MALAT1 knockdown led to the overexpression of miR-194-5p and restrained FOXP2 expression. Furthermore, inhibition of miR-194-5p exerted a rescue effect on MALAT1 knockdown of FOXP2, whereas the overexpression of FOXP2 reversed the effect of MALAT1 knockdown on viability and apoptosis of LPS-stimulated HPAEpiC. CONCLUSION: Our results demonstrated that MALAT1 knockdown alleviated HPAEpiC apoptosis by competitively binding to miR-194-5p and then elevating the inhibitory effect on its target FOXP2. These data provide a novel insight into the role of MALAT1 in the progression of ALI and potential diagnostic and therapeutic strategies for ALI patients.	NA	Front Cell Dev Biol. 2020 Oct 7;8:586869. doi: 10.3389/fcell.2020.586869. eCollection 2020.
4334	LncRNA	MALAT1	miR-22	NA	EOC tissues and cell	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33312345	LncRNA MALAT-1 promotes growth and metastasis of epithelial ovarian cancer via sponging microrna-22.	LncRNAs and miRNAs are emerging players in epithelial ovarian cancer (EOC). LncRNA MALAT-1 and miR-22 play vital roles in the onset and development of multiple cancers. Both of them are abnormally expressed in ovarian cancer, but the molecular basis for their involvement in EOC is unclear. In this study, we found MALAT-1 was up-regulated but miR-22 was down-regulated in EOC tissues and cell lines when compared to normal ovarian epithelial cell line IOSE80. Both of MALAT-1shRNA and miR-22 mimics inhibited ovarian cell proliferation, migration, and invasion, while simultaneously overexpressing MALAT-1 and miR-22 largely canceled out this inhibitory effect. Consistently, MALAT-1 silencing and miR-22 overexpression restrained tumor growth and metastasis to lungs in nude mice, which could be largely counteracted by co-overexpressing MALAT-1 and miR-22. Mechanistically, MALAT-1 targeted and sponged miR-22, counteracting its inhibitory effect on c-myc and c-myc-mediated epithelial-mesenchymal transition. Our findings for the first time demonstrated that MALAT-1 supports EOC progression through sponging miR-22, providing a novel insight into the role of MALAT-1 in ovarian cancer.	NA	Am J Transl Res. 2020 Nov 15;12(11):6977-6987. eCollection 2020.
4335	LncRNA	MAPK8IP1P2	miR-146b-3p	NA	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	qRT-PCR	33489905	Long Non-Coding RNA MAPK8IP1P2 Inhibits Lymphatic Metastasis of Thyroid Cancer by Activating Hippo Signaling via Sponging miR-146b-3p.	The principal issue derived from thyroid cancer is its high propensity to metastasize to the lymph node. Aberrant exprssion of long non-coding RNAs have been extensively reported to be significantly correlated with lymphatic metastasis of thyroid cancer. However, the clinical significance and functional role of lncRNA-MAPK8IP1P2 in lymphatic metastasis of thyroid cancer remain unclear. Here, we reported that MAPK8IP1P2 was downregulated in thyroid cancer tissues with lymphatic metastasis. Upregulating MAPK8IP1P2 inhibited, while silencing MAPK8IP1P2 enhanced anoikis resistance in vitro and lymphatic metastasis of thyroid cancer cells in vivo. Mechanistically, MAPK8IP1P2 activated Hippo signaling by sponging miR-146b-3p to disrupt the inhibitory effect of miR-146b-3p on NF2, RASSF1, and RASSF5 expression, which further inhibited anoikis resistance and lymphatic metastasis in thyroid cancer. Importantly, miR-146b-3p mimics reversed the inhibitory effect of MAPK8IP1P2 overexpression on anoikis resistance of thyroid cancer cells. In conclusion, our findings suggest that MAPK8IP1P2 may serve as a potential biomarker to predict lymphatic metastasis in thyroid cancer, or a potential therapeutic target in lymphatic metastatic thyroid cancer.	NA	Front Oncol. 2021 Jan 7;10:600927. doi: 10.3389/fonc.2020.600927. eCollection 2020.
4336	LncRNA	MCF2L-AS1	miR-874-3p	CCNE1	CRC cells	Colorectal Cancer	Homo sapiens (human)	Luciferase reporter assay;	33037865	Long non-coding RNA MCF2L-AS1 promotes the aggressiveness of colorectal cancer by sponging miR-874-3p and thereby up-regulating CCNE1.	BACKGROUND: Long non-coding RNAs (lncRNAs) have drawn growing attention because of the role which they play in various diseases, including colorectal cancer (CRC). However, the potential functions of lncRNA MCF2L antisense RNA 1 (MCF2L-AS1) in tumors remained largely unclear. The present study aimed to explore the clinical significance and the biological effects of lncRNA MCF2L antisense RNA 1 (MCF2L-AS1) in CRC. METHODS: Reverse transcriptase-polymerase chain reaction was performed to determine the expression of MCF2L-AS1 in CRC. The clinical significance of MCF2L-AS1 in CRC patients was analyzed statistically. In vitro experiments were performed to determine the effects of MCF2L-AS1 on the cellular progression of CRC cells. Bioinformatic assays, luciferase reporter assays and RNA-pulldown assays were performed to predict for potential microRNAs that can interact with MCF2L-AS1 and mRNAs that can interact with miR-874-3p. RESULTS: We identified a novel CRC-related lncRNA, MCF2L-AS1, which is distinctly highly expressed in CRC. Its diagnostic value for CRC patients was also demonstrated. Clinical assays revealed that high MCF2L-AS1 expression is associated with advanced stages, positive metastasis and the poor prognosis of CRC patients. Multivariate assays confirmed that MCF2L-AS1 expression is an independent poor prognostic factor for both 5-year overall survival and 5-year disease-free survival of CRC patients. Functionally, we confirmed that knockdown of MCF2L-AS1 distinctly suppresses the proliferation, migration and invasion of CRC cells and also promotes apoptosis. Mechanistic investigation showed that MCF2L-AS1 functions as an endogenous sponge for miR-874-3p to increase the expression of CCNE1. CONCLUSIONS: Our findings identified a novel CRC-related lncRNA, MCF2L-AS1, which may be used as a potential diagnostic and prognostic biomarker for CRC patients. In addition, the newly identified MCF2L-AS1/miR-874-3p/CCNE1 axis can modulate the initiation and progression of CRC.	NA	J Gene Med. 2021 Jan;23(1):e3285. doi: 10.1002/jgm.3285. Epub 2020 Nov 5.
4337	LncRNA	MCM3AP-AS1	miR-599	ARPP19	CRC cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33613714	Long non-coding RNA MCM3AP-AS1 facilitates colorectal cancer progression by regulating the microRNA-599/ARPP19 axis.	Colorectal cancer (CRC) is one of the most aggressive malignancies worldwide. Increasing evidence has indicated that microRNA (miR)-599 is involved in the occurrence and development of different types of tumors, such as breast cancer and glioma. However, the role of miR-599 in CRC remains unclear. Thus, the present study aimed to identify the regulatory mechanism of miR-599 in CRC progression. Reverse transcription-quantitative PCR was used to analyze the expression levels of MCM3AP-AS1, miR-599 and ARPP19, and Cell Counting Kit-8 and Transwell assays were used to determine the cell proliferation and migration of CRC cells. In addition, a Dual-luciferase reporter assay was used to analyze the direct interaction between miR-599 and MCM3AP-AS1 or ARPP19. Reverse transcription-quantitative PCR analysis demonstrated that miR-599 expression decreased in patients with CRC and in CRC cell lines, while miR-599 overexpression inhibited cell proliferation and migration abilities in vitro. MCM3AP-AS1 was identified as a molecular sponge of miR-599, and further investigation indicated that MCM3AP-AS1 silencing inhibited cell proliferation and migration of the CRC cell lines. In addition, ARPP19 was identified as a target gene of miR-599, and MCM3AP-AS1-knockdown decreased ARPP19 mRNA expression and increased miR-599 expression. Furthermore, silencing ARPP19 inhibited the proliferation and migration of the CRC cell lines. The results also demonstrated that MCM3AP-AS1 promoted CRC cell progression by regulating the miR-599/ARPP19 axis. Taken together, the results of the present study suggest that MCM3AP-AS1 may be a novel therapeutic target for patients with CRC.	NA	Oncol Lett. 2021 Mar;21(3):225. doi: 10.3892/ol.2021.12486. Epub 2021 Jan 24.
4338	LncRNA	MEG3	miR-216a	PD-L1	EC cells	Endometrial Cancer	Homo sapiens (human)	Luciferase reporter assay;	33363153	PD-L1 Is a Tumor Suppressor in Aggressive Endometrial Cancer Cells and Its Expression Is Regulated by miR-216a and lncRNA MEG3.	BACKGROUND: Poorly differentiated endometrioid adenocarcinoma and serous adenocarcinoma represent an aggressive subtype of endometrial cancer (EC). Programmed death-ligand-1 (PD-L1) was known to exhibit a tumor cell-intrinsic function in mediating immune-independent tumor progression. However, the functional relevance of tumor cell-intrinsic PD-L1 expression in aggressive EC cells and the mechanisms regulating its expression remain unknown. METHODS: PD-L1 expression in 65 EC tissues and 18 normal endometrium samples was analyzed using immunohistochemical staining. The effects of PD-L1 on aggressive EC cell growth, migration and invasion were investigated by cell functional assays. Luciferase reporter assays were used to reveal the microRNA-216a (miR-216a)-dependent mechanism modulating the expression of PD-L1. RESULTS: Positive PD-L1 expression was identified in 84% of benign cases but only in 12% of the EC samples, and the staining levels of PD-L1 in EC tissues were significantly lower than those in the normal tissues. Higher PD-L1 expression predicts favorable survival in EC. Ectopic expression of PD-L1 in aggressive EC cells results in decreased cell proliferation and the loss of mesenchymal phenotypes. Mechanistically, PD-L1 exerts the anti-tumor effects by downregulating MCL-1 expression. We found that PD-L1 levels in aggressive EC cells are regulated by miR-216a, which directly targets PD-L1. We further identified a mechanism whereby the long non-coding RNA MEG3 represses the expression of miR-216a, thereby leading to increased PD-L1 expression and significant inhibition of cell migration and invasion. CONCLUSION: These results reveal an unappreciated tumor cell-intrinsic role for PD-L1 as a tumor suppressor in aggressive EC cells, and identify MEG3 and miR-216a as upstream regulators of PD-L1.	NA	Front Cell Dev Biol. 2020 Dec 9;8:598205. doi: 10.3389/fcell.2020.598205. eCollection 2020.
4339	LncRNA	MEG3	miR-4513	PBLD	MCF-7 and MDA-MB-231 cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33121324	Long noncoding RNA MEG3 suppresses cell proliferation, migration and invasion, induces apoptosis and paclitaxel-resistance via miR-4513/PBLD axis in breast cancer cells.	Breast cancer remains a general-threat event in the health of women. Currently, increasing records indicate that long non-coding RNA maternally expressed 3 (MEG3) plays a central role in breast cancer. The current research focused on the function of MEG3 in paclitaxel (PTX)-resistance and human breast cancer growth. Levels of MEG3, microRNA (miR)-4513, and phenazine biosynthesis-like domain-containing protein (PBLD) were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assays. 3-(4.5-dimethylghiazol-2-yl)-2,5-diphenyltetrazolium Bromide (MTT) assay was performed to examine the IC(50) of PTX and cell proliferation in breast cancer cells. In addition, cell apoptosis was determined utilizing flow cytometry. Transwell was conducted to assay cell migration and invasion in MCF-7 and MDA-MB-231 cells. The interaction between miR-4513 and MEG3 or PBLD was expounded via dual-luciferase reporter assay. Levels of MEG3 and PBLD were decreased, but miR-4513 level was triggered in breast cancer tissues and cell lines. Overexpression of MEG3 could reinforce cell apoptosis, impede proliferation, migration, invasion, and the IC50 of PTX in breast cancer cells. Moreover, the impact of miR-4513 inhibitor on cell progression and PTX-resistance was overturned by MEG3 deficiency. Interestingly, miR-4513 mimic could abolish the role of PBLD upregulation in cell behaviors and PTX-resistance in MCF-7 and MDA-MB-231 cells. Finally, the expression of PBLD was co-modulated by miR-4513 and MEG3 in vitro. MEG3/miR-4513/PBLD axis modulated PTX-resistance and the development of breast cancer cells, which might provide a promising therapeutic strategy for breast cancer.	NA	Cell Cycle. 2020 Dec;19(23):3277-3288. doi: 10.1080/15384101.2020.1839700. Epub 2020 Oct 30.
4340	LncRNA	MEG3	miR-214	TXNIP	serum	Osteoporosis	Homo sapiens (human)	qRT-PCR	33393160	Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP.	Studies have shown that long non-coding RNA (lncRNA) MEG3 plays a key role in osteoporosis (OP), but its regulatory mechanism is somewhat incompletely clear. Here, we intend to probe into the mechanism of MEG3 on OP development by modulating microRNA-214 (miR-214) and thioredoxin-interacting protein (TXNIP). Rat models of OP were established. MEG3, miR-214 and TXNIP mRNA expression in rat femoral tissues were detected, along with TXNIP, OPG and RANKL protein expression. BMD, BV/TV, Tb.N and Tb.Th in tissue samples were measured. Ca, P and ALP contents in rat serum were also determined. Primary osteoblasts were isolated and cultured. Viability, COL-I, COL-II and COL-Χ mRNA expression, PCNA, cyclin D1, OCN, RUNX2 and osteolix protein expresion, ALP content and activity, and mineralized nodule area of rat osteoblasts were further detected. Dual-luciferase reporter gene and RNA-pull down assays verified the targeting relationship between MEG3, miR-214 and TXNIP. MEG3 and TXNIP were up-regulated while miR-214 was down-regulated in femoral tissues of OP rats. MEG3 silencing and miR-214 overexpression increased BMD, BV/TV, Tb.N, Tb.Th, trabecular bone area, collagen area and OPG expression, and down-regulated RANKL of femoral tissues in OP rats. MEG3 silencing and miR-214 overexpression elevated Ca and P and reduced ALP in OP rat serum, elevated osteoblast viability, differentiation ability, COL-I and COL-Χ expression and ALP activity, and reduced COL-II expression of osteoblasts. MEG3 specifically bound to miR-214 to regulate TXNIP. MEG3 silencing and miR-214 overexpression promote proliferation and differentiation of osteoblasts in OP by down-regulating TXNIP, which further improves OP.	NA	J Cell Mol Med. 2021 Feb;25(4):2025-2039. doi: 10.1111/jcmm.16096. Epub 2021 Jan 3.
4341	LncRNA	MEG3	miR-214	TXNIP	serum	Osteoporosis	Rattus (rat)	qRT-PCR	33393160	Long non-coding RNA MEG3 silencing and microRNA-214 restoration elevate osteoprotegerin expression to ameliorate osteoporosis by limiting TXNIP.	Studies have shown that long non-coding RNA (lncRNA) MEG3 plays a key role in osteoporosis (OP), but its regulatory mechanism is somewhat incompletely clear. Here, we intend to probe into the mechanism of MEG3 on OP development by modulating microRNA-214 (miR-214) and thioredoxin-interacting protein (TXNIP). Rat models of OP were established. MEG3, miR-214 and TXNIP mRNA expression in rat femoral tissues were detected, along with TXNIP, OPG and RANKL protein expression. BMD, BV/TV, Tb.N and Tb.Th in tissue samples were measured. Ca, P and ALP contents in rat serum were also determined. Primary osteoblasts were isolated and cultured. Viability, COL-I, COL-II and COL-Χ mRNA expression, PCNA, cyclin D1, OCN, RUNX2 and osteolix protein expresion, ALP content and activity, and mineralized nodule area of rat osteoblasts were further detected. Dual-luciferase reporter gene and RNA-pull down assays verified the targeting relationship between MEG3, miR-214 and TXNIP. MEG3 and TXNIP were up-regulated while miR-214 was down-regulated in femoral tissues of OP rats. MEG3 silencing and miR-214 overexpression increased BMD, BV/TV, Tb.N, Tb.Th, trabecular bone area, collagen area and OPG expression, and down-regulated RANKL of femoral tissues in OP rats. MEG3 silencing and miR-214 overexpression elevated Ca and P and reduced ALP in OP rat serum, elevated osteoblast viability, differentiation ability, COL-I and COL-Χ expression and ALP activity, and reduced COL-II expression of osteoblasts. MEG3 specifically bound to miR-214 to regulate TXNIP. MEG3 silencing and miR-214 overexpression promote proliferation and differentiation of osteoblasts in OP by down-regulating TXNIP, which further improves OP.	NA	J Cell Mol Med. 2021 Feb;25(4):2025-2039. doi: 10.1111/jcmm.16096. Epub 2021 Jan 3.
4342	LncRNA	MEG3	miR-181a-2-3p	NA	16HBE cells	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33262837	Long non-coding maternally expressed gene 3 regulates cigarette smoke extract-induced apoptosis, inflammation and cytotoxicity by sponging miR-181a-2-3p in 16HBE cells.	Accumulating evidence has suggested that long non-coding (lnc)RNAs are widely involved in the progression of multiple diseases, including chronic obstructive pulmonary disease (COPD). The aim of the present study was to explore the function and molecule mechanism of maternally expressed gene 3 (MEG3) in cigarette smoke extract (CSE)-treated 16HBE cells. Cell viability and apoptosis were evaluated using Cell Counting Kit-8 analysis and flow cytometry, respectively. Western blot analysis was carried out to determine the protein levels of Bcl-2, Bax and cleaved caspase-3. ELISA assays were utilized to measure the protein levels of IL-1β and IL-6 and TNF-α. Cytotoxicity was assessed using a lactate dehydrogenase release assay. The expression levels of MEG3 and microRNA (miR)-181a-2-3p were detected using reverse transcription-quantitative PCR. The interaction between miR-181a-2-3p and MEG3 was predicted using DIANA tools and verified by a dual-luciferase reporter assay and RNA Immunoprecipitation assay. MEG3 expression was enhanced while miR-181a-2-3p abundance was reduced in the serum of patients with COPD and CSE-treated 16HBE cells. MEG3-knockdown or miR-181a-2-3p-overexpression inhibited CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells. Moreover, miR-181a-2-3p directly bind to MEG3 and its knockdown reversed the inhibitory effect of MEG3 interference on apoptosis, inflammation and cytotoxicity in CSE-treated 16HBE cells. Overall, MEG3-knockdown suppressed CSE-induced apoptosis, inflammation and cytotoxicity in 16HBE cells by upregulating miR-181a-2-3p, providing a promising therapeutic target for treatment of CSE-induced COPD.	NA	Oncol Lett. 2021 Jan;21(1):45. doi: 10.3892/ol.2020.12306. Epub 2020 Nov 17.
4343	LncRNA	MEG3	miR-7a-5p	Nlrp3	traumatic brain injury cells	Traumatic Brain Injury	Homo sapiens (human)	luciferase assay;	33189612	LncRNA-Meg3 promotes Nlrp3-mediated microglial inflammation by targeting miR-7a-5p.	Recent studies have identified neuroinflammation as a significant contributor to the pathological process of traumatic brain injury (TBI) and as a potentially effective target for treatment. LncRNA maternally expressed gene 3 (Meg3) has further been observed to play a critical role in diverse biological processes, including microglial activation and the inflammatory response. However, its target gene and associated signaling pathway require further elucidation. This study found that lipopolysaccharide + ATP upregulated Meg3, promoted microglia activation, Nlrp3/caspase1 activation and inflammation, and markedly reduced miR-7a-5p. Overexpression of miR-7a-5p attenuated Meg3-induced microglial activation, but not Meg3 expression. Bioinformatic analysis and dual-luciferase assays indicated that Meg3 was a direct target of miR-7a-5p that negatively regulates miR-7a-5p expression. Further, we showed that Meg3 acted as a competing endogenous RNA for miR-7a-5p and induced microglial inflammation by regulating nod-like receptor protein 3 (Nlrp3) expression. Our study thus demonstrates Meg3 regulates microglia inflammation by targeting the miR-7a-5p /Nlrp3 pathway.	NA	Int Immunopharmacol. 2021 Jan;90:107141. doi: 10.1016/j.intimp.2020.107141. Epub 2020 Nov 12.
4344	LncRNA	MEG3	miR-21-5p	PTEN	H1299 and PC9 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;luciferase assay;	33495842	Long non-coding RNA MEG3 inhibits cell migration and invasion of non-small cell lung cancer cells by regulating the miR-21-5p/PTEN axis.	Long non-coding RNAs (lncRNAs) are involved in the occurrence and progression of numerous types of cancer. The aim of the present study was to evaluate the effect of the lncRNA maternally expressed gene 3 (MEG3) on the migration and invasion of non-small cell lung cancer (NSCLC) H1299 and PC9 cells. Reverse transcription-quantitative (RT-q)PCR analysis showed that MEG3 was downregulated in NSCLC PC9 and H1299 cells. Additionally, bioinformatics analysis indicated that MEG3 sponges microRNA (miR)-21-5p; miR-21-5p was predicted to target the phosphatase and tensin homolog (PTEN) 3'-untranslated region sequence. MEG3 overexpression led to miR-21-5p suppression and PTEN upregulation in PC9 and H1299 cells, as detected by RT-qPCR. Subsequently, western blot analysis confirmed that MEG3 overexpression enhanced PTEN expression levels and inhibited the PI3K/AKT signaling pathway in NSCLC cells. These effects were attenuated by miR-21-5p. Dual luciferase assay supported the sponging effect of MEG3 on miR-21-5p and validated the direct interaction between miR-21-5p and PTEN. Furthermore, Transwell assay demonstrated that MEG3 overexpression had an inhibitory effect on cell migration and invasion. MEG3 overexpression also mediated epithelial-to-mesenchymal transition by significantly enhancing E-cadherin and decreasing N-cadherin, Vimentin and matrix metalloprotein 9 expression levels in NSCLC cells, as indicated by western blot analysis. These changes were partially reversed by an miR-21-5p mimic. These results indicated that MEG3 acted as a tumor suppressor that inhibited NSCLC cell migration and invasion via sponging miR-21-5p, which, in turn, enhanced the expression levels of PTEN, in part via the PI3K/AKT signaling pathway. The results of the present study have suggested the potential of MEG3 as a novel therapeutic target for NSCLC treatment.	NA	Mol Med Rep. 2021 Mar;23(3):191. doi: 10.3892/mmr.2021.11830. Epub 2021 Jan 26.
4345	LncRNA	MEG3	miR-325-3p	TRPV4	H9c2 cells	Acute Myocardial Infarction	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33179099	Long non-coding RNA MEG3 knockdown alleviates hypoxia-induced injury in rat cardiomyocytes via the miR-325-3p/TRPV4 axis.	Acute myocardial infarction (AMI) is a common cardiac disease. Long non-coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia-inducible factor 1α (HIF1α), MEG3, microRNA (miR)-325-3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia-treated H9c2 cells were detected via reverse transcription-quantitative PCR. The protein expression levels of HIF1α, Bcl-2, Bax, cleaved caspase-3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual-luciferase reporter assay was performed to verify the targeted relationship between miR-325-3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR-325-3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR-325-3p was downregulated by MEG3 compared with the vector group, and miR-325-3p targeted TRPV4 in hypoxia-treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia-stimulated injury in H9c2 cells by regulating miR-325-3p. TRPV4 knockdown also mitigated hypoxia-induced injury in H9c2 cells via miR-325-3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia-treated H9c2 cells by sponging miR-325-3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia-induced injury in rat cardiomyocytes by sponging miR-325-3p.	NA	Mol Med Rep. 2021 Jan;23(1):18. doi: 10.3892/mmr.2020.11656. Epub 2020 Nov 12.
4346	LncRNA	MEG3	miR-325-3p	TRPV4	H9c2 cells	Acute Myocardial Infarction	Rattus (rat)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33179099	Long non-coding RNA MEG3 knockdown alleviates hypoxia-induced injury in rat cardiomyocytes via the miR-325-3p/TRPV4 axis.	Acute myocardial infarction (AMI) is a common cardiac disease. Long non-coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia-inducible factor 1α (HIF1α), MEG3, microRNA (miR)-325-3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia-treated H9c2 cells were detected via reverse transcription-quantitative PCR. The protein expression levels of HIF1α, Bcl-2, Bax, cleaved caspase-3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual-luciferase reporter assay was performed to verify the targeted relationship between miR-325-3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR-325-3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR-325-3p was downregulated by MEG3 compared with the vector group, and miR-325-3p targeted TRPV4 in hypoxia-treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia-stimulated injury in H9c2 cells by regulating miR-325-3p. TRPV4 knockdown also mitigated hypoxia-induced injury in H9c2 cells via miR-325-3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia-treated H9c2 cells by sponging miR-325-3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia-induced injury in rat cardiomyocytes by sponging miR-325-3p.	NA	Mol Med Rep. 2021 Jan;23(1):18. doi: 10.3892/mmr.2020.11656. Epub 2020 Nov 12.
4347	LncRNA	MEG3	miR-1930-5p	Mllt1	Primary brain microvascular endothelial cells	Intracerebral Hemorrhage	Homo sapiens (human)	RACE;	33127454	Long noncoding RNA MEG3 contributes to dysfunction of brain microvascular endothelial cells after intracerebral hemorrhage by regulating the miR-1930-5p/Mllt1 axis.	BACKGROUND: Intracerebral hemorrhage (ICH) is a subtype of stroke and causes disability and death worldwide. The roles of long noncoding RNAs (lncRNAs) in brain function and neurological diseases have been revealed. LncRNA maternally expressed gene 3 (MEG3) is involved in neurological impairment, but its role in ICH remains unknown. AIMS: The aim of this research is to explore the role of MEG3 in ICH. METHODS AND RESULTS: Here, we established an ICH mouse model via intracerebral injection of autologous blood. Primary brain microvascular endothelial cells (BMECs) were treated with oxygen-and-glucose-deprivation (OGD) plus hemin to establish the model in vitro. We observed that MEG3 expression was significantly upregulated in both ICH mouse model and OGD/hemin (OGD/H) induced BMECs. The downregulation of MEG3 suppressed cell apoptosis and the activation of NOD-like receptor family protein 3 (NLRP3) inflammasome in OGD/H-induced BMECs. In ICH mice, MEG3 downregulation inhibited cell apoptosis and improved brain dysfunction. Mechanistically, MEG3 was confirmed to act as a molecular sponge for microRNA (miR)-1930-5p, and Mllt1 was a downstream target for miR-1930-5p. MEG3 competitively bound with miR-1930-5p to upregulate Mllt1. We further verified that Mllt1 overexpression reversed the inhibitory effect of miR-1930-5p in OGD/H-induced BMECs. CONCLUSIONS: In conclusion, lncRNA MEG3 promoted the dysfunction of BMECs by modulating the miR-1930-5p/Mllt1 axis, which provides a potential target in gene therapy for brain injury following ICH.	NA	Brain Res Bull. 2021 Jan;166:1-11. doi: 10.1016/j.brainresbull.2020.10.002. Epub 2020 Oct 27.
4348	LncRNA	MEG3	miR-1930-5p	Mllt1	Primary brain microvascular endothelial cells	Intracerebral Hemorrhage	Mus musculus (mouse)	RACE;	33127454	Long noncoding RNA MEG3 contributes to dysfunction of brain microvascular endothelial cells after intracerebral hemorrhage by regulating the miR-1930-5p/Mllt1 axis.	BACKGROUND: Intracerebral hemorrhage (ICH) is a subtype of stroke and causes disability and death worldwide. The roles of long noncoding RNAs (lncRNAs) in brain function and neurological diseases have been revealed. LncRNA maternally expressed gene 3 (MEG3) is involved in neurological impairment, but its role in ICH remains unknown. AIMS: The aim of this research is to explore the role of MEG3 in ICH. METHODS AND RESULTS: Here, we established an ICH mouse model via intracerebral injection of autologous blood. Primary brain microvascular endothelial cells (BMECs) were treated with oxygen-and-glucose-deprivation (OGD) plus hemin to establish the model in vitro. We observed that MEG3 expression was significantly upregulated in both ICH mouse model and OGD/hemin (OGD/H) induced BMECs. The downregulation of MEG3 suppressed cell apoptosis and the activation of NOD-like receptor family protein 3 (NLRP3) inflammasome in OGD/H-induced BMECs. In ICH mice, MEG3 downregulation inhibited cell apoptosis and improved brain dysfunction. Mechanistically, MEG3 was confirmed to act as a molecular sponge for microRNA (miR)-1930-5p, and Mllt1 was a downstream target for miR-1930-5p. MEG3 competitively bound with miR-1930-5p to upregulate Mllt1. We further verified that Mllt1 overexpression reversed the inhibitory effect of miR-1930-5p in OGD/H-induced BMECs. CONCLUSIONS: In conclusion, lncRNA MEG3 promoted the dysfunction of BMECs by modulating the miR-1930-5p/Mllt1 axis, which provides a potential target in gene therapy for brain injury following ICH.	NA	Brain Res Bull. 2021 Jan;166:1-11. doi: 10.1016/j.brainresbull.2020.10.002. Epub 2020 Oct 27.
4349	LncRNA	MEG3	miR-129-5p	HMGB1	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33175458	MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR-129-5p/HMGB1 axis.	The apoptosis of renal tubular epithelial cells (TECs) during ischemia/reperfusion (I/R) facilitates the progression of acute kidney injury (AKI). This study aimed to probe the role of long noncoding RNA maternally expressed 3 (MEG3) in I/R-induced apoptosis of TECs. In this study, with CoCl(2) and hypoxia/reoxygenation treatments, cell models were established to mimic I/R using the human kidney tubular cell line HK-2. In HK-2 cells, expression of MEG3 detected using quantitative real-time polymerase chain reaction (qRT-PCR), was significantly upregulated after CoCl(2) treatment and hypoxia/reoxygenation treatment. The results of cell counting kit-8 assay and flow cytometry suggested that knockdown of MEG3 significantly increased the viability of HK-2 cells but inhibited its apoptosis, while overexpression of MEG3 exerted the reverse effects. Additionally, expression levels of interleukin 6 and tumor necrosis factor-α in the medium were elevated after MEG3 was overexpressed in HK-2 cells. Together with qRT-PCR and Western blot analysis, a dual-luciferase reporter gene assay was used to verify the interactions among MEG3, miR-129-5p, and HMGB1. The results demonstrated that in HK-2 cells, miR-129-5p was a target of MEG3, and HMGB1 served as a target gene of miR-129-5p. Besides this, compared with the control group, the expression levels of MEG3 and HMGB1 in samples derived from AKI patients were remarkably upregulated, and the expression of miR-129-5p was downregulated. Therefore, taken together, we conclude that the overexpression of MEG3 induced by I/R promotes apoptosis of TECs via regulating the miR-129-5p/HMGB1 axis.	NA	J Biochem Mol Toxicol. 2021 Feb;35(2):e22649. doi: 10.1002/jbt.22649. Epub 2020 Nov 11.
4350	LncRNA	MEG3	miR-214	EGFR	A549 and H460 cells	Primary Hypertension	Homo sapiens (human)	luciferase assay;	33635564	Rs884225 polymorphism is associated with primary hypertension by compromising interaction between epithelial growth factor receptor (EGFR) and miR-214.	Genetic variations in the 3'UTR of mRNAs as well as sequences of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) can affect gene expression by interfering with the binding between them. In this study, we investigated the role of the following polymorphisms in the risk of hypertension: the 774T > C (rs17337023) polymorphism located in the EGFR 3' untranslated region (3'UTR), the rs884225 polymorphism located in the sequence of miR-214, and the single nucleotide polymorphisms (SNPs) rs325797437, rs344501106, rs81286029 and rs318656749 located in the promoter of lncRNA MEG3. Taqman genotyping assays and haplotype analysis tools were used to measure the MEG3 haplotypes and the rs17337023 and rs884225 polymorphisms genotypes. The relationship between MEG3, miR-214 and EGFR was validated using computational analysis and luciferase assays. Unlike other polymorphisms, only patients grouped according to their rs884225 genotypes exhibited varied EGFR mRNA and protein levels, which indicated that the rs884225 genotype is associated with the expression of EGFR mRNA and protein levels. MiR-214 was confirmed to bind to MEG3 and 3'UTR of EGFR by showing that the transfection of exogenous miR-214 significantly down-regulated the luciferase activity of A549 and H460 cells transfected with wild-type MEG3 or wild-type EGFR 3' UTR. Additionally, MEG3 overexpression inhibited miR-214 expression while elevating the EGFR mRNA and protein expressions. Meanwhile, MEG3 down-regulation demonstrated an opposite result, thus establishing the MEG3/miR-214/EGRF signalling pathway. Our study confirmed that the T > C substitution of rs884225 polymorphism located in miR-214 binding site in the 3'UTR of EGFR is associated with increased risk of primary hypertension.	NA	J Cell Mol Med. 2021 Apr;25(8):3714-3723. doi: 10.1111/jcmm.15976. Epub 2021 Feb 26.
4351	LncRNA	MEG3	miR-103a-3p	PDHB	CC tumor tissues and cells	Colorectal Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33118833	LncRNA MEG3 promotes endoplasmic reticulum stress and suppresses proliferation and invasion of colorectal carcinoma cells through the MEG3/miR-103a-3p/PDHB ceRNA pathway.	LncRNA maternally expressed gene 3 (MEG3) is a potential prognostic and diagnostic biomarker in colorectal carcinoma (CC). However, its cellular functions and mechanism remain not fully uncovered. Relative expression of MEG3, miRNA (miR)-103a-3p, and pyruvate dehydrogenase E1 subunit beta (PDHB) was detected by RT-qPCR and western blotting. Cell proliferation was measured by CCK-8 assay, colony formation assay, and flow cytometry, as well as xenograft tumor assay. Transwell assay examined cell invasion. Endoplasmic reticulum (ER) stress was evaluated by western blotting. Dual-luciferase reporter assay and RNA immunoprecipitation determined the relationship between miR-103a-3p and MEG3 or PDHB. Expression of MEG3 was downregulated in human CC tumor tissues and cells (SW620 and HCT116), accompanied by higher miR-103a-3p and lower PDHB. Restoring MEG3 suppressed cell viability, colony formation ability, and invasion, arrested cell cycle, and induced apoptosis rate in SW620 and HCT116 cells, as well as promoted expression of ER stress-related proteins (GRP78, ATF6, CHOP, caspase-3, and caspase-9). Furthermore, MEG3 overexpression hindered tumor growth and facilitated ER stress in vivo. Molecularly, miR-103a-3p was a target of MEG3, and further targeted PDHB. Similarly, in function, blocking miR-103a-3p suppressed CC in vitro by affecting proliferation, invasion, and ER stress; in addition, restoring miR-103a-3p partially counteracted the suppressive role of MEG3 in CC cells. MEG3 sponged miR-103a-3p to suppress CC malignancy by inducing ER stress and inhibiting cell proliferation and invasion via upregulating PDHB, suggesting a novel MEG3/miR-103a-3p/PDHB ceRNA pathway.	NA	Neoplasma. 2021 Mar;68(2):362-374. doi: 10.4149/neo_2020_200813N858. Epub 2020 Oct 30.
4352	LncRNA	MEG3	miR-421	NA	Oral cancer stem cells	Oral Cancer	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33012637	LncRNA MEG3 inhibits self-renewal and invasion abilities of oral cancer stem cells by sponging miR-421.	BACKGROUND/PURPOSE: Oral cancer stem cells (CSCs) have been considered as the key cells that are implicated in tumor recurrence and metastasis. In recent years, great attention has been paid to the significance of various non-coding RNAs due to their regulatory roles in oral CSCs. Although the function of long non-coding RNA MEG3 in various cancers has been investigated, its effects on the features of oral CSCs remained to be determined. METHODS: The expression levels of MEG3 in tongue squamous cell carcinomas and prognostic effect have been evaluated. We assessed the expression of MEG3 in sphere cells (oral CSCs) using qRT-PCR. Secondary sphere formation and invasion assays were conducted to evaluate the self-renewal and metastatic abilities, respectively. Bioinformatics software and luciferase reporter assay were used to predict and verify the relationship between MEG3 and miR-421. RESULTS: MEG3 was downregulated in the tissues of oral cancer and associated with a poor prognosis. In oral CSCs, the expression of MEG3 was repressed and overexpression of MEG3 resulted in suppression of self-renewal and invasion abilities. Luciferase reporter assay showed that miR-421 directly interacted with MEG3, and our subsequent experiment demonstrated that elevation of miR-421 reversed the MEG3-inhibited characteristics of oral CSCs. CONCLUSION: Our findings suggest that MEG3 can serve as a tumor suppressor in oral CSCs by impeding the action of miR-421. Moreover, targeting MEG3-miR-421 axis has the potential to mitigate the tumor recurrence and metastasis.	NA	J Formos Med Assoc. 2021 Apr;120(4):1137-1142. doi: 10.1016/j.jfma.2020.09.006. Epub 2020 Oct 2.
4353	LncRNA	MEG3	miR-29c	AKAP12	MEN cells	Meningioma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33251130	Long Non-Coding RNA MEG3 Modifies Cell-Cycle, Migration, Invasion, and Proliferation Through AKAP12 by Sponging miR-29c in Meningioma Cells.	Meningioma (MEN) is a common central nervous system disease. Accumulating evidence indicated that long non-coding RNA maternally expressed gene 3 (MEG3) participated in the progression of MEN. However, the potential mechanisms of MEG3 in altering the aggressive phenotypes of MEN need further exploration. Levels of MEG3, microRNA (miR)-29c, and A-kinase anchor protein 12 (AKAP12) were determined using quantitative real-time Polymerase Chain Reaction (qRT-PCR) assay. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify the relationship between miR-29c and MEG3 or AKAP12. The protein level of AKAP12 was detected by western blot. Moreover, cell-cycle arrest, migration, invasion, and proliferation were assessed by flow cytometry, wound healing, transwell assays, and CCK-8 assay, respectively. Levels of MEG3 and AKAP12 were downregulated, while miR-29c was effectively increased in MEN tissues and cell line. Mechanically, MEG3 was a sponge of miR-29c to regulate the expression of AKAP12. Functionally, increase of MEG3 diminished cell-cycle, migration, invasion, and proliferation in MEN cells, and reintroduction of miR-29c could eliminate these effects. In addition, AKAP12 depletion overturned the inhibitory effects of miR-29c absence on cell-cycle, migration, invasion, and proliferation in vitro. Also, AKAP12 was co-regulated by MEG3/miR-29c axis. MEG3 mediated the aggressive behaviors of MEN cells via miR-29c/AKAP12 axis, supporting that MEG3 served as a promising biomarker for the diagnosis and treatment of human MEN.	NA	Front Oncol. 2020 Nov 4;10:537763. doi: 10.3389/fonc.2020.537763. eCollection 2020.
4354	LncRNA	MEG8	miR-367-3p	TGFbR1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	33147050	LncRNA MEG8 plays an oncogenic role in hepatocellular carcinoma progression through miR-367-3p/14-3-3ζ/TGFβR1 axis.	Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and it carries a poor prognosis. Clarifying the pathologic mechanisms of this disease will be beneficial for the diagnosis and treatment of HCC. LncRNA MEG8 is involved in several tumors but its role in HCC progression remains unknown. This study was designed to explore the role and regulatory mechanisms of MEG8 in HCC progression. MTT, EdU, wound-healing, and transwell assays were employed to analyze the proliferation, migration, and invasion of HCC cells. A luciferase assay was utilized to confirm the predicted binding site. RNA immunoprecipitation and co-immunoprecipitation were employed to verify the binding between MEG8 and miR-367-3p as well as 14-3-3ζ and TGFβR1. Real-time PCR and western blot were employed to detect the expression of interesting genes. Results revealed that MEG8 was increased in HCC tissues and cells, and was correlated with the poor prognosis of HCC patients. Inhibiting MEG8 significantly repressed the HCC cells' ability to proliferate, migrate, and invade. Moreover, MEG8 sponged miR-367-3p to upregulate 14-3-3ζ, the binding of which suppressed TGFβR1 degradation, thereby enhancing TGFβ signaling. In conclusion, this work exposed a novel role and regulatory mechanism of MEG8 in HCC and provided new insight into the treatment of HCC.	NA	Neoplasma. 2021 Mar;68(2):273-282. doi: 10.4149/neo_2020_200730N785. Epub 2020 Nov 5.
4355	LncRNA	MEG8	miR-14-3-3p	TGFbR1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	33147050	LncRNA MEG8 plays an oncogenic role in hepatocellular carcinoma progression through miR-367-3p/14-3-3ζ/TGFβR1 axis.	Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and it carries a poor prognosis. Clarifying the pathologic mechanisms of this disease will be beneficial for the diagnosis and treatment of HCC. LncRNA MEG8 is involved in several tumors but its role in HCC progression remains unknown. This study was designed to explore the role and regulatory mechanisms of MEG8 in HCC progression. MTT, EdU, wound-healing, and transwell assays were employed to analyze the proliferation, migration, and invasion of HCC cells. A luciferase assay was utilized to confirm the predicted binding site. RNA immunoprecipitation and co-immunoprecipitation were employed to verify the binding between MEG8 and miR-367-3p as well as 14-3-3ζ and TGFβR1. Real-time PCR and western blot were employed to detect the expression of interesting genes. Results revealed that MEG8 was increased in HCC tissues and cells, and was correlated with the poor prognosis of HCC patients. Inhibiting MEG8 significantly repressed the HCC cells' ability to proliferate, migrate, and invade. Moreover, MEG8 sponged miR-367-3p to upregulate 14-3-3ζ, the binding of which suppressed TGFβR1 degradation, thereby enhancing TGFβ signaling. In conclusion, this work exposed a novel role and regulatory mechanism of MEG8 in HCC and provided new insight into the treatment of HCC.	NA	Neoplasma. 2021 Mar;68(2):273-282. doi: 10.4149/neo_2020_200730N785. Epub 2020 Nov 5.
4356	LncRNA	MIAT	miR-488-3p	SOX11	LPS-treated C28/I2 cells	Chondrocytes Inflammatory Injury	Homo sapiens (human)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34124371	lncRNA myocardial infarction-associated transcript (MIAT) knockdown alleviates LPS-induced chondrocytes inflammatory injury via regulating miR-488-3p/sex determining region Y-related HMG-box 11 (SOX11) axis.	Long noncoding RNA (lncRNA) has been shown to be involved in the development of osteoarthritis (OA), an age-related bone and joint disease. However, the function and possible molecular mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in lipopolysaccharide (LPS)-induced chondrocytes injury model remain unexplored. Cell viability and apoptosis were detected by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. Western blot was used to detect protein expression. The concentrations of inflammatory factors were estimated by enzyme-linked immunosorbent assay (ELISA). Abundances of MIAT, microRNA-488-3p (miR-488-3p), and sex determining region Y-related HMG-box 11 (SOX11) were examined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to analyze the interaction between miR-488-3p and MIAT or SOX11. LPS caused chondrocytes injury by reducing cell activity and increasing apoptosis rate and inflammatory factor secretions. Higher levels of MIAT and SOX11 and lower miR-488-3p were observed in LPS-treated C28/I2 cells. Importantly, knockdown of MIAT attenuated the LPS-induced cell injury by targeting miR-488-3p, and miR-488-3p overexpression weakened the LPS-induced cell injury by targeting SOX11. Additionally, repression of MIAT inactivated the LPS-induced NF-κB signaling pathway by decreasing SOX11 and increasing miR-488-3p. Knockdown of MIAT alleviated the LPS-induced chondrocytes injury by inhibiting the NF-κB signaling pathway mediated by the miR-488-3p/SOX11 axis.	NA	Open Life Sci. 2021 May 31;16(1):511-522. doi: 10.1515/biol-2021-0023. eCollection 2021.
4357	LncRNA	MIAT	miR-495	Prox1	adipose-derived mesenchymal stem cells	Lymphedema	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	33760182	lncRNA-MIAT facilitates the differentiation of adipose-derived mesenchymal stem cells into lymphatic endothelial cells via the miR-495/Prox1 axis.	The development of novel treatments for lymphedema is hindered by the poorly understood pathophysiology of the disease. To improve the therapeutic success of treating the disease, the present study aimed to investigate the effects and mechanism of long non-coding RNA myocardial infarction-associated transcript (MIAT) in terms of the differentiation of adipose-derived mesenchymal stem cells (ADMSCs) into lymphatic endothelial cells (LECs). The expression levels of (MIAT), microRNA (miR)-495 and Prospero-related homeobox 1 (Prox1) were measured by reverse transcription-quantitative PCR. The protein expression levels of Prox1, lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), vascular endothelial growth factor receptor-3 (VEGFR-3) and podoplanin (PDPL) were detected by western blotting and immunofluorescence. A dual-luciferase reporter assay was also used to detect the interaction between MIAT, miR-495 and Prox1. In addition, migration and tube-formation capabilities were measured by Transwell assay and tube-formation assay, respectively. The results obtained demonstrated that VEGF-C156S (recombinant VEGF-C in which Cys156 was replaced by Ser residue) treatment could efficiently induce the differentiation of ADMSCs into LECs. MIAT expression was upregulated and miR-495 was downregulated during differentiation. Mechanistically, MIAT upregulated Prox1 expression possibly by acting as a molecular sponge for miR-495. Functional analyses indicated that the expression levels of Prox1, LYVE-1, VEGFR-3 and PDPL, and the migration and tube-formation capabilities of ADMSCs induced by VEGF-C156S, were significantly inhibited by silencing MIAT and overexpressing miR-495. Moreover, miR-495 inhibition and Prox1 overexpression reversed the effects of MIAT downregulation and miR-495 upregulation, respectively, on the differentiation of ADMSCs into LECs. Taken together, these results suggested that MIAT may be involved in the differentiation of ADMSCs into LECs, and that the MIAT/miR-495/Prox1 axis may be a novel regulatory mechanism and therapeutic target for the treatment of lymphedema.	NA	Mol Med Rep. 2021 May;23(5):323. doi: 10.3892/mmr.2021.11962. Epub 2021 Mar 24.
4358	LncRNA	MIAT	miR-490-3p	ICAM1	oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells	Atherosclerosis	Homo sapiens (human)	RNA immunoprecipitation;RNA pull-down assay;Western blot;RNA immunoprecipitation;RNA pull-down;	33165137	Myocardial Infarction-associated Transcript Knockdown Inhibits Cell Proliferation, Migration, and Invasion Through miR-490-3p/Intercellular Adhesion Molecule 1 Axis in Oxidized Low-density Lipoprotein-induced Vascular Smooth Muscle Cells.	Emerging evidence has demonstrated that long noncoding RNAs are related to the pathogenesis of atherosclerosis. We aimed to investigate the roles and molecular mechanisms of myocardial infarction-associated transcript (MIAT) in the proliferation, migration, and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p), and intercellular adhesion molecule 1 (ICAM1). Cell Counting Kit-8 assay was performed to assess cell proliferation. Transwell assay was used to evaluate cell migration and invasion. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen, N-cadherin, matrix metalloprotein-9, and ICAM1. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays were conducted to verify the relationship between miR-490-3p and MIAT or ICAM1. MIAT was elevated in atherosclerosis patients' serum and ox-LDL-induced VSMCs. MIAT knockdown suppressed cell proliferation, migration, and invasion in ox-LDL-stimulated VSMCs. MIAT acted as a sponge of miR-490-3p, and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration, and invasion. ICAM1 was a direct target of miR-490-3p, and ICAM1 silencing repressed the proliferation, migration, and invasion of ox-LDL-stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL-induced VSMC proliferation, migration, and invasion. MIAT knockdown could depress cell proliferation, migration, and invasion through miR-490-3p/ICAM1 axis in ox-LDL-induced VSMCs.	NA	J Cardiovasc Pharmacol. 2020 Nov;76(5):617-626. doi: 10.1097/FJC.0000000000000901.
4359	LncRNA	MIAT	miR-147a	NKAP	mouse lung epithelial TC-1 cells	Pneumonia	Mus musculus (mouse)	FISH;microarray;qRT-PCR;FISH;	33318298	Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis.	PURPOSE: Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS: Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2506-2518. doi: 10.18632/aging.202284. Epub 2020 Dec 9.
4360	LncRNA	MIAT	miR-147a	NFkB	mouse lung epithelial TC-1 cells	Pneumonia	Homo sapiens (human)	FISH;microarray;qRT-PCR;FISH;	33318298	Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis.	PURPOSE: Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS: Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2506-2518. doi: 10.18632/aging.202284. Epub 2020 Dec 9.
4361	LncRNA	MIAT	miR-147a	NKAP	mouse lung epithelial TC-1 cells	Pneumonia	Mus musculus (mouse)	FISH;microarray;qRT-PCR;FISH;	33318298	Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis.	PURPOSE: Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS: Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2506-2518. doi: 10.18632/aging.202284. Epub 2020 Dec 9.
4362	LncRNA	MIAT	miR-147a	NFkB	mouse lung epithelial TC-1 cells	Pneumonia	Homo sapiens (human)	FISH;microarray;qRT-PCR;FISH;	33318298	Silencing of lncRNA MIAT alleviates LPS-induced pneumonia via regulating miR-147a/NKAP/NF-κB axis.	PURPOSE: Pneumonia is a respiratory disease with an increasing incidence in recent years. More and more studies have revealed that lncRNAs can regulate the transcriptional expression of target genes at different stage. Herein, we aimed to explore the effect of lncRNA MIAT in LPS-induced pneumonia, and further illuminate the possible underlying mechanisms. METHOD AND RESULTS: Mice were intraperitoneally injected with LPS, and the lung inflammation was evaluated. Microarray showed lncRNA MIAT was up-regulated in LPS-induced pulmonary inflammation. And qRT-PCR and FISH assay indicated that MIAT was increased in mice with LPS injection. Functional analysis showed sh-MIAT inhibited LPS-induced inflammation response, inhibited apoptosis level and protected lung function. As well, si-MIAT removed the injury of LPS on mouse lung epithelial TC-1 cells, and inhibited the activation of NF-κB signaling. Furthermore, MIAT acted as a sponge of miR-147a, and miR-147a directly targeted NKAP. Functionally, AMO-147a or NKAP remitted the beneficial effects of si-MIAT on LPS-induced inflammation response of TC-1 cells. CONCLUSION: Deletion of MIAT protected against LPS-induced lung inflammation via regulating miR-147a/NKAP, which might provide new insight for pneumonia treatment.	NA	Aging (Albany NY). 2020 Dec 9;13(2):2506-2518. doi: 10.18632/aging.202284. Epub 2020 Dec 9.
4363	LncRNA	MIAT	miR-488-3p	IGF1R	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	RNA pull-down assay;Western blot;RNA pull-down;	33085926	Downregulation of Long Noncoding RNA Myocardial Infarction Associated Transcript Suppresses Cell Proliferation, Migration, Invasion, and Glycolysis by Regulation of miR-488-3p/IGF1R Pathway in Colorectal Cancer.	Background: Colorectal cancer (CRC) is a significant public problem and the third cause of cancer-induced death all over the world. In addition, long noncoding RNA (lncRNA) has been reported as a vital mediator in human cancer. However, the precise role of lncRNA myocardial infarction associated transcript (MIAT) in CRC is unclear. Methods: The abundance of MIAT, miR-488-3p, and the type 1 insulin-like growth factor receptor (IGF1R) was measured by real-time quantitative polymerase chain reaction assay. The western blot assay was carried out to assess the protein level in CRC samples or control group. The cell activity, abilities of migration and invasion, and glycolysis were evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), transwell, and testing glucose consumption and lactate product, correspondingly. The target association between miR-488-3p, MIAT, or IGF1R was predicted and established by bioinformatics tools, dual-luciferase reporter, and RNA pull-down assays, correspondingly. The effects of MIAT silencing in vivo were analyzed by animal experiments. Results: LncRNA MIAT was upregulated in CRC sample and that was positively correlated with IGF1R expression. Loss-of-functional assay suggested that knockdown of MIAT impeded cell activity, migration, invasion, and glycolysis of CRC cells in vivo, along with xenograft growth in vivo. Moreover, silencing of IGF1R inhibited the progression of CRC. Therefore, overexpression of IGF1R could abolish silencing of MIAT-induced effects on CRC cells. Mechanistically, MIAT was a sponge for miR-488-3p, thereby regulating IGF1R expression in CRC. Conclusion: The present study confirmed that the "MIAT/miR-488-3p/IGF1R" pathway was involved in the development of CRC, which may be the target for developing therapeutic approaches for CRC.	NA	Cancer Biother Radiopharm. 2020 Oct 21. doi: 10.1089/cbr.2020.3671.
4364	LncRNA	MIAT	miR-140-3p	ZAK	293T cells	Blood-Tumor Barrier	Homo sapiens (human)	ChIP;luciferase assay;	33127881	Long non-coding RNA MIAT regulates blood tumor barrier permeability by functioning as a competing endogenous RNA.	Blood-tumor barrier (BTB) presents a major obstacle to brain drug delivery. Therefore, it is urgent to enhance BTB permeability for the treatment of glioma. In this study, we demonstrated that MIAT, ZAK, and phosphorylated NFκB-p65 (p-NFκB-p65) were upregulated, while miR-140-3p was downregulated in glioma-exposed endothelial cells (GECs) of BTB compared with those in endothelial cells cocultured with astrocytes (ECs) of blood-brain barrier (BBB). MIAT inhibited miR-140-3p expression, increased the expression of ZAK, enhanced the ratio of p-NFκB-p65:NFκB-p65, and promoted the endothelial leakage of BTB. Our current study revealed that miR-140-3p was complementary to the ZAK 3'untranslated regions (3'-UTR), and luciferase activity of ZAK was inhibited by miR-140-3p in 293T cells. MiR-140-3p silencing resulted in an increase in BTB permeability by targeting ZAK, while overexpression of miR-140-3p had the opposite results in GECs of BTB. Overexpression of ZAK induced an increase in BTB permeability, and this effect was related to ZAK's ability to mediate phosphorylation of NFκB-p65. Conversely, ZAK silencing get opposite results in GECs of BTB. As a molecular sponge of miR-140-3p, MIAT attenuated its negative regulation of the target gene ZAK by adsorbing miR-140-3p. P-NFκB-p65 as a transcription factor negatively regulated the expression of TJ-associated proteins by means of chip assay and luciferase assay. Single or combined application of MIAT and miR-140-3p effectively promoted antitumor drug doxorubicin (Dox) across BTB to induce apoptosis of glioma cells. In summary, MIAT functioned as a miR-140-3p sponge to regulate the expression of its target gene ZAK, which contribution to phosphorylation of NFκB-p65 was associated with an increase in BTB permeability by down-regulating the expression of TJ associated proteins, thereby promoting Dox delivery across BTB. These results might provide a novel strategy and target for chemotherapy of glioma.	NA	Cell Death Dis. 2020 Oct 30;11(10):936. doi: 10.1038/s41419-020-03134-0.
4365	LncRNA	MIAT	miR-342-3p	CASP1	diabetic retinopathy cells	Diabetic Retinopathy	Homo sapiens (human)	Luciferase reporter assay;	33065089	Long noncoding RNA MIAT regulates primary human retinal pericyte pyroptosis by modulating miR-342-3p targeting of CASP1 in diabetic retinopathy.	Diabetic retinopathy (DR) is the leading cause of visual impairment and acquired blindness among adults worldwide. Retinal microvascular pericyte deficiency is one of the earliest pathological changes associated with DR, and long noncoding RNA myocardial infarction-associated transcript (MIAT) has been implicated as a crucial regulator of microvascular dysfunction in DR. Pyroptosis is a caspase-1-dependent proinflammatory form of cell death, and in the present study, we investigated the potential pyroptosis of primary human retinal pericytes (HRPCs) and the mechanism by which MIAT is involved in this process. We applied advanced glycation end product modified bovine serum albumin (AGE-BSA) to simulate the DR environment. The results suggested that AGE-BSA induced the active cleavage of caspase-1 and gasdermin D, the release of IL-1β, IL-18 and LDH, and reduced cell viability, which was prevented by the inhibition of caspase-1, indicating the occurrence of caspase-1-mediated pyroptosis in HRPCs. Immunofluorescence images revealed the phenotypic characteristics of pyroptosis, including pyknosis, swelling and hyperpermeability in plasmolemma. MIAT and CASP1 expression were substantially increased, while that of miR-342-3p was decreased in AGE-BSA-treated HRPCs. MIAT knockdown inhibited pyroptosis in HRPCs, which was reinforced by cotreatment with miR-342-3p mimic but relieved by cotreatment with miR-342-3p inhibitor. Furthermore, HRPC pyroptosis was inhibited by treatment with the miR-342-3p mimic alone but enhanced by the miR-342-3p inhibitor. Luciferase reporter assay results demonstrated binding between MIAT and miR-342-3p, as well as between miR-342-3p and CASP1. MIAT antagonized the effect of miR-342-3p on the depression of its target CASP1 and promoted AGE-BSA-induced pericyte pyroptosis. These findings may promote a better understanding of retinal pericyte depletion pathogenesis and the development of new therapeutic strategies for the treatment of diabetic retinopathy.	NA	Exp Eye Res. 2021 Jan;202:108300. doi: 10.1016/j.exer.2020.108300. Epub 2020 Oct 13.
4366	LncRNA	MIAT	miR-29a-5p	NA	hypoxic pulmonary hypertension model 	Hypoxic Pulmonary Hypertension	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	32964992	LncRNA MIAT stimulates oxidative stress in the hypoxic pulmonary hypertension model by sponging miR-29a-5p and inhibiting Nrf2 pathway.	OBJECTIVE: To elucidate the potential biological functions of long non-coding RNA (lncRNA) MIAT in the development of hypoxic pulmonary hypertension (HPH) and the underlying mechanism. MATERIALS AND METHODS: Twenty Sprague Dawley (SD) rats were randomly assigned into normoxia group (n=10) and hypoxia group (n=10), respectively. In vivo HPH model in rats was established by hypoxic induction. Expression levels of MIAT and miR-29a-5p in rats were detected. Meanwhile, hemodynamic indicators in rats were examined. In vitro HPH model was conducted in hypoxia-induced HPAECs. The interaction between MIAT and miR-29a-5p was assessed by Dual-Luciferase reporter assay. Moreover, their regulatory effects on viability, migratory ability, oxidative stress, and the Nrf2 pathway in hypoxia-induced HPAECs were examined. RESULTS: MIAT was upregulated in both in vivo and in vitro HPH models, while miR-29a-5p was downregulated. Knockdown of MIAT suppressed viability, migratory ability, and oxidative stress in hypoxia-induced HPAECs. MiR-29a-5p was the target gene binding MIAT, and silence of miR-29a-5p partially relieved the inhibitory effects of MIAT on the above regulations in HPAECs. CONCLUSIONS: MIAT promotes proliferative and migratory abilities, as well as oxidative stress in hypoxia-induced HPAECs by targeting miR-29a-5p, thus aggravating the development of HPH.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):9022-9029. doi: 10.26355/eurrev_202009_22845.
4367	LncRNA	MIAT	miR-1246	NA	non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	32965021	Long non-coding RNA MIAT promotes non-small cell lung cancer progression by sponging miR-1246.	Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long non-coding RNA MIAT promotes non-small cell lung cancer progression by sponging miR-1246, by D. Lin, H.-P. Xu, J.-H. Lin, H.-H. Hu, Q. Wang, J. Zhang, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5795-5801-DOI: 10.26355/eurrev_201907_18318-PMID: 31298331" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18318.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(17):8626. doi: 10.26355/eurrev_202009_22762.
4368	LncRNA	MIAT	miR-147a	E2F3	mesangial cells	Diabetic Nephropathy	Homo sapiens (human)	RACE;Luciferase reporter assay;	33009725	Loss of lncRNA MIAT ameliorates proliferation and fibrosis of diabetic nephropathy through reducing E2F3 expression.	Diabetic nephropathy (DN) is a serious kidney disease resulted from diabetes. Dys-regulated proliferation and extracellular matrix (ECM) accumulation in mesangial cells contribute to DN progression. In this study, we tested expression level of MIAT in DN patients and mesangial cells treated by high glucose (HG). Up-regulation of MIAT was observed in DN. Then, functional assays displayed that silence of MIAT by siRNA significantly repressed the proliferation and cycle progression in mesangial cells induced by HG. Meanwhile, we found that collagen IV, fibronectin and TGF-β1 protein expression was obviously triggered by HG, which could be rescued by loss of MIAT. Then, further assessment indicated that MIAT served as sponge harbouring miR-147a. Moreover, miR-147a was decreased in DN, which exhibited an antagonistic effect of MIAT on modulating mesangial cell proliferation and fibrosis. Moreover, bioinformatics analysis displayed that E2F transcription factor 3 (E2F3) could act as direct target of miR-147a. We demonstrated that E2F3 was greatly increased in DN and the direct binding association between miR-147a and E2F3 was evidenced using luciferase reporter assay. In summary, our data explored the underlying mechanism of DN pathogenesis validated that MIAT induced mesangial cell proliferation and fibrosis via sponging miR-147a and regulating E2F3.	NA	J Cell Mol Med. 2020 Nov;24(22):13314-13323. doi: 10.1111/jcmm.15949. Epub 2020 Oct 3.
4369	LncRNA	MIAT	miR-130a-3p	TLR4	nephropathy cells	Diabetic Nephropathy	Homo sapiens (human)	qRT-PCR	32972755	Ablation of lncRNA MIAT mitigates high glucose-stimulated inflammation and apoptosis of podocyte via miR-130a-3p/TLR4 signaling axis.	Podocyte injury has been considered as a major contributor to the progression of diabetic nephropathy (DN). Long non-coding RNAs (lncRNAs) are being found to be involved in DN pathogenesis. The current research was designed to elucidate the potential role and latent molecular mechanism of long non-coding RNA MIAT in HG-induced podocyte injury. Our data demonstrated that MIAT expression was substantially elevated but miR-130a-3p was diminished in HG-challenged podocytes. Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β. Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes. Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p. More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage. Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.	NA	Biochem Biophys Res Commun. 2020 Dec 10;533(3):429-436. doi: 10.1016/j.bbrc.2020.09.034. Epub 2020 Sep 21.
4370	LncRNA	MIR100HG	miR-5590-3p	OTX1	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Immunohistochemistry;luciferase assay;RNA immunoprecipitation;	33088216	Long non-coding RNA MIR100HG promotes the migration, invasion and proliferation of triple-negative breast cancer cells by targeting the miR-5590-3p/OTX1 axis.	BACKGROUND: As an aggressive subtype of breast cancer with a high risk of recurrence, triple-negative breast cancer (TNBC) lacks available treatment targets. LncRNA MIR100HG promotes cell proliferation in TNBC. However, few studies have investigated the molecular mechanism of MIR100HG in TNBC. Thus, additional in-depth investigations are needed to unravel its associated regulatory mechanism. METHODS: MIR100HG and miR-5590-3p expression in TNBC tissue samples and cell lines was detected by RT-qPCR. Flow cytometry, transwell, wound-healing, CCK8 and colony formation assays were performed to analyse cell apoptosis, cell cycle, invasion, migration and proliferation. The protein expression of orthodenticle homeobox 1 (OTX1) and proteins in the ERK/MAPK signalling pathway were assessed by western blot analysis. Bioinformatics and luciferase assay were performed to predict and validate the interaction between MIR100HG and miR-5590-3p as well as OTX1 and miR-5590-3p. RNA immunoprecipitation (RIP) was used to detect the interaction between MIR100HG and miR-5590-3p. Subcutaneous tumour growth was observed in nude mice. Immunohistochemistry (IHC) analysis was used to assess OTX1 expression in tumour tissues. RESULTS: MIR100HG expression was upregulated, whereas that of miR-5590-3p was downregulated in TNBC. MIR100HG was shown to directly interact with miR-5590-3p. Furthermore, MIR100HG knockdown could promote TNBC cell apoptosis and cell cycle arrest in G0/G1 phase while inhibiting migration, invasion and proliferation. Furthermore, miR-5590-3p inhibition showed the opposite results and could reverse the effect of MIR100HG knockdown in TNBC cells. MiR-5590-3p downregulated the ERK/MAPK signalling pathway, suppressed the migration, invasion and proliferation of TNBC cells and promoted their apoptosis and cell cycle arrest in G0/G1 phase by targeting OTX1. In addition, MIR100HG knockdown inhibited OTX1 expression by upregulating miR-5590-3p in vivo, thereby inhibiting tumour growth. CONCLUSIONS: MIR100HG promotes the progression of TNBC by sponging miR-5590-3p, thereby upregulating OTX1, suggesting a new potential treatment target for TNBC.	NA	Cancer Cell Int. 2020 Oct 16;20:508. doi: 10.1186/s12935-020-01580-6. eCollection 2020.
4371	LncRNA	MIR194-2HG	miR-1207-5p	TCF19	HepG2 and Huh7 cells	Liver Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33116574	LncRNA MIR194-2HG Promotes Cell Proliferation and Metastasis via Regulation of miR-1207-5p/TCF19/Wnt/β-Catenin Signaling in Liver Cancer.	PURPOSE: LncRNAs play an important role in tumorigenesis and cancer progression in liver cancer. Although many lncRNAs have been reported, the role of MIR194-2HG and the underlying mechanism mediated by it are still largely unknown in HCC. This study aimed to investigate the biological role and mechanism of MIR194-2HG in liver cancer. MATERIALS AND METHODS: The expression of MIR194-2HG was determined in liver cancer tissues and cells by RT-qPCR. The overall survival rate of MIR194-2HG was analyzed by Kaplan-Meier survival analysis. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and Transwell assays were carried out to detect cell migration and invasion. Western blotting was used to quantify the levels of all proteins. The regulatory mechanism of the MIR194-2HG/miR-1207-5p/TCF19 axis in liver cancer was investigated by dual-luciferase activity reporter assay, Kaplan-Meier survival analysis, and Western blotting. RESULTS: MIR194-2HG was upregulated in liver cancer tissues and cell lines. Liver cancer patients with higher expression of MIR194-2HG revealed poor overall survival compared with those who had lower expression of MIR194-2HG. MIR194-2HG promoted the proliferation, migration, and invasion of HepG2 and Huh7 cells by acting as a ceRNA mechanism for the miR-1207-5p/TCF19 axis to activate the Wnt/β-catenin signaling pathway. CONCLUSION: MIR194-2HG acts in an oncogenic role and activates the Wnt/β-catenin signaling pathway via a miR-1207-5p/TCF19 axis-mediated mechanism, which provides a novel avenue for diagnostic or therapeutic interventions in liver cancer.	NA	Onco Targets Ther. 2020 Oct 6;13:9887-9899. doi: 10.2147/OTT.S264614. eCollection 2020.
4372	LncRNA	MIR4435-2HG	miR-22-3p	YWHAZ	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33194037	Long noncoding RNA MIR4435-2HG promotes hepatocellular carcinoma proliferation and metastasis through the miR-22-3p/YWHAZ axis.	Long noncoding RNAs (lncRNAs) play the critical biological role in many malignant tumours. MIR4435-2HG has been proven to be a novel oncogenic lncRNA. However, the exact role and mechanism of MIR4435-2HG in hepatocellular carcinoma (HCC) remain unclear. Here, we found that MIR4435-2HG is overexpressed in HCC tissue compared to normal controls and that high level of MIR4435-2HG indicates a poorer prognosis in HCC patients. MIR4435-2HG enhances the growth and metastasis ability of HCC cells. MIR4435-2HG promotes the expression of YWHAZ by sponging miR-22-3p to liberate YWHAZ mRNA transcripts. MIR4435-2HG facilitates the proliferation and metastasis of HCC by modulating the miR-22-3p/YWHAZ axis. These results demonstrated the role and mechanism of MIR4435-2HG in malignant progression of HCC. MIR4435-2HG may be used as the prognostic marker and treatment target for the patient with HCC.	NA	Am J Transl Res. 2020 Oct 15;12(10):6381-6394. eCollection 2020.
4373	LncRNA	MIR4713HG	let-7c-5p	TMC7	OTSCC cell lines	Oral Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR	33760127	Long non-coding RNA MIR4713HG aggravates malignant behaviors in oral tongue squamous cell carcinoma via binding with microRNA let-7c-5p.	Oral tongue squamous cell carcinoma (OTSCC) is one of the most aggressive pathological types of head and neck squamous cell carcinoma, and presents with rapid local invasion and metastasis. The present study confirmed that the long non-coding (lnc) RNA MIR4713HG was markedly upregulated in both OTSCC tissues and cell lines and associated with poor survival. The present study performed a series of experiments to investigate the impact of MIR4713HG on OTSCC and revealed that upregulation of MIR4713HG had a crucial role in promoting cell proliferation and metastasis of OTSCC cell lines both in vitro and in vivo. By applying bioinformatics analyses, micro RNA let-7c-5p was observed to physically bind with MIR4713HG, and the knockdown of let-7c-5p could counteract the influence of MIR4713HG on OTSCC. Furthermore, the present study demonstrated that let-7c-5p performed its regulating role in OTSCC via affecting the expression level of transmembrane channel like 7 (TMC7). In conclusion, the present study demonstrated that lncRNA MIR4713HG acted as a pro-tumor factor facilitating cell proliferation and metastasis of OTSCC via affecting the let-7c-5p/TMC7 signaling pathway, which presents as a promising therapeutic target in OTSCC.	NA	Int J Mol Med. 2021 May;47(5):84. doi: 10.3892/ijmm.2021.4917. Epub 2021 Mar 24.
4374	LncRNA	MIR497HG	miR-497	E2F4	BCa cell line	Bladder Cancer	Homo sapiens (human)	qRT-PCR	33363213	Silencing of lncRNA MIR497HG via CRISPR/Cas13d Induces Bladder Cancer Progression Through Promoting the Crosstalk Between Hippo/Yap and TGF-β/Smad Signaling.	A subset of long non-coding RNAs (lncRNAs), categorized as miRNA-host gene lncRNAs (lnc-miRHGs), is processed to produce miRNAs and involved in cancer progression. This work aimed to investigate the influences and the molecular mechanisms of lnc-miRHGs MIR497HG in bladder cancer (BCa). The miR-497 and miR-195 were derived from MIR497HG. We identified that lnc-miRHG MIR497HG and two harbored miRNAs, miR-497 and miR-195, were downregulated in BCa by analyzing The Cancer Genome Atlas and our dataset. Silencing of MIR497HG by CRISPR/Cas13d in BCa cell line 5637 promoted cell growth, migration, and invasion in vitro. Conversely, overexpression of MIR497HG suppressed cell progression in BCa cell line T24. MiR-497/miR-195 mimics rescued significantly the oncogenic roles of knockdown of MIR497HG by CRISPR/Cas13d in BCa. Mechanistically, miR-497 and miR-195 co-ordinately suppressed multiple key components in Hippo/Yap and transforming growth factor β signaling and particularly attenuated the interaction between Yap and Smad3. In addition, E2F4 was proven to be critical for silencing MIR497HG transcription in BCa cells. In short, we propose for the first time to reveal the function and mechanisms of MIR497HG in BCa. Blocking the pathological process may be a potential strategy for the treatment of BCa.	NA	Front Mol Biosci. 2020 Dec 9;7:616768. doi: 10.3389/fmolb.2020.616768. eCollection 2020.
4375	LncRNA	miR503HG	miR-15b	PDCD4	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Cell transfection;Cell transfection;Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	33046427	LncRNA miR503HG inhibits epithelial-mesenchymal transition and angiogenesis in hepatocellular carcinoma by enhancing PDCD4 via regulation of miR-15b.	OBJECTIVE: To reveal the effect of lncRNA miR503HG on epithelial-mesenchymal transition (EMT) and angiogenesis in hepatocellular carcinoma (HCC). METHODS: The expressions of miR503HG, miR-15b and PDCD4 in HCC tissues and cell lines were measured. After cell transfection, Transwell assay tested the migration and invasion ability of HCC cells. qRT-PCR and Western blot detected the expressions of EMT markers (E-cad, N-cad, Vim and Snail-1). Matrigel-based tube formation assay assessed the angiogenesis capacity of human umbilical vein endothelial cells (HUVECs) cultured in conditioned medium of treated HCC cells. ELISA detected the level of VEGF in supernatant of HUVECs. RIP, RNA pulldown and dual-luciferase reporter assay were applied to verify the binding of miR-15b to miR503HG or PDCD4. pcDNA3.1-miR503HG-BEL-7404 cells or pcDNA3.1-BEL-7404 cells were implanted into nude mice for construction of HCC model in vivo. RESULTS: miR503HG and PDCD4 were under-expressed and miR-15b was over-expressed in HCC cells and tissues. Up-regulation of miR503HG and PDCD4 or inhibition of miR-15b hindered migration, invasion and EMT of HCC cells and angiogenesis of HUVECs. Both miR503HG and PDCD4 could bind to miR-15b. Over-expression of miR503HG suppressed HCC growth and angiogenesis in nude mice. CONCLUSION: LncRNA miR503HG suppresses EMT and angiogenesis in HCC via miR-15b/PDCD4 axis.	NA	Dig Liver Dis. 2021 Jan;53(1):107-116. doi: 10.1016/j.dld.2020.09.008. Epub 2020 Oct 10.
4376	LncRNA	MRPL43	miR-608	NA	HCT-116 cell line	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33171811	Molecular and Functional Roles of MicroRNAs in the Progression of Hepatocellular Carcinoma-A Review.	Liver cancer is the fourth leading cause of cancer deaths globally, of which hepatocellular carcinoma (HCC) is the major subtype. Viral hepatitis B and C infections, alcohol abuse, and metabolic disorders are multiple risk factors for liver cirrhosis and HCC development. Although great therapeutic advances have been made in recent decades, the prognosis for HCC patients remains poor due to late diagnosis, chemotherapy failure, and frequent recurrence. MicroRNAs (miRNAs) are endogenous, non-coding RNAs that regulate various molecular biological phenomena by suppressing the translation of target messenger RNAs (mRNAs). miRNAs, which often become dysregulated in malignancy, control cell proliferation, migration, invasion, and development in HCC by promoting or suppressing tumors. Exploring the detailed mechanisms underlying miRNA-mediated HCC development and progression can likely improve the outcomes of patients with HCC. This review summarizes the molecular and functional roles of miRNAs in the pathogenesis of HCC. Further, it elucidates the utility of miRNAs as novel biomarkers and therapeutic targets.	NA	Int J Mol Sci. 2020 Nov 7;21(21):8362. doi: 10.3390/ijms21218362.
4377	LncRNA	MRUL	miR-17-5p	SRSF2	NSCLC cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33123591	lncRNA MRUL Suppressed Non-Small Cell Lung Cancer Cells Proliferation and Invasion by Targeting miR-17-5p/SRSF2 Axis.	The two broad histological subtypes of lung cancer are small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC), which are the leading causes of cancer-related death in the world. Long noncoding RNAs (lncRNAs) have been verified to be critical in the regulation of cancer development. The present study identified and elucidated the regulatory roles of a novel lncRNA MRUL in NSCLC. The results showed that MRUL was overexpressed in NSCLC samples and correlated with the poor prognosis of patients who had NSCLC. Moreover, this research has for the first time demonstrated that MRUL acted as an oncogenetic lncRNA in NSCLC. Knockdown of MRUL considerably repressed NSCLC cell proliferation, invasion, and migration. The bioinformatics analysis showed that MRUL was involved in regulating multiple RNA splicing and proliferation-related biological processes, such as mRNA splicing, RNA splicing, mRNA processing, mRNA 3'-end processing, mRNA splice site selection, and DNA replication. By combining bioinformatics analysis and experimental validation, we found that MRUL regulated NSCLC progression through promoting SRSF2 by sponging miR-17 in NSCLC cells. The discoveries indicated that MRUL could be a therapeutic target and a potential diagnostic for NSCLC.	NA	Biomed Res Int. 2020 Oct 7;2020:9567846. doi: 10.1155/2020/9567846. eCollection 2020.
4378	LncRNA	MSC-AS1	miR-373-3p	CPEB4	glioma cells	Glioma	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33106913	MSC-AS1 knockdown inhibits cell growth and temozolomide resistance by regulating miR-373-3p/CPEB4 axis in glioma through PI3K/Akt pathway.	Long non-coding RNAs (lncRNAs) have been widely reported to regulate the development and chemoresistance of a variety of tumors. Temozolomide (TMZ) is a first-line chemotherapy for treatment of glioma. However, the effect and the regulatory mechanism of lncRNA MSC-AS1 (MSC-AS1) in TMZ-resistant glioma remain unrevealed. Levels of MSC-AS1, microRNA-373-3p (miR-373-3p), and cytoplasmic polyadenylation element binding protein 4 (CPEB4) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). All protein expression was detected by western blot. Cell viability and the half maximal inhibitory concentration (IC(50)) value of TMZ was assessed by cell counting kit-8 (CCK-8) assay. Cell cloning ability and apoptosis were examined by colony formation and flow cytometry assays, respectively. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to verify the correlation between miR-373-3p and MSC-AS1 or CPEB4. The xenograft models were established to determine the effect of MSC-AS1 in vivo. MSC-AS1 was up-regulated in TMZ-resistant glioma tissues and cells, and glioma patients with high MSC-AS1 expression tend to have lower overall survival rate. MSC-AS1 suppression reduced the IC(50) value of TMZ and proliferation, promoted apoptosis and TMZ sensitivity, and affected PI3K/Akt pathway in TMZ-resistant glioma cells. MSC-AS1 acted as miR-373-3p sponge, and miR-373-3p directly targeted CPEB4. Silencing miR-373-3p reversed the promoting effect of MSC-AS1 or CPEB4 knockdown on TMZ sensitivity. Furthermore, MSC-AS1 knockdown inhibited TMZ-resistant glioma growth in vivo by regulating miR-373-3p/CPEB4 axis through PI3K/Akt pathway. Collectively, MSC-AS1 knockdown suppressed cell growth and the chemoresistance of glioma cells to TMZ by regulating miR-373-3p/CPEB4 axis in vitro and in vivo through activating PI3K/Akt pathway.	NA	Mol Cell Biochem. 2021 Feb;476(2):699-713. doi: 10.1007/s11010-020-03937-x. Epub 2020 Oct 26.
4379	LncRNA	MSC-AS1	miR-429	COL4A	laryngeal cancer cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA sequencing;	33079247	Identification of MSC-AS1, a novel lncRNA for the diagnosis of laryngeal cancer.	PURPOSE: Our study was aimed to identify potential lncRNAs related to laryngeal cancer (LC) and explore their potential regulatory mechanisms. METHODS: RNA sequencing data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to identify differentially expressed genes (DEGs). Receiver operating characteristic (ROC) curve analysis was performed to analyze the sensitivity and specificity of differentially expressed lncRNAs (DElncRNAs) as biomarkers. Weighted gene co-expression network analysis (WGCNA) was applied to identify co-expressed DElncRNAs and differentially expressed mRNAs (DEmRNAs) associated with clinical indicators. We performed functional enrichment analysis on target genes and constructed a lncRNA-miRNA-mRNA ceRNA network. The expression of lncRNA and mRNAs in ceRNA network were validated via RT-qPCR. RESULTS: By differential expression analyzing TCGA and GEO data, 6 up-regulated DElncRNAs were consistently identified, and their predictive performance were suggested to be considerable via ROC curve. 1998 DEmRNAs and 6 lncRNAs were involved in the construction of WGCNA network, in which the MEblue module was positively correlated with clinical stage. Functional enrichment analysis of this module suggested that the functions of DEmRNAs were closely involved in PI3K/Akt pathway. A ceRNA network composed of MSC-AS1, miR-429, COL4A1 and ITGAV was constructed. It was verified by RT-qPCR that the lncRNA and mRNAs in the ceRNA network were highly expressed in multiple LC tissues. CONCLUSIONS: This study identified lncRNA MSC-AS1 as a potential biomarker of LC. Besides, we constructed a ceRNA network, which provides a basis for the research of ceRNA in LC.	NA	Eur Arch Otorhinolaryngol. 2021 Apr;278(4):1107-1118. doi: 10.1007/s00405-020-06427-4. Epub 2020 Oct 20.
4380	LncRNA	MSC-AS1	miR-429	ITGAV	laryngeal cancer cells	Laryngeal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA sequencing;	33079247	Identification of MSC-AS1, a novel lncRNA for the diagnosis of laryngeal cancer.	PURPOSE: Our study was aimed to identify potential lncRNAs related to laryngeal cancer (LC) and explore their potential regulatory mechanisms. METHODS: RNA sequencing data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases were used to identify differentially expressed genes (DEGs). Receiver operating characteristic (ROC) curve analysis was performed to analyze the sensitivity and specificity of differentially expressed lncRNAs (DElncRNAs) as biomarkers. Weighted gene co-expression network analysis (WGCNA) was applied to identify co-expressed DElncRNAs and differentially expressed mRNAs (DEmRNAs) associated with clinical indicators. We performed functional enrichment analysis on target genes and constructed a lncRNA-miRNA-mRNA ceRNA network. The expression of lncRNA and mRNAs in ceRNA network were validated via RT-qPCR. RESULTS: By differential expression analyzing TCGA and GEO data, 6 up-regulated DElncRNAs were consistently identified, and their predictive performance were suggested to be considerable via ROC curve. 1998 DEmRNAs and 6 lncRNAs were involved in the construction of WGCNA network, in which the MEblue module was positively correlated with clinical stage. Functional enrichment analysis of this module suggested that the functions of DEmRNAs were closely involved in PI3K/Akt pathway. A ceRNA network composed of MSC-AS1, miR-429, COL4A1 and ITGAV was constructed. It was verified by RT-qPCR that the lncRNA and mRNAs in the ceRNA network were highly expressed in multiple LC tissues. CONCLUSIONS: This study identified lncRNA MSC-AS1 as a potential biomarker of LC. Besides, we constructed a ceRNA network, which provides a basis for the research of ceRNA in LC.	NA	Eur Arch Otorhinolaryngol. 2021 Apr;278(4):1107-1118. doi: 10.1007/s00405-020-06427-4. Epub 2020 Oct 20.
4381	LncRNA	MYLK-AS1	miR-424-5p	E2F7	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	FISH;qPCR;qRT-PCR;RIP assay;Western blot;FISH;	33168027	LncRNA MYLK-AS1 facilitates tumor progression and angiogenesis by targeting miR-424-5p/E2F7 axis and activating VEGFR-2 signaling pathway in hepatocellular carcinoma.	BACKGROUND: Long non-coding RNAs (lncRNAs) are crucial in the invasion, angiogenesis, progression, and metastasis of hepatocellular carcinoma (HCC). The lncRNA MYLK-AS1 promotes the growth and invasion of HCC through the EGFR/HER2-ERK1/2 signaling pathway. However, the clinical significance of MYLK-AS1 in HCC still needs to be further determined. METHODS: Bioinformatic analysis was performed to determine the potential relationship among MYLK-AS1, miRNAs and mRNAs. A total of 156 samples of normal liver and paired HCC tissues from HCC patients were used to evaluate MYLK-AS1 expression by qRT-PCR. Human HCC cell lines were used to evaluate the colony formation, cell proliferation, migration, invasion, cell cycle and apoptosis after transfection of lentiviral short-hairpin RNAs (shRNAs) targeting MYLK-AS1 or MYLK-AS1 vectors. The competitive endogenous RNA (ceRNA) mechanism was clarified using fluorescence in situ hybridization (FISH), Western blotting, qPCR, RNA binding protein immunoprecipitation (RIP), and dual luciferase reporter analysis. RESULTS: MYLK-AS1 up-regulation was detected in the HCC tumor tissues and cell lines associated with the enhancement of the angiogenesis and tumor progression. The down-regulation of MYLK-AS1 reversed the effects on angiogenesis, proliferation, invasion and metastasis in the HCC cells and in vivo. MYLK-AS1 acted as ceRNA, capable of regulating the angiogenesis in HCC, while the microRNA miR-424-5p was the direct target of MYLK-AS1. Promoting the angiogenesis and the tumor proliferation, the complex MYLK-AS1/miR-424-5p activated the VEGFR-2 signaling through E2F7, whereas the specific targeting of E2F transcription factor 7 (E2F7) by miR-424-5p, was indicated by the mechanism studies. CONCLUSIONS: MYLK-AS1 and E2F7 are closely related to some malignant clinicopathological features and prognosis of HCC, thus the MYLK-AS1/ miR-424-5p/E2F7 signaling pathway might represent a promising treatment strategy to combat HCC.	NA	J Exp Clin Cancer Res. 2020 Nov 9;39(1):235. doi: 10.1186/s13046-020-01739-z.
4382	LncRNA	NCK1-AS1	miR-137	NA	SK-MES-1 and H1299 cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Luciferase reporter assay;	33194081	Long non-coding RNA NCK1-AS1 promotes the proliferation, migration and invasion of non-small cell lung cancer cells by acting as a ceRNA of miR-137.	Long noncoding RNAs (lncRNAs) have been shown to play important roles in carcinogenesis and progression. In this study, we mainly investigate the potential influence of lncRNA NCK1 antisense RNA 1 (NCK1-AS1) on the progression of non-small cell lung cancer (NSCLC). RT-PCR was performed to determine the expression of NCK1-AS1 and miR-137 in NSCLC specimens and cell lines. The clinical significance of NCK1-AS1 in 148 patients was analyzed statistically. The receiver operating characteristic (ROC) curve was performed to estimate the diagnostic value of NCK1-AS1 and miR-137. Regulatory effects of NCK1-AS1 on proliferative, colony formation abilities, metastasis and apoptosis of SK-MES-1 and H1299 cells were assessed through a series of functional experiments. RNA-pull down and Dual-Luciferase reporter assay was performed to verify the sponge effect of NCK1-AS1 on miR-137. We observed that NCK1-AS1 expression was upregulated, while miR-137 expression was down-regulated in NSCLC specimens and cell lines. Increased NCK1-AS1 expression was positively correlated with TNM stage and lymph node metastasis and poor clinical outcome. The diagnostic value of NCK1-AS1 and miR-137 expression was also confirmed. Functionally, knockdown of NCK1-AS1 suppressed the proliferation, migration and invasion of NSCLC cells, and promoted apoptosis. Moreover, NCK1-AS1 was able to adsorb miR-137 via a sponge effect. Overall, our findings suggested that NCK1-AS1 may be a candidate biomarker and a target for new therapies in NSCLC patients.	NA	Am J Transl Res. 2020 Oct 15;12(10):6908-6920. eCollection 2020.
4383	LncRNA	NCK1-AS1	miR-100	NA	Oral squamous cell carcinoma cells	Oral Squamous Cell Cancer 	Homo sapiens (human)	Cell transfection;Cell transfection;qPCR;RT-qPCR;	33194849	LncRNA NCK1-AS1 in plasma distinguishes oral ulcer from early-stage oral squamous cell carcinoma.	BACKGROUND: Oral squamous cell carcinoma (OSCC) at early stages can be misdiagnosed as an oral ulcer (OU) due to similar symptoms, such as chronic and indurated ulcer. LncRNA NCK1-AS1 has been characterized as a key player in cervical cancer, while its role in OSCC is unknown. METHODS: All participants were selected at Jiangxi Province Tumor Hospital from December 2016 to December 2018. Expression levels of NCK1-AS1 and miR-100 in plasma from both OSCC and OU patients were measured by RT-qPCR. Diagnostic analysis was performed through ROC curve. Potential interactions between NCK1-AS1 and miR-100 were detected by cell transfection experiments. Cell invasion and migration were assessed by Transwell assays. RESULTS: The expression of NCK1-AS1 was upregulated in early-stage OSCC patients but not in OU patients. Upregulation of NCK1-AS1 distinguished OSCC patients from OU patients. The expression of miR-100 was inversely correlated with the expression of NCK1-AS1. Overexpression of NCK1-AS1 was followed by promoted OSCC cell invasion and migration. Overexpression of miR-100 did not affect the expression of NCK1-AS1 but inhibited the role of NCK1-AS1. CONCLUSIONS: Therefore, NCK1-AS1 may promote the metastasis of OSCC by downregulating miR-100.	NA	J Biol Res (Thessalon). 2020 Nov 11;27:16. doi: 10.1186/s40709-020-00126-1. eCollection 2020 Dec.
4384	LncRNA	NEAT1	miR-204-5p	NA	RA-FLSs cell	Rheumatoid Arthritis	Homo sapiens (human)	qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;luciferase assay;RNA pull-down;	33394349	LncRNA NEAT1 regulates the proliferation and production of the inflammatory cytokines in rheumatoid arthritis fibroblast-like synoviocytes by targeting miR-204-5p.	Rheumatoid arthritis (RA) is a chronic inflammatory disease, featured by erosive arthritis, which will eventually lead to deprivation normal functions of the joint and joint malformations. Continued illness also results in more serious complications, such as cardiovascular diseases and disability. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) function in various conditions, including RA. LncRNA NEAT1 was reported to promote migration and invasion in RA-FLSs, functioning as a promising diagnostic and therapeutic indicator in RA. The present work focused on the role of lncRNA NEAT1 in RA and the related mechanism. We collected the synovial tissue samples of 30 RA patients and 20 healthy controls. Moreover, RA fibroblast-like synoviocytes (RA-FLSs) cell line was bought and treated with tumor necrosis factor-α (TNF-α) to establish in vitro model of RA. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of NEAT1 in synovial tissue and RA-FLSs. NEAT1 silencing plasmid were synthesized and co-trasnfected with miR-204-5p inhibitor into RA-FLSs. MTT and 5-Ethynyl-2'-deoxyuridine staining were used to assess cell proliferation. Flow cytometry and TUNEL assay were used to determine the cell apoptosis. miR-204-5p has been predicted as a target miRNA of NEAT1, and the interaction between NEAT1 and miR-204-5p was verified by dual-luciferase assay and RNA pull-down assay. qRT-PCR and enzyme-linked immunosorbent assay were used to determine the mRNA and protein concentration of interleukin-1β and interleukin-6. Finally, western blot assay was applied to measure the effect of NEAT1 and on p53, NF-κB, and p-NF-κB expressions. We found that NEAT1 was up-regulated, and miR-204-5p was down-regulated in the RA patients' synovial tissue and TNF-α treated RA-FLSs. TNF-α increased NEAT1 level and decreased miR-204-5p level in RA-FLSs. There was no significant variance of p53 after transfected with NEAT1 in RA-FLSs. Meanwhile, Knockdown of NEAT1 attenuated TNF-α-induced RA-FLSs cell proliferation and inflammatory cytokine production while promoted cell apoptosis by targeting miR-204-5p through NF-κB pathway. These findings indicated that NEAT1 may be developed as a potential target for patients with RA.	NA	Hum Cell. 2021 Mar;34(2):372-382. doi: 10.1007/s13577-020-00461-4. Epub 2021 Jan 4.
4385	LncRNA	NEAT1	miR-27b-3p	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	33292252	Long noncoding RNA NEAT1 regulates radio-sensitivity via microRNA-27b-3p in gastric cancer.	BACKGROUND: Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) exhibits an oncogenic role in multiple cancers, including gastric cancer (GC). But, the functions of NEAT1 in modulating radio-sensitivity of GC and its potential molecular mechanisms have not been totally elucidated. METHODS: qRT-PCR was performed to detect the expressions of NEAT1 and microRNA-27b-3p (miR-27b-3p). Kaplan-Meier survival curves for NEAT1 expression in GC created using KM Plotter. Colony formation assay was used to determine the survival fraction. Cell apoptosis was evaluated by flow cytometry. Luciferase reporter assay was used to verify the relationship between miR-27b-3p and NEAT1. RESULTS: NEAT1 was highly expressed while miR-27b-3p was downregulated in GC tissues and cells. NEAT1 was negatively correlated with that of miR-27b-3p and associated with poor overall survival. Moreover, NEAT1 and miR-27b-3p varied inversely after radiation in GC tissues and cells. Loss of NEAT1 or upregulation of miR-27b-3p increased the effect of radiation on cell survival fraction inhibition and apoptosis promotion. In addition, NEAT1 negatively regulated the expression of miR-27b-3p in GC cells. Interestingly, the depletion of miR-27b-3p dramatically attenuated the NEAT1 knockdown-mediated function in AGS and MKN-45 cells treated with radiation in vitro. Similarly, downregulation of NEAT1 enhanced the radiation-mediated inhibition of tumor growth, which was mitigated by decrease of miR-27b-3p. CONCLUSION: NEAT1 depletion enhanced radio-sensitivity of GC by negatively regulating miR-27b-3p in vitro and in vivo.	NA	Cancer Cell Int. 2020 Dec 3;20(1):581. doi: 10.1186/s12935-020-01655-4.
4386	LncRNA	NEAT1	miR-503	SMO	HCC cell line	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33398379	Silencing of long non-coding RNA NEAT1 inhibits hepatocellular carcinoma progression by downregulating SMO by sponging microRNA-503.	Hepatocellular carcinoma (HCC) poses an increasing threat to humans, due to its poor prognosis. Nuclear-enriched abundant transcript 1 (NEAT1), a type of long non-coding (lnc)RNA, has been found to function in a variety of cancer types. However, the role of NEAT1 in HCC is poorly understood. Reverse transcription-quantitative PCR was used to detect the expression levels of NEAT1, microRNA (miR)-503 and Smoothened (SMO) mRNA in HCC tissues and cells. MTT and flow cytometry assays were used to investigate cell viability and apoptosis, respectively, while Transwell assays were performed to investigate cell invasion and migration. StarBase and TargetScan were utilized to predict the target sequence between miR-503 and NEAT1 or SMO, the results of which were verified using a dual-luciferase reporter assay. The protein expression level of SMO was measured using western blot. The RNA expression level of NEAT1 and SMO was significantly elevated in HCC tissues and cells compared with that in the corresponding healthy tissues and cells, which was contrary to miR-503 expression level. NEAT1 silencing was found to restrict the viability, migration and invasion of the cells, while simultaneously induced apoptosis in the HCC cell line. Further studies found that miR-503 expression was negatively correlated with NEAT1 or SMO. It was also confirmed that NEAT1 directly interacted with miR-503 and miR-503 could bind to the 3'-untranslated region of SMO. Furthermore, overexpression of NEAT1 or SMO could reverse the effects of miR-503-mediated inhibition on cell viability, invasion, migration and promotion of apoptosis in the HCC cell lines. These results demonstrated that downregulation of NEAT1 impeded the viability, migration, invasion and induced apoptosis through the NEAT1/miR-503/SMO axis in the HCC cell line.	NA	Mol Med Rep. 2021 Mar;23(3):168. doi: 10.3892/mmr.2020.11807. Epub 2021 Jan 5.
4387	LncRNA	NEAT1	miR-195-5p	VEGFA	sinonasal squamous cell carcinoma cells	Sinonasal Squamous Cell Carcinoma 	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33146672	Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of sinonasal squamous cell carcinoma cells via miR-195-5p/VEGFA axis.	The role of long non-coding RNA nuclear-enriched abundant transcript 1 (lncRNA NEAT1) in sinonasal squamous cell carcinoma (SNSCC) remained obscure. Target genes and potential binding sites of NEAT1, microRNA (miR)-195-5p and VEGFA were predicted using StarBase and TargetScan, and confirmed by dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expressions of NEAT1, vascular endothelial growth factor A (VEGFA) and miR-195-5p. Pearson's correlation analysis of NEAT1, miR-195-5p and VEGFA was conducted. Cell viability, apoptosis and tube formation capability were assessed by MTT assay, flow cytometry and capillary-like tube formation assay, respectively. Expressions of VEGFA and proteins related to the phosphatidylinositide 3-kinase/Protein Kinase B (PI3K/AKT) pathway were measured by Western blot. In SNSCC tissues and cells, the expressions of NEAT1 and VEGFA were up-regulated while the expression of miR-195-5p was down-regulated, and NEAT1 was negatively correlated with miR-195-5p yet positively correlated with VEGFA. Overexpressed VEGFA promoted the viability and capillary-like tube formation of SNSCC cells yet suppressed their apoptosis, while silencing VEGFA led to the opposite results. MiR-195-5p could bind to NEAT1, and down-regulating miR-195-5p reversed the effects of silencing NEAT1 on the expressions of NEAT1 and miR-195-5p, cell viability, apoptosis and capillary-like tube formation as well as PI3K/AKT pathway activation. VEGFA was the target of miR-195-5p, and overexpressed VEGFA reversed the effects of miR-195-5p. Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of SNSCC cells yet promoted their apoptosis via the miR-195-5p/VEGFA axis, providing a possible therapeutic target for SNSCC treatment.	NA	Biosci Rep. 2020 Nov 27;40(11):BSR20201373. doi: 10.1042/BSR20201373.
4388	LncRNA	NEAT1	miR-365	FGF9	OC cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33545926	LncRNA NEAT1 promotes proliferation of ovarian cancer cells and angiogenesis of co-incubated human umbilical vein endothelial cells by regulating FGF9 through sponging miR-365: An experimental study.	OBJECTIVE: To uncover the function of lncRNA NEAT1 in ovarian cancer (OC) cells and its mechanism. METHODS: The expression patterns of lncRNA NEAT1 and FGF9 in human OC cells and human ovarian epithelial cells was determined. OC cells were transfected with sh-NEAT1, pcDNA3.1-NEAT1, miR-365 mimic, miR-365 inhibitor or pcDNA3.1-NEAT1 + sh-NEAT1 before cell proliferation rate and cell clone formation rate were measured. After the transfected OC cells were co-cultivated with human umbilical vein endothelial cells (HUVECs), Matrigel angiogenesis assay tested angiogenesis of HUVECs; qRT-PCR and Western blot tested the expressions of vascular endothelial growth factor (VEGF), angiogenin 1 (Ang-1) and matrix metalloproteinase 2 (MMP2). Dual-luciferase reporter assay determined the targeted binding of NEAT1 and FGF9 to miR-365. RESULTS: LncRNA NEAT1 and FGF9 are over-expressed in OC cells. Knockdown of NEAT1 or FGF9, or over-expression of miR-365 results in decreased proliferation rate and cell clones as well as inhibited angiogenesis and down-regulated expressions of VEGF, Ang-1 and MMP2. Over-expression of NEAT1 or knockdown of miR-365 can reverse the effect caused by FGF9 knockdown. NEAT1 can down-regulate the expression of miR-365 while up-regulating that of FGF9. Dual-luciferase reporter assay determined that NEAT1 competes with FGF9 for binding to miR-365. CONCLUSION: LncRNA NEAT1 up-regulates FGF9 by sponging miR-365, thus promoting OC cell proliferation and angiogenesis of HUVECs.	NA	Medicine (Baltimore). 2021 Jan 22;100(3):e23423. doi: 10.1097/MD.0000000000023423.
4389	LncRNA	NEAT1	miR-3619-5p	LASP1	RB cells	Retinoblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33281873	LncRNA NEAT1 Knockdown Inhibits Retinoblastoma Progression by miR-3619-5p/LASP1 Axis.	Retinoblastoma (RB) is the most common intraocular tumor in childhood. Long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NTAT1) has been reported to be related to RB progression. This study aims to study the molecular mechanism of NEAT1 in regulating cell cycle, proliferation, apoptosis, migration, and invasion in RB. The expression levels of NEAT1 and miR-3619-5p were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression of LIM and SH3 domain protein 1 (LASP1) was measured by western blot. The proliferation of RB cells was analyzed by cell counting kit-8 (CCK-8) and cell colony formation assays. Cell migration and invasion were evaluated by transwell assay. Cell cycle and apoptosis were assessed by flow cytometry analysis. The association between miR-3619-5p and NEAT1 or LASP1 was predicted by starBase 3.0 database and identified by dual-luciferase reporter assay. The effects of NEAT1 knockdown on the tumor growth in vivo were detected by in vivo tumor formation assay. NEAT1 expression was dramatically up-regulated, and miR-3619-5p expression was obviously downregulated in RB tissues and cells compared with control groups. The protein level of LASP1 was obviously increased in RB tissues or cells relative to paracancerous normal tissues or cells, respectively. Functionally, NEAT1 silencing inhibited RB cell migration, invasion, and proliferation, whereas induced cell apoptosis and cell cycle arrest in RB; this phenomenon was partially abolished by miR-3619-5p inhibitor. Mechanistically, NEAT1 acted as a sponge of miR-3619-5p, and miR-3619-5p was associated with LASP1. In addition, NEAT1 knockdown decreased the volume and weight of RB tumor in vivo. Together, NEAT1 silencing repressed cell migration, invasion, and proliferation, whereas induced cell apoptosis and cycle arrest by sponging miR-3619-5p to inhibit LASP1 expression in RB cells. This study may provide a theoretical basis for RB therapy.	NA	Front Genet. 2020 Nov 17;11:574145. doi: 10.3389/fgene.2020.574145. eCollection 2020.
4390	LncRNA	NEAT1	miR-129-5p	SOCS2	AML-12 cells	Alcoholic Steatohepatitis	Homo sapiens (human)	qRT-PCR	33228663	LncRNA NEAT1/microRNA-129-5p/SOCS2 axis regulates liver fibrosis in alcoholic steatohepatitis.	BACKGROUND: Long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to play an essential role in non-alcoholic fatty liver disease. However, the role of NEAT1 in regulation of alcoholic steatohepatitis (ASH) remains largely unknown. This study aims to explore the role of NEAT1 in ASH by mediating microRNA-129-5p (miR-129-5p) targeting suppressor of cytokine signaling 2 (SOCS2). METHODS: NEAT1, miR-129-5p and SOCS2 expression in serum of ASH patients were assessed. In the in vitro cellular experiment, we transfected siRNAs, oligonucleotides or plasmids into ethanol-induced AML-12 mouse hepatocytes to alter NEAT1 and miR-129-5p expression, and inflammatory factors and lipid content were determined. In the in vivo animal experiment, we injected lentiviruses carrying siRNAs, oligonucleotides or plasmids onto ASH mice (ASH induced by feeding mice a Lieber-DeCarli ethanol diet) to alter NEAT1 and miR-129-5p expression through the tail vein. Serum liver function, blood lipids and inflammatory factors were detected; liver histopathology, liver cell apoptosis, and fibrosis were observed. The relationship between NEAT1 and miR-129-5p, or between miR-129-5p and SOCS2 was verified. RESULTS: MiR-129-5p was reduced while NEAT1 and SOCS2 were elevated in ASH. Inhibited NEAT1 or elevated miR-129-5p suppressed the elevated lipid metabolism and restrained inflammation reaction in ethanol-stimulated AML-12 cells. The promoted miR-129-5p and inhibited NEAT1 could improve the liver function and repress blood lipid, inflammation reaction, hepatocyte apoptosis and liver fibrosis in ethanol-induced ASH mice. Furthermore, NEAT1 could negatively regulate miR-129-5p to target SOCS2. CONCLUSION: We have found that the inhibited NEAT1 could suppress liver fibrosis in ASH mice by promoting miR-129-5p and restraining SOCS2, thereby decelerating the development of ASH.	NA	J Transl Med. 2020 Nov 24;18(1):445. doi: 10.1186/s12967-020-02577-5.
4391	LncRNA	NEAT1	miR-129-5p	SOCS2	AML-12 cells	Alcoholic Steatohepatitis	Mus musculus (mouse)	qRT-PCR	33228663	LncRNA NEAT1/microRNA-129-5p/SOCS2 axis regulates liver fibrosis in alcoholic steatohepatitis.	BACKGROUND: Long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to play an essential role in non-alcoholic fatty liver disease. However, the role of NEAT1 in regulation of alcoholic steatohepatitis (ASH) remains largely unknown. This study aims to explore the role of NEAT1 in ASH by mediating microRNA-129-5p (miR-129-5p) targeting suppressor of cytokine signaling 2 (SOCS2). METHODS: NEAT1, miR-129-5p and SOCS2 expression in serum of ASH patients were assessed. In the in vitro cellular experiment, we transfected siRNAs, oligonucleotides or plasmids into ethanol-induced AML-12 mouse hepatocytes to alter NEAT1 and miR-129-5p expression, and inflammatory factors and lipid content were determined. In the in vivo animal experiment, we injected lentiviruses carrying siRNAs, oligonucleotides or plasmids onto ASH mice (ASH induced by feeding mice a Lieber-DeCarli ethanol diet) to alter NEAT1 and miR-129-5p expression through the tail vein. Serum liver function, blood lipids and inflammatory factors were detected; liver histopathology, liver cell apoptosis, and fibrosis were observed. The relationship between NEAT1 and miR-129-5p, or between miR-129-5p and SOCS2 was verified. RESULTS: MiR-129-5p was reduced while NEAT1 and SOCS2 were elevated in ASH. Inhibited NEAT1 or elevated miR-129-5p suppressed the elevated lipid metabolism and restrained inflammation reaction in ethanol-stimulated AML-12 cells. The promoted miR-129-5p and inhibited NEAT1 could improve the liver function and repress blood lipid, inflammation reaction, hepatocyte apoptosis and liver fibrosis in ethanol-induced ASH mice. Furthermore, NEAT1 could negatively regulate miR-129-5p to target SOCS2. CONCLUSION: We have found that the inhibited NEAT1 could suppress liver fibrosis in ASH mice by promoting miR-129-5p and restraining SOCS2, thereby decelerating the development of ASH.	NA	J Transl Med. 2020 Nov 24;18(1):445. doi: 10.1186/s12967-020-02577-5.
4392	LncRNA	NEAT1	miR-373	FLT1	trophoblast cells	Preeclampsia	Homo sapiens (human)	qRT-PCR	33093438	Long Non-Coding RNA Nuclear-Enriched Abundant Transcript 1 (NEAT1) Represses Proliferation of Trophoblast Cells in Rats with Preeclampsia via the MicroRNA-373/FLT1 Axis.	BACKGROUND Preeclampsia (PE) remains one of the primary causes of maternal morbidity and mortality worldwide. This study was designed to investigate the relevance of long non-coding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) and downstream molecules in trophoblast cell proliferation and apoptosis. MATERIAL AND METHODS NEAT1 expression in the placental tissues of rats with PE was analyzed by reverse transcriptionquantitative polymerase chain reaction. The role of NEAT in trophoblast cell proliferation, migration, invasion, and apoptosis was assessed by transfecting pcDNA-NEAT1 and siRNA-NEAT1 into trophoblast cells. The microRNA (miRNA) binding to NEAT1 and the genes targeted by the screened miRNAs were predicted by Starbase, and the mechanism of action of NEAT1 in PE was further investigated. RESULTS The expression of NEAT1 lncRNA was markedly higher in placental samples of PE than control rats. Ectopic expression of NEAT1 repressed trophoblast cell proliferation, migration, invasion, and colony formation, but facilitated cell apoptosis, whereas NEAT1 downregulation resulted in the opposite effects. NEAT1 was found to act as a molecular sponge for miR-373, regulating Fms-like tyrosine kinase-1 (FLT-1) to modulate PE development. CONCLUSIONS NEAT1 may contribute to PE development by regulating trophoblast cell proliferation and apoptosis. These findings may provide a new perspective for understanding the etiology and pathogenesis of PE.	NA	Med Sci Monit. 2020 Oct 23;26:e927305. doi: 10.12659/MSM.927305.
4393	LncRNA	NEAT1	miR-212-3p	AXIN1	MPP(+)-stimulated SK-N-SH cells	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33241432	LncRNA NEAT1 Regulates the Development of Parkinson's Disease by Targeting AXIN1 Via Sponging miR-212-3p.	Long non-coding RNA (lncRNA) nuclear-enriched assembly transcript 1 (NEAT1) has been reported to be highly expressed in Parkinson's disease (PD). However, the mechanism of NEAT1 in PD progression has not been fully elucidated. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine injection (MPTP) was used to construct PD mouse models in vivo, and 1-methyl-4-phenyl pyridine (MPP(+)) was used to build PD cell models in vitro. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to test the expression of NEAT1, microRNA (miR)-212-3p and axis inhibition protein 1 (AXIN1). The viability, apoptosis and inflammation of cells were determined using cell counting kit 8 (CCK8) assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA), respectively. Then, the protein levels of apoptosis-related markers and AXIN1 were measured by western blot (WB) analysis. Furthermore, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the interaction between miR-212-3p and NEAT1 or AXIN1. NEAT1 was upregulated in PD mouse models and cell models. Function experiments confirmed that NEAT1 knockdown could promote the viability, suppress the apoptosis and inflammation of MPP(+)-stimulated SK-N-SH cells to restrain PD progression. MiR-212-3p was downregulated in PD, and its inhibitor could reverse the suppression effect of NEAT1 knockdown on PD progression. Additionally, AXIN1 was a target of miR-212-3p, and its overexpression could invert the inhibition effect of miR-212-3p mimic on PD progression. Furthermore, AXIN1 expression was inhibited by NEAT1 silencing and promoted by NEAT1 overexpression, while these effect could be recovered by miR-212-3p inhibitor and mimic, respectively. Our results demonstrated that NEAT1 knockdown suppressed PD progression through regulating the miR-212-3p/AXIN1 pathway, indicating that NEAT1 might be a therapeutic target for neuroprotection in PD.	NA	Neurochem Res. 2021 Feb;46(2):230-240. doi: 10.1007/s11064-020-03157-1. Epub 2020 Nov 26.
4394	LncRNA	NEAT1	miR-212-3p	AXIN1	MPP(+)-stimulated SK-N-SH cells	Parkinsons Disease	Mus musculus (mouse)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33241432	LncRNA NEAT1 Regulates the Development of Parkinson's Disease by Targeting AXIN1 Via Sponging miR-212-3p.	Long non-coding RNA (lncRNA) nuclear-enriched assembly transcript 1 (NEAT1) has been reported to be highly expressed in Parkinson's disease (PD). However, the mechanism of NEAT1 in PD progression has not been fully elucidated. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine injection (MPTP) was used to construct PD mouse models in vivo, and 1-methyl-4-phenyl pyridine (MPP(+)) was used to build PD cell models in vitro. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to test the expression of NEAT1, microRNA (miR)-212-3p and axis inhibition protein 1 (AXIN1). The viability, apoptosis and inflammation of cells were determined using cell counting kit 8 (CCK8) assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA), respectively. Then, the protein levels of apoptosis-related markers and AXIN1 were measured by western blot (WB) analysis. Furthermore, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the interaction between miR-212-3p and NEAT1 or AXIN1. NEAT1 was upregulated in PD mouse models and cell models. Function experiments confirmed that NEAT1 knockdown could promote the viability, suppress the apoptosis and inflammation of MPP(+)-stimulated SK-N-SH cells to restrain PD progression. MiR-212-3p was downregulated in PD, and its inhibitor could reverse the suppression effect of NEAT1 knockdown on PD progression. Additionally, AXIN1 was a target of miR-212-3p, and its overexpression could invert the inhibition effect of miR-212-3p mimic on PD progression. Furthermore, AXIN1 expression was inhibited by NEAT1 silencing and promoted by NEAT1 overexpression, while these effect could be recovered by miR-212-3p inhibitor and mimic, respectively. Our results demonstrated that NEAT1 knockdown suppressed PD progression through regulating the miR-212-3p/AXIN1 pathway, indicating that NEAT1 might be a therapeutic target for neuroprotection in PD.	NA	Neurochem Res. 2021 Feb;46(2):230-240. doi: 10.1007/s11064-020-03157-1. Epub 2020 Nov 26.
4395	LncRNA	NEAT1	miR-221-3p	Sirt2	mesenchymal stem cells	Cardiac Senescence	Homo sapiens (human)	luciferase assay;	33129330	Exosomal LncRNA-NEAT1 derived from MIF-treated mesenchymal stem cells protected against doxorubicin-induced cardiac senescence through sponging miR-221-3p.	BACKGROUND: The chemotherapy drug doxorubicin (Dox) is widely used for treating a variety of cancers. However, its high cardiotoxicity hampered its clinical use. Exosomes derived from stem cells showed a therapeutic effect against Dox-induced cardiomyopathy (DIC). Previous studies reported that exosomes derived from mesenchymal stem cells (MSCs) pretreated with macrophage migration inhibitory factor (MIF) (exosome(MIF)) showed a cardioprotective effect through modulating long noncoding RNAs/microRNAs (lncRNAs/miRs). This study aimed to investigate the role of exosome(MIF) in the treatment of DIC. RESULTS: Exosomes were isolated from control MSCs (exosome) and MIF-pretreated MSCs (exosome(MIF)). Regulatory lncRNAs activated by MIF pretreatment were explored using genomics approaches. Fluorescence-labeled exosomes were tracked in vitro by fluorescence imaging. In vivo and in vitro, miR-221-3p mimic transfection enforced miR-221-3p overexpression, and senescence-associated β-galactosidase assay was applied to test cellular senescence. Exosomal delivering LncRNA-NEAT1 induced therapeutic effect in vivo was confirmed by echocardiography. It demonstrated that exosomes(MIF) recovered the cardiac function and exerted the anti-senescent effect through LncRNA-NEAT1 transfer against Dox. TargetScan and luciferase assay showed that miR-221-3p targeted the Sirt2 3'-untranslated region. Silencing LncRNA-NEAT1 in MSCs, miR-221-3p overexpression or Sirt2 silencing in cardiomyocytes decreased the exosome(MIF)-induced anti-senescent effect against Dox. CONCLUSIONS: The results indicated exosome(MIF) serving as a promising anti-senescent effector against Dox-induced cardiotoxicity through LncRNA-NEAT1 transfer, thus inhibiting miR-221-3p and leading to Sirt2 activation. The study proposed that exosome(MIF) might have the potential to serve as a cardioprotective therapeutic agent during cancer chemotherapy.	NA	J Nanobiotechnology. 2020 Oct 31;18(1):157. doi: 10.1186/s12951-020-00716-0.
4396	LncRNA	NEAT1	miR-486-5p	TGF-b2	lens epithelial cells	Posterior Capsular Opacification	Drosophila (flies)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33292220	LncRNA NEAT1 promotes proliferation, migration, invasion and epithelial-mesenchymal transition process in TGF-β2-stimulated lens epithelial cells through regulating the miR-486-5p/SMAD4 axis.	BACKGROUND: Abnormal proliferation, metastasis and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) are direct factors of posterior capsular opacification (PCO). Nuclear enriched abundant transcript 1 (NEAT1) has been shown to promote cell proliferation, metastasis and EMT, but whether it affects the progression of PCO is unclear. METHODS: The expression of NEAT1, microRNA-486-5p (miR-486-5p) and Drosophila mothers against decapentaplegic 4 (SMAD4) was determined using quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation of cells was measured via 3-(4, 5-dimethyl-2 thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Transwell assay was employed to detect the migration and invasion of cells. The levels of EMT marker proteins, SMAD4 protein and transforming growth factor-β (TGF-β)/SMAD signaling pathway-related proteins were assessed by western blot (WB) analysis. Further, the relationship between miR-486-5p and NEAT1 or SMAD4 was confirmed by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and biotin-labeled RNA pull-down assay. RESULTS: NEAT1 is upregulated and miR-486-5p is downregulated in the posterior capsular tissues of PCO patients and TGF-β2-induced LECs. Interference of NEAT1 reverses the promoting effect of TGF-β2 on the proliferation, migration, invasion and EMT of LECs. MiR-486-5p can be sponged by NEAT1, and its inhibitor reverses the suppression effect of NEAT1 silencing on the progression of TGF-β2-induced LECs. SMAD4 functions as a target of miR-486-5p, and its overexpression recovers the inhibition effect of miR-486-5p overexpression on the progression of TGF-β2-induced LECs. The activity of the TGF-β/SMAD signaling pathway is regulated by the NEAT1/miR-486-5p/SMAD4 axis. CONCLUSION: Our study shows that NEAT1 has a positive effect on the progression of PCO and is expected to become a new target for PCO treatment.	NA	Cancer Cell Int. 2020 Oct 31;20(1):529. doi: 10.1186/s12935-020-01619-8.
4397	LncRNA	NEAT1	miR-339-5p	ITGA3	TSCCA, CAL27, SCC15 and HN13. CAL27 cell lines	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;MTT assay;	33043343	[LncRNA NEAT1 regulates proliferation, migration and invasion of tongue squamous cell carcinoma cells by regulating miR-339-5p/ITGA3 axis].	PURPOSE: To investigate the molecular mechanism of LncRNA NEAT1 regulating proliferation, migration and invasion of tongue squamous cell carcinoma cells by regulating miR-339-5p/ITGA3 axis. METHODS: qRT-PCR and Western blot were used to detect the expression of NEAT1, miR-339-5p, ITGA3 mRNA and ITGA3 protein in 25 cases of human tongue squamous cell carcinoma, its corresponding adjacent tissues, human normal oral mucosal cell line HOK and human tongue squamous cell carcinoma cell lines TSCCA, CAL27, SCC15 and HN13. CAL27 cell lines that inhibited NEAT1 and overexpressed miR-339-5p were constructed, respectively. Cell viability was detected by MTT assay, cell numbers of migration and invasion were detected by Transwell assay, and the expression of Cyclin D1 and MMP-9 proteins were detected by Western blotting. The dual luciferase reporter gene was used to verify the targeting relationship of NEAT1, miR-339-5p and ITGA3, and the regulatory relationship was detected by Western blotting and qRT-PCR. SPSS 17.0 software package was used for statistical analysis of the data. RESULTS: Compared with normal human oral mucosal cell line HOK, the expression of NEAT1 and ITGA3 was up-regulated, while the expression of miR-339-5p was down-regulated in human tongue squamous cell carcinoma cell lines. Inhibition of NEAT1 or over-expression of miR-339-5p significantly inhibited proliferation, migration and invasion of CAL27 cells, and significantly inhibited expression of Cyclin D1 and MMP-9 proteins. Dual luciferase reporter gene assay confirmed that NEAT1 directly interacted with miR-339-5p and suppressed its expression. miR-339-5p negatively regulated ITGA3 expression. Inhibition of NEAT1 reversed the inhibitory effect of the inhibition of miR-339-5p on proliferation, migration and invasion of CAL27 cells. CONCLUSIONS: LncRNA NEAT1 promotes proliferation, migration and invasion of tongue squamous cell carcinoma cells by down-regulating miR-339-5p/ITGA3 axis.	NA	Shanghai Kou Qiang Yi Xue. 2020 Jun;29(3):267-274.
4398	LncRNA	NEAT1	miR-1277-5p	ARHGAP26	SK-N-SH cells	Neurodegenerative Diseases	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33069733	Deficiency of NEAT1 prevented MPP(+)-induced inflammatory response, oxidative stress and apoptosis in dopaminergic SK-N-SH neuroblastoma cells via miR-1277-5p/ARHGAP26 axis.	Noncoding RNAs including long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) have been documented to play prominent role in neurodegenerative diseases including Parkinson's disease (PD). This study intended to investigate the role of lncRNA nuclear enriched assembly transcript 1 (NEAT1) in MPP(+)-induced PD model in dopaminergic neuronblastoma SK-N-SH cells, as well as its mechanism through sponging miRNA (miR)-1277-5p. Real-time PCR and western blotting revealed that NEAT1 and ARHGAP26 were upregulated, and miR-1277-5p was downregulated in MPP(+)-treated SK-N-SH cells in a certain of concentration- and time- dependent manner. MPP(+) induced apoptosis in SK-N-SH cells, as evidenced by decreased cell viability and Bcl-2 expression, and elevated apoptosis rate and levels of Bax and cleaved caspase-3, which were examined by MTT assay, flow cytometry and western blotting. Moreover, commercial assay kits indicated that inflammatory response and oxidative stress were provoked in response to MPP(+), due to promoted contents of interleukin (IL)-6, IL-1β, tumor necrosis factor-α, malondialdehyde, and lactate dehydrogenase, accompanied with suppressed superoxide dismutase and glutathione peroxidase levels. Notably, MPP(+)-induced apoptosis, inflammatory response and oxidative stress in SK-N-SH cells were mitigated by NEAT1 knockdown and/or miR-1277-5p overexpression. Moreover, silencing of miR-1277-5p could abrogate the suppression of NEAT1 deficiency on MPP(+)-induced cell injury. Similarly, upregulating miR-1277-5p-elicited neuroprotection in MPP(+)-induced SK-N-SH cells was reversed by ARHGAP26 restoration. Dual-luciferase reporter assay demonstrated a direct interaction between miR-1277-5p and NEAT1 or ARHGAP26. Collectively, NEAT1 upregulation might contribute to MPP(+)-induced neuron injury via NEAT1-miR-1277-5p-ARHGAP26 competing endogenous RNAs (ceRNAs) pathway.	NA	Brain Res. 2021 Jan 1;1750:147156. doi: 10.1016/j.brainres.2020.147156. Epub 2020 Oct 16.
4399	LncRNA	NEAT1	let-7g-5p	MAP3K1	glioma stem cells	Glioblastoma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33057597	LncRNA NEAT1 promotes malignant phenotypes and TMZ resistance in glioblastoma stem cells by regulating let-7g-5p/MAP3K1 axis.	Glioblastoma multiforme (GBM) is one of the most malign brain tumors in adults. Temozolomide (TMZ) is an oral chemotherapy drug constituting the backbone of chemotherapy regimens utilized as first-line treatment of GBM. However, resistance to TMZ often leads to treatment failure. In the present study, we explored the expression and related mechanisms of nuclear enriched abundant transcript 1 (NEAT1) in glioma stem cells (GSCs). Quantitative real-time PCR (qRT-PCR) showed that NEAT1 was up-regulated in serum samples of GBM patients and GSCs isolated from U87, U251 cell lines. Functional experiments showed that NEAT1 knockdown restrained malignant behaviors of GSC, including proliferation, migration and invasion. Dual-luciferase assays identified let-7g-5p was a downstream target and negatively adjusted by NEAT1. Restoration of let-7g-5p impeded tumor progression by inhibiting proliferation, migration and invasion. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1), as a direct target of let-7g-5p, was positively regulated by NEAT1 and involved to affect the regulation of NEAT1 on GSCs' behaviors. In conclusion, our results suggested that NEAT1 promoted GSCs progression via NEAT1/let-7g-5p/MAP3K1 axis, which provided a depth insight into TMZ resistance mechanism.	NA	Biosci Rep. 2020 Oct 30;40(10):BSR20201111. doi: 10.1042/BSR20201111.
4400	LncRNA	NEAT1	miR-18a-5p	ESRa	HTR-8/SVneo cells	Preeclampsia	Homo sapiens (human)	qRT-PCR	32998583	Up-regulation of LncRNA NEAT1 induces apoptosis of human placental trophoblasts.	The trophoblast apoptosis induced by placental oxidative stress is a contributor to the pathological development of preeclampsia (PE), whereas the molecular mechanism remains unclear. In this study, we explored the role and mechanism of Long non-coding RNA (LncRNA) NEAT1 in trophoblasts apoptosis. In the placenta tissues of PE patients and H(2)O(2)-treated human trophoblast cell line HTR-8/SVneo, the expressions of LncRNA NEAT1, p53, and estrogen receptor α (ESRα) were increased whereas miR-18a-5p expression was decreased. ESRα expression was up-regulated by LncRNA NEAT1 overexpression and down-regulated by miR-18a-5p overexpression in HTR-8/SVneo cells. LncRNA NEAT1 could release ESRα expression through sponging miR-18a-5p and the transcription of LncRNA NEAT1 was promoted by p53. miR-18a-5p overexpression suppressed H(2)O(2)-induced cell apoptosis in HTR-8/SVneo cells, while the inhibitory effect of miR-18a-5p overexpression on cell apoptosis was abrogated by LncRNA NEAT1 overexpression. In summary, LncRNA NEAT1 transcription was induced by p53 under oxidative stress condition, the high expression of LncRNA NEAT1 subsequently increased ESRα expression by sponging miR-18a-5p, thus inducing trophoblasts apoptosis.	NA	Free Radic Res. 2020 Sep;54(8-9):678-686. doi: 10.1080/10715762.2020.1826468. Epub 2020 Oct 1.
4401	LncRNA	NEAT1	miR-1224-5p	RSF1	Gastric Cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;	33244266	LncRNA NEAT1 Promotes the Progression of Gastric Cancer Through Modifying the miR-1224-5p/RSF1 Signaling Axis.	INTRODUCTION: The therapy of patients with advanced phase gastric cancer is still a huge threat, with extremely imperfect therapies authorized. Even if the amassed indications have validated the significance of lncRNA in gastric cancer, few understandings are stated concerning nuclear paraspeckle assembly transcript 1 (NEAT1) practical functions and molecular mechanisms. METHODS: In this research, the expression of NEAT1 and miR-1224-5p in gastric cancer tissues was measured by qRT-PCR analysis, and the expression of remodeling and spacing factor 1 (RSF1) was measured by IHC assay. Then, the bioinformatics prediction software ENCORI was applied to envisage the assumed binding sites. The monitoring roles of NEAT1 or miR-1224-5p on the cell proliferation and migration capacity were verified by CCK-8, wound healing and transwell assay, correspondingly. The interactions among NEAT1, miR-1224-5p and RSF1 were investigated via luciferase analysis. RESULTS: Our findings revealed high expression levels of NEAT1, RSF1 and a decreased expression level of miR-1224-5p in gastric cancer. Upregulation of NEAT1 or knockdown of miR-1224-5p elevated gastric cancer cell proliferation, and migration. Bioinformatics and luciferase analyses simplified that NEAT1 directly cooperated with miR-1224-5p to weaken miR-1224-5p binding to the RSF1 3'-UTR region. Likewise, the mechanical inquiries ratified that initiation of the miR-1224-5p/RSF1 regulatory loop by miR-1224-5p knockdown or overexpressed RSF1 validated the functions of NEAT1 in endorsing gastric cancer cell malignancy. DISCUSSION: Our research initially validated that NEAT1 may regulate the expression of RSF1 competitive sponge to miR-1224-5p, contributed to the supervision of gastric cancer evolution, which exposed new brightness for diagnosis and therapy of gastric cancer.	NA	Cancer Manag Res. 2020 Nov 19;12:11845-11855. doi: 10.2147/CMAR.S267666. eCollection 2020.
4402	LncRNA	NEAT1	miR-216b	MAP2K6	AP cells	Acute Pancreatitis	Homo sapiens (human)	qRT-PCR	33051781	Quercetin inhibits caerulein-induced acute pancreatitis through regulating miR-216b by targeting MAP2K6 and NEAT1.	Acute pancreatitis (AP) is a common acute abdominal disease with high mortality and mortality rates. Increasing evidences clarified that Traditional Chinese Medicine (TCM) adjuvant therapy for AP can be used and it gives a positive effect. Quercetin (3,3',4',5,7-pentahydroxyflavone, QE) is a type of flavone compound with positive effect on cancer and inflammation prevention. The current study aims to identify the effect of QE on AP and potential molecular effect. In this case, caerulein (CAE) induced AP cell and mice model were used. QE alleviated inflammatory mediators TNF-α, IL-6, and IL-10 in experiments. In addition, miR-216b was increased based on QE treatment. In further study, MAP2K6 of p38/MAPK signaling pathway was identified as a direct target of miR-216b, and QE inhibited p38/MAPK signaling pathway through up-regulating miR-216b. Our study also first confirmed that long non-coding RNA NEAT1 is a direct target of miR-216b and can be suppressed by QE. Because of the target, NEAT1, miR-216b, and MAP2K6 formed a competitive endogenous RNA (ceRNA) network. Besides direct target mediated by QE, it also decreased TNF-α which down-regulated TRAF2 and MAP3K5 located on upstream of p38/MAPK signaling and formed a feedback loop. In conclusion, QE has a protective effect on AP through inhibiting p38/MAPK signaling pathway by up-regulating miR-216b and suppressing TNF-α.	NA	Inflammopharmacology. 2021 Apr;29(2):549-559. doi: 10.1007/s10787-020-00767-7. Epub 2020 Oct 13.
4403	LncRNA	NEAT1	miR-543	PLA2G4A	chondrocyte	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33040229	LncRNA NEAT1 regulates chondrocyte proliferation and apoptosis via targeting miR-543/PLA2G4A axis.	Osteoarthritis (OA), which is characterized by articular cartilage degeneration, shows a gradually increasing incidence with age. This study explored the molecular mechanism underlying the proliferation and apoptosis of chondrocytes during OA progression. In this study, chondrocytes were isolated from human knee cartilages. The targeted relationship among nuclear enriched abundant transcript 1 (NEAT1), microRNA-543 (miR-543) and PLA2G4A was predicted on TargetScan V7.2 and starBase and validated by performing dual-luciferase reporter assay. High-expressed NEAT1 was detected in OA cartilage and chondrocytes. NEAT1 was negatively correlated with miR-543 and was low-expressed in OA cartilage and PLA2G4A was negatively correlated with miR-543 and was high-expressed in OA cartilage. In OA chondrocytes, the overexpressed NEAT1 inhibited the expressions of p-Akt1 and Bcl-2 and upregulated that of matrix metalloprotease (MMP)-3, MMP-9, MMP-13, interleukin (IL)-6 and IL-8, but such effects of overexpressed NEAT1 were reversed by miR-543 mimic. SiRNA-NEAT1 exerted an opposite effect to NEAT1 overexpression on OA chondrocytes, but this could be reversed by miR-543 inhibitor. The effect of PLA2G4A overexpression was the opposite to miR-543 mimic on OA chondrocytes. In conclusion, NEAT1 could sponge miR-543 to induce PLA2G4A expression, inhibit chondrocyte proliferation and promote apoptosis.	NA	Hum Cell. 2021 Jan;34(1):60-75. doi: 10.1007/s13577-020-00433-8. Epub 2020 Oct 10.
4404	LncRNA	NEAT1	miR-146b-5p	NOTCH1	T-ALL cells	T Cell Acute Lymphoblastic Leukemia	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Luciferase reporter assay;MTT assay;	33010698	LncRNA-NEAT1 promotes proliferation of T-ALL cells via miR-146b-5p/NOTCH1 signaling pathway.	BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) is a malignant tumor of the hematopoietic system, which can develop at any age, with the symptoms of weakness, fatigue, enlarged lymph nodes, or weight loss. Nuclear paraspeckle assembly transcript 1 (NEAT1) is involved in the process of T-ALL, but the regulatory mechanism is still not known clearly. METHODS: The expression levels of NEAT1 and miR-146b-5p in T-ALL cells were performed by qRT-PCR and NOTCH1 protein level- wwWwas determined by western blot assay. Dual-luciferase reporter assay was used to detect the interaction between NEAT1 and miR-146b-5p, as well as miR-146b-5p and NOTCH1. The cell proliferation was measured by using MTT assay and colony formation assay. RESULTS: The expression levels of NEAT1 were markedly increased, but miR-146b-5p levels were reduced in T-ALL cells. Knockdown of NEAT1 or overexpression of miR-146b-5p decreased NOTCH1 expression, inhibited the proliferation of T-ALL cells. MiR-146b-5p bound both NEAT1 and NOTCH1 3'-UTR directly. Finally, inhibition of miR-146b-5p could abrogate the effects of NEAT1 knockdown on the proliferation of T-ALL cells. CONCLUSION: NEAT1 promotes the proliferation of T-ALL cells by sponging miR-146b-5p to upregulate the expression of NOTCH1. The results of this study provide new insight into the action mechanism of NEAT1 modulating T-ALL progression.	NA	Pathol Res Pract. 2020 Nov;216(11):153212. doi: 10.1016/j.prp.2020.153212. Epub 2020 Sep 13.
4405	LncRNA	Nespas	miR-615-3p	Psmd11	epileptiform hippocampal neurons	Neurological Disease	Homo sapiens (human)	Rescue assay;	33212147	Long noncoding RNA Nespas inhibits apoptosis of epileptiform hippocampal neurons by inhibiting the PI3K/Akt/mTOR pathway.	Epilepsy is one of the most common neurological diseases with spontaneous recurrent seizures. Long noncoding RNAs (lncRNAs) are crucial modulators in numerous diseases, including epilepsy. However, the functional role and potential mechanism of lncRNA Nespas in epilepsy remain unknown. Our study clarified that Nespas was underexpressed in epileptiform hippocampal tissues and neurons. Furthermore, Nespas promoted hippocampal neuron viability and proliferation, and inhibited hippocampal neuron apoptosis. Mechanistically, Nespas interacted with microRNA 615-3p (miR-615-3p) in epileptiform hippocampal neurons. 26S proteasome non-ATPase regulatory subunit 11 (Psmd11) was a downstream target of miR-615-3p, and Nespas elevated Psmd11 expression via competitively binding to miR-615-3p in epileptiform hippocampal neurons. In addition, rescue assays suggested that Nespas promoted hippocampal neuron viability and proliferation, and suppressed hippocampal neuron apoptosis by upregulation of Psmd11. Furthermore, Nespas suppressed the PI3K/Akt/mTOR pathway via upregulating Psmd11 in epileptiform hippocampal neurons. This report explored the function and regulatory mechanism of Nespas in epileptiform hippocampal neurons for the first time. Our findings revealed that Nespas suppressed the apoptosis of epileptiform hippocampal neurons by inhibiting the PI3K/Akt/mTOR pathway via upregulation of Psmd11 at a miR-615-3p dependent way, indicating that Nespas may offer a new direction for the treatment of epilepsy.	NA	Exp Cell Res. 2021 Jan 1;398(1):112384. doi: 10.1016/j.yexcr.2020.112384. Epub 2020 Nov 17.
4406	LncRNA	NORAD	miR-144-3p	MYCN	renal cancer tissues	Renal Cancer	Homo sapiens (human)	luciferase assay;	33155199	LncRNA NORAD stimulates proliferation and migration of renal cancer via activating the miR-144-3p/MYCN axis.	OBJECTIVE: The purpose of this study was to clarify the potential role of long non-coding RNA (lncRNA) NORAD in the development of renal cancer. PATIENTS AND METHODS: Expression levels of NORAD, miR-144-3p, and MYCN in renal cancer tissues and cell lines were detected. After overexpression of NORAD, proliferative and migratory changes in ACHN and A498 cells were evaluated by Cell Counting Kit-8 (CCK-8) and transwell assay, respectively. Thereafter, Luciferase assay was conducted to determine the interaction in the NORAD/miR-144-3p/MYCN axis. Besides, its biological function in influencing phenotype changes of renal cancer cells was finally demonstrated by rescue experiments. RESULTS: The results manifested that NORAD and MYCN were upregulated, while miR-144-3p was downregulated in renal cancer tissues. Overexpression of NORAD stimulated proliferative and migratory potentials in ACHN and A498 cells, which were partially abolished by co-overexpression of miR-144-3p. Moreover, NORAD/miR-144-3p/MYCN axis was found to be responsible for stimulating the malignant development of renal cancer. CONCLUSIONS: LncRNA NORAD stimulates proliferative and migratory potentials in renal cancer by sponging miR-144-3p to upregulate MYCN.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10426-10432. doi: 10.26355/eurrev_202010_23394.
4407	LncRNA	NR2F1-AS1	miR-140-5p	HK2	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33488124	NR2F1-AS1/miR-140/HK2 Axis Regulates Hypoxia-Induced Glycolysis and Migration in Hepatocellular Carcinoma.	BACKGROUND: Hypoxia is an important feature for the progression of hepatocellular carcinoma (HCC). Long noncoding RNA nuclear receptor subfamily 2 group F member 1 antisense RNA 1 (NR2F1-AS1) is dysregulated in HCC. However, the role and mechanism of N2RF1-AS1 in hypoxia-induced glycolysis and migration remain unclear. MATERIALS AND METHODS: Tumor tissues and adjacent samples were harvested from 40 HCC patients. HCC cells were treated by hypoxia. The levels of NR2F1-AS1, microRNA (miR)-140, and hexokinase 2 (HK2) were examined via quantitative reverse transcription polymerase chain reaction or Western blot. Glycolysis was analyzed via glucose uptake, lactate production, and adenosine triphosphate (ATP) levels. Cell migration was analyzed via transwell assay. The target association was analyzed via dual-luciferase reporter assay and RNA immunoprecipitation. RESULTS: NR2F1-AS1 level was enhanced in HCC tissues and cells. High expression of NR2F1-AS1 indicated poor overall survival. Silence of NR2F1-AS1 repressed hypoxia-induced glycolysis and migration in HCC cells. NR2F1-AS1 could regulate HK2 expression by modulating miR-140. miR-140 down-regulation or HK2 up-regulation mitigated the influence of NR2F1-AS1 silence on hypoxia-induced glycolysis and migration in HCC cells. CONCLUSION: NR2F1-AS1 knockdown restrained hypoxia-induced glycolysis and migration in HCC cells via increasing miR-140 and decreasing HK2.	NA	Cancer Manag Res. 2021 Jan 15;13:427-437. doi: 10.2147/CMAR.S266797. eCollection 2021.
4408	LncRNA	NUTM2A-AS1	miR-376a	TET1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;MTT assay;	33089970	LncRNA NUTM2A-AS1 positively modulates TET1 and HIF-1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR-376a.	Long noncoding RNA NUTM2A-AS1 has been shown to be dysregulated in non-small cell lung carcinoma. To date, it is unclear whether NUTM2A-AS1 plays a role in gastric cancer progression. The purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A-AS1 in gastric cancer. mRNA and protein levels were measured by RT-qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dual-luciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR-376a and NUTM2A-AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A-AS1 in vivo and human clinical setting. Our results suggested that NUTM2A-AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR-376a. More interestingly, TET1 and HIF-1A were negatively regulated by miR-376a. TET1 could interact with HIF-1A to modulate PD-L1. Finally, we revealed that PD-L1 was key to NUTM2A-AS1- and miR-376a-mediated tumorigenesis and drug resistance. In summary, our conclusions facilitate us understand the underlying mechanism and develop novel treatment strategy for gastric cancer.	NA	Cancer Med. 2020 Dec;9(24):9499-9510. doi: 10.1002/cam4.3544. Epub 2020 Oct 22.
4409	LncRNA	NUTM2A-AS1	miR-376a	HIF-1a	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	MTT assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;MTT assay;	33089970	LncRNA NUTM2A-AS1 positively modulates TET1 and HIF-1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR-376a.	Long noncoding RNA NUTM2A-AS1 has been shown to be dysregulated in non-small cell lung carcinoma. To date, it is unclear whether NUTM2A-AS1 plays a role in gastric cancer progression. The purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A-AS1 in gastric cancer. mRNA and protein levels were measured by RT-qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dual-luciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR-376a and NUTM2A-AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A-AS1 in vivo and human clinical setting. Our results suggested that NUTM2A-AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR-376a. More interestingly, TET1 and HIF-1A were negatively regulated by miR-376a. TET1 could interact with HIF-1A to modulate PD-L1. Finally, we revealed that PD-L1 was key to NUTM2A-AS1- and miR-376a-mediated tumorigenesis and drug resistance. In summary, our conclusions facilitate us understand the underlying mechanism and develop novel treatment strategy for gastric cancer.	NA	Cancer Med. 2020 Dec;9(24):9499-9510. doi: 10.1002/cam4.3544. Epub 2020 Oct 22.
4410	LncRNA	OIP5-AS1	miR-34a	NA	OC cells	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33092644	LncRNA OIP5-AS1 upregulates snail expression by sponging miR-34a to promote ovarian carcinoma cell invasion and migration.	BACKGROUND: Although OIP5-AS1 has been characterized as an oncogenic lncRNA in many types of cancer, its role and underlying mechanism in ovarian carcinoma (OC) remains unknown. This study aimed to investigate the role of OIP5-AS1 in OC. METHODS: OC tissues and non-tumor tissues (ovary tissues within 3 cm around tumors) were collected from 58 OC patients (age range 36 to 67 years old, mean age 51.4 ± 5.9 years old). The expression of OIP5-AS1 and snail in paired tissues were determined by RT-qPCR. The interaction between OIP5-AS1 and miR-34a was predicted by IntaRNA2.0 and confirmed by dual luciferase reporter assay. The effects of overexpression of OIP5-AS1 and miR-34a on the expression of snail were analyzed by RT-qPCR and Western blotting. Cell invasion and migration were analyzed by Transwell assay. RESULTS: We observed that the expression of OIP5-AS1 and snail was upregulated and positively correlated with each other in OC. RNA-RNA interaction analysis showed that OIP5-AS1 might sponge miR-34a. In OC cells, overexpression of OIP5-AS1 resulted in the upregulated expression of snail, while overexpression of miR-34a downregulated the expression of snail. In addition, overexpression of miR-34a reduced the effects of overexpression of OIP5-AS1 on the expression of snail. In cell invasion and migration assay, overexpression of OIP5-AS1 and snail resulted in increased OC cell invasion and migration, while overexpression of miR-34a decreased OC cell invasion and migration. Moreover, overexpression of miR-34a attenuated the effects of OIP5-AS1 overexpression on OC cell invasion and migration. CONCLUSIONS: Therefore, OIP5-AS1 may upregulate snail expression in OC by sponging miR-34a to promote OC cell invasion and migration.	NA	Biol Res. 2020 Oct 22;53(1):49. doi: 10.1186/s40659-020-00315-1.
4411	LncRNA	OIP5-AS1	miR-34a	SIRT1	H9c2 cells	Diabetic Cardiomyopathy	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Luciferase reporter assay;MTT assay;	33380310	Long noncoding RNA OIP5-AS1 overexpression promotes viability and inhibits high glucose-induced oxidative stress of cardiomyocytes by targeting microRNA-34a/SIRT1 axis in diabetic cardiomyopathy.	OBJECTIVE: Diabetic cardiomyopathy (DCM) is an important complication of diabetes. This study was attempted to discover the effects of long noncoding RNA OIP5-AS1 (OIP5-AS1) on the viability and oxidative stress of cardiomyocyte in DCM. METHODS: The expression of OIP5-AS1 and microRNA-34a (miR-34a) in DCM was detected by qRT-PCR. In vitro, DCM was simulated by high glucose (HG, 30 mM) treatment in H9c2 cells. The viability of HG (30 mM)-treated H9c2 cells was examined by MTT assay. The reactive oxygen species (ROS), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were used to evaluate the oxidative stress of HG (30 mM)-treated H9c2 cells. Dual-luciferase reporter assay was used to confirm the interactions among OIP5-AS1, miR-34a and SIRT1. Western blot was applied to analyze the protein expression of SIRT1. RESULTS: The expression of OIP5-AS1 was down-regulated in DCM, but miR-34a was up-regulated. The functional experiment stated that OIP5-AS1 overexpression increased the viability and SOD level, while decreased the ROS and MDA levels in HG (30 mM)-treated H9c2 cells. The mechanical experiment confirmed that OIP5-AS1 and SIRT1 were both targeted by miR-34a with the complementary binding sites at 3'UTR. MiR-34a overexpression inhibited the protein expression of SIRT1. In the feedback experiments, miR-34a overexpression or SIRT1 inhibition weakened the promoting effect on viability, and mitigated the reduction effect on oxidative stress caused by OIP5-AS1 overexpression in HG (30 mM)-treated H9c2 cells. CONCLUSIONS: OIP5-AS1 overexpression enhanced viability and attenuated oxidative stress of cardiomyocyte via regulating miR-34a/SIRT1 axis in DCM, providing a new therapeutic target for DCM.	NA	Endocr Metab Immune Disord Drug Targets. 2020 Dec 29. doi: 10.2174/1871530321666201230090742.
4412	LncRNA	OIP5-AS1	miR-186-5p	NGFR	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33820868	Downregulation of OIP5-AS1 affects proNGF-induced pancreatic cancer metastasis by inhibiting p75NTR levels.	We aimed to explore the mechanism by which long non-coding RNA (lncRNA) OIP5-AS1 affects proNGF (precursor nerve growth factor)-induced pancreatic cancer metastasis by targeting the miR-186-5p/NGFR axis. Bioinformatics was used to analyse whether OIP5-AS1 targets miR-186-5p/NGFR and their expression characteristics in pancreatic cancer. OIP5-AS1 and NGFR were overexpressed in pancreatic cancer, and their levels showed a significant positive correlation. Clinical trials also demonstrated that high expression of OIP5-AS1 and NGFR and low expression of miR-186-5p played a pro-cancer role in pancreatic cancer. MiR-186-5p inhibited the migration and invasion of colon cancer cells by targeting NGFR-regulated p75NTR. OIP5-AS1 regulated the action of miR-186-5p on NGFR mRNA and p75NTR by targeting miR-186-5p. Downregulation of NGFR inhibited the expression of p75NTR protein and blocked the role of proNGF in promoting the migration and invasion of pancreatic cancer cells. Animal experiments also showed that the knockdown of miR-186-5p promoted cancer via the expression of NGFR mRNA and p75NTR protein, while the downregulation of proNGF blocked the effects. OIP5-AS1, as a ceRNA, promotes the progression of pancreatic cancer by targeting miR-186-5p/NGFR and affecting the prognosis of patients, which may be related to the action of proNGF.	NA	Aging (Albany NY). 2021 Apr 3;13(7):10688-10702. doi: 10.18632/aging.202847. Epub 2021 Apr 3.
4413	LncRNA	OIP5-AS1	miR-98-5p	HMGB1	endothelial cells	Endothelial Cell Injury	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	32990894	LncRNA OIP5-AS1 facilitates ox-LDL-induced endothelial cell injury through the miR-98-5p/HMGB1 axis.	Cerebrovascular diseases have a high mortality and disability rate in developed countries. Endothelial cell injury is the main cause of atherosclerosis and cerebrovascular disease. Long non-coding RNA (lncRNA) has been proved to participate in the progression of endothelial cell. Our study aimed to develop the function of lncRNA opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in oxidative low-density lipoprotein (ox-LDL)-induced endothelial cell injury. The expression of OIP5-AS1, miR-98-5p and High-mobility group protein box-1 (HMGB1) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry were used to detect the cell proliferation and apoptosis. The levels of cyclinD1, Bcl-2 Associated X Protein (Bax), Cleaved-caspase-3, Toll like receptors 4 (TLR4), phosphorylation of p65 (p-P65), phosphorylation of nuclear factor-kappa B inhibitor α (p-IκB-α) and HMGB1 were measured by Western blot. The concentrations of Interleukin-6 (IL-6), Interleukin-1β (IL-1β) and Tumor necrosis factor-α (TNF-α) were detected by Enzyme-linked immunosorbent assay (ELISA). The production of Reactive oxygen species (ROS), Superoxide Dismutase (SOD) and malondialdehyde (MDA) was detected by the corresponding kit. The targets of OIP5-AS and miR-98-5p were predicted by starBase 3.0 and TargetScan and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The expression of OIP5-AS1 was upregulated, while miR-98-5p was downregulated in ox-LDL-induced human umbilical vein endothelial cells (HUVECs). Functionally, knockdown of OIP5-AS1 induced proliferation and inhibited apoptosis, inflammatory injury and oxidative stress injury in ox-LDL-induced HUVEC cells. Interestingly, miR-98-5p was a target of OIP5-AS1 and miR-98-5p inhibition abolished the effects of OIP5-AS1 downregulation on ox-LDL-induced HUVECs injury. More importantly, miR-98-5p directly targeted HMGB1, and OIP5-AS1 regulated the expression of HMGB1 by sponging miR-98-5p. Finally, OIP5-AS1 regulated the TLR4/nuclear factor-kappa B (NF-κB) signaling pathway through miR-98-5p/HMGB1 axis. LncRNA OIP5-AS1 accelerates ox-LDL-induced endothelial cell injury through regulating HMGB1 mediated by miR-98-5p via the TLR4/NF-κB signaling pathway.	NA	Mol Cell Biochem. 2021 Jan;476(1):443-455. doi: 10.1007/s11010-020-03921-5. Epub 2020 Sep 29.
4414	LncRNA	OIP5-AS1	miR-27b-3p	TRIM14	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Luciferase reporter assay;MTT assay;	33692839	Long non-coding RNA OIP5-AS1 contributes to cisplatin resistance of oral squamous cell carcinoma through the miR-27b-3p/TRIM14 axis.	Oral squamous cell carcinoma (OSCC) accounts for 90% of oral cavity cancer types, but the overall prognosis for patients with OSCC remains unfavorable. Cisplatin (DDP) is an effective drug in OSCC treatment, but DDP resistance weakens its therapeutic effect. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) can trigger DDP resistance. The purpose of the current study was to explore the role and mechanism ofOIP5-AS1 in OSCC DDP resistance. In the present study, the expression levels of OIP5-AS1, microRNA (miR)-27b-3p and tripartite motif-containing 14 (TRIM14) were detected by reverse transcription-quantitative PCR. DDP resistance was measured using an MTT assay. Moreover, cell proliferation, migration and invasion were assessed by MTT, Transwell, and Matrigel assays. Protein expression levels of TRIM14, E-cadherin, N-cadherin and Vimentin were detected by western blot analysis. Putative binding sites between miR-27b-3p andOIP5-AS1 or TRIM14werepredicted with starBase and verified using a dual-luciferase reporter assay. The role of OIP5-AS1 in DDP resistance of OSCC in vivo was measured using a xenograft tumor model. It was observed that OIP5-AS1 was upregulated in DDP-resistant OSCC cells, and the knockdown of OIP5-AS1 improved DDP sensitivity in DDP-resistant OSCC cells. The present study identified that miR-27b-3p was a target of OIP5-AS1. Furthermore, miR-27b-3p silencing reversed the effect of OIP5-AS1 knockdown on DDP sensitivity in DDP-resistant OSCC cells. TRIM14was shown to be a direct target of miR-27b-3p, and TRIM14 overexpression abolished the effect of miR-27b-3p on DDP sensitivity in DDP-resistant OSCC cells. The results suggested that OIP5-AS1 increased TRIM14 expression by sponging miR-27b-3p. In addition, OIP5-AS1 knockdown enhanced DDP sensitivity of OSCC in vivo. Data from the present study indicated that OIP5-AS1 may improve DDP resistance through theupregulationTRIM14 mediated bymiR-27b-3p, providing a possible therapeutic strategy for OSCC treatment.	NA	Exp Ther Med. 2021 Apr;21(4):408. doi: 10.3892/etm.2021.9839. Epub 2021 Feb 25.
4415	LncRNA	OTUD6B-AS1	miR-3171	NA	HCT116 cells	Colorectal Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;Rescue assay;	33574932	Long non-coding RNA OTUD6B-AS1 overexpression inhibits the proliferation, invasion and migration of colorectal cancer cells via downregulation of microRNA-3171.	Colorectal cancer (CRC) is a common digestive system malignancy and a major cause of cancer-associated mortality worldwide. Aberrant expression of long non-coding RNAs has been reported in several types of cancer. The aim of the present study was to investigate the role of ovarian tumor domain containing 6B antisense RNA1 (OTUD6B-AS1) in CRC and its underlying mechanisms. OTUD6B-AS1 expression in CRC cell lines was examined using reverse transcription-quantitative PCR. Furthermore, The Cancer Genome Atlas database was utilized to examine the expression levels of OTUD6B-AS1 in CRC tissues. Following OTUD6B-AS1 overexpression, Cell Counting Kit-8 and colony formation assays were used to detect the proliferation ability of HCT116 cells. The expression levels of proliferation-related protein Ki67 were determined using immunofluorescence staining. Subsequently, Transwell and wound healing assays were used to evaluate the invasion and migration of HCT116 cells, respectively. The expression levels of migration-related proteins (MMP2 and MMP9) were measured using western blotting. Additionally, a luciferase reporter assay was used to verify the potential interaction between OTUD6B-AS1 and microRNA-3171 (miR-3171). Subsequently, rescue assays were performed to clarify the regulatory effects of OTUD6B-AS1 and miR-3171 on CRC development. The results demonstrated that OTUD6B-AS1 expression was low in CRC cells and tissues. Overexpression of OTUD6B-AS1 inhibited the proliferation, invasion and migration of HCT116 cells. Furthermore, miR-3171 was demonstrated to be a direct target of OTUD6B-AS1 using a luciferase reporter assay. The rescue assays revealed that miR-3171 mimics markedly reversed the inhibitory effects of OTUD6B-AS1 overexpression on proliferation, invasion and migration of CRC cells. Overall, these findings demonstrated that OTUD6B-AS1 overexpression inhibited the proliferation, invasion and migration of HCT116 cells via downregulation of miR-3171, suggesting that OTUD6B-AS1 may serve as a novel biomarker for CRC treatment.	NA	Oncol Lett. 2021 Mar;21(3):193. doi: 10.3892/ol.2021.12454. Epub 2021 Jan 8.
4416	LncRNA	PCAT1	miR-216a-3p	BCL3	CCA cells	Cholangiocarcinoma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Western blot;	33544468	PCAT1 induced by transcription factor YY1 promotes cholangiocarcinoma proliferation, migration and invasion by sponging miR-216a-3p to up-regulate oncogene BCL3.	This study was designed to illustrate the function and role of PCAT1 in CCA. The relative expression was confirmed by RT-qPCR and western blot. The biological function of PCAT1 was evaluated by CCK8, EdU, colony formation, wound healing, transwell, and subcutaneous tumor formation assays. Protein levels of EMT markers were measured by western blot. The binding relationship was predicted by JASPAR and starBase. The binding of YY1 to PCAT1 promoter was assessed by ChIP and luciferase reporter. The binding capacity between miR-216a-3p and PCAT1 as well as BCL3 was assessed by luciferase reporter and AGO2-RIP assays. In this study, we found that PCAT1 was up-regulated in CCA tissues and cells, and the PCAT1 overexpression was associated with poor prognosis. Moreover, PCAT1 was assessed as an independent risk factor of prognosis for CCA patients. Amplified PCAT1 was found to promote tumor proliferation, migration, invasion and EMT process, whereas PCAT1 knockdown inhibited these malignant phenotypes. Mechanistically, PCAT1 was predominantly localized in the cytoplasm and competitively bound miR-216a-3p to increase BCL3 expression. In addition, PCAT1 was activated by transcription factor YY1. This study revealed that PCAT1 acted as an oncogene in CCA, and the YY1/PCAT1/miR-216a-3p/BCL3 axis exhibited critical functions in CCA progression.	NA	Biol Chem. 2020 Oct 23;402(2):207-219. doi: 10.1515/hsz-2020-0276. Print 2021 Jan 27.
4417	LncRNA	PCAT18	miR-759	SPRR3	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33204157	Long Noncoding RNA PCAT18 Upregulates SPRR3 to Promote Colorectal Cancer Progression by Binding to miR-759.	BACKGROUND: Long noncoding RNAs (lncRNAs) play essential functions in the development of several cancers, including colorectal cancer (CRC). Nevertheless, how PCAT18 regulates CRC tumorigenesis remains unclear. In this research, we aimed to investigate the roles of PCAT18 in CRC. MATERIALS AND METHODS: qRT-PCR and Western blot were used to analyze RNA and protein levels. CCK8, colony formation, transwell and wound healing assays were utilized to analyze proliferation, migration and invasion. Luciferase reporter assay was used to analyze RNA interactions. RESULTS: PCAT18 was found to be highly expressed in CRC tissues and cells. PCAT18 level was positively correlated with lymph node metastasis and TNM stage. Functionally, PCAT18 silencing induced impairment of CRC proliferation, migration and invasion. Besides, PCAT18 was identified to inhibit miR-759. PCAT18 promotes SPRR3 expression through binding to miR-759. Furthermore, miR-759 inhibitors or SPRR3 ectopic expression partially rescued the abilities of proliferation, migration and invasion in CRC cells transfected with sh-PCAT18. CONCLUSION: Therefore, our study demonstrated that PCAT18 contributes to CRC progression through regulating miR-759/SPRR3 axis, which provides a new theoretical basis of explaining CRC tumorigenesis.	NA	Cancer Manag Res. 2020 Nov 9;12:11445-11452. doi: 10.2147/CMAR.S272652. eCollection 2020.
4418	LncRNA	PCAT19	miR-142-5p	MELK	glioma cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32980991	Suppression of long non-coding RNA PCAT19 inhibits glioma cell proliferation and invasion, and increases cell apoptosis through regulation of MELK targeted by miR-142-5p.	BACKGROUND: Glioma has the chief type of primary brain tumors worldwide. The glioma may be controlled by regulators including some lncRNAs, miRNAs, and proteins. OBJECTIVE: Our study aims to discover the underlying mechanism for lncPCAT19/miR-142-5p/MELK axis in glioma progression. METHODS: The clinical samples were from patients with gliomas in our Hospital. Hematoxylin-eosin staining (H&E) was applied to determine the clinical pathological changes. Real time PCR was performed to measure the levels of lncPCAT19, miR-142-5p, MELK, and expression of other genes. Western blot was conducted to detect the protein level of MELK. RIP assay was performed to analyze the interaction between lncPCAT19 and miR-142-5p, and dual-luciferase reporter assay was used to determine the binding site between lncPCAT19 and miR-142-5p. CCK-8, colony formation assay, flow cytometry, and trans-well assay were carried out to confirm cell proliferation, colony formation, apoptosis, and invasion, respectively. RESULTS: LncPCAT19 was increased in cancer tissues. Then, lncPCAT19 could interact with and down-regulate miR-142-5p. Knockdown of lncPCAT19 distinctly inhibited tumor growth in vivo. Interfering lncPCAT19/overexpression of miR-142-5p decreased glioma cell proliferation, colony formation and invasion, and promoted cell apoptosis by down-regulating expression of Cyclin B1, CDK2, N-cadherin, Bcl-2, and by up-regulating expression of Bax and E-cadherin. Moreover, overexpression of lncPCAT19 overturned tumor-suppressing role of miR-142-5p in cells. Additionally, lncPCAT19 and miR-142-5p synergistically regulated expression of MELK. In conclusion, lncPCAT19 enhanced glioma development via increasing MELK by performing as a sponge of miR-142-5p. CONCLUSIONS: LncPCAT19 promotes glioma progression by sponging miR-142-5p to upregulate MELK levels. Thus, lncPCAT19/miR-142-5p/MELK signaling would be a potential target for glioma treatment.	NA	Genes Genomics. 2020 Nov;42(11):1299-1310. doi: 10.1007/s13258-020-01003-w. Epub 2020 Sep 26.
4419	LncRNA	PCAT19	miR-128	GOLM1	CC tissues and cells	Cervical Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Luciferase reporter assay;MTT assay;	33116617	Knockdown of lncRNA PCAT1 Enhances Radiosensitivity of Cervical Cancer by Regulating miR-128/GOLM1 Axis.	PURPOSE: Cervical cancer (CC) is the fourth most common cancer with high death rate in females. The study aims to detect the mechanism of long non-coding RNA (LncRNA) PCAT1 on radiosensitivity of CC. METHODS: The expression of PCAT1, miR-128 and GOLM1 in CC tissues and cells was measured by qRT-PCR. Different doses of X-ray were used for radiation treatment of CC cells and 6 Gy was chosen to perform the following experiments. The proliferation, migration and invasion of CC cells were measured by MTT assay, wound healing assay and transwell assay, respectively. The target relationships among PCAT1, miR-128 and GOLM1 were predicted by StarBase and TargetScan and verified by luciferase reporter assay. The protein level of GOLM1 was determined by Western blot. The xenograft tumor model was constructed in nude mice to verify the effect of PCAT1 on radiosensitivity of CC in vivo. RESULTS: The PCAT1 expression was upregulated in CC tissues and cells. PCAT1 silencing enhances radiosensitivity of CC cells on proliferation, migration and invasion. MiR-128 was the target of PCAT1 and was negatively regulated by PCAT1. Upregulation of miR-128 enhances radiosensitivity of CC cells on proliferation, migration and invasion. GOLM1 was a target of miR-128 and was negatively regulated by miR-128. Upregulation of GOLM1 and downregulation of miR-128 both reversed the enhanced effect of PCAT1 knockdown on radiosensitivity of CC cells, which partly promoted the proliferation, migration and invasion of CC cells. CONCLUSION: Silencing of PCAT1 enhanced radiosensitivity of CC via targeting miR-128/GOLM1, which provided a new idea for treating CC.	NA	Onco Targets Ther. 2020 Oct 13;13:10373-10385. doi: 10.2147/OTT.S263728. eCollection 2020.
4420	LncRNA	PCAT6	miR-513a-5p	NA	BC cells	Bladder Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;	33090394	LncRNA PCAT6 aggravates the progression of bladder cancer cells by targeting miR-513a-5p.	OBJECTIVE: Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in tumorigenesis of bladder cancer (BC). Our research aimed to explore the underlying mechanisms of lncRNA prostate cancer-associated transcript 6 (PCAT6) in BC. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain reaction (RT-qPCR) was used to measure the levels of PCAT6 and miR-513a in BC tissues and cells. The Kaplan-Meier analysis was utilized to evaluate the overall survival time of BC patients. Besides, cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were evaluated by wound healing and transwell assays. Furthermore, starBase and Dual-Luciferase reporter assay were used to determine the interaction between PCAT6 and miR-513a in BC cells. RESULTS: PCAT6 expression was upregulated, while miR-513a was downregulated in BC tissues and cell lines. BC patients with high expression of PCAT6 exhibited a shorter overall survival time compared with those patients with low expression of PCAT6. Moreover, PCAT6 knockdown notably suppressed cell progression. In addition, PCAT6 inhibited miR-513a expression through direct interaction, and the silencing of PCAT6 remarkably increased the expression of miR-513a. Finally, the knockdown of miR-513a partly abolished PCAT6 silencing-induced inhibitory effects on BC progression. CONCLUSIONS: Our study illustrated that PCAT6 knockdown inhibited cell progression of BC by regulating miR-513a, suggesting that PCAT6 might act as a prognostic biomarker and therapeutic target for BC patients.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(19):9908-9914. doi: 10.26355/eurrev_202010_23201.
4421	LncRNA	PCAT6	miR-513	IGF2BP1	glioblastoma cells	Glioblastoma	Homo sapiens (human)	qRT-PCR	32990800	LncRNA PCAT6 Regulated by YY1 Accelerates the Progression of Glioblastoma via miR-513/IGF2BP1.	Glioblastoma is one of the most frequent and aggressive primary tumor of glial brain tumors. Long non-coding RNA Prostate cancer-associated ncRNA transcript 6 (PCAT6) has been identified to influence the progression of many cancers, but its expression and functions in glioblastoma remain unclear. In this study, we intended to investigate the expression, functions and the corresponding mechanisms of PCAT6 in glioblastoma. We observed that PCAT6 expression was upregulated in glioblastoma tissues and cell lines and its high expression was due to the transcriptional activation by Yin Yang 1. miR-513 was a target of PCAT6 and Insulin like growth factor 2 mRNA binding protein 1 (IGF2BP1) was a target of miR-513. Hence, PCAT6 upregulated IGF2BP1 expression via miR-513 in a competing endogenous RNAs manner. PCAT6 and IGF2BP1 functioned as oncogenes while miR-513 acted as a tumor suppressor gene in glioblastoma. PCAT6 and miR-513 modulated the proliferation and survival of glioblastoma cells via AKT signaling by mediating IGF2BP1. IGF2BP1 raised the expression of PCAT6 by increasing its stability. In conclusion, our results indicate that PCAT6/miR-513/IGF2BP1 positive feedback loop plays a crucial role in facilitating glioblastoma progression.	NA	Neurochem Res. 2020 Dec;45(12):2894-2902. doi: 10.1007/s11064-020-03138-4. Epub 2020 Sep 29.
4422	LncRNA	PCED1B-AS1	miR-194-5p	PD-L1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33219943	Dual targeting of PD-L1 and PD-L2 by PCED1B-AS1 via sponging hsa-miR-194-5p induces immunosuppression in hepatocellular carcinoma.	BACKGROUND: PD-L1 and PD-L2 are PD-1 ligands (PD-Ls). PD-Ls over-expression is associated with poor prognosis in hepatocellular carcinoma (HCC). However, little is known about how PD-Ls expression is regulated. Here, we investigated the involvement of lncRNA-microRNA network in the regulation of PD-Ls in HCC. METHODS: The expression of PD-Ls, PCED1B-AS1 and hsa-miR-194-5p was measured in 45 pairs of HCC samples. The interaction between PCED1B-AS1 and hsa-miR-194-5p was measured by microRNA pull down and in vitro binding assay. The effects of PCED1B-AS1 knockdown and over-expression on hsa-miR-194-5p and PD-Ls expression were investigated in HCC cell lines. Immunosuppression was evaluated in co-culture of HCC cell line and human T cells. Exosomes were isolated from HCC cells and their effects on receipt cells were investigated. Tumor behaviors were evaluated by in vitro and in vivo assays. RESULTS: PD-L1 expression was highly correlated with PD-L2 expression in HCC. PCED1B-AS1 and hsa-miR-194-5p expression was up-regulated in HCC. PCED1B-AS1 was positively correlated with PD-Ls but negatively correlated hsa-miR-194-5p in HCC. These correlations were cross-validated by TCGA-LIHC dataset. PCED1B-AS1 interacted with hsa-mir-194-5p which inhibited PD-Ls expression. PCED1B-AS1 enhanced the expression of PD-Ls via sponging hsa-mir-194-5p. PCED1B-AS1-induced PD-Ls-mediated immunosuppression in co-cultured T cells. HCC cells released PCED1B-AS1 containing exosomes and the exosomal PCED1B-AS1 enhanced PD-Ls expression in receipt HCC cells while inhibited receipt T cells and macrophages. Blood exosomal PCED1B-AS1 was correlated with HCC PD-Ls expression. Finally, PCED1B-AS1 promoted cell proliferation, colony formation and in vivo tumor formation in xenografted nude mice while inhibited apoptosis. CONCLUSIONS: PCED1B-AS1 enhances the expression and function of PD-Ls via sponging hsa-miR-194-5p to induce immunosuppression in HCC.	NA	Hepatol Int. 2021 Apr;15(2):444-458. doi: 10.1007/s12072-020-10101-6. Epub 2020 Nov 21.
4423	LncRNA	PCED1B-AS1	miR-194-5p	PD-L2	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33219943	Dual targeting of PD-L1 and PD-L2 by PCED1B-AS1 via sponging hsa-miR-194-5p induces immunosuppression in hepatocellular carcinoma.	BACKGROUND: PD-L1 and PD-L2 are PD-1 ligands (PD-Ls). PD-Ls over-expression is associated with poor prognosis in hepatocellular carcinoma (HCC). However, little is known about how PD-Ls expression is regulated. Here, we investigated the involvement of lncRNA-microRNA network in the regulation of PD-Ls in HCC. METHODS: The expression of PD-Ls, PCED1B-AS1 and hsa-miR-194-5p was measured in 45 pairs of HCC samples. The interaction between PCED1B-AS1 and hsa-miR-194-5p was measured by microRNA pull down and in vitro binding assay. The effects of PCED1B-AS1 knockdown and over-expression on hsa-miR-194-5p and PD-Ls expression were investigated in HCC cell lines. Immunosuppression was evaluated in co-culture of HCC cell line and human T cells. Exosomes were isolated from HCC cells and their effects on receipt cells were investigated. Tumor behaviors were evaluated by in vitro and in vivo assays. RESULTS: PD-L1 expression was highly correlated with PD-L2 expression in HCC. PCED1B-AS1 and hsa-miR-194-5p expression was up-regulated in HCC. PCED1B-AS1 was positively correlated with PD-Ls but negatively correlated hsa-miR-194-5p in HCC. These correlations were cross-validated by TCGA-LIHC dataset. PCED1B-AS1 interacted with hsa-mir-194-5p which inhibited PD-Ls expression. PCED1B-AS1 enhanced the expression of PD-Ls via sponging hsa-mir-194-5p. PCED1B-AS1-induced PD-Ls-mediated immunosuppression in co-cultured T cells. HCC cells released PCED1B-AS1 containing exosomes and the exosomal PCED1B-AS1 enhanced PD-Ls expression in receipt HCC cells while inhibited receipt T cells and macrophages. Blood exosomal PCED1B-AS1 was correlated with HCC PD-Ls expression. Finally, PCED1B-AS1 promoted cell proliferation, colony formation and in vivo tumor formation in xenografted nude mice while inhibited apoptosis. CONCLUSIONS: PCED1B-AS1 enhances the expression and function of PD-Ls via sponging hsa-miR-194-5p to induce immunosuppression in HCC.	NA	Hepatol Int. 2021 Apr;15(2):444-458. doi: 10.1007/s12072-020-10101-6. Epub 2020 Nov 21.
4424	LncRNA	PCED1B-AS1	miR-484	ZEB1	ccRCC cells	Clear Cell Renal Cancer	Homo sapiens (human)	CCK-8 assay;Cell proliferation assay;qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33469315	Long Non-Coding RNA PCED1B-AS1 Promotes the Progression of Clear Cell Renal Cell Carcinoma Through miR-484/ZEB1 Axis.	BACKGROUND: Long non-coding RNA (lncRNA) has been recognized as the new regulator and biomarker for cancers. However, in clear cell renal cell carcinoma (ccRCC), the functions of lncRNAs are not well characterized. This research aimed to probe the function of lncRNA PCED1B-AS1 in the progression of ccRCC. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression levels of PCED1B-AS1, microRNA-484 (miR-484), and zinc finger E-box binding homeobox 1 (ZEB1) in 40 pairs of human ccRCC tissues and corresponding adjacent kidney tissue samples. Chi-square test was employed to evaluate the association between PCED1B-AS1 expression level and clinicopathological characteristics. The effects of PCED1B-AS1, miR-484 and ZEB1 on the cell proliferation, migration and epithelial-mesenchymal transition (EMT) process of ccRCC cells were studied by CCK-8 assay, EdU cell proliferation assay, wound healing test and Western blotting. The regulatory relationships among PCED1B-AS1, miR-484, ZEB1 were examined by luciferase reporter gene assay and RNA immunoprecipitation assay. RESULTS: PCED1B-AS1 was remarkably up-regulated in ccRCC tissues and cell lines. High expression of PCED1B-AS1 was associated with poor prognosis of the patients. Loss-of-function experiments showed that PCED1B-AS1 could regulate the proliferation, migration and EMT of ccRCC cells. PCED1B-AS1 sponged miR-484 to suppress its expression, and miR-484 targeted the 3'-UTR of ZEB1 to repress the expression of ZEB1. MiR-484 counteracted the functions of PCED1B-AS1 in promoting the proliferation, migration and EMT of ccRCC cells, and PCED1B-AS1 promotes the expression of ZEB1 via repressing miR-484. CONCLUSION: PCED1B-AS1/miR-484/ZEB1 axis is involved in regulating the progression of ccRCC.	NA	Onco Targets Ther. 2021 Jan 13;14:393-402. doi: 10.2147/OTT.S270149. eCollection 2021.
4425	LncRNA	PDCD4-AS1	miR-10b-5p	IQGAP2	TNBC tissues and cells	Triple Negative Breast Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33248413	LncRNA PDCD4-AS1 alleviates triple negative breast cancer by increasing expression of IQGAP2 via miR-10b-5p.	OBJECTIVE: Mounting evidence demonstrates that long non-coding RNA (lncRNA) is dysregulated in breast cancers. This study was designed to detect the influences and regulatory mechanism of lncRNA PDCD4-AS1 in triple-negative breast cancer (TNBC). METHODS: qRT-PCR and Western blot were utilized to investigate the expression levels of PDCD4-AS1, miR-10b-5p and IQGAP2 in TNBC tissues and cells. Online software and luciferase reporter gene system were employed to testify the interactions among these molecules. Loss and gain of function of PDCD4-AS1, miR-10b-5p or IQGAP2 were performed before MTT and colony formation assay, TUNEL staining in addition to Transwell and scratch assays were applied to measure the cell biological functions. RESULTS: In this work, PDCD4-AS1 and IQGAP2 were lowly expressed while miR-10b-5p was strongly expressed in TNBC tissues and cells. PDCD4-AS1 or IQGAP2 overexpression effectively attenuated TNBC cell proliferation, migration and invasion, and increased the apoptosis rate, while this effect was abandoned in response to miR-10b-5p mimics transfection. miR-10b-5p bound to IQGAP2 and acted as a downstream target of PDCD4-AS1. CONCLUSION: Our findings identified lncRNA PDCD4-AS1 as a tumor suppressor in TNBC by regulating IQGAP2 expression via miR-10b-5p, giving a novel insight into the regulatory mechanism of PDCD4-AS1 in the pathogenesis of TNBC.	NA	Transl Oncol. 2021 Jan;14(1):100958. doi: 10.1016/j.tranon.2020.100958. Epub 2020 Nov 25.
4426	LncRNA	PEG10	miR-101-3p	KIF2A	DLBCL cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	32976381	Long Non-Coding RNA Paternally Expressed Imprinted Gene 10 (PEG10) Elevates Diffuse Large B-Cell Lymphoma Progression by Regulating Kinesin Family Member 2A (KIF2A) via Targeting MiR-101-3p.	BACKGROUND Diffuse large B-cell lymphoma (DLBCL) is a common malignant tumor in the immune system with high mortality. We investigated the functional effects of long non-coding RNA paternally expressed imprinted gene 10 (PEG10) on DLBCL progression. MATERIAL AND METHODS Real-time quantitative polymerase chain reaction was used to measure the level of PEG10, kinesin family member 2A (KIF2A) and microRNA-101-3p (miR-101-3p) in DLBCL tissues and cell lines. The relative protein level was detected by western blot analysis. The biological behaviors including cell proliferation, apoptosis, migration, and invasion were determined by MTT assay, flow cytometry analysis, and Transwell assays, respectively. Bioinformatics analysis and dual-luciferase reporter assay were performed to evaluate the interaction among PEG10, miR-101-3p, and KIF2A. RESULTS PEG10 and KIF2A level were significantly upregulated, while miR-101-3p was downregulated in DLBCL tissues and cells. PEG10 positively regulated KIF2A level in DLBCL. PEG10, or KIF2A deletion significantly inhibited the proliferative, migratory, and invasive abilities of DLBCL cells and elevated cell apoptosis in DLBCL cells. KIF2A upregulation partially reversed the effects of PEG10 downregulation on cell growth, metastasis, and apoptosis in DLBCL. Moreover, PEG10 negatively regulated miR-101-3p level and miR-101-3p upregulation exerted inhibition effects on the progression of DLBCL. Besides, miR-101-3p was a target of PEG10 and miR-101-3p could directly target KIF2A. PEG10 promoted KIF2A level by sponging miR-101-3p. CONCLUSIONS Our findings revealed that PEG10 played an oncogenic role in DLBCL progression, which might be a potential target for the treatment of DLBCL.	NA	Med Sci Monit. 2020 Sep 25;26:e922810. doi: 10.12659/MSM.922810.
4427	LncRNA	PGM5-AS1	miR-587	GDF10	PCa cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR	33407592	PGM5-AS1 impairs miR-587-mediated GDF10 inhibition and abrogates progression of prostate cancer.	BACKGROUND: Prostate cancer (PCa) is a leading cause of cancer-related death in males. Aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in various human malignancies, including PCa. This study aims to clarify the inhibitory role of human PGM5 antisense RNA 1 (PGM5-AS1) in the proliferation and apoptosis of PCa cells. METHODS: The regulatory network of PGM5-AS1/microRNA-587 (miR-587)/growth and differentiation factor 10 (GDF10) axis was examined by dual-luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull down assay. We manipulated the expression of PGM5-AS1, miR-587 and GDF10 by transducing expression vectors, mimic, inhibitor, or short hairpin RNA into PCa cells, thus establishing their functions in cell proliferation and apoptosis. Additionally, we measured the tumorigenicity of PCa cells xenografted in nude mice. RESULTS: PGM5-AS1 is expressed at low levels in PCa cell lines. Forced overexpression of PGM5-AS1 restricted proliferation and facilitated apoptosis of PCa cells, manifesting in suppressed xenograft tumor growth in nude mice. Notably, PGM5-AS1 competitively bound to miR-587, which directly targets GDF10. We further validated that the anti-cancer role of PGM5-AS1 in PCa cells was achieved by binding to miR-587 to promote the expression of GDF10. CONCLUSION: PGM5-AS1 upregulates GDF10 gene expression by competitively binding to miR-587, thus inhibiting proliferation and accelerating apoptosis of PCa cells.	NA	J Transl Med. 2021 Jan 6;19(1):12. doi: 10.1186/s12967-020-02572-w.
4428	LncRNA	PlncRNA-1	miR-136-5p	Smad3	BC tissues	Bladder Cancer	Homo sapiens (human)	qRT-PCR	33288752	Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis.	Apart from being potential prognostic biomarkers and therapeutic targets, long non-coding RNAs (lncRNAs) modulate the development and progression of multiple cancers. PlncRNA-1 is a newly discovered lncRNA that exhibits the above properties through multiple regulatory pathways. However, the clinical significance and molecular mechanisms of PlncRNA-1 in bladder cancer have not been established. PlncRNA-1 was found to be overexpressed in 71.43% of bladder cancer tissues. Moreover, the expression level correlated with tumor invasion, T stage, age, and number of tumors, but not with gender, recurrent status, preoperative treatment, pathological grade, and tumor size. The expression level of PlncRNA-1 can, to a certain extent, be used as a predictor of the degree of tumor invasion and T stage among BC patients. Inhibiting PlncRNA-1 expression impaired the proliferation, migration, and invasion of T24 and 5637 bladder cancer cells in vitro and in vivo. Specifically, PlncRNA-1 promoter in BC tissues was found to be hypomethylated at position 131 (36157603 on chromosome 21). PlncRNA-1 promoter hypomethylation induces the overexpression of PlncRNA-1. In addition, PlncRNA-1 modulated the expression of smad3 and has-miR-136-5p (miR-136). Conversely, miR-136 regulated the expression of PlncRNA-1 and smad3. PlncRNA-1 mimics competitive endogenous RNA (ceRNA) in its regulation of smad3 expression by binding miR-136. Rescue analysis further revealed that modulation of miR-136 could reverse the expression of smad3 and epithelial-mesenchymal transition (EMT) marker proteins impaired by PlncRNA-1. In summary, PlncRNA-1 has important clinical predictive values and is involved in the post-transcriptional regulation of smad3. The PlncRNA-1/miR-136/smad3 axis provides insights into the regulatory mechanism of BC, thus may serve as a potential therapeutic target and prognostic biomarker for cancer.	NA	Cell Death Dis. 2020 Dec 7;11(12):1038. doi: 10.1038/s41419-020-03240-z.
4429	LncRNA	PRNCR1	miR-330-5p	TLR4	endothelial cells	Pvec Injury	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;Immunohistochemistry;RNA immunoprecipitation;	33049095	Downregulating lncRNA PRNCR1 ameliorates LPS-induced pulmonary vascular endothelial cell injury by modulating miR-330-5p/TLR4 axis.	Pulmonary vascular endothelial cell (PVEC) injury following acute lung injury or acute respiratory distress syndrome seriously affects disease development. Recently, accumulating evidence has suggested that long noncoding RNA (lncRNA) exerts significant effects in vascular endothelial cell injury. However, PRNCR1, a novel lncRNA, remains scarcely understood in terms of its functions in PVEC injury. Both in vivo and in vitro models of PVEC injury were constructed by lipopolysaccharide (LPS) administration. The relative expressions of PRNCR1, miR-330-5p, and TLR4 were detected by quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry. Besides, gain and loss assays of PRNCR1/miR-330-5p were conducted to verify their effects on LPS-induced PVEC injury. Cell Counting Kit-8 assay used to measure cell viability and flow cytometry was used to detect apoptosis. Besides, the protein levels of caspase 3, nuclear factor-κB (NF-κB), and inflammatory cytokines (including tumor necrosis factor-α, interleukin-1β [IL-1β], and IL-6) were evaluated via Western blot and enzyme-linked immunosorbent assay. Moreover, a dual-luciferase activity experiment and RNA immunoprecipitation were applied to confirm the targeting relationship between PRNCR1 and miR-330-5p, miR-330-5p, and TLR4. PRNCR1 and TLR4 levels were significantly upregulated in LPS-treated PVEC, both in vivo and in vitro, while miR-330-5p were downregulated. Inhibiting PRNCR1 or overexpressing miR-330-5p markedly attenuated LPS-induced PVEC injury, expressions of TLR4, NF-κB, and inflammatory cytokines. Mechanistically, PRNCR1 functioned as a competitive endogenous RNA by sponging miR-330-5p and then promoting TLR4 expression. PRNCR1 was upregulated in LPS-induced PVEC and aggravated its injury via modulating the miR-330-5p/TLR4 axis.	NA	J Biochem Mol Toxicol. 2021 Feb;35(2):e22644. doi: 10.1002/jbt.22644. Epub 2020 Oct 13.
4430	LncRNA	PRR34-AS1	miR-498	FOXO3	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Cell migration and invasion assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33154667	Long Noncoding RNA PRR34-AS1 Aggravates the Progression of Hepatocellular Carcinoma by Adsorbing microRNA-498 and Thereby Upregulating FOXO3.	PURPOSE: Long noncoding RNAs are differentially expressed in hepatocellular carcinoma (HCC) and have been validated as essential regulators in HCC. However, there is limited knowledge regarding the detailed roles and mechanisms of most lncRNAs in HCC cells. In this study, the expression profiles of PRR34 antisense RNA 1 (PRR34-AS1) in HCC tissues and cell lines were determined. In addition, the detailed roles and underlying mechanisms of PRR34-AS1 in HCC cells were comprehensively elucidated. METHODS: Reverse transcription-quantitative polymerase chain reaction (PCR) was performed to measure PRR34-AS1 expression in HCC cells. Cell proliferation, apoptosis, and migration and invasion were evaluated in vitro using the cell counting kit-8 (CCK-8) assay, flow cytometric analysis, and transwell cell migration and invasion assays, respectively. In vivo tumor growth was determined using tumor xenograft experiments. The potential miRNA targets of PRR34-AS1 were predicted via bioinformatic analysis and further confirmed using the luciferase reporter assay, RNA immunoprecipitation assay, and reverse transcription-quantitative PCR. RESULTS: PRR34-AS1 was highly expressed in HCC tissues and cell lines, and its interference suppressed HCC cell proliferation, migration, and invasion but promoted cell apoptosis in vitro. In addition, loss of PRR34-AS1 decreased tumor growth in HCC cells in vivo. Mechanistically, PRR34-AS1 functions as a miR-498 sponge and subsequently increases forkhead box O3 (FOXO3) expression in HCC cells. Rescue experiments revealed that the suppressive effects triggered by PRR34-AS1 knockdown on the malignant characteristics of HCC cells could be abrogated by inhibiting miR-498 or restoring FOXO3 expression. CONCLUSION: The depletion of PRR34-AS1 suppresses the oncogenicity of HCC cells by targeting the miR-498/FOXO3 axis. Therefore, the PRR34-AS1/miR-498/FOXO3 pathway may offer a basis for HCC treatment.	NA	Cancer Manag Res. 2020 Oct 29;12:10749-10762. doi: 10.2147/CMAR.S263619. eCollection 2020.
4431	LncRNA	PTPRG-AS1	miR-200c-3p	TCF4	Non small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Western blot;Immunohistochemistry;Luciferase reporter assay;	33174523	Long Noncoding RNA PTPRG Antisense RNA 1 Reduces Radiosensitivity of Non small cell lung cancer Cells Via Regulating MiR-200c-3p/TCF4.	BACKGROUND: PTPRG antisense RNA 1 has been well-documented to exert an oncogenic role in diverse neoplasms. However, the precise role of PTPRG antisense RNA 1 in regulating radiosensitivity of Non small cell lung cancer cells remains largely elusive. METHODS: Expression levels of PTPRG antisense RNA 1 and miR-200c-3p in Non small cell lung cancer tissues and cells were detected by quantitative real-time polymerase chain reaction, while transcription factor 4 expression was examined by immunohistochemistry and Western blot. After Non small cell lung cancer cells were exposed to X-ray with different doses in vitro, Cell Counting Kit-8 assay and colony formation assay were conducted to determine the influence of PTPRG antisense RNA 1 on cell viability. Interaction between miR-200c-3p and PTPRG antisense RNA 1 as well as transcription factor 4 was investigated by dual luciferase reporter assay. RESULT: In Non small cell lung cancer tissues, the expressions of PTPRG antisense RNA 1 and transcription factor 4 were significantly upregulated, whereas the expression of miR-200c-3p was downregulated. It was also proved that PTPRG antisense RNA 1 and 3'-untranslated region of transcription factor 4 can bind to miR-200c-3p. Under X-ray irradiation, overexpressed PTPRG antisense RNA 1 could promote the viability and enhance the radioresistance of Non small cell lung cancer cells, and this effect was partially weakened by miR-200c-3p mimics. Transcription factor 4 was identified as a target gene of miR-200c-3p, which could be positively regulated by PTPRG antisense RNA 1. CONCLUSION: PTPRG antisense RNA 1 reduces the radiosensitivity of Non small cell lung cancer cells via modulating miR-200c-3p/TCF4 axis.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820942615. doi: 10.1177/1533033820942615.
4432	LncRNA	PTPRG-AS1	miR-545-3p	HDAC4	EOC cells	Ovarian Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA immunoprecipitation;	33099316	Long non-coding RNA PTPRG-AS1 promotes cell tumorigenicity in epithelial ovarian cancer by decoying microRNA-545-3p and consequently enhancing HDAC4 expression.	BACKGROUND: Long non-coding RNA PTPRG antisense RNA 1 (PTPRG-AS1) deregulation has been reported in various human malignancies and identified as an important modulator of cancer development. Few reports have focused on the detailed role of PTPRG-AS1 in epithelial ovarian cancer (EOC) and its underlying mechanism. This study aimed to determine the physiological function of PTPRG-AS1 in EOC. A series of experiments were also performed to identify the mechanisms through which PTPRG-AS1 exerts its function in EOC. METHODS: Reverse transcription-quantitative polymerase chain reaction was used to determine PTPRG-AS1 expression in EOC tissues and cell lines. PTPRG-AS1 was silenced in EOC cells and studied with respect to cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo. The putative miRNAs that target PTPRG-AS1 were predicted using bioinformatics analysis and further confirmed in luciferase reporter and RNA immunoprecipitation assays. RESULTS: Our data verified the upregulation of PTPRG-AS1 in EOC tissues and cell lines. High PTPRG-AS1 expression was associated with shorter overall survival in patients with EOC. Functionally, EOC cell proliferation, migration, invasion in vitro, and tumor growth in vivo were suppressed by PTPRG-AS1 silencing. In contrast, cell apoptosis was promoted by loss of PTPRG-AS1. Regarding the mechanism, PTPRG-AS1 could serve as a competing endogenous RNA in EOC cells by decoying microRNA-545-3p (miR-545-3p), thereby elevating histone deacetylase 4 (HDAC4) expression. Furthermore, rescue experiments revealed that PTPRG-AS1 knockdown-mediated effects on EOC cells were, in part, counteracted by the inhibition of miR-545-3p or restoration of HDAC4. CONCLUSIONS: PTPRG-AS1 functioned as an oncogenic lncRNA that aggravated the malignancy of EOC through the miR-545-3p/HDAC4 ceRNA network. Thus, targeting the PTPRG-AS1/miR-545-3p/HDAC4 pathway may be a novel strategy for EOC anticancer therapy.	NA	J Ovarian Res. 2020 Oct 24;13(1):127. doi: 10.1186/s13048-020-00723-7.
4433	LncRNA	PTTG3P	miR-132	FoxM1	PDAC cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33298873	A novel lncRNA PTTG3P/miR-132/212-3p/FoxM1 feedback loop facilitates tumorigenesis and metastasis of pancreatic cancer.	Pseudogene pituitary tumor-transforming 3 (PTTG3P) is emerging as a key player in the development and progression of cancer. However, the biological role and clinical significance of PTTG3P in pancreatic ductal adenocarcinoma (PDAC) remain unclear. Here, we found that PTTG3P was significantly upregulated in PDAC tissues. Elevated PTTG3P expression correlated with larger tumor size and worse differentiation, and reduced overall survival. Bioinformatics and experimental evidence revealed that PTTG3P promoted malignant phenotypes and FoxM1 signaling pathway in PDAC cells. Mechanistically, PTTG3P functions as a microRNA sponge to positively regulate the expression of FoxM1 through sponging miR-132/212-3p. Moreover, it showed that FoxM1 transcriptionally activated PTTG3P expression, thus forming a feedback loop to promote the aggressiveness of PDAC cells. Taken together, our findings suggest that PTTG3P promotes PDAC progression through PTTG3P/miR-132/212-3p/FoxM1 feedforward circuitry and it may serve as a promising diagnostic marker or target for treatment in PDAC patients.	NA	Cell Death Discov. 2020 Nov 30;6(1):136. doi: 10.1038/s41420-020-00360-5.
4434	LncRNA	PTTG3P	miR-212-3p	FoxM1	PDAC cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33298873	A novel lncRNA PTTG3P/miR-132/212-3p/FoxM1 feedback loop facilitates tumorigenesis and metastasis of pancreatic cancer.	Pseudogene pituitary tumor-transforming 3 (PTTG3P) is emerging as a key player in the development and progression of cancer. However, the biological role and clinical significance of PTTG3P in pancreatic ductal adenocarcinoma (PDAC) remain unclear. Here, we found that PTTG3P was significantly upregulated in PDAC tissues. Elevated PTTG3P expression correlated with larger tumor size and worse differentiation, and reduced overall survival. Bioinformatics and experimental evidence revealed that PTTG3P promoted malignant phenotypes and FoxM1 signaling pathway in PDAC cells. Mechanistically, PTTG3P functions as a microRNA sponge to positively regulate the expression of FoxM1 through sponging miR-132/212-3p. Moreover, it showed that FoxM1 transcriptionally activated PTTG3P expression, thus forming a feedback loop to promote the aggressiveness of PDAC cells. Taken together, our findings suggest that PTTG3P promotes PDAC progression through PTTG3P/miR-132/212-3p/FoxM1 feedforward circuitry and it may serve as a promising diagnostic marker or target for treatment in PDAC patients.	NA	Cell Death Discov. 2020 Nov 30;6(1):136. doi: 10.1038/s41420-020-00360-5.
4435	LncRNA	PVT1	miR-128	VEGFC	lung cancer cell	Lung Cancer	Homo sapiens (human)	Western blot;	33167678	Amplified LncRNA PVT1 promotes lung cancer proliferation and metastasis by facilitating VEGFC expression.	Although the abundance of long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) in lung cancer has been well researched, the underlying mechanisms behind its effects were unknown. Here we investigated the molecular events regulating PVT1 in lung cancer. The pro-proliferative property of PVT1 was examined using a xenograft tumor model. Transwell chambers were used to analyze the impact of PVT1 expression on cell invasiveness and migration. In vivo metastasis was examined by tail-vein-injection in mice. Direct binding of miR-128 to PVT1 was investigated using a probe pulldown assay. The relative expression levels of miR-128 and PVT1 were quantified by real-time polymerase chain reaction and Western blotting. We show here that when PVT1 is amplified, there is a poor survival prognosis for patients with lung cancer. Elevated levels of PVT1 promoted lung cancer cell proliferation and metastasis, both in vitro and in vivo. Mechanistically, we found that PVT1 competes endogenously with miR-128 in the regulation of vascular endothelial growth factor C (VEGFC) expression, which is significantly associated with an unfavorable prognosis in lung cancer. We identified that copy number amplification significantly contributes to the high level of PVT1 transcripts in lung cancer, which promotes cell proliferation and metastatic behavior via modulating VEGFC expression by endogenous competition with miR-128.	NA	Biochem Cell Biol. 2020 Dec;98(6):676-682. doi: 10.1139/bcb-2019-0435. Epub 2020 Nov 9.
4436	LncRNA	PVT1	miR-29	WAVE1	AML cells	Acute Myeloid Leukemia	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33558065	LncRNA PVT1 promotes the malignant progression of Acute myeloid leukemia via sponging miR-29 family to increase WAVE1 expression.	LncRNA PVT1 has been demonstrated to be upregulated in Acute myeloid leukemia (AML) patients and indicates a poor prognosis. Nevertheless, its role in AML remains obscure. This study investigated the regulatory role and potential mechanisms of PVT1 in the progression of AML. Expression of PVT1, miR-29 family and WAVE1 was detected by quantitative real-time polymerase chain reaction. CCK8 and EdU assays were performed to assess the proliferation of AML cells. Cell cycle and apoptosis were determined by propidium iodide (PI) staining and Annexin V/PI staining on a flow cytometer. Transwell assay was carried out to evaluate the migration and invasion abilities. The interaction between miR-29 family and PVT1/WAVE1 was confirmed by dual luciferase reporter assay and RNA immunoprecipitation assay. The protein levels of WAVE1, Bcl-2, Bax, cleaved Caspase 3, cyclin D1, and p21 were detected by western blotting. Xenograft transplantation was performed to determine the tumourigenicity of AML cell in vivo. PVT1 expression was significantly increased in AML patient samples and cells, which positively correlated with WAVE1 expression. Silencing of PVT1 restrained growth, migration and invasion, while inducing apoptosis of AML cells. Moreover, PVT1 acted as a sponge for miR-29 family to increase WAVE1 expression in AML cells. Overexpression of WAVE1 partly counteracted PVT1 knockdown-induced anti-tumour effects on AML cells in vitro and xenograft tumour in vivo. PVT1 facilitated the progression of AML via regulating miR-29 family/WAVE1 axis, which supported the conclusion that PVT1 may be a promising therapeutic target for AML.	NA	Pathology. 2021 Feb 6:S0031-3025(21)00021-0. doi: 10.1016/j.pathol.2020.11.003.
4437	LncRNA	PVT1	miR-423-5p	PAK3	TC cells	Thyroid Cancer	Homo sapiens (human)	Western blot;	33408513	LncRNA PVT1 Acts as a Tumor Promoter in Thyroid Cancer and Promotes Tumor Progression by Mediating miR-423-5p-PAK3.	INTRODUCTION: Thyroid cancer (TC) is an endocrine tumor whose risk of onset has been rising, so the deep understanding of its molecular mechanism helps formulate new treatment strategies. METHODS: This paper was aimed at exploring the regulatory mechanism of long non-coding RNA (LncRNA) plasmacytoma variant translocation 1 (PVT1) in TC. The expression of PVT1, miR-423-5p and p21-activated kinase 3 (PAK3) in TC tissues and cell lines was detected by real-time PCR. PAK3 levels were detected by Western blot. Regulatory relationships between target genes and the proliferation, invasion and apoptosis of cells and genes were analyzed. RESULTS: PVT1 and PAK3 upregulated while miR-423-5p downregulated in the tissues and cell lines. PVT1 downregulation inhibited TC cells from malignantly proliferating and invading, and promoted their apoptosis. PVT1 specifically regulated miR-423-5p, and its overexpression could weaken the anti-tumor effect of this miR on TC cells. In addition, miR-423-5p directly targeted PAK3, and knocking down its expression could weaken the inhibitory effect of PAK3 downregulation on TC progression. Besides, PVT1 acted as a competitive endogenous RNA to sponge this miR and thus regulate PAK3 expression. DISCUSSION: In conclusion, PVT1 can mediate the molecular mechanism of the miR-423-5p-PAK3 axis regulatory network on regulating TC, so it is a new direction of treating the disease.	NA	Cancer Manag Res. 2020 Dec 30;12:13403-13413. doi: 10.2147/CMAR.S283443. eCollection 2020.
4438	LncRNA	PVT1	miR-135a-5p	FOXO1	H9c2 cells	Hypoxia-Induced Cardiomyocyte Injury	Homo sapiens (human)	Flow cytometry assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33093283	Long non-coding RNA plasmacytoma variant translocation 1 linked to hypoxia-induced cardiomyocyte injury of H9c2 cells by targeting miR-135a-5p/forkhead box O1 axis.	BACKGROUND: Myocardial infarction occurs due to insufficient (ischemia) blood supply to heart for long time; plasmacytoma variant translocation 1 (PVT1) is a long non-coding RNAs (lncRNAs) involved in the pathogenesis of various diseases, including heart disease; However, few studies have explored its role. The present study evaluated the effects of lncRNA PVT1 on hypoxic rat H9c2 cells. METHODS: Hypoxic injury was examined by measuring cell viability and apoptosis by using cell counting kit-8 activity and flow cytometry assays. Gene expressions after hypoxia were estimated by quantitative real time polymerase chain reaction and the signaling pathway were explored by Western blot analysis. RNA immunoprecipitation and luciferase reporter assays were applied to examine the interactions among genes. Data were analyzed using t-test with one-way or two-way analysis of variance. RESULTS: The lncRNA PVT1 is up-regulated in hypoxia-stressed H9c2 cells and knockdown of PVT1 mitigates hypoxia-induced injury in H9c2 cells. PVT1 acts as a sponge for miR-135a-5p and knockdown of PVT1 attenuated the increased hypoxia-induced injury by up-regulating miR-135a-5p. Forkhead box O1 (FOXO1) was identified as a target of miR-135a-5p, and the expression was negatively regulated by miR-135a-5p. The exploration of the underlying mechanism demonstrated that knockdown of FOXO1 reversed PVT1/miR-135a-5p mediated hypoxia-induced injury in H9c2 cells. CONCLUSIONS: PVT1 plays a crucial role in hypoxia-injured H9c2 cells through sponging miR-135a-5p and then positively regulating FOXO1.	NA	Chin Med J (Engl). 2020 Oct 21;133(24):2953-2962. doi: 10.1097/CM9.0000000000001147.
4439	LncRNA	PVT1	miR-135a-5p	FOXO1	H9c2 cells	Hypoxia-Induced Cardiomyocyte Injury	Rattus (rat)	Flow cytometry assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33093283	Long non-coding RNA plasmacytoma variant translocation 1 linked to hypoxia-induced cardiomyocyte injury of H9c2 cells by targeting miR-135a-5p/forkhead box O1 axis.	BACKGROUND: Myocardial infarction occurs due to insufficient (ischemia) blood supply to heart for long time; plasmacytoma variant translocation 1 (PVT1) is a long non-coding RNAs (lncRNAs) involved in the pathogenesis of various diseases, including heart disease; However, few studies have explored its role. The present study evaluated the effects of lncRNA PVT1 on hypoxic rat H9c2 cells. METHODS: Hypoxic injury was examined by measuring cell viability and apoptosis by using cell counting kit-8 activity and flow cytometry assays. Gene expressions after hypoxia were estimated by quantitative real time polymerase chain reaction and the signaling pathway were explored by Western blot analysis. RNA immunoprecipitation and luciferase reporter assays were applied to examine the interactions among genes. Data were analyzed using t-test with one-way or two-way analysis of variance. RESULTS: The lncRNA PVT1 is up-regulated in hypoxia-stressed H9c2 cells and knockdown of PVT1 mitigates hypoxia-induced injury in H9c2 cells. PVT1 acts as a sponge for miR-135a-5p and knockdown of PVT1 attenuated the increased hypoxia-induced injury by up-regulating miR-135a-5p. Forkhead box O1 (FOXO1) was identified as a target of miR-135a-5p, and the expression was negatively regulated by miR-135a-5p. The exploration of the underlying mechanism demonstrated that knockdown of FOXO1 reversed PVT1/miR-135a-5p mediated hypoxia-induced injury in H9c2 cells. CONCLUSIONS: PVT1 plays a crucial role in hypoxia-injured H9c2 cells through sponging miR-135a-5p and then positively regulating FOXO1.	NA	Chin Med J (Engl). 2020 Oct 21;133(24):2953-2962. doi: 10.1097/CM9.0000000000001147.
4440	LncRNA	PVT1	miR-23a-3p	CASP10	Dilated cardiomyocytes	Diabetes Mellitus	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33049089	Long noncoding RNA PVT1 facilitates high glucose-induced cardiomyocyte death through the miR-23a-3p/CASP10 axis.	Dilated cardiomyopathy (DCM) is the leading cause of morbidity and mortality in diabetic patients. Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) has been shown to be related to the pathogenesis of DCM. However, the mechanism by which PVT1 regulates DCM pathogenesis is unclear. High glucose level was employed to construct a DCM cell model in vitro. Cell viability was determined via cell counting kit-8 assay. The level of lactate dehydrogenase (LDH) was measured with the corresponding kit. Expression levels of PVT1, miR-23a-3p, and caspase-10 (CASP10) messenger RNA were evaluated with a quantitative real-time polymerase chain reaction. Cell apoptosis was assessed by flow cytometry assay. Protein levels of B-cell lymphoma 2-associated X (Bax), cleaved-caspase-3 (cleaved-casp-3), and CASP10 were examined via western blot analysis. The relationship between PVT1 or CASP10 and miR-23a-3p was verified with dual-luciferase reporter assay. We observed that PVT1 and CASP10 were upregulated while miR-23a-3p was downregulated in high glucose-induced cardiomyocytes. High glucose levels repressed cardiomyocyte activity and induced cardiomyocyte apoptosis, but this influence was antagonized by PVT1 knockdown or miR-23a-3p overexpression. Furthermore, PVT1 acted as a sponge for miR-23a-3p, and miR-23a-3p inhibition counterbalanced the influence of PVT1 silencing on viability and apoptosis of cardiomyocytes under high glucose level treatment. PVT1 could increase CASP10 expression via sponging miR-23a-3p. In conclusion, PVT1 acted as a deleterious lncRNA in DCM. PVT1 facilitated cardiomyocyte death by regulating the miR-23a-3p/CASP10, which offered a new mechanism to comprehend the pathogenesis of DCM.	NA	Cell Biol Int. 2021 Jan;45(1):154-163. doi: 10.1002/cbin.11479. Epub 2020 Oct 29.
4441	LncRNA	PVT1	miR-194-5p	BCLAF1	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33188158	LncRNA PVT1 accelerates malignant phenotypes of bladder cancer cells by modulating miR-194-5p/BCLAF1 axis as a ceRNA.	BACKGROUND: Numerous studies proved that long non-coding RNA (lncRNA) is involved in the progression of multifarious diseases, especially in some carcinomas. As a potential tumor biomarker, plasmacytoma variant translocation 1 gene (PVT1) is involved in the development and progression of multifarious cancers. Nevertheless, the intrinsic and concrete molecular mechanism of PVT1 in bladder cancer still remained unclear, which is also the dilemma faced in many non-coding RNA studies. RESULTS: Our research revealed that PVT1 was significantly higher expression in bladder carcinoma specimens and cell lines. Further experiments indicated that knockdown or overexpression of PVT1 restrained or promoted the malignant phenotype and WNT/β-catenin signaling in bladder cancer cells. Meanwhile miR-194-5p was in contrast and miR-194-5p could partially reverse the function of PVT1 in malignant bladder tumor cells. As a microRNA sponge, PVT1 actively promotes the expression of b-cells lymphoma-2-associated transcription factor 1 (BCLAF1) to sponge miR-194-5p and subsequently increases malignant phenotypes of bladder cancer cells. Therefore, it performs a carcinogenic effect and miR-194-5p as the opposite function, and serves as an antioncogene in the bladder carcinomas pathogenesis. CONCLUSION: PVT1-miR-194-5p-BCLAF1 axis is involved in the malignant progression and development of bladder carcinomas. Experiments revealed that PVT1 has a significant regulatory effect on bladder cancer (BC) and can be used as a clinical diagnostic marker and a therapeutic molecular marker for patients suffering from BC. METHODS: In urothelial bladder carcinoma specimens and cell lines, the relative expression levels of PVT1 and miR-194-5p were detected by quantitative reverse transcription PCR (RT-qPCR). Through experiments such as loss-function and over-expression, the biological effects of PVT1 and miR-194-5p on the proliferation, migration, apoptosis and tumorigenicity were explored in bladder cancer cells. Co-immunoprecipitation, proteomics experiments, dual luciferase reporter gene analysis, western blot and other methods were adopted to investigate the PVT1 potential mechanism in bladder carcinomas.	NA	Aging (Albany NY). 2020 Nov 16;12(21):22291-22312. doi: 10.18632/aging.202203. Epub 2020 Nov 16.
4442	LncRNA	PVT1	miR-503	ARL2	CC cells	Cervical Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33817293	LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression.	Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.	NA	Open Life Sci. 2021 Jan 21;16(1):1-13. doi: 10.1515/biol-2021-0002. eCollection 2021.
4443	LncRNA	PVT1	miR-503	ARL2	CC cells	Cervical Cancer	Mus musculus (mouse)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33817293	LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression.	Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.	NA	Open Life Sci. 2021 Jan 21;16(1):1-13. doi: 10.1515/biol-2021-0002. eCollection 2021.
4444	Circular RNA	PVT1	miR-149-5p	FOXM1	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR	33391456	Circular PVT1 regulates cell proliferation and invasion via miR-149-5p/FOXM1 axis in ovarian cancer.	Long non-coding RNA plasmacytoma variant translocation 1 (PVT1) is a dysregulated gene in malignancy and is associated with oncogenesis. In this study, we found PVT1 RNA was an ovarian specific expressing gene, and overexpressed in multiple cancer types, including ovarian cancer (OV). Higher expression levels of PVT1 are related to shorter survival time in OV patients, especially in patients with advanced stage and grade. Recent studies indicated circular PVT1 also had an important role in cancer progression, whose roles in OV remain unclear. Knockdown of circular PVT1 significantly suppressed OV cell proliferation, migration and invasion. Bioinformatics analysis demonstrated that circular PVT1 was involved in regulating angiogenesis, osteoblast differentiation, regulation of cell growth, type B pancreatic cell proliferation, negative regulation of apoptotic process, phospholipid homeostasis, regulation of neurogenesis, definitive hemopoiesis, cell migration, regulation of glucose metabolic process, central nervous system development and type 2 immune response. Our data showed miR-149-5p targeted FOXM1, which was regulated by circular PVT1. Forkhead Box M1 (FOXM1) expression in ovarian cancer exhibited high level when compared with normal tissues, and had relation with relatively poor survival. FOXM1 promoted cell viability and reduced FOXM1 could rescue circular influence of circular PVT1-caused carcinoma induction. In conclusion, circular PVT1 increased FOXM1 level via binding to miR-149-5p and thus affected ovarian cancer cell viability and migration.	NA	J Cancer. 2021 Jan 1;12(2):611-621. doi: 10.7150/jca.52234. eCollection 2021.
4445	LncRNA	PVT1	miR-15a-5p	PI3K	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4446	LncRNA	PVT1	miR-29c-3p	PI3K	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4447	LncRNA	PVT1	miR-15a-5p	AKT	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4448	LncRNA	PVT1	miR-29c-3p	AKT	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4449	LncRNA	PVT1	miR-15a-5p	mTOR	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4450	LncRNA	PVT1	miR-29c-3p	mTOR	CD(4+)T cells	Ozone-Triggered Asthma	Homo sapiens (human)	qRT-PCR	33223504	Exposure to ozone impacted Th1/Th2 imbalance of CD(4+) T cells and apoptosis of ASMCs underlying asthmatic progression by activating lncRNA PVT1-miR-15a-5p/miR-29c-3p signaling.	This investigation attempted to elucidate whether lncRNA PVT1-led miRNA axes participated in aggravating ozone-triggered asthma progression. One hundred and sixty-eight BALB/c mice were evenly divided into saline+air group, ovalbumin+air group, saline+ozone group and ovalbumin+ozone group. Correlations were evaluated between PVT1 expression and airway smooth muscle function/inflammatory cytokine release among the mice models. Furthermore, pcDNA3.1-PVT1 and si-PVT1 were, respectively, transfected into CD(4+)T cells and airway smooth muscle cells (ASMCs), and activities of the cells were observed. Ultimately, a cohort of asthma patients was recruited to estimate the diagnostic performance of PVT1. It was demonstrated that mice of ovalbumin+ozone group were associated with higher PVT1 expression, thicker trachea/airway smooth muscle and smaller ratio of Th1/Th2-like cytokines than mice of ovalbumin+air group and saline+ozone group (P<0.05). Moreover, pcDNA3.1-PVT1 significantly brought down Th1/Th2 ratio in CD(4+) T cells by depressing miR-15a-5p expression and activating PI3K-Akt-mTOR signaling (P<0.05). The PVT1 also facilitated ASMC proliferation by sponging miR-29c-3p and motivating PI3K-Akt-mTOR signaling (P<0.05). Additionally, PVT1 seemed promising in diagnosis of asthma, with favorable sensitivity (i.e. 0.844) and specificity (i.e. 0.978). Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	NA	Aging (Albany NY). 2020 Nov 20;12(24):25229-25255. doi: 10.18632/aging.104124. Epub 2020 Nov 20.
4451	LncRNA	PVT1	miR-93-5p	HMGB1	C28/I2 cells	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;Western blot;Luciferase reporter assay;	33174011	Knockdown of exosome-mediated lnc-PVT1 alleviates lipopolysaccharide-induced osteoarthritis progression by mediating the HMGB1/TLR4/NF-κB pathway via miR-93-5p.	Osteoarthritis is a chronic degenerative joint disease. Long non-coding RNA plasmacytoma variant translocation 1 (PVT1) is involved in the progression of osteoarthritis and exosomes serve a central role in intercellular communication. However, whether PVT1 can be mediated by exosomes in osteoarthritis has not been reported. Whole blood was drawn from osteoarthritis patients and healthy volunteers. Lipopolysaccharide (LPS) was used to stimulate human normal chondrocytes (C28/I2) to construct a cell damage model in vitro. Protein levels were examined via western blot analysis. eThe expression of PVT1, microRNA (miR)-93-5p and high mobility groupprotein B1 (HMGB1) was evaluated through reverse transcription-quantitative PCR. Cell viability and apoptosis were determined through CCK-8 or flow cytometric assay. Inflammatory cytokines were measured via ELISA. The relationship between PVT1 or HMGB1 and miR-93-5p was confirmed by dual-luciferase reporter assay. PVT1, HMGB1 and exosomal PVT1 were upregulated while miR-93-5p was downregulated in osteoarthritis patient serum and LPS-induced C28/I2 cells. Exosomes from osteoarthritis patient serum and LPS-treated C28/I2 cells increased PVT1 expression in C28/I2 cells. PVT1 depletion reversed the decrease of viability and the increase of apoptosis, inflammation responses and collagen degradation of C28/I2 cells induced by LPS. PVT1 regulated HMGB1 expression via sponging miR-93-5p. miR-93-5p inhibition abolished PVT1 silencing-mediated viability, apoptosis, inflammation responses and collagen degradation of LPS-stimulated C28/I2 cells. HMGB1 increase overturned miR-93-5p upregulation-mediated viability, apoptosis, inflammation responses and collagen degradation of LPS-stimulated C28/I2 cells. Furthermore, PVT1 modulated the Toll-like receptor 4/NF-κB pathway through an miR-93-5p/HMGB1 axis. In summary, exosome-mediated PVT1 regulated LPS-induced osteoarthritis progression by modulating the HMGB1/TLR4/NF-κB pathway via miR-93-5p, providing a new route for possible osteoarthritis treatment.	NA	Mol Med Rep. 2020 Dec;22(6):5313-5325. doi: 10.3892/mmr.2020.11594. Epub 2020 Oct 14.
4452	LncRNA	PWRN2	miR-325	DDX5	PTC cells	Papillary Thyroid Cancer	Homo sapiens (human)	luciferase assay;	33090407	LncRNA PWRN2 stimulates the proliferation and migration in papillary thyroid carcinoma through the miR-325/DDX5 axis.	OBJECTIVE: The objective of this study was to illustrate the role of long non-coding RNA (lncRNA) PWRN2 in the development of papillary thyroid carcinoma (PTC) and the potential mechanism. PATIENTS AND METHODS: Expression levels of PWRN2, miR-325 and DDX5 in 32 PTC tissues and paired normal ones were detected. The interaction in the PWRN2/miR-325/DDX5 axis was assessed by Luciferase assay. At last, the roles of the PWRN2/miR-325/DDX5 axis in regulating proliferative and migratory potentials in PTC were examined. RESULTS: It was found that PWRN2 was upregulated and miR-325 was downregulated in PTC tissues and cell lines. MiR-325 level was negatively correlated with PWRN2 level in PTC samples, and the overexpression of PWRN2 stimulated proliferative and migratory potentials in PTC cells, which were partially abolished by overexpression of miR-325. In addition, DDX5 was the target gene binding to miR-325, and its level was negatively regulated by miR-325. Moreover, Luciferase assay and rescue experiments confirmed that the PWRN2/miR-325/DDX5 axis aggravated the development of PTC. CONCLUSIONS: LncRNA PWRN2 stimulates proliferative and migratory potentials in PTC through sponging miR-325 to upregulate DDX5.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(19):10022-10027. doi: 10.26355/eurrev_202010_23216.
4453	LncRNA	RAMP2-AS1	miR-296-5p	MACF1	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33281971	Identification of key genes in lung adenocarcinoma based on a competing endogenous RNA network.	Lung adenocarcinoma (LUAD) is the most commonly diagnosed type of lung cancer and exhibits a high morbidity. The present study aimed to investigate the long non-coding RNA (lncRNA)-associated competing endogenous RNA (ceRNA) mechanisms in LUAD. The receptor activity modifying protein 2-antisense RNA 1 (RAMP2-AS1) was identified using GSE113852 and GSE130779 datasets downloaded from the Gene Expression Omnibus database, and the downregulation of RAMP2-AS1 was the most significant in LUAD. In addition, microRNA (miR)-296-5p was identified to bind to RAMP2-AS1 via bioinformatics analysis. Subsequently, CD44, cyclin D3 (CCND3), neurocalcin δ (NCALD), microtubule actin crosslinking factor 1 (MACF1) and potassium channel tetramerization domain containing 15 were obtained by intersecting the predicted target genes of miR-296-5p and 368 differentially expressed mRNAs in LUAD. According to the Gene Expression Profiling Interactive Analysis and UALCAN databases, these five mRNAs were downregulated in LUAD, and their expression levels were positively correlated with those of RAMP2-AS1. CD44, CCND3, NCALD and MACF1 were selected as key mRNAs in LUAD based on prognostic analyses. Furthermore, functional enrichment analyses were performed and an interaction network was constructed to reveal the functions of the RAMP2-AS1-associated ceRNA in LUAD. The results indicated that the functions were mainly enriched in generic transcription pathways, cyclin D-associated events in G(1) and epithelial stromal transformation. Reverse transcription-quantitative PCR assays revealed that RAMP2-AS1, CD44, CCND3, NCALD and MACF1 expression was lower in tumor tissues than in normal tissues, while miR-296-5p expression was higher in tumor tissues compared with in normal tissues. The association between RAMP2-AS1 and MACF1 was further confirmed using in vitro experiments. Overall, the present results indicated that RAMP2-AS1, miR-296-5p, CD44, CCND3, NCALD and MACF1 may be involved in LUAD progression and may therefore serve as potential biomarkers and provide a theoretical basis for the study of the pathogenesis of LUAD.	NA	Oncol Lett. 2021 Jan;21(1):60. doi: 10.3892/ol.2020.12322. Epub 2020 Nov 19.
4454	Circular RNA	RASGRF2	miR-1224	FAK	HCC cell lines	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33312757	circRASGRF2 functions as an oncogenic gene in hepatocellular carcinoma by acting as a miR-1224 sponge.	Circular RNAs (circRNAs) are a class of non-coding RNAs broadly expressed in cells of various species. However, the contributions and molecular mechanisms of circRNAs to hepatocellular carcinoma (HCC) remain largely unknown. In the present study, we compared the expression of circRNAs between five paired HCC and adjacent noncancerous liver (ANL) tissues by using RNA-sequencing (RNA-seq). circRASGRF2 (a circRNA located on chromosome 5 and derived from RASGRF2, hsa_circ_0073181) was identified and validated by quantitative reverse transcriptase PCR. The role of circRASGRF2 in HCC progression was assessed both in vitro and in vivo. Mechanistically, RNA immunoprecipitation and luciferase reporter assays were performed to confirm the interaction between circRASGRF2 and miR-1224 in HCC. circRASGRF2 was found to be significantly upregulated in HCC tissues and HCC cell lines compared with paired ANL tissues and normal cells. Our in vivo and in vitro data indicated that knockdown of circRASGRF2 inhibits the proliferation and migration of HCC cells. Mechanistically, we found that circRASGRF2 could promote the expression of focal adhesion kinase (FAK) by sponging miR-1224. Our data showed that circRASGRF2 is a central component linking circRNAs to progression of HCC, making it a potential therapeutic target.	NA	Mol Ther Nucleic Acids. 2020 Oct 27;23:13-26. doi: 10.1016/j.omtn.2020.10.035. eCollection 2021 Mar 5.
4455	LncRNA	RNA01134	miR-4784	SSRP1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	32970959	Long intergenic noncoding RNA01134 accelerates hepatocellular carcinoma progression by sponging microRNA-4784 and downregulating structure specific recognition protein 1.	Dysregulation of long noncoding RNAs (lncRNAs) has been suggested to foster the carcinogenesis of hepatocellular carcinoma (HCC). To date, the role of long intergenic noncoding RNA01134 (LINC01134) in HCC have never been researched yet. Herein, we found that LINC01134 was highly expressed in HCC tissues in comparison with the matched normal liver tissues and increased LINC01134 expression correlated with shorter overall survival of patients with HCC. Additionally, we demonstrated LINC01134 downregulation significantly suppressed the proliferation ability and colony formation capacity of HCC cells. Furthermore, we revealed that LINC01134 functioned as a competitive endogenous RNA (ceRNA) for miR-4784 to upregulate structure-specific recognition protein 1 (SSRP1) in HCC cells. Meanwhile, miR-4784 inhibitor or restoration of SSRP1 could markedly attenuate the inhibitory effect of LINC01134 downregulation on HCC cells. Taken together, LINC01134 may promote the carcinogenesis of HCC at least partly via the miR-4784/SSRP1 axis. Therefore, LINC01134/miR-4784/SSRP1 axis should be developed as the promising therapeutic target for HCC.	NA	Bioengineered. 2020 Dec;11(1):1016-1026. doi: 10.1080/21655979.2020.1818508.
4456	LncRNA	RNF144A-AS1	miR-455-5p	SOX11	BC cell	Bladder Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA pull-down assay;Luciferase reporter assay;RNA pull-down;	33177836	LncRNA RNF144A-AS1 Promotes Bladder Cancer Progression via RNF144A-AS1/miR-455-5p/SOX11 Axis.	BACKGROUND: Bladder cancer (BC) is the most commonly occurring malignant tumor of the urinary system worldwide. Long non-coding RNAs (lncRNAs), including lncRNA RNF144A-AS1 (RNF144A-AS1), perform an oncogenic role in BC progression. However, how RNF144A-AS1 is regulated in BC has not been fully investigated, and its role in BC is mostly obscure. In this study, we explore its role in BC progression. MATERIALS AND METHODS: The expression level of RNF144A-AS1 in BC tissues was explored via bioinformatics analysis and quantitative real-time PCR (qRT-PCR). We used RNF144A-AS1 siRNA (si-RNF144A-AS1) to inhibit the RNF144A-AS1 level in BC cell lines (J82 and 5637 cells). A series of experimental studies in vitro (CCK-8 assay, colony formation assay and Transwell assay) was performed to explore the role of si-RNF144A-AS1 on the proliferation, migration and invasion of J82 and 5637 cells. A BC xenograft model was established, and the effect of si-RNF144A-AS1 on xenograft growth was explored in vivo. The interactions among RNF144A-AS1, miR-455-5p and SOX11 were predicted by bioinformatics miRanda and Targetscan database, and verified by the luciferase reporter assay and RNA pull-down assay. Finally, miR-455-5p inhibitor and si-RNF144A-AS1 were cotransfected into J82 and 5637 cells. RESULTS: RNF144A-AS1 is overexpressed in BC tumors and cells, and its overexpression is correlated with poor prognosis. Knockdown of RNF144A-AS1 markedly suppressed the proliferation, migration and invasion of J82 and 5637 cells and significantly inhibited xenograft growth in nude mice, compared to si-NC. We found that RNF144A-AS1 serves as a sponge for miR-455-5p. Furthermore, a binding site of miR-455-5p was found in 3' UTR of SOX11 gene, and overexpression of miR-455-5p suppressed SOX11 levels. RNF144A-AS1 knockdown markedly decreased SOX11 expression levels, while miR-455-5p inhibitor restored this repressive effect. Restoration of SOX11 could reverse this repressive effect of RNF144A-AS1 on cell proliferation, migration and invasion abilities. CONCLUSION: Overall, our findings underline the critical role of RNF144A-AS1 in BC development, and our study reveals for the first time that RNF144A-AS1 promotes BC progression via the RNF144A-AS1/miR-455-5p/SOX11 axis.	NA	Onco Targets Ther. 2020 Nov 4;13:11277-11288. doi: 10.2147/OTT.S266067. eCollection 2020.
4457	LncRNA	ROR1-AS1	miR-670-3p	STC2	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Rescue assay;	33081599	Long noncoding RNA ROR1-AS1 enhances STC2-mediated cell growth and autophagy in cervical cancer through miR-670-3p.	PURPOSE: Cervical cancer (CC) ranks the fourth among female malignancies and has become a dominating cause for tumor-associated death nowadays. More and more documents have proposed that long noncoding RNAs (lncRNAs), which emerge as pivotal biomarkers, actively participate in the regulation of human carcinomas. LncRNA ROR1-AS1 is a recently identified RNA that is highlighted for its crucial role in the biological processes of cancers. However, the role and molecular mechanism of ROR1-AS1 in CC have not been clarified yet. METHODS AND RESULTS: In the current study, RT-qPCR analysis uncovered that ROR1-AS1 expression was evidently upregulated in CC tissues and cell lines. Functional experiments (CCK-8, EdU, TUNEL, wound healing and Transwell assays as well as western blot analysis) revealed that knockdown of ROR1-AS1 markedly suppressed the malignant phenotypes of CC cells via decreasing cell viability, proliferation, migration, invasion and autography, and facilitating cell apoptosis. Subsequently, by performing luciferase reporter and RNA pulldown assays, miR-670-3p was identified to be sponged by ROR1-AS1. Additionally, STC2 was disclosed to be targeted by miR-670-3p in CC cells. Rescue assays illuminated that upregulation of STC2 counteracted ROR1-AS1 knockdown-induced suppression on CC cell growth. CONCLUSIONS: These data suggested that ROR1-AS1 contributed to the malignant properties of CC cells through sponging miR-670-3p and upregulating of STC2.	NA	J Recept Signal Transduct Res. 2020 Oct 20:1-11. doi: 10.1080/10799893.2020.1836495.
4458	LncRNA	ROR1-AS1	miR-4686	NA	glioma cells	Glioma	Homo sapiens (human)	microarray;MTT assay;qRT-PCR;RIP assay;luciferase assay;MTT assay;	33204092	Exosomal lncRNA ROR1-AS1 Derived from Tumor Cells Promotes Glioma Progression via Regulating miR-4686.	OBJECTIVE: Glioma is one of the most common central nervous system malignant tumors, accounting for 45%-60% of adult intracranial tumors. However, the clinical treatment of glioma is limited. It is of great significance to seek new therapeutic methods for glioma via gene therapy. MATERIALS AND METHODS: Microarray is used to identify the lncRNAs that are differentially expressed in glioma. The expression of long non-coding RNA (lncRNA) ROR1-AS1 and miR-4686 was detected by qRT-PCR. Exosomes were isolated from the supernatant of normal and cancerous cells, and TEM was used for exosomes identification. MTT assay, wound healing assay, transwell assay, and colony formation assay were used to detect the exo-ROR1-AS1 function on proliferation, migration, and invasion in glioma cells. Luciferase assay and RIP assay were used to identify the relationship between lncRNA ROR1-AS1 and miR-4686. The effect of exo-ROR1-AS1 on tumorigenesis of glioma was confirmed by the xenograft nude mice model. RESULTS: ROR1-AS1 was up-regulated in glioma tissues, and the high expression of ROR1-AS1 indicated a poor prognosis in glioma patients. Interestingly, ROR1-AS1 was packaged into exosomes and derived from tumor cells. Functional analysis showed exo-ROR1-AS1 promoted the progression of glioma cell lines SHG44 and U251. Furthermore, ROR1-AS1 acted as a sponge of miR-4686 and inhibited its expression. Functionally, forced expression of miR-4686 removed the promoted effects of lncRNA ROR1-AS1 on glioma development. In vivo tumorigenesis experiments showed that exo-ROR1-AS1 promoted glioma development via miR-4686 axis. CONCLUSION: Our study suggested tumor cells derived exo-ROR1-AS1 promoted glioma progression by inhibiting miR-4686, which might be a potential therapeutic target for glioma clinical treatment.	NA	Int J Nanomedicine. 2020 Nov 10;15:8863-8872. doi: 10.2147/IJN.S271795. eCollection 2020.
4459	LncRNA	RP11-757G1.5	miR-139-5p	YAP1	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	FISH;ISH;qPCR;RT-qPCR;RNA pull-down assay;Western blot;FISH;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33023613	Long noncoding RNA RP11-757G1.5 sponges miR-139-5p and upregulates YAP1 thereby promoting the proliferation and liver, spleen metastasis of colorectal cancer.	BACKGROUND: Accumulating evidence indicates that long non-coding RNAs (lncRNAs) acting as crucial regulators in tumorigenesis. However, its biological functions of lncRNAs in colorectal cancer (CRC) have not been systematically clarified. METHODS: An unbiased screening was performed to identify disregulated lncRNAs revealed to be implicated in CRC carcinogenesis according to an online-available data dataset. In situ hybridization (ISH), RT-qPCR and RNA fluorescence in situ hybridization (RNA-FISH) were applied to detect RP11-757G1.5 expression in CRC tissues and cell lines. The associations of RP11-757G1.5 with clinicopathological characteristics were analyzed. Their effects on prognosis were analyzed by the Kaplan-Meier analysis, Log-rank test, Univariate and Multivariate Cox regression analysis. The potential biological function of RP11-757G1.5 in CRC was investigated by Colony formation, Edu cell proliferation, Flow cytometry, Wound healing and Transwell assays. Bioinformatics binding site analysis, Luciferase reporter assay, Ago2 immunoprecipitation assays, RNA pull-down assay, RT-qPCR and Western blotting were utilized to demonstrate the mechanism of RP11-757G1.5 acts as a molecular sponge of miR-139-5p to regulate the expression of YAP1. Finally, we further explore the potential role of RP11-757G1.5 in CRC orthotopic xenografts in vivo. RESULTS: We discovered a novel oncogenic lncRNA RP11-757G1.5, that was overexpressed in CRC tissues, especially in aggressive cases. Moreover, up-regulation of RP11-757G1.5 strongly correlated with poor clinical outcomes of patients with CRC. Functional analyses revealed that RP11-757G1.5 promoted cell proliferation in vitro and in vivo. Furthermore, RP11-757G1.5 stimulated cell migration and invasion in vitro and in vivo. Mechanistic studies illustrated that RP11-757G1.5 regulated the expression of YAP1 through sponging miR-139-5p and inhibiting its activity thereby promoting CRC progression and development. CONCLUSIONS: Altogether, these results reveal a novel RP11-757G1.5/miR-139-5p/YAP1 regulatory axis that participates in CRC carcinogenesis and progression.	NA	J Exp Clin Cancer Res. 2020 Oct 6;39(1):207. doi: 10.1186/s13046-020-01717-5.
4460	Circular RNA	SETD3	miR-615-5p	MAPRE1	NPC cells	Nasopharyngeal Cancer	Homo sapiens (human)	ISH;qRT-PCR;RNA sequencing;	33122825	circSETD3 regulates MAPRE1 through miR-615-5p and miR-1538 sponges to promote migration and invasion in nasopharyngeal carcinoma.	Circular RNAs (circRNAs) play an essential role in tumorigenesis and development. However, they have rarely been investigated in nasopharyngeal carcinoma (NPC). This study aimed to investigate the role of circRNA in the invasion and metastasis of NPC. We screened and verified the high expression of circSETD3 in NPC cell lines using RNA sequencing (RNA-Seq) and verified the results of NPC biopsy samples using real-time quantitative polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH). In vivo and in vitro experiments indicated that circSETD3 could promote NPC cell invasion and migration. We compared the proteomic data of NPC cells before and after the overexpression or knockdown of circSETD3 in combination with bioinformatics prediction and experimental verification. It was found that circSETD3 competitively adsorbs to miR-615-5p and miR-1538 and negates their inhibitory effect on MAPRE1 mRNA, thereby upregulating the expression of MAPRE1. The upregulated MAPRE1 then inhibits the acetylation of α-tubulin, promotes the dynamic assembly of microtubules, and enhances the invasion and migration capabilities of NPC cells. The results of this study suggest that circSETD3 is a novel molecular marker and a potential target for NPC diagnosis and treatment.	NA	Oncogene. 2021 Jan;40(2):307-321. doi: 10.1038/s41388-020-01531-5. Epub 2020 Oct 29.
4461	Circular RNA	SETD3	miR-1538	MAPRE1	NPC cells	Nasopharyngeal Cancer	Homo sapiens (human)	ISH;qRT-PCR;RNA sequencing;	33122825	circSETD3 regulates MAPRE1 through miR-615-5p and miR-1538 sponges to promote migration and invasion in nasopharyngeal carcinoma.	Circular RNAs (circRNAs) play an essential role in tumorigenesis and development. However, they have rarely been investigated in nasopharyngeal carcinoma (NPC). This study aimed to investigate the role of circRNA in the invasion and metastasis of NPC. We screened and verified the high expression of circSETD3 in NPC cell lines using RNA sequencing (RNA-Seq) and verified the results of NPC biopsy samples using real-time quantitative polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH). In vivo and in vitro experiments indicated that circSETD3 could promote NPC cell invasion and migration. We compared the proteomic data of NPC cells before and after the overexpression or knockdown of circSETD3 in combination with bioinformatics prediction and experimental verification. It was found that circSETD3 competitively adsorbs to miR-615-5p and miR-1538 and negates their inhibitory effect on MAPRE1 mRNA, thereby upregulating the expression of MAPRE1. The upregulated MAPRE1 then inhibits the acetylation of α-tubulin, promotes the dynamic assembly of microtubules, and enhances the invasion and migration capabilities of NPC cells. The results of this study suggest that circSETD3 is a novel molecular marker and a potential target for NPC diagnosis and treatment.	NA	Oncogene. 2021 Jan;40(2):307-321. doi: 10.1038/s41388-020-01531-5. Epub 2020 Oct 29.
4462	LncRNA	SH3PXD2A-AS1	miR-330-5p	UBA2	CRC cells	Colorectal Cancer	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;	33073888	SH3PXD2A-AS1/miR-330-5p/UBA2 ceRNA network mediates the progression of colorectal cancer through regulating the activity of the Wnt/β-catenin signaling pathway.	Long non-coding RNAs have important roles in the occurrence and progression of various cancers. However, the molecular mechanism of lncRNAs in colorectal cancer (CRC) is not well illustrated. Thus, we used bioinformatics methods to find potential lncRNAs associated with CRC progression, and chose SH3PXD2A-AS1 as a candidate for further analysis. The roles of SH3PXD2A-AS1 in CRC cells were determined by CCK-8, transwell invasion, wound healing and flow cytometry assays. Besides, we established the CRC tumor models in nude mice to study the effect of SH3PXD2A-AS1 on the tumor growth. Based on the ceRNA hypothesis, we used miRDB and miRTarBase websites to identify the SH3PXD2A-AS1-related ceRNA regulatory network, and measured the roles of this network in CRC cells. The results revealed that the expression profiles of SH3PXD2A-AS1 from GEO and TCGA databases showed an aberrant high level in CRC tissues compared with colorectal normal tissues. SH3PXD2A-AS1 over-expression was also found in CRC cells. SH3PXD2A-AS1 knockdown inhibited the CRC cellular proliferation, invasion and migration but induced apoptosis. Besides, SH3PXD2A-AS1 knockdown also suppressed the growth of CRC tumors. Furthermore, SH3PXD2A-AS1 could function as a ceRNA of miR-330-5p. Additionally, UBA2 was proved to be a target gene of miR-330-5p. Moreover, SH3PXD2A-AS1 knockdown downregulated UBA2 expression through sponging miR-330-5p to inactivate the Wnt/β-catenin signaling pathway, thereby inhibiting the cell growth and promoting apoptosis. Therefore, the SH3PXD2A-AS1/miR-330-5p/UBA2 network could regulate the progression of CRC through the Wnt/β-catenin pathway. These findings offer new sights for understanding the pathogenesis of CRC and provide potential biomarkers for CRC treatment.	NA	Environ Toxicol. 2020 Oct 19. doi: 10.1002/tox.23038.
4463	Circular RNA	SIPA1L1	miR-204-5p	ALPL	stem cells from apical papilla (SCAPs)	Osteogenic Differentiation	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;Flow cytometry assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33138854	Circular RNA SIPA1L1 regulates osteoblastic differentiation of stem cells from apical papilla via miR-204-5p/ALPL pathway.	BACKGROUND: Osteogenesis is a complex biological process which requires the coordination of multiple molecular mechanisms. This research aimed to explore the biological role and underlying regulatory mechanism of circSIPA1L1 during the osteogenic differentiation of stem cells from apical papilla (SCAPs). METHODS: EdU retention assay, flow cytometry assay, and CCK-8 assay were used to evaluate the proliferation capacity of SCAPs. Western blot assay, alkaline phosphatase (ALP), and alizarin red staining (ARS) were conducted to investigate the biological roles of circSIPA1L1 and miR-204-5p. Fluorescence in situ hybridization was applied for circSIPA1L1 localization. Dual-luciferase reporter assay was performed to prove the interaction of circSIPA1L1 and miR-204-5p. RESULTS: CircSIPA1L1 had no significant effect on the proliferative capacity of SCAPs. CircSIPA1L1 promotes osteogenic differentiation of SCAPs by serving as a miRNA sponge for miR-204-5p. Either knockdown of circSIPA1L1 or overexpression of miR-204-5p significantly suppresses osteogenic differentiation of SCAPs. CONCLUSIONS: CircSIPA1L1 upregulates ALPL through targeting miR-204-5p and promotes the osteogenic differentiation of SCAPs.	NA	Stem Cell Res Ther. 2020 Nov 2;11(1):461. doi: 10.1186/s13287-020-01970-7.
4464	LncRNA	SLC16A1-AS1	miR-149	NA	GBM cells	Glioblastoma	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;	33603467	LncRNA SLC16A1-AS1 is Upregulated in Glioblastoma and Promotes Cancer Cell Proliferation by Regulating miR-149 Methylation.	INTRODUCTION: LncRNA SLC16A1-AS1 has been characterized as a critical player in lung cancer, while its role in glioblastoma (GBM) is unknown. By analyzing the TCGA dataset, we observed the upregulation of SLC16A1-AS1 expression in GBM. Therefore, we aimed to investigate the role of SLC16A1-AS1 in this cancer. METHODS: GBM tissues and paired non-tumor tissues were collected from 62 GBM patients through biopsy. RT-qPCR was performed to determine the expression of SLC16A1-AS1 and miR-149. Linear regression was used to analyze their correlations. The relationship between SLC16A1-AS1 and miR-149 was assessed by gain and loss of function experiments. Methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP) were performed to analyze the methylation status of miR-149. Cell proliferation was evaluated by CCK-8 assay and colony formation experiments in GBM cells. RESULTS: We found that SLC16A1-AS1 expression was upregulated in GBM tissues, and the upregulated expression of SLC16A1-AS1 predicted poor survival of GBM patients. MiR-149 was downregulated in GBM tissues and inversely correlated with the expression of SLC16A1-AS1. In GBM cells, overexpression of SLC16A1-AS1 downregulated the expression of miR-149 and increased the methylation of miR-149 gene. In cell proliferation and colony formation assay, overexpression of SLC16A1-AS1 reduced the inhibitory effects of miR-149 on GBM cell proliferation. CONCLUSION: SLC16A1-AS1 may promote GBM cell proliferation by regulating miR-149 methylation. SLC16A1-AS1 can be considered as a potential diagnostic marker in GBM.	NA	Cancer Manag Res. 2021 Feb 10;13:1215-1223. doi: 10.2147/CMAR.S264613. eCollection 2021.
4465	LncRNA	SNHG1	miR-195	Cdc42	EC cells	Oesophageal Cancer	Homo sapiens (human)	qRT-PCR	33171523	Downregulation of the long noncoding RNA SNHG1 inhibits tumor cell migration and invasion by sponging miR-195 through targeting Cdc42 in oesophageal cancer.	Despite the poor prognosis of oesophageal cancer (EC), the molecular mechanisms of EC are still unclear. In recent years, role of lncRNA in cancer development attracted much attention. The present study aimed to investigate the effects of the long noncoding RNA SNHG1 on the migration and invasion of EC cells and the possible mechanisms involved. The effects of SNHG1 on cell proliferation, migration, and invasion were determined and its relationship with miR-195/Cdc42 axis was investigated. It was found SNHG1 and Cdc42 were significantly upregulated, and miR-195 was significantly downregulated in both EC tissues and cell lines. In addition, the inhibition of either SNHG1 or Cdc42 resulted in suppression of cell proliferation, migration, and invasion, while inhibition of miR-195 led to opposite results and reversed the effects of si-SNHG1. We also observed that higher SNHG1 predicted poorer prognosis of EC patients. In summary, inhibition of SNHG1 can suppress the cell migration and invasion of EC cells by sponging miR-195 through targeting Cdc42. This study might provide deeper insights into the SNHG1/miR-195/Cdc42 axis in EC.	NA	Kaohsiung J Med Sci. 2021 Mar;37(3):181-191. doi: 10.1002/kjm2.12318. Epub 2020 Nov 10.
4466	LncRNA	SNHG1	miR-320b	IFNGR1	ligament fibroblastic cells	Ossification Of Posterior Longitudinal Ligament	Homo sapiens (human)	microarray;	33017569	Promoting effect of long non-coding RNA SNHG1 on osteogenic differentiation of fibroblastic cells from the posterior longitudinal ligament by the microRNA-320b/IFNGR1 network.	Long non-coding RNAs (lncRNAs) have been noted to influence the progression of ossification of posterior longitudinal ligament (OPLL). The work aims to probe the effect of lncRNA SNHG1 on osteogenic differentiation of ligament fibroblastic cells (LFCs). Aberrantly expressed lncRNAs in ossified PLL tissues were screened out by microarray analysis. Gain- and loss-of function experiments of SNHG1 were performed to identify its role in osteogenic differentiation of LFCs. The downstream molecules of SNHG1 were explored. Altered expression of miR-320b was introduced in LFCs as well. The interactions among SNHG1, miR-320b and IFNGR1 were identified. Consequently, SNHG1 was found highly expressed in OPLL patients. Silencing of SNHG1 inhibited BMP-2, RUNX2 and OCN expression and the ALP activity and reduced osteogenic differentiation of LFCs. Importantly, SNHG1 could and upregulate IFNGR1 through serving as a sponge for miR-320b. Over-expression of miR-320b inhibited osteogenic differentiation of LFCs and inactivated the JAK/STAT signaling pathway. Further administration of Fedratinib, a JAK2-specific agonist, increased osteogenic differentiation of LFCs. To conclude, the study suggested that SNHG1 could upregulate IFNGR1 by sequestering miR-320b and activate the JAK/STAT signaling. Silencing of SNHG1 could reduce the osteogenic differentiation and mineralization of LFCs. The study may offer new insights into OPLL treatment.	NA	Cell Cycle. 2020 Nov;19(21):2836-2850. doi: 10.1080/15384101.2020.1827188. Epub 2020 Oct 5.
4467	LncRNA	SNHG1	miR-154-5p	TLR5	SH-SY5Y cells	Epilepsy	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33096314	SP1 activated-lncRNA SNHG1 mediates the development of epilepsy via miR-154-5p/TLR5 axis.	BACKGROUND: Epilepsy is a one of the most frequent serious neurological disorders characterized by enduring and unprovoked seizures. The treatments to epilepsy are very limited and many patients are even resistant to current medications due to the elusive pathogenesis. Here, we sought to investigate the functions of lncRNA SNHG1 and miR-154-5p in epilepsy. METHODS: We employed both in vivo mouse model and in vitro cell model to study epilepsy. H&E staining and Nissl staining were used to examine the morphology of hippocampus and measure neuronal injury, respectively. TUNEL staining and flow cytometry were performed to determine cell apoptosis. Caspase-3 activity assay kit was used to assess caspase-3 activity. RT-qPCR and western blot were conducted to measure the levels of SNHG1, miR-154-5p, TLR5, and SP1, respectively. Dual luciferase reporter assay was employed to validate the binding relationship of SNHG1/miR-154-5p and miR-154-5p/TLR5. ChIP assay was performed to confirm the transcriptional regulation of SP1 on SNHG1. RESULTS: Elevated SNHG1 and decreased miR-154-5p were observed in both in vivo mouse model and in vitro cell model of epilepsy. Knockdown of SNHG1 or transfection with miR-154-5p mimics significantly ameliorated Mg(2+) free-induced neuronal injury in SH-SY5Y cells. SNHG1 acted as a sponge of miR-154-5p. Moreover, SNHG1 promoted neuronal injury via acting as a miR-154-5p sponge to disinhibit TLR5. Additionally, SP1 activated the transcriptional activity of SNHG1. CONCLUSION: In summary, SP1 transcriptionally activated-SNHG1 contributes to the development of epilepsy via directly regulating miR-154-5p/TLR5 axis, which provides novel targets in treatment of epilepsy.	NA	Epilepsy Res. 2020 Dec;168:106476. doi: 10.1016/j.eplepsyres.2020.106476. Epub 2020 Sep 25.
4468	LncRNA	SNHG1	miR-154-5p	TLR5	SH-SY5Y cells	Epilepsy	Mus musculus (mouse)	ChIP;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33096314	SP1 activated-lncRNA SNHG1 mediates the development of epilepsy via miR-154-5p/TLR5 axis.	BACKGROUND: Epilepsy is a one of the most frequent serious neurological disorders characterized by enduring and unprovoked seizures. The treatments to epilepsy are very limited and many patients are even resistant to current medications due to the elusive pathogenesis. Here, we sought to investigate the functions of lncRNA SNHG1 and miR-154-5p in epilepsy. METHODS: We employed both in vivo mouse model and in vitro cell model to study epilepsy. H&E staining and Nissl staining were used to examine the morphology of hippocampus and measure neuronal injury, respectively. TUNEL staining and flow cytometry were performed to determine cell apoptosis. Caspase-3 activity assay kit was used to assess caspase-3 activity. RT-qPCR and western blot were conducted to measure the levels of SNHG1, miR-154-5p, TLR5, and SP1, respectively. Dual luciferase reporter assay was employed to validate the binding relationship of SNHG1/miR-154-5p and miR-154-5p/TLR5. ChIP assay was performed to confirm the transcriptional regulation of SP1 on SNHG1. RESULTS: Elevated SNHG1 and decreased miR-154-5p were observed in both in vivo mouse model and in vitro cell model of epilepsy. Knockdown of SNHG1 or transfection with miR-154-5p mimics significantly ameliorated Mg(2+) free-induced neuronal injury in SH-SY5Y cells. SNHG1 acted as a sponge of miR-154-5p. Moreover, SNHG1 promoted neuronal injury via acting as a miR-154-5p sponge to disinhibit TLR5. Additionally, SP1 activated the transcriptional activity of SNHG1. CONCLUSION: In summary, SP1 transcriptionally activated-SNHG1 contributes to the development of epilepsy via directly regulating miR-154-5p/TLR5 axis, which provides novel targets in treatment of epilepsy.	NA	Epilepsy Res. 2020 Dec;168:106476. doi: 10.1016/j.eplepsyres.2020.106476. Epub 2020 Sep 25.
4469	LncRNA	SNHG1	miR-140-5p	CDK4	HCC tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	RNA immunoprecipitation;Chromatin immunoprecipitation;luciferase assay;RNA immunoprecipitation;	33009370	Epigenetic silencing of CDKN1A and CDKN2B by SNHG1 promotes the cell cycle, migration and epithelial-mesenchymal transition progression of hepatocellular carcinoma.	Enhanced SNHG1 (small nucleolar RNA host gene 1) expression has been found to play a critical role in the initiation and progression of hepatocellular carcinoma (HCC) with its detailed mechanism largely unknown. In this study, we show that SNHG1 promotes the HCC progression through epigenetically silencing CDKN1A and CDKN2B in the nucleus, and competing with CDK4 mRNA for binding miR-140-5p in the cytoplasm. Using bioinformatics analyses, we found hepatocarcinogenesis is particularly associated with dysregulated expression of SNHG1 and activation of the cell cycle pathway. SNHG1 was upregulated in HCC tissues and cells, and its knockdown significantly inhibited HCC cell cycle, growth, metastasis, and epithelial-mesenchymal transition (EMT) both in vitro and in vivo. Chromatin immunoprecipitation and RNA immunoprecipitation assays demonstrate that SNHG1 inhibit the transcription of CDKN1A and CDKN2B through enhancing EZH2 mediated-H3K27me3 in the promoter of CDKN1A and CDKN2B, thus resulting in the de-repression of the cell cycle. Dual-luciferase assay and RNA pulldown revealed that SNHG1 promotes the expression of CDK4 by competitively binding to miR-140-5p. In conclusion, we propose that SNHG1 formed a regulatory network to confer an oncogenic function in HCC and SNHG1 may serve as a potential target for HCC diagnosis and treatment.	NA	Cell Death Dis. 2020 Oct 2;11(10):823. doi: 10.1038/s41419-020-03031-6.
4470	LncRNA	SNHG10	miR-532-3p	FBXL19	glioma cells	Glioma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;	33298070	ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p/FBXL19 axis.	BACKGROUND: In past few years, long non-coding RNAs (lncRNAs) have been reported to play regulatory roles during cancer progression. LncRNA SNHG10 has been explored in several sorts of cancers. However, its detailed role and mechanism are still not well understood in glioma. METHODS: Expression levels of genes were evaluated by RT-qPCR. EdU, TUNEL, sphere formation, wound healing and transwell assays appraised the effect of SNHG10 on glioma cellular processes. The interaction between molecules was examined by ChIP, RIP, RNA pull down and luciferase reporter assays. RESULTS: High level of SNHG10 was detected in glioma cells. Functional assay confirmed that SNHG10 promoted the proliferation, migration, invasion and stemness of glioma cells. Moreover, miR-532-3p was validated to bind with SNHG10 and expressed at a low level in glioma cells. Importantly, miR-532-3p exerted inhibitory functions in glioma. Furthermore, it was found that FBXL19 targeted by miR-532-3p facilitated cell growth and stemness in glioma, and that SNHG10 worked in glioma by increasing FBXL19 expression through sequestering miR-532-3p. More importantly, ETS1 promoted the transcription of SNHG10 and it mediated contribution to the malignant behaviors of glioma cells by SNHG10/miR-532-3p/FBXL19 signaling. CONCLUSION: SNHG10 was transcriptionally activated by ETS1 and played an oncogenic role in glioma by sponging miR-532-3p and up-regulating FBXL19.	NA	Cancer Cell Int. 2020 Dec 9;20(1):589. doi: 10.1186/s12935-020-01649-2.
4471	LncRNA	SNHG10	miR-182-5p	FZD3	OS cells	Osteosarcoma	Homo sapiens (human)	FISH;RIP assay;RNA immunoprecipitation;FISH;Luciferase reporter assay;RNA immunoprecipitation;	33251045	lncRNA SNHG10 Promotes the Proliferation and Invasion of Osteosarcoma via Wnt/β-Catenin Signaling.	Uncontrolled growth and an enforced epithelial-mesenchymal transition (EMT) process contribute to the poor survival rate of patients with osteosarcoma (OS). Long noncoding RNAs (lncRNAs) have been reported to be involved in the development of OS. However, the significant role of lncRNA SNHG1O on regulating proliferation and the EMT process of OS cells remains unclear. In this study, quantitative real-time PCR and fluorescence in situ hybridization (FISH) results suggested that SNHG10 levels were significantly increased in OS compared with healthy tissues. In vitro experiments (including colony formation, CCK-8, wound healing, and transwell assays) and in vivo experiments indicated that downregulation of SNHG10 significantly suppressed the proliferation and invasion of OS cells. Luciferase reporter assay and RNA immunoprecipitation (RIP) assay confirmed that SNHG10 could regulate FZD3 levels through sponging microRNA 182-5p (miR-182-5p). In addition, the SNHG10/miR-182-5p/FZD3 axis could further promote the β-catenin transfer into nuclear accumulation to maintain the activation of the Wnt singling pathway. Together, our results established that SNHG10 has an important role in promoting OS growth and invasion. By sponging miR-182-5p, SNHG10 can increase FZD3 expression and further maintain the activation of Wnt/β-catenin singling pathway in OS cells.	NA	Mol Ther Nucleic Acids. 2020 Oct 15;22:957-970. doi: 10.1016/j.omtn.2020.10.010. eCollection 2020 Dec 4.
4472	LncRNA	SNHG10	miR-21	NA	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;	33081752	LncRNA SNHG10 is downregulated in non-small cell lung cancer and predicts poor survival.	BACKGROUND: LncRNA SNHG10 has been reported to be an oncogenic lncRNA in liver cancer. However, its roles in non-small cell lung cancer (NSCLC) remains unknown. METHODS: Tumor and paired non-tumor tissues were harvested from 62 NSCLC patients. RT-qPCR was used to detect the expression of SNHG10 and miR-21 in tissues. Overexpression experiments were used to evaluate the interaction between SNHG10 and miR-21 in NSCLC cells. CCK-8 assay was used to detect the cell proliferation. RESULTS: We observed the expression of SNHG10 was down-regulated in non-small cell lung cancer (NSCLC) compared with that in non-tumor tissues. Moreover, we found that high expression levels of SNHG10 predicted favorable survival of NSCLC patients, and the expression of miR-21 were increased in NSCLC and inversely correlated with SNHG10 expression. In NSCLC cells, overexpression of SNHG10 resulted in increased miR-21 gene methylation and decreased miR-21 expression. Moreover, overexpression of SNHG10 attenuated the enhancing effect of miR-21 overexpression on cell proliferation. CONCLUSIONS: SNHG10 may involve in NSCLC cell proliferation by regulating the miR-21 gene methylation.	NA	BMC Pulm Med. 2020 Oct 20;20(1):273. doi: 10.1186/s12890-020-01281-w.
4473	LncRNA	SNHG11	miR-483-3p	CTNNB1	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33068778	lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.	Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNHG11. SNHG11 induced GSK-3β ubiquitination through interacting with Cullin 4A (CUL4A) to further activate the Wnt/β-catenin pathway. Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/β-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. Finally, SNHG11 upregulation in GC cells was shown to be transcriptionally induced by TCF7L2. In conclusion, we reveal that SNHG11 is an onco-lncRNA in GC and might be a promising prognostic and therapeutic target for GC.	NA	Mol Ther. 2021 Mar 3;29(3):1258-1278. doi: 10.1016/j.ymthe.2020.10.011. Epub 2020 Oct 15.
4474	LncRNA	SNHG11	miR-1276	CTNNB1	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33068778	lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.	Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNHG11. SNHG11 induced GSK-3β ubiquitination through interacting with Cullin 4A (CUL4A) to further activate the Wnt/β-catenin pathway. Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/β-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. Finally, SNHG11 upregulation in GC cells was shown to be transcriptionally induced by TCF7L2. In conclusion, we reveal that SNHG11 is an onco-lncRNA in GC and might be a promising prognostic and therapeutic target for GC.	NA	Mol Ther. 2021 Mar 3;29(3):1258-1278. doi: 10.1016/j.ymthe.2020.10.011. Epub 2020 Oct 15.
4475	LncRNA	SNHG11	miR-483-3p	ATG12	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33068778	lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.	Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNHG11. SNHG11 induced GSK-3β ubiquitination through interacting with Cullin 4A (CUL4A) to further activate the Wnt/β-catenin pathway. Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/β-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. Finally, SNHG11 upregulation in GC cells was shown to be transcriptionally induced by TCF7L2. In conclusion, we reveal that SNHG11 is an onco-lncRNA in GC and might be a promising prognostic and therapeutic target for GC.	NA	Mol Ther. 2021 Mar 3;29(3):1258-1278. doi: 10.1016/j.ymthe.2020.10.011. Epub 2020 Oct 15.
4476	LncRNA	SNHG11	miR-1276	ATG12	GC cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33068778	lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt/β-Catenin Pathway and Oncogenic Autophagy.	Long non-coding RNAs (lncRNAs) are under active investigation in the development of cancers, including gastric cancer (GC). Oncogenic autophagy is required for cancer cell survival. The present study aimed to investigate the regulatory role of lncRNA small nucleolar host gene 11 (SNHG11) in GC. We show that SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. Functionally, SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC. Mechanistically, SNHG11 post-transcriptionally upregulated catenin beta 1 (CTNNB1) and autophagy related 12 (ATG12) through miR-483-3p/miR-1276, while the processing of precursor (pre-)miR-483/pre-miR-1276 was hindered by SNHG11. SNHG11 induced GSK-3β ubiquitination through interacting with Cullin 4A (CUL4A) to further activate the Wnt/β-catenin pathway. Intriguingly, SNHG11 regulated autophagy in a manner dependent on ATG12 rather than the Wnt/β-catenin pathway, whereas SNHG11 contributed to the malignant behaviors of GC cells via both pathways. Finally, SNHG11 upregulation in GC cells was shown to be transcriptionally induced by TCF7L2. In conclusion, we reveal that SNHG11 is an onco-lncRNA in GC and might be a promising prognostic and therapeutic target for GC.	NA	Mol Ther. 2021 Mar 3;29(3):1258-1278. doi: 10.1016/j.ymthe.2020.10.011. Epub 2020 Oct 15.
4477	LncRNA	SNHG12	miR-148a	CDK1	CC cells	Cervical Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33292254	LncRNA SNHG12 regulates the radiosensitivity of cervical cancer through the miR-148a/CDK1 pathway.	BACKGROUND: Radiation resistance is a major obstacle to the prognosis of cervical cancer (CC) patients. Many studies have confirmed that long non-coding RNAs (lncRNAs) are involved in the regulation of radiosensitivity of cancers. However, whether small nucleolar RNA host gene 12 (SNHG12) regulates the radiosensitivity of CC remains unknown. METHODS: Quantitative real-time polymerase chain reaction was used to measure the expression levels of SNHG12 and microRNA-148a (miR-148a). The radiosensitivity of cells was evaluated by clonogenic assay. Flow cytometry and caspase-3 activity assay were performed to assess the apoptosis ability and cell cycle distribution of cells. Besides, dual-luciferase reporter and RNA immunoprecipitation assay were used to verify the interaction between miR-148a and SNHG12 or cyclin-dependent kinase 1 (CDK1). Also, the protein levels of CDK1, CCND1 and γ-H2AX were detected by western blot analysis. Furthermore, in vivo experiments were conducted to verify the effect of SNHG12 on CC tumor growth. Ki-67 and TUNEL staining were employed to evaluate the proliferation and apoptosis rates in vivo. The hematoxylin and eosin (HE) staining were employed to evaluate the tumor cell morphology. RESULTS: SNHG12 was upregulated in CC tissues and cells, and its knockdown improved the radiosensitivity by promoting the radiation-induced apoptosis and cell cycle arrest of CC cells. Also, miR-148a could be sponged by SNHG12 and could target CDK1. MiR-148a inhibitor or CDK1 overexpression could invert the promotion effect of silenced-SNHG12 on CC radiosensitivity. Meanwhile, SNHG12 interference reduced the tumor growth of CC, increased miR-148a expression, and inhibited CDK1 level in vivo. CONCLUSION: LncRNA SNHG12 promoted CDK1 expression to regulate the sensitivity of CC cells to radiation through sponging miR-148a, indicating that SNHG12 could be used as a potential biomarker to treat the radiotherapy resistance of CC patients.	NA	Cancer Cell Int. 2020 Dec 1;20(1):554. doi: 10.1186/s12935-020-01654-5.
4478	LncRNA	SNHG14	miR-330-5p	NA	HTR-8/SVneo cells	Preeclampsia	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;	33161910	lncRNA SNHG14 involved in trophoblast cell proliferation, migration, invasion and epithelial-mesenchymal transition by targeting miR-330-5p in preeclampsia.	Preeclampsia (PE), a pregnancy-specific disease, has become one of the leading causes of maternal and neonatal morbidity and mortality. Pathogenesis of PE has still not been fully addressed and there is a great need to develop early diagnosis markers and effective therapy. This study aimed to determine if lncRNA SNHG14 has a protective effect on placental trophoblast and prevents PE. SNHG14 levels in the peripheral blood from patients with PE or from women with healthy pregnancies were detected using RT-qPCR. The relationship between SNHG14 and miR-330-5p was determined using a dual-luciferase reporter assay. In addition, cell proliferation and cell cycle were evaluated by performing CCK8 assays and flow-cytometric analysis, respectively. Wound-healing and transwell assays were performed to assess cell migration and invasion ability. lncRNA SNHG14 was downregulated in PE patients; it was involved in trophoblast proliferation and regulated cell proliferation during G1/S transition. In addition, lncRNA SNHG14 promoted migration, invasion and epithelial-mesenchymal transition (EMT) in HTR-8/SVneo cells. Luciferase reporter assay indicated that lncRNA SNHG14 served as a molecular sponge for miR-330-5p and negatively regulated miR-330-5p expression in PE. Furthermore, the effects of silenced SNHG14 on trophoblast proliferation, migration, invasion and EMT were reversed by addition of miR-330-5p inhibitor, suggesting that in PE lncRNA SNHG14 functions by competitively binding to miR-330-5p. Taken together, the current study demonstrated that in PE lncRNA SNHG14 is a vital regulator by binding to miR-330-5p. SNHG14 might serve as a therapeutic application in PE progression.	NA	Zygote. 2021 Apr;29(2):108-117. doi: 10.1017/S0967199420000507. Epub 2020 Nov 9.
4479	LncRNA	SNHG14	miR-613	NA	LUAD cellss	Lung Cancer	Homo sapiens (human)	qRT-PCR	33155262	Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613.	Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA SNHG14 exerts oncogenic functions in lung adenocarcinoma through acting as a sponge to miR-613, by Z.-N. Xu, Z.-X. Wang, L. Xu, H.-X. Yu, K. Chao, L.-L. Yang, X.-L. Han, H.-B. Sun, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10810-10817-DOI: 10.26355/eurrev_201912_19784-PMID: 31858549" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19784.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10304. doi: 10.26355/eurrev_202010_23357.
4480	LncRNA	SNHG14	miR-655-3p	NA	EC tissues and cells	Endometrial Cancer	Homo sapiens (human)	qPCR;qRT-PCR;	33155197	LncRNA SNHG14 promotes proliferation of endometrial cancer through regulating microRNA-655-3p.	OBJECTIVE: Previous studies have shown that long non-coding RNA (lncRNA) SNHG14 can act as a cancer-promoting gene, but the role of SNHG14 in the development of endometrial carcinoma (EC) has not been reported. This study was designed to investigate the expression characteristics of SNHG14 in EC tissues and cells and to specify whether SNHG14 promotes the malignant progression of EC by modulating microRNA-655-3P. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qPCR) was carried out to examine SNHG14 expression in tumor tissue specimens and paracancerous tissue specimens collected from 52 patients with EC, and the relationship between SNHG14 expression and clinical indicators or prognosis of these subjects was analyzed as well. Further, the expression level of SNHG14 in EC cell lines was also verified by qRT-PCR. In addition, SNHG14 knockdown and the overexpression models were constructed using lentivirus in EC cell lines, Ishikawa, and KLE, and the influence of SNHG14 on EC cell biological functions was evaluated by Cell Counting Kit-8 (CCK-8), plate cloning, 5-ethynyl-2'-deoxyuridine (EdU) and flow apoptosis assays. Finally, in vitro recovery experiments were conducted to explore the mechanism by which SNHG14 interacts with microRNA-655-3P to exert its effect on the progression of EC. RESULTS: qPCR results indicated that SHHG14 expression in EC tumor tissues was remarkably higher than that in adjacent tissues. Compared with patients with low expression of SNHG14, patients with high expression of SNHG14 had larger tumor size, lower overall survival, and more advanced pathological stage. In vitro, compared with those in the control group, the overexpression of SNHG14 markedly enhanced EC cell proliferation while inhibited cell apoptosis, and the opposite result was observed in SNHG14 silencing group. Subsequently, qRT-PCR verified that microRNA-655-3P expression was significantly reduced in EC tissues and negatively correlated with SNHG14. In addition, recovery experiment revealed a mutual regulation between SNHG14 and microRNA-655-3P, the two of which may together modulate the malignant progression of EC. CONCLUSIONS: EC tumor tissues contain a significantly high expression of LncRNA SNHG14, which has been confirmed to be remarkably associated with tumor size, pathological stage, and poor prognosis of EC patients. Additionally, lncRNA SNHG14 is capable of accelerating malignant progression of EC by regulating microRNA-655-3P expression.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10410-10418. doi: 10.26355/eurrev_202010_23391.
4481	LncRNA	SNHG14	miR-124-3p	TGFBR2	A549 cells	Acute Lung Injury	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33652176	Blocking SNHG14 Antagonizes Lipopolysaccharides-Induced Acute Lung Injury via SNHG14/miR-124-3p Axis.	BACKGROUND: Emerging evidence show that long noncoding RNAs (lncRNAs) are crucial regulators in pathophysiology of acute lung injury (ALI). Small nucleolar RNA host gene 14 (SNHG14) is a novel oncogenic lncRNA, and has been associated with inflammation-related cell injuries. Thus, we wondered the role and mechanism of SNHG14 in lipopolysaccharides (LPS)-induced ALI cell model. METHODS: Expression of SNHG14, miRNA (miR)-124-3p, and transforming growth factor β type 2 receptor (TGFBR2) was detected by RT-qPCR and western blotting. Cell apoptosis was determined by methyl thiazolyl tetrazolium assay, flow cytometry, western blotting, and lactate dehydrogenase activity kit. Inflammation was measured by enzyme-linked immunosorbent assay. The interaction among SNHG14, miR-124-3p, and TGFBR2 was validated by dual-luciferase reporter assay and RNA immunoprecipitation. RESULTS: LPS administration attenuated human lung epithelial cell viability and B-cell lymphoma-2 expression, but augmented apoptosis rate, cleaved-caspase-3 expression, lactate dehydrogenase activity, and secretions of tumor necrosis factor-α, interleukin-1β, and IL-6 in A549 cells. Thus, LPS induced A549 cells apoptosis and inflammation, wherein SNHG14 was upregulated and miR-124-3p was downregulated. However, silencing SNHG14 could suppress LPS-induced apoptosis and inflammation depending on upregulating miR-124-3p via target binding. Similarly, overexpressing miR-124-3p attenuated LPS-induced A549 cells injury through inhibiting its downstream target TGFBR2. Furthermore, SNHG14 knockdown could also affect TGFBR2 expression via miR-124-3p. CONCLUSIONS: SNHG14 knockdown prevents A549 cells from LPS-induced apoptosis and inflammation through regulating miR-124-3p and TGFBR2, suggesting a novel SNHG14/miR-124-3p/TGFBR2 circuit in alveolar epithelial cells on the set of ALI.	NA	J Surg Res. 2021 Jul;263:140-150. doi: 10.1016/j.jss.2020.10.034. Epub 2021 Feb 27.
4482	LncRNA	SNHG14	miR-193b-3p	MCL1	AML cells	Childhood Acute Myeloid Leukemia	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;	33300066	Long non-coding RNA SNHG14 affects the proliferation and apoptosis of childhood Acute myeloid leukemia cells by modulating the miR-193b-3p/MCL1 axis.	The purpose of the present study was to determine the biological function and associated regulatory mechanism of small nucleolar RNA host gene 14 (SNHG14) in childhood Acute myeloid leukemia (AML). SNHG14 expression was measured via RT-qPCR in bone marrow tissues from 57 patients with AML and 57 healthy donors. The clinicopathological features of AML patients with low and high SNHG14 expression were analysed. AML cell viability and apoptosis were assessed using MTT and flow cytometry analyses. The starBase online database, and RNA-binding protein immunoprecipitation and dual luciferase reporter gene assays were employed to analyse the interactions among SNHG14, microRNA (miR)-193b-3p and MCL1 apoptosis regulator BCL2 family member (MCL1). SNHG14 was found to be overexpressed in the bone marrow tissues of patients with AML. The French-American-British classification and cytogenetics were significantly different between patients with high and low expression of SNHG14. Silencing SNHG14 decreased AML cell proliferation and facilitated apoptosis. SNHG14 functioned as a sponge for miR-193b-3p, and miR-193b-3p decreased the viability and accelerated the apoptosis rate of AML cells. In addition, miR-193b-3p targeted MCL1. Furthermore, silencing SNHG14 resulted in the sponging of miR-193b-3p to regulate cell viability, apoptosis, and MCL1 expression in AML. SNHG14 silencing decreased the viability and promoted apoptosis of AML cells by modulating the miR-193b-3p/MCL1 axis.	NA	Mol Med Rep. 2021 Feb;23(2):90. doi: 10.3892/mmr.2020.11729. Epub 2020 Dec 10.
4483	LncRNA	SNHG14	miR-93-5p	NA	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR	33505213	lncRNA SNHG14 Plays a Role in Sepsis-Induced Acute Kidney Injury by Regulating miR-93.	Acute kidney injury (AKI) is a common organ injury in sepsis, which leads to poor prognosis. Long noncoding RNA (lncRNA) small nucleolus RNA host gene 14 (SNHG14) was recognized to induce cell injury in LPS-induced acute lung injury and Parkinson's disease. We want to investigate the functions and mechanisms of SNHG14 in sepsis-induced AKI. Increased expression of SNHG14 was observed in LPS-induced HK-2 cells, and this was due to the activation of the TLR4/NF-κB pathway. In vitro studies showed that SNHG14 was involved in the oxidative stress, inflammation, and apoptosis of LPS-induced HK-2 cells. Further investigations confirmed that SNHG14 exerted the functions via miR-93 which could regulate the activation of NF-κB and STAT3 signaling by targeting IRAK4 and IL-6R. We also found that silencing SNHG14 also alleviated cellular injury processes of IL-1β and IL-6 in HK-2 cells via miR-93. We demonstrate that SNHG14 accelerates cellular injury in sepsis-induced AKI by activating IRAK4/NF-κB and IL-6R/STAT3 signaling via miR-93.	NA	Mediators Inflamm. 2021 Jan 6;2021:5318369. doi: 10.1155/2021/5318369. eCollection 2021.
4484	LncRNA	SNHG15	miR-188-5p	PTEN	cardiomyocyte	Cure Myocardial Infarction	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32970504	Long non-coding RNA SNHG15 regulates cardiomyocyte apoptosis after hypoxia/reperfusion injury via modulating miR-188-5p/PTEN axis.	Nowadays the most effective way to cure myocardial infarction (MI) is reperfusion, which inevitably leads to cardiomyocyte apoptosis. In this study, we discussed the functions of SNHG15 in regulating cardiomyocyte apoptosis through the modulation of miR-188-5p/PTEN axis. We examined the links between SNHG15 and miR-188-5p/PTEN in mice with MI. Extensive experiments, measurements and comparisons were performed, including RT-PCR, western blotting, luciferase reporter assay, flow cytometry analysis etc. Through a series of comparisons and analysis, we discovered that SNHG15 could interact with the miR-188-5p/PTEN axis and impact the cellular physiology of cardiomyocyte apoptosis. PTEN was upregulated in hypoxia cells, but this effect was attenuated by miR-188-5p. MiR-188-5p could combine with SNHG15 and PTEN, and form a SNHG15-miR-188-5p-PTEN axis, which regulated the apoptosis of MCs. These results suggest that LncRNA SNHG15 regulates cardiomyocyte apoptosis induced by hypoxia or reperfusion injury through modulating of miR-188-5p/PTEN axis.	NA	Arch Physiol Biochem. 2020 Sep 24:1-8. doi: 10.1080/13813455.2020.1819336.
4485	LncRNA	SNHG16	miR-15b-5p	PRPS1	neuroblastoma tissues and cells	Neuroblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33105440	SNHG16 knockdown inhibits tumorigenicity of neuroblastoma in children via miR-15b-5p/PRPS1 axis.	Neuroblastoma is an important problem in children. Long noncoding RNAs (lncRNAs) exhibit important roles in tumorigenicity of neuroblastoma. However, the role and mechanism of lncRNA small nucleolar RNA host gene 16 (SNHG16) in neuroblastoma tumorigenicity remain poorly understood. Forty-six neuroblastoma samples and 28 normal tissues were harvested. The levels of SNHG16, microRNA-15b-5p (miR-15b-5p), and phosphoribosyl pyrophosphate synthetase 1 (PRPS1) were detected via quantitative reverse transcription PCR or western blot. Cell proliferation as well as cycle distribution were measured via 3-(4, 5-Dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide or flow cytometry. Cell metastasis was investigated via epithelial-mesenchymal transition or transwell assay. The target relationship of miR-15b-5p and SNHG16 or PRPS1 was explored via starBase and dual-luciferase reporter assay. The role of SNHG16 in neuroblastoma in vivo was analyzed using a xenograft model. We found SNHG16 and PRPS1 levels were increased in neuroblastoma tissues and cells. SNHG16 knockdown inhibited cell proliferation, increased the cell cycle distribution at G0/G1 phase, and decreased the cells at S phase. SNHG16 overexpression caused an opposite effect. SNHG16 silence suppressed neuroblastoma cell metastasis. PRPS1 knockdown constrained cell proliferation and metastasis and regulated cell cycle distribution. miR-15b-5p was sponged by SNHG16 and directly targeted PRPS1. miR-15b-5p knockdown or PRPS1 overexpression mitigated the influence of SNHG16 silence on cell cycle, proliferation, and metastasis. SNHG16 knockdown reduced xenograft tumor growth. In conclusion, SNHG16 downregulation suppressed neuroblastoma tumorigenicity by regulating cell cycle, proliferation, and metastasis via miR-15b-5p/PRPS1 axis.	NA	Neuroreport. 2020 Dec 9;31(17):1225-1235. doi: 10.1097/WNR.0000000000001537.
4486	LncRNA	SNHG16	miR-520	VEGF	lung cancer cells	Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33015794	LncRNA SNHG16 drives proliferation, migration, and invasion of lung cancer cell through modulation of miR-520/VEGF axis.	OBJECTIVE: Long non-coding RNAs (lncRNAs) have been shown to have important effects on various biological behavior of human diseases. Although increasing lncRNAs have been explored in human cancers, there are still countless lncRNA to be mined. The purpose of this study was to investigate the effect of lncRNA SNHG16 on the proliferation and metastasis of lung cancer cells. PATIENTS AND METHODS: RT-qPCR was used to analyze the expression patterns of SNHG16, miR-520 and VEGF. MTT and transwell methods were used to detect the effect of SNHG16 on cell migration. The association between SNHG16, miR-520 and VEGF was analyzed by bioinformatics analysis and Dual-Luciferase verification reporter analysis. Finally, lung cancer cells have demonstrated the role of SNHG16-miR-520-VEGF in the cell biological behavior axis. RESULTS: Compared with normal cells, SNHG16 is highly expressed in lung cancer cells. Silent SNHG16 has a negative effect on the migration of lung cancer cells. CONCLUSIONS: LncRNA SNHG16 as ceRNA up-regulates VEGF in lung cancer cells by binding to miR-520. LncRNA SNHG16 as ceRNA promotes the migration of lung cancer cells by regulating the miR-520/VEGF axis.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9522-9531. doi: 10.26355/eurrev_202009_23037.
4487	LncRNA	SNHG17	miR-23a-3p	CXCL12	CRA cells	Colorectal Adenocarcinoma	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;	33292246	SNHG17 promotes the proliferation and migration of colorectal adenocarcinoma cells by modulating CXCL12-mediated angiogenesis.	BACKGROUND: Colorectal adenocarcinoma (CRA) is one of the leading causes of cancer-related deaths in the world. Long non-coding RNAs (lncRNAs) have been implicated to be effective regulators in the disease course of human cancers, including CRA. Small nucleolar RNA host gene 17 (SNHG17) belongs to lncRNAs, and it has been reported in breast cancer and gastric cancer. However, the function of SNHG17 and its mechanism in CRA progression remain largely unknown. In this study, we attended to shedding some light on the role of SNHG17 in CRA. METHODS: RT-qPCR was used to assess SNHG17 expression in CRA cells. CCK-8 assay, colony formation and transwell assay were carried out to detect the regulatory effect of SNHG17 silencing on CRA cell proliferation and migration. The angiogenesis of SNHG7-downregulated CRA cells was analyzed by tube formation assay. Mechanism experiments were conducted to identify the interaction between miR-23a-3p and SNHG17 or C-X-C motif chemokine ligand 12 (CXCL12). RESULTS: SNHG17 possessed with high expression in CRA cells. Knockdown of SNHG17 caused the inhibition on CRA cell proliferation and migration. SNHG17 promoted CRA cell proliferation and migration by sponging miR-23a-3p to upregulate CXCL12. CONCLUSION: SNHG17 promotes the proliferation and migration of CRA cells by inhibiting miR-23a-3p to modulate CXCL12-mediated angiogenesis.	NA	Cancer Cell Int. 2020 Nov 26;20(1):566. doi: 10.1186/s12935-020-01621-0.
4488	LncRNA	SNHG17	miR-485-5p	WLS	LUAD cells	Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33109341	SNHG17 upregulates WLS expression to accelerate lung adenocarcinoma progression by sponging miR-485-5p.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been uncovered to be essential regulators in the biological processes of human cancers, including lung adenocarcinoma (LUAD). Recently, small nucleolar RNA host gene 17 (SNHG17) has been identified as one novel oncogenic lncRNA in gastric cancer. However, it remains unclear whether SNHG7 exert functions in LUAD progression. METHODS: The expression levels of SNHG17, miR-485-5p and Wnt ligand secretion mediator (WLS) in LUAD cells was evaluated by RT-qPCR. The effect of SNHG7 silencing on LUAD cell proliferation was assessed by colony formation and EdU assays. The apoptosis of LUAD cells was measured by flow cytometry analysis. Transwell assays were applied to detect cell migration and invasion. The relationship between SNHG17 and miR-485-5p was validated by RIP, RNA pull down and luciferase reporter assays. RESULTS: SNHG17 and WLS were up-regulated in LUAD cell lines. Down-regulation of SNHG17 curbed LUAD cell proliferation, migration and invasion but facilitated apoptosis. SNHG17 acted as miR-485-5p sponge to upregulate WLS expression. CONCLUSION: SNHG17 triggers the progression of LUAD via sponging miR-485-5p to upregulate WLS expression.	NA	Biochem Biophys Res Commun. 2020 Dec 17;533(4):1435-1441. doi: 10.1016/j.bbrc.2020.09.130. Epub 2020 Oct 24.
4489	LncRNA	SNHG17	miR-324-3p	NA	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	32933241	LncRNA SNHG17 acts as a ceRNA of miR-324-3p to contribute the progression of osteosarcoma.	unknown	NA	J Biol Regul Homeost Agents. 2020 Jul-Aug;34(4):1529-1533. doi: 10.23812/20-302-L.
4490	LncRNA	SNHG17	miR-375	PAX6	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32924983	LncRNA SNHG17 promotes the progression of oral squamous cell carcinoma by modulating miR-375/PAX6 axis.	BACKGROUND: The prognosis of patients with recurrent and/or metastatic oral squamous cell carcinoma (OSCC) remains poor, and its incidence is especially high in developing countries. Multiple long non-coding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors. This study aimed to probe into the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) on the progression of OSCC. METHODS: The expression level of SNHG17 in OSCC samples was tested using quantitative real-time polymerase chain reaction (qRT-PCR). Human OSCC cell lines CAL-27 and Tca8113 were used in in vitro studies. Cell counting kit-8 (CCK-8) and BrdU assays were used to assess the effect of SNHG17 on OSCC cell proliferation. Flow cytometry was used to study the effect of SNHG17 on OSCC cell apoptosis. Transwell assay was conducted to detect the effect of SNHG17 on migration and invasion. Moreover, luciferase reporter assay was employed to confirm targeting relationship between miR-375 and SNHG17. Additionally, Western blot was used to observe the regulatory function of SNHG17 on PAX6. RESULTS: SNHG17 expression in OSCC clinical samples was significantly increased and was correlated with unfavorable pathological indexes. Its overexpression remarkably accelerated proliferation and metastasis of OSCC cells, while reduced apoptosis. Accordingly, knockdown of SNHG17 suppressed the malignant phenotypes of OSCC cells. Overexpression of SNHG17 significantly reduced the expression of miR-375 by sponging it, but enhanced the expression of PAX6. CONCLUSION: SNHG17 is a sponge of tumor suppressor miR-375 in OSCC, enhances the expression of PAX6 indirectly, and functions as an oncogenic lncRNA.	NA	Cancer Biomark. 2021;30(1):1-12. doi: 10.3233/CBM-191070.
4491	LncRNA	SNHG20	miR-338-3p	MCL1	OC cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33552251	Long non-coding RNA SNHG20 promotes ovarian cancer development by targeting microRNA-338-3p to regulate MCL1 expression.	Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs) were reported to be associated with the development of ovarian cancer (OC). Increasing evidence demonstrated that lncRNA SNHG20 and miR-338-3p were involved in OC. However, the functional mechanism of lncRNA SNHG20 and miR-338-3p in OC development remains unknown. The expression of SNHG20, miR-338-3p and myeloid cell leukemia 1 (MCL1) was detected by reverse transcription-quantitative PCR. MTT assay, flow cytometry and transwell migration and invasion assays were used to assess cell proliferation, apoptosis, migration and invasion, respectively. The relative protein expression was detected by western blot analysis. The interaction between miR-338-3p and SNHG20 or MCL1 was predicted by starBase v3.0, and subsequently confirmed by dual-luciferase reporter assay. Besides, mouse xenograft assay was carried out to explore the effect of SNHG20 on tumor growth in vivo. The levels of SNHG20 and MCL1 were upregulated, while miR-338-3p level was downregulated in OC tissues and cells. SNHG20 knockdown repressed OC cell proliferation, migration, invasion and epithelial-mesenchymal transition, and induced apoptosis. Interestingly, SNHG20 targeted miR-338-3p to regulate MCL1 expression. miR-338-3p depletion or MCL1 overexpression could reverse the effects of SNHG20 knockdown on OC cells. Besides, SNHG20 knockdown impeded tumor growth in vivo. In conclusion, the present study demonstrated that SNHG20 regulates OC development via modulation of the miR-338-3p/MCL1 axis, providing the theoretical basis for the treatment of OC.	NA	Oncol Lett. 2021 Feb;21(2):130. doi: 10.3892/ol.2020.12391. Epub 2020 Dec 18.
4492	LncRNA	SNHG20	miR-338-3p	MCL1	OC cells	Ovarian Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33552251	Long non-coding RNA SNHG20 promotes ovarian cancer development by targeting microRNA-338-3p to regulate MCL1 expression.	Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs/miRs) were reported to be associated with the development of ovarian cancer (OC). Increasing evidence demonstrated that lncRNA SNHG20 and miR-338-3p were involved in OC. However, the functional mechanism of lncRNA SNHG20 and miR-338-3p in OC development remains unknown. The expression of SNHG20, miR-338-3p and myeloid cell leukemia 1 (MCL1) was detected by reverse transcription-quantitative PCR. MTT assay, flow cytometry and transwell migration and invasion assays were used to assess cell proliferation, apoptosis, migration and invasion, respectively. The relative protein expression was detected by western blot analysis. The interaction between miR-338-3p and SNHG20 or MCL1 was predicted by starBase v3.0, and subsequently confirmed by dual-luciferase reporter assay. Besides, mouse xenograft assay was carried out to explore the effect of SNHG20 on tumor growth in vivo. The levels of SNHG20 and MCL1 were upregulated, while miR-338-3p level was downregulated in OC tissues and cells. SNHG20 knockdown repressed OC cell proliferation, migration, invasion and epithelial-mesenchymal transition, and induced apoptosis. Interestingly, SNHG20 targeted miR-338-3p to regulate MCL1 expression. miR-338-3p depletion or MCL1 overexpression could reverse the effects of SNHG20 knockdown on OC cells. Besides, SNHG20 knockdown impeded tumor growth in vivo. In conclusion, the present study demonstrated that SNHG20 regulates OC development via modulation of the miR-338-3p/MCL1 axis, providing the theoretical basis for the treatment of OC.	NA	Oncol Lett. 2021 Feb;21(2):130. doi: 10.3892/ol.2020.12391. Epub 2020 Dec 18.
4493	LncRNA	SNHG20	miR-495	STAT3	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Luciferase reporter assay;Rescue assay;	33179110	Long non-coding RNA SNHG20 promotes colorectal cancer cell proliferation, migration and invasion via miR-495/STAT3 axis.	Colorectal cancer (CRC) is one of the primary causes of cancer-associated mortality worldwide. However, the potential molecular mechanism of CRC progression remains unknown. Long non-coding RNA small nucleolar RNA host gene 20 (SNHG20) has been demonstrated to be involved in the development and progression of a variety of tumors, including CRC. However, the involvement of SNHG20 in CRC progression remains unclear. The aim of the present study was to investigate the functional role and molecular mechanism of SNHG20 in CRC progression. In the present study, SNHG20 expression was found to be significantly upregulated in CRC tissues and cell lines. Association analysis indicated that high SNHG20 expression was significantly association with greater tumor size (P=0.014), tumor invasion depth (P=0.019), positive lymph node status (P=0.022), distant metastasis (P=0.017) and advanced tumor node metastasis stage (P=0.038). Loss-of-function experiments indicated that SNHG20 knockdown could significantly suppress proliferation, migration and invasion in vitro. Notably, SNHG20 knockdown significantly inhibited tumor growth and lung metastasis in vivo. Bioinformatics analysis and luciferase reporter assays confirmed that microRNA (miR)-495 was a direct target of SNHG20. Rescue assays indicated that miR-495 inhibitor reversed the suppressive effects of SNHG20 knockdown on CRC progression. Moreover, STAT3 was identified as a downstream target of miR-495 in CRC. STAT3 overexpression partially rescued the inhibitory effects of SNHG20 knockdown on CRC progression. Taken together, the results revealed that SNHG20 facilitated CRC progression by regulating STAT3 expression and by sponging miR-495.	NA	Mol Med Rep. 2021 Jan;23(1):31. doi: 10.3892/mmr.2020.11669. Epub 2020 Nov 12.
4494	LncRNA	SNHG20	miR-342	DDX49	A549 cells	Lung Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33089952	LncRNA SNHG20 promoted proliferation, invasion and inhibited cell apoptosis of lung adenocarcinoma via sponging miR-342 and upregulating DDX49.	BACKGROUND: There is increasing evidence that long non-coding RNA (lncRNA) small nucleolar RNA host gene 20 (SNHG20) plays an important role in cancer. However, the function of SNHG20 in lung adenocarcinoma is unclear. The aim of our study was to investigate the roles of SNHG20 in lung adenocarcinoma. METHODS: Real-time quantitative polymerasechain reaction (RT-qPCR) was used to calculate the expression of SNHG20, miR-342 and DEAD-box helicase 49 (DDX49). Dual luciferase reporter gene assay was applied to verify whether miR-342 binding to SNHG20 and DDX49. The expression correlation between miR-342 and SNHG20 or DDX49 was assessed using Pearson's correlation analysis. RESULTS: SNHG20 and DDX49 were overexpressed, while miR-342 was lowly expressed in lung adenocarcinoma tissues and cell lines. Knockdown of SNHG20 suppressed cell proliferation, invasion and enhanced cell apoptosis. SNHG20 was found to directly bind to miR-342 and regulate the expression of miR-342. MiR-342 directly targeted DDX49 and the expression of miR-342 had negative connection with DDX49 in lung adenocarcinoma tissues. Knockdown of DDX49 inhibited the progression of lung adenocarcinoma. DDX49 partially restored the functions of SNHG20 in A549 cells. CONCLUSIONS: SNHG20 regulated lung adenocarcinoma cell proliferation, invasion and promoted cell apoptosis via miR-342/DDX49 axis. Our findings demonstrate that SNHG20/miR-342/DDX49 axis plays an important role in lung adenocarcinoma, providing a novel insight into the treatment of lung adenocarcinoma.	NA	Thorac Cancer. 2020 Dec;11(12):3510-3520. doi: 10.1111/1759-7714.13693. Epub 2020 Oct 22.
4495	LncRNA	SNHG20	miR-520f-3p	NA	CCA tumor cells	Cholangiocarcinoma	Homo sapiens (human)	Luciferase reporter assay;	32907346	Knockdown of lncRNA SNHG20 Suppressed the Proliferation of Cholangiocarcinoma by Sponging miR-520f-3p.	Objective: A large number of studies had found that small nucleolar RNA host gene 20 (SNHG20) was a long noncoding RNA (lncRNA) that played important regulatory functions in numerous tumors. Nevertheless, the expression and pathophysiological role of SNHG20 in cholangiocarcinoma (CCA) are currently unclear. The objective of this study is to reveal the clinical significance and pathophysiological function of SNHG20 in CCA. Methods: The tumor tissues and adjacent normal tissues of CCA were obtained to determine the expression and clinical significance of SNHG20, and the targets of related genes were predicted through bioinformatics analysis. The function and regulatory mechanism of SNHG20 in CCA were evaluated by transfection, CCK-8 experiment, and luciferase reporter assay. Result: In CCA, SNHG20 was highly expressed. Overexpressed SNHG20 was markedly interrelated with the lymph node invasion and TNM stage. In addition, it could be used as indicator to evaluate the prognosis of patients. SNHG20 sponging miR-520f-3p could accelerate the proliferation of CCA tumor cells. MiR-520f-3p acted as a tumor suppressor in CCA and could also serve as a prognostic indicator. Abolition of miR-520f-3p caused an antagonistic effect and diminished the impacts of SNHG20 knockdown. SNHG20 combined with miR-520f-3p could better predict the prognosis of CCA patients. Conclusion: These data confirmed the knockdown SNHG20 expression in CCA could inhibit the proliferation by means of sponging miR-520f-3p.	NA	Cancer Biother Radiopharm. 2020 Sep 9. doi: 10.1089/cbr.2020.4042.
4496	LncRNA	SNHG3	miR-139-5p	Notch1	OVCAR3 cells	Ovarian Cancer	Drosophila (flies)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33552243	lncRNA SNHG3 acts as oncogene in ovarian cancer through miR-139-5p and Notch1.	Ovarian cancer (OC) is a common malignant tumor of the female reproductive system. Long non-coding RNAs (lncRNAs) play an important role in OC occurrence and development. Thus, the function and potential mechanism of lncRNA small nucleolar RNA host gene 3 (SNHG3) was explored in the development of OC. The expression of SNHG3, microRNA (miR)-139-5p and Notch homolog 1, translocation-associated (Drosophila) (Notch1) in OC were detected by RT-qPCR or western blot assay. In addition, CCK-8 and wound-healing assays were used to detect OVCAR3 proliferation and migration ability. The targeting relationship of miR-139-5p with SNHG3 or Notch1 was verified through luciferase reporter assay. Rescue experiments were performed to confirm whether SNHG3 could mediate OVCAR3 proliferation and migration through miR-139-5p and Notch1. In OC tissues and cell lines, the expression of SNHG3 and Notch1 were significantly increased, and the expression of miR-139-5p was significantly decreased. SNHG3 inhibition suppressed the proliferation and migration of OVCAR3 cells. Luciferase reporter experiment confirmed that miR-139-5p could target SNHG3 and Notch1. Transfection of miR-139-5p inhibitor significantly reversed the inhibitory effect of SNHG3 knockdown on OVCAR3 proliferation and migration. Moreover, SNHG3 inhibition or miR-139-5p mimic abolished the promotion of Notch1 overexpression on OVCAR3 proliferation and migration. In conclusion, SNHG3 could accelerate the proliferation and migration of OC cells by regulating miR-139-5p and Notch1.	NA	Oncol Lett. 2021 Feb;21(2):122. doi: 10.3892/ol.2020.12383. Epub 2020 Dec 17.
4497	LncRNA	SNHG3	miR-3619-5p	ARL2	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Chromatin immunoprecipitation;Luciferase reporter assay;	32930970	Long non-coding RNA SNHG3, induced by IL-6/STAT3 transactivation, promotes stem cell-like properties of gastric cancer cells by regulating the miR-3619-5p/ARL2 axis.	BACKGROUND: Chemotherapy is, next to surgery and radiotherapy, the mainstay regimen for the clinical management of gastric cancer. This therapy is, however, heavily compromised by the acquisition of resistance. Here, we aimed to clarify the potential involvement of long non-coding RNA SNGH3 in the acquisition of cisplatin resistance and stemness in gastric cancer. METHODS: Cell viability and proliferation were measured using Cell Counting Kit-8 and colony formation assays, respectively. Stem cell-like cell growth was evaluated using a mammosphere formation assay. RNA levels of SNHG2, OCT-4, SOX-2, CD44, miR-3619-5p and ARL2 were determined using qRT-PCR, whereas protein levels of OCT-4, SOX-2, CD44, ARL2, STAT3 and pSTAT3 were determined using Western blotting. Dual luciferase reporter assays were employed to interrogate regulatory interactions between STAT3, SNHG3, miR-3619-5p and ARL2, respectively. Direct binding of STAT3 to the SNHG3 promoter was investigated using a chromatin immunoprecipitation assay. RESULTS: We found that IL-6 triggered stem cell-like properties in cisplatin-treated gastric cancer cells and activated STAT3, which in turn transcriptionally regulated SNHG3 expression. SNHG3 expression up-regulation positively correlated with cisplatin resistance and stemness of gastric cancer cells, while SNHG3 down-regulation inhibited stem cell-like properties. In addition, we found that SNHG3 up-regulated ARL2 expression through sponging miR-3619-5p, which predominantly mediated the oncogenic properties of SNHG3 in this disease. CONCLUSIONS: Our data indicate an involvement of aberrant SNHG3 over-expression in the acquisition of both cisplatin resistance and stemness of gastric cancer cells, and of the IL-6/STAT3/SNHG3/miR-3619-5p/ARL2 signaling cascade in the oncogenic properties of SNHG3.	NA	Cell Oncol (Dordr). 2021 Feb;44(1):179-192. doi: 10.1007/s13402-020-00560-2. Epub 2020 Sep 15.
4498	LncRNA	SNHG4	miR-204-5p	RUNX2	renal cell carcinoma cells	Renal Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33088220	Long noncoding RNA SNHG4 promotes renal cell carcinoma tumorigenesis and invasion by acting as ceRNA to sponge miR-204-5p and upregulate RUNX2.	BACKGROUND: Long noncoding RNAs (lncRNAs) are involved in the tumorigenesis and progression of human cancers, including renal cell carcinoma (RCC). Small nucleolar RNA host gene 4 (SNHG4) is reported to play an essential role in tumor growth and progression. However, the molecular mechanisms and function of SNHG4 in RCC remain undocumented. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine expression levels of SNHG4 in RCC tissue samples and cell lines. Cell counting kit-8, western blotting, activities of caspase-3, -8, and -9, wound-healing, and transwell invasion assays were performed to explore cell proliferation, apoptosis, migration, and invasion. The interaction among SNHG4, miR-204-5p, and RUNX2 was verified by bioinformatic analysis, a luciferase gene report, qRT-PCR, western blot analysis, and RNA immunoprecipitation assays. Xenograft mouse models were carried out to examine the role of SNHG4 in RCC in vivo. RESULTS: SNHG4 was highly expressed in RCC tissue samples and cell lines, and its upregulation was significantly involved in node involvement, distant metastasis, and reduced overall and relapse-free survival of patients with RCC. SNHG4 acted as an oncogenic lncRNA with promoted RCC cell proliferation, migration, invasion, and inhibited apoptosis. SNHG4 boosted tumor growth in xenograft mouse models. Mechanistically, SNHG4 functioned as a competing endogenous RNA (ceRNA) for sponging miR-204-5p, leading to the upregulation of its target RUNX2 to promote RCC cell proliferation and invasion. CONCLUSION: SNHG4 and miR-204-5p might be indicated in RCC progression via RUNX2, suggesting the potential use of SNHG4/miR-204-5p/RUNX2 axis in RCC treatment.	NA	Cancer Cell Int. 2020 Oct 19;20:514. doi: 10.1186/s12935-020-01606-z. eCollection 2020.
4499	LncRNA	SNHG4	miR-204-5p	RUNX2	renal cell carcinoma cells	Renal Cancer	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33088220	Long noncoding RNA SNHG4 promotes renal cell carcinoma tumorigenesis and invasion by acting as ceRNA to sponge miR-204-5p and upregulate RUNX2.	BACKGROUND: Long noncoding RNAs (lncRNAs) are involved in the tumorigenesis and progression of human cancers, including renal cell carcinoma (RCC). Small nucleolar RNA host gene 4 (SNHG4) is reported to play an essential role in tumor growth and progression. However, the molecular mechanisms and function of SNHG4 in RCC remain undocumented. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine expression levels of SNHG4 in RCC tissue samples and cell lines. Cell counting kit-8, western blotting, activities of caspase-3, -8, and -9, wound-healing, and transwell invasion assays were performed to explore cell proliferation, apoptosis, migration, and invasion. The interaction among SNHG4, miR-204-5p, and RUNX2 was verified by bioinformatic analysis, a luciferase gene report, qRT-PCR, western blot analysis, and RNA immunoprecipitation assays. Xenograft mouse models were carried out to examine the role of SNHG4 in RCC in vivo. RESULTS: SNHG4 was highly expressed in RCC tissue samples and cell lines, and its upregulation was significantly involved in node involvement, distant metastasis, and reduced overall and relapse-free survival of patients with RCC. SNHG4 acted as an oncogenic lncRNA with promoted RCC cell proliferation, migration, invasion, and inhibited apoptosis. SNHG4 boosted tumor growth in xenograft mouse models. Mechanistically, SNHG4 functioned as a competing endogenous RNA (ceRNA) for sponging miR-204-5p, leading to the upregulation of its target RUNX2 to promote RCC cell proliferation and invasion. CONCLUSION: SNHG4 and miR-204-5p might be indicated in RCC progression via RUNX2, suggesting the potential use of SNHG4/miR-204-5p/RUNX2 axis in RCC treatment.	NA	Cancer Cell Int. 2020 Oct 19;20:514. doi: 10.1186/s12935-020-01606-z. eCollection 2020.
4500	LncRNA	SNHG4	miR-204-5p	NA	GC cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33236157	lncRNA SNHG4 promotes cell proliferation, migration, invasion and the epithelial-mesenchymal transition process via sponging miR-204-5p in gastric cancer.	Long non-coding (lnc)RNAs and microRNAs (miRNAs/miRs) have physiological and pathological functions in various diseases, including gastric cancer (GC). The current study explored the association between lncRNA small nucleolar RNA host gene 4 (SNHG4) and miR-148a-3p, and their functions in GC cells. SNHG4 expression and overall survival data were analyzed using bioinformatics, and the interaction of SNHG4 and miR-148a-3p was predicted using starBase and confirmed via a dual-luciferase reporter assay. Cell viability, colony formation ability and apoptosis rate were detected using Cell Counting Kit-8, colony formation and flow cytometry assays, respectively. Cell migration and invasion were determined via wound-healing and Transwell assays. mRNA and protein expression levels were determined via reverse transcription-quantitative PCR and western blotting. The results demonstrated that in GC tissues and cell lines, SNHG4 was highly expressed, while miR-204-5p expression was decreased, and that the expression levels of SNHG4 and miR-204-5p were negatively correlated. The downregulated expression of SNHG4 decreased the effects of miR-204-5p inhibitor on promoting cell proliferation, migration, invasion and epithelial-mesenchymal transition, but enhanced the inhibitory effect of miR-204-5p on GC cell apoptosis. The findings of the current study revealed the potential mechanism of the SNHG4-miR-204-5p pathway in GC, which may be conducive to the development of novel drugs against GC growth.	NA	Mol Med Rep. 2021 Jan;23(1):85. doi: 10.3892/mmr.2020.11724. Epub 2020 Nov 25.
4501	LncRNA	SNHG5	miR-26b	CTGF	umbilical vein endothelial cells	Acute Myelogenous Leukemia	Homo sapiens (human)	qRT-PCR	33318617	LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia.	Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.	NA	Lab Invest. 2021 Mar;101(3):341-352. doi: 10.1038/s41374-020-00519-9. Epub 2020 Dec 14.
4502	LncRNA	SNHG5	miR-26b	VEGFA	umbilical vein endothelial cells	Acute Myelogenous Leukemia	Homo sapiens (human)	qRT-PCR	33318617	LncRNA SNHG5 upregulation induced by YY1 contributes to angiogenesis via miR-26b/CTGF/VEGFA axis in acute myelogenous leukemia.	Acute myelogenous leukemia (AML) is the most common acute leukemia in adults. Despite great progress has been made in this field, the pathogenesis of AML is still not fully understood. We report here the biological role of lncRNA small nucleolar RNA host gene 5 (SNHG5) in the pathogenesis of AML and the underlying mechanisms. The results showed that lncRNA SNHG5 was highly expressed in AML cancer cell lines. In vitro studies displayed that inhibition of SNHG5 with shRNA resulted in suppression of survival, cell cycle progression, migration/invasion of AML and capacity of adhesion and angiogenesis in human umbilical vein endothelial cells. Mechanistic studies revealed a SNHG5/miR-26b/connective tissue growth factor (CTGF)/vascular endothelial growth factor A (VEGFA) axis in the regulation of AML angiogenesis. Finally, Yin Yang 1 (YY1) was found to transactivate and interact with SNHG5 promoter, leading to the upregulation of SNHG5 in AML. Collectively, upregulation of lncRNA SNHG5 mediated by YY1, activates CTGF/VEGFA via targeting miR-26b to regulate angiogenesis of AML. Our work provides new insights into the molecular mechanisms of AML.	NA	Lab Invest. 2021 Mar;101(3):341-352. doi: 10.1038/s41374-020-00519-9. Epub 2020 Dec 14.
4503	LncRNA	SNHG5	miR-205	COMMD1	A549 cells	Acute Respiratory Distress Syndrome 	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;MTT assay;	33170429	Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis.	Previous studies have reported the important roles of long non-coding RNAs (lncRNAs) in acute respiratory distress syndrome (ARDS). Here, we focus on the role and regulatory mechanism of lncRNA SNHG5 in ARDS. LPS was used to induce mice to establish ARDS model in vivo and to induce A549 cells to establish ARDS model in vitro. qRT-PCR was performed to determine the expressions of SNHG5, miR-205, and inflammatory cytokines. MTT assay was applied to detect cell viability. Dual-luciferase reporter (DLR) assay was performed to test the interactions among SNHG5, miR-205 and COMMD1. Western blot was used to detect the protein expression of COMMD1. Lung injury was evaluated by evaluating the score of lung injury, lung wet/dry weight ratio, and myeloperoxidase (MPO) activity. SNHG5 was downregulated, while miR-205 was upregulated in the serum of ARDS patients and lung tissues of LPS-induced mice. Upregulation of SNHG5 or down-regulation of miR-205 inhibited inflammation and promoted the viability of LPS-induced A549 cells. SNHG5 alleviated the lung injury of ARDS mice. MiR-205 was a target of SNHG5 and inversely correlated with SNHG5. COMMD1 was targeted by miR-205, and was positively regulated by SNHG5. MiR-205 mimics or sh-COMMD1 reversed the promoting effect of SNHG5 on cell viability and the suppressing effect of SNHG5 on inflammation in cellular model of ARDS. Meantime, miR-205 mimics reversed the relieving effect of SNHG5 on lung injury in mouse model of ARDS. SNHG5 acted as a sponge for miR-205 to ameliorate LPS-induced ARDS by regulating COMMD1.	NA	Mol Cell Biochem. 2021 Feb;476(2):1063-1074. doi: 10.1007/s11010-020-03972-8. Epub 2020 Nov 10.
4504	LncRNA	SNHG5	miR-205	COMMD1	A549 cells	Acute Respiratory Distress Syndrome 	Mus musculus (mouse)	MTT assay;qRT-PCR;Western blot;MTT assay;	33170429	Long non-coding RNA SNHG5 suppresses the development of acute respiratory distress syndrome by targeting miR-205/COMMD1 axis.	Previous studies have reported the important roles of long non-coding RNAs (lncRNAs) in acute respiratory distress syndrome (ARDS). Here, we focus on the role and regulatory mechanism of lncRNA SNHG5 in ARDS. LPS was used to induce mice to establish ARDS model in vivo and to induce A549 cells to establish ARDS model in vitro. qRT-PCR was performed to determine the expressions of SNHG5, miR-205, and inflammatory cytokines. MTT assay was applied to detect cell viability. Dual-luciferase reporter (DLR) assay was performed to test the interactions among SNHG5, miR-205 and COMMD1. Western blot was used to detect the protein expression of COMMD1. Lung injury was evaluated by evaluating the score of lung injury, lung wet/dry weight ratio, and myeloperoxidase (MPO) activity. SNHG5 was downregulated, while miR-205 was upregulated in the serum of ARDS patients and lung tissues of LPS-induced mice. Upregulation of SNHG5 or down-regulation of miR-205 inhibited inflammation and promoted the viability of LPS-induced A549 cells. SNHG5 alleviated the lung injury of ARDS mice. MiR-205 was a target of SNHG5 and inversely correlated with SNHG5. COMMD1 was targeted by miR-205, and was positively regulated by SNHG5. MiR-205 mimics or sh-COMMD1 reversed the promoting effect of SNHG5 on cell viability and the suppressing effect of SNHG5 on inflammation in cellular model of ARDS. Meantime, miR-205 mimics reversed the relieving effect of SNHG5 on lung injury in mouse model of ARDS. SNHG5 acted as a sponge for miR-205 to ameliorate LPS-induced ARDS by regulating COMMD1.	NA	Mol Cell Biochem. 2021 Feb;476(2):1063-1074. doi: 10.1007/s11010-020-03972-8. Epub 2020 Nov 10.
4505	LncRNA	SNHG5	miR-655-3p	FZD4	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33093919	lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR-655-3p/FZD4 axis.	Recently, previous studies have shown that long non-coding RNA (lncRNA) can act as a tumor promoter or inhibitor in the pathogenesis of oral squamous cell carcinoma (OSCC). However, the regulatory mechanism of lncRNA SNHG5 is unknown in OSCC. Therefore, the functional mechanism of lncRNA SNHG5 in OSCC was initially revealed in this study. Here, RT-qPCR and western blot analysis were used to assess mRNA and protein expression. The functional mechanism of SNHG5 was investigated by MTT, Transwell and luciferase reporter assays. The results showed that SNHG5 expression was upregulated in OSCC and promoted the viability, migration and invasion of OSCC cells. In addition, SNHG5 is the sponge of miR-655-3p in OSCC. And miR-655-3p was found to play an inhibitory effect in OSCC by interacting with SNHG5. Moreover, miR-655-3p directly targets FZD4 and negatively regulates its expression in OSCC. Functionally, FZD4 promoted the progression of OSCC by interacting with the SNHG5/miR-655-3p axis. In conclusion, lncRNA SNHG5 promotes cell proliferation, migration and invasion in OSCC by regulating miR-655-3p/FZD4 axis.	NA	Oncol Lett. 2020 Dec;20(6):310. doi: 10.3892/ol.2020.12173. Epub 2020 Sep 30.
4506	LncRNA	SNHG5	miR-10a-5p	H3F3B	Chondrocytes	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	32967481	LncRNA SNHG5 promotes chondrocyte proliferation and inhibits apoptosis in osteoarthritis by regulating miR-10a-5p/H3F3B axis.	BACKGROUND: Osteoarthritis (OA) is a common degenerative joint disease in the elderly. Increasing evidence suggested that long non-coding RNAs (lncRNAs) played vital roles in OA progression. This study aimed to explore the role and mechanism of lncRNA small nucleolar RNA host gene 5 (SNHG5) in OA development. METHODS: Chondrocytes were stimulated with interleukin-1β (IL-1β) in vitro. The levels of SNHG5, miR-10a-5p, and H3 histone family 3B (H3F3B) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and colony formation assay. Cell apoptosis was tested by flow cytometry. The levels of apoptosis-related and cartilage-related markers were detected by western blot. The interaction among SNHG5, miR-10a-5p, and H3F3B was confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: SNHG5 and H3F3B were downregulated, while miR-10a-5p was upregulated in OA cartilage tissues. Knockdown of SNHG5 enhanced IL-1β-induced apoptosis in chondrocytes. Rescue experiments verified that SNHG5 hindered apoptosis in IL-1β-stimulated chondrocytes by sponging miR-10a-5p. Moreover, H3F3B was a target of miR-10a-5p, and miR-10a-5p promoted IL-1β-induced chondrocyte apoptosis by regulating H3F3B. In addition, SNHG5 regulated H3F3B expression via sponging miR-10a-5p in IL-1β-treated chondrocytes. CONCLUSION: SNHG5 suppressed chondrocytes apoptosis in OA by regulating the miR-10a-5p/H3F3B axis, which provided a promising biomarker for OA treatment.	NA	Connect Tissue Res. 2020 Sep 23:1-10. doi: 10.1080/03008207.2020.1825701.
4507	LncRNA	SNHG6	miR-101-3p	EZH2	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33192074	LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma.	BACKGROUND: The long non-coding RNA (lncRNA) SNHG6 was significantly upregulated in esophageal squamous-cell carcinoma (ESCC), and it promoted ESCC cell proliferation, invasion, and migration. However, the effects of SNHG6 on cell apoptosis and the corresponding underlying mechanisms have not yet reported. METHODS: Apoptosis was detected by flow cytometric analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for mRNA and protein quantification, respectively. A luciferase reporter assay was performed to verify downstream target genes for SNHG6 and miR-101-3p. RESULTS: Dysregulation of SNHG6 inhibited apoptosis in ESCC cells and regulated the expression of apoptosis-related proteins such as Bcl-2, Mcl-1, Bax and Caspase-3. Functionally, miR-101-3p could compete binding with 3'-untranslated region of SNHG6 and downregulation of miR-101-3p reversed its effect on cell apoptosis in SNHG6 knockdown cells. EZH2 was confirmed as a downstream target gene of miR-101-3p, silencing EZH2 expression had the same effect on apoptosis and protein expression as knocking down SNHG6. Overexpression of EZH2 reversed the effects of miR-101-3p overexpression on cell apoptosis in ESCC cells. CONCLUSION: In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/EZH2 axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.	NA	Onco Targets Ther. 2020 Nov 6;13:11411-11420. doi: 10.2147/OTT.S275135. eCollection 2020.
4508	LncRNA	SNHG6	miR-186-5p	NA	Human induced pluripotent stem cell-derived cardiomyocytes (HiPSC-CMs)	Severe Cardiac Failure	Homo sapiens (human)	qRT-PCR;Luciferase activity assay;	32968636	Downregulation of long noncoding RNA SNHG6 rescued propofol-induced cytotoxicity in human induced pluripotent stem cell-derived cardiomyocytes.	BACKGROUND: Propofol (PPF) overdose is a rare but lethal condition, which may lead to severe cardiac failure. In this study, we established an in vitro PPF-induced cardiac cytotoxicity model, and investigate the functional role of long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6). METHODS: Human induced pluripotent stem cell-derived cardiomyocytes (HiPSC-CMs) were exposed to PPF in vitro. PPF-induced cytotoxic effects were measured. PPF-induced SNHG6 expression change in HiPSC-CMs were monitored by qRT-PCR. SNHG6 was downregulated in HiPSC-CMs to examine its role in PPF-induced cardiac cytotoxicity. The expression of competing endogenous RNA (ceRNA) candidate of SNHG6, human microRNA-186-5p (hsa-miR-186-5p) was also investigated in PPF-exposed HiPSC-CMs. Functions of hsa-miR-186-5p were further investigated in PPF-exposed and SNHG6-downregulated HiPSC-CMs. RESULTS: PPF induced significant cytotoxicity, as well as SNHG6 upregulation in HiPSC-CMs. SNHG6 downregulation had rescuing effects on PPF-induced cardiac cytotoxicity. Dual-luciferase activity assay confirmed that hsa-miR-186-5p was the ceRNA candidate of SNHG6. QRT-PCR showed hsa-miR-186-5p expression was reversely correlated with SNHG6 in PPF-exposed HiPSC-CMs. Suppressing hsa-miR-186-5p reduced the rescuing effects of SNHG6-downregulation on PPF-induced cardiac cytotoxicity. CONCLUSIONS: SNHG6/hsa-miR-186-5p can modulate PPF-induced cardiac cytotoxicity in HiPSC-CMs, and thus may be a future drug target to prevent PPF infusion syndrome.	NA	Cardiovasc Diagn Ther. 2020 Aug;10(4):811-819. doi: 10.21037/cdt-20-443.
4509	LncRNA	SNHG6	miR-944	RAB11A	HP75 cells,PA cells,IPA cells	Pituitary Adenoma	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	32935999	LncRNA SNHG6 Induces Epithelial-Mesenchymal Transition of Pituitary Adenoma Via Suppressing MiR-944.	Background: Pituitary adenoma (PA) is a kind of common primary brain tumor with invasive properties. Although the fact that long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) exerts oncogenic function in cancer cells and that miR-944 inhibits epithelial-mesenchymal transition (EMT) of cancer cells are well documented, few studies explore the function and mechanism of SNHG6 and miR-944 in invasive pituitary adenoma (IPA). Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of SNHG6 and miR-944 in PA samples. Human PA cell line HP75 was used as a cell model. The biological effects of SNHG6 and miR-944 on HP75 cells were investigated with cell counting kit-8 (CCK-8) assay, Transwell assay, and scratch healing assay in vitro, respectively. Markers of EMT, including E-cadherin and vimentin, were detected by western blot. Interactions between SNHG6 and miR-944, miR-944 and RAB11A were determined by bioinformatics analysis, qRT-PCR, and dual luciferase reporter assay. Results: SNHG6 was significantly upregulated in IPA samples, whereas miR-944 was downregulated. SNHG6 markedly promoted viability, migration, invasion, and EMT of PA cells, whereas miR-944 transfection had the opposite effects. SNHG6 could downregulate miR-944, and there was a negative correlation between SNHG6 expression and miR-944 expression in IPA samples. Besides, it was confirmed that miR-944 could pair with the 3'-untranslated region of RAB11A and repress its expression. Conclusions: This study authenticates that the SNHG6/miR-994/RAB11A axis plays a crucial role in regulating proliferation, migration, invasion, and EMT of IPA cells. SNHG6 and miR-994 can serve as novel valuable therapeutic targets for IPA.	NA	Cancer Biother Radiopharm. 2020 Sep 16. doi: 10.1089/cbr.2020.3587.
4510	LncRNA	SNHG7	miR-15a	NA	MCF7 and T47D	Breast Cancer	Homo sapiens (human)	Cell proliferation assay;Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33099915	LncRNA SNHG7 inhibits proliferation and invasion of breast cancer cells by regulating miR-15a expression.	PURPOSE: To explore the inhibition of proliferation and invasion of breast cancer cells by LncRNA SNHG7 via regulating the expression of miR-15a and its mechanism. METHODS: The expression of SNHG7 in breast cancer and adjacent tissues and different breast cancer cells was measured by qRT-PCR and the relationship between SNHG7 and clinicopathological parameters of breast cancer patients was analyzed. The interaction of SNHG7 with miR-15a was explored by dual-luciferase reporter assay. The change in the proliferation of breast cancer cells after silencing SNHG7 was examined by cell proliferation assay. The change in the invasion of breast cancer cells after silencing SNHG7 was examined by Transwell invasion assay. Subcutaneous tumor formation in nude mice was detected to record the tumor size and volume of tumor cells. RESULTS: Compared with adjacent normal tissues, the expression of SNHG7 was significantly increased in breast cancer tissues; the expression of SNHG7 was the highest in breast cancer cells MCF7 and T47D; the expression level of SNHG7 was not notably different among breast cancer patients of different genders and age groups, and the difference was not statistically significant (p>0.05). The expression level of SNHG7 was higher in patients with a higher stage of breast cancer and patients with lymph node metastasis, and the difference was statistically significant. SNHG7 could specifically bind to the 3' UTR of miR-15a. The inhibition of SNHG7 led to constrained proliferation and invasion of breast cancer cells. The tumor volume and weight of the tumor-bearing mice in the si-SNHG7 group were significantly lower than those in the non-specific control (NC) group. CONCLUSION: SNHG7 plays an important role in the development of breast cancer. SNHG7 can affect the proliferation and invasion of breast cancer cells through its targeted regulation of miR-15a activity.	NA	J BUON. 2020 Jul-Aug;25(4):1792-1798.
4511	LncRNA	SNHG7	miR-214-5p	PPARGC1B	osteoarthritis cells	Osteoarthritis	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;	33296783	LncRNA SNHG7 alleviates IL-1β-induced osteoarthritis by inhibiting miR-214-5p-mediated PPARGC1B signaling pathways.	BACKGROUND: As a common joint disease, osteoarthritis (OA) is the main cause of limited joint mobility and disability. The role of lncRNAs in the regulation of OA is increasingly discovered. Therefore, further exploring the function of SNHG7 in OA is of great significance for understanding its occurrence and development. METHODS: We used interleukin-1β (IL-1β) to treat to establish an OA model primary on chondrocytes in vitro, and gain- and loss of function assays of SNHG7 and miR-214-5p were conducted. The cell viability and apoptosis of chondrocytes were detected by CCK8 assay, BrdU assay and flow cytometry. The inflammatory cytokines (IL-1β, IL-6 and TNF-α), NLRP3 inflammasome, protein level of PPARGC1B, PPARγ, P38 and NF-κB were determined by RT-PCR and/or western blot. RESULTS: The results showed that SNHG7 was distinctly downregulated, while miR-214-5p was significantly upregulated in OA patients and primary chondrocytes treated with IL-1β. In addition, SNHG7 enhanced cell viability, inhibited apoptosis and inflammation of IL-1β-mediated chondrocytes. In contrast, miR-214-5p upregulation reduced viability, promoted apoptosis and inflammation of chondrocytes. Mechanistically, SNHG7 served as a competitive endogenous RNA by sponging miR-214-5p, which targeted PPARGC1B. Besides, the results of the compensation experiment affirmed that miR-214-5p attenuates SNHG7-mediated protective effects on IL-1β-mediated chondrocytes against apoptosis and inflammation, and activating PPARγ pathway markedly dampened the cytotoxic effects of miR-214-5p. CONCLUSIONS: Collectively, The above results confirmed that SNHG7 prevents IL-1β induced OA by inhibiting NLRP3 inflammasome and apoptosis through miR-214-5p/PPARGC1B axis.	NA	Int Immunopharmacol. 2021 Jan;90:107150. doi: 10.1016/j.intimp.2020.107150. Epub 2020 Dec 6.
4512	LncRNA	SNHG7	miR-34a	LDHA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	luciferase assay;	33074217	LncRNA-SNHG7 interferes with miR-34a to de-sensitize gastric cancer cells to cisplatin.	Gastric cancer (GC) remains poor prognosis and survival issues due to the resistance of chemotherapies, such as cisplatin. The long non-coding RNA small nucleolar RNA host gene 7 (lncRNA-SNHG7) is known as an oncogenic molecule in diverse cancers. Here, we demonstrate that SNHG7 was significantly upregulated in gastric cancer and positively correlated with cisplatin resistance of gastric cancer cells that SNHG7 was significantly upregulated in cisplatin resistant cells. Silencing SNHG7 dramatically sensitized cisplatin resistant cells. In contrast, a negative correlation between lncRNA-SNHG7 and miR-34a was found that miR-34a was downregulated in gastric cancer patient tissues and significantly sensitized cisplatin resistant gastric cancer cells. Intriguingly, bioinformatical analysis indicated miR-34a has putative biding site for SNHG7 and such negative association between SNHG7 and miR-34a was verified in gastric cancer tissues. The cisplatin resistant cells displayed increased glycolysis rate and SNHG7 promoted cellular glycolysis rate of gastric cancer cells. Luciferase assay illustrated LDHA, a glycolysis enzyme, was the direct target of miR-34a. Importantly, inhibiting SNHG7 successfully suppressed LDHA expressions and sensitized cisplatin resistant cells and such inhibitory effects could be recovered by further anti-miR-34a. These findings suggest an important regulator mechanism for the SNHG7-mediated cisplatin resistance via miR-34a/LDHA-glycolysis axis.	NA	Cancer Biomark. 2021;30(1):127-137. doi: 10.3233/CBM-201621.
4513	LncRNA	SNHG7	miR-9	SIRT1	PC12 cells	Ischemic Stroke	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	33262598	Long Non-Coding RNA SNHG7 Alleviates Oxygen and Glucose Deprivation/Reoxygenation-Induced Neuronal Injury by Modulating miR-9/SIRT1 Axis in PC12 Cells: Potential Role in Ischemic Stroke.	OBJECTIVE: The roles of long non-coding RNA (lncRNAs) in ischemic stroke (IS) have been widely illustrated. Here, we focused on the function and mechanism of lncRNA SNHG7 in IS. METHODS: Middle cerebral artery occlusion (MCAO) was used for inducing mice to establish IS models in vivo. Oxygen and glucose deprivation/reoxygenation (OGD/R) was used for treating PC12 cells to establish IS models in vitro. Relative expression of SNHG7 and miR-9 was determined by qRT-PCR. The neuronal injury was assessed by measuring relative activity of ROS, malondialdehyde (MDA) level and cell viability. Cell viability was determined by MTT assay. Dual-luciferase reporter (DLR) assay was employed to test the target of SNHG7 or miR-9. Western blot was used to determine the protein expression of SIRT1. Apoptosis rate was measured by flow cytometry. RESULTS: SNHG7 was down-regulated and miR-9 was up-regulated by MCAO treatment in brain tissues of mice and by OGD/R treatment in PC12 cells. Overexpression of SNHG7 or suppression of miR-9 decreased the relative activity of ROS and the MDA level as well as enhancing cell viability, and SNHG7 reduced apoptosis rate in OGD/R-induced PC12 cells (IS cells). MiR-9 was targeted by SNHG7 and SIRT1 was targeted by miR-9. The protein expression of SIRT1 was reduced by OGD/R treatment in PC12 cells. The suppressive effects of SNHG7 on the relative activity of ROS, the MDA level and apoptosis rate as well as the promotion effect of SNHG7 on cell viability were reversed by miR-9 mimics or sh-SIRT1 in IS cells. CONCLUSION: LncRNA SNHG7 alleviated OGD/R-induced neuronal injury by mediating miR-9/SIRT1 axis in vitro.	NA	Neuropsychiatr Dis Treat. 2020 Nov 24;16:2837-2848. doi: 10.2147/NDT.S273421. eCollection 2020.
4514	LncRNA	SNHG7	miR-34a	NA	BC cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33330080	LncRNA SNHG7 Mediates the Chemoresistance and Stemness of Breast Cancer by Sponging miR-34a.	Chemoresistance is considered to be a major cause of the recurrence and metastasis of breast cancer (BC). LncRNA SNHG7 has been reported to be upregulated in breast cancer and to promote tumor progression and metastasis. Nevertheless, the function and potential regulatory mechanism of SNHG7 in BC drug resistance are still largely unclear. This study indicated that SNHG7 was highly expressed in chemoresistant BC tissues and cells. Upregulated SNHG7 might predict a low pCR rate and poor clinical outcome in BC patients. Knockdown of SNHG7 enhanced drug sensitivity and drug-induced apoptosis in chemoresistant BC cells. In terms of the mechanism, miR-34a was found to be a target of SNHG7 and its expression in breast cancer tissues and chemoresistant cell lines was negatively correlated with SNHG7 expression. Importantly, sh-SNHG7 upregulated miR-34a expression, reduced the percentages of CD44(+)/CD24(-)cells, and inhibited sphere-formation and stem cell factor (Oct4, Nanog, SOX2) expression. Functional loss experiments showed that the repressive effect of SNHG7 knockdown on BC cell stemness was partially reversed by transfection with miR-34a inhibitors. In summary, this study indicated that SNHG7 contributed to the chemoresistance of BC and mediated chemoresistance and cancer stemness by sponging miR-34a.	NA	Front Oncol. 2020 Nov 24;10:592757. doi: 10.3389/fonc.2020.592757. eCollection 2020.
4515	LncRNA	SOX21-AS1	miR-7-5p	IRS2	OS cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;RNA pull-down;	33341286	LncRNA SOX21-AS1 Promotes the Growth and Invasiveness of Osteosarcoma Cells Through miR-7-5p/IRS2 Regulatory Network.	BACKGROUND: Osteosarcoma (OS) is commonly known as a bone malignancy, causing a mass of lethality worldwide. Long coding RNAs (lncRNAs) have been widely reported by documents that they exert important functions in the development of cancers. However, the relative mechanism of lncRNA SOX21-AS1 needs to be fully discovered in OS, as it has never been studied in the past. AIM OF THE STUDY: To find out how SOX21-AS1 materializes its function in OS. METHODS: qRT-PCR detected RNA expression, and western blot tested the protein level. CCK8 and TUNEL assays were performed to assess cell viability and apoptosis. Next, Transwell analyses were applied to identify OS cell migration and invasion. Luciferase reporter, RIP and RNA pull-down experiments were employed for investigating the relationships among RNAs. RESULTS: SOX21-AS1 had high expression in OS, and its presence accelerated OS cell proliferation, migration and invasion. Interestingly, we evidenced that SOX21-AS1 sponged miR-7-5p, which then targeted IRS2 in OS cells. SOX21-AS1 competed with IRS2 in binding to miR-7-5p, which formulated the ceRNA signaling in OS. SOX21-AS1 could negatively regulate miR-7-5p expression. Rescue experiments certified that the enhancement of IRS2 would neutralize the inhibition of SOX21-AS1 depletion on OS cell proliferation and metastasis. CONCLUSIONS: SOX21-AS1 enhances IRS2 level by absorbing miR-7-5p, so as to boost the progression of OS.	NA	Arch Med Res. 2021 Apr;52(3):294-303. doi: 10.1016/j.arcmed.2020.11.007. Epub 2020 Dec 17.
4516	LncRNA	SPINT1-AS1	let-7a	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Flow Cytometry assay;	33246290	LncRNA SPINT1-AS1 promotes breast cancer proliferation and metastasis by sponging let-7 a/b/i-5p.	BACKGROUND: A growing number of studies have shown that long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of tumors. In this study, we explored the function and molecular mechanism of lncRNA SPINT1-AS1 in breast cancer progression. METHODS: A total of 30 patients and 25 healthy controls were enrolled to detect the expression of SPINT1-AS1 in the serum by RT-qPCR. CCK-8 assay, clone formation assay, EdU assay, Transwell assay, Flow cytometry for apoptosis assay and wound healing assays were used to explore the effects of SPINT1-AS1 on the proliferation and migration of breast cancer cells. Bioinformatics analysis were used to enrich the downstream target genes and related pathways of miRNAs interacting with SPINT1-AS1, construct a competitive endogenous RNA (ceRNA) network diagram. RESULTS: SPINT1-AS1 is up-regulated in the serum of breast cancer patients and breast cancer cell lines. The proliferation and migration ability of breast cancer cells were decreased significantly after SPINT1-AS1 knockdown, and it may inhibit its expression by sponging miR-let-7a/b/i-5p, thereby promoting breast cancer progression. CONCLUSIONS: SPINT1-AS1 can promote the proliferation and migration of breast cancer cells by regulating miR-let-7a/b/i-5p, suggesting that it may be an important regulator of breast cancer progression.	NA	Pathol Res Pract. 2021 Jan;217:153268. doi: 10.1016/j.prp.2020.153268. Epub 2020 Nov 4.
4517	LncRNA	SPINT1-AS1	let-7b	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Flow Cytometry assay;	33246290	LncRNA SPINT1-AS1 promotes breast cancer proliferation and metastasis by sponging let-7 a/b/i-5p.	BACKGROUND: A growing number of studies have shown that long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of tumors. In this study, we explored the function and molecular mechanism of lncRNA SPINT1-AS1 in breast cancer progression. METHODS: A total of 30 patients and 25 healthy controls were enrolled to detect the expression of SPINT1-AS1 in the serum by RT-qPCR. CCK-8 assay, clone formation assay, EdU assay, Transwell assay, Flow cytometry for apoptosis assay and wound healing assays were used to explore the effects of SPINT1-AS1 on the proliferation and migration of breast cancer cells. Bioinformatics analysis were used to enrich the downstream target genes and related pathways of miRNAs interacting with SPINT1-AS1, construct a competitive endogenous RNA (ceRNA) network diagram. RESULTS: SPINT1-AS1 is up-regulated in the serum of breast cancer patients and breast cancer cell lines. The proliferation and migration ability of breast cancer cells were decreased significantly after SPINT1-AS1 knockdown, and it may inhibit its expression by sponging miR-let-7a/b/i-5p, thereby promoting breast cancer progression. CONCLUSIONS: SPINT1-AS1 can promote the proliferation and migration of breast cancer cells by regulating miR-let-7a/b/i-5p, suggesting that it may be an important regulator of breast cancer progression.	NA	Pathol Res Pract. 2021 Jan;217:153268. doi: 10.1016/j.prp.2020.153268. Epub 2020 Nov 4.
4518	LncRNA	SPINT1-AS1	let-7i-5p	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Flow Cytometry assay;	33246290	LncRNA SPINT1-AS1 promotes breast cancer proliferation and metastasis by sponging let-7 a/b/i-5p.	BACKGROUND: A growing number of studies have shown that long non-coding RNAs (lncRNAs) play an important role in the occurrence and development of tumors. In this study, we explored the function and molecular mechanism of lncRNA SPINT1-AS1 in breast cancer progression. METHODS: A total of 30 patients and 25 healthy controls were enrolled to detect the expression of SPINT1-AS1 in the serum by RT-qPCR. CCK-8 assay, clone formation assay, EdU assay, Transwell assay, Flow cytometry for apoptosis assay and wound healing assays were used to explore the effects of SPINT1-AS1 on the proliferation and migration of breast cancer cells. Bioinformatics analysis were used to enrich the downstream target genes and related pathways of miRNAs interacting with SPINT1-AS1, construct a competitive endogenous RNA (ceRNA) network diagram. RESULTS: SPINT1-AS1 is up-regulated in the serum of breast cancer patients and breast cancer cell lines. The proliferation and migration ability of breast cancer cells were decreased significantly after SPINT1-AS1 knockdown, and it may inhibit its expression by sponging miR-let-7a/b/i-5p, thereby promoting breast cancer progression. CONCLUSIONS: SPINT1-AS1 can promote the proliferation and migration of breast cancer cells by regulating miR-let-7a/b/i-5p, suggesting that it may be an important regulator of breast cancer progression.	NA	Pathol Res Pract. 2021 Jan;217:153268. doi: 10.1016/j.prp.2020.153268. Epub 2020 Nov 4.
4519	LncRNA	ST7-AS1	miR-181b-5p	KPNA4	LUAD cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	33327962	LncRNA ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of lung adenocarcinoma.	BACKGROUND: Growing evidence suggests that suppressor of tumorigenicity 7 antisense RNA 1 (ST7-AS1) is an oncogenic long noncoding RNA (lncRNA). However, little is known on its clinical significance, biological functions, or molecular mechanisms in lung adenocarcinoma (LUAD). METHODS: The expression of ST7-AS1 and miR-181b-5p were examined by qRT-PCR. The correlations between ST7-AS1 level and different clinicopathological features were analysed. In vitro, LUAD cells were examined for cell viability, migration and invasion by MTT, wound healing and Transwell assay, respectively. Epithelial-mesenchymal transition (EMT) biomarkers were detected by Western blot. The regulations between ST7-AS1, miR-181b-5p, and KPNA4 were examined by luciferase assay, RNA immunoprecipitation, RNA pulldown. Both gain- and loss-of-function strategies were used to assess the importance of different signalling molecules in malignant phenotypes of LUAD cells. The in vivo effect was analysed using the xenograft and the experimental metastasis mouse models. RESULTS: ST7-AS1 was upregulated in LUAD tissues or cell lines, correlated with tumours of positive lymph node metastasis or higher TNM stages, and associated with shorter overall survival of LUAD patients. ST7-AS1 essentially maintained the viability, migration, invasion, and EMT of LUAD cells. The oncogenic activities of ST7-AS1 were accomplished by sponging miR-181b-5p and releasing the suppression of the latter on KPNA4. In LUAD tissues, ST7-AS1 level positively correlated with that of KPNA4 and negatively with miR-181b-5p level. In vivo, targeting ST7-AS1 significantly inhibited xenograft growth and metastasis. CONCLUSIONS: ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of LUAD cells. Targeting ST7-AS1 and KPNA4 or up-regulating miR-181b-5p, therefore, may benefit the treatment of LUAD.	NA	Cancer Cell Int. 2020 Dec 17;20(1):568. doi: 10.1186/s12935-020-01652-7.
4520	LncRNA	ST7-AS1	miR-181b-5p	KPNA4	LUAD cells	Lung Cancer	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	33327962	LncRNA ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of lung adenocarcinoma.	BACKGROUND: Growing evidence suggests that suppressor of tumorigenicity 7 antisense RNA 1 (ST7-AS1) is an oncogenic long noncoding RNA (lncRNA). However, little is known on its clinical significance, biological functions, or molecular mechanisms in lung adenocarcinoma (LUAD). METHODS: The expression of ST7-AS1 and miR-181b-5p were examined by qRT-PCR. The correlations between ST7-AS1 level and different clinicopathological features were analysed. In vitro, LUAD cells were examined for cell viability, migration and invasion by MTT, wound healing and Transwell assay, respectively. Epithelial-mesenchymal transition (EMT) biomarkers were detected by Western blot. The regulations between ST7-AS1, miR-181b-5p, and KPNA4 were examined by luciferase assay, RNA immunoprecipitation, RNA pulldown. Both gain- and loss-of-function strategies were used to assess the importance of different signalling molecules in malignant phenotypes of LUAD cells. The in vivo effect was analysed using the xenograft and the experimental metastasis mouse models. RESULTS: ST7-AS1 was upregulated in LUAD tissues or cell lines, correlated with tumours of positive lymph node metastasis or higher TNM stages, and associated with shorter overall survival of LUAD patients. ST7-AS1 essentially maintained the viability, migration, invasion, and EMT of LUAD cells. The oncogenic activities of ST7-AS1 were accomplished by sponging miR-181b-5p and releasing the suppression of the latter on KPNA4. In LUAD tissues, ST7-AS1 level positively correlated with that of KPNA4 and negatively with miR-181b-5p level. In vivo, targeting ST7-AS1 significantly inhibited xenograft growth and metastasis. CONCLUSIONS: ST7-AS1, by regulating miR-181b-5p/KPNA4 axis, promotes the malignancy of LUAD cells. Targeting ST7-AS1 and KPNA4 or up-regulating miR-181b-5p, therefore, may benefit the treatment of LUAD.	NA	Cancer Cell Int. 2020 Dec 17;20(1):568. doi: 10.1186/s12935-020-01652-7.
4521	LncRNA	ST8SIA6-AS1	miR-125a-3p	NNMT	LUAD cell lines	Lung Cancer	Homo sapiens (human)	qRT-PCR	33363573	Long Non-coding RNA ST8SIA6-AS1 Promotes Lung Adenocarcinoma Progression Through Sponging miR-125a-3p.	Emerging evidence suggests that long non-coding RNA (lncRNA) plays a critical role in human disease progression. Recently, a novel lncRNA ST8SIA6-AS1 was shown as an important driver in various cancer types. Nevertheless, its contribution to lung adenocarcinoma (LUAD) remains undocumented. Herein, we found that ST8SIA6-AS1 was frequently overexpressed in LUAD cell lines, tissues, and plasma. Depletion of ST8SIA6-AS1 significantly inhibited LUAD cell proliferation and invasion in vitro and tumor growth in vivo. In term of mechanism, ST8SIA6-AS1 was transcriptionally repressed by tumor suppressor p53, and ST8SIA6-AS1 was mainly located in the cytoplasm and could abundantly sponge miR-125a-3p to increase nicotinamide N-methyltransferase (NNMT) expression, thereby facilitating LUAD malignant progression. Clinically, high ST8SIA6-AS1 was positively correlated with larger tumor size, lymph node metastasis, and later TNM stage. Moreover, ST8SIA6-AS1 was identified as an excellent indicator for MM diagnosis and prognosis. Collectively, our data demonstrate that ST8SIA6-AS1 is a carcinogenic lncRNA in LUAD, and targeting the axis of ST8SIA6-AS1/miR-125a-3p/NNMT may be a promising treatment for LUAD patients.	NA	Front Genet. 2020 Dec 8;11:597795. doi: 10.3389/fgene.2020.597795. eCollection 2020.
4522	LncRNA	ST8SIA6-AS1	miR-4252	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	microarray;qRT-PCR;	33037712	Profiling of specific long non-coding RNA signatures identifies ST8SIA6-AS1 AS a novel target for breast cancer.	BACKGROUND: Breast cancer is the most commonly diagnosed cancer among women and is also the leading cause of cancer death for which the treatment and methods of diagnosis remain unsatisfied. Long non-coding RNA (lncRNA) plays an important role in the occurrence and development of tumors, including breast cancer. We aimed to seek new and efficient treatment targets by analyzing the lncRNA expression profiles of breast cancer. METHODS: A competitive endogenous RNA microarray was used to investigate the profiles of differentially expressed lncRNAs. Quantitative real-time polymerase chain reaction analysis (qRT-PCR) validated the top differentially expressed lncRNAs in 107 pairs of breast cancer tissues and adjacent normal tissues. cis- and trans-regulation mRNAs of lncRNAs were used to perform enrichment analysis. Cell function assays were used to explore the functions of ST8SIA6-AS1. RESULTS: Seven lncRNAs, comprising ST8SIA6-AS1, lnc-HIST1H2BJ-5:1, lnc-PRICKLE2-3:2, RP1-86C11.7, RP11-15F12.1, ZNF670-ZNF695 and lnc-STRN3-12:1, were shown to be significantly up-regulated in breast cancer. lncRNA ST8SIA6-AS1 was associated with TNM staging and Ki-67 index. The cell function assays showed that ST8SIA6-AS1 can promote the proliferation, migration and invasion of breast cancer cells. The functions of ST8SIA6-AS1 were explored and the competing endogenous RNA mode showed that miR-4252 was a potential candidate. Its target genes were further predicted. The lncRNA-protein mode showed three potential candidate RNA binding proteins: NONO, QKI and RBMX. CONCLUSIONS: lncRNA ST8SIA6-AS1 can promote the proliferation, migration and invasion of breast cancer cells. By hypothesizing two different functional modes of ST8SIA6-AS1, we found lncRNA ST8SIA6-AS1 may contribute to breast cancer progression through miR-4252 or interacting with RNA binding proteins: NONO, QKI and RBMX.	NA	J Gene Med. 2021 Feb;23(2):e3286. doi: 10.1002/jgm.3286. Epub 2021 Jan 5.
4523	LncRNA	ST8SIA6-AS1	miR-129-5p	MAGEA3	HCC in-house tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33012505	LncRNA ST8SIA6-AS1 promotes hepatocellular carcinoma progression by regulating MAGEA3 and DCAF4L2 expression.	Hepatocellular carcinoma (HCC) is the most prevalent type of liver cancer. In this study, we aimed to explore the role and mechanism of lncRNA ST8SIA6-AS1 in HCC. We found that ST8SIA6-AS1 was upregulated in HCC tissues and associated with poorer overall survival of HCC patients from TCGA. Moreover, ST8SIA6-AS1 was highly expressed in HCC in-house tissues and cells, and ST8SIA6-AS1 upregulation was related to aggressive tumor phenotypes and the poor overall survival of HCC patients. Downregulation of ST8SIA6-AS1 suppressed HCC cell proliferation, migration and invasion in vitro and restrained HCC tumorigenesis in vivo. In terms of mechanism, ST8SIA6-AS1 regulated melanoma-associated antigen (MAGE)-A3 (MAGEA3) and DDB1-and Cul4-associated factor 4-like 2 (DCAF4L2) expression, and rescue experiments verified that ST8SIA6-AS1 played a protumorigenic role in HCC via the regulation of MAGEA3 and DCAF4L2. ST8SIA6-AS1 partly directly bound to miR-129-5p and functioned as a competing endogenous RNA (ceRNA), subsequently facilitating the expression of the miR-129-5p target gene DCAF4L2 to play its role in HCC. In summary, our results identified ST8SIA6-AS1 as an oncogenic lncRNA predicting poor clinical outcomes of patients with HCC. These findings suggest that ST8SIA6-AS1 is a potential therapeutic target for HCC.	NA	Biochem Biophys Res Commun. 2020 Dec 17;533(4):1039-1047. doi: 10.1016/j.bbrc.2020.09.115. Epub 2020 Oct 1.
4524	LncRNA	ST8SIA6-AS1	miR-129-5p	DCAF4L2	HCC in-house tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33012505	LncRNA ST8SIA6-AS1 promotes hepatocellular carcinoma progression by regulating MAGEA3 and DCAF4L2 expression.	Hepatocellular carcinoma (HCC) is the most prevalent type of liver cancer. In this study, we aimed to explore the role and mechanism of lncRNA ST8SIA6-AS1 in HCC. We found that ST8SIA6-AS1 was upregulated in HCC tissues and associated with poorer overall survival of HCC patients from TCGA. Moreover, ST8SIA6-AS1 was highly expressed in HCC in-house tissues and cells, and ST8SIA6-AS1 upregulation was related to aggressive tumor phenotypes and the poor overall survival of HCC patients. Downregulation of ST8SIA6-AS1 suppressed HCC cell proliferation, migration and invasion in vitro and restrained HCC tumorigenesis in vivo. In terms of mechanism, ST8SIA6-AS1 regulated melanoma-associated antigen (MAGE)-A3 (MAGEA3) and DDB1-and Cul4-associated factor 4-like 2 (DCAF4L2) expression, and rescue experiments verified that ST8SIA6-AS1 played a protumorigenic role in HCC via the regulation of MAGEA3 and DCAF4L2. ST8SIA6-AS1 partly directly bound to miR-129-5p and functioned as a competing endogenous RNA (ceRNA), subsequently facilitating the expression of the miR-129-5p target gene DCAF4L2 to play its role in HCC. In summary, our results identified ST8SIA6-AS1 as an oncogenic lncRNA predicting poor clinical outcomes of patients with HCC. These findings suggest that ST8SIA6-AS1 is a potential therapeutic target for HCC.	NA	Biochem Biophys Res Commun. 2020 Dec 17;533(4):1039-1047. doi: 10.1016/j.bbrc.2020.09.115. Epub 2020 Oct 1.
4525	LncRNA	STARD13-AS	miR-1248	C3A	lung squamous carcinoma cells	Lung Squamous Carcinoma	Homo sapiens (human)	luciferase assay;	32949706	LncRNA STARD13-AS blocks lung squamous carcinoma cells growth and movement by targeting miR-1248/C3A.	BACKGROUND: This research aims to illustrate the effect of lncRNA StAR Related Lipid Transfer Domain Containing 13 antisense RN (STARD13-AS)/miR-1248/C3A on lung squamous carcinoma cells growth and metastasis. METHODS: Bioinformatics analysis was applied to detect the expression of STARD13-AS/miR-1248/C3A in lung cancer samples and establish the ceRNA network. Transfection was performed to construct over-expression or knockdown models. PCR was implemented to examine the transfection efficiency. The biological function including growth, invasion and migration of LUSC cells were estimated by CCK-8 analysis, colony formation assay and transwell assay. Luciferase assay was executed to analyze the relationship between C3A and miR-1248, as well as miR-1248 and STARD13-AS. RESULTS: By consulting the TCGA database and GEPIA website, we found that C3A expression was significantly reduced in LUSC samples. Additionally, we also discovered that miR-1248, which was a downstream target of STARD13-AS, was presented as an upstream regulator of C3A. Moreover, STARD13-AS was under expressed in LUSC cells and has a negative effect on LUSC cells growth ability. C3A expression was co-regulated by miR-1248 and STARD13-AS. Importantly, the inhibitory effect of C3A or the promoting effect of miR-1248 on LUSC cells growth, invasion and migration abilities can be regulated by STARD13-AS. CONCLUSIONS: Our findings revealed that overexpression of STARD13-AS restricted the growth and aggressiveness of LUSC cells via regulating miR-1248/C3A.	NA	Pulm Pharmacol Ther. 2020 Oct;64:101949. doi: 10.1016/j.pupt.2020.101949. Epub 2020 Sep 17.
4526	LncRNA	TALNEC2	miR-650	APAF1	neuroblastoma cells	Neuroblastoma	Homo sapiens (human)	Luciferase reporter assay;	33075457	Long Non-coding RNA TALNEC2 Aggravates Cerebral Ischemia/Reperfusion Injury via Acting as a Competing Endogenous RNAs for miR-650 to Target Apoptotic Peptidase Activating Factor 1.	Increasing evidence has indicated that long non-coding RNAs (lncRNAs) play a vital role for adjusting RNA transcripts as competing endogenous RNAs (ceRNAs) for microRNAs (miRNAs). The present study was intended to explore the probable regulation of lncRNA TALNEC2 in ischemic stroke. In this study, we measured the up-regulation of TALNEC2 and down-regulation of miR-650 in mice brains after cerebral ischemia/reperfusion (I/R) operation and in cultured neuroblastoma cells of neuro-2A (N2a) treated with oxygen glucose deprivation/reoxygenation (OGD/R). Then we verified the common predicted binding sites of miR-650 in TALNEC2 and 3'-UTR of apoptotic peptidase activating factor 1 (APAF1), a critical regulator in ischemic neuronal death, with bioinformatics. Overexpression of miR-650 reduced N2a cell apoptosis induced by OGD/R. MiR-650 was confirmed to be a directly target of APAF1 by luciferase reporter assay. It was found that TALNEC2 played a critical role as a ceRNA for miR-650 and bound directly to miR-650 to mediate the APAF1. In result, overexpression of TALNEC2 antagonized the inhibition impact of miR-650 on APAF1 expression and N2a cell apoptosis induced by OGD/R, while TALNEC2 knockdown aggravated the impact. Furthermore, TALNEC2 knockdown reversed brain injury and neurological deficits induced by I/R in vivo. In conclusion, we verified a TALNEC2/miR-650/APAF1 signaling pathway as a key mechanism monitoring cerebral I/R injury.	NA	Neuroscience. 2021 Mar 15;458:64-76. doi: 10.1016/j.neuroscience.2020.10.010. Epub 2020 Oct 17.
4527	LncRNA	TATDN1	miR-26b	NA	TNBC cells	Triple Negative Breast Cancer	Homo sapiens (human)	Cell proliferation assay;Cell transfection;Cell transfection;microarray;qPCR;RT-qPCR;	33192097	Overexpression of lncRNA TATDN1 Promotes Cancer Cell Proliferation in Triple Negative Breast Cancer by Regulating miR-26b Methylation.	BACKGROUND: Long non-coding RNA (lncRNA) TatD DNase Domain Containing 1 (TATDN1) is a recently characterized oncogenic lncRNA in several types of cancer including breast cancer. Our preliminary microarray analysis revealed its upregulation in triple negative breast cancer (TNBC) and its inverse correlation with microRNA-26b (miR-26b), which is a tumor suppressive miRNA in breast cancer. This study was therefore carried out to investigate the interaction between TATDN1 and miR-26b in TNBC. METHODS: A total of 66 pairs of TNBC and non-tumor tissues were collected from 66 patients (45.8 ± 10.5 years old) with TNBC through biopsy under the guidance of MRI before initiation of any therapies. Quantitative reverse transcription PCR (RT-qPCR), transient cell transfection, methylation specific PCR (MSP) and cell proliferation assay were carried out in this study. RESULTS: We found that TATDN1 was upregulated and miR-26b was downregulated in TNBC. Correlation analysis showed that the expression of TATDN1 and miR-26b was inversely correlated. In TNBC cells, overexpression of TATDN1 mediated the downregulation of miR-26b. Knockdown of TATDN1 led to the upregulation of miR-26b. Methylation-specific PCR showed that TATDN1 positively regulated the methylation of miR-26b gene. Cell proliferation analysis showed that TATDN1 positively regulated the proliferation of TNBC cells. Overexpression of miR-26b attenuated the effects of TATDN1 overexpression on cell proliferation. CONCLUSION: Therefore, overexpression of TATDN1 promotes cancer cell proliferation in TNBC by regulating the methylation of miR-26b gene.	NA	Cancer Manag Res. 2020 Nov 6;12:11403-11410. doi: 10.2147/CMAR.S258191. eCollection 2020.
4528	LncRNA	TCONS_00026334	miR-548n	TP53INP1	CRC cells	Colorectal Cancer	Homo sapiens (human)	microarray;	32986920	Long noncoding RNA TCONS_00026334 is involved in suppressing the progression of colorectal cancer by regulating miR-548n/TP53INP1 signaling pathway.	Recently, long noncoding RNAs (lncRNAs) were recognized as significant therapeutic targets in tumors. Our previous microarray analysis showed that lncRNA TCONS_000026334 expression was reduced in metastatic colorectal cancer (CRC) tissues. The objective of this study was to research the biological functions of TCONS_000026334 and the potential mechanism during the development of CRC. TCONS_00026334 transcription levels were detected in CRC tissues from 86 patients and different CRC cell lines. The clinical prognosis factors related to TCONS_00026334 expression were then analyzed. TCONS_000026334 was overexpressed from plasmid pcDNA3.1-TCONS_ 000026334 or knocked down using a small interfering RNA (siRNA). Furthermore, bioinformatics approach and luciferase reporter gene assays were utilized to search for candidate miRNAs of TCONS_00026334 and identify the downstream target genes. The results indicated that TCONS_00026334 expression in 86 CRC tissues was markedly lower than that in non-cancerous tissues. The aberrant expression of TCONS_00026334 correlated negatively with larger tumor size, distant metastasis, serological carcinoembryonic antigen level, and unfavorable survival of patients with CRC. TCONS_00026334 overexpression could inhibit the aggressive phenotypes of CRC in vitro and in vivo. Conversely, TCONS_00026334 silencing accelerated CRC cell proliferation and invasion. We then verified that TCONS_00026334 upregulated the expression level of TP53INP1, a target gene of miR-548n, via direct binding to miR-548n as a competing endogenous RNA. Taken together, our study showed that TCONS_00026334 acts as an anti-tumor and anti-metastatic gene by regulating the miR548n/TP53INP1 axis in the development of CRC.	NA	Cancer Med. 2020 Nov;9(22):8639-8649. doi: 10.1002/cam4.3473. Epub 2020 Sep 28.
4529	LncRNA	TCONS_00814106	miR-1343	TGFBR1	porcine granulosa cells	High-Fecundity Sow Ovarian	Homo sapiens (human)	Luciferase reporter assay;	33091558	Long non-coding RNA TCONS_00814106 regulates porcine granulosa cell proliferation and apoptosis by sponging miR-1343.	Recent evidence shows that long non-coding RNAs (lncRNAs), a class of non-coding RNAs, are involved in the regulation of reproductive processes. In this study, we identified a lncRNA, TCONS_00814106, that was upregulated in high-fecundity sow ovarian tissues and influenced by reproductive hormones. Bioinformatics analyses and luciferase reporter assays showed that TCONS_00814106 is a miR-1343 target. Cell counting kit (CCK)-8 and apoptosis assays showed that TCONS_00814106 promotes proliferation and inhibits apoptosis in porcine granulosa cells (GCs), and that this could be reversed by miR-1343. Also, we observed that transforming growth factor-β receptor type I (TGFBR1) is a functional target of miR-1343 in GCs. TCONS_00814106 serves as a competing endogenous RNA to regulate TGFBR1 expression by sponging miR-1343, thereby exerting regulatory functions in GCs. Overall, these results provide new insights into the biological function of the lncRNA TCONS_00814106.	NA	Mol Cell Endocrinol. 2021 Jan 15;520:111064. doi: 10.1016/j.mce.2020.111064. Epub 2020 Oct 19.
4530	Circular RNA	TGFBR2	miR-25-3p	TWIST1	Human aortic valve interstitial cells	Calcific Aortic Valve Disease	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33070258	CircRNA TGFBR2/MiR-25-3p/TWIST1 axis regulates osteoblast differentiation of human aortic valve interstitial cells.	INTRODUCTION: Calcified aortic valve disease (CAVD) is characterized by valve thickening and calcification. Osteoblast differentiation is one of the key steps of valve calcification. CircRNAs is involved in osteogenic differentiation of multiple mesenchymal cells. However, the function of circRNA TGFBR2 (TGFBR2) in CAVD remained unclear. We explored the effect and mechanism of TGFBR2 in modulating CAVD. MATERIALS AND METHODS: Human aortic valve interstitial cells (VICs) were subjected to osteogenic induction, and transfected with TGFBR2, miR-25-3p mimic and siTWIST1. The relationship between miR-25-3p and GFBR2 was predicted by starBase and confirmed by luciferase reporter and Person's correlation test. The relationship between miR-25-3p and TWIST1 was predicted by TargetScan and confirmed by luciferase reporter assay. The expressions of TGFBR2, miR-25-3p, TWIST1, osteoblast markers (RUNX2 and OPN) were detected by Western blot or/and qRT-PCR. Alkaline phosphatase (ALP) activity and calcium nodule was determined by colorimetric method and Alizarin Red S staining. RESULTS: The expression of TGFBR2 was down-regulated and that of miR-25-3p was up-regulated in calcific valves and osteogenic VICs. TGFBR2 was inversely correlated with miR-25-3p expression in calcific valves. TGFBR2 sponged miR-25-3p to regulate TWIST1 expression in osteogenic VICs. During osteogenic differentiation, ALP activity, calcium nodule, the levels of osteoblast markers were increased in VICs. MiR-25-3p overexpression or TWIST1 knockdown reversed the inhibitory effect of TGFBR2 overexpression on ALP activity, calcium nodule, the expressions of RUNX2 and OPN in osteogenic VICs. CONCLUSION: The findings indicated that TGFBR2/miR-25-3p/TWIST1 axis regulates osteoblast differentiation in VICs, supporting the fact that TGFBR2 is a miRNA sponge in CAVD.	NA	J Bone Miner Metab. 2021 May;39(3):360-371. doi: 10.1007/s00774-020-01164-4. Epub 2020 Oct 18.
4531	LncRNA	TINCR	miR-503-5p	EGFR	breast cancer cells	Breast Cancer	Homo sapiens (human)	Chromatin immunoprecipitation;	33446634	LncRNA TINCR favors tumorigenesis via STAT3-TINCR-EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer.	The long noncoding RNA (lncRNA) TINCR has recently been found to be associated with the progression of human malignancies, but the molecular mechanism of TINCR action remains elusive, particularly in breast cancer. The oncogenic role of TINCR was examined in vitro and in vivo in breast cancer. Next, the interaction between TINCR, DNMT1, and miR-503-5p methylation was explored. Moreover, the mechanism by which TINCR enhances EGFR expression and downstream signaling via an RNA-RNA interaction was comprehensively investigated. Furthermore, upstream transcriptional regulation of TINCR expression by STAT3 was examined by performing chromatin immunoprecipitation. Finally, feedback signaling in the STAT3-TINCR-EGFR downstream cascade was also investigated. TINCR is upregulated in human breast cancer tissues, and TINCR knockdown suppresses tumorigenesis in vitro and in vivo. Mechanistically, TINCR recruits DNMT1 to the miR-503-5p locus promoter, which increases the methylation and suppresses the transcriptional expression of miR-503-5p. Furthermore, TINCR also functions as a competing endogenous RNA to upregulate EGFR expression by sponging miR-503-5p. In addition, TINCR stimulates JAK2-STAT3 signaling downstream from EGFR, and STAT3 reciprocally enhances the transcriptional expression of TINCR. Our findings broaden the current understanding of the diverse manners in which TINCR functions in cancer biology. The newly identified STAT3-TINCR-EGFR-feedback loop could serve as a potential therapeutic target for human cancer.	NA	Cell Death Dis. 2021 Jan 14;12(1):83. doi: 10.1038/s41419-020-03188-0.
4532	Circular RNA	TMEM87A	miR-142-5p	ULK1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;qRT-PCR;Western blot;FISH;Luciferase reporter assay;RNA pull-down;RNA sequencing;	33155080	Circular RNA TMEM87A promotes cell proliferation and metastasis of gastric cancer by elevating ULK1 via sponging miR-142-5p.	BACKGROUND: Circular RNAs (circRNAs) act as vital regulators of gene expression in a variety of cancers. However, the role of circRNAs in gastric cancer (GC) remains largely unexplored. Herein, we identified that circTMEM87A sponges miR-142-5p to promote GC progression through up-regulating ULK1 expression. METHODS: The expression of circTMEM87A in GC was determined by RNA sequencing and quantitative real-time PCR (qRT-PCR). The effects of knockdown or exogenous expression of circTMEM87A on GC cell phenotypes were evaluated both in vitro and in vivo. The interacting miRNA of circTMEM87A was predicted by bioinformatics and confirmed by RNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization (FISH). The mechanism by which circTMEM87A/miR-142-5p/ULK1 axis promotes GC was determined by western blot, GFP/mRFP-LC3 puncta analysis, transmission electron microscope (TEM). RESULTS: CircTMEM87A was dramatically elevated in GC tissues and cell lines, and high circTMEM87A expression was closely correlated with poor prognosis of GC patients. Knockdown of circTMEM87A suppressed cell growth, migration, invasion and induced apoptosis in vitro, as well as inhibited GC tumorigenicity and lung metastasis potential in vivo. Meanwhile, circTMEM87A overexpression had the opposite effects. Furthermore, we demonstrated that circTMEM87A could act as a sponge of miR-142-5p to regulate ULK1 expression and GC progression. CONCLUSIONS: Our findings suggest that circTMEM87A functions as an oncogene through the miR-142-5p/ULK1 axis in GC. CircTMEM87A might be a prognostic biomarker as well as a promising therapeutic target for GC.	NA	J Gastroenterol. 2021 Feb;56(2):125-138. doi: 10.1007/s00535-020-01744-1. Epub 2020 Nov 6.
4533	LncRNA	TMPO-AS1	miR-383-5p	NA	Glioma Cells	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33262650	LncRNA TMPO-AS1 Promotes Proliferation and Invasion by Sponging miR-383-5p in Glioma Cells.	PURPOSE: Glioma is one of the most common malignant tumors affecting human health. Long non-coding RNA (lncRNA) TMPO-AS1 participates in the pathogenesis of various cancers. However, the role of lncRNA TMPO-AS1 in glioma remains largely unknown. This study aims to uncover the role of TMPO-AS1 and explore its potential mechanism in glioma. METHODS: Expression levels of TMPO-AS1 and miR-383-5p in glioma cell lines were measured by real-time quantitative PCR (RT-qPCR). CCK-8, colony formation, wound-healing, and Transwell assays were conducted to determine cell proliferation, migration and invasion abilities, respectively. Western blotting was applied to detect the expression of corresponding proteins. Immunofluorescence assay was performed to measure the expression of Ki67. The binding condition between TMPO-AS1 and miR-383-5p was verified by dual-luciferase reporter assay. RESULTS: We found that TMPO-AS1 was up-regulated while miR-383-5p was down-regulated in glioma cell lines, and knockdown of TMPO-AS1 significantly suppressed glioma cell proliferation, migration and invasion abilities. miR-383-5p was demonstrated to be a direct target of TMPO-AS1. Besides, inhibition of miR-383-5p abolished the effects of TMPO-AS1 knockdown on glioma cells. CONCLUSION: In summary, our study revealed that inhibition of lncRNA TMPO-AS1 could suppress glioma progression through targeting miR-383-5p. TMPO-AS1 might be used as a therapeutic target for glioma treatment.	NA	Cancer Manag Res. 2020 Nov 23;12:12001-12009. doi: 10.2147/CMAR.S282539. eCollection 2020.
4534	LncRNA	TMPO-AS1	miR-326	SOX12	LUAD cells	Lung Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;qPCR;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33293866	TMPO-AS1, a Novel E2F1-Regulated lncRNA, Contributes to the Proliferation of Lung Adenocarcinoma Cells via Modulating miR-326/SOX12 Axis.	BACKGROUND: TMPO-AS1, an antisense lncRNA located at human chromosome 12p23.1, has been identified as an oncogene involved in cell proliferation in various cancers, including LUAD. In this study, we aimed to explore the novel molecular mechanism of TMPO-AS1 underlying LUAD growth. MATERIALS AND METHODS: The transcription levels of TMPO-AS1, miR-326, and SOX12 in LUAD tissues and cell lines were detected by quantitative real-time PCR (qRT-PCR). The cell proliferation ability was evaluatect 3d by cell counting kit-8 (CCK-8) assay. Cell cycle and apoptosis analysis was assessed by flow cytometry. The target relationship among TMPO-AS1, miR-326, and SOX12 and promoter activity of TMPO-AS1 was measured using dual-luciferase reporter assay. The protein levels of SOX12 in LUAD cells were determined by Western blot. ChIP-qPCR assay was performed to validate the direct binding between E2F1 and TMPO-AS1 promoter. RESULTS: TMPO-AS1 was up-regulated in LUAD tissues as well as cell lines. Boosted TMPO-AS1 expression was positively correlated with poor prognosis and pathological stage in LUAD. Down-regulation of TMPO-AS1 could restrain the proliferation of LUAD cells through arresting the cell cycle at G0/G1 phase and inducing apoptosis in vitro. Mechanically, we demonstrated that TMPO-AS1 could modulate the proliferation of LUAD cells through increasing SOX12 expression level via sponging miR-326 in accordance with bioinformatics analysis and experimental validation. Furthermore, we identified that TMPO-AS1 could be activated by E2F transcription factor 1 (E2F1) as a novel target gene. CONCLUSION: TMPO-AS1 can modulate LUAD cell proliferation through E2F1/miR-326/SOX12 pathway.	NA	Cancer Manag Res. 2020 Dec 2;12:12403-12414. doi: 10.2147/CMAR.S269269. eCollection 2020.
4535	LncRNA	TMPO-AS1	miR-204-3p	ERBB2	NSCLC cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	32969763	LncRNA TMPO-AS1 facilitates the proliferation and metastasis of NSCLC cells by up-regulating ERBB2 via sponging miR-204-3p.	INTRODUCTION: This study aims at probing into the expression and biological function of long non-coding RNA (lncRNA) TMPO-AS1 in non-small cell lung cancer (NSCLC), and exploring its regulatory role for miR-204-3p and erb-b2 receptor tyrosine kinase 2 (ERBB2). METHODS: In this study, paired NSCLC samples were collected, and the expression levels of TMPO-AS1, miR-204-3p and ERBB2 were examined by quantitative real-time polymerase chain reaction (qRT-PCR); proliferative ability and colony formation ability were detected by CCK-8 assay and plate colony formation assay, respectively; flow cytometry was performed to detect the effect of TMPO-AS1 on apoptosis; Transwell assay was used to detect the changes of migration and invasion; qRT-PCR and Western blot were utilised to analyse the changes of miR-204-3p and ERBB2 regulated by TMPO-AS1; luciferase reporter gene assay and RNA immunoprecipitation assay were employed to determine the regulatory relationship between TMPO-AS1 and miR-204-3p. RESULTS: We demonstrated that TMPO-AS1 was significantly up-regulated in cancerous tissues of NSCLC samples, and positively correlated with the expression of ERBB2, while negatively correlated with miR-204-3p. After transfection of TMPO-AS1 shRNAs into NSCLC cells, the malignant phenotypes of NSCLC cells were significantly inhibited, while overexpression of TMPO-AS1 had opposite effects; TMPO-AS1 was also demonstrated to regulate the expression of miR-204-3p by sponging it, and indirectly modulate the expression of ERBB2. CONCLUSION: Collectively, we conclude that TMPO-AS1 has the potential to be the 'ceRNA' to regulate the expression of ERBB2 by sponging miR-204-3p in NSCLC.	NA	Int J Immunopathol Pharmacol. 2020 Jan-Dec;34:2058738420958947. doi: 10.1177/2058738420958947.
4536	LncRNA	TMPO-AS1	miR-140-5p	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;	33235626	Long non-coding RNA TMPO-AS1 promotes tumor progression via sponging miR-140-5p in breast cancer.	Long non-coding RNAs (lncRNAs) are involved in carcinogenesis and tumor suppression, and are novel biological tumor regulators. However, the functional roles of lncRNAs and their underlying dysregulation mechanisms in breast cancer are not completely understood. The aim of the present study was to investigate the clinical significance and biological functions of lncRNA TMPO antisense RNA 1 (TMPO-AS1) in breast cancer. TMPO-AS1 levels were measured in human cancer tissues and breast cancer cell lines, and the functional roles of TMPO-AS1 in breast cancer cells were investigated by performing in vitro and in vivo assays. Additionally, luciferase reporter assays were conducted to detect the association between microRNA (miR)-140-5p and TMPO-AS1. TMPO-AS1 expression levels were significantly increased in breast cancer tissues and cell lines compared with adjacent non-cancerous tissues and MCF-10A cells, respectively. In vitro and in vivo studies indicated that TMPO-AS1 knockdown significantly suppressed breast cancer cell viability at 48 and 72 h compared with the small interfering (si)RNA negative control group (NC; siNC). TMPO-AS1 knockdown in vitro inhibited MCF-7 and T47D cell migration and invasion compared with the siNC group. TMPO-AS1 knockdown in metastatic breast cancer cells also decreased metastatic colonization in the mouse lung compared with the short hairpin RNA NC group. Mechanistically, TMPO-AS1 promoted cellular viability and migration as a competing endogenous RNA by sponging miR-140-5p. The results suggested that TMPO-AS1 may serve as a potential therapeutic target in patients with breast cancer.	NA	Exp Ther Med. 2021 Jan;21(1):17. doi: 10.3892/etm.2020.9449. Epub 2020 Nov 5.
4537	LncRNA	TMPO-AS1	miR-140-5p	NA	breast cancer cells	Breast Cancer	Mus musculus (mouse)	Luciferase reporter assay;	33235626	Long non-coding RNA TMPO-AS1 promotes tumor progression via sponging miR-140-5p in breast cancer.	Long non-coding RNAs (lncRNAs) are involved in carcinogenesis and tumor suppression, and are novel biological tumor regulators. However, the functional roles of lncRNAs and their underlying dysregulation mechanisms in breast cancer are not completely understood. The aim of the present study was to investigate the clinical significance and biological functions of lncRNA TMPO antisense RNA 1 (TMPO-AS1) in breast cancer. TMPO-AS1 levels were measured in human cancer tissues and breast cancer cell lines, and the functional roles of TMPO-AS1 in breast cancer cells were investigated by performing in vitro and in vivo assays. Additionally, luciferase reporter assays were conducted to detect the association between microRNA (miR)-140-5p and TMPO-AS1. TMPO-AS1 expression levels were significantly increased in breast cancer tissues and cell lines compared with adjacent non-cancerous tissues and MCF-10A cells, respectively. In vitro and in vivo studies indicated that TMPO-AS1 knockdown significantly suppressed breast cancer cell viability at 48 and 72 h compared with the small interfering (si)RNA negative control group (NC; siNC). TMPO-AS1 knockdown in vitro inhibited MCF-7 and T47D cell migration and invasion compared with the siNC group. TMPO-AS1 knockdown in metastatic breast cancer cells also decreased metastatic colonization in the mouse lung compared with the short hairpin RNA NC group. Mechanistically, TMPO-AS1 promoted cellular viability and migration as a competing endogenous RNA by sponging miR-140-5p. The results suggested that TMPO-AS1 may serve as a potential therapeutic target in patients with breast cancer.	NA	Exp Ther Med. 2021 Jan;21(1):17. doi: 10.3892/etm.2020.9449. Epub 2020 Nov 5.
4538	LncRNA	TNK2-AS1	miR-4319	WDR1	OS cells	Osteosarcoma	Homo sapiens (human)	Rescue assay;	33164271	TNK2-AS1 upregulated by YY1 boosts the course of osteosarcoma through targeting miR-4319/WDR1.	Mounting research papers have suggested that long non-coding RNAs (lncRNAs) elicit important functions in the progression of osteosarcoma (OS). This study focused on the role of TNK2-AS1 in OS. TNK2-AS1 was powerfully expressed in OS tissues and cell lines. In addition, TNK2-AS1 downregulation inhibited proliferative, migratory, and invasive capacities while promoting apoptosis in OS cells. miR-4319 was removed by TNK2-AS1 and therefore TNK2-AS1 elevated WDR1 expression in OS cells. miR-4319 had an inhibitory influence on OS progression, while WDR1 was a contributor to OS progression. Rescue assays certified that TNK2-AS1 promoted malignant phenotypes in vitro and the growth in vivo of OS cells by upregulating WDR1. In depth, we found that YY1 accelerated the transcription of TNK2-AS1 in OS cells, and that its role in OS also depended on TNK2-AS1-regulated WDR1. In conclusion, TNK2-AS1 was positively modulated by YY1 and aggravated the development of OS by 'sponging' miR-4319 to elevate WDR1. The findings highlighted that TNK2-AS1 might be a promising target for the treatment of OS.	NA	Cancer Sci. 2021 Feb;112(2):893-905. doi: 10.1111/cas.14727. Epub 2020 Dec 1.
4539	LncRNA	TPTEP1	miR-106a-5p	P38	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR	33173989	lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR-106a-5p-mediated P38 MAPK signaling.	Glioma is diagnosed as the most common intracranial malignant tumor. Cancer stem cells determine stemness and radioresistance, and may facilitate glioma recurrence. The present study aimed to investigate whether the long non-coding RNA (lncRNA) transmembrane phosphatase with tensin homology pseudogene 1 (TPTEP1) regulated cell stemness and radioresistance of glioma, and determine the underlying molecular mechanism of TPTEP1 in the modulation of glioma progression. Cell and molecular biology techniques were applied for investigating the role of TPTEP1 in glioma cell lines, animal model, and clinical samples. The results demonstrated that TPTEP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo. In addition, TPTEP1 augmented MAPK14 expression by competitively interacting with microRNA (miR)-106a-5p, thus activating the P38 MAPK signaling pathway, and suppressing glioma stemness and radioresistance. TPTEP1 functionally bound to miR-106a-5p, which formed a reciprocal regulatory loop to stimulate the P38 MAPK signaling pathway. Low TPTEP1 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues, and were positively associated with poor prognosis of patients with glioma. Furthermore, analysis using data from The Cancer Genome Atlas database confirmed the molecular mechanism and biological significance of dysregulation of TPTEP1 in glioma progression. Taken together, the results of the present study suggest that TPTEP1 may be applied as a diagnostic and prognostic indicator for glioma, and may be an alternative target for the treatment of glioma.	NA	Mol Med Rep. 2020 Dec;22(6):4857-4867. doi: 10.3892/mmr.2020.11542. Epub 2020 Sep 28.
4540	LncRNA	TSPEAR-AS2	miR-1207-5p	CLDN4	GC cells	Gastric Cancer	Homo sapiens (human)	RNA immunoprecipitation;Chromatin immunoprecipitation;RNA immunoprecipitation;	33294297	BTEB2-Activated lncRNA TSPEAR-AS2 Drives GC Progression through Suppressing GJA1 Expression and Upregulating CLDN4 Expression.	Long non-coding RNAs (lncRNAs) are characterized as key layers of the genome in various cancers. TSPEAR-AS2 was highlighted to be a candidate lncRNA potentially involved in gastric cancer (GC) progression. However, the clinical significance and mechanism of TSPEAR-AS2 in GC required clarification. The clinical significance of TSPEAR-AS2 was elucidated through Kaplan-Meier Plotter. The mechanism of TSPEAR-AS2 in GC was clarified in vitro and in vivo using luciferase reporter, chromatin immunoprecipitation, RNA immunoprecipitation assays, and animal models. TSPEAR-AS2 elevation was closely correlated with overall survival of GC patients. A basic transcription element-binding protein 2 (BTEB2)-activated TSPEAR-AS2 model was first explored in this study. TSPEAR-AS2 silencing substantially reduced tumorigenic capacities of GC cells, while TSPEAR-AS2 elevation had the opposite effect. Mechanistically, TSPEAR-AS2 bound with both polycomb repressive complex 2 (PRC2) and argonaute 2 (Ago2). TSPEAR-AS2 knockdown significantly decreased H3K27me3 levels at promoter regions of gap junction protein alpha 1 (GJA1). Ago2 was recruited by TSPEAR-AS2, which was defined to sponge miR-1207-5p, contributing to the repression of claudin 4 (CLDN4) translation. The axis of EZH2/GJA1 and miR-1207-5p/CLDN4 mediated by BTEB2-activated-TSPEAR-AS2 plays an important role in GC progression, suggesting a new therapeutic direction in GC treatment.	NA	Mol Ther Nucleic Acids. 2020 Oct 22;22:1129-1141. doi: 10.1016/j.omtn.2020.10.022. eCollection 2020 Dec 4.
4541	LncRNA	TTN-AS1	miR-16-5p	Cyclin-E1	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;	33378944	LncRNA TTN-AS1 intensifies sorafenib resistance in hepatocellular carcinoma by sponging miR-16-5p and upregulation of cyclin E1.	Drug resistance has always been an important problem affecting the therapeutic effect of hepatocellular carcinoma (HCC). To investigate the potential role of lncRNA TTN-AS1 in HCC cells with sorafenib (SOR) resistance, and explore the underlying pathways, quantitative real time polymerase chain reaction (qRT-PCR) was used to test the expression of TTN-AS1 in HCC tissues and cells. Then, the expression of TTN-AS1 was down-regulated by shRNA, the activity changes, apoptosis and related protein expression in HCC cells with/without SOR treatment were observed in succession. Expression levels of the downstream target of TTN-AS1, miR-16-5p were studied by dual-luciferase binding assay, cell proliferation, and western blotting analysis. Nude mice models of human HCC with TTN-AS1 gene knockdown were established to observe the tumor growth. As the results revealed, TTN-AS1 silencing in HCC cells induced apoptosis by enhancing the sensitivity of cells to SOR, and the tumor in nude mice became smaller. The mechanism study showed that miR-16-5p was affected by TTN-AS1 sponge, up-regulated cyclin E1 expression, and regulated PTEN/Akt signaling pathway, thereby significantly alleviating the inhibition of apoptosis of HCC cells induced by TTN-AS1 gene. Collectively, our results provided TTN-AS1 as a potential therapeutic target for sorafenib resistance in HCC.	NA	Biomed Pharmacother. 2021 Jan;133:111030. doi: 10.1016/j.biopha.2020.111030. Epub 2020 Nov 28.
4542	LncRNA	TTN-AS1	miR-140-5p	NA	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	32934725	Long non-coding RNA TTN-AS1 promotes breast cancer cell migration and invasion via sponging miR-140-5p.	[This retracts the article DOI: 10.3892/ol.2019.11222.].	NA	Oncol Lett. 2020 Nov;20(5):157. doi: 10.3892/ol.2020.12018. Epub 2020 Aug 25.
4543	LncRNA	TTTY15	miR-29a-3p	DVL3	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;	33016900	LncRNA testis-specific transcript, Y-linked 15 (TTTY15) promotes proliferation, migration and invasion of colorectal cancer cells via regulating miR-29a-3p/DVL3 axis.	BACKGROUND: Long non-coding RNA testis-specific transcript, Y-linked 15 (TTTY15) is oncogenic in prostate cancer, however its expression and function in colorectal cancer remain largely unknown. METHODS: Paired colorectal cancer samples/normal tissues were collected, and the expression levels of TTTY15, miR-29a-3p and disheveled segment polarity protein 3 (DVL3) were examined by quantitative real-time polymerase chain reaction (qRT-PCR); TTTY15 shRNA and overexpression plasmids were transfected into HT29 and HCT-116 cell lines using lipofectamine reagent, respectively; the proliferation and colony formation were detected by CCK-8 assay and plate colony formation assay; qRT-PCR and Western blot were used to analyze the changes of miR-29a-3p and DVL3; dual-luciferase reporter gene assay was used to determine the regulatory relationships between miR-29a-3p and TTTY15, miR-29a-3p and DVL3. RESULTS: TTTY15 was significantly up-regulated in cancerous tissues of colorectal cancer samples, positively correlated with the expression of DVL3, while negatively correlated with the expression of miR-29a-3p. After TTTY15 shRNAs were transfected into colorectal cancer cells, the proliferation and metastasis of cancer cells were significantly inhibited, while TTTY15 overexpression had opposite biological effects. TTTY15 shRNA could reduce the expression of DVL3 on both mRNA and protein levels, and the luciferase activity of TTTY15 sequence was also inhibited by miR-29a-3p. DVL3 was also validated as a target gene of miR-29a-3p, and it could be repressed by miR-29a-3p mimics or TTTY15 shRNA. CONCLUSION: TTTY15 is abnormally upregulated in colorectal cancer tissues, and it can modulate the proliferation and metastasis of colorectal cancer cells. It functions as the ceRNA to regulate the expression of DVL3 by sponging miR-29a-3p.	NA	Cancer Biomark. 2021;31(1):1-11. doi: 10.3233/CBM-201709.
4544	LncRNA	TUG1	miR-29a-3p	NA	AC16 Cells	Hypoxia-Induced Myocardial Cell Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33165134	LncRNA TUG1 Contributes to Hypoxia-Induced Myocardial Cell Injury Through Downregulating miR-29a-3p in AC16 Cells.	Myocardial ischemia is a common reason that causes human death globally. Long noncoding RNA taurine upregulated 1 (TUG1) serves as an oncogene in a variety of cancers. In this article, we aimed to investigate the role of TUG1 and its underlying signal pathway in hypoxia-induced myocardial cell injury. Cell viability, apoptosis, and lactate dehydrogenase (LDH) release were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, western blot assay, and LDH cytotoxicity assay. Quantitative real-time polymerase chain reaction was applied to measure the enrichment of TUG1 and miR-29a-3p. MiR-29a-3p was predicted as a target of TUG1 by StarBase bioinformatic software, and the target relationship between TUG1 and miR-29a-3p was verified by dual-luciferase reporter assay. Hypoxia treatment induced the apoptosis and LDH release while inhibited the viability of AC16 cells. TUG1 was markedly upregulated while the level of miR-29a-3p was notably decreased in hypoxia-stimulated AC16 cells. TUG1 contributed to hypoxia-induced AC16 injury. MiR-29a-3p depletion intensified hypoxia-induced AC16 damage. TUG1 negatively regulated the expression of miR-29a-3p through their direct interaction in AC16 cells. TUG1 silencing-mediated influences in hypoxia-induced AC16 cells were partly reversed by the interference of miR-29a-3p. In conclusion, TUG1 accelerated hypoxia-induced AC16 injury through inversely modulating the level of miR-29a-3p. TUG1/miR-29a-3p axis might be an underlying therapeutic target for myocardial ischemia.	NA	J Cardiovasc Pharmacol. 2020 Nov;76(5):533-539. doi: 10.1097/FJC.0000000000000906.
4545	LncRNA	TUG1	miR-141-3p	CTNNB1	HK-2 cells	Renal Interstitial Fibrosis	Homo sapiens (human)	RACE;Western blot;	33135476	Silencing of the lncRNA TUG1 attenuates the epithelial-mesenchymal transition of renal tubular epithelial cells by sponging miR-141-3p via regulating β-catenin.	Renal interstitial fibrosis (RIF) is characterized by excessive extracellular matrix deposition and involves epithelial-mesenchymal transition (EMT). The lncRNA taurine-upregulated gene 1 (TUG1) participates in EMT in several cancers; however, the effect and underlying mechanism of TUG1 in RIF-related EMT remain unclear. Here, we explored the mechanisms by which TUG1 modulates RIF. An in vivo model of renal fibrosis was established by unilateral ureteral obstruction in Balb/c mice. Human renal proximal tubular epithelial (HK-2) cells treated with transforming growth factor (TGF)-β1 were used to induce the in vitro model. Morphological changes and TUG1 expression were assessed. HK-2 cells were transfected with siRNA to silence TUG1. Western blot analysis, immunofluorescence staining, cell proliferation, and migration assays were performed to examine TGF-β1-induced changes in EMT markers and EMT-like cell behaviors. TUG1 and β-catenin (CTNNB1) levels were significantly upregulated, whereas miR-141-3p was significantly downregulated, during EMT in vitro and in vivo. TUG1 knockdown or miR-141-3p overexpression supported the epithelioid morphology of HK-2 cells while enhancing the downregulation of E-cadherin and upregulation of vimentin, α-smooth muscle actin, and β-catenin levels in TGF-β1-treated HK-2 cells. TUG1 knockdown promoted the proliferation and decreased the migration of HK-2 cells and enhanced the downregulation of miR-141-3p levels in TGF-β1-treated HK-2 cells. TUG1 directly targeted miR-141-3p, and miR-141-3p was directly bound to CTNNB1. Downregulation of miR-141-3p inhibited TUG1 silencing-induced suppression of EMT. In conclusion, TUG1 promotes EMT in TGF-β1-induced HK-2 cells via upregulation of β-catenin levels by sponging miR-141-3p, suggesting a novel therapeutic candidate for RIF.	NA	Am J Physiol Renal Physiol. 2020 Dec 1;319(6):F1125-F1134. doi: 10.1152/ajprenal.00321.2020. Epub 2020 Nov 2.
4546	LncRNA	TUG1	miR-497	MEF2C	transverse abdominal aortic	Cardiac Hypertrophy	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33817315	Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis.	The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatment in vitro. Levels of lncRNA TUG1, miR-497 and myocyte enhancer factor 2C (MEF2C) mRNA were assessed by quantitative reverse transcriptase PCR (qRT-PCR). Western blot assay was performed to determine the expression of MEF2C protein. The endogenous interactions among TUG1, miR-497 and MEF2C were confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that TUG1 was upregulated and miR-497 was downregulated in the TAC rat model and Ang II-induced cardiomyocytes. TUG1 knockdown or miR-497 overexpression alleviated the hypertrophy induced by Ang II in cardiomyocytes. Moreover, TUG1 acted as a sponge of miR-497, and MEF2C was directly targeted and repressed by miR-497. miR-497 overexpression mediated the protective role of TUG1 knockdown in Ang II-induced cardiomyocyte hypertrophy. MEF2C was a functional target of miR-497 in regulating Ang II-induced cardiomyocyte hypertrophy. In addition, TUG1 regulated MEF2C expression through sponging miR-497. Knockdown of TUG1 rescued Ang II-induced hypertrophy in cardiomyocytes at least partly through targeting the miR-497/MEF2C axis, highlighting a novel promising therapeutic target for cardiac hypertrophy treatment.	NA	Open Life Sci. 2021 Mar 16;16(1):242-251. doi: 10.1515/biol-2021-0025. eCollection 2021.
4547	LncRNA	TUG1	miR-497	MEF2C	transverse abdominal aortic	Cardiac Hypertrophy	Rattus (rat)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33817315	Knockdown of TUG1 rescues cardiomyocyte hypertrophy through targeting the miR-497/MEF2C axis.	The aim of this study was to investigate the detailed role and molecular mechanism of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in cardiac hypertrophy. Cardiac hypertrophy was established by transverse abdominal aortic constriction (TAC) in vivo or angiotensin II (Ang II) treatment in vitro. Levels of lncRNA TUG1, miR-497 and myocyte enhancer factor 2C (MEF2C) mRNA were assessed by quantitative reverse transcriptase PCR (qRT-PCR). Western blot assay was performed to determine the expression of MEF2C protein. The endogenous interactions among TUG1, miR-497 and MEF2C were confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that TUG1 was upregulated and miR-497 was downregulated in the TAC rat model and Ang II-induced cardiomyocytes. TUG1 knockdown or miR-497 overexpression alleviated the hypertrophy induced by Ang II in cardiomyocytes. Moreover, TUG1 acted as a sponge of miR-497, and MEF2C was directly targeted and repressed by miR-497. miR-497 overexpression mediated the protective role of TUG1 knockdown in Ang II-induced cardiomyocyte hypertrophy. MEF2C was a functional target of miR-497 in regulating Ang II-induced cardiomyocyte hypertrophy. In addition, TUG1 regulated MEF2C expression through sponging miR-497. Knockdown of TUG1 rescued Ang II-induced hypertrophy in cardiomyocytes at least partly through targeting the miR-497/MEF2C axis, highlighting a novel promising therapeutic target for cardiac hypertrophy treatment.	NA	Open Life Sci. 2021 Mar 16;16(1):242-251. doi: 10.1515/biol-2021-0025. eCollection 2021.
4548	LncRNA	TUG1	miR-145-5p	TRPC6	CRC cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	32985219	The lncRNA TUG1 promotes cell growth and migration in colorectal cancer via the TUG1-miR-145-5p-TRPC6 pathway.	Colorectal cancer (CRC) is the third-most prevalent malignant tumor. Taurine upregulated gene 1 (TUG1), a long non-coding RNA (lncRNA), is reportedly involved in the physiological and pathological processes of CRC. However, the role of TUG1 in the progression of CRC and its underlying mechanisms are largely unknown. Here, we measured the expression of TUG1 in clinical samples from CRC patients and found that the expression level of TUG1 was higher in CRC tissues compared with the normal adjacent tissues. We then performed knockdown of TUG1 with siRNAs in two CRC cell lines and found that TUG1 knockdown inhibited the viability, proliferation, and migration of CRC cells, and reduced the ability of CRC cells to form subcutaneous tumors. Furthermore, we discovered that TUG1 affects the cellular processes in CRC cells by sponging miR-145-5p. We further found that miR-145-5p inhibits the expression of the protein-encoding gene Transient Receptor Potential Cation Channel Subfamily C Member 6 (TRPC6), and that overexpression of TRPC6 restored the inhibitory role of miR-145-5p in CRC cells. In conclusion, we have demonstrated that TUG1 exerts its role by modulating the TUG1-miR-145-5p-TRPC6 regulatory axis, thus revealing a novel molecular mechanism for the effects of TUG1 in the progression of CRC. Our data indicate that the TUG1-miR-145-5p-TRPC6 signaling pathway could serve as a target for the diagnosis and treatment of CRC.	NA	Biochem Cell Biol. 2021 Apr;99(2):249-260. doi: 10.1139/bcb-2020-0017. Epub 2020 Sep 27.
4549	LncRNA	TUG1	miR-29c-3p	PDGF-BB	endothelial progenitor cells	Diabetes Mellitus	Mus musculus (mouse)	Western blot;Flow Cytometry assay;luciferase assay;	33059750	TUG1 enhances high glucose-impaired endothelial progenitor cell function via miR-29c-3p/PDGF-BB/Wnt signaling.	BACKGROUND: Diabetes is associated with the dysfunction of endothelial progenitor cells (EPCs), characterized as impaired angiogenesis, a phenomenon thought to be involved in the development of diabetic foot. lncRNA plays an essential role in microvascular dysfunction and signaling pathways in patients with diabetes. lncRNA taurine upregulated gene 1 (TUG1) participates in angiogenesis in various cells. However, the mechanisms of TUG1 activity in EPCs have not been elucidated. METHODS: We isolated and then characterized EPCs from the peripheral blood of mice using immunofluorescence and flow cytometry. Western blot detected the wnt/β-catenin pathway in high glucose-treated EPCs. Bioinformatics analysis predicted a putative binding site for TUG1 on miR-29c-3p. The interactions among TUG1, platelet-derived growth factor-BB (PDGF-BB), and miR-29c-3p were analyzed by luciferase assays. In vivo, diabetic mouse ischemic limb was treated with normal saline or TUG1 overexpression lentiviruses. RESULTS: We found that EPC migration, invasion, and tube formation declined after treatment with high glucose, but improved with TUG1 overexpression. Mechanically, wnt/β-catenin pathway and autophagy were involved in the function of TUG1 overexpression in high glucose-treated EPCs. Moreover, TUG1 regulates the PDGF-BB/wnt pathway and function of high glucose-treated EPCs via miR-29c-3p. In vivo, injection of TUG1 lentivirus in a diabetic mouse ischemic limb model stimulated angiogenesis. CONCLUSIONS: Our findings suggest that TUG1 restores high glucose-treated EPC function by regulating miR-29c-3p/PDGF-BB/Wnt signaling.	NA	Stem Cell Res Ther. 2020 Oct 15;11(1):441. doi: 10.1186/s13287-020-01958-3.
4550	LncRNA	TUG1	miR-421	mTOR	neuronal cells	Status Epilepticus	Rattus (rat)	qRT-PCR	33007387	LncRNA TUG1 inhibits neuronal apoptosis in status epilepticus rats via targeting the miR-421/mTOR axis.	Status epilepticus (SE) induces apoptosis of hippocampal neurons. However, the underlying mechanism in SE is not fully understood. Recently, lncRNA TUG1 is reported as a significant mediator in neuronal development. In present study, we aimed to investigate whether lncRNA TUG1 induces apoptosis of hippocampal neurons in SE rat models. TUG1 expression in serum of normal volunteers and SE patients, SE rats and neurons with epileptiform discharge was detected. SE rat model was established and intervened with TUG1 to evaluate hippocampal neuronal apoptosis. The experiments in vitro were further performed in neurons with epileptiform discharge to verify the effects of TUG1 on neuronal apoptosis of SE rats. The downstream mechanism of TUG1 was predicted and verified. miR-421 was intervened to perform the rescue experiments. Levels of oxidative stress and inflammation-related factors and mTOR pathway-related proteins in SE rats and hippocampal neurons were detected. TUG1 was highly expressed in serum of SE patients, SE rats and neurons with epileptiform discharge. Inhibition of TUG1 relieved pathological injury, oxidative stress and inflammation and reduced neuronal apoptosis in SE rats, which were further verified in hippocampal neurons. TUG1 upregulated TIMP2 expression by targeting miR-421. Overexpressed miR-421 inhibited hippocampal neuronal apoptosis. TUG1 knockout inactivated the mTOR pathway via the miR-421/TIMP2 axis to relieve neuronal apoptosis, oxidative stress and inflammation in SE rats and hippocampal neurons. Taken together, these findings showed that downregulation of lncRNA TUG1 inhibited apoptosis of hippocampal neurons in SE rats, and attenuated oxidative stress and inflammation damage through regulating the miR-421/mTOR axis.	NA	Cell Signal. 2020 Dec;76:109787. doi: 10.1016/j.cellsig.2020.109787. Epub 2020 Sep 30.
4551	LncRNA	TUG1	miR-29a-3p	ELN	MLE-12 cells	Bronchopulmonary Dysplasia	Mus musculus (mouse)	ELISA;qRT-PCR;Western blot;	33194901	Long Non-coding RNA TUG1 Modulates Expression of Elastin to Relieve Bronchopulmonary Dysplasia via Sponging miR-29a-3p.	Objective: Multiple studies have highlighted that long non-coding RNAs (lncRNAs) may exert paramount roles in relieving bronchopulmonary dysplasia (BPD). The aim of our investigation is to probe the role and mechanism of lncRNA taurine upregulated gene 1 (TUG1) in BPD. Methods: The current mouse model of BPD was simulated by induction of hyperoxia, and hyperoxia-induced mouse type II alveolar epithelial (MLE-12) (MLE-12) cells were established as a cellular model. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to determine relative expressions of TUG1, miR-29a-3p, and elastin (ELN). We assessed cell apoptosis by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining. Western blot was used for detection of apoptosis-related proteins. Moreover, cell viability was tested by cell counting kit-8 (CCK-8) assay. Inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter (DLR) assay was employed to confirm relationship between genes. Results: Upregulation of miR-29a-3p was found in lung tissues of BPD mice compared with lung tissues without BPD, while downregulations of TUG1 and ELN were discovered in BPD tissues in comparison with tissues without BPD. Increasing TUG1 was shown to alleviate lung injury of BPD mice and promote proliferation of hyperoxia-induced MLE-12 cells. Meanwhile, TUG1 inhibited inflammatory response and cell apoptosis in lung tissues of BPD mice and hyperoxia-induced MLE-12 cells. miR-29a-3p was targeted by TUG1 and negatively modulated by TUG1. ELN was inversely regulated by miR-29a-3p. Meantime, suppressive effects of TUG1 on apoptosis and inflammation were reversed by decreasing ELN or increasing miR-29a-3p in hyperoxia-induced MLE-12 cells. Conclusion: lncRNA TUG1 relieved BPD through regulating the miR-29a-3p/ELN axis, which provided a therapeutic option to prevent or ameliorate BPD.	NA	Front Pediatr. 2020 Oct 30;8:573099. doi: 10.3389/fped.2020.573099. eCollection 2020.
4552	LncRNA	TUG1	miR-421	mTOR	neuronal cells	Status Epilepticus	Homo sapiens (human)	qRT-PCR	33007387	LncRNA TUG1 inhibits neuronal apoptosis in status epilepticus rats via targeting the miR-421/mTOR axis.	Status epilepticus (SE) induces apoptosis of hippocampal neurons. However, the underlying mechanism in SE is not fully understood. Recently, lncRNA TUG1 is reported as a significant mediator in neuronal development. In present study, we aimed to investigate whether lncRNA TUG1 induces apoptosis of hippocampal neurons in SE rat models. TUG1 expression in serum of normal volunteers and SE patients, SE rats and neurons with epileptiform discharge was detected. SE rat model was established and intervened with TUG1 to evaluate hippocampal neuronal apoptosis. The experiments in vitro were further performed in neurons with epileptiform discharge to verify the effects of TUG1 on neuronal apoptosis of SE rats. The downstream mechanism of TUG1 was predicted and verified. miR-421 was intervened to perform the rescue experiments. Levels of oxidative stress and inflammation-related factors and mTOR pathway-related proteins in SE rats and hippocampal neurons were detected. TUG1 was highly expressed in serum of SE patients, SE rats and neurons with epileptiform discharge. Inhibition of TUG1 relieved pathological injury, oxidative stress and inflammation and reduced neuronal apoptosis in SE rats, which were further verified in hippocampal neurons. TUG1 upregulated TIMP2 expression by targeting miR-421. Overexpressed miR-421 inhibited hippocampal neuronal apoptosis. TUG1 knockout inactivated the mTOR pathway via the miR-421/TIMP2 axis to relieve neuronal apoptosis, oxidative stress and inflammation in SE rats and hippocampal neurons. Taken together, these findings showed that downregulation of lncRNA TUG1 inhibited apoptosis of hippocampal neurons in SE rats, and attenuated oxidative stress and inflammation damage through regulating the miR-421/mTOR axis.	NA	Cell Signal. 2020 Dec;76:109787. doi: 10.1016/j.cellsig.2020.109787. Epub 2020 Sep 30.
4553	LncRNA	TUG1	miR-29a-3p	ELN	MLE-12 cells	Bronchopulmonary Dysplasia	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;	33194901	Long Non-coding RNA TUG1 Modulates Expression of Elastin to Relieve Bronchopulmonary Dysplasia via Sponging miR-29a-3p.	Objective: Multiple studies have highlighted that long non-coding RNAs (lncRNAs) may exert paramount roles in relieving bronchopulmonary dysplasia (BPD). The aim of our investigation is to probe the role and mechanism of lncRNA taurine upregulated gene 1 (TUG1) in BPD. Methods: The current mouse model of BPD was simulated by induction of hyperoxia, and hyperoxia-induced mouse type II alveolar epithelial (MLE-12) (MLE-12) cells were established as a cellular model. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to determine relative expressions of TUG1, miR-29a-3p, and elastin (ELN). We assessed cell apoptosis by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining. Western blot was used for detection of apoptosis-related proteins. Moreover, cell viability was tested by cell counting kit-8 (CCK-8) assay. Inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA). Dual-luciferase reporter (DLR) assay was employed to confirm relationship between genes. Results: Upregulation of miR-29a-3p was found in lung tissues of BPD mice compared with lung tissues without BPD, while downregulations of TUG1 and ELN were discovered in BPD tissues in comparison with tissues without BPD. Increasing TUG1 was shown to alleviate lung injury of BPD mice and promote proliferation of hyperoxia-induced MLE-12 cells. Meanwhile, TUG1 inhibited inflammatory response and cell apoptosis in lung tissues of BPD mice and hyperoxia-induced MLE-12 cells. miR-29a-3p was targeted by TUG1 and negatively modulated by TUG1. ELN was inversely regulated by miR-29a-3p. Meantime, suppressive effects of TUG1 on apoptosis and inflammation were reversed by decreasing ELN or increasing miR-29a-3p in hyperoxia-induced MLE-12 cells. Conclusion: lncRNA TUG1 relieved BPD through regulating the miR-29a-3p/ELN axis, which provided a therapeutic option to prevent or ameliorate BPD.	NA	Front Pediatr. 2020 Oct 30;8:573099. doi: 10.3389/fped.2020.573099. eCollection 2020.
4554	LncRNA	TUG1	miR-29b-3p	CDK	colonic epithelial YAMC cells	Ulcerative Colitis	Homo sapiens (human)	MTT assay;RIP assay;Western blot;Flow Cytometry assay;Luciferase activity assay;MTT assay;RNA pull-down;	33047284	LncRNA TUG1 regulates the balance of HuR and miR-29b-3p and inhibits intestinal epithelial cell apoptosis in a mouse model of ulcerative colitis.	This study aimed to investigate the role of long non-coding RNA (lncRNA) taurine up-regulated 1 (TUG1) in the development of ulcerative colitis (UC) and to explore the underlying mechanisms. A murine model of UC was induced by dextran sodium sulfate (DSS) exposure. The colonic epithelial YAMC cells were treated with TNF-α to simulate the inflammatory environment of intestinal epithelial cells (IECs). RNA pull-down and RIP assays were performed to analyze the interaction between TUG1 and HuR. Luciferase activity assay was conducted to evaluate the interaction between TUG1 and miR-29b-3p. Cell proliferation was evaluated by MTT assay. Cell apoptosis was assessed by flow cytometry and western blot analysis of apoptosis-related proteins. TUG1 overexpression promoted cell proliferation and inhibited cell apoptosis in the TNF-α-stimulated YAMC cells. The mechanistic analysis showed that TUG1 positively regulated the HuR/c-myc axis via its interaction with HuR, leading to upregulation of c-myc expression; meanwhile, TUG1 negatively regulated the miR-29b-3p/CDK2 signaling via binding to miR-29b-3p, leading to derepression of CDK2 expression. Further animal experiments showed that TUG1 overexpression attenuated UC progression in the DSS-induced UC in mice. Collectively, TUG1 inhibits IEC apoptosis and UC progression by regulating the balance of HuR and miR-29b-3p.	NA	Hum Cell. 2021 Jan;34(1):37-48. doi: 10.1007/s13577-020-00428-5. Epub 2020 Oct 12.
4555	LncRNA	TUSC7	miR-181a	RASSF6	OS cell lines	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33416181	lncRNA TUSC7 inhibits osteosarcoma progression through the miR-181a/RASSF6 axis.	Osteosarcoma (OS) is one of the most aggressive malignancies, accompanied by an elevated incidence and a decreased rate of healing. Recently, several long non-coding RNAs (lncRNAs) have been reported to be involved in OS progression. Although tumor suppressor candidate 7 (TUSC7) was reported as a novel lncRNA, little is known about its biological functions in OS. The present study was designed to explore whether TUSC7 was involved in the pathological development of OS using various methods, including hematoxylin and eosin staining, Cell Counting Kit-8 assay, colony formation assay and Transwell assay. The present study revealed that TUSC7 expression was downregulated in OS tissues and cell lines compared with in normal tissues and cell lines. Functionally, the current results revealed that overexpression of TUSC7 inhibited OS cell proliferation, migration and invasion, while promoting apoptosis in vitro and in vivo. Next, the subcellular distribution of TUSC7 was examined by nuclear/cytoplasmic RNA fractionation and reverse transcription-quantitative PCR. Mechanistic studies revealed that TUSC7 exerted its role by sponging microRNA (miR)-181a in OS cell lines. Ras association domain family member 6 (RASSF6) was confirmed as a target gene of miR-181a, and the expression levels of RASSF6 were negatively regulated by miR-181a. Additionally, the results of rescue experiments suggested that overexpression of miR-181a neutralized the inhibitory effects of TUSC7 overexpression on OS cells. Overall, the present study demonstrated that the tumor suppressor role of TUSC7 in OS progression was mediated through the miR-181a/RASSF6 axis, which may represent a new therapeutic target for OS.	NA	Int J Mol Med. 2021 Feb;47(2):583-594. doi: 10.3892/ijmm.2020.4825. Epub 2020 Dec 18.
4556	LncRNA	UCA1	miR-513a-3p	CYP1B1	GC cells	Gastric Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	33469378	LncRNA UCA1 Enhances Cisplatin Resistance by Regulating CYP1B1-mediated Apoptosis via miR-513a-3p in Human Gastric Cancer.	BACKGROUND: Chemoresistance contributes to treatment failure of gastric cancer (GC) patients but the molecular mechanism of chemoresistance in GC is still unclear. Long-chain noncoding RNA (lncRNA) urothelial cancer associated 1 (UCA1) is associated with resistance to chemotherapy drugs. METHODS: We detected the expression of UCA1 in 53 pairs of GC tumor tissue and adjacent normal tissue, human normal gastric mucosa cells (GES-1) and human GC cells (HGC-27, SNU-5, AGS, SGC-7901, and NCI-N87) using RT-qPCR. Small RNA interference technology was used to knock down the expression of UCA1 in gastric cancer cells. CCK8 solution was used to detect cell viability. Flow cytometry was used to detect apoptosis, and Western blotting was used to detect protein expression. RESULTS: UCA1 was highly expressed in GC tissues and cells, and knockdown of UCA1 increased chemosensitivity to cisplatin by inducing cell apoptosis. Furthermore, UCA1 promoted CYP1B1 expression by binding to miR-513a-3p in human GC cells in vitro, and UCA1/CYP1B1 expression was negatively related to miR-513a-3p expression, while UCA1 expression was positively related to CYP1B1 expression in human GC tissues. Moreover, overexpression of miR-513a-3p or knockdown of CYP1B1 increased chemosensitivity to cisplatin, and knockdown of miR-513a-3p or overexpression of CYP1B1 decreased chemosensitivity to cisplatin by inducing cell apoptosis in human GC cells. Importantly, overexpression of CYP1B1 reduced chemosensitivity to cisplatin which increased by knockdown of UCA1, and knockdown of CYP1B1 increased chemosensitivity to cisplatin which decreased by knockdown of miR-513a-3p in human GC cells. CONCLUSION: The lncRNA UCA1/miR-513a-3p/CYP1B1 axis regulates cisplatin resistance in human GC cells; hence, it is a potential target for treating chemoresistance in GC.	NA	Cancer Manag Res. 2021 Jan 14;13:367-377. doi: 10.2147/CMAR.S277399. eCollection 2021.
4557	LncRNA	UCA1	miR-143	BCL-2	cardiac microvascular endothelial cells	H/R Injury	Homo sapiens (human)	qRT-PCR	33591946	Transfer of lncRNA UCA1 by hUCMSCs-derived exosomes protects against hypoxia/reoxygenation injury through impairing miR-143-targeted degradation of Bcl-2.	Ischemia results in neuronal damage via alterations in gene transcription and protein expression. Long noncoding RNAs (LncRNAs) are pivotal in the regulation of target protein expression in hypoxia/reoxygenation (H/R). In this study, we observed the function of exosomes-carried lncRNA UCA1 in H/R-induced injury of cardiac microvascular endothelial cells (CMECs). In H/R cell model, CMECs were co-cultured with human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-ex). The loss-of-function experiments were conducted to assess the effect of lncRNA UCA1 on H/R injury by assessing the biological behaviors of CMECs. The relationship among lncRNA UCA1, miR-143 and Bcl-2 were verified. An ischemia-reperfusion (I/R) rat model was established. Then hUCMSC-ex was injected into I/R rats to identify its effects on apoptosis and autophagy. Functional rescue experiments were performed to verify the sponge system. In vitro and in vivo experiments showed that hUCMSC-ex protected I/R rats and H/R CMECs against injury. Silencing UCA1 in hUCMSC-ex or miR-143 overexpression aggravated H/R injury in CMECs. LncRNA UCA1 competitively bound to miR-143 to upregulate Bcl-2. And hUCMSCs-ex/si-UCA1+inhi-miR-143 treatment protected CMECs against H/R injury and inhibited hyperautophagy. Together, hUCMSC-ex-derived lncRNA UCA1 alleviates H/R injury through the miR-143/Bcl-2/Beclin-1 axis. Hence, this study highlights a stem cell-based approach against I/R injury.	NA	Aging (Albany NY). 2021 Feb 11;13(4):5967-5985. doi: 10.18632/aging.202520. Epub 2021 Feb 11.
4558	LncRNA	UCA1	miR-143	BCL-2	cardiac microvascular endothelial cells	H/R Injury	Rattus (rat)	qRT-PCR	33591946	Transfer of lncRNA UCA1 by hUCMSCs-derived exosomes protects against hypoxia/reoxygenation injury through impairing miR-143-targeted degradation of Bcl-2.	Ischemia results in neuronal damage via alterations in gene transcription and protein expression. Long noncoding RNAs (LncRNAs) are pivotal in the regulation of target protein expression in hypoxia/reoxygenation (H/R). In this study, we observed the function of exosomes-carried lncRNA UCA1 in H/R-induced injury of cardiac microvascular endothelial cells (CMECs). In H/R cell model, CMECs were co-cultured with human umbilical cord mesenchymal stem cell-derived exosomes (hUCMSC-ex). The loss-of-function experiments were conducted to assess the effect of lncRNA UCA1 on H/R injury by assessing the biological behaviors of CMECs. The relationship among lncRNA UCA1, miR-143 and Bcl-2 were verified. An ischemia-reperfusion (I/R) rat model was established. Then hUCMSC-ex was injected into I/R rats to identify its effects on apoptosis and autophagy. Functional rescue experiments were performed to verify the sponge system. In vitro and in vivo experiments showed that hUCMSC-ex protected I/R rats and H/R CMECs against injury. Silencing UCA1 in hUCMSC-ex or miR-143 overexpression aggravated H/R injury in CMECs. LncRNA UCA1 competitively bound to miR-143 to upregulate Bcl-2. And hUCMSCs-ex/si-UCA1+inhi-miR-143 treatment protected CMECs against H/R injury and inhibited hyperautophagy. Together, hUCMSC-ex-derived lncRNA UCA1 alleviates H/R injury through the miR-143/Bcl-2/Beclin-1 axis. Hence, this study highlights a stem cell-based approach against I/R injury.	NA	Aging (Albany NY). 2021 Feb 11;13(4):5967-5985. doi: 10.18632/aging.202520. Epub 2021 Feb 11.
4559	LncRNA	UCA1	miR-613	SPOCK1	GBC cells	Gallbladder Cancer	Homo sapiens (human)	Flow cytometry assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33090888	Knockdown of Long Noncoding RNA Urothelial Carcinoma-Associated 1 Represses Gallbladder Cancer Advancement by Regulating SPOCK1 Expression Through Sponging miR-613.	Background: Gallbladder cancer (GBC) is the most common biliary tract malignancy. Long noncoding RNA urothelial carcinoma-associated 1 (UCA1) and MicroRNA-613 (miR-613) have been reported to be involved in the progression of various cancers. However, the regulatory mechanism between UCA1 and miR-613 in GBC is unclear. Materials and Methods: The expression levels of UCA1, miR-613, and secreted protein/osteonectin, cwcv, and kazal-like domains proteoglycan 1 (SPOCK1) mRNA were detected using quantitative real-time polymerase chain reaction. Cell proliferation, migration, invasion, and apoptosis were determined with MTT, transwell, or flow cytometry assays. The levels of SPOCK1 protein, Bax, cleaved-casp-3, and Bcl-2 were determined by western blot analysis. The relationship between miR-613 and UCA1 or SPOCK1 was verified through dual-luciferase reporter and/or RNA immunoprecipitation assays. Xenograft assay was performed to verify the role of UCA1 in vivo. Results: UCA1 and SPOCK1 were upregulated, whereas miR-613 was downregulated in GBC tissues and cells. UCA1 silencing decreased tumor growth in vivo and impeded proliferation, migration, invasion, and induced apoptosis of GBC cells in vitro. Notably, UCA1 acted as a sponge for miR-613, which targeted SPOCK1 in GBC cells. Moreover, UCA1 enhancement reversed the repressive impact of miR-613 mimic on the malignancy of GBC cells. UCA1 regulated SPOCK1 expression through adsorbing miR-613. Furthermore, SPOCK1 elevation overturned UCA1 silencing mediated the malignant behaviors of GBC cells. Conclusion: UCA1 knockdown suppressed GBC progression through downregulating SPOCK1 via sponging miR-613, providing an evidence for UCA1 as a target for GBC treatment.	NA	Cancer Biother Radiopharm. 2020 Oct 22. doi: 10.1089/cbr.2020.4290.
4560	LncRNA	UCA1	miR-203	HK2	EC cells	Esophageal Cancer	Homo sapiens (human)	Luciferase activity assay;	33204264	Upregulated Long Noncoding RNA UCA1 Enhances Warburg Effect via miR-203/HK2 Axis in Esophagal Cancer.	Reprogrammed glucose metabolism of enhanced aerobic glycolysis, also known as Warburg effect, which exerts a significant contributor to cancer progression, is regarded as a hallmark of cancer. The roles of long noncoding RNAs (lncRNA) in regulating cancer via metabolic reprogramming are mostly unknown, including esophagal cancer (EC). Here, we showed that how the lncRNA urothelial carcinoma associated 1 (UCA1) exerts pro-oncogene in regulating EC glucose metabolism. Firstly, we found that upregulated UCA1 expression enhances the malignant phenotypes of EC, including poor outcome, larger tumor size, positive lymphatic invasion, and advanced pathological stages. UCA1 silencing could suppress EC cell proliferation and metastasis. Following, bioinformatics analyses revealed that UCA1 regulated the HK2 expression through functioning as a competing endogenous RNA (ceRNA). Mechanistically, UCA1 overexpression could elevate the activation of HK2 oncogenes via inhibition of miR-203 activity, as evidenced by the positive correlation of UCA1 with HK2 and inverse correlation with miR-203 expression. Luciferase activity assay further verified the targeting relationship between UCA1, miR-203, and HK2. Upregulated UCA1 in EC cells significantly suppressed the degradation of HK2 by miR-203. Further research showed that upregulated UCA1 effectively increased the rate of glucose uptake, lactate output, and ECAR value, all of which can be attenuate by HK2 interference and 2-DG, whereas knockdown of UCA1 had the opposite effect. In sum, our findings suggest that the UCA1/miR-203/HK2 axis contributes to EC development by reprogramming tumor glucose metabolism, providing new insight into the management of EC patients.	NA	J Oncol. 2020 Nov 4;2020:8847687. doi: 10.1155/2020/8847687. eCollection 2020.
4561	LncRNA	UCA1	miR-455	RUNX2	TR-8/SVneo cells	Spontaneous Abortion	Homo sapiens (human)	qPCR;	33085763	Urothelial cancer associated 1 (UCA1) regulates trophoblast viability, proliferation, and migration via modulating the UCA1/miR-455/RUNX2 signaling pathway.	Spontaneous abortion (SA) is the spontaneous loss of a pregnancy before 20 gestational weeks. The causes of SA are still largely unknown. Long noncoding RNA (lncRNA) urothelial cancer associated 1 (UCA1) plays an important role in cellular progress. However, there is no report focusing on the role of UCA1 in SA. Here, we revealed that, compared with that in clinical samples from elective induced abortion, UCA1 expression was decreased in samples from SA patients as shown by qPCR method. The results demonstrated that UCA1 might be involved in the progress of SA. Then, we found that knockdown of UCA1 reduced cell viability and inhibited cell proliferation and migration of HTR-8/SVneo trophoblast cells as shown by CCK8, EdU, and Transwell methods. Furthermore, we demonstrated that UCA1 could act as a molecular sponge for miR-455 in HTR-8/SVneo cells as shown by luciferase reporter system method. In addition, miR-455 inhibited cell viability, cell proliferation and migration via regulating RUNX2 in HTR-8/SVneo cells. Ultimately, we illustrated that UCA1 plays its role via absorbing miR-455, thus promoting RUNX2 expression in HTR-8/SVneo cells. Collectively, this study first revealed the role and mechanism of UCA1 in the growth and migration of HTR-8/SVneo cells, indicating its potential as a diagnostic biomarker and therapeutic target for SA.	NA	Acta Biochim Biophys Sin (Shanghai). 2020 Oct 19;52(10):1120-1130. doi: 10.1093/abbs/gmaa096.
4562	LncRNA	UCA1	miR-331-3p	EIF4G1	PCa tissues and cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	32943997	Down-regulation of lncRNA UCA1 enhances radiosensitivity in prostate cancer by suppressing EIF4G1 expression via sponging miR-331-3p.	BACKGROUND: We aimed to explore the role of long noncoding RNA urothelial carcinoma-associated 1 (lncRNA UCA1) and its underlying mechanism in the radioresistance of prostate cancer (PCa). METHODS: QRT-PCR was conducted to measure the expression of UCA1, microRNA-331-3p (miR-331-3p) and eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) in PCa tissues and cells. The relative protein level was determined by western blot assay. Cell proliferation and apoptosis were detected by MTT, colony formation assay, and flow cytometry, respectively. The target interaction between miR-331-3p and UCA1 or EIF4G1 was predicted through bioinformatics analysis, and verified by dual-luciferase reporter gene assay system. RESULTS: The high levels of UCA1 and EIF4G1 as well as the low level of miR-331-3p were observed in PCa tissues and cell lines. UCA1 and EIF4G1 expression were significantly upregulated by Gy radiation treatement. UCA1 or EIF4G1 knockdown repressed cell growth and enhanced cell apoptosis in 22RV1 and DU145 cells under radiation. Moreover, overexpression of EIF4G1 abolished UCA1 knockdown-induced effect on 6 Gy irradiated PCa cells. UCA1 sponged miR-331-3p to regulate EIF4G1 expression. CONCLUSIONS: LncRNA UCA1 deletion suppressed the radioresistance to PCa by suppressing EIF4G1 expression via miR-331-3p. UCA1 acted as a potential regulator of radioresistance of PCa, providing a promising therapeutic target for PCa.	NA	Cancer Cell Int. 2020 Sep 11;20:449. doi: 10.1186/s12935-020-01538-8. eCollection 2020.
4563	LncRNA	UPK1A-AS1	miR-138-5p	EZH2	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;RNA sequencing;	33121524	Long noncoding RNA UPK1A-AS1 indicates poor prognosis of hepatocellular carcinoma and promotes cell proliferation through interaction with EZH2.	BACKGROUND: Dysregulation of long non-coding RNAs (lncRNAs) is responsible for cancer initiation and development, positioning lncRNAs as not only biomarkers but also promising therapeutic targets for cancer treatment. A growing number of lncRNAs have been reported in hepatocellular carcinoma (HCC), but their functional and mechanistic roles remain unclear. METHODS: Gene Set Enrichment Analysis was used to investigate the molecular mechanism of UPK1A antisense RNA 1 (UPK1A-AS1). Cell Counting Kit-8 assays, EdU assays, flow cytometry, western blotting, and xenograft assays were used to confirm the role of UPK1A-AS1 in the proliferation of HCC cells in vitro and in vivo. Bioinformatics analyses and quantitative polymerase chain reaction (qRT-PCR) were performed to explore the interplay between UPK1A-AS1 and enhancer of zeste homologue 2 (EZH2). RNA immunoprecipitation (RIP), RNA pull-down assays, western blotting, and qRT-PCR were conducted to confirm the interaction between UPK1A-AS1 and EZH2. The interaction between UPK1A-AS1 and miR-138-5p was examined by luciferase reporter and RIP assays. Finally, the expression level and prognosis value of UPK1A-AS1 in HCC were analyzed using RNA sequencing data from The Cancer Genome Atlas datasets. RESULTS: We showed that UPK1A-AS1, a newly identified lncRNA, promoted cellular proliferation and tumor growth by accelerating cell cycle progression. Cell cycle-related genes, including CCND1, CDK2, CDK4, CCNB1, and CCNB2, were significantly upregulated in HCC cells overexpressing UPK1A-AS1. Furthermore, overexpression of UPK1A-AS1 could protect HCC cells from cis-platinum toxicity. Mechanistically, UPK1A-AS1 interacted with EZH2 to mediate its nuclear translocation and reinforce its binding to SUZ12, leading to increased H27K3 trimethylation. Targeting EZH2 with specific small interfering RNA impaired the UPK1A-AS1-mediated upregulation of proliferation and cell cycle progression-related genes. Moreover, miR-138-5p was identified as a direct target of UPK1A-AS1. Additionally, UPK1A-AS1 was significantly upregulated in HCC, and the upregulation of UPK1A-AS1 predicted poor prognosis for patients with HCC. CONCLUSIONS: Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.	NA	J Exp Clin Cancer Res. 2020 Oct 29;39(1):229. doi: 10.1186/s13046-020-01748-y.
4564	LncRNA	VENTXP1	miR-205-5p	NA	head and neck squamous cell carcinoma cells	Head And Neck Squamous  Carcinoma	Homo sapiens (human)	qRT-PCR	33037177	Epigenetic regulation of VENTXP1 suppresses tumor proliferation via miR-205-5p/ANKRD2/NF-kB signaling in head and neck squamous cell carcinoma.	An increasing number of studies have shown that long noncoding RNAs (lncRNAs) play important roles in tumor development and progression. However, their involvement in head and neck squamous cell carcinoma (HNSCC) remains largely unknown. Epigenetic regulation is one major mechanism utilized by cancer cells to control lncRNA expression. We identified that lncRNA VENTXP1 was epigenetically silenced in multiple cancer types, and its lower expression was correlated with poorer survival in HNSCC patients. Through in silico analysis and experimental validation, we identified miR-205-5p and its direct interacting partner of VENTXP1, which regulates HNSCC cell proliferation and tumorigenicity. Using RNA-seq and differential gene expression analysis, we further identified ANKRD2 as a miR-205-5p target, which plays an essential role in modulating NF-kB signaling. These findings suggest that VENTXP1 inhibits tumor growth via suppressing miR-205-5p/ANKRD2-mediated NF-kB signaling in HNSCC. Thus, pharmaceutical targeting of DNA methylation to restore VENTXP1 expression might constitute a therapeutic strategy for HNSCC.	NA	Cell Death Dis. 2020 Oct 9;11(10):838. doi: 10.1038/s41419-020-03057-w.
4565	LncRNA	Vi4	miR-185-5p	Igfbp3	neuronal cells	Neonatal Hypoxic Ischemic Encephalopathy	Homo sapiens (human)	Luciferase reporter assay;	33262982	Vi4-miR-185-5p-Igfbp3 Network Protects the Brain From Neonatal Hypoxic Ischemic Injury via Promoting Neuron Survival and Suppressing the Cell Apoptosis.	Neonatal hypoxic ischemic encephalopathy (HIE) due to birth asphyxia is common and causes severe neurological deficits, without any effective therapies currently available. Neuronal death is an important driving factors of neurological disorders after HIE, but the regulatory mechanisms are still uncertain. Long non-coding RNA (lncRNA) or ceRNA network act as a significant regulator in neuroregeneration and neuronal apoptosis, thus owning a great potential as therapeutic targets in HIE. Here, we found a new lncRNA, is the most functional in targeting the Igfbp3 gene in HIE, which enriched in the cell growth and cell apoptosis processes. In addition, luciferase reporter assay showed competitive regulatory binding sites to the target gene Igfbp3 between TCONS00044054 (Vi4) and miR-185-5p. The change in blood miR-185-5p and Igfbp3 expression is further confirmed in patients with brain ischemia. Moreover, Vi4 overexpression and miR-185-5p knock-out promote the neuron survival and neurite growth, and suppress the cell apoptosis, then further improve the motor and cognitive deficits in rats with HIE, while Igfbp3 interfering got the opposite results. Together, Vi4-miR-185-5p-Igfbp3 regulatory network plays an important role in neuron survival and cell apoptosis and further promote the neuro-functional recovery from HIE, therefore is a likely a drug target for HIE therapy.	NA	Front Cell Dev Biol. 2020 Nov 9;8:529544. doi: 10.3389/fcell.2020.529544. eCollection 2020.
4566	LncRNA	VPS9D1-AS1	miR-525-5p	HMGA1	CRC cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33116849	Long Noncoding RNA VPS9D1-AS1 Sequesters microRNA-525-5p to Promote the Oncogenicity of Colorectal Cancer Cells by Upregulating HMGA1.	BACKGROUND: The long noncoding RNA VPS9D1 antisense RNA 1 (VPS9D1-AS1) has emerged as a critical regulator in non-small-cell lung, gastric, and prostate cancers. In this study, we measured the expression levels of VPS9D1-AS1 in colorectal cancer (CRC) and determined the role of VPS9D1-AS1 in regulating the biological activities of CRC cells. In addition, we thoroughly elucidated the molecular mechanism mediating the oncogenic activities of VPS9D1-AS1 in CRC. METHODS: The expression levels of VPS9D1-AS1 in CRC tissues and cell lines were detected via quantitative reverse transcription-polymerase chain reaction. Loss-of-function experiments were performed to detect the effects of VPS9D1-AS1 silencing on CRC cell proliferation, apoptosis, migration, and invasion as well as on tumor growth in vivo. Bioinformatics analysis predicted the potential microRNAs (miRNAs) interacting with VPS9D1-AS1, and this prediction was further confirmed via RNA immunoprecipitation and luciferase reporter assays. RESULTS: Our results demonstrated the upregulated expression of VPS9D1-AS1 in CRC tissues and cell lines. Functionally, VPS9D1-AS1 interference suppressed CRC cell proliferation, migration, and invasion and promoted cell apoptosis in vitro. In addition, the loss of VPS9D1-AS1 hindered tumor growth in vivo. Mechanistic studies identified VPS9D1-AS1 as a competing endogenous RNA in CRC cells, in which VPS9D1-AS1 acted as a molecular sponge of miR-525-5p and consequently increased the expression of high-mobility group AT-hook 1 (HMGA1). Moreover, rescue experiments revealed that the regulatory effects of VPS9D1-AS1 deficiency on CRC cells were abolished after miR-525-5p inhibition or HMGA1 restoration. CONCLUSION: The newly identified competing endogenous RNA pathway involving VPS9D1-AS1, miR-525-5p, and HMGA1 is implicated in the control of CRC progression and may provide an effective target for CRC diagnosis and therapy.	NA	Cancer Manag Res. 2020 Oct 9;12:9915-9928. doi: 10.2147/CMAR.S273687. eCollection 2020.
4567	LncRNA	WWOX-AS1	miR-20b-5p	WWOX	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	Rescue assay;	32931356	LncRNA WWOX-AS1 sponges miR-20b-5p in hepatocellular carcinoma and represses its progression by upregulating WWOX.	Increasing evidence has revealed that long noncoding RNAs (lncRNAs) emerge as pivotal regulators in diverse cancers, including hepatocellular carcinoma (HCC). This study was conducted to investigate the role of lncRNA WWOX antisense RNA 1 (WWOX-AS1) in HCC progression. Our present study illustrated that WWOX-AS1 was lowly expressed in HCC tissues and cell lines. High WWOX-AS1 expression was further confirmed to predict a favorable prognosis in HCC patients. Through functional assays, we observed that upregulated WWOX-AS1 was correlated with decreased cell proliferation, migration, epithelial to mesenchymal transition (EMT) process and increased cell apoptosis, suggesting that WWOX-AS1 exerted anti-carcinogenic role in the development of HCC. Moreover, WWOX, the nearby gene of WWOX-AS1, was found at a low level in HCC tissues and cell lines. Furthermore, there was a positive relationship between WWOX-AS1 and WWOX. Additionally, WWOX overexpression hampered cell proliferation, migration, EMT process and induced cell apoptosis in HCC. Mechanically, WWOX-AS1 was identified as a cytoplasmic RNA in HCC cells and sponged miR-20b-5p to regulate WWOX expression. Rescue assays further indicated that WWOX knockdown counteracted WWOX-AS1 overexpression-mediated suppressive function on HCC progression. Collectively, WWOX-AS1/miR-20b-5p/WWOX axis suppresses HCC tumorigenesis, hinting a potential molecular mechanism for the therapy of HCC patients.	NA	Cancer Biol Ther. 2020 Oct 2;21(10):927-936. doi: 10.1080/15384047.2020.1806689. Epub 2020 Sep 15.
4568	LncRNA	XIST	miR-98-5p	PAPPA	HUVECs	Atherosclerosis	Homo sapiens (human)	Flow cytometry assay;qPCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33542956	LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs.	Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.	NA	Open Med (Wars). 2021 Jan 8;16(1):117-127. doi: 10.1515/med-2021-0200. eCollection 2021.
4569	LncRNA	XIST	miR-497-5p	FOXK1	colorectal cancer cell	Colorectal Cancer 	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33298041	The lncRNA XIST promotes colorectal cancer cell growth through regulating the miR-497-5p/FOXK1 axis.	BACKGROUND: Recent studies suggest that long noncoding RNAs (lncRNAs) play an important role in tumorigenesis. As a newly identified lncRNA, the role of XIST in colorectal cancer (CRC) has not been established. Here, we sought to characterize the role of XIST and its associated regulatory network in CRC cells. METHODS: Expression of XIST mRNA, miR-497-5p, and forkhead box k1 (FOXK1) in CRC cells and tissues were detected using quantitative real-time polymerase chain reaction (qRT-PCR). Proliferation and apoptosis of CRC cells were determined using the CCK-8 cell counting assay and flow cytometry. The rate of cell migration and invasion was determined using a transwell assay. The relationships between XIST, miR-497-5p, and FOXK1 were predicted and confirmed using a dual-luciferase reporter assay. Expression of FOXK1 protein was quantified by Western blot. RESULTS: XIST and FOXK1 expression were significantly upregulated in CRC tissues and cell lines, while miR-497-5p expression was downregulated. XIST knockdown significantly suppressed CRC cell proliferation, migration, and invasion. Silencing of XIST also reversed the downregulation of miR-497-5p and upregulation of FOXK1. Moreover, blocking XIST expression was shown to inhibit CRC tumor growth in vivo and the effects were antagonized by the loss of miR-497-5p. miR-497-5p was shown to act as a sponge of XIST and also targeted FOXK1 in CRC cells. CONCLUSIONS: XIST was shown to promote the malignancy of CRC cells by competitively binding to miR-497-5p, resulting in an increase in FOXK1 expression. These results suggest that targeting of XIST may represent a possible treatment for CRC.	NA	Cancer Cell Int. 2020 Dec 10;20(1):553. doi: 10.1186/s12935-020-01647-4.
4570	LncRNA	XIST	miR-361-3p	STX17	retinoblastoma cells	Retinoblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33155266	Long non-coding RNA XIST confers aggressive progression via miR-361-3p/STX17 in retinoblastoma cells.	OBJECTIVE: Retinoblastoma (RB) is a frequent intraocular tumor in children. Long-non-coding RNA X inactive specific transcript (XIST) has been reported to participate in the RB process, while its potential role remains largely unknown. PATIENTS AND METHODS: The expression patterns of XIST, microRNA (miR)-361-3p, and Syntaxin 17 (STX17) were determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, and transwell assays were employed to reckon cell viability, apoptosis, and mobility in RB cells, respectively. Besides, the levels of STX17 and autophagy-related proteins were detected utilizing Western blot. Dual-Luciferase reporter assay was implemented to evaluate the interaction between miR-361-3p and XIST or STX17, and the role of XIST in tumor growth was analyzed through xenograft tumor model. RESULTS: The expression levels of XIST and STX17 were higher in RB tissues and cells, but miR-361-3p was downregulated. Loss of XIST was inversely connected with aggressive characteristics, showing as the curb of cell proliferation, migration, invasion, autophagy, and enhancement of apoptosis in RB cells. Also, the deficiency of XIST caused the decrease of tumor growth in vivo. Meanwhile, miR-361-3p inhibitor partially rescued XIST detection-mediated cell behaviors in vitro. Similarly, miR-361-3p mimic-mediated suppressive effect on aggressive phenotypes was abolished after overexpression of STX17 in RB cells. Mechanically, XIST was a sponge of miR-361-3p to regulate STX17. CONCLUSIONS: XIST functioned as an oncogenic lncRNA via miR-361-3p/STX17 axis in the progression of RB, which might provide a promising theoretical basis for the clinical therapy of RB.	NA	Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10433-10444. doi: 10.26355/eurrev_202010_23395.
4571	LncRNA	XIST	miR-124-3p	ITGB1	renal cells	Renal Ischemia Reperfusion Injury	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33299380	Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury.	OBJECTIVE: Renal ischemia/reperfusion injury (RI/RI) is the main cause of acute kidney injury. Total glucosides of paeony (TGP) are a traditional Chinese medicine. This study was aimed at exploring the role of TGP in RI/RI and its underlying mechanism of action. METHODS: Rat RI/RI models were constructed by surgical operation. Serum creatinine (Scr) and blood urea nitrogen (BUN) were used to evaluate renal function. The levels of proinflammatory cytokines were detected by ELISA. RI/RI was simulated by hypoxia/reoxygenation (H/R) treatment in renal cells in vitro. The lncRNA XIST (XIST) expression was analyzed by qRT-PCR. Then, the viability and apoptosis of renal cells were detected by MTT and flow cytometry assay. Additionally, dual-luciferase reporter assay was used to determine the interactions among XIST, microRNA-124-3p (miR-124-3p), and ITGB1. RESULTS: TGP improved renal function and inhibited inflammatory responses after RI/RI. XIST expression was highly expressed in rat RI/RI models and H/R-treated renal cells, whereas treatment with TGP downregulated the XIST expression. Additionally, TGP increased viability and attenuated apoptosis and inflammation of H/R-treated renal cells via inhibiting XIST. Moreover, XIST was competitively bound to miR-124-3p, and ITGB1 was a target of miR-124-3p. miR-124-3p overexpression or ITGB1 inhibition rescued the reduction effect on viability and mitigated the promoting effects on cell apoptosis and inflammation caused by XIST overexpression in H/R-treated renal cells. CONCLUSIONS: In vivo, TGP attenuated renal dysfunction and inflammation in RI/RI rats. In vitro, TGP inhibited XIST expression to modulate the miR-124-3p/ITGB1 axis, alleviating the apoptosis and inflammation of H/R-treated renal cells.	NA	Mediators Inflamm. 2020 Nov 24;2020:8869511. doi: 10.1155/2020/8869511. eCollection 2020.
4572	LncRNA	XIST	miR-124-3p	ITGB1	renal cells	Renal Ischemia Reperfusion Injury	Rattus (rat)	Dual-luciferase reporter assay;ELISA;Flow cytometry assay;qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	33299380	Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury.	OBJECTIVE: Renal ischemia/reperfusion injury (RI/RI) is the main cause of acute kidney injury. Total glucosides of paeony (TGP) are a traditional Chinese medicine. This study was aimed at exploring the role of TGP in RI/RI and its underlying mechanism of action. METHODS: Rat RI/RI models were constructed by surgical operation. Serum creatinine (Scr) and blood urea nitrogen (BUN) were used to evaluate renal function. The levels of proinflammatory cytokines were detected by ELISA. RI/RI was simulated by hypoxia/reoxygenation (H/R) treatment in renal cells in vitro. The lncRNA XIST (XIST) expression was analyzed by qRT-PCR. Then, the viability and apoptosis of renal cells were detected by MTT and flow cytometry assay. Additionally, dual-luciferase reporter assay was used to determine the interactions among XIST, microRNA-124-3p (miR-124-3p), and ITGB1. RESULTS: TGP improved renal function and inhibited inflammatory responses after RI/RI. XIST expression was highly expressed in rat RI/RI models and H/R-treated renal cells, whereas treatment with TGP downregulated the XIST expression. Additionally, TGP increased viability and attenuated apoptosis and inflammation of H/R-treated renal cells via inhibiting XIST. Moreover, XIST was competitively bound to miR-124-3p, and ITGB1 was a target of miR-124-3p. miR-124-3p overexpression or ITGB1 inhibition rescued the reduction effect on viability and mitigated the promoting effects on cell apoptosis and inflammation caused by XIST overexpression in H/R-treated renal cells. CONCLUSIONS: In vivo, TGP attenuated renal dysfunction and inflammation in RI/RI rats. In vitro, TGP inhibited XIST expression to modulate the miR-124-3p/ITGB1 axis, alleviating the apoptosis and inflammation of H/R-treated renal cells.	NA	Mediators Inflamm. 2020 Nov 24;2020:8869511. doi: 10.1155/2020/8869511. eCollection 2020.
4573	LncRNA	XIST	miR-29a	MYC	AML KG-1 cells	Acute Myeloid Leukemia	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	33228517	Silencing long non-coding RNA XIST suppresses drug resistance in acute myeloid leukemia through down-regulation of MYC by elevating microRNA-29a expression.	BACKGROUND: Long non-coding RNAs (lncRNAs) are biomarkers participating in multiple disease development including acute myeloid leukemia (AML). Here, we investigated molecular mechanism of X Inactive-Specific Transcript (XIST) in regulating cellular viability, apoptosis and drug resistance in AML. METHODS: XIST, miR-29a and myelocytomatosis oncogene (MYC) expression in AML bone marrow cells collected from 62 patients was evaluated by RT-qPCR and Western blot analysis. Besides, the relationship among XIST, miR-29a and MYC was analyzed by dual luciferase reporter assay, RIP, and RNA pull down assays. AML KG-1 cells were treated with anti-tumor drug Adriamycin. The role of XIST/miR-29a/MYC in cellular viability, apoptosis and drug resistance in AML was accessed via gain- and loss-of-function approaches. At last, we evaluated role of XIST/miR-29a/MYC on tumorigenesis in vivo. RESULTS: XIST and MYC were up-regulated, and miR-29a was down-regulated in AML bone marrow cells. Silencing XIST inhibited cellular activity and drug resistance but promoted cellular apoptosis of KG-1 cells by down-regulating MYC. XIST inhibited miR-29a expression to up-regulate MYC. Moreover, silencing XIST inhibited tumorigenesis of AML cells in vivo. CONCLUSIONS: Overall, down-regulation of XIST decreased MYC expression through releasing the inhibition on miR-29a, thereby reducing drug resistance, inhibiting viability and promoting apoptosis of AML cells.	NA	Mol Med. 2020 Nov 24;26(1):114. doi: 10.1186/s10020-020-00229-4.
4574	LncRNA	XIST	miR-27b-3p	ADAMTS-5	synovium-derived mesenchymal stem cells	Temporomandibular Joint Osteoarthritis	Homo sapiens (human)	qPCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33128918	Long non-coding RNA XIST regulates chondrogenic differentiation of synovium-derived mesenchymal stem cells from temporomandibular joint via miR-27b-3p/ADAMTS-5 axis.	OBJECTIVE: Temporomandibular joint osteoarthritis (TMJOA) is a common degenerative disease in jaw joint, accompanied by articular cartilage destruction. Differentiation of stem cells to cartilage has important therapeutic implications in TMJ cartilage repair. Previous studies revealed that lncRNA XIST participated in various biological processes. However, the effect of XIST on chondrogenic differentiation of synovium-derived mesenchymal stem cells (SMSCs) remains unclear. Our study aimed to investigate the function of XIST in chondrogenic differentiation of human SMSCs from TMJ. METHODS: Alcian blue staining was performed to determine proteoglycan in SMSCs. qPCR, western blotting and immunofluorescence assays were allowed to assess sex determining region Y-box 9 (SOX9), Collagen type II alpha 1 chain (COL2A1) and Aggrecan (ACAN) expression. The direct interaction between miR-27b-3p and XIST or ADAMTS-5 was confirmed by dual luciferase reporter assay or RNA immunoprecipitation (RIP) assay. RESULTS: XIST was remarkably down-regulated in chondrogenic differentiation of SMSCs. Functional analysis demonstrated that XIST silencing promoted chondrogenic differentiation of SMSCs. Dual luciferase reporter and RIP assays identified that XIST acted as a sponge for miR-27b-3p. Moreover, XIST regulated ADAMTS-5 expression by directly binding miR-27b-3p. More importantly, miR-27b-3p/ADAMTS-5 rescued the effects of XIST on chondrogenic differentiation of SMSCs. CONCLUSION: The results suggest that XIST modulates SMSCs chondrogenic differentiation via the miR-27b-3p/ADAMTS-5 axis, which provides new targets for TMJOA treatment.	NA	Cytokine. 2021 Jan;137:155352. doi: 10.1016/j.cyto.2020.155352. Epub 2020 Oct 28.
4575	LncRNA	XIST	miR-142-5p	NA	RB cells	Retinoblastoma	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;RNA pull-down;	33015766	LncRNA XIST promotes proliferation and epithelial-mesenchymal transition of retinoblastoma cells through sponge action of miR-142-5p.	OBJECTIVE: The aim of the study was to investigate the effect of lncRNA XIST on the proliferation and epithelial-mesenchymal transition (EMT) of retinoblastoma (RB) and its relevant mechanism. PATIENTS AND METHODS: 60 RB patients who were treated in our hospital were collected. The expression of XIST in tissues and cells was detected by qRT-PCR, and the effect of XIST on the prognosis of RB cells was observed. Stable and transient over-expression and suppression vectors were established and transfected into RB cells WERI-RB1 and Y79. CCK-8, transwell, and flow cytometry were used to evaluate the proliferation, invasion, and apoptosis of transfected cells. Western Blot was used to detect apoptosis-related proteins and EMT-related proteins. Dual-Luciferase report was used to determine the relationship between XIST and miR-142-5p. RNA pull-down and RIP experiments were used to determine the relationship between XIST and miR-142-5p. RESULTS: XIST was highly expressed in RB patients, which had a high diagnostic value. Patients with XIST high expression had a poor prognosis. After overexpression of XIST, the proliferation, invasion and EMT of cells increased, and apoptosis rate decreased, while inhibition of Ptv1 had the opposite effect. Dual-Luciferase report confirmed that XIST could target miR-142-5p. Functional analysis showed that the overexpression of miR-142-5p inhibited the proliferation, invasion and EMT of RB cells and promoted cell apoptosis. Rescue experiments showed that miR-142-5p could eliminate the inhibition of miR-142-5p on the proliferation, invasion, and EMT of RB cells by upregulating XIST expression. CONCLUSIONS: Ptv1 can promote the proliferation, invasion, and EMT of RB cells by regulating miR-142-5p.	NA	Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9256-9264. doi: 10.26355/eurrev_202009_23007.
4576	LncRNA	XIST	miR-152	KLF4	GBM cells	Glioblastoma	Homo sapiens (human)	qRT-PCR	33090636	Steroid receptor coactivator-1 enhances the stemness of glioblastoma by activating long noncoding RNA XIST/miR-152/KLF4 pathway.	Glioblastoma (GBM) recurrence is attributed to the presence of therapy-resistant glioblastoma stem cells. Steroid receptor coactivator-1 (SRC-1) acts as an oncogenic regulator in many human tumors. The relationship between SRC-1 and GBM has not yet been studied. Herein, we investigate the role of SRC-1 in GBM. In this study, we found that SRC-1 expression is positively correlated with grades of glioma and inversely correlated with glioma patient's prognosis. Steroid receptor coactivator-1 promotes the proliferation, migration, and tumor growth of GBM cells. Notably, SRC-1 knockdown suppresses the stemness of GBM cells. Mechanistically, long noncoding RNA X-inactive specific transcript (XIST) is regulated by SRC-1 at the posttranscriptional level and mediates the function of SRC-1 in promoting stemness-like properties of GBM. Steroid receptor coactivator-1 can promote the expression of Kruppel-like factor 4 (KLF4) through the XIST/microRNA (miR)-152 axis. Additionally, arenobufagin and bufalin, SRC small molecule inhibitors, can reduce the proliferation and stemness of GBM cells. This study reveals SRC-1 promotes the stemness of GBM by activating the long noncoding RNA XIST/miR-152/KLF4 pathway and provides novel markers for diagnosis and therapy of GBM.	NA	Cancer Sci. 2021 Feb;112(2):604-618. doi: 10.1111/cas.14685. Epub 2020 Dec 14.
4577	LncRNA	XIST	miR-let-7b	NA	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33009035	Long non-coding RNA X-inactive-specific transcript contributes to cisplatin resistance in gastric cancer by sponging miR-let-7b.	X-inactive-specific transcript (XIST) is a 19 kb noncoding RNA which is oncogenic in many cancers including gastric cancer. It is reported that XIST contributes to gastric cancer cells resistant to cisplatin, but specific mechanisms governing this resistance remain unclear. We firstly examined the XIST level in gastric cancer cells and tumor specimens. We confirmed that XIST is overexpressed in gastric cancer cells and tumors, which further contributed to the poor prognosis of patients with gastric cancer. We also confirmed that high XIST level contributes to the cisplatin resistance in gastric cancer cells. Subsequently, we predicted microRNAs that have the potential to interact with XIST and found that Let-7b-5p may directly interact with XIST. We confirmed the direct interaction between XIST and Let-7b-5p and identified a negative correlation between the level of Let-7b-5p and XIST in gastric cancer tumors. Meanwhile, Let-7b-5p inhibitor treatment can partially rescued the effect of XIST-specific small interfering RNA on cell proliferation and apoptosis by regulating Aurora kinase B expression. XIST functions as an oncogene in gastric cancer which contributes to the cisplatin resistance by interacting with Let-7b-5p.	NA	Anticancer Drugs. 2020 Nov;31(10):1018-1025. doi: 10.1097/CAD.0000000000000942.
4578	LncRNA	XIST	miR-30b-5p	CCL16	WI-38 cells	Lps-Induced Acute Lung Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33817304	Silencing XIST mitigated lipopolysaccharide (LPS)-induced inflammatory injury in human lung fibroblast WI-38 cells through modulating miR-30b-5p/CCL16 axis and TLR4/NF-κB signaling pathway.	BACKGROUND: Emerging evidence shows that long noncoding RNA (lncRNA) has been a novel insight in various diseases, including pneumonia. Even though lncRNA X-inactive-specific transcript (XIST) is well studied, its role in pneumonia remains to be largely unrevealed. METHODS: Expression of XIST, miRNA-30b-5p (miR-30b-5p), and CC chemokine ligand 16 (CCL16) was detected using reverse transcriptase quantitative polymerase chain reaction and western blotting; their interaction was confirmed by dual-luciferase reporter assay. Apoptosis, inflammation, and toll-like receptor 4 (TLR4)/NF-κB signaling pathway were measured using methyl thiazolyl tetrazolium assay, flow cytometry, western blotting, and enzyme-linked immunosorbent assay. RESULTS: Lipopolysaccharide (LPS) stimulation decreased cell viability and B cell lymphoma (Bcl)-2 expression, and increased cell apoptosis rate and expression of Bcl-2-associated X protein (Bax), cleaved-caspase-3, interleukin (IL)-6, IL-1β, and tumor necrosis factor α (TNF-α) in WI-38 cells. Expression of XIST and CCL16 was upregulated in the serum of patients with pneumonia and LPS-induced WI-38 cells, respectively; silencing XIST and CCL16 could suppress LPS-induced apoptosis and inflammation in WI-38 cells, and this protection was abolished by miR-30b-5p downregulation. Moreover, XIST and CCL16 could physically bind to miR-30b-5p, and XIST regulated CCL16 expression via sponging miR-30b-5p. TLR4 and phosphorylated P65 (p-P65) and p-IκB-α were highly induced by LPS treatment, and this upregulation was diminished by blocking XIST, accompanied with CCL16 downregulation and miR-30b-5p upregulation. CONCLUSIONS: Silencing XIST could alleviate LPS-induced inflammatory injury in human lung fibroblast WI-38 cells through modulating miR-30b-5p/CCL16 axis and inhibiting TLR4/NF-κB signaling pathway.	NA	Open Life Sci. 2021 Feb 6;16(1):108-127. doi: 10.1515/biol-2021-0005. eCollection 2021.
4579	LncRNA	XIST	miR-199a-3p	Sp1	brain tissue	Parkinsons Disease	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33494069	LncRNA XIST sponges miR-199a-3p to modulate the Sp1/LRRK2 signal pathway to accelerate Parkinson's disease progression.	In vitro and in vivo models of Parkinson's disease were established to investigate the effects of the lncRNA XIST/miR-199a-3p/Sp1/LRRK2 axis. The binding between XIST and miR-199a-3p as well as miR-199a-3p and Sp1 were examined by luciferase reporter assay and confirmed by RNA immunoprecipitation analysis. Following the Parkinson's disease animal behavioural assessment by suspension and swim tests, the brain tissue injuries were evaluated by hematoxylin and eosin, TdT-mediated dUTP-biotin nick end labelling, and tyrosine hydroxylase stainings. The results indicated that miR-199a-3p expression was downregulated, whereas that of XIST, Sp1 and LRRK2 were upregulated in Parkinson's disease. Moreover, miR-199a-3p overexpression or XIST knockdown inhibited the cell apoptosis induced by MPP(+) treatment and promoted cell proliferation. The neurodegenerative defects were significantly recovered by treating the cells with shXIST or shSp1, whereas miR-199a-3p inhibition or Sp1 and LRRK2 overexpression abrogated these beneficial effects. Furthermore, the results of our in vivo experiments confirmed the neuroprotective effects of shXIST and miR-199a-3p against MPTP-induced brain injuries, and the Parkinson's disease behavioural symptoms were effectively alleviated upon shXIST or miR-199a-3p treatment. In summary, the results of the present study showed that lncRNA XIST sponges miR-199a-3p to modulate Sp1 expression and further accelerates Parkinson's disease progression by targeting LRRK2.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4115-4137. doi: 10.18632/aging.202378. Epub 2021 Jan 20.
4580	LncRNA	XIST	miR-199a-3p	LRRK2	brain tissue	Parkinsons Disease	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33494069	LncRNA XIST sponges miR-199a-3p to modulate the Sp1/LRRK2 signal pathway to accelerate Parkinson's disease progression.	In vitro and in vivo models of Parkinson's disease were established to investigate the effects of the lncRNA XIST/miR-199a-3p/Sp1/LRRK2 axis. The binding between XIST and miR-199a-3p as well as miR-199a-3p and Sp1 were examined by luciferase reporter assay and confirmed by RNA immunoprecipitation analysis. Following the Parkinson's disease animal behavioural assessment by suspension and swim tests, the brain tissue injuries were evaluated by hematoxylin and eosin, TdT-mediated dUTP-biotin nick end labelling, and tyrosine hydroxylase stainings. The results indicated that miR-199a-3p expression was downregulated, whereas that of XIST, Sp1 and LRRK2 were upregulated in Parkinson's disease. Moreover, miR-199a-3p overexpression or XIST knockdown inhibited the cell apoptosis induced by MPP(+) treatment and promoted cell proliferation. The neurodegenerative defects were significantly recovered by treating the cells with shXIST or shSp1, whereas miR-199a-3p inhibition or Sp1 and LRRK2 overexpression abrogated these beneficial effects. Furthermore, the results of our in vivo experiments confirmed the neuroprotective effects of shXIST and miR-199a-3p against MPTP-induced brain injuries, and the Parkinson's disease behavioural symptoms were effectively alleviated upon shXIST or miR-199a-3p treatment. In summary, the results of the present study showed that lncRNA XIST sponges miR-199a-3p to modulate Sp1 expression and further accelerates Parkinson's disease progression by targeting LRRK2.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4115-4137. doi: 10.18632/aging.202378. Epub 2021 Jan 20.
4581	LncRNA	XIST	miR-155-5p	NA	human cardiac fibroblast cells	Acute Myocardial Infarction	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33767772	Long non-coding RNA XIST promotes the proliferation of cardiac fibroblasts and the accumulation of extracellular matrix by sponging microRNA-155-5p.	Acute myocardial infarction (AMI) is characterized by cardiomyocyte death followed by myocardial fibrosis, eventually leading to heart failure. Long non-coding (lnc)RNA X-inactive specific transcript (XIST) serves a vital role in the regulation of fibrosis. The aim of the present study was to determine whether myocardial fibrosis may be regulated by XIST and to elucidate the underlying mechanism. The relative mRNA expression levels of the target genes were evaluated using reverse transcription-quantitative polymerase chain reaction. Cell viability and apoptosis were determined using a Cell Counting Kit-8 assay and flow cytometry, respectively. The apoptosis and fibrosis-related protein expression levels were detected using western blot analysis. Finally, the interaction between XIST and microRNA (miR)-155-5p was analyzed using a luciferase reporter assay. XIST-overexpression increased proliferation and the expression level of the fibrosis-related proteins in the human cardiac fibroblast cells (HCFs). XIST directly targeted miR-155-5p and downregulated its expression, while miR-155-5p downregulation abolished the effect of XIST-silencing on cell viability and the expression level of the fibrosis-related proteins in the HCFs. XIST promoted cell proliferation and the expression level of fibrosis-related proteins by sponging miR-155-5p. Therefore, XIST may represent a novel effective target for AMI treatment.	NA	Exp Ther Med. 2021 May;21(5):477. doi: 10.3892/etm.2021.9908. Epub 2021 Mar 12.
4582	LncRNA	XIST	miR-335	NA	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	RNA pull-down assay;RNA pull-down;	32919956	Platycodin D (PD) regulates LncRNA-XIST/miR-335 axis to slow down bladder cancer progression in vitro and in vivo.	Recently, increasing evidences indicated that Platycodin D (PD) served as an effective anti-tumor drug for cancer treatment in clinic. However, the molecular mechanisms are still unclear. In the present study, we proved that PD regulated LncRNA-XIST/miR-335 axis to hamper the development of bladder cancer in vitro and in vivo. Mechanistically, PD inhibited malignant phenotypes, including cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT), and promoted cell apoptosis in bladder cancer cells in a time- and dose-dependent manner. In addition, the following experiments validated that PD inhibited LncRNA-XIST expressions, while increased miR-335 expression levels in bladder cancer cells. Next, by conducting the dual-luciferase reporter gene system assay and RNA pull-down assay, we validated that LncRNA-XIST inhibited miR-335 expressions through acting as RNA sponges, and the promoting effects of PD stimulation on miR-335 levels were abrogated by upregulating LncRNA-XIST. Interestingly, both silencing LncRNA-XIST and miR-335 overexpression enhanced the inhibiting effects of PD on the malignant phenotypes in bladder cancer cells. Consistently, the xenograft tumor-bearing mice models were established, and the data indicated that PD slowed down tumor growth and inhibited tumorigenesis in vivo, which were also aggravated by downregulating LncRNA-XIST. In general, analysis of data proved that targeting LncRNA-XIST/miR-335 axis was novel to enhance the anti-tumor effects of PD in bladder cancer in vitro and in vivo, and this study provided alternative therapeutic strategies for bladder cancer treatment in clinic.	NA	Exp Cell Res. 2020 Nov 1;396(1):112281. doi: 10.1016/j.yexcr.2020.112281. Epub 2020 Sep 10.
4583	LncRNA	XIST	miR-455-3p	BTG2	OSCC cells	Oral Squamous Cell Cancer	Homo sapiens (human)	FISH;Western blot;FISH;Luciferase reporter assay;	33177835	LncRNA XIST Inhibits the Progression of Oral Squamous Cell Carcinoma via Sponging miR-455-3p/BTG2 Axis.	OBJECTIVE: Oral squamous cell carcinoma (OSCC) is one of the most common cancers, accounting for over 90% of malignant lesions in the oral cavity. Long non-coding RNAs play an important role in the development of OSCC. This study aimed to investigate the effects of lncRNA XIST on the malignant behaviors of OSCC cells and its possible molecular mechanisms. METHODS: Real-time quantitative PCR and Western blot were used to detect the RNA and protein level, respectively. CAL27 and SCC25 cells with the lowest expression level of XIST were used for further study. MTT, transwell assay, colony formation, and xenograft model were applied to examine the effect of XIST on the progression of OSCC. FISH assay was performed to investigate the co-location of XIST and miR-455-3p in OSCC cells. The bioinformatics analysis, luciferase, and RNA pull down assay were utilized to predict and verify the target genes of miR-455-3p. RESULTS: XIST was downregulated in OSCC tissues and cell lines. Overexpression of XIST inhibited the proliferation, migration, and invasion ability of OSCC cells. Bioinformatics analysis and luciferase reporter assay confirmed XIST could bind to miR-455-3p. Besides, miR-455-3p directly targeted BTG2 in OSCC cells. Rescue experiments further confirmed the positive interaction between miR-455-3p and XIST as well as between miR-455-3p and BTG2. CONCLUSION: XIST was down-regulated in OSCC. XIST regulated the expression of BTG2 via sponging miR-455-3p. XIST/miR-455-3p/BTG2 signal axis inhibited the malignant progression of OSCC.	NA	Onco Targets Ther. 2020 Nov 3;13:11211-11220. doi: 10.2147/OTT.S267937. eCollection 2020.
4584	LncRNA	XIST	miR-194-5p	PD-L1	Huh-7 cell line	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33442449	Pivotal role of long non-coding ribonucleic acid-X-inactive specific transcript in regulating immune checkpoint programmed death ligand 1 through a shared pathway between miR-194-5p and miR-155-5p in hepatocellular carcinoma.	BACKGROUND: Anti-programmed death therapy has thrust immunotherapy into the spotlight. However, such therapy has a modest response in hepatocellular carcinoma (HCC). Epigenetic immunomodulation is a suggestive combinatorial therapy with immune checkpoint blockade. Non-coding ribonucleic acid (ncRNA) driven regulation is a major mechanism of epigenetic modulation. Given the wide range of ncRNAs that co-opt in programmed cell-death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) regulation, and based on the literature, we hypothesized that miR-155-5p, miR-194-5p and long non-coding RNAs (lncRNAs) X-inactive specific transcript (XIST) and MALAT-1 are involved in a regulatory upstream pathway for PD-1/PD-L1. Recently, nutraceutical therapeutics in cancers have received increasing attention. Thus, it is interesting to study the impact of oleuropein on the respective study key players. AIM: To explore potential upstream regulatory ncRNAs for the immune checkpoint PD-1/PD-L1. METHODS: Bioinformatics tools including microrna.org and lnCeDB software were adopted to detect targeting of miR-155-5p, miR-194-5p and lncRNAs XIST and MALAT-1 to PD-L1 mRNA, respectively. In addition, Diana tool was used to predict targeting of both aforementioned miRNAs to lncRNAs XIST and MALAT-1. HCC and normal tissue samples were collected for scanning of PD-L1, XIST and MALAT-1 expression. To study the interaction among miR-155-5p, miR-194-5p, lncRNAs XIST and MALAT-1, as well as PD-L1 mRNA, a series of transfections of the Huh-7 cell line was carried out. RESULTS: Bioinformatics software predicted that miR-155-5p and miR-194-5p can target PD-L1, MALAT-1 and XIST. MALAT-1 and XIST were predicted to target PD-L1 mRNA. PD-L1 and XIST were significantly upregulated in 23 HCC biopsies compared to healthy controls; however, MALAT-1 was barely detected. MiR-194 induced expression elevated the expression of PD-L1, XIST and MALAT-1. However, overexpression of miR-155-5p induced the upregulation of PD-L1 and XIST, while it had a negative impact on MALAT-1 expression. Knockdown of XIST did have an impact on PD-L1 expression; however, following knockdown of the negative regulator of X-inactive specific transcript (TSIX), PD-L1 expression was elevated, and abolished MALAT-1 activity. Upon co-transfection of miR-194-5p with siMALAT-1, PD-L1 expression was elevated. Co-transfection of miR-194-5p with siXIST did not have an impact on PD-L1 expression. Upon co-transfection of miR-194 with siTSIX, PD-L1 expression was upregulated. Interestingly, the same PD-L1 expression pattern was observed following miR-155-5p co-transfections. Oleuropein treatment of Huh-7 cells reduced the expression profile of PD-L1, XIST, and miR-155-5p, upregulated the expression of miR-194-5p and had no significant impact on the MALAT-1 expression profile. CONCLUSION: This study reported a novel finding revealing that opposing acting miRNAs in HCC, have the same impact on PD-1/PD-L1 immune checkpoint by sharing a common signaling pathway.	NA	World J Hepatol. 2020 Dec 27;12(12):1211-1227. doi: 10.4254/wjh.v12.i12.1211.
4585	LncRNA	MALAT1	miR-194-5p	PD-L1	Huh-7 cell line	Hepatocellular Carcinoma	Homo sapiens (human)	RACE;	33442449	Pivotal role of long non-coding ribonucleic acid-X-inactive specific transcript in regulating immune checkpoint programmed death ligand 1 through a shared pathway between miR-194-5p and miR-155-5p in hepatocellular carcinoma.	BACKGROUND: Anti-programmed death therapy has thrust immunotherapy into the spotlight. However, such therapy has a modest response in hepatocellular carcinoma (HCC). Epigenetic immunomodulation is a suggestive combinatorial therapy with immune checkpoint blockade. Non-coding ribonucleic acid (ncRNA) driven regulation is a major mechanism of epigenetic modulation. Given the wide range of ncRNAs that co-opt in programmed cell-death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) regulation, and based on the literature, we hypothesized that miR-155-5p, miR-194-5p and long non-coding RNAs (lncRNAs) X-inactive specific transcript (XIST) and MALAT-1 are involved in a regulatory upstream pathway for PD-1/PD-L1. Recently, nutraceutical therapeutics in cancers have received increasing attention. Thus, it is interesting to study the impact of oleuropein on the respective study key players. AIM: To explore potential upstream regulatory ncRNAs for the immune checkpoint PD-1/PD-L1. METHODS: Bioinformatics tools including microrna.org and lnCeDB software were adopted to detect targeting of miR-155-5p, miR-194-5p and lncRNAs XIST and MALAT-1 to PD-L1 mRNA, respectively. In addition, Diana tool was used to predict targeting of both aforementioned miRNAs to lncRNAs XIST and MALAT-1. HCC and normal tissue samples were collected for scanning of PD-L1, XIST and MALAT-1 expression. To study the interaction among miR-155-5p, miR-194-5p, lncRNAs XIST and MALAT-1, as well as PD-L1 mRNA, a series of transfections of the Huh-7 cell line was carried out. RESULTS: Bioinformatics software predicted that miR-155-5p and miR-194-5p can target PD-L1, MALAT-1 and XIST. MALAT-1 and XIST were predicted to target PD-L1 mRNA. PD-L1 and XIST were significantly upregulated in 23 HCC biopsies compared to healthy controls; however, MALAT-1 was barely detected. MiR-194 induced expression elevated the expression of PD-L1, XIST and MALAT-1. However, overexpression of miR-155-5p induced the upregulation of PD-L1 and XIST, while it had a negative impact on MALAT-1 expression. Knockdown of XIST did have an impact on PD-L1 expression; however, following knockdown of the negative regulator of X-inactive specific transcript (TSIX), PD-L1 expression was elevated, and abolished MALAT-1 activity. Upon co-transfection of miR-194-5p with siMALAT-1, PD-L1 expression was elevated. Co-transfection of miR-194-5p with siXIST did not have an impact on PD-L1 expression. Upon co-transfection of miR-194 with siTSIX, PD-L1 expression was upregulated. Interestingly, the same PD-L1 expression pattern was observed following miR-155-5p co-transfections. Oleuropein treatment of Huh-7 cells reduced the expression profile of PD-L1, XIST, and miR-155-5p, upregulated the expression of miR-194-5p and had no significant impact on the MALAT-1 expression profile. CONCLUSION: This study reported a novel finding revealing that opposing acting miRNAs in HCC, have the same impact on PD-1/PD-L1 immune checkpoint by sharing a common signaling pathway.	NA	World J Hepatol. 2020 Dec 27;12(12):1211-1227. doi: 10.4254/wjh.v12.i12.1211.
4586	LncRNA	XLOC_006390	miR-338-3p	SOX4	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33613979	Silver nanoparticles achieve cytotoxicity against breast cancer by regulating long-chain noncoding RNA XLOC_006390-mediated pathway.	The specific cytotoxic effect of nanoparticles on tumor cells may be used in future antitumor clinical applications. Silver nanoparticles (AgNPs) have been reported to have potent cytotoxic effect, but the mechanism is unclear. Here, AgNPs were synthesized, and the particle average size was 63.1 ± 8.3 nm and showed a nearly circular shape, which were determined by transmission electron microscopy and field emission scanning electron microscopy. The selected area electron diffraction patterns showed that the nanoparticles were crystalline. The energy-dispersive X-ray spectrum proved that silver is the main component of nanoparticles. The AgNPs showed potent cytotoxicity in breast cancer cells, no matter whether they were tamoxifen sensitive or resistant. Next, we found that a long noncoding RNA, XLOC_006390, was decreased in AgNPs-treated breast cancer cells, coupled to inhibited cell proliferation, altered cell cycle and apoptotic phenotype. Downstream of AgNPs, XLOC_006390 was recognized to target miR-338-3p and modulate the SOX4 expression. This signaling pathway also mediates the AgNPs function of sensitizing tamoxifen-resistant breast cancer cells to tamoxifen. These results provide a new clue for the antitumor mechanism of AgNPs, and a new way for drug development by using AgNPs.	NA	Toxicol Res (Camb). 2021 Jan 22;10(1):123-133. doi: 10.1093/toxres/tfaa090. eCollection 2021 Jan.
4587	Circular RNA	Circ_XP01	miR-23a-3p	XPO1	OS cells	Osteosarcoma	Homo sapiens (human)	microarray;qRT-PCR;Rescue assay;	33091396	Circ-XPO1 upregulates XPO1 expression by sponging multiple miRNAs to facilitate osteosarcoma cell progression.	Circular RNAs (circRNAs) act as a key role in mediating carcinogenesis. Nevertheless, the functions and mechanisms of circRNAs in osteosarcoma (OS) are still not fully understood. In the present study, we aim to investigate the functions of circ-XPO1 in OS and its potential mechanism underlying OS progression. CircRNA microarray indicated elevation of circ-XPO1 in OS specimens relative to normal samples. Elevation of circ-XPO1 and XPO1 mRNA was identified in OS tissue specimens and cells by qRT-PCR. In addition, enhanced expression of circ-XPO1 and XPO1 mRNA both correlated with poor prognosis for the patients with OS, as estimated by Kaplan-Meier analysis. Functionally, circ-XPO1 and XPO1 both facilitated the growth and invasion and decreased the apoptosis of OS cells. Moreover, we constructed the circ-XPO1-miRNAs-XPO1 3'-UTR interaction network and verified that circ-XPO1 could sponge miR-23a-3p, miR-23b-3p, miR-23c, and miR-130a-5p to regulate XPO1 expression. Furthermore, rescue assay indicated that the effect of circ-XPO1 on cell progression was partly relying on these miRNAs. Taken together, we found that circ-XPO1 regulated the expression of XPO1 through sponging miRNAs as a competing endogenous (ceRNA), providing the possibility that circ-XPO1 might play as a new therapeutic target for OS.	NA	Exp Mol Pathol. 2020 Dec;117:104553. doi: 10.1016/j.yexmp.2020.104553. Epub 2020 Oct 19.
4588	Circular RNA	Circ_XP01	miR-23b-3p	XPO1	OS cells	Osteosarcoma	Homo sapiens (human)	microarray;qRT-PCR;Rescue assay;	33091396	Circ-XPO1 upregulates XPO1 expression by sponging multiple miRNAs to facilitate osteosarcoma cell progression.	Circular RNAs (circRNAs) act as a key role in mediating carcinogenesis. Nevertheless, the functions and mechanisms of circRNAs in osteosarcoma (OS) are still not fully understood. In the present study, we aim to investigate the functions of circ-XPO1 in OS and its potential mechanism underlying OS progression. CircRNA microarray indicated elevation of circ-XPO1 in OS specimens relative to normal samples. Elevation of circ-XPO1 and XPO1 mRNA was identified in OS tissue specimens and cells by qRT-PCR. In addition, enhanced expression of circ-XPO1 and XPO1 mRNA both correlated with poor prognosis for the patients with OS, as estimated by Kaplan-Meier analysis. Functionally, circ-XPO1 and XPO1 both facilitated the growth and invasion and decreased the apoptosis of OS cells. Moreover, we constructed the circ-XPO1-miRNAs-XPO1 3'-UTR interaction network and verified that circ-XPO1 could sponge miR-23a-3p, miR-23b-3p, miR-23c, and miR-130a-5p to regulate XPO1 expression. Furthermore, rescue assay indicated that the effect of circ-XPO1 on cell progression was partly relying on these miRNAs. Taken together, we found that circ-XPO1 regulated the expression of XPO1 through sponging miRNAs as a competing endogenous (ceRNA), providing the possibility that circ-XPO1 might play as a new therapeutic target for OS.	NA	Exp Mol Pathol. 2020 Dec;117:104553. doi: 10.1016/j.yexmp.2020.104553. Epub 2020 Oct 19.
4589	Circular RNA	Circ_XP01	miR-23c	XPO1	OS cells	Osteosarcoma	Homo sapiens (human)	microarray;qRT-PCR;Rescue assay;	33091396	Circ-XPO1 upregulates XPO1 expression by sponging multiple miRNAs to facilitate osteosarcoma cell progression.	Circular RNAs (circRNAs) act as a key role in mediating carcinogenesis. Nevertheless, the functions and mechanisms of circRNAs in osteosarcoma (OS) are still not fully understood. In the present study, we aim to investigate the functions of circ-XPO1 in OS and its potential mechanism underlying OS progression. CircRNA microarray indicated elevation of circ-XPO1 in OS specimens relative to normal samples. Elevation of circ-XPO1 and XPO1 mRNA was identified in OS tissue specimens and cells by qRT-PCR. In addition, enhanced expression of circ-XPO1 and XPO1 mRNA both correlated with poor prognosis for the patients with OS, as estimated by Kaplan-Meier analysis. Functionally, circ-XPO1 and XPO1 both facilitated the growth and invasion and decreased the apoptosis of OS cells. Moreover, we constructed the circ-XPO1-miRNAs-XPO1 3'-UTR interaction network and verified that circ-XPO1 could sponge miR-23a-3p, miR-23b-3p, miR-23c, and miR-130a-5p to regulate XPO1 expression. Furthermore, rescue assay indicated that the effect of circ-XPO1 on cell progression was partly relying on these miRNAs. Taken together, we found that circ-XPO1 regulated the expression of XPO1 through sponging miRNAs as a competing endogenous (ceRNA), providing the possibility that circ-XPO1 might play as a new therapeutic target for OS.	NA	Exp Mol Pathol. 2020 Dec;117:104553. doi: 10.1016/j.yexmp.2020.104553. Epub 2020 Oct 19.
4590	LncRNA	ZFAS1	miR-296-5p	MMP-15	TNF-α-stimulated MH7A cells	Rheumatoid Arthritis	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33191176	Long noncoding RNA ZFAS1 silencing alleviates rheumatoid arthritis via blocking miR-296-5p-mediated down-regulation of MMP-15.	Rheumatoid arthritis (RA), a chronic inflammatory disease, deprives patients' walking ability and reduces their life quality worldwide. Though recent studies have indicated the role of long noncoding RNA (lncRNA) ZFAS1 in several diseases, however, its role in RA remains uncharacterized. The present study aimed to unravel the the effect of ZFAS1 on RA. Herein, the RA mouse model and the human RA synoviocyte MH7A cell lines stimulated with TNF-α were established. ZFAS1 was next determined to be highly expressed in the mice with RA-like symptoms and TNF-α-stimulated MH7A cells while inhibiting ZFAS1 was demonstrated to promote proliferation and suppress apoptosis of MH7A cells. Furthermore, ZFAS1 knockdown exerted anti-inflammation effect in vitro and in vivo and reduced the arthritis index value. Moreover, RNA immunoprecipitation and dual-luciferase reporter assays identified the binding of ZFAS1 to microRNA (miR)-296-5p as well as the binding of miR-296-5p to matrix metalloproteinase-15 (MMP-15). Of note, ZFAS1 could bind miR-296-5p to up-regulate the expression of MMP-15. Our results from in vitro and in vivo experiments demonstrated silencing ZFAS1 mitigated RA-like symptoms such as inflammation and hyperplasia via miR-296-5p-dependent inhibition of MMP-15. Taken altogether, our study confirmed that ZFAS1 involved in RA progression by competitively binding to miR-296-5p and regulating MMP-15 expression.	NA	Int Immunopharmacol. 2021 Jan;90:107061. doi: 10.1016/j.intimp.2020.107061. Epub 2020 Nov 13.
4591	LncRNA	ZFAS1	miR-296-5p	MMP-15	TNF-α-stimulated MH7A cells	Rheumatoid Arthritis	Mus musculus (mouse)	Dual-luciferase reporter assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33191176	Long noncoding RNA ZFAS1 silencing alleviates rheumatoid arthritis via blocking miR-296-5p-mediated down-regulation of MMP-15.	Rheumatoid arthritis (RA), a chronic inflammatory disease, deprives patients' walking ability and reduces their life quality worldwide. Though recent studies have indicated the role of long noncoding RNA (lncRNA) ZFAS1 in several diseases, however, its role in RA remains uncharacterized. The present study aimed to unravel the the effect of ZFAS1 on RA. Herein, the RA mouse model and the human RA synoviocyte MH7A cell lines stimulated with TNF-α were established. ZFAS1 was next determined to be highly expressed in the mice with RA-like symptoms and TNF-α-stimulated MH7A cells while inhibiting ZFAS1 was demonstrated to promote proliferation and suppress apoptosis of MH7A cells. Furthermore, ZFAS1 knockdown exerted anti-inflammation effect in vitro and in vivo and reduced the arthritis index value. Moreover, RNA immunoprecipitation and dual-luciferase reporter assays identified the binding of ZFAS1 to microRNA (miR)-296-5p as well as the binding of miR-296-5p to matrix metalloproteinase-15 (MMP-15). Of note, ZFAS1 could bind miR-296-5p to up-regulate the expression of MMP-15. Our results from in vitro and in vivo experiments demonstrated silencing ZFAS1 mitigated RA-like symptoms such as inflammation and hyperplasia via miR-296-5p-dependent inhibition of MMP-15. Taken altogether, our study confirmed that ZFAS1 involved in RA progression by competitively binding to miR-296-5p and regulating MMP-15 expression.	NA	Int Immunopharmacol. 2021 Jan;90:107061. doi: 10.1016/j.intimp.2020.107061. Epub 2020 Nov 13.
4592	LncRNA	ZFAS1	miR-647	NA	CC cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	33235466	ZFAS1 Exerts an Oncogenic Role via Suppressing miR-647 in an m(6)A-Dependent Manner in Cervical Cancer.	BACKGROUND: Cervical cancer (CC) is the second serious health threat in women worldwide. LncRNA (ZNFX1 antisense RNA 1) ZFAS1 has been observed to abnormally express in human cancers. However, the expression pattern, clinical significance and molecular mechanism of ZFAS1 have not been thoroughly studied in CC. METHODS: qRT-PCR was performed to examine the differential expression of ZFAS1 in CC tissues and adjacent normal cervical tissues. Gain- and loss-of-function experiments were constructed to test the functional role of ZFAS1 in CC by CCK-8, colony formation, transwell and xenograft models assays. Luciferase reporter, RNA immunoprecipitation (RIP), methylated RNA immunoprecipitation (MeRIP), RNA pull-down assays were used to reveal the underlying mechanisms. RESULTS: We found that ZFAS1 was significantly upregulated in CC tissues. Elevation of ZFAS1 correlated with advanced FIGO stage, lymph node and distant metastasis, and also indicated poor overall survival in patients with CC. Functional experiments demonstrated that ZFAS1 promoted CC cell proliferation, migration and invasion in vitro, and facilitated tumor growth and metastasis in vivo. Mechanistic investigation revealed that ZAFS1 sequestered miR-647, and this RNA-RNA interaction is regulated by METLL3-mediated m(6)A modification. CONCLUSION: Our findings elucidate the functional roles of ZFAS1 and its m(6)A modification in CC cells and indicate that ZFAS1 may be a promising target for CC treatment.	NA	Onco Targets Ther. 2020 Nov 17;13:11795-11806. doi: 10.2147/OTT.S274492. eCollection 2020.
4593	LncRNA	ZFAS1	miR-590-3p	NLRP3	Mice with cecal ligation and puncture (CLP)-induced sepsis	Sepsis	Homo sapiens (human)	ChIP;ELISA;MTT assay;Western blot;Flow Cytometry assay;Immunohistochemistry;Luciferase reporter assay;MTT assay;	33002446	SP1-induced ZFAS1 aggravates sepsis-induced cardiac dysfunction via miR-590-3p/NLRP3-mediated autophagy and pyroptosis.	BACKGROUND: Sepsis-induced cardiac dysfunction is one of the leading complications of sepsis, contributing to the high morbidity and mortality of septic patients. Several lines of evidence have demonstrated that autophagy and pyroptosis may be involved in septic cardiac dysfunction. In this study, we examined the impact of zinc finger antisense 1 (ZFAS1) on sepsis-induced myocardial dysfunction via regulating pyroptosis and autophagy. METHOD: Mice with cecal ligation and puncture (CLP)-induced sepsis was constructed in vivo. Myocardial injury was assessed by H&E staining, immunohistochemistry (IHC) for NLRP3, caspase 1, and interleukin (IL)-1β, as well as ELISA assay for serum levels of creatine kinase (CK), CK-MB, tumor necrosis factor α (TNF-α), and IL-1β. Primary cardiomyocytes exposed to lipopolysaccharide (LPS) were established to simulate sepsis-induced cardiac dysfunction in vitro. Cell viability was examined by MTT assay and concentration of TNF-α and IL-1β was measured by ELISA. Flow cytometry, immunofluorescent staining and western blotting were performed to assess pyroptosis and autophagy. The transcriptional regulation of SP1 on ZFAS1 was determined using ChIP assay. Luciferase reporter assay was performed to verify the ZFAS1/miR-590-3p interaction. Besides, activation of AMPK/mTOR signaling was detected using western blotting. RESULTS: Highly expressed ZFAS1 was observed in sepsis-induced cardiac dysfunction in the in vivo and in vitro model. Knockdown of ZFAS1 robustly abolished LPS-induced pyroptosis and attenuated the inhibition of autophagy. SP1 was identified to be an essential transcription factor to positively regulate ZFAS1 expression. Moreover, miR-590-3p functioned as a downstream effector to reverse ZFAS1-mediated sepsis-induced cardiac dysfunction. AMPK/mTOR signaling was involved in miR-590-3p-regulated autophagy and pyroptosis of cardiomyocytes. Furthermore, the regulatory network of ZFAS1/miR-590-3p on AMPK/mTOR signaling was verified in vivo. CONCLUSION: ZFAS1, activated by SP1, aggravates the progression of sepsis-induced cardiac dysfunction via targeting miR-590-3p/AMPK/mTOR signaling-mediated autophagy and pyroptosis of cardiomyocytes.	NA	Arch Biochem Biophys. 2020 Nov 30;695:108611. doi: 10.1016/j.abb.2020.108611. Epub 2020 Sep 29.
4594	LncRNA	ZFAS1	miR-1271-5p	HK2	glioma tissues and cells	Glioma	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	32964288	LncRNA ZFAS1/miR-1271-5p/HK2 Promotes Glioma Development Through Regulating Proliferation, Migration, Invasion and Apoptosis.	Glioma is the common type of malignant tumor with high mortality worldwide. Survival rate of patients with glioma remains poor, and almost half of patients died within 15 months. The increasing researches indicated that long non-coding RNA (lncRNA) Zinc finger antisense 1 (ZFAS1) played essential roles in tumor initiation and progression. Therefore, it is worth clarifying potential role of ZFAS1 in glioma. The expression levels of ZFAS1, miR-1271-5p, and Hexokinase 2 (HK2) in glioma tissues and cells were examined by real-time quantitative polymerase chain reaction (RT-qPCR). Kaplan-Meier curve was employed to analyze the relationship between cumulative survival time of glioma patients and expression level of ZFAS1. The cell proliferation, apoptosis, and mobility ability were assessed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT), flow cytometry, and transwell assays. The relationship among ZFAS1, miR-1271-5p, and HK2 was analyzed by bioinformatics assay, dual-luciferase reporter and Pearson's correlation analyses. The protein expression level of HK2 was examined by western blot assay. Finally, a xenograft experiment was established to assess the effects of ZFAS1 silencing in vivo. ZFAS1 was highly expressed in glioma tissues and cells, besides, the expression level of ZFAS1 was associated with survival time of glioma patients. Functional experiments suggested that knockdown of ZFAS1 or upregulation of miR-1271-5p constrained proliferation, migration and induced apoptosis of glioma cells. In addition, miR-1271-5p, interacted with HK2, was a target of ZFAS1. The gain of HK2 could overturn ZFAS1 silencing-induced effects on glioma cells. Besides, deficiency of ZFAS1 hindered tumor growth in vivo. ZFAS1 was involved in proliferation, migration, and apoptosis of glioma cells via regulating miR-1271-5p/HK2 axis.	NA	Neurochem Res. 2020 Dec;45(12):2828-2839. doi: 10.1007/s11064-020-03131-x. Epub 2020 Sep 22.
4595	LncRNA	ZFPM2-AS1	miR-137	TRIM24	CRC cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33300060	Long non-coding RNA ZFPM2-AS1 promotes colorectal cancer progression by sponging miR-137 to regulate TRIM24.	Accumulating evidence indicates that long non-coding RNAs (lncRNAs) may serve essential roles during tumorigenesis of colorectal cancer (CRC). The lncRNA ZFPM2-AS1 was observed to be involved in the progression of numerous types of cancer, such as lung adenocarcinoma and cervical cancer. The aim of the present study was to investigate the expression levels and function of ZFPM2-AS1 in CRC. Expression levels of ZFPM2-AS1 in tissue and CRC cells were measured by reverse transcription-quantitative PCR. Furthermore, cell proliferation and Transwell assays were conducted to investigate the functional role of ZFPM2-AS1 in vitro. In addition, bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation assay and western blotting were performed to explore the possible underlying mechanism. The expression levels of ZFPM2-AS1 were significantly upregulated in tissue samples from patients with CRC and CRC cell lines compared with normal tissue and normal human colorectal mucosa cell line. Notably, the upregulation of ZFPM2-AS1 was significantly associated with tumor size, histological differentiation, lymph node metastasis and TNM stage. In addition, ZFPM2-AS1 knockdown significantly inhibited cell proliferation, migration and invasion compared with the control group in vitro. Moreover, it was found that ZFPM2-AS1 positively regulated tripartite motif containing 24 (TRIM24) expression by sponging miR-137. In conclusion, the present study indicated that ZFPM2-AS1 may serve as an oncogene in CRC by regulating the miR-137/TRIM24 axis.	NA	Mol Med Rep. 2021 Feb;23(2):98. doi: 10.3892/mmr.2020.11737. Epub 2020 Dec 10.
4596	LncRNA	AFAP1-AS1	miR-497-5p	CELF1	nasopharyngeal carcinoma tissues and cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR	33400247	SP1-induced AFAP1-AS1 contributes to proliferation and invasion by regulating miR-497-5p/CELF1 pathway in nasopharyngeal carcinoma.	Nasopharyngeal carcinoma is a type of otolaryngological malignancy with high incidence. Long non-coding RNAs (lncRNAs) are closely related to nasopharyngeal carcinoma. LncRNA AFAP1-AS1 (AFAP1-AS1) has been found to play important roles in nasopharyngeal carcinoma progression and poor prognosis. However, the mechanism underlying AFAP1-AS1 in regulating nasopharyngeal carcinoma is still unclear. In current study, AFAP1-AS1 was found to be up-regulated in nasopharyngeal carcinoma tissues and cells. AFAP1-AS1 overexpression and knockdown were conducted in nasopharyngeal carcinoma cells. The results proved that AFAP1-AS1 promoted the survival and migration of nasopharyngeal carcinoma cells. Additionally, specificity protein 1 (SP1) was enhanced in nasopharyngeal carcinoma tissues and cells, and induced AFAP1-AS1 expression. The interaction between AFAP1-AS1 and miR-497-5p was confirmed. AFAP1-AS1 was demonstrated to regulate CELF1, a target gene of miR-497-5p. Further functional analysis revealed that AFAP1-AS1 knockdown attenuated SP1-induced nasopharyngeal carcinoma progression. These results indicate that SP1-induced AFAP1-AS1 facilitates nasopharyngeal carcinoma progression by regulating miR-497-5p/CELF1 pathway, which provides a new target for nasopharyngeal carcinoma treatment.	NA	Hum Cell. 2021 Mar;34(2):491-501. doi: 10.1007/s13577-020-00475-y. Epub 2021 Jan 5.
4597	Circular RNA	ARL3	miR-1305	METTL3	Hepatitis B virus(+) hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	microarray;	33372396	N(6) -methyladenosine modification of circular RNA circ-ARL3 facilitates Hepatitis B virus-associated hepatocellular carcinoma via sponging miR-1305.	Hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC), whether circular RNA (circRNA) is involved in this process remains unknown. In this study, we performed circRNA microarray profile and found an HBV-related circRNA, circ-ARL3 (hsa_circ_0092493). Stable knockdown of circ-ARL3 inhibited the proliferation and invasion of HBV(+) HCC cells. High circ-ARL3 was positively correlated with malignant clinical features and poor prognosis. In terms of mechanism, HBx protein upregulated N(6) -methyladenosine (m(6) A) methyltransferases METTL3 expression, increasing the m(6) A modification of circ-ARL3; then, m(6) A reader YTHDC1 bound to m(6) A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV(+) HCC progression. Importantly, depletion of circ-ARL3 significantly retarded HBV(+) HCC cell growth in vivo, whereas this effect was evidently blocked after silencing of miR-1305. Collectively, our data suggest that circ-ARL3 is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/miR-1305 may be a promising treatment for HBV(+) HCC patients.	NA	IUBMB Life. 2021 Feb;73(2):408-417. doi: 10.1002/iub.2438. Epub 2020 Dec 28.
4598	Circular RNA	ARL3	miR-1305	YTHDC1	Hepatitis B virus(+) hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	microarray;	33372396	N(6) -methyladenosine modification of circular RNA circ-ARL3 facilitates Hepatitis B virus-associated hepatocellular carcinoma via sponging miR-1305.	Hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC), whether circular RNA (circRNA) is involved in this process remains unknown. In this study, we performed circRNA microarray profile and found an HBV-related circRNA, circ-ARL3 (hsa_circ_0092493). Stable knockdown of circ-ARL3 inhibited the proliferation and invasion of HBV(+) HCC cells. High circ-ARL3 was positively correlated with malignant clinical features and poor prognosis. In terms of mechanism, HBx protein upregulated N(6) -methyladenosine (m(6) A) methyltransferases METTL3 expression, increasing the m(6) A modification of circ-ARL3; then, m(6) A reader YTHDC1 bound to m(6) A-modified of circ-ARL3 and favored its reverse splicing and biogenesis. Furthermore, circ-ARL3 was able to sponge miR-1305, antagonizing the inhibitory effects of miR-1305 on a cohort of target oncogenes, thereby promoting HBV(+) HCC progression. Importantly, depletion of circ-ARL3 significantly retarded HBV(+) HCC cell growth in vivo, whereas this effect was evidently blocked after silencing of miR-1305. Collectively, our data suggest that circ-ARL3 is a critical regulator in HBV-related HCC, targeting the axis of circ-ARL3/miR-1305 may be a promising treatment for HBV(+) HCC patients.	NA	IUBMB Life. 2021 Feb;73(2):408-417. doi: 10.1002/iub.2438. Epub 2020 Dec 28.
4599	LncRNA	ASAP1-IT1	miR-2278	YAP	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	luciferase assay;	33576454	Long non-coding RNA ASAP1-IT1 suppresses ovarian cancer progression by regulating Hippo/YAP signaling.	Long non-coding RNAs (lncRNAs) are a class of non-protein coding transcripts that are involved in the regulation of gene expression in mammalian cells. Transcriptional co-activator Yes associated protein 1 (YAP1) plays a key role in the progression of ovarian cancer. However, the regulation of Hippo/YAP signaling in ovarian cancer remains elusive. In the present study, the expression levels of lncRNA ASAP1-IT1 were investigated. The analysis indicated that lncRNA ASAP1-IT1 expression was downregulated in ovarian tumor samples and ovarian cancer cells. The overexpression of ASAP1-IT1 inhibited ovarian cancer cell proliferation and induced cell apoptosis. Bioinformatics analysis predicted that miR-2278, a previously reported upregulated miRNA in ovarian tumors, may bind to ASAP1-IT1. Dual luciferase assay confirmed the direct regulatory association between ASAP1-IT1 and miR-2278. In addition, the data demonstrated that large tumor suppressor 2 (LATS2) was a target gene of miR-2278, whose expression was upregulated by ASAP1-IT1 in ovarian cancer cells. By regulating the expression of LATS2, ASAP1-IT1 induced the downregulation of YAP1 expression in ovarian cancer cells. Moreover, the silencing of LATS2 attenuated the inhibition of cell proliferation and the apoptosis induced by ASAP1-IT1 overexpression in ovarian cancer cells. The association among the expression levels of ASAP1-IT1, miR-2278 and LATS2 was observed in specimens obtained from patients with ovarian cancer. Taken together, the data presented herein demonstrate that ASAP1-IT1 functions as a potential tumor suppressor lncRNA by upregulating LATS2 expression in ovarian cancer.	NA	Int J Mol Med. 2021 Apr;47(4):44. doi: 10.3892/ijmm.2021.4877. Epub 2021 Feb 12.
4600	LncRNA	BC037916	miR-3145-3p	JAK2	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;Western blot;	33447050	Overexpression of a Long Non-Coding RNA BC037916 is Associated with Pancreatic Tumorigenesis and Poor Prognosis.	BACKGROUND: Pancreatic cancer is one of the most lethal malignancies. Accumulating evidence supports for the critical contribution of long noncoding RNAs (lncRNAs) to the cancer development and progression. We tried to identify novel lncRNAs involved in the pancreatic carcinogenesis. MATERIALS AND METHODS: Two independent datasets (Gene Expression Omnibus datasets: GSE16515 and GSE32688) were obtained from the Gene Expression Omnibus (GEO). The level of BC037916 was detected in pancreatic cancer tissues and adjacent no-tumorous tissues (n=86) by qRT-PCR. Effects of BC037916 on proliferation, apoptosis, and invasion of pancreatic cancer cells were examined. RESULTS: We identified a novel lncRNA BC037916 involved in the pancreatic carcinogenesis by analyzing GEO datasets. Quantitative RT-PCR analysis showed that 86.0% (74/86) pancreatic cancer tissues had increased BC037916 expression as compared with normal counterparts. Further, positive correlation was observed between BC037916 expression and clinical stage, primary tumor, and regional lymph node invasion. Importantly, BC037916 was an independent prognostic factor of pancreatic cancer. Functionally, knockdown of BC037916 repressed cell proliferation, inhibited cell invasion, halted cell cycle progression, and promoted apoptosis in both PANC-1 and SW1990 cells. In contrast, overexpression of BC037916 in CAPAN-1 had opposite effects. Moreover, silencing of BC037916 significantly inhibited the tumor growth of xenografted SW1990 cells in vivo. Results of Western blot assays suggested that BC037916 knockdown also suppressed the activation of JAK2/STAT3 and TGF-β signaling. Further experiments suggested that BC037916 positively regulated the expression of Twist through miR-3145-3p. CONCLUSION: BC037916 exhibited oncogenic potential in pancreatic cancer development.	NA	Onco Targets Ther. 2021 Jan 5;13:13451-13463. doi: 10.2147/OTT.S282350. eCollection 2020.
4601	LncRNA	BC037916	miR-3145-3p	STAT3	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;Western blot;	33447050	Overexpression of a Long Non-Coding RNA BC037916 is Associated with Pancreatic Tumorigenesis and Poor Prognosis.	BACKGROUND: Pancreatic cancer is one of the most lethal malignancies. Accumulating evidence supports for the critical contribution of long noncoding RNAs (lncRNAs) to the cancer development and progression. We tried to identify novel lncRNAs involved in the pancreatic carcinogenesis. MATERIALS AND METHODS: Two independent datasets (Gene Expression Omnibus datasets: GSE16515 and GSE32688) were obtained from the Gene Expression Omnibus (GEO). The level of BC037916 was detected in pancreatic cancer tissues and adjacent no-tumorous tissues (n=86) by qRT-PCR. Effects of BC037916 on proliferation, apoptosis, and invasion of pancreatic cancer cells were examined. RESULTS: We identified a novel lncRNA BC037916 involved in the pancreatic carcinogenesis by analyzing GEO datasets. Quantitative RT-PCR analysis showed that 86.0% (74/86) pancreatic cancer tissues had increased BC037916 expression as compared with normal counterparts. Further, positive correlation was observed between BC037916 expression and clinical stage, primary tumor, and regional lymph node invasion. Importantly, BC037916 was an independent prognostic factor of pancreatic cancer. Functionally, knockdown of BC037916 repressed cell proliferation, inhibited cell invasion, halted cell cycle progression, and promoted apoptosis in both PANC-1 and SW1990 cells. In contrast, overexpression of BC037916 in CAPAN-1 had opposite effects. Moreover, silencing of BC037916 significantly inhibited the tumor growth of xenografted SW1990 cells in vivo. Results of Western blot assays suggested that BC037916 knockdown also suppressed the activation of JAK2/STAT3 and TGF-β signaling. Further experiments suggested that BC037916 positively regulated the expression of Twist through miR-3145-3p. CONCLUSION: BC037916 exhibited oncogenic potential in pancreatic cancer development.	NA	Onco Targets Ther. 2021 Jan 5;13:13451-13463. doi: 10.2147/OTT.S282350. eCollection 2020.
4602	LncRNA	BCRT1	miR-1303	FGF7	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	34102610	LncRNA BCRT1 facilitates osteosarcoma progression via regulating miR-1303/FGF7 axis.	Growing studies noted that lncRNA was closely related with the initiation and progression of tumors. However, the role of BCRT1 in the progression of osteosarcoma remains unknown. We noted that BCRT1 is significantly upregulated in osteosarcoma specimens and cells. Elevated expression of BCRT1 promotes cell growth and cell cycle in osteosarcoma cell. Moreover, BCRT1 induces EMT and secretion of inflammatory mediators in osteosarcoma cell. We illustrated that elevated expression of BCRT1 decreases miR-1303 expression in MG-63 cell. The expression of miR-1303 is lower in osteosarcoma specimens than in non-tumor specimens. There is an inverse interrelation between miR-1303 levels and BCRT1 levels in osteosarcoma specimens. Furthermore, we identified FGF7 is one direct target gene of miR-1303 in osteosarcoma cell. Ectopic expression of miR-1303 suppresses FGF7 expression and elevated expression of BCRT1 enhanced FGF7 expression in MG-63 cell. Finally, we illustrated that BCRT1 induces osteosarcoma cell cycle and proliferation and promotes EMT progression and inflammatory mediators secretion via modulating FGF7 expression. Our study suggested that BCRT1 acts as one oncogene in osteosarcoma progression.	NA	Aging (Albany NY). 2021 Jun 8;13(11):15501-15510. doi: 10.18632/aging.203106. Epub 2021 Jun 8.
4603	LncRNA	BLACAT1	miR-519d-3p	CREB1	Colorectal Cancer tissues and cells	Colorectal Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	33376405	LncRNA BLACAT1/miR-519d-3p/CREB1 Axis Mediates Proliferation, Apoptosis, Migration, Invasion, and Drug-Resistance in Colorectal Cancer Progression.	BACKGROUND: Colorectal cancer (CRC) is a common severe disease around the world. The merging papers reported that long noncoding RNAs (lncRNAs) took part in the diversified pathological processes of CRC. This study aimed to uncover the role and the potential mechanism of lncRNA bladder cancer-associated transcript 1 (BLACAT1) in CRC progression. METHODS: LncRNA BLACAT1, micro-519d-3p (miR-519d-3p), and cAMP-responsive element binding protein 1 (CREB1) levels were detected by quantitative real-time polymerase chain reaction (qRT-PCR) in CRC tissues and cells. The bio-functional effects were examined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry assay, and transwell assay. The susceptibility testing was determined by oxaliplatin (OXA) administration. The potential binding sites between miR-519d-3p and BLACAT1 or CREB1 were predicted by online software starBase and confirmed by dual-luciferase reporter analysis. The relative proteins expression in CRC cells was determined by Western blot analysis. Xenograft tumor model was used to evaluate biological function of BLACAT1 in vivo. RESULTS: The expression of BLACAT1 was promoted in CRC tissues and cells, and correlated to the TNM (tumor, node, metastasis) stage, distant metastasis, and overall survival rate. Silencing of BLACAT1 limited the proliferation, migration, and invasion, facilitated the apoptosis, and re-sensitized OXA-resistance in CRC cells. MiR-519d-3p was a target of BLACAT1. Furthermore, miR-519d-3p deletion reversed the positive effects of BLACAT1 deletion on CRC cells. Moreover, our data showed that miR-519d-3p directly targeted CREB1 and BLACAT1 sponged miR-519d-3p to regulate CREB1 expression. Besides, CREB1 disrupted the bio-functional results above from BLACAT1 suppression. Additionally, BLACAT1 knockdown promoted CRC cells sensitivity to OXA in vivo. CONCLUSION: BLACAT1 mediated the progression of CRC and OXA-resistance by miR-519d-3p/CREB1 axis.	NA	Cancer Manag Res. 2020 Dec 22;12:13137-13148. doi: 10.2147/CMAR.S274447. eCollection 2020.
4604	LncRNA	C2dat2	miR-30d-5p	DDIT4	Neuro-2a cells	Cerebral Ischemia-Reperfusion Injury	Homo sapiens (human)	qRT-PCR	33833132	lncRNA C2dat2 facilitates autophagy and apoptosis via the miR-30d-5p/DDIT4/mTOR axis in cerebral ischemia-reperfusion injury.	Cerebral ischemia-reperfusion injury (CIRI) is an important pathophysiological process of ischemic stroke associated with various physiological and pathological processes, including autophagy and apoptosis. In this study, we examined the role and mechanism of long noncoding RNA CAMK2D-associated transcript 2 (C2dat2) in regulating CIRI in vivo and in vitro. C2dat2 up-regulation facilitated neuronal autophagy and apoptosis induced by CIRI. Mechanistically, C2dat2 acts as a competing endogenous RNA (ceRNA) to negatively regulate miR-30d-5p expression. More specifically, miR-30d-5p targeted the 3'-untranslated region of DNA damage-inducible transcript 4 (DDIT4) and silenced its target mRNA DDIT4. Additionally, C2dat2 binding with heat shock cognate 70/heat shock protein 90 blocked RNA-induced silencing complex assembly to abolish the miR-30d-5p targeting of DDIT4 and inhibited miR-30d-5p to silence its target mRNA DDIT4. Further analysis showed that C2dat2 knockdown conspicuously inhibited the up-regulation of DDIT4 and Beclin-1 levels and LC3B II/I ratio and the down-regulation of P62 and phosphorylated mammalian target of rapamycin (mTOR)/mTOR and phosphorylated-P70S6K/P70S6K ratio in Neuro-2a cells after oxygen-glucose deprivation/reoxygenation. This study first revealed that C2dat2/miR-30d-5p/DDIT4/mTOR forms a novel signaling pathway to facilitate autophagy and apoptosis induced by CIRI, contributing to the better understanding of the mechanisms of CIRI and enriching the ceRNA hypothesis in CIRI.	NA	Aging (Albany NY). 2021 Apr 4;13(8):11315-11335. doi: 10.18632/aging.202824. Epub 2021 Apr 4.
4605	LncRNA	CASC15	miR-582-5p	HMGB2	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR;Luciferase activity assay;	33395735	Tumor promoting long non-coding RNA CASC15 affects HMGB2 expression by sponging miR-582-5p in colorectal cancer.	BACKGROUND: The importance of long non-coding RNAs (lncRNAs) in regulating tumorigenesis has been gradually recognized. Roles of lncRNA cancer susceptibility candidate 15 (CASC15) in cancers have been validated by several independent groups, however, its role in colorectal cancer (CRC) remains to be explored. METHODS: Levels of CASC15 in CRC cells and normal cells were measured with the qRT-PCR method. In vitro functional assays were performed to detect the effects of CASC15 on cell proliferation, invasion, and apoptosis. Bioinformatic analyses and luciferase activity assays were conducted to investigate the targets for CASC15. Animal experiments were conducted to analyze the effect of CASC15 on tumor growth in vivo. RESULTS: CASC15 level is revealed to be significantly elevated in CRC cells compared with normal cells. In vitro assays revealed that CASC15 overexpression stimulates cell growth and invasion, while its down-expression has opposite effects. Furthermore, CASC15 can bind with microRNA-582-5p (miR-582-5p) to modulate high mobility group box 2 (HMGB2) expression. We also showed that silencing of CASC15 inhibits tumor growth. CONCLUSIONS: In summary, CASC15 overexpression could promote CRC carcinogenesis, indicating knockdown of CASC15 might be a possible therapeutic measure to hinder carcinogenesis. This work could help us to understand the mechanisms behind CRC progression.	NA	J Gene Med. 2021 Jan 4:e3308. doi: 10.1002/jgm.3308.
4606	LncRNA	CASC9	miR-370	EGFR	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Luciferase reporter assay;	33478874	Long non-coding RNA CASC9 promotes the progression and development of gastric cancer via regulating miR-370/EGFR axis.	lncRNA cancer susceptibility 9 (CASC9) is a pivotal modulator in various cancers, such as colorectal cancer, breast cancer and esophageal cancer. However, its exact role in gastric cancer (GC) has not been systematically studied. Here, using a combination of molecular and cell biology approaches, we found that CASC9 also acts as a factor promoting the progression of GC. First, mRNA and protein expression levels were quantified by real-time quantitative reverse transcription PCR (qRT-PCR) and western blot, respectively. Second, CCK-8 assay, colony formation assay and cell cycle analysis were performed to compare the cell growth abilities when CASC9 was knocked down. Third, the proliferative cells were determined by labeling Edu and the regulatory effect of CASC9 on miR-370 was detected by RNA-protein pull-down and luciferase reporter assays. Finally, in vivo mice model was established to verify the role of CASC9 in promoting GC progression. Our results showed that CASC9 was up-regulated significantly in both GC tissues and cell lines. Conversely, CASC9 knockdown inhibited GC growth in vitro. Further analysis indicated that CASC9 directly targeted miR-370 and negatively regulated miR-370 expression in GC. Besides, EGFR (epidermal growth factor receptor) was identified as a direct target gene of miR-370. Taken together our results support a model in which CASC9 promotes GC progression through miR-370/EGFR/ERK/AKT pathway. Finally, in vivo CASC9 knockdown resulted in impaired GC growth. In sum, this study firstly demonstrates that lncRNA CASC9 acts as an oncogene through altering EGFR expression level via negatively regulating miR-370 expression.	NA	Dig Liver Dis. 2021 Apr;53(4):509-516. doi: 10.1016/j.dld.2020.12.115. Epub 2021 Jan 18.
4607	LncRNA	CCAT2	miR-143	NA	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;Western blot;Cell Invasion Assay;Luciferase reporter assay;	33664828	Inhibiting proliferation and metastasis of osteosarcoma cells by downregulation of long non-coding RNA colon cancer-associated transcript 2 targeting microRNA-143.	Osteosarcoma is a malignant bone tumor, which has a high incidence in children and adolescents. However, the pathogenesis of osteosarcoma remains unclear. Long noncoding RNA (lncRNA) is a new potential therapeutic target and diagnostic biomarker for osteosarcoma. Hence, the present study aimed to explore the effect of lncRNA colon cancer-associated transcript (CCAT2) on osteosarcoma and its potential underlying mechanisms. For this purpose, the proliferation of osteosarcoma cells was measured using the CCK-8 assay. The scratch-wound and cell invasion assays were used to determine the migration and invasion of osteosarcoma cells, respectively. LncRNA CCAT2 and microRNA (miR)-143 binding sites were identified by the dual-luciferase reporter assay. RNA and protein expression levels were detected by reverse-transcription quantitative PCR and western blotting, respectively. Downregulation of lncRNA CCAT2 inhibited the proliferation, migration, and invasion of osteosarcoma cells. The findings also revealed that miR-143 bound directly to lncRNA CCAT2. The expression of miR-143 was upregulated by the knockdown of lncRNA CCAT2. Downregulation of the FOS-like antigen 2 was also observed after knockdown of lncRNA CCAT2. The function of lncRNA CCAT2 in osteosarcoma cells was attenuated by co-transfection with anti-miR-143 oligodeoxyribonucleotide. In conclusion, downregulation of lncRNA CCAT2 inhibited the proliferation and metastasis of osteosarcoma cells by targeting miR-143. lncRNA CCAT2 was identified as a potential target for osteosarcoma treatment.	NA	Oncol Lett. 2021 Apr;21(4):265. doi: 10.3892/ol.2021.12526. Epub 2021 Feb 8.
4608	LncRNA	CCDC144NL-AS1	miR-490-3p	HMGA2	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33442262	Long Noncoding RNA CCDC144NL-AS1 Promotes the Oncogenicity of Osteosarcoma by Acting as a Molecular Sponge for microRNA-490-3p and Thereby Increasing HMGA2 Expression.	PURPOSE: The long noncoding RNA CCDC144NL antisense RNA 1 (CCDC144NL-AS1) exhibits important functions in gastric cancer. In this study, we aimed to investigate the roles of CCDC144NL-AS1 in modulating the phenotype of osteosarcoma (OS) cells in vitro and in vivo and elucidate its underlying mechanisms. METHODS: Reverse transcription quantitative polymerase chain reaction (PCR) was performed to determine the expression level of CCDC144NL-AS1 in OS tissues and cell lines. The proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were determined in OS cells using the Cell Counting Kit 8 assay, flow cytometric analysis, transwell migration and invasion assays, and xenograft experiments, respectively. Bioinformatics analysis was performed to identify the potential microRNA targets of CCDC144NL-AS1, which were subsequently confirmed using the luciferase reporter assay, RNA immunoprecipitation assay, reverse transcription quantitative PCR, Western blotting, and rescue experiments. RESULTS: CCDC144NL-AS1 expression was upregulated in OS tissues and cell lines. Patients with OS who exhibited high CCDC144NL-AS1 expression had shorter overall survival than those who exhibited low CCDC144NL-AS1 expression. Functionally, interference in CCDC144NL-AS1 expression led to a notable decrease in the proliferation, migration, and invasion of OS cells and an increase in cell apoptosis in vitro. Furthermore, CCDC144NL-AS1 knockdown impaired OS tumor growth in vivo. Mechanistically, CCDC144NL-AS1 directly bound to miR-490-3p in OS cells, where it functioned as a molecular sponge and subsequently increased the expression of high-mobility group AT-hook 2 (HMGA2). Rescue experiments further demonstrated that miR-490-3p suppression or HMGA2 restoration abated CCDC144NL-AS1 deficiency-induced cancer-inhibitory actions in OS cells. CONCLUSION: CCDC144NL-AS1 exhibits pro-oncogenic roles in OS by functioning as a sponge for miR-490-3p and increasing HMGA2 expression. Our findings suggest that greater understanding of the CCDC144NL-AS1/miR-490-3p/HMGA2 pathway can provide useful information for OS diagnosis, prognosis, and therapy.	NA	Onco Targets Ther. 2021 Jan 6;14:1-13. doi: 10.2147/OTT.S280912. eCollection 2021.
4609	LncRNA	CERS6-AS1	miR-15a-5p	FGFR1	pancreatic ductal adenocarcinoma cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33581689	Long non-coding RNA CERS6-AS1 facilitates the oncogenicity of pancreatic ductal adenocarcinoma by regulating the microRNA-15a-5p/FGFR1 axis.	The long non-coding RNA CERS6 antisense RNA 1 (CERS6-AS1) has critical regulatory roles in breast cancer progression. Here, we determined CERS6-AS1 expression in pancreatic ductal adenocarcinoma (PDAC) and the roles of CERS6-AS1 in PDAC carcinogenesis. The mechanisms underlying the regulatory actions of CERS6-AS1 in PDAC cells were elucidated in detail. CERS6-AS1 expression was evidently increased in PDAC tissues and cell lines. Patients with PDAC having high CERS6-AS1 expression had shorter overall survival periods than those having low CERS6-AS1 expression. Functionally, the knockdown of CERS6-AS1 attenuated the proliferation, migration, and invasion and stimulated apoptosis of PDAC cells in vitro. Additionally, CERS6-AS1 depletion decreased PDAC tumor growth in vivo. Mechanistically, CERS6-AS1 could competitively bind to microRNA-15a-5p (miR-15a-5p) and effectively work as a molecular sponge in PDAC cells, resulting in the upregulation of fibroblast growth factor receptor 1 (FGFR1), a direct target of miR-15a-5p. Rescue experiments revealed that miR-15a-5p downregulation or FGFR1 restoration rescued the effects of CERS6-AS1 knockdown on the behaviors of PDAC cells. In conclusion, CERS6-AS1 promoted the oncogenicity of PDAC by serving as a competing endogenous RNA to sequester miR-15a-5p and increase FGFR1 expression, which highlights the potential of the CERS6-AS1/miR-15a-5p/FGFR1 pathway as an effective target for cancer therapy.	NA	Aging (Albany NY). 2021 Feb 13;13(4):6041-6054. doi: 10.18632/aging.202540. Epub 2021 Feb 13.
4610	Circular RNA	Circ_0000337	miR-942-5p	MAT2A	glioma cells	Malignant Glioma	Homo sapiens (human)	qRT-PCR	33336744	Hsa_circ_0000337 promotes proliferation, migration and invasion in glioma by competitively binding miRNA-942-5p and thus upregulates MAT2A.	OBJECTIVE: CircRNAs are vital factors involved in the pathological processes. This study aims to elucidate the biological functions of hsa_circ_0000337 in affecting the malignant progress of glioma. PATIENTS AND METHODS: Relative levels of hsa_circ_0000337 in 45 cases of glioma and 24 cases of normal tissues were tested. The correlation between hsa_circ_0000337 and clinical features of glioma was assessed. Proliferative and metastatic abilities of U87 and U251 cells regulated by hsa_circ_0000337 were examined by 5-Ethynyl-2'-deoxyuridine (EdU) and transwell assay, respectively. Potential molecular mechanism of hsa_circ_0000337 on regulating glioma cell functions was clarified by bioinformatic analysis, which was further verified through rescue experiments. RESULTS: Hsa_circ_0000337 was highly expressed in glioma cases. Its level was correlated to poor prognosis of glioma. In vitro experiments obtained the conclusion that hsa_circ_0000337 accelerated proliferative and metastatic abilities of glioma cells. Serving as a ceRNA, hsa_circ_0000337 sponged miRNA-942-5p to upregulate MAT2A, thus inducing the malignant phenotypes of glioma. CONCLUSIONS: Hsa_circ_0000337/miRNA-942-5p / MAT2A axis is responsible for the deterioration of glioma. Hsa_circ_0000337 may be a potential therapeutic target for glioma.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12251-12257. doi: 10.26355/eurrev_202012_24017.
4611	Circular RNA	Circ_0000429	miR-1197	MADD	Non-small-cell lung carcinoma cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	CCK-8 assay;FISH;qRT-PCR;FISH;	33542659	CircRNA_0000429 Regulates Development of NSCLC by Acting as a Sponge of miR-1197 to Control MADD.	BACKGROUND: Non-small-cell lung carcinoma (NSCLC) is the most common type of lung cancer. Circular RNA_0000429 (circ_0000429) is an identified circular RNA (circRNA) that is correlated with cancer progression. However, the role of circ_0000429 in NSCLC remains unknown. In the present study, we aimed to investigate the function of circ_0000429 in NSCLC and the underlying mechanism. METHODS: The expression patterns of circ_0000429 were determined using qRT-PCR in NSCLC samples and cell lines. The subcellular distribution of circ_0000429 in NSCLC cells was analyzed by fluorescence in situ hybridization (FISH). Cell proliferation was examined utilizing the CCK-8 assay. Cell migration and invasion were evaluated using the transwell assay. We used the bioinformatics software TargetScan and miRanda to predict circRNA-miRNA and miRNA-mRNA interactions. RESULTS: Our results showed that circ_0000429 expressions were significantly upregulated in NSCLC tissues and cell lines. Knockdown of circ_0000429 significantly inhibited the cell proliferation, migration, and invasion of NSCLC cells in vitro. Furthermore, we demonstrated that circ_0000429 acted as a sponge to absorb microRNA-1197 (miR-1197) and promoted MADD expression. CONCLUSION: Collectively, our results demonstrated that circ_0000429 exhibited a carcinogenic role by sponging miR-1197 and regulating CMADD expression in NSCLC. These findings provided evidence for understanding the role of circ_0000429 in NSCLC tumorigenesis.	NA	Cancer Manag Res. 2021 Jan 29;13:861-870. doi: 10.2147/CMAR.S270790. eCollection 2021.
4612	Circular RNA	Circ_0000714	miR-370-3p	CDK6	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	microarray;Western blot;Flow Cytometry assay;	33380810	Knockdown of Circular RNA Hsa_circ_0000714 Can Regulate RAB17 by Sponging miR-370-3p to Reduce Paclitaxel Resistance of Ovarian Cancer Through CDK6/RB Pathway.	PURPOSE: Paclitaxel resistance in ovarian cancer has become an urgent clinical problem. This study investigated the regulatory effects of RAB17 on the non-coding RNA network of the paclitaxel-resistant ovarian cancer cell A2780/PTX. METHODS: Microarray analysis was used to identify differentially expressed genes in paclitaxel-resistant cell A2780/PTX compared to the parent paclitaxel-sensitive cell A2780. Quantitative real-time PCR and Western blot were used to measure the expression of related mRNAs and proteins. The CCK8 assay was used to determine cell survival ratios and drug resistance indices in ovarian cancer cells. The clone forming assay was used to analyze the cell clone proliferation. Flow cytometry was used to analyze the cell cycle. Dual-luciferase reporter gene assays evaluated the relationship between the genes. RESULTS: RAB17 is highly expressed in A2780/PTX cells. RAB17 knockdown increased the cell sensitivity to paclitaxel, inhibited proliferation, and caused cell cycle arrest in the G1 phase in A2780/PTX. Western blot confirmed that RAB17 influenced cell behavior by activating the CDK6/RB signaling pathway. Bioinformatics analyses identified RAB17 as a new target by the microRNA miR-370-3p, and the latter was predicted to interact with circular RNA hsa_circ_0000714. Hsa_circ_0000714 indeed acted as a miRNA sponge for miR-370-3p allowing its regulation of RAB17 expression. This regulation was accomplished through the CDK6/RB signaling pathway. CONCLUSION: Hsa_circ_0000714 acts as a sponge for miR-370-3p, and regulates RAB17 expression through the CDK6/RB signaling pathway, which plays a role in the malignant progression of the paclitaxel-resistant ovarian cancer cell A2780/PTX.	NA	Onco Targets Ther. 2020 Dec 24;13:13211-13224. doi: 10.2147/OTT.S285153. eCollection 2020.
4613	Circular RNA	Circ_0000714	miR-370-3p	RB	ovarian cancer cells	Ovarian Cancer	Homo sapiens (human)	microarray;Western blot;Flow Cytometry assay;	33380810	Knockdown of Circular RNA Hsa_circ_0000714 Can Regulate RAB17 by Sponging miR-370-3p to Reduce Paclitaxel Resistance of Ovarian Cancer Through CDK6/RB Pathway.	PURPOSE: Paclitaxel resistance in ovarian cancer has become an urgent clinical problem. This study investigated the regulatory effects of RAB17 on the non-coding RNA network of the paclitaxel-resistant ovarian cancer cell A2780/PTX. METHODS: Microarray analysis was used to identify differentially expressed genes in paclitaxel-resistant cell A2780/PTX compared to the parent paclitaxel-sensitive cell A2780. Quantitative real-time PCR and Western blot were used to measure the expression of related mRNAs and proteins. The CCK8 assay was used to determine cell survival ratios and drug resistance indices in ovarian cancer cells. The clone forming assay was used to analyze the cell clone proliferation. Flow cytometry was used to analyze the cell cycle. Dual-luciferase reporter gene assays evaluated the relationship between the genes. RESULTS: RAB17 is highly expressed in A2780/PTX cells. RAB17 knockdown increased the cell sensitivity to paclitaxel, inhibited proliferation, and caused cell cycle arrest in the G1 phase in A2780/PTX. Western blot confirmed that RAB17 influenced cell behavior by activating the CDK6/RB signaling pathway. Bioinformatics analyses identified RAB17 as a new target by the microRNA miR-370-3p, and the latter was predicted to interact with circular RNA hsa_circ_0000714. Hsa_circ_0000714 indeed acted as a miRNA sponge for miR-370-3p allowing its regulation of RAB17 expression. This regulation was accomplished through the CDK6/RB signaling pathway. CONCLUSION: Hsa_circ_0000714 acts as a sponge for miR-370-3p, and regulates RAB17 expression through the CDK6/RB signaling pathway, which plays a role in the malignant progression of the paclitaxel-resistant ovarian cancer cell A2780/PTX.	NA	Onco Targets Ther. 2020 Dec 24;13:13211-13224. doi: 10.2147/OTT.S285153. eCollection 2020.
4614	Circular RNA	Circ_0002874	miR-1273f	MDM2	lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33612481	Overexpression of hsa_circ_0002874 promotes resistance of non-small cell lung cancer to paclitaxel by modulating miR-1273f/MDM2/p53 pathway.	BACKGROUND: This study aimed to investigate the aberrant expression of hsa_circ_0002874 in non-small cell lung cancer (NSCLC) and elucidate associated molecular mechanisms that influence apoptosis and induce paclitaxel (PTX) resistance. METHODS: Inhibitors were used to downregulate circRNA or miRNA expression. pCDNA plasmid transfection and mimics were used to upregulate circRNA or miRNA expression. Dual-luciferase reporter assays were conducted to evaluate interactions between miR1273f and MDM2. Xenograft tumor models were used to assess the effect of hsa_circ_0002874 and miR1273f on tumor growth. NSCLC tissues and matched non-cancerous tissues were also collected for correlation analysis. RESULTS: hsa_circ_0002874 acts as a sponge for miR1273f which targets MDM2/P53. The stability of the hsa_circ_0002874/miR1273f/MDM2/P53 pathway was verified by upregulating and downregulating the expression of hsa_circ_0002874 and miR1273f. hsa_circ_0002874 downregulation or miR1273f upregulation reversed the resistance of the A549/Taxol cells in xenograft models. The expression of hsa_circ_0002874 was high, and the level of MDM2 was low in NSCLC tissues. P53 was only weakly expressed in NSCLC tissues with high expression of MDM2. CONCLUSIONS: hsa_circ_0002874 is strongly expressed in NSCLC tissues and maybe a potential marker for PTX resistance. hsa_circ_0002874 downregulation could regulate miR1273f/MDM2/P53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis in vitro and vivo.	NA	Aging (Albany NY). 2021 Feb 17;13(4):5986-6009. doi: 10.18632/aging.202521. Epub 2021 Feb 17.
4615	Circular RNA	Circ_0002874	miR-1273f	P53	lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33612481	Overexpression of hsa_circ_0002874 promotes resistance of non-small cell lung cancer to paclitaxel by modulating miR-1273f/MDM2/p53 pathway.	BACKGROUND: This study aimed to investigate the aberrant expression of hsa_circ_0002874 in non-small cell lung cancer (NSCLC) and elucidate associated molecular mechanisms that influence apoptosis and induce paclitaxel (PTX) resistance. METHODS: Inhibitors were used to downregulate circRNA or miRNA expression. pCDNA plasmid transfection and mimics were used to upregulate circRNA or miRNA expression. Dual-luciferase reporter assays were conducted to evaluate interactions between miR1273f and MDM2. Xenograft tumor models were used to assess the effect of hsa_circ_0002874 and miR1273f on tumor growth. NSCLC tissues and matched non-cancerous tissues were also collected for correlation analysis. RESULTS: hsa_circ_0002874 acts as a sponge for miR1273f which targets MDM2/P53. The stability of the hsa_circ_0002874/miR1273f/MDM2/P53 pathway was verified by upregulating and downregulating the expression of hsa_circ_0002874 and miR1273f. hsa_circ_0002874 downregulation or miR1273f upregulation reversed the resistance of the A549/Taxol cells in xenograft models. The expression of hsa_circ_0002874 was high, and the level of MDM2 was low in NSCLC tissues. P53 was only weakly expressed in NSCLC tissues with high expression of MDM2. CONCLUSIONS: hsa_circ_0002874 is strongly expressed in NSCLC tissues and maybe a potential marker for PTX resistance. hsa_circ_0002874 downregulation could regulate miR1273f/MDM2/P53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis in vitro and vivo.	NA	Aging (Albany NY). 2021 Feb 17;13(4):5986-6009. doi: 10.18632/aging.202521. Epub 2021 Feb 17.
4616	Circular RNA	Circ_0005795	miR-1231	caspase3	basal cell carcinoma tissues and cells	Basal Cell Carcinoma	Homo sapiens (human)	luciferase assay;	33433717	Circular RNA hsa_Circ_0005795 mediates cell proliferation of cutaneous basal cell carcinoma via sponging miR-1231.	Growing evidence has revealed that circular RNAs (circRNA) play critical roles in cancer progression. Here, we examined the function of a novel circRNA, Circ_0005795, in basal cell carcinoma (BCC) and explored the possible molecular mechanism. Nodular BCC and adjacent non-tumor tissues derived from 30 patients and 2 BCC cell lines were applied to analyze gene expression. Circ_0005795 loss- and gain-of-function were constructed to investigate BCC progression. Nuclear and cytoplasmic fractionation and luciferase assay were carried out to determine cellular localization and molecular interaction of Circ_0005795. Circ_0005795 expression was significantly elevated in BCC tissues and cells. Knockdown of Circ_0005795 dramatically reduced cell viability, colony formation, and anti-apoptotic protein levels, while increased caspase-3 activity. Circ_0005795 located in cytoplasm, which exerted its tumor-promoting effect through targeting and sponging miR-1231 in BCC cells. In summary, Circ_0005795 works as an oncogene in BCC, which might be used as a promising biomarker and a potential therapeutic target for BCC diagnosis and treatment.	NA	Arch Dermatol Res. 2021 Jan 12. doi: 10.1007/s00403-020-02174-y.
4617	Circular RNA	Circ_0005909	miR-338-3p	HMGA1	Osteoarthritis cells	Osteosarcoma	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;luciferase assay;	33536787	CircRNA hsa_circ_0005909 Promotes Cell Proliferation of Osteosarcoma Cells by Targeting miR-338-3p/HMGA1 Axis.	OBJECTIVE: Osteosarcoma (OS) is the most common malignant bone tumor in the pediatric population. The main goal of this study is to investigate the role of hsa_circ_0005909 and the underlying signaling pathway involved in OS. METHODS: Cell proliferation was measured using a CCK-8 assay kit and clone formation assay. Change of RNA and protein expression was determined using RNA extract and quantitative real time PCR (RT-qPCR) assay and Western blotting, respectively. CircInteractome was used to predict the target of circRNA and starBase v2.0 was used to predict the target of miRNAs. Luciferase assay was used to confirm the predicted results from CircInteractome, starBase v2.0, and MirTarget2. RESULTS: Expression of circ_0005909 was upregulated in both OS tissues and cell lines. The predicted results from CircInteractome, starBase v2.0, and MirTarget2 demonstrated that circ_0005909 could sponge miR-338-3p and that HGMA1 was the direct target of miR-338-3p. Cell viability and cell clones were inhibited by knockdown of circ_0005909 but increased by dual inhibition of circ_0005909 and miR-338-3p. Phosphorylation of ERK, Akt, and PI3K was inhibited by sh-circ_0005909, while this inhibition was repressed by co-transfection of sh-circ_0005909 and HGMA1. CONCLUSION: Expression of circ_0005909 was upregulated in both OS tissues and cell lines which upregulated expression of HGMA1 through sponging miR-338-3p, resulting in the activation of MAPK-ERK and PI3K-Akt signaling pathways to promote the development of OS.	NA	Cancer Manag Res. 2021 Jan 27;13:795-803. doi: 10.2147/CMAR.S285118. eCollection 2021.
4618	Circular RNA	Circ_0009172	miR-485-3p	NTRK3	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	luciferase assay;	33531648	Circular RNA hsa_circ_0009172 suppresses gastric cancer by regulation of microRNA-485-3p-mediated NTRK3.	Gastric cancer is the third leading cause of cancer-related death worldwide, with relapse and metastasis being major contributors to the mortality. Circular RNAs (circRNAs) have been at the center of several researches and some circRNAs have been indicated to be involved in gastric cancer as sponges. Nevertheless, the mechanism underlying the function of circRNA remains largely unclear. Therefore, this study was conducted with the main objective of screening the associated circRNA in gastric cancer and exploring its mechanism. Expression of hsa_circRNA_0009172 was validated in gastric cancer tissues and cell lines after the correlation between hsa_circRNA_0009172 and prognosis was determined. Moreover, the binding site between miR-485-3p and hsa_circRNA_0009172 or NTRK3 was verified using dual luciferase assay and RNA pull down. Function-gain and -loss experiments were performed for the purpose of detecting the effect of hsa_circRNA_0009172 in vivo and in vitro as well as its mechanism with microRNA (miRNA)-485-3p and NTRK3 in gastric cancer. The hsa_circRNA_0009172 expression was downregulated in gastric cancer tissues and cell lines, indicating a positive association with patient prognosis. Functionally, hsa_circ_0009172 overexpression inhibited proliferative, invasive and migrative potential of gastric cancer cells as well as epithelial-mesenchymal transition (EMT)-related proteins by sponging miR-485-3p to inhibit NTRK3, while miR-485-3p overexpression could reverse the inhibitory effect of hsa_circ_0009172 on gastric cancer. Furthermore, either up-regulation of hsa_circ_0009172 or down-regulation of miR-485-3p led to the suppression of xenograft tumor growth in nude mice. In conclusion, hsa_circ_0009172 serves as a tumor suppressor in gastric cancer by targeting miR-485-3p/NTRK3 axis.	NA	Cancer Gene Ther. 2021 Feb 2. doi: 10.1038/s41417-020-00280-7.
4619	Circular RNA	Circ_0014717	miR-668-3p	BTG2	hepatocellular carcinoma tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Rescue assay;	33598424	Circular RNA circ_0014717 Suppresses Hepatocellular Carcinoma Tumorigenesis Through Regulating miR-668-3p/BTG2 Axis.	Recent studies have reported a close association between circRNAs and cancer development. CircRNAs have been recognized to be involved in various biological processes. Up to now, the function of circRNAs in hepatocellular carcinoma (HCC) is still poorly known. qRT-PCR was used to test circ_0014717 expression in HCC tissue samples and cells was determined. It was shown that circ_0014717 was significantly decreased in HCC. Then, we observed overexpression of circ_0014717 obviously repressed HCC cell growth, migration and invasion. Next, we predicted circ_0014717 acted as a sponge of miR-668-3p. miR-668-3p has been reported to participate in several diseases. In our work, it was shown miR-668-3p was greatly increased in HCC and the direct binding sites between circ_0014717 and miR-668-3p were validated. In addition, B-cell translocation gene 2 (BTG2) is closely involved in cellular carcinogenic processes. BTG2 was predicted as a target for miR-668-3p. By performing rescue assays, we demonstrated that circ_0014717 repressed HCC progression via inhibiting BTG2 expression and sponging miR-668-3p. It was manifested loss of circ_0014717 induced HCC progression, which was reversed by BTG2 in Hep3B cells. In conclusion, our findings illustrated a novel circ_0014717/miR-668-3p/BTG2 regulatory signaling pathway in HCC.	NA	Front Oncol. 2021 Jan 27;10:592884. doi: 10.3389/fonc.2020.592884. eCollection 2020.
4620	Circular RNA	Circ_0030018	miR-1297	RAB21	glioma tissues and cells	Glioma	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33440987	CircRNA hsa_circ_0030018 regulates the development of glioma via regulating the miR-1297/RAB21 axis.	Circular RNAs (circRNAs) play a crucial role in tumor occurrence and progression. And the dysregulated circRNAs are reported to be relevant to glioma development. Nevertheless, the function and regulatory mechanism of hsa_circ_0030018 in glioma progression are largely indistinct. The abundances of hsa_circ_0030018, miR-1297, and RAB21 were detected using quantitative real-time polymerase chain reaction or western blot. Cell proliferation was assessed via colony formation assay and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell apoptosis and cell cycle progression were evaluated by flow cytometry. Cell migration and invasion were examined using transwell assay and wound healing assay. The protein levels were measured by western blot. The interaction between miR-1297 and hsa_circ_0030018 or RAB21 was validated via dual-luciferase reporter analysis, RNA immunoprecipitation (RIP), and RNA pull-down assays. A xenograft model experiment was performed to analyze the function of hsa_circ_0030018 on tumor growth in vivo. hsa_circ_0030018 and RAB21 levels were enhanced, and the miR-1297 level was reduced in glioma tissues and cells. The silence of hsa_circ_0030018 or overexpression of miR-1297 impeded cell proliferation, metastasis, and expedited cell apoptosis and cycle arrest in glioma cells. Furthermore, hsa_circ_0030018 modulated glioma malignant behaviors via sponging miR-1297, and miR-1297 suppressed glioma development via targeting RAB21. Moreover, hsa_circ_0030018 knockdown inhibited tumor growth in vivo. The hsa_circ_0030018 knockdown repressed glioma progression by mediating the miR-1297/RAB21 pathway, providing potential therapeutic targets for glioma treatment.	NA	Neoplasma. 2021 Mar;68(2):391-403. doi: 10.4149/neo_2020_200702N682. Epub 2021 Jan 14.
4621	Circular RNA	Circ_0038383	miR-196b-5p	HOXA9	NA	Recurrent Implantation Failure	Homo sapiens (human)	qPCR;RT-qPCR;	33611311	Hsa_circ_0038383-mediated competitive endogenous RNA network in recurrent implantation failure.	BACKGROUND: Inadequate endometrial receptivity contributes to recurrent implantation failure (RIF) during IVF-embryo transfer. Though multiple circRNAs have been confirmed differentially expression in RIF, the potential function of novel circRNAs needed to be detected. RESULTS: The top ten DEcircRNAs were selected as initial candidates. A ceRNA network was conducted on the basis of circRNA-miRNA-mRNA potential interaction, consisting of 10 DEcircRNAs, 28 DEmiRNAs and 59 DEmRNAs. Three down-regulation circRNAs with high degree of connectivity were verified by RT-qPCR, and results suggested that only hsa_circ_0038383 was significantly downregulation in RIF compared with control group. Subsequently, three hub genes (HOXA3, HOXA9 and PBX1) were identified as hub genes. Ultimately, a subnetwork was determined based on one DEcircRNA (hsa_circ_0038383), two DEmiRNAs (has-miR-196b-5p and has-miR-424-5p), and three DEmRNAs (HOXA3, HOXA9 and PBX1). Following verification, hsa_circ_0038383/miR-196b-5p/HOXA9 axis may be a key pathway in affecting RIF. CONCLUSION: In summary, a hsa_circ_0038383-mediated ceRNA network related to RIF was proposed. This network provided new insight into exploring potential biomarkers for diagnosis and clinical treatment of RIF. METHODS: We retrieved the expression profiles of RIF from GEO databases (circRNA, microRNA and mRNA) and constructed a competing endogenous RNAs (ceRNA) network based on predicted circRNA-miRNA and miRNA-mRNA pairs. The expression levels of three hub DEcircRNAs identified by cytoscape were validated by RT-qPCR.	NA	Aging (Albany NY). 2021 Feb 20;13(4):6076-6090. doi: 10.18632/aging.202590. Epub 2021 Feb 20.
4622	Circular RNA	Circ_0107702	miR-876-3p	CDKL3	colorectal cancer tissues	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33232736	CircTP53 promotes colorectal cancer by acting as a miR-876-3p sponge to increase cyclin-dependent kinase-like 3 expression.	According to ceRNA theory, circular RNAs could regulate certain protein expression through targeting corresponding microRNAs to affect the progression of multiple diseases, including colorectal cancer. CircTP53 (hsa_circ_0107702), highly expressed in thyroid cancer tissues, could promote the proliferation of thyroid cancer. However, the function of circTP53 in colorectal cancer is still unclear. In our study, we found circTP53 was significantly up-regulated in colorectal cancer tissues from patients and in colorectal cell lines. Next, using colorectal cell lines, we confirmed that circTP53 promoted the proliferation, migration and invasion, and reduced the apoptotic rate. Furthermore, through bioinformatics analysis and experimental confirmation, we found circTP53 functioned as the sponge of miR-876-3p, and miR-876-3p reversed the phenotype of circTP53 on the facilitation of colorectal cancer. Additionally, we found circTP53 promoted the progression of colorectal cancer by elevating the expression of CDKL3. At last, we suggested that circTP53 knockdown could inhibit colorectal cancer progression in vivo. In conclusion, circTP53 was highly expressed in colorectal cancer tissues, and promoted colorectal cancer progression via modulating miR-876-3p/CDKL3 axis.	NA	Cell Signal. 2021 Feb;78:109845. doi: 10.1016/j.cellsig.2020.109845. Epub 2020 Nov 21.
4623	Circular RNA	Circ_0123190	miR-483-3p	APLNR	Renal tissues	Lupus Nephritis	Homo sapiens (human)	qRT-PCR;Immunohistochemistry;Luciferase reporter assay;	33436040	Hsa_circ_0123190 acts as a competitive endogenous RNA to regulate APLNR expression by sponging hsa-miR-483-3p in lupus nephritis.	BACKGROUND: Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus (SLE). Circular RNAs (circRNAs) can act as competitive endogenous RNAs (ceRNAs) to regulate gene transcription, which is involved in mechanism of many diseases. However, the role of circRNA in lupus nephritis has been rarely reported. In this study, we aim to investigate the clinical value of circRNAs and explore the mechanism of circRNA involvement in the pathogenesis of LN. METHODS: Renal tissues from three untreated LN patients and three normal controls (NCs) were used to identify differently expressed circRNAs by next-generation sequencing (NGS). Validated assays were used by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The interactions between circRNA and miRNA, or miRNA and mRNA were further determined by luciferase reporter assay. The extent of renal fibrosis between the two groups was assessed by Masson-trichome staining and immunohistochemistry (IHC) staining. RESULTS: 159 circRNAs were significantly dysregulated in LN patients compared with NCs. The expression of hsa_circ_0123190 was significantly decreased in the renal tissues of patients with LN (P = 0.014). Bio-informatics analysis and luciferase reporter assay illustrated that hsa_circ_0123190 can act as a sponge for hsa-miR-483-3p, which was also validated to interact with APLNR. APLNR mRNA expression was related with chronicity index (CI) of LN (P = 0.033, R(2) = 0.452). Moreover, the fibrotic-related protein, transforming growth factor-β1 (TGF-β1), which was regulated by APLNR, was more pronounced in the LN group (P = 0.018). CONCLUSION: Hsa_circ_0123190 may function as a ceRNA to regulate APLNR expression by sponging hsa-miR-483-3p in LN.	NA	Arthritis Res Ther. 2021 Jan 13;23(1):24. doi: 10.1186/s13075-020-02404-8.
4624	Circular RNA	Circ_100984	miR-432-3p	YBX-1	Bladder cancer cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR	33314480	circ_100984-miR-432-3p axis regulated c-Jun/YBX-1/β-catenin feedback loop promotes bladder cancer progression.	Bladder cancer (BC) is one of the most commonly diagnosed cancers globally. Recently, circular RNAs (circRNAs) have been revealed to participate in BC progression with diverse mechanisms. However, mechanisms of circ_100984 in BC have not been determined. Here, we found that circ_100984 and YBX-1 were high presented, while miR-432-3p was low presented in BC. Silencing of circ_100984 and YBX-1 repressed BC tumor growth, migration, and invasion in vitro and in vivo. Mechanistically, we revealed that circ_100984 served as a competing endogenous RNA that sponged miR-432-3p to indirectly regulate YBX-1 and epithelial-mesenchymal transition (EMT)-related molecules. Moreover, we confirmed that YBX-1 or c-Jun acted as a transcription regulatory factor for β-catenin or YBX-1, respectively, in BC cells. Knockdown of YBX-1 inhibited the expression of β-catenin and c-Jun, whereas downregulated c-Jun inversely repressed the expression of YBX-1 and β-catenin. Our results suggested that circ_100984-miR-432-3p axis regulated c-Jun/YBX-1/β-catenin feedback loop promotes BC progression, providing a potential therapeutic axis for BC progression.	NA	Cancer Sci. 2021 Apr;112(4):1429-1442. doi: 10.1111/cas.14774. Epub 2021 Feb 10.
4625	Circular RNA	Circ_LRIG3	miR-449a	RNF38	hepatocellular carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	33880997	circ_LRIG3 contributes to the progression of hepatocellular carcinoma by elevating RNF38 via sponging miR-449a.	Circular RNAs (circRNAs) play crucial roles in multiple cancers, including hepatocellular carcinoma (HCC). However, the effects and molecular mechanisms of circ_LRIG3 in HCC remain barely unknown. qRT-PCR assay was employed to detect the levels of circ_LRIG3, LRIG3, miR-449a and ring finger protein 38 (RNF38). RNase R assay and Actinomycin D assay were performed to analyze the characteristics of circ_LRIG3. Colony formation assay and MTT assay were used to evaluate cell proliferation. Flow cytometry analysis and transwell assay were adopted for cell apoptosis and metastasis, respectively. Western blot assay was carried out for the protein levels of Ki67, Snail, E-cadherin, RNF38, Smad2/3 and p-Smad2/3. Murine xenograft model assay was used to explore the role of circ_LRIG3 in vivo. circ_LRIG3 expression was upregulated in HCC tissues and cells. Knockdown of circ_LRIG3 suppressed proliferation, migration and invasion and facilitated cell apoptosis in HCC cells in vitro and blocked tumor growth of HCC in vivo. RNF38 overexpression reversed the effects of circ_LRIG3 knockdown on the malignant behaviors of HCC cells. Moreover, circ_LRIG3 could sponge miR-449a to positively modulate RNF38 expression in HCC cells. circ_LRIG3 knockdown inhibited the progression of HCC cells by sponging miR-449a. In addition, circ_LRIG3 silencing might inhibit the Smad2/3 pathway. circ_LRIG3 facilitated HCC progression by modulation of miR-449a/LRIG3 axis, which might provide a novel method for HCC therapy.	NA	Gen Physiol Biophys. 2021 Mar;40(2):103-114. doi: 10.4149/gpb_2020044.
4626	Circular RNA	Circ_NOTCH3	miR-205-5p	KLF12	basal-like breast carcinoma cells	Basal-Like Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33552974	circ_NOTCH3 Functions as a Protooncogene Competing With miR-205-5p, Modulating KLF12 Expression and Promoting the Development and Progression of Basal-Like Breast Carcinoma.	Breast cancer is the most common type of cancer diagnosed among women, and basal-like breast carcinoma (BLBC) has been associated with a more aggressive histology, poorer prognosis, and non-responsiveness to hormone therapy. In the present study, the role and molecular mechanism of circular (circ)_NOTCH3 in the development and progression for BLBC was identified. circ_RNAs array was used to screen the ectopic expression of hsa_circ_0109177 (circ_NOTCH3) in BLBC. RT-qPCR was conducted to evaluate the circ_NOTCH3 expression in BLBC tissues and paired normal tissues, as well as related cell lines. Cell function changes were analyzed following circ_NOTCH3 or micro (mi)RNA overexpression or co-expression. Bioinformatics analysis and dual-luciferase reporter assay were performed to predict and verify the binding sites between circ_NOTCH3 and miRNAs. Gene expression changes were assessed using western blotting. circ_NOTCH3 had a significantly higher expression in BLBC tissues and cell lines. The upregulation of circ_NOTCH3 promoted the proliferation, migration, invasion and inhibited the apoptosis for BLBC cells. The opposite results were observed following miR-205-5p overexpression. However, the co-expression of circ_NOTCH3 and miR-205-5p resulted in those restoration. circ_NOTCH3 is capable of binding to miR-205-5p, and upregulating its target gene KLF12, which can be downregulated by miR-205-5p overexpression and restored by the co-expression of circ_NOTCH3 and miR205-5p. circ_NOTCH3, being an protooncogene and a powerful biomarker, can function as a sponge, compete with miR-205-5p, modulate KLF12 expression, and promote the development and progression of BLBC.	NA	Front Oncol. 2021 Jan 20;10:602694. doi: 10.3389/fonc.2020.602694. eCollection 2020.
4627	Circular RNA	CircCUX1	miR-338-3p	PHF20	Neuroblastoma tissues and cells	Neuroblastoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RACE;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33655888	circCUX1 promotes neuroblastoma progression and glycolysis by regulating the miR-338-3p/PHF20 axis.	Neuroblastoma (NB) is an extracranial solid malignancy in childhood. More and more studies have demonstrated that circRNAs are essential regulators of various tumors. This study conducted to explore the role and mechanism of circular RNA CUT-like homeobox 1 (circCUX1) in NB. The levels of circCUX1, miR-338-3p and plant homeodomain finger protein 20 (PHF20) were detected by qRT-PCR or Western blot. Cell proliferation and apoptosis were evaluated by colony formation assay, flow cytometry and Western blot analysis. Cell migration and invasion were examined via transwell assay. Glycolysis was expressed by measuring the extracellular acidification rate (ECAR). The interaction among circCUX1, miR-338-3p and PHF20 were validated by dual-luciferase reporter assay and RNA Immunoprecipitation assay. Besides, xenograft experiment was performed to assess tumor growth in vivo. circCUX1 and PHF20 were up-regulated, while miR-338-3p was down-regulated in NB tissues and cells. Knockdown of circCUX1 suppressed the progression and glycolysis of NB cells. circCUX1 triggered NB progression and glycolysis by regulating miR-338-3p. Additionally, down-regulation of miR-338-3p promoted NB progression and glycolysis via targeting PHF20. Moreover, circCUX1 sponged miR-338-3p to regulate PHF20 expression. Furthermore, circCUX1 silencing hindered tumor growth in vivo. circCUX1 depletion suppressed tumor progression and glycolysis in NB by regulating miR-338-3p/PHF20 axis, suggesting a potential biomarker for NB treatment.	NA	Gen Physiol Biophys. 2021 Jan;40(1):17-29. doi: 10.4149/gpb_2020041.
4628	Circular RNA	CircNEIL3	miR-137	KLF12	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33413360	CircNEIL3 promotes cervical cancer cell proliferation by adsorbing miR-137 and upregulating KLF12.	BACKGROUND: CircRNAs play crucial roles in multiple tumours. However, the functions of most circRNAs in cervical cancer remain unclear. METHODS: This study collected GSE113696 data from the GEO database to search for differentially expressed circRNAs in cervical cancer. Quantitative reverse transcription PCR was used to detect the expression level of circNEIL3 in cervical cancer cells and tissues. Then, functional experiments in vitro and in vivo were performed to evaluate the effects of circNEIL3 in cervical cancer. RESULTS: CircNEIL3 was highly expressed in cervical cancer. In vivo and in vitro experiments verified that circNEIL3 enhanced the proliferation capacity of cervical cancer cells. RNA immunoprecipitation, luciferase reporter assay, pull-down assay, and fluorescent in situ hybridization confirmed the interaction between circNEIL3 and miR-137 in cervical cancer. A luciferase reporter assay showed that circNEIL3 adsorbed miR-137 and upregulated KLF12 to regulate the proliferation of cervical cancer cells. CONCLUSIONS: CircNEIL3 is an oncogene in cervical cancer and might serve as a ceRNA that competitively binds to miR-137, thereby indirectly upregulating the expression of KLF12 and promoting the proliferation of cervical cancer cells.	NA	Cancer Cell Int. 2021 Jan 7;21(1):34. doi: 10.1186/s12935-020-01736-4.
4629	Circular RNA	Circ-PRMT5	miR-509-3p	TCF7L2	breast cancer cells	Breast Cancer	Homo sapiens (human)	Flow Cytometry assay;Rescue assay;	33277756	Circ-PRMT5 promotes breast cancer by the miR-509-3p/TCF7L2 axis activating the PI3K/AKT pathway.	BACKGROUND: Breast cancer is the most prevalent malignancy occurring in females. In recent years, emerging evidence has suggested that circular RNAs are involved in the development of multiple cancers. Circ-PRMT5 has recently attracted attention as a tumor-promoting circular RNA. In the present study, we focused on exploring the biological effects of circ-PRMT5 in breast cancer. METHODS: A quantitative real-time polymerase chain reaction was used to determine the expression of circ-PRMT5 in breast cancer. In vitro experiments, including cell-counting kit-8, 5-ethynyl-2'-deoxyuridine, flow cytometry and tube formation assays, were performed to test the effects of circ-PRMT5 on the cellular progression of breast cancer. Bioinformatic analysis, luciferase reporter, radioimmunoprecipitation and RNA-pull down assays were performed to predict the potential microRNAs interacting with circ-PRMT5 and mRNAs that can be targeted by miR-509-3p. RESULTS: Circ-PRMT5 is up-regulated in breast cancer tissues and cells. Importantly, an elevation of circ-PRMT5 indicates a poor prognosis in patients with breast cancer. Functionally, knockdown of circ-PRMT5 suppresses cell proliferation and angiogenesis and increases cell apoptosis in breast cancer. Mechanistically, we identified that circ-PRMT5 up-regulates TCF7L2 expression by acting as a miR-509-3p sponge. The negative expression correlation between miR-509-3p and circ-PRMT5 or TCF7L2 in clinical tissues was further demonstrated. Rescue assays showed that TCF7L2 overexpression reverses the antitumoral effects of circ-PRMT5 knockdown on breast cancer cell processes. Additionally, we demonstrated that circ-PRMT5 activates the phosphoinositide 3-kinase (PI3K)/AKT pathway by up-regulation of TCF7L2. CONCLUSIONS: Overall, our data indicate that the circ-PRMT5/miR-509-3p/TCF7L2 axis can aggravate the malignant character of breast cancer cells by the regulation of the PI3K/AKT pathway.	NA	J Gene Med. 2021 Feb;23(2):e3300. doi: 10.1002/jgm.3300. Epub 2020 Dec 27.
4630	Circular RNA	CircRILPL1	miR-145	IGF1R	myoblast	Myoblast Proliferation And Apoptosis	Homo sapiens (human)	RNA immunoprecipitation;luciferase assay;RNA immunoprecipitation;	33542215	CircRILPL1 promotes muscle proliferation and differentiation via binding miR-145 to activate IGF1R/PI3K/AKT pathway.	Many novel non-coding RNAs, such as microRNAs (miRNAs) and circular RNAs (circRNAs), are involved in various physiological and pathological processes. The PI3K/AKT signaling pathway is important for its role in regulating skeletal muscle development. In this study, molecular and biochemical assays were used to confirm the role of miRNA-145 (miR-145) in myoblast proliferation and apoptosis. Based on sequencing data and bioinformatics analysis, we identified a new circRILPL1, which acts as a sponge for miR-145. The interactions between circRILPL1 and miR-145 were examined by bioinformatics, a luciferase assay, and RNA immunoprecipitation. Mechanistically, knockdown or exogenous expression of circRILPL1 in the primary myoblasts was performed to prove the functional significance of circRILPL1. We investigated the inhibitory effect of miR-145 on myoblast proliferation by targeting IGF1R to regulate the PI3K/AKT signaling pathway. A novel circRILPL1 was identified that could sponge miR-145 and is related to AKT activation. In addition, circRILPL1 was positively correlated with muscle proliferation and differentiation in vitro and could inhibit cell apoptosis. The newly identified circRILPL1 functions as a miR-145 sponge to regulate the IGF1R gene and rescue the inhibitory effect of miR-145 on the PI3K/AKT signaling pathway, thereby promoting myoblast growth.	NA	Cell Death Dis. 2021 Feb 1;12(2):142. doi: 10.1038/s41419-021-03419-y.
4631	Circular RNA	CircRILPL1	miR-145	PI3K	myoblast	Myoblast Proliferation And Apoptosis	Homo sapiens (human)	RNA immunoprecipitation;luciferase assay;RNA immunoprecipitation;	33542215	CircRILPL1 promotes muscle proliferation and differentiation via binding miR-145 to activate IGF1R/PI3K/AKT pathway.	Many novel non-coding RNAs, such as microRNAs (miRNAs) and circular RNAs (circRNAs), are involved in various physiological and pathological processes. The PI3K/AKT signaling pathway is important for its role in regulating skeletal muscle development. In this study, molecular and biochemical assays were used to confirm the role of miRNA-145 (miR-145) in myoblast proliferation and apoptosis. Based on sequencing data and bioinformatics analysis, we identified a new circRILPL1, which acts as a sponge for miR-145. The interactions between circRILPL1 and miR-145 were examined by bioinformatics, a luciferase assay, and RNA immunoprecipitation. Mechanistically, knockdown or exogenous expression of circRILPL1 in the primary myoblasts was performed to prove the functional significance of circRILPL1. We investigated the inhibitory effect of miR-145 on myoblast proliferation by targeting IGF1R to regulate the PI3K/AKT signaling pathway. A novel circRILPL1 was identified that could sponge miR-145 and is related to AKT activation. In addition, circRILPL1 was positively correlated with muscle proliferation and differentiation in vitro and could inhibit cell apoptosis. The newly identified circRILPL1 functions as a miR-145 sponge to regulate the IGF1R gene and rescue the inhibitory effect of miR-145 on the PI3K/AKT signaling pathway, thereby promoting myoblast growth.	NA	Cell Death Dis. 2021 Feb 1;12(2):142. doi: 10.1038/s41419-021-03419-y.
4632	Circular RNA	CircRILPL1	miR-145	AKT	myoblast	Myoblast Proliferation And Apoptosis	Homo sapiens (human)	RNA immunoprecipitation;luciferase assay;RNA immunoprecipitation;	33542215	CircRILPL1 promotes muscle proliferation and differentiation via binding miR-145 to activate IGF1R/PI3K/AKT pathway.	Many novel non-coding RNAs, such as microRNAs (miRNAs) and circular RNAs (circRNAs), are involved in various physiological and pathological processes. The PI3K/AKT signaling pathway is important for its role in regulating skeletal muscle development. In this study, molecular and biochemical assays were used to confirm the role of miRNA-145 (miR-145) in myoblast proliferation and apoptosis. Based on sequencing data and bioinformatics analysis, we identified a new circRILPL1, which acts as a sponge for miR-145. The interactions between circRILPL1 and miR-145 were examined by bioinformatics, a luciferase assay, and RNA immunoprecipitation. Mechanistically, knockdown or exogenous expression of circRILPL1 in the primary myoblasts was performed to prove the functional significance of circRILPL1. We investigated the inhibitory effect of miR-145 on myoblast proliferation by targeting IGF1R to regulate the PI3K/AKT signaling pathway. A novel circRILPL1 was identified that could sponge miR-145 and is related to AKT activation. In addition, circRILPL1 was positively correlated with muscle proliferation and differentiation in vitro and could inhibit cell apoptosis. The newly identified circRILPL1 functions as a miR-145 sponge to regulate the IGF1R gene and rescue the inhibitory effect of miR-145 on the PI3K/AKT signaling pathway, thereby promoting myoblast growth.	NA	Cell Death Dis. 2021 Feb 1;12(2):142. doi: 10.1038/s41419-021-03419-y.
4633	Circular RNA	CircRNA_0068481	miR-646	EYA3	AC16 cells	Ventricular Hypertrophy	Homo sapiens (human)	qPCR;Western blot;luciferase assay;	33710774	Up-regulation of circRNA_0068481 promotes right ventricular hypertrophy in PAH patients via regulating miR-646/miR-570/miR-885.	CircRNA-0068481 and several miRNAs are important in the pathogenesis of right ventricular hypertrophy (VH), while the inhibition of eye absent transcriptional coactivator and phosphatase 3 (EYA3) was proved to reverse vascular remodelling in rats. In this study, we tried to study the diagnostic value and mechanistic role of circRNA_0068481 in the diagnosis of RVH in PAH patients. qPCR was done to measure circRNA-0068481, miR-646, miR-750, miR-885 and EYA3 mRNA expression. Luciferase assay was done to explore the regulatory relationship between circRNA-0068481/EYA3 and the miRNAs. Western blot was done to measure EYA3 expression in AC16 cells. The expression of circRNA-0068481, miR-646 and miR-570 showed a considerable capability to diagnose RVH in PAH patients. The luciferase activity of circRNA-0068481 was remarkably suppressed by miR-646, miR-570 or miR-885. The luciferase signal of EYA3 was also inhibited by miR-646, miR-570 and miR-885. Up-regulation of circRNA-0068481 expression in AC16 significantly decreased miR-646, miR-570 and miR-885 expression, and up-regulated EYA3 expression, whereas circRNA-0068481 down-regulation significantly increased miR-646, miR-570 and miR-885 expression, and repressed EYA3 expression. CircRNA_0068481 sponged several miRNAs including miR-646, miR-570 and miR-885. These miRNAs were all found to target the expression of EYA3 mRNA, which is involved in the onset of right ventricular hypertrophy. Therefore, it can be concluded that the up-regulation of circRNA_0068481 can predict the diagnosis of right ventricular hypertrophy in pulmonary arterial hypertension patients.	NA	J Cell Mol Med. 2021 Apr;25(8):3735-3743. doi: 10.1111/jcmm.16164. Epub 2021 Mar 12.
4634	Circular RNA	CircRNA_0068481	miR-570	EYA3	AC16 cells	Ventricular Hypertrophy	Homo sapiens (human)	qPCR;Western blot;luciferase assay;	33710774	Up-regulation of circRNA_0068481 promotes right ventricular hypertrophy in PAH patients via regulating miR-646/miR-570/miR-885.	CircRNA-0068481 and several miRNAs are important in the pathogenesis of right ventricular hypertrophy (VH), while the inhibition of eye absent transcriptional coactivator and phosphatase 3 (EYA3) was proved to reverse vascular remodelling in rats. In this study, we tried to study the diagnostic value and mechanistic role of circRNA_0068481 in the diagnosis of RVH in PAH patients. qPCR was done to measure circRNA-0068481, miR-646, miR-750, miR-885 and EYA3 mRNA expression. Luciferase assay was done to explore the regulatory relationship between circRNA-0068481/EYA3 and the miRNAs. Western blot was done to measure EYA3 expression in AC16 cells. The expression of circRNA-0068481, miR-646 and miR-570 showed a considerable capability to diagnose RVH in PAH patients. The luciferase activity of circRNA-0068481 was remarkably suppressed by miR-646, miR-570 or miR-885. The luciferase signal of EYA3 was also inhibited by miR-646, miR-570 and miR-885. Up-regulation of circRNA-0068481 expression in AC16 significantly decreased miR-646, miR-570 and miR-885 expression, and up-regulated EYA3 expression, whereas circRNA-0068481 down-regulation significantly increased miR-646, miR-570 and miR-885 expression, and repressed EYA3 expression. CircRNA_0068481 sponged several miRNAs including miR-646, miR-570 and miR-885. These miRNAs were all found to target the expression of EYA3 mRNA, which is involved in the onset of right ventricular hypertrophy. Therefore, it can be concluded that the up-regulation of circRNA_0068481 can predict the diagnosis of right ventricular hypertrophy in pulmonary arterial hypertension patients.	NA	J Cell Mol Med. 2021 Apr;25(8):3735-3743. doi: 10.1111/jcmm.16164. Epub 2021 Mar 12.
4635	Circular RNA	CircRNA_0068481	miR-885	EYA3	AC16 cells	Ventricular Hypertrophy	Homo sapiens (human)	qPCR;Western blot;luciferase assay;	33710774	Up-regulation of circRNA_0068481 promotes right ventricular hypertrophy in PAH patients via regulating miR-646/miR-570/miR-885.	CircRNA-0068481 and several miRNAs are important in the pathogenesis of right ventricular hypertrophy (VH), while the inhibition of eye absent transcriptional coactivator and phosphatase 3 (EYA3) was proved to reverse vascular remodelling in rats. In this study, we tried to study the diagnostic value and mechanistic role of circRNA_0068481 in the diagnosis of RVH in PAH patients. qPCR was done to measure circRNA-0068481, miR-646, miR-750, miR-885 and EYA3 mRNA expression. Luciferase assay was done to explore the regulatory relationship between circRNA-0068481/EYA3 and the miRNAs. Western blot was done to measure EYA3 expression in AC16 cells. The expression of circRNA-0068481, miR-646 and miR-570 showed a considerable capability to diagnose RVH in PAH patients. The luciferase activity of circRNA-0068481 was remarkably suppressed by miR-646, miR-570 or miR-885. The luciferase signal of EYA3 was also inhibited by miR-646, miR-570 and miR-885. Up-regulation of circRNA-0068481 expression in AC16 significantly decreased miR-646, miR-570 and miR-885 expression, and up-regulated EYA3 expression, whereas circRNA-0068481 down-regulation significantly increased miR-646, miR-570 and miR-885 expression, and repressed EYA3 expression. CircRNA_0068481 sponged several miRNAs including miR-646, miR-570 and miR-885. These miRNAs were all found to target the expression of EYA3 mRNA, which is involved in the onset of right ventricular hypertrophy. Therefore, it can be concluded that the up-regulation of circRNA_0068481 can predict the diagnosis of right ventricular hypertrophy in pulmonary arterial hypertension patients.	NA	J Cell Mol Med. 2021 Apr;25(8):3735-3743. doi: 10.1111/jcmm.16164. Epub 2021 Mar 12.
4636	Circular RNA	CircRNA_072697	miR-3150a-3p	KRAS	diabetic foot ulcers tissues	Diabetic Foot Ulcers	Homo sapiens (human)	qPCR;RT-qPCR;	33314661	Identification of potential circRNAs and circRNA-miRNA-mRNA regulatory network in the development of diabetic foot ulcers by integrated bioinformatics analysis.	We aimed to explore the mechanism of circular RNAs (circRNAs) and provide potential biomarkers for molecular therapy of diabetic foot ulcers (DFU). Gene expression profile of GSE114248, including five normal samples and five DFU samples, was downloaded from GEO database. Differentially expressed circRNAs (DEcircRNAs) between two groups were identified. Then, DEcircRNA-miRNA and miRNA-mRNA interaction was revealed, followed by the circRNA-miRNA-mRNA network construction. Moreover, functional and pathway analysis were performed based on mRNAs, followed by the DM-related pathway exploration. Specific binding sites for key circRNAs and associated miRNAs were under investigation. Finally, RT-qPCR was used to verify the candidate the relative expression level of circRNA between normal tissues and DFU. Totally, 65 DEcircRNAs were revealed between two groups, followed by 113 circRNA-miRNA-mRNA interactions explored. The mRNAs in these interactions were mainly assembled in functions like cell proliferation and pathways. Moreover, a total of 11 DM-related pathways were revealed. Finally, circRNA-miRNA specific binding-site analysis revealed two key circRNAs, for example, circRNA_072697 and circRNA_405463, corresponding to their miRNAs. These two circRNAs were novel biomarkers for DFU. circRNA_072697 acted as a sponge of miR-3150a-3p in the progression of DFU via regulating KRAS. MAPK signaling pathway might contribute to the development of DFU.	NA	Int Wound J. 2021 Jun;18(3):323-331. doi: 10.1111/iwj.13535. Epub 2020 Dec 13.
4637	Circular RNA	CircRNA_103809	miR-377-3p	GOT1	non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qPCR;Western blot;Immunohistochemistry;	33276753	A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC).	BACKGROUND: Cisplatin is the first-line chemotherapeutic drug for non-small cell lung cancer (NSCLC), and emerging evidences suggests that targeting circular RNAs (circRNAs) is an effective strategy to increase cisplatin-sensitivity in NSCLC, but the detailed mechanisms are still not fully delineated. METHODS: Cell proliferation, viability and apoptosis were examined by using the cell counting kit-8 (CCK-8) assay, trypan blue staining assay and Annexin V-FITC/PI double staining assay, respectively. The expression levels of cancer associated genes were measured by using the Real-Time qPCR and Western Blot analysis at transcriptional and translated levels. Dual-luciferase reporter gene system assay was conducted to validated the targeting sites among hsa_circRNA_103809, miR-377-3p and 3' untranslated region (3'UTR) of GOT1 mRNA. The expression status, including expression levels and localization, were determined by immunohistochemistry (IHC) assay in mice tumor tissues. RESULTS: Here we identified a novel hsa_circRNA_103809/miR-377-3p/GOT1 signaling cascade which contributes to cisplatin-resistance in NSCLC in vitro and in vivo. Mechanistically, parental cisplatin-sensitive NSCLC (CS-NSCLC) cells were subjected to continuous low-dose cisplatin treatment to generate cisplatin-resistant NSCLC (CR-NSCLC) cells, and we found that hsa_circRNA_103809 and GOT1 were upregulated, while miR-377-3p was downregulated in CR-NSCLC cells but not in CS-NSCLC cells. In addition, hsa_circRNA_103809 sponged miR-337-3p to upregulate GOT1 in CS-NSCLC cells, and knock-down of hsa_circRNA_103809 enhanced the inhibiting effects of cisplatin on cell proliferation and viability, and induced cell apoptosis in CR-NSCLC cells, which were reversed by downregulating miR-377-3p and overexpressing GOT1. Consistently, overexpression of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells by regulating the miR-377-3p/GOT1 axis. Finally, silencing of hsa_circRNA_103809 aggravated the inhibiting effects of cisplatin treatment on NSCLC cell growth in vivo. CONCLUSIONS: Analysis of data suggested that targeting the hsa_circRNA_103809/miR-377-3p/GOT1 pathway increased susceptibility of CR-NSCLC cells to cisplatin, and this study provided novel targets to improve the therapeutic efficacy of cisplatin for NSCLC treatment in clinic.	NA	BMC Cancer. 2020 Dec 4;20(1):1190. doi: 10.1186/s12885-020-07680-w.
4638	Circular RNA	CircRNA_104348	miR-187-3p	RTKN2	hepatocellular carcinoma tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33311442	CircRNA hsa_circRNA_104348 promotes hepatocellular carcinoma progression through modulating miR-187-3p/RTKN2 axis and activating Wnt/β-catenin pathway.	Circular RNAs (circRNAs) have confirmed to participate in diverse biological functions in cancer. However, the expression patterns of circRNAs on hepatocellular carcinoma (HCC) remains unclear. In the present study, we clarified that hsa_circRNA_104348 was dramatically upregulated in HCC tissues and cells. Patients with HCC displaying high hsa_circRNA_104348 level possessed poor prognosis. Has_circ_104348 facilitated proliferation, migration, and invasion, meanwhile suppressed apoptosis of HCC cell. Furthermore, hsa_circRNA_104348 directly targeted miR-187-3p, could regulate miR-187-3p to affect proliferation, migration, invasion, and apoptosis of HCC cells, and may have effect on Wnt/β-catenin signaling pathway. Moreover, RTKN2 could be a direct target of miR-187-3p. In addition, knockdown of hsa_circRNA_104348 attenuated HCC tumorigenesis and lung metastasis in vivo. Taken together, these findings indicated that circular RNA hsa_circRNA_104348 might function as a competing endogenous RNA (ceRNA) to promotes HCC progression by targeting miR-187-3p/RTKN2 axis and activating Wnt/β-catenin pathway.	NA	Cell Death Dis. 2020 Dec 14;11(12):1065. doi: 10.1038/s41419-020-03276-1.
4639	Circular RNA	CircRNA_141539	miR-4469	CDK3	esophageal squamous cell carcinoma cells	Esophageal Squamous Cancer	Homo sapiens (human)	ChIP;Dual-luciferase reporter assay;luciferase assay;Luciferase reporter assay;	33504681	circRNA_141539 can serve as an oncogenic factor in esophageal squamous cell carcinoma by sponging miR-4469 and activating CDK3 gene.	The abnormal expression and regulation of circular RNA (circRNA) is involved in the occurrence and development of a variety of tumors. The current study aimed to determine the role of circRNA_141539 in esophageal squamous cell carcinoma (ESCC). CircRNA_141539 expression in ESCC was detected via circRNA chip analysis and verified via reverse transcription-quantitative PCR. Associations between circRNA_141539, patient clinicopathological characteristics and prognosis were also statistically analyzed. Additionally, the effects of circRNA_141539 on ESCC cell proliferation and invasion were assessed. A dual-luciferase assay was performed to analyze the interaction between circRNAs, microRNAs (miRs) and mRNAs. The results revealed that circRNA_141539 was significantly up-regulated in patients with ESCC. Furthermore, high circRNA_141539 expressions were significantly associated with TNM stage, differentiation and poor prognosis, revealing high diagnostic value (P<0.05). Furthermore, circRNA_141539 overexpression promoted cell proliferation and invasion, while circRNA_141539 silencing inhibited cell proliferation and invasion (P<0.05). The dual-luciferase reporter assay identified that circRNA_141539 directly binds to miR-4469 and also revealed that cyclin-dependent kinase-3 (CDK3) was negatively regulated by miR-4469. The results indicated that circRNA_141539 served as an oncogenic factor in ESCC by sponging miR-4469 and activating CDK3 expression. circRNA_141539 may present as a novel diagnostic and prognostic biomarker and a therapeutic target for patients with ESCC.	NA	Aging (Albany NY). 2021 Jan 27;13(8):12179-12193. doi: 10.18632/aging.103071. Epub 2021 Jan 27.
4640	Circular RNA	CircRNA_30032	miR-96-5p	HBEGF	TGF-β1-treated BUMPT cells	Renal Fibrosis	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33973871	CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis.	In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as in vitro and in vivo models. CircRNA_30032 expression was significantly increased by 9.15- and 16.6-fold on days 3 and 7, respectively, in the renal tissues of UUO model mice. In TGF-β1-treated BUMPT cells, circRNA_30032 expression was induced by activation of the p38 mitogen-activated protein kinase signaling pathway. Quantitative real-time PCR, western blotting and dual luciferase reporter assays showed that circRNA_30032 mediated TGF-β1-induced and UUO-induced renal fibrosis by sponging miR-96-5p and increasing the expression of profibrotic proteins, including HBEGF, KRAS, collagen I, collagen III and fibronectin. CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.	NA	Aging (Albany NY). 2021 May 11;13(9):12780-12799. doi: 10.18632/aging.202947. Epub 2021 May 11.
4641	Circular RNA	CircRNA_30032	miR-96-5p	KRAS	TGF-β1-treated BUMPT cells	Renal Fibrosis	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33973871	CircRNA_30032 promotes renal fibrosis in UUO model mice via miRNA-96-5p/HBEGF/KRAS axis.	In this study, we investigated the role of circular RNA_30032 (circRNA_30032) in renal fibrosis and the underlying mechanisms. The study was carried out using TGF-β1-induced BUMPT cells and unilateral ureteral obstruction (UUO)-induced mice, respectively, as in vitro and in vivo models. CircRNA_30032 expression was significantly increased by 9.15- and 16.6-fold on days 3 and 7, respectively, in the renal tissues of UUO model mice. In TGF-β1-treated BUMPT cells, circRNA_30032 expression was induced by activation of the p38 mitogen-activated protein kinase signaling pathway. Quantitative real-time PCR, western blotting and dual luciferase reporter assays showed that circRNA_30032 mediated TGF-β1-induced and UUO-induced renal fibrosis by sponging miR-96-5p and increasing the expression of profibrotic proteins, including HBEGF, KRAS, collagen I, collagen III and fibronectin. CircRNA_30032 silencing significantly reduced renal fibrosis in UUO model mice by increasing miR-96-5p levels and decreasing levels of HBEGF and KRAS. These results demonstrate that circRNA_30032 promotes renal fibrosis via the miR-96-5p/HBEGF/KRAS axis and suggest that circRNA_30032 is a potential therapeutic target for treatment of renal fibrosis.	NA	Aging (Albany NY). 2021 May 11;13(9):12780-12799. doi: 10.18632/aging.202947. Epub 2021 May 11.
4642	Circular RNA	CircRNA051239	miR-509-5p	PRSS3	epithelial ovarian cancer SKOV3 cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;RACE;Luciferase activity assay;	33841644	Tumor-derived exosomal circRNA051239 promotes proliferation and migration of epithelial ovarian cancer.	Recent studies have shown the involvement of exosomes in intercellular communication during tumor progression. Circular RNAs (circRNAs) can be packaged into exosomes for extracellular communication, however, the possible effects of exosomal circRNAs in epithelial ovarian cancer (EOC) cells with high metastatic potential have been rarely studied. In this study, we identified exosomal circRNA051239 from high-metastatic ovarian cancer SKOV3.ip cells and subsequently analyzed circRNA051239 levels in both EOC tissues and exosomes derived from plasma and cells by qRT-PCR. A variety of in vitro assays were employed to observe the effects of exosomal circRNA051239 derived from high-metastatic ovarian cancer SKOV3.ip cells on low-metastatic ovarian cancer SKOV3 cells. Bioinformatics analysis and luciferase activity assays were further utilized to confirm the relationship between circRNA051239, miR-509-5p and PRSS3. As a result, circRNA051239 expression was increased in tissues and plasma exosomes from EOC patients. Moreover, si-circRNA051239-Exo (exosomes derived from circRNA051239 knockdown SKOV3.ip cells) inhibited the proliferation, migration as well as invasion of SKOV3 cells. Mechanistically, circRNA051239 functioned as a competitive endogenous RNA (ceRNA) by sponging miR-509-5p to facilitate PRSS3 expression. Exosomal circRNA051239 derived from high-metastatic ovarian cancer SKOV3.ip cells promoted the progression of low-metastatic ovarian cancer SKOV3 cells. Collectively, these outcomes implicated that higher metastatic EOC cells can confer this potential to lower metastatic potential via exosomal circRNA051239, causing enhanced proliferative, migratory and invasive capacities in recipient cells.	NA	Am J Transl Res. 2021 Mar 15;13(3):1125-1139. eCollection 2021.
4643	Circular RNA	CircRUNX1	miR-296-3p	DDHD2	Papillary thyroid cancer cells	Papillary Thyroid Cancer	Homo sapiens (human)	FISH;FISH;Luciferase reporter assay;	33479208	Circular RNA circRUNX1 promotes papillary thyroid cancer progression and metastasis by sponging MiR-296-3p and regulating DDHD2 expression.	Papillary thyroid cancer (PTC) has a continuously increasing incidence and imposes a heavy medical burden to individuals and society due to its high proportion of lymph node metastasis and recurrence in recent years. Circular RNAs, a class of noncoding RNAs, participate in the progression of many cancers, but the role of circRNAs in PTC is still rarely reported. In this study, circRNA deep sequencing was performed to identify differentially expressed circRNAs in PTC. CircRUNX1 was selected for its high expression in PTC, and circRUNX1 silencing was directly associated with the week potential for migration, invasion and proliferation of PTC in vivo and in vitro. Fluorescence in situ hybridization (FISH) was further used to confirm the cytoplasmic localization of circRUNX1, indicating the possible function of circRUNX1 as a ceRNAs in PTC progression through miRNA binding. MiR-296-3p was then confirmed to be regulated by circRUNX1 and to target DDHD domain containing 2 (DDHD2) by luciferase reporter assays. The strong antitumor effect of miR-296-3p and the tumor-promoting effect of DDHD2 were further investigated in PTC, indicating that circRUNX1 modulates PTC progression through the miR-296-3p/DDHD2 pathway. Overall, circRUNX1 plays an oncogenic role in PTC and provides a potentially effective therapeutic strategy for PTC progression.	NA	Cell Death Dis. 2021 Jan 21;12(1):112. doi: 10.1038/s41419-020-03350-8.
4644	Circular RNA	Circ-UBR1	miR-1299	CCND1	breast cancer cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33259864	Circ-UBR1 facilitates proliferation, metastasis, and inhibits apoptosis in breast cancer by regulating the miR-1299/CCND1 axis.	AIMS: Circular RNA (circRNA) is abnormally expressed in cancers and has been linked to cancer progression, including breast cancer (BC). However, the role and mechanism of circ-UBR1 in BC progression remains to be further studied. MATERIALS AND METHODS: Quantitative real-time PCR (qRT-PCR) was conducted to analyze the expression of circ-UBR1, miR-1299 and Cyclin D1 (CCND1). Cell counting kit 8 (CCK8) assay was used to measure cell viability. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Then, the migration and invasion of cells were determined by transwell assay. Moreover, BC tumor xenograft model was built to evaluate the function of circ-UBR1 silencing on BC tumor volume and weight. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to illuminate the interaction between miR-1299 and circ-UBR1 or CCND1. In addition, relative CCND1 protein expression was assessed using western blot (WB) analysis. KEY FINDINGS: Our results revealed that circ-UBR1 was upregulated in BC, and its silencing could inhibit BC cell proliferation, metastasis, and promote apoptosis in vitro, as well as restrain BC tumor growth in vivo. Meanwhile, we found that circ-UBR1 could sponge miR-1299, and miR-1299 inhibitor could reverse the effect of circ-UBR1 knockdown on BC cell progression. Furthermore, CCND1 was a target of miR-1299, and CCND1 overexpression could reverse the effect of miR-1299 mimic on BC cell progression. Also, the downregulation of circ-UBR1 could inhibit CCND1 expression, while this effect could be inverted by miR-1299 inhibitor. SIGNIFICANCE: Our data indicated that circ-UBR1 might play a pro-cancer role in BC progression by regulating the miR-1299/CCND1 axis.	NA	Life Sci. 2021 Feb 1;266:118829. doi: 10.1016/j.lfs.2020.118829. Epub 2020 Nov 28.
4645	LncRNA	CYTOR	miR-1252-5p	FOXD1	oral squamous cell carcinoma tissues	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR	33352248	Forkhead box D1 promotes EMT and chemoresistance by upregulating lncRNA CYTOR in oral squamous cell carcinoma.	Chemotherapy regimens containing cisplatin remain the first-line treatments for patients with oral squamous cell cancer (OSCC); however, the treatment effect is often transient because of chemoresistance and recurrence. Understanding the mechanisms of chemoresistance in OSCC might provide novel targetable vulnerabilities. In the present study, we revealed that Forkhead box D1 (FOXD1) is upregulated in OSCC and predicted poor prognosis. Moreover, ectopic expression of FOXD1 promoted, while silencing of FOXD1 inhibited, the epithelial-mesenchymal transition (EMT) and chemoresistance of OSCC, both in vitro and in vivo. Mechanistically, FOXD1 binds to the promoter of long non-coding RNA Cytoskeleton Regulator RNA (CYTOR) and activates its transcription. CYTOR then acts as a competing endogenous RNA to inhibit miR-1252-5p and miR-3148, thus upregulating lipoma preferred partner (LPP) expression. Importantly, the CYTOR/LPP axis was proven to be essential for FOXD1-induced EMT and chemoresistance in OSCC. These findings reveal a novel mechanism for the chemotherapy resistance of OSCC, suggesting that FOXD1 might be a potential prognostic marker and anti-resistance therapeutic target.	NA	Cancer Lett. 2021 Apr 10;503:43-53. doi: 10.1016/j.canlet.2020.11.046. Epub 2020 Dec 19.
4646	LncRNA	DANCR	miR-214-5p	TGF-b	prostate carcinoma	Prostate Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;RNA pull-down;	34017385	miR-214-5p targeted by LncRNA DANCR mediates TGF-β signaling pathway to accelerate proliferation, migration and inhibit apoptosis of prostate cancer cells.	OBJECTIVE: This research was designed to probe into the regulatory mechanism of long non-coding RNA (LncRNA) differentiation antagonizing non-protein coding RNA (DANCR) in potential applications and molecular mechanisms of prostate carcinoma (PC). METHODS: The DANCR and miR-214-5p levels in PC tissues and cell lines were tested via real-time PCR, and those of transforming growth factor-β (TGF-β) signaling pathway related proteins were evaluated via Western Blot (WB). Cell proliferation, migration, apoptosis and the regulatory relationship between target genes were assessed via MTT method, scratch test, flow cytometry, dual-luciferase report, RNA co-immunoprecipitation and RNA pull-down test, respectively. RESULTS: DANCR was up-regulated in PC patients' serum and cell lines, while miR-214-5p was opposite, showing negative correlation. Besides, DANCR was significantly correlated with PSA, Gleason score and T stage in PC patients. The area under the curve (AUC) of DANCR and miR-214-5p for diagnosing PC was not less than 0.850, while the AUC for predicting poor prognosis was more than 0.800. Cox analysis results also revealed that the two might be prognostic indicators of PC patients. We found that DANCR high levels or miR-214-5p low levels were related to PC patients' poor prognosis. Up-regulating DANCR or down-regulating miR-214-5p could promote PC cells' malignant proliferation and migration, prevent apoptosis, and activate TGF-β signaling pathway, while reverse treatment of DANCR or miR-214-5p can reverse the above results. DANCR regulates miR-214-5p in a targeted manner, and DANCR over-expression can reduce the cancer inhibitory effect of miR-214-5p on PC cells. CONCLUSION: DANCR-miR-214-5p-TGF-β axis regulatory network plays a key regulatory part in PC progression. It may provide new strategies for the screening and treatment of patients.	NA	Am J Transl Res. 2021 Apr 15;13(4):2224-2240. eCollection 2021.
4647	LncRNA	DDX11-AS1	miR-499b-5p	RWDD4	glioma tissues and cells	Glioma	Homo sapiens (human)	qRT-PCR;luciferase assay;	33447057	LncRNA DDX11-AS1 Exerts Oncogenic Roles in Glioma Through Regulating miR-499b-5p/RWDD4 Axis.	BACKGROUND: Long noncoding RNAs (lncRNA) exert essential functions during tumorigenesis. However, how lncRNAs participate in glioma development remains poorly researched. This study aimed to determine how DDX11-AS1 affects glioma progression. METHODS: Gene expression was analyzed by qRT-PCR. Survival rate curve was plotted in 56 glioma patients. Loss-of-function assays were performed to analyze proliferation, migration, and invasion through CCK8, colony formation, and transwell assays. Luciferase assay and RNA pulldown assays were conducted to illustrate the underlying molecular mechanism. RESULTS: DDX11-AS1 expression was upregulated in glioma tissues and cells. DDX11-AS1 overexpression was linked with poor prognostic value. DDX11-AS1 knockdown suppressed proliferation, migration, and invasion while inducing apoptosis. DDX11-AS1 interacted with miR-499b-5p to eliminate it, leading to upregulation of RWDD4 expression. RWDD4 was upregulated in glioma while miR-499b-5p was downregulated. CONCLUSION: DDX11-AS1 upregulation promotes glioma progression through acting as a competing endogenous RNA for miR-499b-5p to upregulate RWDD4.	NA	Onco Targets Ther. 2021 Jan 8;14:157-164. doi: 10.2147/OTT.S278986. eCollection 2021.
4648	LncRNA	DGCR5	miR-3163	TOP2A	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	ChIP;	33613108	DGCR5 is activated by PAX5 and promotes pancreatic cancer via targeting miR-3163/TOP2A and activating Wnt/β-catenin pathway.	Long noncoding RNA DiGeorge syndrome critical region gene 5 (DGCR5) has been shown to be highly associated with cancer development. However, the biological role and molecular mechanism of DGCR5 in pancreatic cancer (PC) remains largely unknown. This study aimed to explore the role of DGCR5 in PC. It was revealed that DGCR5 was highly expressed in PC tissues compared with adjacent normal tissues and was associated with poor prognosis in PC patients. Furthermore, DGCR5 depletion inhibited the proliferation, migration and invasion by increasing apoptosis and inducing G0/G1 cell cycle arrest in vitro. Moreover, xenograft assay validated that DGCR5 promotes PC tumor growth in vivo. Mechanistically, DGCR5 was found to act as a ceRNA by sponging miR-3163 to regulate DNA topoisomerase 2-alpha (TOP2A) and inhibit Wnt/β-catenin pathway. In addition, it was found that DGCR5 downregulation could enhance the sensitivity of PC cells to gemcitabine, and ChIP assay showed that PAX5 (Paired Box 5) could bind to the promoter region of DGCR5 and increase its transcription. The results of the present study indicated that DGCR5 may be a potential diagnostic biomarker and therapeutic target for PC.	NA	Int J Biol Sci. 2021 Jan 1;17(2):498-513. doi: 10.7150/ijbs.55636. eCollection 2021.
4649	LncRNA	DHRS4-AS1	miR-224-3p	TP53	Non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33425890	LncRNA DHRS4-AS1 Inhibits the Stemness of NSCLC Cells by Sponging miR-224-3p and Upregulating TP53 and TET1.	Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death. This study aimed to examine the roles of DHRS4-AS1/miR-224-3p signaling in the cancer cell stemness of NSCLC. Real-time PCR showed that DHRS4-AS1 was downregulated in cancerous tissues, and bioinformatics analysis revealed that high DHRS4-AS1 expression indicated a good prognosis for NSCLC patients. Sphere and colony formation assays showed that DHRS4-AS1 overexpression significantly suppressed NSCLC cell colony formation and stem cell-like properties. DHRS4-AS1 also abrogated the expression of OCT4, SOX2, CD34, and CD133, markedly inhibited the expression of epithelial-mesenchymal transition (EMT)-related factors, N-cadherin, ZEB1, and Vimentin, and increased E-cadherin expression in spheres. Furthermore, luciferase reporter assays and real-time PCR analysis demonstrated that DHRS4-AS1 and miR-224-3p were antagonistically repressed in NSCLC cells. RNA immunoprecipitation (RIP) analysis revealed that DHRS4-AS1 interacted with miR-224-3p. DHRS4-AS1 partially reversed the miR-224-3p-decreased TP53 and TET1, resulting in the inhibition of tumor growth in vivo. Finally, TP53 and TET1 were antagonistically regulated by DHRS4-AS1 and miR-224-3p in NSCLC cells. In conclusion, TP53- and TET1-associated DHRS4-AS1/miR-224-3p axis is an essential mechanism by which NSCLC modulates cancer cell stemness.	NA	Front Cell Dev Biol. 2020 Dec 23;8:585251. doi: 10.3389/fcell.2020.585251. eCollection 2020.
4650	LncRNA	DHRS4-AS1	miR-224-3p	TET1	Non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33425890	LncRNA DHRS4-AS1 Inhibits the Stemness of NSCLC Cells by Sponging miR-224-3p and Upregulating TP53 and TET1.	Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death. This study aimed to examine the roles of DHRS4-AS1/miR-224-3p signaling in the cancer cell stemness of NSCLC. Real-time PCR showed that DHRS4-AS1 was downregulated in cancerous tissues, and bioinformatics analysis revealed that high DHRS4-AS1 expression indicated a good prognosis for NSCLC patients. Sphere and colony formation assays showed that DHRS4-AS1 overexpression significantly suppressed NSCLC cell colony formation and stem cell-like properties. DHRS4-AS1 also abrogated the expression of OCT4, SOX2, CD34, and CD133, markedly inhibited the expression of epithelial-mesenchymal transition (EMT)-related factors, N-cadherin, ZEB1, and Vimentin, and increased E-cadherin expression in spheres. Furthermore, luciferase reporter assays and real-time PCR analysis demonstrated that DHRS4-AS1 and miR-224-3p were antagonistically repressed in NSCLC cells. RNA immunoprecipitation (RIP) analysis revealed that DHRS4-AS1 interacted with miR-224-3p. DHRS4-AS1 partially reversed the miR-224-3p-decreased TP53 and TET1, resulting in the inhibition of tumor growth in vivo. Finally, TP53 and TET1 were antagonistically regulated by DHRS4-AS1 and miR-224-3p in NSCLC cells. In conclusion, TP53- and TET1-associated DHRS4-AS1/miR-224-3p axis is an essential mechanism by which NSCLC modulates cancer cell stemness.	NA	Front Cell Dev Biol. 2020 Dec 23;8:585251. doi: 10.3389/fcell.2020.585251. eCollection 2020.
4651	LncRNA	DLG1-AS1	miR-497-5p	SSRP1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Luciferase reporter assay;	33407499	DLG1-AS1 is activated by MYC and drives the proliferation and migration of hepatocellular carcinoma cells through miR-497-5p/SSRP1 axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to be biological regulators in hepatocellular carcinoma (HCC). DLG1 antisense RNA 1 (DLG1-AS1) has been found to be up-regulated in cervical cancer. However, its function and underlying mechanism in HCC remains unknown. METHODS: DLG1-AS1 expression was assessed in HCC cells and normal cell by RT-qPCR. Luciferase reporter assay, RNA pull down assay and RIP assay were used to demonstrate the interaction between DLG1-AS1 and miR-497-5p. RESULTS: DLG1-AS1 was highly expressed in HCC cells. Silencing of DLG1-AS1 led to the inhibition of HCC cell growth and migration. Besides, MYC induced the transcriptional activation of DLG1-AS1. MYC could facilitate HCC cellular processes by up-regulating DLG1-AS1. MiR-497-5p could interact with DLG1-AS1 in HCC cells. Down-regulation of miR-497-5p could reverse the impacts of DLG1-AS1 silencing on HCC cells. SSRP1 expression could be positively regulated by DLG1-AS1 but was negatively regulated by miR-497-5p. Knockdown of DLG1-AS1 suppressed tumor growth in nude mice. CONCLUSIONS: DLG1-AS1 is activated by MYC and functions as an oncogene in HCC via miR-497-5p/SSRP1 axis.	NA	Cancer Cell Int. 2021 Jan 6;21(1):16. doi: 10.1186/s12935-020-01667-0.
4652	LncRNA	DLGAP1-AS2	miR-505	GALNT10	Cholangiocarcinoma cells	Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR;RT-PCR;luciferase assay;	33301605	The long noncoding RNA DLGAP1-AS2 facilitates cholangiocarcinoma progression via miR-505 and GALNT10.	Cholangiocarcinoma (CCA) is a highly invasive malignant tumor with high mortality. Most cases of CCA are already advanced when they are detected, resulting in poor prognosis. As such, there is an ongoing need for the identification of effective biomarkers for CCA. The long noncoding RNA DLGAP1-AS2 has been reported to have prognostic value in glioma and Wilms' tumor. Here, we investigated the function of DLGAP1-AS2 in CCA. The differential expression of DLGAP1-AS2 in CCA tissues and normal tissues was first examined using data from the The Cancer Genome Atlas database and then in CCA cell lines by quantitative RT-PCR (qRT-PCR). The target gene was predicted by bioinformatics analysis, and the binding sites were confirmed using luciferase assay. DLGAP1-AS2 is up-regulated in CCA, and high DLGAP1-AS2 expression promotes cell viability and is associated with poor prognosis. Notably, DLGAP1-AS2 acts as a sponge to suppress miR-505 expression, and miR-505 reduces the expression of N-acetylgalactosaminyltransferase 10 (GALNT10) in CCA cells. Biofunctional experiments revealed that a miR-505 inhibitor almost completely removed the inhibitory effect of si-DLGAP1-AS2 on CCA cell malignant progression, whereas the malignant phenotype of cells cotransfected with si-DLGAP1-AS2 and si-GALNT10 was significantly reduced as compared with the control. In summary, the DLGAP1-AS2/miR-505/GALNT10 axis may contribute to regulating the malignant progression of CCA and may have potential as a novel target for CCA therapy.	NA	FEBS Open Bio. 2021 Feb;11(2):413-422. doi: 10.1002/2211-5463.13061. Epub 2020 Dec 31.
4653	LncRNA	DQ786243	miR-15b-5p	Wnt3A	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;luciferase assay;	33760109	lncRNA DQ786243 promotes hepatocellular carcinoma cell invasion and proliferation by regulating the miR-15p-5p/Wnt3A axis.	Increasing evidence suggests that long noncoding RNAs (lncRNAs) influence the pathogenesis and progression of hepatocellular carcinoma (HCC). The authors of the present study previously reported that abnormal upregulation of lncRNA DQ786243 (lncDQ) was associated with poor prognoses for patients with HCC. However, the elucidation of underlying mechanisms which influenced these results was not completed. Thus, the current study aimed to characterize the mechanisms and functions of lncDQ that facilitate its promotion of HCC progression. lncDQ, miR-15b-5p and Wnt3A expression levels were characterized in HCC and portal vein tumor thrombus tissue samples and for liver cancer and liver cancer cell lines using reverse transcription-quantitative PCR. Bioinformatics software was used for the analysis of interactions between lncDQ and miR-15b-5p, miR-15b-5p and Wnt3A. Luciferase assays confirmed the binding relationships between miR-15b-5p and the 3' untranslated region (UTR) of Wnt3A. Using online databases, prognostic values of miR-15b-5p and Wnt3A were also assessed. Proliferation and invasion assays were used to assess liver cancer and HCC cell functions after individually silencing lncDQ and miR-15b-5p expression in the cells. Western blotting was used for the investigation of alterations of the expression of Wnt3A/β-catenin and epithelial-mesenchymal transition (EMT) signal pathways. lncDQ and Wnt3A expression were significantly increased in HCC tissues, whereas miR-15b-5p was downregulated in HCC tissues. Low expression of miR-15b-5p was also associated with poor prognoses for patients with HCC. lncDQ was able to bind with miR-15b-5p and served as a competing endogenous RNA. As the target gene of miR-15b-5p, Wnt3A was correlated with poor prognoses for patients with HCC. Silencing of lncDQ expression significantly attenuated proliferation and invasion of liver cancer and HCC cells, however the inhibition of miR-15b-5p was able to reverse this effect. However, silencing of lncDQ and miR-15b-5p expression simultaneously resulted in the partial rescue of the inhibitory effect in the liver cancer and HCC cells. lncDQ inhibited miR-15b-5p so as to promote HCC cell invasion and proliferation through activation of the Wnt3A/β-catenin/EMT pathway. Taken together, the results of the present study suggested that the lncDQ/miR-15b-5p axis modulates the progression of HCC.	NA	Mol Med Rep. 2021 May;23(5):318. doi: 10.3892/mmr.2021.11957. Epub 2021 Mar 24.
4654	LncRNA	DRAIC	miR-18a-3p	H3K4me3	glioma cells	Gastric Cancer	Homo sapiens (human)	ChIP;qPCR;Luciferase reporter assay;	33336743	SET7/9 promotes H3K4me3 at lncRNA DRAIC promoter to modulate growth and metastasis of glioma.	OBJECTIVE: We aimed at investigating the expression levels of SET7/9 in glioma and the relationship between SET7/9 and LncRNA DRAIC. Further, we explored the relationship between SET7/9 and glioma cell metastasis and mood. PATIENTS AND METHODS: The expression levels of DRAIC and miR-18a-3p in gastric cancer cells were measured by quantitative polymerase chain reaction (qPCR). The binding site of the promoter of DRAIC by H3K4me3 was confirmed by ChIP-Real-time PCR. The direct target of DRAIC and miR-18a-3p in gastric cancer cells was measured by a Luciferase reporter assay. Cell proliferation was detected by Cell counting kit-8 (CCK8), and cell invasion and migration were measured by transwell assays. RESULTS: Compared with adjacent non-cancerous normal tissues, SET7/9 and DRAIC were both downregulated and miR-18a-3p was upregulated in glioma cells. Meanwhile, silencing of SET7/9 enhanced cell proliferation, migration, and invasion in U251 cells. H3K4me3 protein can bind to DRAIC promoter directly. Inhibition of SET7/9 and downregulation of DRAIC in U251 cells reversed the effect of SET7/9 silencing on the growth and metastasis of glioma cells. In U251 cells, SET7/9 and DRAIC overexpression inhibited cell proliferation, migration and invasion. In addition, miR-18a-3p interacts with DRAIC through direct binding. The inhibition of DRAIC promoted the growth and metastasis of U251 cells, while the co-transfection of si- DRAIC and miR-18a-3p further promoted the growth and metastasis of U251 cells. Overexpression of DRAIC inhibited the growth and metastasis of cells, completely reversing the co-transfection of Lnc-DRAIC and miR-18a-3p. CONCLUSIONS: In this research, we discovered that the expression of SET7/9 was low in glioma cells and SET7/9-mediated H3K4me3 enrichment on the DRAIC promoter regulated the growth and metastasis of glioma cells by targeting miR-18a-3p. It potentially provides a new therapeutic marker targeting glioma.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12241-12250. doi: 10.26355/eurrev_202012_24016.
4655	LncRNA	DUXAP8	miR-20b-5p	SOS1	Papillary thyroid carcinoma cells	Papillary Thyroid Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	33760128	lncRNA DUXAP8 inhibits papillary thyroid carcinoma cell apoptosis via sponging the miR-20b-5p/SOS1 axis.	Papillary thyroid carcinoma (PTC) is the most common type of cancer in the endocrine system. Long non-coding RNAs (lncRNAs) are associated with PTC progression. Therefore, the present study aimed to identify a novel lncRNA involved in PTC. Herein, dysregulated lncRNAs were analyzed in The Cancer Genome Atlas (TCGA)-thyroid cancer (THCA) data. Furthermore, the association between double homeobox A pseudogene 8 (DUXAP8) gene expression and disease stage, and prognosis of patients with PTC was evaluated using the GEPIA online database, while the correlation between DUXAP8 expression and the clinicopathological characteristics of patients with PTC was analyzed by Chi-square test. In addition, the biological effect of DUXAP8 expression on cell proliferation and apoptosis was also investigated. The protein and mRNA/microRNA (miRNA)/lncRNA expression levels were assessed by western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR), respectively. The interaction between miR-20b-5p and DUXAP8 was verified using bioinformatics analysis, RNA RIP assay, dual luciferase reporter assay, western blot analysis and RT-qPCR. The analysis of the TCGA-THCA data revealed that DUXAP8 was one of the most significantly upregulated lncRNAs in PTC. This finding was further confirmed in tissues from patients with PTC. Increased DUXAP8 expression was associated with higher grade and poorer prognosis in patients with PTC. In PTC cell lines, silencing of DUXAP8 expression with small interfering RNA-DUXAP8 (si-DUXAP8) induced cell apoptosis and attenuated cell proliferation. Additionally, transfection of PTC cells with si-DUXAP8 decreased the phosphorylation levels of MEK1/2 and ERK1/2, as well as downregulated the expression of son of sevenless 1 (SOS1), cyclin D1 (CCND1) and c-Myc. The results of the present study also revealed that miR-20b-5p could directly target DUXAP8. DUXAP8 expression was positively associated with that of SOS1, c-Myc and CCND1 in the TCGA-THCA data, and DUXAP8 level was positively correlated with that of SOS1 in PTC tumor tissues. Finally, transfection of PTC cells with the SOS1 overexpression plasmid, pcDNA3.1-SOS1, rescued the effects of si-DUXAP8 on cell proliferation and apoptosis. The present study was the first to identify DUXAP8 as a novel upregulated lncRNA in PTC, and provided new insights in understanding the effect of the lncRNA-miRNA-mRNA network in PTC.	NA	Oncol Rep. 2021 May;45(5):64. doi: 10.3892/or.2021.8015. Epub 2021 Mar 24.
4656	LncRNA	EGFR-AS1	miR-133b	EGFR	Colorectal cancer tissues	Colorectal Cancer	Homo sapiens (human)	ELISA;Immunohistochemistry;	33211633	Long non-coding RNA EGFR-AS1 in colorectal cancer: potential role in tumorigenesis and survival via miRNA-133b sponge and EGFR/STAT3 axis regulation.	BACKGROUND: Colorectal cancer is one of the most common cancers worldwide and a major cause of cancer-related death. Thus molecular biomarkers for colorectal cancer have been proposed. The role of long non-coding RNA EGFR-AS1 in colorectal cancer is still unclear. We aimed to evaluate its expression in different stages of colorectal cancer and determine any possible role in regulating the miR-133b/EGFR/STAT3 signalling pathway. MATERIALS AND METHODS: The relative expression of EGFR-AS1 and miR-133b were evaluated by quantitative real-time RT-transcription PCR in 130 colorectal cancer samples and 30 normal tissues. EGFR expression was assessed using immunohistochemistry. Furthermore, levels of p-EGFR, p-STAT3, and apoptotic proteins were determined by ELISA. RESULTS: Both EGFR-AS1 and EGFR overexpression were positively linked with colorectal cancer status (both p < 0.01), grade (both p < 0.01), and metastasis (P < 0.01 and p = 0.019 respectively). EGFR-AS1 and miR-133b were significantly inversely correlated (P < 0.01). Low expression of miR-133b was inversely associated with overexpressed EGFR and increased p-STAT3 levels. EGFR-AS1 was an independent prognostic factor for survival of colorectal cancer patients (P < 0.01, HR 2.06; 95% CI 1.32-3.19) where low EGFR-AS1 expression was associated with higher survival rate (p = 0.003). CONCLUSION: EGFR-AS1 may have a role in colorectal cancer by regulation of miR-133b/EGFR/STAT3 signalling. It may be a potential biomarker for early diagnosis and predicting the survival rate of colorectal cancer.	NA	Br J Biomed Sci. 2021 Jul;78(3):122-129. doi: 10.1080/09674845.2020.1853913. Epub 2021 Apr 14.
4657	LncRNA	EGFR-AS1	miR-133b	STAT3	Colorectal cancer tissues	Colorectal Cancer	Homo sapiens (human)	ELISA;Immunohistochemistry;	33211633	Long non-coding RNA EGFR-AS1 in colorectal cancer: potential role in tumorigenesis and survival via miRNA-133b sponge and EGFR/STAT3 axis regulation.	BACKGROUND: Colorectal cancer is one of the most common cancers worldwide and a major cause of cancer-related death. Thus molecular biomarkers for colorectal cancer have been proposed. The role of long non-coding RNA EGFR-AS1 in colorectal cancer is still unclear. We aimed to evaluate its expression in different stages of colorectal cancer and determine any possible role in regulating the miR-133b/EGFR/STAT3 signalling pathway. MATERIALS AND METHODS: The relative expression of EGFR-AS1 and miR-133b were evaluated by quantitative real-time RT-transcription PCR in 130 colorectal cancer samples and 30 normal tissues. EGFR expression was assessed using immunohistochemistry. Furthermore, levels of p-EGFR, p-STAT3, and apoptotic proteins were determined by ELISA. RESULTS: Both EGFR-AS1 and EGFR overexpression were positively linked with colorectal cancer status (both p < 0.01), grade (both p < 0.01), and metastasis (P < 0.01 and p = 0.019 respectively). EGFR-AS1 and miR-133b were significantly inversely correlated (P < 0.01). Low expression of miR-133b was inversely associated with overexpressed EGFR and increased p-STAT3 levels. EGFR-AS1 was an independent prognostic factor for survival of colorectal cancer patients (P < 0.01, HR 2.06; 95% CI 1.32-3.19) where low EGFR-AS1 expression was associated with higher survival rate (p = 0.003). CONCLUSION: EGFR-AS1 may have a role in colorectal cancer by regulation of miR-133b/EGFR/STAT3 signalling. It may be a potential biomarker for early diagnosis and predicting the survival rate of colorectal cancer.	NA	Br J Biomed Sci. 2021 Jul;78(3):122-129. doi: 10.1080/09674845.2020.1853913. Epub 2021 Apr 14.
4658	LncRNA	ELFN1-AS1	miR-4270	SBK1	retinoblastoma tissues and cells	Retinoblastoma	Homo sapiens (human)	qRT-PCR;	33574704	LncRNA ELFN1-AS1 Promotes Retinoblastoma Growth and Invasion via Regulating miR-4270/SBK1 Axis.	BACKGROUND: Long noncoding RNA (lncRNA) has been reported to play important roles in tumor initiation. However, how lncRNA ELFN1-AS1 affects retinoblastoma development remains unclear. Thus, we sought to elucidate its functions in retinoblastoma progression. METHODS: ELFN1-AS1 expression was measured in retinoblastoma tissues and normal tissues by qRT-PCR. CCK8, colony formation and Transwell assay were carried out to investigate the effects of ELFN1-AS1 knockdown on cell malignant behaviors. Bioinformatics analyses were performed to predict the relationship among ELFN1-AS1, miR-4270 and SBK1. RESULTS: ELFN1-AS1 was highly expressed in retinoblastoma tissues and cell lines. ELFN1-AS1 was positively correlated with retinoblastoma progression and prognosis. ELFN1-AS1 knockdown curtailed retinoblastoma proliferation, migration and invasion. ELFN1-AS1 was the competing endogenous RNA for miR-4270 and promoted SBK1expression. CONCLUSION: Altogether, our findings demonstrated that ELFN1-AS1 promotes retinoblastoma progression through mediating miR-4270/SBK1 axis and might be a promising therapeutic target.	NA	Cancer Manag Res. 2021 Feb 5;13:1067-1073. doi: 10.2147/CMAR.S281536. eCollection 2021.
4659	LncRNA	ENST00000609755.1	miR-150	ELK1	coronary heart tissues	Coronary Heart Disease	Homo sapiens (human)	microarray;qRT-PCR;	33279591	Preliminary verification of lncRNA ENST00000609755.1 potential ceRNA regulatory network in coronary heart disease.	BACKGROUND: This study aims to explore the possible ceRNA regulatory network of lncRNA ENST00000609755.1 in CHD patients based on the population; reveal the possible regulatory mechanism of lncRNA ENST00000609755.1. METHOD: Microarray analysis were used to identify differentially expressed miRNA, and mRNA profiles between 5 CHD and 5 healthy controls. The lncRNA ENST00000609755.1-miRNA-mRNA ceRNA regulatory network was constructed with lncRNA ENST00000609755.1 as the core based on microarray data and related prediction software (RNAhybird, miRanda, miRWalk 2.0). Furthermore, qRT-PCR was used to verify the expression levels of miRNA and mRNA. t-test and pearson correlation analysis were used to compare the expression differences and correlations of lncRNA, miRNA and mRNA. The receiver operating characteristic (ROC) curve was used to determine the discriminative ability of lncRNA ENST00000609755.1 and its downstream targets. RESULTS: Totally 25 miRNAs and 953 mRNAs were differentially expressed between CHD and healthy control. The lncRNA ENST00000609755.1- miRNA- mRNA ceRNA regulatory network was constructed (5 miRNA and 58 mRNA). qRT-PCR results suggest that the expression of lncRNA ENST00000609755.1 and ELK1 were up-regulated in CHD group and positively correlated, the expression of miR-150 was down-regulated in CHD, which was negatively correlated with lncRNA ENST00000609755.1 and ELK1. The AUC was 0.777(95%CI, 0.659-0.895) when miRNA-150 and ELK1 was added, which was higher than that of lncRNA ENST00000609755.1 single indicator. CONCLUSION: LncRNA ENST00000609755.1, miR-150 and ELK1 may have a potential ceRNA regulatory network relationship which could be considered to have a good combined diagnostic value for CHD. Also, preliminarily reveal the possible mechanism of lncRNA ENST00000609755.1 involved in CHD.	NA	Int J Cardiol. 2021 Apr 1;328:165-175. doi: 10.1016/j.ijcard.2020.11.064. Epub 2020 Dec 3.
4660	LncRNA	FAM225A	miR-130a-5p	CCNG1	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33245102	FAM225A promotes sorafenib resistance in hepatocarcinoma cells through modulating miR-130a-5p-CCNG1 interaction network.	Chemotherapy resistance is still a key hurdle in current hepatocellular carcinoma (HCC) treatment. Therefore, clarifying the molecular mechanisms contributing to this acquired resistance is urgent for the effective treatment of liver cancer. In this research, we observed that lncRNA FAM225A expression is dramatically upregulated not only in hepatocellular carcinoma tissues and cell lines but also in sorafenib-resistant HepG2/SOR cells. Moreover, FAM225A knockdown significantly weakened HepG2/SOR cells resistance to sorafenib treatment by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. Similar results were obtained from the tumor xenograft model in mice. Further mechanistic researches revealed that the direct interaction between FAM225A and miR-130a-5p, while miR-130a-5p negatively modulated CCNG1 expression by targeting 3'UTR of CCNG1. MiR-130a-5p inhibition or CCNG1 overexpression could partially offset FAM225A knockdown-induced increased viability of HepG2/SOR cells in response to sorafenib challenge. Collectively, our findings provide evidence that FAM225A/miR-130a-5p/CCNG1 interaction network regulates the resistance of HCC cells to sorafenib treatment and could supply a possible strategy for restoring sorafenib sensitivity in HCC therapy.	NA	Biosci Rep. 2020 Nov 27;40(12):BSR20202054. doi: 10.1042/BSR20202054.
4661	LncRNA	FAM83A-AS1	miR-214	CDC25B	esophageal cell squamous carcinoma cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;Cell cycle assay;Rescue assay;	33442418	LncRNA FAM83A-AS1 promotes ESCC progression by regulating miR-214/CDC25B axis.	Background: Recent researches have pinpointed that long non-coding RNA (lncRNA) was tightly related to the carcinogenesis. However, the function of lncRNA in esophageal cell squamous carcinoma (ESCC) remains to be explored. In the current study, we assessed the expression pattern and the biological function of FAM83A-AS1 in ESCC. Methods: qRT-PCR was used to detect the expression of FAM83A-AS1, miR-214, and CDC25B expression in ESCC tissues and cell lines. CCK-8, transwell, apoptosis and cell cycle assays were performed to define the function of FAM83A-AS1 in ESCC cells. Furthermore, the regulation of miR-214 by FAM83A-AS1 was defined by qRT- PCR and rescue assays. In addition, the association between CDC25B, miR-214, CDC25B was confirmed by qRT-PCR. Results: Here, we discovered that FAM83A-AS1 was strongly expressed in ESCC tissues. FAM83A-AS1 abundance was associated with TNM stages and the differentiation grade of ESCC patients. The receiver operating characteristic curve (ROC) analysis indicated the high accuracy of FAM83A-AS1 in ESCC diagnosis. Functionally, inhibiting FAM83A-AS1 repressed cell proliferation, migration, and invasion in ESCC. In addition, we found that FAM83A-AS1 accelerated the cell cycle while inhibited cell apoptosis. Mechanistically, we found that FAM83A-AS1 regulated miR-214 expression, and there was a negative correlation between miR-214 and FAM83A-AS1 in ESCC. Rescue assay indicated that miR-214 could impair the suppressing effect of cell migration induced by FAM83A-AS1 depletion. Furthermore, CDC25B was a direct target of miR-214, and FAM83A-AS1 enhanced CDC25B expression while miR-214 positively CDC25B expression in ESCC. Conclusions: Collectively, we concluded that FAM83A-AS1 facilitated ESCC progression by regulating the miR-214/CDC25B axis. Our study showed FAM83A-AS1 may act as a promising target for ESCC diagnosis and therapy.	NA	J Cancer. 2021 Jan 1;12(4):1200-1211. doi: 10.7150/jca.54007. eCollection 2021.
4662	LncRNA	FAM83H-AS1	miR-22-3p	NA	nucleus pulposus cells	Intervertebral Disc Degeneration	Homo sapiens (human)	qRT-PCR	33313263	LncRNA FAM83H-AS1 maintains intervertebral disc tissue homeostasis and attenuates inflammation-related pain via promoting nucleus pulposus cell growth through miR-22-3p inhibition.	BACKGROUND: Intervertebral disc degeneration (IVDD) is regarded as the leading cause of low back pain, resulting in disability and a heavy burden on public health. Several studies have unveiled that long noncoding RNAs (lncRNAs) play a key role in the pathogenesis and progression of IVDD. In this study, we aimed to investigate the biological function and latent molecular mechanism of the lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) in IVDD development. METHODS: Firstly, we established an IVDD model in rats using advanced glycation end products (AGEs) intradiscal injection. Subsequently, gain-of-function assays were conducted to investigate the role of FAM83H-AS1 in the progression of IVDD. Bioinformatics analysis, RNA pull down assay and rescue experiments were employed to shed light on the molecular mechanism underlying FAM83H-AS1 involving in IVDD. RESULTS: Our findings verified that AGEs treatment aggravated IVDD damage, and FAM83H-AS1 was downregulated in the IVDD group. Additionally, overexpression of FAM83H-AS1 contributed to the growth of nucleus pulposus (NP) cells and ameliorated IVDD injury. It was revealed that FAM83H-AS1 possessed the speculated binding sites of miR-22-3p. More importantly, we confirmed that FAM83H-AS1 functioned as a sponge of miR-22-3p in IVDD. Lastly, we demonstrated that miR-22-3p mediated the impact of FAM83H-AS1 on cell proliferation, ECM degradation, and inflammation. CONCLUSIONS: Our study indicated that FAM83H-AS1 relieved IVDD deterioration through sponging miR-22-3p, and provides novel insights into the mechanisms underlying FAM83H-AS1 in IVDD progression.	NA	Ann Transl Med. 2020 Nov;8(22):1518. doi: 10.21037/atm-20-7056.
4663	LncRNA	FAM83H-AS1	miR-15a	CCNE2	Prostate cancer cells	Prostate Cancer	Homo sapiens (human)	qRT-PCR	33614501	A Novel Androgen-Induced lncRNA FAM83H-AS1 Promotes Prostate Cancer Progression via the miR-15a/CCNE2 Axis.	Prostate cancer (PCa) is one of the most common types of tumors among males worldwide. However, the roles of long noncoding RNAs (lncRNAs) in PCa remain unclear. This study shows that lncRNA FAM83H-AS1 is upregulated in prostate adenocarcinoma, bladder urothelial carcinoma, and kidney renal papillary cell carcinoma samples. Androgen receptor (AR) signaling plays the most important role in PCa tumorigenesis and development. In this study, the results validate that AR signaling is involved in upregulating FAM83H-AS1 expression in PCa cells. Loss-of-function assays demonstrate that FAM83H-AS1 acts as an oncogene in PCa by modulating cell proliferation, cell cycle, and migration. Bioinformatics analysis demonstrates that FAM83H-AS1 is remarkably related to the regulation of the cell cycle and DNA replication through affecting multiple regulators related to these pathways, such as CCNE2. Mechanically, we found that FAM83H-AS1 plays its roles through sponging miR-15a to promote CCNE2 expression. These findings indicate that FAM83H-AS1 is a novel diagnostic and therapeutic marker for PCa.	NA	Front Oncol. 2021 Feb 4;10:620306. doi: 10.3389/fonc.2020.620306. eCollection 2020.
4664	LncRNA	FENDRR	miR-424-5p	NA	Colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33356998	FENDRR Sponges miR-424-5p to Inhibit Cell Proliferation, Migration and Invasion in Colorectal Cancer.	OBJECTIVE: LncRNAs are non-coding RNAs exerting vital roles in the occurrence and development of various cancer types. This study tended to describe the expression pattern of FENDRR in colorectal cancer (CRC), and further investigate the role of FENDRR in CRC cell biological behaviors. METHODS: Gene expression profile of colon cancer was accessed from the TCGA database, and then processed for differential analysis for identification of differentially expressed lncRNAs and miRNAs. Some in vitro experiments like qRT-PCR, MTT, colony formation assay, wound healing assay and Transwell assay were performed to assess the effect of FENDRR on cell biological behaviors. Dual-luciferase reporter assay was conducted to further validate the targeting relationship between FENDRR and miR-424-5p, and rescue experiments were carried out for determining the mechanism of FENDRR/miR-424-5p underlying the proliferation, migration and invasion of CRC cells. RESULTS: Bioinformatics analysis suggested that FENDRR was significantly down-regulated in CRC tissue, and low FENDRR was intimately correlated to poor prognosis. FENDRR overexpression could greatly inhibit cell proliferation, migration and invasion. Besides, there was a negative correlation between FENDRR and miR-424-5p. Dual-luciferase reporter assay indicated that miR-424-5p was a direct target of FENDRR. Rescue experiments discovered that FENDRR exerted its role in cell proliferation, migration and invasion in CRC via targeting miR-424-5p. CONCLUSION: FENDRR is poorly expressed in CRC tissue and cells, and low FENDRR is responsible for the inhibition of cell proliferation, migration and invasion of CRC by means of targeting miR-424-5p.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820980102. doi: 10.1177/1533033820980102.
4665	LncRNA	FEZF1-AS1	miR-363-3p	PAX6	retinoblastoma tissues and cells	Retinoblastoma	Homo sapiens (human)	qRT-PCR	33432525	Long Non-coding RNA FEZF1-AS1 Promotes Growth and Reduces Apoptosis Through Regulation of miR-363-3p/PAX6 Axis in Retinoblastoma.	Retinoblastoma is the most common malignancy in children's eyes with high incidence. Long non-coding RNAs (lncRNAs) play important roles in the progression of retinoblastoma. LncRNA FEZF1 antisense RNA 1 (FEZF1-AS1) has been found to stimulate retinoblastoma. However, the mechanism of FEZF1-AS1 underlying progression of retinoblastoma is still unclear. In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells. FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. In conclusion, FEZF1-AS1 elevated growth and inhibited apoptosis by regulating miR-363-3p/PAX6 in retinoblastoma, which provide a new target for retinoblastoma treatment.	NA	Biochem Genet. 2021 Jun;59(3):637-651. doi: 10.1007/s10528-020-10026-7. Epub 2021 Jan 11.
4666	LncRNA	Ftx	miR-382-5p	Nrg1	microglial cells	Spinal Cord Injury	Homo sapiens (human)	qRT-PCR	33359189	The lncRNA Ftx/miR-382-5p/Nrg1 axis improves the inflammation response of microglia and spinal cord injury repair.	During spinal cord injury (SCI), a quick and sustained decline of Neuregulin-1 (Nrg1) has been observed, exerting a significant positive effect in modulating the proliferation of astrocytes and the formation of glial scars within the damaged spinal cord. In this study, we revealed the abnormal downregulation of lncRNA Ftx and Nrg1 and upregulation of miR-382-5p after SCI, which contributed to the inflammatory response in microglial cells and affected SCI repair. Ftx overexpression was significantly reduced, and Ftx knockdown further promoted LPS effects on the inflammatory factors, indicating that lncRNA Ftx might affect the microglial inflammatory response. miR-382-5p targeted both lncRNA Ftx and Nrg1, and lncRNA Ftx competed with Nrg1 for miR-382-5p binding to act as a ceRNA, therefore counteracting miR-382-5p-mediated inhibition of Nrg1. miR-382-5p overexpression was significantly enhanced, and Nrg1 overexpression attenuated LPS effects on inflammatory factors within the microglia. Under LPS stimulation, the effects of Ftx overexpression were significantly reversed by overexpression of miR-382-5p, and the effects of miR-382-5p overexpression were significantly reversed by Nrg1 overexpression. In summary, the lncRNA Ftx/miR-382-5p/Nrg1 axis improves the inflammation response of the microglia, which might improve SCI repair.	NA	Neurochem Int. 2021 Feb;143:104929. doi: 10.1016/j.neuint.2020.104929. Epub 2020 Dec 23.
4667	LncRNA	FUT8-AS1	miR-145-5p	NRAS	melanoma cells	Melanoma	Homo sapiens (human)	Rescue assay;	34094894	FUT8-AS1 Inhibits the Malignancy of Melanoma Through Promoting miR-145-5p Biogenesis and Suppressing NRAS/MAPK Signaling.	Melanoma is the major lethal skin malignancy. However, the critical molecular drivers governing melanoma progression and prognosis are still not clear. By analyzing The Cancer Genome Atlas (TCGA) data, we identified FUT8-AS1 as a prognosis-related long non-coding RNA (lncRNA) in melanoma. We further confirmed that FUT8-AS1 is downregulated in melanoma. Reduced expression of FUT8-AS1 is correlated with aggressive clinical factors and inferior overall survival. Using in vitro functional assays, our findings demonstrated that ectopic expression of FUT8-AS1 represses melanoma cell proliferation, migration, and invasion. FUT8-AS1 silencing promotes melanoma cell proliferation, migration, and invasion. Furthermore, in vivo functional assays demonstrated that FUT8-AS1 represses melanoma growth and metastasis. Mechanistically, FUT8-AS1 was found to bind NF90, repress the interaction between NF90 and primary miR-145 (pri-miR-145), relieve the repressive roles of NF90 on mature miR-145-5p biogenesis, and thus promote miR-145-5p biogenesis and upregulate mature miR-145-5p level. The expression of FUT8-AS1 is positively correlated with miR-145-5p in melanoma tissues. Via upregulating miR-145-5p, FUT8-AS1 reduces the expression of NRAS, a target of miR-145-5. FUT8-AS1 further represses MAPK signaling via downregulating NRAS. Functional rescue assays demonstrated that inhibition of miR-145-5p reverses the tumor suppressive roles of FUT8-AS1 in melanoma. The oncogenic roles of FUT8-AS1 silencing are also blocked by MAPK signaling inhibitor MEK162. In conclusion, these findings demonstrate that FUT8-AS1 exerts tumor suppressive roles in melanoma via regulating NF90/miR-145-5p/NRAS/MAPK signaling axis. Targeting FUT8-AS1 and its downstream molecular signaling axis represent promising therapeutic strategies for melanoma.	NA	Front Oncol. 2021 May 19;10:586085. doi: 10.3389/fonc.2020.586085. eCollection 2020.
4668	LncRNA	FUT8-AS1	miR-145-5p	MAPK	melanoma cells	Melanoma	Homo sapiens (human)	Rescue assay;	34094894	FUT8-AS1 Inhibits the Malignancy of Melanoma Through Promoting miR-145-5p Biogenesis and Suppressing NRAS/MAPK Signaling.	Melanoma is the major lethal skin malignancy. However, the critical molecular drivers governing melanoma progression and prognosis are still not clear. By analyzing The Cancer Genome Atlas (TCGA) data, we identified FUT8-AS1 as a prognosis-related long non-coding RNA (lncRNA) in melanoma. We further confirmed that FUT8-AS1 is downregulated in melanoma. Reduced expression of FUT8-AS1 is correlated with aggressive clinical factors and inferior overall survival. Using in vitro functional assays, our findings demonstrated that ectopic expression of FUT8-AS1 represses melanoma cell proliferation, migration, and invasion. FUT8-AS1 silencing promotes melanoma cell proliferation, migration, and invasion. Furthermore, in vivo functional assays demonstrated that FUT8-AS1 represses melanoma growth and metastasis. Mechanistically, FUT8-AS1 was found to bind NF90, repress the interaction between NF90 and primary miR-145 (pri-miR-145), relieve the repressive roles of NF90 on mature miR-145-5p biogenesis, and thus promote miR-145-5p biogenesis and upregulate mature miR-145-5p level. The expression of FUT8-AS1 is positively correlated with miR-145-5p in melanoma tissues. Via upregulating miR-145-5p, FUT8-AS1 reduces the expression of NRAS, a target of miR-145-5. FUT8-AS1 further represses MAPK signaling via downregulating NRAS. Functional rescue assays demonstrated that inhibition of miR-145-5p reverses the tumor suppressive roles of FUT8-AS1 in melanoma. The oncogenic roles of FUT8-AS1 silencing are also blocked by MAPK signaling inhibitor MEK162. In conclusion, these findings demonstrate that FUT8-AS1 exerts tumor suppressive roles in melanoma via regulating NF90/miR-145-5p/NRAS/MAPK signaling axis. Targeting FUT8-AS1 and its downstream molecular signaling axis represent promising therapeutic strategies for melanoma.	NA	Front Oncol. 2021 May 19;10:586085. doi: 10.3389/fonc.2020.586085. eCollection 2020.
4669	LncRNA	GAN1	miR-26a-5p	PTEN	non-small cell lung cancer	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;microarray;qRT-PCR;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33407724	Lnc-GAN1 expression is associated with good survival and suppresses tumor progression by sponging mir-26a-5p to activate PTEN signaling in non-small cell lung cancer.	BACKGROUND: Long non-coding RNAs (lncRNAs) play vital roles in the development and progression of non-small-cell lung cancer (NSCLC); however, the role of most lncRNAs in NSCLC remains unknown. This study explored the clinical significance, biological function and underlying mechanism of lnc-GAN1 in NSCLC. METHODS: With a custom lncRNA microarray we found that lnc-GAN1 is markedly downregulated in NSCLC tissues. Then lnc-GAN1 expression level was measured using qRT-PCR in NSCLC tissues and cell lines. Survival was assessed using the Kaplan-Meier method. The biological functions of lnc-GAN1 in lung cancer cells were evaluated in vitro and in vivo. RNA fluorescence in situ hybridization and subcellular localization assays revealed the subcellular distribution of lnc-GAN1 in cells. Bioinformatic analysis was adopted to predict miRNAs and signaling pathways regulated by lnc-GAN1. RNA immunoprecipitation and Dual-luciferase reporter assays were used to assess the interaction between lnc-GAN1 and miR-26a-5p in lung cancer cells. RESULTS: lnc-GAN1 is downregulated in HCC tissues and associated with larger tumor size and poor overall survival and disease-free survival; its ectopic expression suppresses cell proliferation, colony formation, and cell cycle progression and induces apoptosis in NSCLC cells; it also inhibits tumor growth in the NSCLC xenograft model. We further proved that lnc-GAN1 is localized in cytoplasm and transcribed independently from its parental gene GAN. Mechanistically, lnc-GAN1 acts as a sponge for miR-26a-5p by two seed sequences, and the two non-coding RNAs have a negative relationship in NSCLC tissues; we further prove that PTEN is a direct target of miR-26a-5p and lnc-GAN1 inhibits cell cycle signaling pathway by activating PTEN, whose expression level correlated negatively with miR-26a-5p level but positively with lnc-GAN1 level in NSCLC samples. CONCLUSIONS: Lnc-GAN1 is downregulated and associated with poor survival of NSCLC patients, and mechanistically acts as a tumor suppressor via sponging and inhibiting miR-26a-5p to upregulate PTEN. This study provides a potential prognostic biomarker and treatment target for NSCLC.	NA	J Exp Clin Cancer Res. 2021 Jan 6;40(1):9. doi: 10.1186/s13046-020-01819-0.
4670	LncRNA	GAS5	miR-140-5p	Th1	HTR-8/SVneo cells	Recurrent Pregnancy Loss	Homo sapiens (human)	luciferase assay;	33511769	LncRNA-GAS5 related to the processes of recurrent pregnancy loss by regulating Th1/Th2 balance.	Recurrent pregnancy loss (RPL) is defined as three or more consecutive spontaneous loss of pregnancy and the reason of 50% RPL is unknown. GAS5 is a long non-coding RNA, which has been found to be an immune responses regulator and to be relate to autoimmune diseases. However, the roles of GAS5 during the pathophysiological processes of RPL is unclear. In the present study, the levels of GAS5 were examined in the plasma and trophoblasts from 30 patients with RPL and 15 healthy controls. GAS5 was found overexpressed in patients with RPL and positively correlated with the protein levels of TNF-α in the plasma and trophoblasts. Predicted by bioinformatics tools and confirmed by luciferase assay, GAS5 was identified to function as a competing endogenous RNA (ceRNA) binding with miR-140-5p and protects TNF-α expression in HTR-8/SVneo cells and primary trophoblasts. Activated Naïve T cells co-cultured with the medium from GAS5 overexpression HTR-8/SVneo cells or primary trophoblasts exhibited Th1 bias by expression more IFN-γ, TNF-α and less IL-4, IL-10. In conclusion, GAS5 was overexpressed in the plasma and trophoblasts from RPL patients, which contributes to Th1 bias by binding with miR-140-5p.	NA	Kaohsiung J Med Sci. 2021 Jun;37(6):479-486. doi: 10.1002/kjm2.12360. Epub 2021 Jan 28.
4671	LncRNA	GAS5	miR-140-5p	Th2	HTR-8/SVneo cells	Recurrent Pregnancy Loss	Homo sapiens (human)	luciferase assay;	33511769	LncRNA-GAS5 related to the processes of recurrent pregnancy loss by regulating Th1/Th2 balance.	Recurrent pregnancy loss (RPL) is defined as three or more consecutive spontaneous loss of pregnancy and the reason of 50% RPL is unknown. GAS5 is a long non-coding RNA, which has been found to be an immune responses regulator and to be relate to autoimmune diseases. However, the roles of GAS5 during the pathophysiological processes of RPL is unclear. In the present study, the levels of GAS5 were examined in the plasma and trophoblasts from 30 patients with RPL and 15 healthy controls. GAS5 was found overexpressed in patients with RPL and positively correlated with the protein levels of TNF-α in the plasma and trophoblasts. Predicted by bioinformatics tools and confirmed by luciferase assay, GAS5 was identified to function as a competing endogenous RNA (ceRNA) binding with miR-140-5p and protects TNF-α expression in HTR-8/SVneo cells and primary trophoblasts. Activated Naïve T cells co-cultured with the medium from GAS5 overexpression HTR-8/SVneo cells or primary trophoblasts exhibited Th1 bias by expression more IFN-γ, TNF-α and less IL-4, IL-10. In conclusion, GAS5 was overexpressed in the plasma and trophoblasts from RPL patients, which contributes to Th1 bias by binding with miR-140-5p.	NA	Kaohsiung J Med Sci. 2021 Jun;37(6):479-486. doi: 10.1002/kjm2.12360. Epub 2021 Jan 28.
4672	LncRNA	GAS5	miR-26a	EGR1	hippocampal tissues	Depression	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33341564	Downregulation of lncRNA GAS5 Alleviates Hippocampal Neuronal Damage in Mice with Depression-Like Behaviors Via Modulation of MicroRNA-26a/EGR1 Axis.	BACKGROUND: Accumulating evidences have demonstrated the roles of several long non-coding RNAs (lncRNAs) in depression. We aim to examine the capabilities of lncRNA growth arrest-specific transcript 5 (GAS5) on mice with depression-like behaviors and the mechanism of action. METHODS: Fifty-six healthy mice were selected for model establishment. Morris water maze test and trapeze test were performed for evaluating learning and memory ability. The binding relationship between lncRNA GAS5 and microRNA-26a (miR-26a) and the target relationship between miR-26a and EGR1 were verified by dual-luciferase reporter gene assay. The apoptosis of neurons in the hippocampal CA1 region of mice was detected by TUNEL staining. The expression of inflammatory factors, lncRNA GAS5, miR-26a, early growth response gene 1 (EGR1), phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway- and apoptosis-related factors in hippocampal tissues was tested by RT-qPCR and western blot analysis. RESULTS: miR-26a expression was down-regulated while EGR1 and lncRNA GAS5 expression were up-regulated in hippocampal tissues of mice with depression-like behaviors. LncRNA GAS5 specifically bound to miR-26a and miR-26a targeted EGR1. Silencing of lncRNA GAS5 curtailed the release of inflammatory factors and the apoptosis of hippocampal neuron of mice with depression-like behaviors. EGR1 suppressed PI3K/AKT pathway activation to promote the release of inflammatory factors and the apoptosis of hippocampal neurons in mice with depression-like behaviors. CONCLUSION: Our study provides evidence that silencing of lncRNA GAS5 could activate PI3K/AKT pathway to protect hippocampal neurons against damage in mice with depression-like behaviors by regulating the miR-26a/EGR1 axis.	NA	J Stroke Cerebrovasc Dis. 2021 Mar;30(3):105550. doi: 10.1016/j.jstrokecerebrovasdis.2020.105550. Epub 2020 Dec 18.
4673	LncRNA	GAS5	miR-452-5p	CELF2	spinal cord homogenates	Neuropathic Pain	Homo sapiens (human)	ELISA;Rescue assay;	33264082	Long noncoding RNA GAS5 ameliorates chronic constriction injury induced neuropathic pain in rats by modulation of the miR-452-5p/CELF2 axis.	Neuropathic pain is a type of spontaneous pain that causes damage to the central nervous system. Long noncoding RNAs (lncRNAs) participate in the progression of various nervous system diseases, including neuropathic pain. However, the biological function of GAS5 in neuropathic pain remains unclear. Our findings revealed that GAS5 was downregulated in chronic constriction injury (CCI) rats. Besides, ELISA showed that the concentration of IL-6, TNF-α, and IL-1β were reduced by overexpressed GAS5 in spinal cord homogenates of CCI rats. Moreover, mechanical allodynia and thermal hyperalgesia in CCI rats were inhibited by GAS5 overexpression, suggesting that GAS5 overexpression attenuated neuropathic pain. Subsequently, we found that GAS5 served as a sponge for miR-452-5p in CCI rats and CELF2 was the downstream target of miR-452-5p. Finally, through a rescue assay, we found that GAS5 ameliorated neuropathic pain in CCI rats by sponging miR-452-5p to regulate CELF2 expression. Our study confirmed that GAS5 ameliorated neuropathic pain in rats by modulation of the miR-452-5p/CELF2 axis, which may provide some clues for neuropathic pain treatment.	NA	Can J Physiol Pharmacol. 2020 Dec;98(12):870-877. doi: 10.1139/cjpp-2020-0036. Epub 2020 Dec 2.
4674	LncRNA	GAS5	miR-221-3p	CDKN2B	Follicular thyroid carcinoma cells	Follicular Thyroid Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34130294	Long Noncoding RNA GAS5 Targeting miR-221-3p/Cyclin-Dependent Kinase Inhibitor 2B Axis Regulates Follicular Thyroid Carcinoma Cell Cycle and Proliferation.	INTRODUCTION: Follicular thyroid carcinoma (FTC) is more aggressive than the most common papillary thyroid carcinoma (PTC). However, the current research on FTC is less than PTC. Here, we investigated the effects of long noncoding RNA (lncRNA) GAS5 and miR-221-3p in FTC. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect GAS5 and miR-221-3p expression in the FTC tissues and cells. Cell proliferation was assessed by CCK8 and EdU assays. Flow cytometry was performed to determine the cell cycle. The dual-luciferase reporter assay was employed to validate the binding relationship of GAS5/miR-221-3p and miR-221-3p/cyclin-dependent kinase inhibitor 2B (CDKN2B). Western blot was conducted to measure the protein level of CDKN2B. RESULTS: Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells. What's more, overexpression of GAS5 or miR-221-3p inhibition induced G0/G1 phase arrest and inhibited cell proliferation of FTC cells. GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p. Additionally, GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression. CONCLUSION: GAS5 induced G0/G1 phase arrest and inhibited cell proliferation via targeting miR-221-3p/CDKN2B axis in FTC. Thus, GAS5 may be a potential therapeutic target for the treatment of FTC.	NA	Pathobiology. 2021 Jun 15:1-12. doi: 10.1159/000513338.
4675	LncRNA	GAS5	miR-222-3p	Sirt1	Rheumatoid arthritis tissues	Rheumatoid Arthritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33215529	LncRNA GAS5 alleviates rheumatoid arthritis through regulating miR-222-3p/Sirt1 signalling axis.	INTRODUCTION: Rheumatoid arthritis (RA) is an autoimmune disease that affects millions of people. Fibroblast-like synoviocytes (FLSs) located in rheumatoid panni play a pivotal role in the formation of RA. The long noncoding RNA (lncRNA) GAS5 is reportedly downregulated in rheumatoid arthritis. However, its detailed mechanism in RA remains to be explored. This study investigated the roles and related mechanisms of GAS5 in RA. METHODS: The expression levels of GAS5, miR-222-3p, and sirtuin 1 (Sirt1) were evaluated by quantitative PCR (qPCR). Cell proliferation was analyzed by CCK-8 and BrdU assays. Cell apoptosis was assessed by flow cytometry and western blotting. Enzyme-linked immunosorbent assay (ELISA) was utilized to evaluate the levels of TNF-α, IL-1β, and IL-6. The interaction between GAS5 or Sirt1 and miR-222-3p was predicted by starBase and validated by dual-luciferase reporter assay. RESULTS: GAS5 expression was found to be downregulated in the serum samples of RA patients and in RA-FLSs. GAS5 overexpression or the inhibition of miR-222-3p impeded the activity of RA-FLSs by repressing their proliferation and inflammation and by promoting apoptosis. Mechanistically, GAS5 indirectly regulates Sirt1 expression by binding miR-222-3p. Further experiments confirmed that Sirt1 overexpression restored the anti-RA activity of GAS5 under miR-222-3p mimic. CONCLUSIONS: The miR-222-3p/Sirt1 axis was found to be critical for the function of GAS5 in regulating the proliferation, inflammation, and apoptosis of RA-FLSs. These data indicate GAS5 activation as a potential therapeutic strategy for RA progression.	NA	Autoimmunity. 2021 Feb;54(1):13-22. doi: 10.1080/08916934.2020.1846183. Epub 2020 Nov 20.
4676	LncRNA	GIHCG	miR-29b-3p	ANO1	esophageal cancer cells	Esophageal Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	33408485	LncRNA GIHCG Promotes the Development of Esophageal Cancer by Modulating miR-29b-3p/ANO1 Axis.	BACKGROUND: Esophageal cancer is one of the most frequent cancers with a higher mortality worldwide. Although many long non-coding RNAs (LncRNAs) are reported to play important roles in the progression of esophageal cancer, the function of lncRNA GIHCG in esophageal cancer remains unclear. METHODS: The expression of GIHCG in esophageal cancer tissues and cancer cell lines was detected by qRT-PCR. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, EdU staining assay and colony formation assay. Cell invasion and migration were measured by transwell assay. Cell apoptosis was detected by a flow cytometer. Luciferase reporter assay and RIP assay were used to determine the interaction between GIHCG and miR-29b-3p, and their subsequent regulation of anoctamin 1 (ANO1). The expression of ANO1 in esophageal cancer tissues and cell lines was detected by Western blot. The effect of GIHCG/miR-29b-3p in tumor formation was assessed by the xenograft nude mice model in vivo. RESULTS: GIHCG was significantly upregulated in esophageal cancer tissues and relevant cancer cell lines. Downregulation of GIHCG significantly inhibited the growth, colony formation, invasion, migration and induced apoptosis of esophageal cancer cells in vitro. Bioinformatic analysis and RIP assay determined that GIHCG was a sponge of miR-29b-3p, and ANO1 was a direct target of miR-29b-3p. Moreover, functional experiments showed that GIHCG upregulated ANO1 expression by directly sponging miR-29b-3p. Furthermore, in vivo experiment revealed that knockdown of GIHCG significantly inhibited tumor growth in nude mice. CONCLUSION: Our study revealed that lncRNA GIHCG promoted the progression of esophageal cancer by targeting the miR-29b-3p/ANO1 axis, suggesting that GIHCG might be a novel therapeutic target for esophageal cancer.	NA	Onco Targets Ther. 2020 Dec 31;13:13387-13400. doi: 10.2147/OTT.S282348. eCollection 2020.
4677	LncRNA	H19	miR-769-5p	EIF3A	keloid tissues and fibroblasts	Keloid	Homo sapiens (human)	RACE;	33389493	LncRNA H19 promotes keloid formation through targeting the miR-769-5p/EIF3A pathway.	Keloid is a skin disease characterized by fibrous hyperplasia, which is often difficult to cure. Long non-coding RNAs (lncRNAs) have been shown to be associated with the development of many diseases. However, the role and mechanism of lncRNA H19 in keloid has been less studied. Our study found that lncRNA H19 expression was increased in keloid tissues and fibroblasts. Besides, H19 knockdown hindered the proliferation, migration, invasion, extracellular matrix (ECM) deposition, and enhanced the apoptosis of keloid fibroblasts. Further experiments showed that microRNA (miR)-769-5p could be sponged by H19, and its knockdown reversed the suppression effect of H19 knockdown on keloid formation. Eukaryotic initiation factor 3A (EIF3A) was found to be a target of miR-769-5p, and its overexpression inverted the inhibition effect of miR-769-5p overexpression on keloid formation. Moreover, the expression of EIF3A was regulated by H19 and miR-769-5p in keloid fibroblasts. Collectively, LncRNA H19 might play an active role in keloid formation, which might provide a new target for the treatment of keloid.	NA	Mol Cell Biochem. 2021 Mar;476(3):1477-1487. doi: 10.1007/s11010-020-04024-x. Epub 2021 Jan 3.
4678	LncRNA	H19	miR-324-3p	TNF-a	A549 cells	Pulmonary Inflammatory Response	Homo sapiens (human)	Cell apoptosis assay;ELISA;RT-PCR;Western blot;	33413425	Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade.	OBJECTIVE: To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under dexamethasone (Dex) treatment. METHODS: IL-1β (10 ng/mL) and LPS (1 μg/mL) was used to construct inflammatory cell models with A549 cells; IL-1β performed better against LPS. Different concentrations of Dex were used to attenuate the inflammation induced by IL-1β, and its effect was assessed via RT-PCR to detect inflammatory cytokine-related mRNA levels, including those of IKβ-α, IKKβ, IL-6, IL-8, and TNF-α. Furthermore, ELISA was used to detect the levels of the inflammatory cytokines TNF-α, IL-6, and IL-8. RT-PCR was used to quantify the levels of lncRNAs, including lncMALAT1, lncHotair, lncH19, and lncNeat1. LncH19 was most closely associated with the inflammatory response, which was induced by IL-1β and attenuated by Dex. Among the lncRNAs, the level of lncH19 showed the highest increase following treatment with 1 and 10 μM Dex. Therefore, lncH19 was selected for further functional studies. LncH19 expression was inhibited by shRNA transduced with lentivirus. Cell assays for cell proliferation and apoptosis as well as RT-PCR, western blot, and ELISA for inflammatory genes were conducted to confirm the functions of lncH19. The predicted target miRNAs of lncH19 were hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p, and hsa-miR-19a-3p. Following estimation via RT-PCR, hsa-miR-346, hsa-miR-18a-3p, and hsa-miR-324-3p showed consistent patterns in A549 NC and A549 shlncH19. An miRNA inhibitor was transfected into A549 NC and A549 shlncH19 cells, and the expression levels were determined via RT-PCR. hsa-miR-324-3p was inhibited the most compared with hsa-miR-346 and hsa-miR-18a-3p and was subjected to further functional studies. RT-PCR, ELISA, and western blotting for inflammatory gene detection were conducted to validate the functions of the target hsa-miR-324-3p. RESULTS: Treatment with 1 and 10 μM Dex could effectively attenuate the inflammatory response. During this process, lncH19 expression significantly increased (P < 0.05). Therefore, treatment with 1 μM Dex was used for further study. Under IL-1β treatment with or without Dex, lncH19 inhibition led to an increase in cell proliferation; a decrease in cell apoptosis; an increase in the protein levels of inflammatory genes; phosphorylation of P65, ICAM-1, and VCAM-1; and increase inflammatory cytokines. Prediction of the targets of lncH19 and validation via RT-PCR revealed that miR-346, miR-18a-3p, and miR-324-3p negatively correlate with lncH19. Additionally, Dex increased the lncH19 expression but reduced that of the miRNAs. Among the miRNAs, miR-324-3p was the most markedly downregulated miRNA following treatment of miRNA inhibitors. The MTS assay and cell apoptosis assay showed that the miR-324-3p inhibitor inhibited cell proliferation and induced cell apoptosis, thereby significantly attenuating the inflammatory response, which reversed the effect of lncH19 in regulating cell proliferation and the secretion of inflammatory cytokines (P < 0.05). Therefore, lncH19 might regulate miR-324-3p in pulmonary inflammatory response under Dex treatment. CONCLUSION: Dex can attenuate the pulmonary inflammatory response by regulating the lncH19/miR-324-3p cascade.	NA	J Inflamm (Lond). 2021 Jan 7;18(1):1. doi: 10.1186/s12950-020-00266-0.
4679	LncRNA	H19	miR-324-3p	IL-6	A549 cells	Pulmonary Inflammatory Response	Homo sapiens (human)	Cell apoptosis assay;ELISA;RT-PCR;Western blot;	33413425	Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade.	OBJECTIVE: To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under dexamethasone (Dex) treatment. METHODS: IL-1β (10 ng/mL) and LPS (1 μg/mL) was used to construct inflammatory cell models with A549 cells; IL-1β performed better against LPS. Different concentrations of Dex were used to attenuate the inflammation induced by IL-1β, and its effect was assessed via RT-PCR to detect inflammatory cytokine-related mRNA levels, including those of IKβ-α, IKKβ, IL-6, IL-8, and TNF-α. Furthermore, ELISA was used to detect the levels of the inflammatory cytokines TNF-α, IL-6, and IL-8. RT-PCR was used to quantify the levels of lncRNAs, including lncMALAT1, lncHotair, lncH19, and lncNeat1. LncH19 was most closely associated with the inflammatory response, which was induced by IL-1β and attenuated by Dex. Among the lncRNAs, the level of lncH19 showed the highest increase following treatment with 1 and 10 μM Dex. Therefore, lncH19 was selected for further functional studies. LncH19 expression was inhibited by shRNA transduced with lentivirus. Cell assays for cell proliferation and apoptosis as well as RT-PCR, western blot, and ELISA for inflammatory genes were conducted to confirm the functions of lncH19. The predicted target miRNAs of lncH19 were hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p, and hsa-miR-19a-3p. Following estimation via RT-PCR, hsa-miR-346, hsa-miR-18a-3p, and hsa-miR-324-3p showed consistent patterns in A549 NC and A549 shlncH19. An miRNA inhibitor was transfected into A549 NC and A549 shlncH19 cells, and the expression levels were determined via RT-PCR. hsa-miR-324-3p was inhibited the most compared with hsa-miR-346 and hsa-miR-18a-3p and was subjected to further functional studies. RT-PCR, ELISA, and western blotting for inflammatory gene detection were conducted to validate the functions of the target hsa-miR-324-3p. RESULTS: Treatment with 1 and 10 μM Dex could effectively attenuate the inflammatory response. During this process, lncH19 expression significantly increased (P < 0.05). Therefore, treatment with 1 μM Dex was used for further study. Under IL-1β treatment with or without Dex, lncH19 inhibition led to an increase in cell proliferation; a decrease in cell apoptosis; an increase in the protein levels of inflammatory genes; phosphorylation of P65, ICAM-1, and VCAM-1; and increase inflammatory cytokines. Prediction of the targets of lncH19 and validation via RT-PCR revealed that miR-346, miR-18a-3p, and miR-324-3p negatively correlate with lncH19. Additionally, Dex increased the lncH19 expression but reduced that of the miRNAs. Among the miRNAs, miR-324-3p was the most markedly downregulated miRNA following treatment of miRNA inhibitors. The MTS assay and cell apoptosis assay showed that the miR-324-3p inhibitor inhibited cell proliferation and induced cell apoptosis, thereby significantly attenuating the inflammatory response, which reversed the effect of lncH19 in regulating cell proliferation and the secretion of inflammatory cytokines (P < 0.05). Therefore, lncH19 might regulate miR-324-3p in pulmonary inflammatory response under Dex treatment. CONCLUSION: Dex can attenuate the pulmonary inflammatory response by regulating the lncH19/miR-324-3p cascade.	NA	J Inflamm (Lond). 2021 Jan 7;18(1):1. doi: 10.1186/s12950-020-00266-0.
4680	LncRNA	H19	miR-324-3p	IL-8	A549 cells	Pulmonary Inflammatory Response	Homo sapiens (human)	Cell apoptosis assay;ELISA;RT-PCR;Western blot;	33413425	Dexamethasone can attenuate the pulmonary inflammatory response via regulation of the lncH19/miR-324-3p cascade.	OBJECTIVE: To investigate lncRNAs and their roles in regulating the pulmonary inflammatory response under dexamethasone (Dex) treatment. METHODS: IL-1β (10 ng/mL) and LPS (1 μg/mL) was used to construct inflammatory cell models with A549 cells; IL-1β performed better against LPS. Different concentrations of Dex were used to attenuate the inflammation induced by IL-1β, and its effect was assessed via RT-PCR to detect inflammatory cytokine-related mRNA levels, including those of IKβ-α, IKKβ, IL-6, IL-8, and TNF-α. Furthermore, ELISA was used to detect the levels of the inflammatory cytokines TNF-α, IL-6, and IL-8. RT-PCR was used to quantify the levels of lncRNAs, including lncMALAT1, lncHotair, lncH19, and lncNeat1. LncH19 was most closely associated with the inflammatory response, which was induced by IL-1β and attenuated by Dex. Among the lncRNAs, the level of lncH19 showed the highest increase following treatment with 1 and 10 μM Dex. Therefore, lncH19 was selected for further functional studies. LncH19 expression was inhibited by shRNA transduced with lentivirus. Cell assays for cell proliferation and apoptosis as well as RT-PCR, western blot, and ELISA for inflammatory genes were conducted to confirm the functions of lncH19. The predicted target miRNAs of lncH19 were hsa-miR-346, hsa-miR-324-3p, hsa-miR-18a-3p, hsa-miR-18b-5p, hsa-miR-146b-3p, hsa-miR-19b-3p, and hsa-miR-19a-3p. Following estimation via RT-PCR, hsa-miR-346, hsa-miR-18a-3p, and hsa-miR-324-3p showed consistent patterns in A549 NC and A549 shlncH19. An miRNA inhibitor was transfected into A549 NC and A549 shlncH19 cells, and the expression levels were determined via RT-PCR. hsa-miR-324-3p was inhibited the most compared with hsa-miR-346 and hsa-miR-18a-3p and was subjected to further functional studies. RT-PCR, ELISA, and western blotting for inflammatory gene detection were conducted to validate the functions of the target hsa-miR-324-3p. RESULTS: Treatment with 1 and 10 μM Dex could effectively attenuate the inflammatory response. During this process, lncH19 expression significantly increased (P < 0.05). Therefore, treatment with 1 μM Dex was used for further study. Under IL-1β treatment with or without Dex, lncH19 inhibition led to an increase in cell proliferation; a decrease in cell apoptosis; an increase in the protein levels of inflammatory genes; phosphorylation of P65, ICAM-1, and VCAM-1; and increase inflammatory cytokines. Prediction of the targets of lncH19 and validation via RT-PCR revealed that miR-346, miR-18a-3p, and miR-324-3p negatively correlate with lncH19. Additionally, Dex increased the lncH19 expression but reduced that of the miRNAs. Among the miRNAs, miR-324-3p was the most markedly downregulated miRNA following treatment of miRNA inhibitors. The MTS assay and cell apoptosis assay showed that the miR-324-3p inhibitor inhibited cell proliferation and induced cell apoptosis, thereby significantly attenuating the inflammatory response, which reversed the effect of lncH19 in regulating cell proliferation and the secretion of inflammatory cytokines (P < 0.05). Therefore, lncH19 might regulate miR-324-3p in pulmonary inflammatory response under Dex treatment. CONCLUSION: Dex can attenuate the pulmonary inflammatory response by regulating the lncH19/miR-324-3p cascade.	NA	J Inflamm (Lond). 2021 Jan 7;18(1):1. doi: 10.1186/s12950-020-00266-0.
4681	LncRNA	H19	miR-130a-3p	SATB1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33324070	H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells.	PURPOSE: Breast cancer (BC) is the most common cancer in women. Emerging evidence has demonstrated that lncRNAs play an important role in BC. The objective of this study was to investigate the impact of the long non-coding RNA (lncRNA), H19/miRNA-130a-3P/special AT-rich sequence-binding protein-1 (SATB1) axis on BC progression. MATERIALS AND METHODS: Expression of lncRNA and RNA was quantified via RT-qPCR. CCK-8, colony formation, wound healing, transwell, and flow cytometric analyses were used to analyze the proliferation, migration, invasion and apoptosis of cells. A dual-luciferase reporter assay and a RNA immunoprecipitation (RIP) assay were used to assess molecular binding. Protein levels were measured by Western blotting. The function of the lncRNA H19 (hereafter referred to as H19) was examined by xenotransplantation. RESULTS: We demonstrated that H19 expression was higher in cancer tissues and cancer cell lines than in adjacent non-tumor tissues and normal cell lines, respectively. H19 silencing inhibited the proliferation, migration and invasion of BC cells, and induced apoptosis. In addition, H19 directly bound to miR-130a-3p and downregulated its expression. We further demonstrated that H19 sponged miRNA-130a-3p, which resulted in SATB1 upregulation, thus promoting BC progression. Silencing of H19 substantially suppressed BC tumorigenesis in vivo. CONCLUSION: Our data uncovered a novel mechanism of BC progression based on the H19-miR-130a-3p-SATB1 axis.	NA	Onco Targets Ther. 2020 Dec 7;13:12501-12513. doi: 10.2147/OTT.S280142. eCollection 2020.
4682	LncRNA	HCG11	miR-620	ELK4	Vestibular schwannoma cells	Vestibular Schwannoma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;	33402177	HCG11 up-regulation induced by ELK4 suppressed proliferation in vestibular schwannoma by targeting miR-620/ELK4.	BACKGROUND: Vestibular schwannoma (VS) is a kind of benign tumor deriving from the acoustic nerve sheath. Substantial long non-coding RNAs (lncRNAs) were illustrated to have crucial roles in multiple cancers. However, few lncRNAs were elucidated in VS. METHODS: HCG11, miR-620 and ELK4 expression were tested by RT-qPCR. Gain-of-function experiments were conducted to confirm the effect of HCG11 on VS. RESULTS: HCG11 possessed a low expression in VS cell lines. Overexpression of HCG11 repressed cell proliferation but accelerated apoptosis of VS cells. Moreover, we identified ELK4 stimulated the transcription of HCG11 and their affinity was verified by ChIP assays. MiR-620 was chosen to be a target of HCG11 and it was tested to have a high expression in VS cell lines. Moreover, depletion of miR-620 could inhibit cell proliferative ability while fostering apoptosis rate of VS cells. ELK4 was low expressed in VS cell lines and knockdown of ELK4 could rescue the effects made by HCG11 overexpression on progression of VS. CONCLUSIONS: HCG11 could inhibit the growth of VS by targeting miR-620/ELK4 in VS cells. HCG11 was a novel therapeutic target for VS treatment.	NA	Cancer Cell Int. 2021 Jan 5;21(1):5. doi: 10.1186/s12935-020-01691-0.
4683	LncRNA	HCP5	miR-106b-5p	p21	gactric cells	Gastric Cancer	Homo sapiens (human)	ChIP;qRT-PCR;Chromatin immunoprecipitation;Luciferase reporter assay;	33613117	MEF2A-mediated lncRNA HCP5 Inhibits Gastric Cancer Progression via MiR-106b-5p/p21 Axis.	Background: Long non-coding RNAs (lncRNAs) are deemed to be relevant to the tumorigenesis and development of a variety of tumors, containing gastric cancer (GC). The purpose of our investigations is to explore the character of HCP5 in GC. Methods: HCP5 expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in 62 matched GC tissues and corresponding para-carcinoma tissues. In vitro and in vivo functional assays were subjected to verify the biological effects of HCP5 after alteration of HCP5. Chromatin immunoprecipitation assay (CHIP) assays were conducted to confirm that myocyte enhancer factor 2A (MEF2A) could bind to HCP5 promoter regions and thereby induce HCP5 expression. Analysis of the latent binding of miR-106b-5p to HCP5 and p21 was made by bioinformatics prediction and luciferase reporter assays. Results: Significant downregulation of HCP5 was detected in GC tissues. Negative correlation was determined between HCP5 expression level and tumor size and overall survival in GC patients. HCP5 depletion had a facilitating impact on proliferation, migration and invasion of GC cells. Consistently, overexpression of HCP5 came into an opposite effect. Moreover, we demonstrated that MEF2A could combine with the promoter region of HCP5 and thereby induce HCP5 transcription. Luciferase reporter assays revealed that HCP5 could compete with miR-106b-5p as a competing endogenous RNA (ceRNA) and upregulated p21 expression in GC. Conclusions: MEF2A-mediated HCP5 could exert an anti-tumor effect among the development of GC via miR-106b-5p/p21 axis, which provides a novel target for GC therapy.	NA	Int J Biol Sci. 2021 Jan 16;17(2):623-634. doi: 10.7150/ijbs.55020. eCollection 2021.
4684	LncRNA	HCP5	miR-519d	HMGA1	Gastric Cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33536786	HCP5 Promotes Proliferation and Contributes to Cisplatin Resistance in Gastric Cancer Through miR-519d/HMGA1 Axis.	INTRODUCTION: The long-non-coding RNA HCP5 (HLA complex P5) has been extensively linked to the ability of cancer cells to resist chemotherapeutic interventions. Here, we investigated the role of HCP5 in gastric cancer (GC) which to-date has been poorly characterized. Our results indicated that HCP5 expression was up-regulated in GC cells. METHODS: HCP5, miR-519d, and high mobility group A1 (HMGA1) expression levels in GC cells were measured using quantitative real-time PCR (qRT-PCR) and Western blot analysis. Drug sensitivity and apoptosis of tumor cells were assessed using cell counting kit-8, flow cytometry, and caspase activity assay. Bioinformatics and luciferase reporter assays were employed for analyzing the interactions between HCP5, miR-519d, and HMGA1. RESULTS: HCP5 knockdown suppressed proliferation and weakened the resistance to cisplatin (DDP) of GC cells. miR-519d was down-regulated in GC cells and sponged by HCP5. HMGA1 was directly inhibited by miR-519d and its expression was up-regulated in GC cells. HCP5 exacerbated the resistance to cisplatin of GC cells in vitro by enhancing HMGA1 expression via sponging miR-519d. CONCLUSION: In summary, HCP5 promoted proliferation and contributed to DDP resistance in GC cells through miR-519d/HMGA1 axis.	NA	Cancer Manag Res. 2021 Jan 27;13:787-794. doi: 10.2147/CMAR.S289997. eCollection 2021.
4685	LncRNA	HCP5	miR-299-3p	SMAD5	Gastric Cancer cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33371778	Silencing of long non-coding RNA HCP5 inhibits proliferation, invasion, migration, and promotes apoptosis via regulation of miR-299-3p/SMAD5 axis in gastric cancer cells.	Gastric cancer (GC) is a common malignant gastrointestinal tumor with high mortality. Previous study has reported that the overexpression of lncRNA HCP5 was observed in gastric cancer tissues. The purpose of this study was to investigate the molecular mechanism underlying the effect of lncRNA HCP5 on the proliferative, migratory, and invasive abilities of GC cells. The relative mRNA expression of HCP5, miR-299-3p, and SMAD5 were determined by RT-qPCR. The expressions of proteins associated with apoptosis and invasion were detected by western blot. The interaction of HCP5 with miR-299-3p and SMAD5 with miR-299-3p was confirmed by luciferase reporter assay. The cellular behaviors of AGS cells were, respectively, detected by CCK-8 assays, colony formation assays, migration and invasion assays, and flow cytometry. In our study, lncRNA HCP5 was highly expressed in GC cell lines compared with normal gastric epithelial cell. LncRNA HCP5 silencing inhibited AGS cells proliferation, migration, and invasion, while promoted cell apoptosis. Moreover, miR-299-3p downregulation could abolish the effect of HCP5 knockdown on cellular behaviors of AGS cells. Interestingly, SMAD5 is identified as the downstream target of miR-299-3p, and its expression was inhibited by miR-299-3p. More importantly, SMAD5 silencing inhibited proliferation, migration, and invasion of GC cells, and promoted cell apoptosis. In a word, lncRNA HCP5 silencing inhibits GC cell proliferation, invasion, and migration while promoting its apoptosis via regulation of miR-299-3p/SMAD5 axis. Hence, lncRNA HCP5 could be a novel and promising target for GC treatment.	NA	Bioengineered. 2021 Dec;12(1):225-239. doi: 10.1080/21655979.2020.1863619.
4686	LncRNA	HIF1A-AS2	miR-429	PD-L1	Gastric Cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;Luciferase reporter assay;	33555514	HIF1A-AS2 Promotes the Proliferation and Metastasis of Gastric Cancer Cells Through miR-429/PD-L1 Axis.	BACKGROUND: Gastric cancer (GC) is a common leading cause of cancer-related mortality of all malignancies. LncRNA hypoxia-inducible factor-1 alpha antisense RNA-2 (HIF1A-AS2) has been identified to involve in the development of GC. Therefore, we further explored the detailed molecular mechanism of HIF1A-AS2 in GC progression. METHODS: The expression of HIF1A-AS2, microRNA-429 (miR-429), and programmed cell death ligand 1 (PD-L1) was measured using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell proliferation, migration, and invasion abilities were detected by Cell Counting Kit-8 (CCK-8) or transwell assay. The interaction between miR-429 and HIF1A-AS2 or PD-L1 was confirmed by luciferase reporter assay. Murine xenograft model was established to investigate the role of HIF1A-AS2 in vivo. RESULTS: HIF1A-AS2 was elevated in GC tissues and cell lines. Functional experiments showed that HIF1A-AS2 knockdown inhibited GC cell proliferation, migration, and invasion in vitro, as well as hindered tumor growth in vivo. Moreover, HIF1A-AS2 directly bound to miR-429 based on bioinformatics prediction and luciferase assay, and inhibition of miR-429 abolished the effects of HIF1A-AS2 knockdown on GC cells. Furthermore, miR-429 directly targeted PD-L1, and overexpression of miR-429 suppressed GC tumorigenesis via PD-L1. Besides that, PD-L1 also performed an oncogenic role in GC cell proliferation and metastasis. Additionally, HIF1A-AS2 could indirectly regulate PD-L1 expression via sponging miR-429. CONCLUSION: HIF1A-AS2 is a dependable predictor of malignancy and prognosis in GC and functions as an oncogene to promote GC cell proliferation and metastasis by regulating miR-429/PD-L1 axis, indicating a new insight into the search for novel biomarkers and therapeutic strategies.	NA	Dig Dis Sci. 2021 Feb 8. doi: 10.1007/s10620-020-06819-w.
4687	LncRNA	HLA-F-AS1	miR-375	PFN1	Colorectal cancer tissues and cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qPCR;RT-qPCR;RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33531647	LncRNA HLA-F-AS1 promotes colorectal cancer metastasis by inducing PFN1 in colorectal cancer-derived extracellular vesicles and mediating macrophage polarization.	Colorectal cancer (CRC) is a prevalent malignancy with high incidence and low 5-year survival. Long non-coding RNAs (lncRNAs), a kind of specific RNA transcript, are increasingly implicated in tumor growth, metastasis, invasion, and prognosis by regulating the tumor microenvironment in extracellular vesicles (EVs). This study aims at investigating the potential effect of lncRNA HLA-F-AS1 on CRC by affecting the profilin 1 (PFN1) expression pattern in the tumor EVs. The expression patterns of HLA-F-AS1 and miR-375 were determined by RT-qPCR in the CRC tissues and cells. CCK-8 and Transwell assays were conducted to detect the cell proliferation and migration, and invasion, respectively. Western blot analysis was performed to measure the expression pattern of the epithelial-mesenchymal transition (EMT) markers. Bioinformatics prediction website and dual-luciferase reporter assay were conducted to verify the interaction between HLA-F-AS1 and miR-375. The CRC-derived EVs were extracted with the expression pattern of PFN1 determined by ELISA, while its effect on the macrophage polarization was assessed by flow cytometry. The effect of PFN1-treated macrophages on CRC cell proliferation and migration was observed by subcutaneous tumorigenesis experiments in nude mice. The results indicated that the HLA-F-AS1 expression pattern was increased in the CRC tissues and cells, which promoted the migration, invasion, and EMT of CRC cells in vitro. Mechanistically, HLA-F-AS1 competitively bound to miR-375 and inversely regulated miR-375 expression pattern. Interestingly, PFN1 was identified as a direct target of miR-375, and positively modulated by HLA-F-AS1 by binding to miR-375. Overexpression of HLA-F-AS1 repressed miR-375 and promoted the PFN1 expression pattern in CRC cells and CRC-derived EVs, further promoting M2 polarization of macrophages. Furthermore, macrophages treated with PFN1 in CRC-derived EVs stimulated CRC cell proliferation and migration in vitro and in vivo. Collectively, these outcomes highlight that HLA-F-AS1 promotes the expression pattern of PFN1 in CRC-EVs by inhibiting miR-375, thereby polarizing macrophages toward M2 phenotype, and aggravating the tumorigenesis of CRC, eliciting that HLA-F-AS1 may serve as a viable and promising therapeutic strategy for CRC.	NA	Cancer Gene Ther. 2021 Feb 2. doi: 10.1038/s41417-020-00276-3.
4688	LncRNA	HNF1A-AS1	miR-32-5p	RNF38	Triple-negative breast cancer cells	Triple Negative Breast Cancer 	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	33603481	GATA1-Activated HNF1A-AS1 Facilitates the Progression of Triple-Negative Breast Cancer via Sponging miR-32-5p to Upregulate RNF38.	BACKGROUND: Triple-negative breast cancer (TNBC) is a highly invasive subtype of breast cancer with a high mortality rate. Recently, long non-coding RNAs (lncRNAs) are confirmed to modulate the progression of assorted cancers, including TNBC. However, the functions of lncRNA HNF1 homeobox A antisense RNA 1 (HNF1A-AS1) in TNBC are still unclear. AIM: We aimed to investigate the function and mechanism of HNF1A-AS1 in TNBC. METHODS: The expression of genes in TNBC cells was tested by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. In vitro loss-of-function assays and in vivo xenograft experiments were conducted for evaluating the impact of HNF1A-AS1 on TNBC progression. RNA pull-down, luciferase reporter and RNA immunoprecipitation (RIP) assays were utilized for assessing the correlations between molecules. RESULTS: We discovered that HNF1A-AS1 was highly expressed in TNBC tissues and cells. Knockdown of HNF1A-AS1 restrained cell proliferation but accelerated cell apoptosis. Besides, GATA-binding protein 1 (GATA1) activated HNF1A-AS1 transcription in TNBC. MicroRNA-32-5p (miR-32-5p) was slowly expressed in TNBC cells and sponged by HNF1A-AS1, and its overexpression hinders TNBC cell growth. Ring finger protein 38 (RNF38) was verified as the target of miR-32-5p, and HNF1A-AS1 was a competing endogenous RNA (ceRNA) of RNF38 through sponging miR-32-5p. Rescue experiments indicated that upregulation of RNF38 reversed the inhibited impacts of silencing HNF1A-AS1 on TNBC cell growth. CONCLUSION: GATA1-activated HNF1A-AS1 facilitated TNBC progression via miR-32-5p/RNF38 axis. The findings may provide new roads for developing targeted therapies of TNBC.	NA	Cancer Manag Res. 2021 Feb 11;13:1357-1369. doi: 10.2147/CMAR.S274204. eCollection 2021.
4689	LncRNA	HOTAIR	miR-193a	EZH2	SKOV3 cells	Ovarian Cancer	Homo sapiens (human)	RT-PCR;Western blot;Flow Cytometry assay;	33502891	LncRNA HOTAIR regulates anoikis-resistance capacity and spheroid formation of ovarian cancer cells by recruiting EZH2 and influencing H3K27 methylation.	This study aims to investigate the role of the long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) in the regulation of anoikis resistance of ovarian cancer cells, a prerequisite for metastasis and chemoresistance in ovarian cancer cells. Ovarian cancer SKOV3 cells were cultured in an ultra-low attachment system to establish an anoikis model. The relationship between cellular anoikis capability and HOTAIR expression level was studied by flow cytometry and RT-PCR. The ability of spheroid formation, migration, and invasion of the suspended cells was assessed following the knockdown of HOTAIR expression. The expression of EZH2, H3K27me3, representative targets of EZH2, and anoikis-related biomarkers was also detected. An increase in the duration of suspension culture time rendered the SKOV3 cells anoikis-resistant with a significantly lower apoptotic rate compared to the adherent cells. HOTAIR expression in the suspension cells increased significantly, while that in the adherent cells did not. Following small interfering RNA (siRNA)-mediated knockdown of HOTAIR expression, the abilities of anoikis resistance, migration, and invasion decreased in the suspension cells. Knockdown of HOTAIR levels also reduced the spheroid forming ability of the tumor cells in continuous suspension cultures. Moreover, EZH2 expression correlated with HOTAIR expression, thus regulating the expression of miR-193a and DOK2 via introducing H3K27me3. Western blot analysis of anoikis-related markers showed that N-cadherin, ZEB1, and TWIST1 were downregulated following inhibition of HOTAIR, while E-cadherin and ErbB3 were upregulated. In conclusion, HOTAIR enhances the anoikis resistance and spheroid forming ability of ovarian cancer cells by recruiting EZH2 and influencing H3K27 methylation that may contribute to migration, invasion, and chemoresistance of ovarian cancer cells.	NA	Neoplasma. 2021 May;68(3):509-518. doi: 10.4149/neo_2021_201112N1212. Epub 2021 Jan 28.
4690	LncRNA	HOTAIR	miR-1277-5p	SGTB	CHON-001 chondrocytes	Osteoarthritis	Homo sapiens (human)	ELISA;Western blot;Flow Cytometry assay;	33721916	LncRNA HOTAIR modulates chondrocyte apoptosis and inflammation in osteoarthritis via regulating miR-1277-5p/SGTB axis.	Osteoarthritis (OA) is a common degenerative joint disease in the elderly. This study aimed to investigate the role and mechanism of lncRNA HOX transcript antisense RNA (HOTAIR) in lipopolysaccharide (LPS)-treated chondrocytes in OA. CHON-001 chondrocytes treated with LPS were used as a cell model of OA. The levels of HOTAIR, miR-1277-5p and small glutamine rich tetratricopeptide repeat containing beta (SGTB) were measured via quantitative real-time polymerase chain reaction or western blot. Cell viability and apoptosis were assessed using Cell Counting Kit-8 and flow cytometry. The levels of inflammation-related factors were examined via enzyme-linked immunosorbent assay (ELISA). Aggrecan and Collagen II protein levels were detected using western blot. The interaction among HOTAIR, miR-1277-5p and SGTB were validated by dual-luciferase reporter analysis. HOTAIR and SGTB were up-regulated, while miR-1277-5p was down-regulated in OA cartilages and LPS-stimulated CHON-001 chondrocytes. HOTAIR depletion inhibited LPS-induced apoptosis and inflammation in chondrocytes. Moreover, down-regulation of HOTAIR attenuated LPS-triggered chondrocyte apoptosis and inflammation via sponging miR-1277-5p. Also, miR-1277-5p repressed LPS-induced chondrocyte apoptosis and inflammation by targeting SGTB. Furthermore, HOTAIR enhanced SGTB expression by sponging miR-1277-5p. HOTAIR aggravated chondrocyte apoptosis and inflammation in OA via regulating miR-1277-5p/SGTB pathway.	NA	Wound Repair Regen. 2021 May;29(3):495-504. doi: 10.1111/wrr.12908. Epub 2021 Mar 15.
4691	LncRNA	HOTAIR	miR-148b	DNMT1	gastric cancers tissues	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33527791	HOTAIR Induces Methylation of PCDH10, a Tumor Suppressor Gene, by Regulating DNMT1 and Sponging with miR-148b in Gastric Adenocarcinoma.	PURPOSE: HOX transcript antisense intergenic RNA (HOTAIR), as a long non-coding RNA, has been reported to regulate carcinogenesis by epigenetic mechanism in various cancers. Protocadherin 10 (PCDH10) is one of the well-known tumor suppressor genes, and is frequently methylated in gastric cancers (GC). We aimed to investigate the detailed pathway of how HOTAIR contributes to the target gene in gastric carcinogenesis. MATERIALS AND METHODS: We investigated the mechanism of HOTAIR on carcinogenesis and metastasis of GC. Methylation-specific PCR was performed to identify the interaction between HOTAIR and PCDH10. In addition, we investigated the interaction between miR-148b and HOTAIR by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. RESULTS: The expression of HOTAIR was significantly upregulated in GC tissues (p<0.05) and GC cell lines (p<0.01), while PCDH10 was downregulated in GC tissues (p<0.05). The knockdown of HOTAIR (si-HOTAIR1 and 2) significantly upregulated the mRNA/protein expression of PCDH10 and reduced the methylation of PCDH10 compared to the control in MKN 28 and MKN 74. Si-HOTAIR1 and 2 significantly reduced DNA methyltransferase 1 (DNMT1) expression, and overexpression of HOTAIR increased DNMT1 expression. In RIP, we found that miR-148b interacted with HOTAIR. Si-HOTAIRs increased miR-148b expression, and miR-148b mimic inversely reduced HOTAIR expression. Si-HOTAIRs and miR-148b mimic reduced DNMT1 expression and increased PCDH10 expression compared to the control. CONCLUSION: This study demonstrated that HOTAIR interacts with miR-148b and DNMT1, eventually leading to PCDH10 methylation, which contributes to the progression of GC. Our findings provide a better understanding for detailed pathway of HOTAIR in epigenetic mechanism of GC.	NA	Yonsei Med J. 2021 Feb;62(2):118-128. doi: 10.3349/ymj.2021.62.2.118.
4692	LncRNA	HOTAIR	miR-17-5p	p21	HL-60 cells	Acute Myeloid Leukemia	Homo sapiens (human)	ChIP;qRT-PCR;Chromatin immunoprecipitation;Flow Cytometry assay;	33241756	Long non-coding RNA HOTAIR regulates myeloid differentiation through the upregulation of p21 via miR-17-5p in Acute myeloid leukemia.	Long non-coding RNA HOTAIR has been reported to play a key role in regulating various biological processes in various cancers. However, the roles and mechanisms of HOTAIR in Acute myeloid leukemia (AML) are still unclear and need to be investigated. In this study, we induced differentiation of four AML cell lines by all-trans retinoic acid (ATRA) and found HOTAIR was significantly upregulated in the process. Chromatin immunoprecipitation (ChIP) assays indicated that C/EBPβ upregulated HOTAIR during ATRA induced differentiation in HL-60 cells. By gain- and loss-of-function analysis, we then observed that HOTAIR expression was positively correlated with ATRA-induced differentiation and negatively regulated G1 phase arrest in HL-60 cells. In addition, we found that HOTAIR promoted ATRA-induced differentiation via the regulation of the cell cycle regulator p21 via miR-17-5p. Moreover, we detected the expression of HOTAIR in 84 de novo AML patients, HOTAIR was found significantly downregulated in the AML patients compared to the iron deficiency anaemia (IDA) control group, negatively correlated with the platelet level in M2 patients. In all, our data suggest that HOTAIR may be subtype-specific in AML-M2 patients, also HOTAIR regulates AML differentiation by C/EBPBβ/HOTAIR/miR-17-5p/p21 pathway. The findings of the present study provide a novel insight into the mechanism of lncRNA-mediated differentiation and indicate that HOTAIR may be a promising therapeutic target for leukaemia, especially for AML with M2 type.Abbreviation: AML: Acute myeloid leukemia; APL: acute promyelocytic leukaemia; ATRA: all-trans retinoic acid; CCK8: cell Counting Kit-8; CDKs: cyclin-dependent kinases ; CeRNA: competing endogenous RNAs; ChIP: chromatin immunoprecipitation; CHX: cycloheximide; FAB: French-American-British; FCM: flow cytometry; HOTAIR: HOX transcript antisense RNA; IDA: iron-deficiency anemia; lncRNA: long non-coding RNA; 3'UTR: 3'untranslated region; MT: Mutation type; WT: Wild type; qRT-PCR: Quantitative real-time PCR.	NA	RNA Biol. 2020 Dec 9:1-11. doi: 10.1080/15476286.2020.1854520.
4693	LncRNA	HOTTIP	miR-663a	FRK	osteoarthritis cells	Osteoarthritis	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	33435956	LncRNA HOTTIP leads to osteoarthritis progression via regulating miR-663a/ Fyn-related kinase axis.	BACKGROUND: Long non-coding RNA (lncRNA) has been implicated in the progression of osteoarthritis (OA). This study was aimed to explore the role and molecular mechanism of lncRNA HOXA terminal transcriptional RNA (HOTTIP) in the development of OA. METHODS: The expression of HOTTIP, miR-663a and Fyn-related kinase (FRK) in the OA articular cartilage and OA chondrocyte model induced by IL-1β was determined by qRT-PCR. CCK-8, colony formation and flow cytometry were used to determine the cell proliferation and apoptosis of OA chondrocytes. The specific molecular mechanism of HOTTIP in OA chondrocytes was determined by dual luciferase reporter assay, qRT-PCR, western blotting and RNA pull-down. RESULTS: The expression of HOTTIP and FRK were up-regulated, while miR-663a was down-regulated in OA cartilage tissues. Knockdown of HOTTIP decreased the proliferation and induced the apoptosis of OA cartilage model cells, while overexpression of HOTTIP increased the proliferation and reduced the apoptosis of OA cartilage model cells. Moreover, HOTTIP could bind to miR-663a as competitive endogenous RNA. Inhibition of miR-663a expression could alleviate the effect of HOTTIP knockdown on the proliferation and apoptosis of OA cartilage model cells. Furthermore, FRK was found to be a direct target of miR-663a, which could markedly down-regulate the expression of FRK in OA chondrocytes, while HOTTIP could remarkably up-regulate the expression of FRK. In addition, miR-663a inhibition increased the proliferation and reduced the apoptosis of OA cells, while FRK knockdown reversed the effect of miR-663a inhibition on the proliferation and apoptosis of OA cells. Meanwhile, overexpression of miR-663a decreased the proliferation and induced the apoptosis of OA cells, while overexpression of FRK reversed the effect of miR-663a overexpression on the proliferation and apoptosis of OA cells. CONCLUSION: HOTTIP was involved in the proliferation and apoptosis of OA chondrocytes via miR-663a/ FRK axis, and HOTTIP/miR-663a/FRK might be a potential target for the treatment of OA.	NA	BMC Musculoskelet Disord. 2021 Jan 12;22(1):67. doi: 10.1186/s12891-020-03861-7.
4694	LncRNA	HOXA11-AS	miR-152-3p	ITGA9	cutaneous melanoma cells	Cutaneous Melanoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33564267	Long Non-Coding RNA HOXA11-AS Modulates Proliferation, Apoptosis, Metastasis and EMT in Cutaneous Melanoma Cells Partly via miR-152-3p/ITGA9 Axis.	BACKGROUND: Long non-coding RNA homeobox A11 antisense RNA (HOXA11-AS) was showed to participate in the progression of different kinds of tumors, but the specific role of HOXA11-AS in cutaneous melanoma is not entirely unambiguous. METHODS: The levels of HOXA11-AS, microRNA-152-3p (miR-152-3p) and integrin alpha9 (ITGA9) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was detected via 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT), and apoptosis was measured by flow cytometry. The assessment of cell metastasis was performed by transwell migration and invasion assays. The protein levels were detected through Western blot. Dual-luciferase reporter assay was utilized to explore the target relationship among HOXA11-AS, miR-152-3p and ITGA9. The effect of HOXA11-AS on melanoma in vivo was investigated via xenograft experiment. RESULTS: HOXA11-AS and ITGA9 were up-regulated while miR-152-3p was down-regulated in melanoma. Knockdown of HOXA11-AS refrained cell proliferation, metastasis and epithelial-mesenchymal transition (EMT) but induced apoptosis in melanoma cells. HOXA11-AS targeted miR-152-3p and overexpression of HOXA11-AS mitigated the miR-152-3p-induced effects on melanoma cellular behaviors. ITGA9 was a target of miR-152-3p and miR-152-3p inhibitor relieved the repression on proliferation, metastasis and EMT while elevation on apoptosis caused by si-ITGA9 via elevating ITGA9. HOXA11-AS knockdown restrained ITGA9 expression via up-regulating miR-152-3p. Suppression of HOXA11-AS inhibited melanoma progression in part through increasing miR-152-3p and decreasing ITGA9 expression in vivo. CONCLUSION: HOXA11-AS modulated proliferation, apoptosis, metastasis and EMT in melanoma cells by regulating miR-152-3p/ITGA9 axis in part. HOXA11-AS could promote melanoma development and be used as a promising biomarker in the diagnosis and treatment for cutaneous melanoma.	NA	Cancer Manag Res. 2021 Feb 2;13:925-939. doi: 10.2147/CMAR.S281920. eCollection 2021.
4695	LncRNA	HOXA11-AS	miR-124-3p	FSTL1	microglia	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Western blot;Luciferase reporter assay;	33839699	Inhibition of long non-coding RNA HOXA11-AS against neuroinflammation in Parkinson's disease model via targeting miR-124-3p mediated FSTL1/NF-κB axis.	BACKGROUND: Studies have revealed that lncRNA HOXA11-AS contributes to regulating inflammation, while the role of HOXA11-AS in Parkinson's disease (PD) remains unclear. METHODS: Both in vivo and in vitro PD models were induced. Gain- or loss-assays of HOXA11-AS and miR-124-3p were conducted. The neurological functions, dopaminergic neurons damage, microglia activation of PD mice were measured. Afterwards, the expressions of inflammatory factors were examined with RT-PCR. Western blot was employed to detect the level of FSTL1, NF-κB and NLRP3 inflammasome. Meanwhile, bioinformatics analysis and dual-luciferase reporter assay were utilized to confirm the targeting relationships among miR-124-3p, HOXA11-AS and FSTL1. RESULTS: HOXA11-AS promoted MPTP-mediated SH-SY5Y neuronal injury and LPS-induced microglia activation, while miR-124-3p had the opposite effects. Additionally, miR-124-3p was the target of HOXA11-AS and FSTL1. HOXA11-AS overexpression enhanced the expression of inflammatory factors and FSTL1, NF-κB and NLRP3 inflammasome, while inhibiting NF-κB weakened HOXA11-AS-mediated neuronal damage and microglia activation. Moreover, HOXA11-AS1 downregulation ameliorated MPTP-induced neurological damages and neuroinflammation in mice. CONCLUSION: Inhibition of HOXA11-AS protects mice against PD through repressing neuroinflammation and neuronal apoptosis through miR-124-3p-FSTL1-NF-κB axis.	NA	Aging (Albany NY). 2021 Apr 4;13(8):11455-11469. doi: 10.18632/aging.202837. Epub 2021 Apr 4.
4696	LncRNA	HOXA11-AS	miR-124-3p	NF-kB	microglia	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Western blot;Luciferase reporter assay;	33839699	Inhibition of long non-coding RNA HOXA11-AS against neuroinflammation in Parkinson's disease model via targeting miR-124-3p mediated FSTL1/NF-κB axis.	BACKGROUND: Studies have revealed that lncRNA HOXA11-AS contributes to regulating inflammation, while the role of HOXA11-AS in Parkinson's disease (PD) remains unclear. METHODS: Both in vivo and in vitro PD models were induced. Gain- or loss-assays of HOXA11-AS and miR-124-3p were conducted. The neurological functions, dopaminergic neurons damage, microglia activation of PD mice were measured. Afterwards, the expressions of inflammatory factors were examined with RT-PCR. Western blot was employed to detect the level of FSTL1, NF-κB and NLRP3 inflammasome. Meanwhile, bioinformatics analysis and dual-luciferase reporter assay were utilized to confirm the targeting relationships among miR-124-3p, HOXA11-AS and FSTL1. RESULTS: HOXA11-AS promoted MPTP-mediated SH-SY5Y neuronal injury and LPS-induced microglia activation, while miR-124-3p had the opposite effects. Additionally, miR-124-3p was the target of HOXA11-AS and FSTL1. HOXA11-AS overexpression enhanced the expression of inflammatory factors and FSTL1, NF-κB and NLRP3 inflammasome, while inhibiting NF-κB weakened HOXA11-AS-mediated neuronal damage and microglia activation. Moreover, HOXA11-AS1 downregulation ameliorated MPTP-induced neurological damages and neuroinflammation in mice. CONCLUSION: Inhibition of HOXA11-AS protects mice against PD through repressing neuroinflammation and neuronal apoptosis through miR-124-3p-FSTL1-NF-κB axis.	NA	Aging (Albany NY). 2021 Apr 4;13(8):11455-11469. doi: 10.18632/aging.202837. Epub 2021 Apr 4.
4697	LncRNA	HOXA11-AS	miR-124-3p	NLRP3	microglia	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Western blot;Luciferase reporter assay;	33839699	Inhibition of long non-coding RNA HOXA11-AS against neuroinflammation in Parkinson's disease model via targeting miR-124-3p mediated FSTL1/NF-κB axis.	BACKGROUND: Studies have revealed that lncRNA HOXA11-AS contributes to regulating inflammation, while the role of HOXA11-AS in Parkinson's disease (PD) remains unclear. METHODS: Both in vivo and in vitro PD models were induced. Gain- or loss-assays of HOXA11-AS and miR-124-3p were conducted. The neurological functions, dopaminergic neurons damage, microglia activation of PD mice were measured. Afterwards, the expressions of inflammatory factors were examined with RT-PCR. Western blot was employed to detect the level of FSTL1, NF-κB and NLRP3 inflammasome. Meanwhile, bioinformatics analysis and dual-luciferase reporter assay were utilized to confirm the targeting relationships among miR-124-3p, HOXA11-AS and FSTL1. RESULTS: HOXA11-AS promoted MPTP-mediated SH-SY5Y neuronal injury and LPS-induced microglia activation, while miR-124-3p had the opposite effects. Additionally, miR-124-3p was the target of HOXA11-AS and FSTL1. HOXA11-AS overexpression enhanced the expression of inflammatory factors and FSTL1, NF-κB and NLRP3 inflammasome, while inhibiting NF-κB weakened HOXA11-AS-mediated neuronal damage and microglia activation. Moreover, HOXA11-AS1 downregulation ameliorated MPTP-induced neurological damages and neuroinflammation in mice. CONCLUSION: Inhibition of HOXA11-AS protects mice against PD through repressing neuroinflammation and neuronal apoptosis through miR-124-3p-FSTL1-NF-κB axis.	NA	Aging (Albany NY). 2021 Apr 4;13(8):11455-11469. doi: 10.18632/aging.202837. Epub 2021 Apr 4.
4698	LncRNA	HOXA-AS2	miR-885-5p	RBBP4	glioblastoma tissues and cells	Glioblastoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;luciferase assay;RNA pull-down;	33430870	LncRNA HOXA-AS2 promotes glioblastoma carcinogenesis by targeting miR-885-5p/RBBP4 axis.	BACKGROUND: LncRNA HOXA-AS2 has been found in the literature to deteriorate glioblastoma. However, its regulatory mechanism is yet to be fully investigated. Our study focused chiefly on the interaction and role of the HOXA-AS2/miR-885-5p/RBBP4 axis in the development of glioblastoma. METHODS: qRT-PCR analysis was performed to detect the expression of lncRNA, miRNA and mRNA in glioblastoma tissues and cells. Dual-luciferase assay, RIP assay and RNA pull-down assay were later carried out to reveal the interactions among HOXA-AS2, miR-885-5p and RBBP4. After that, CCK-8 assay, BrdU assay, nude mice xenografting assay, western blot assay, and flow cytometry were carried out to analyze the effect of the HOXA-AS2/miR-885-5p/RBBP4 axis on glioblastoma samples. RESULTS: HOXA-AS2 and RBBP4 were found to be overexpressed in glioblastoma. Experimental results showed that HOXA-AS2 and RBBP4 contributed to the tumorigenesis of glioblastoma cells. However, miR-885-5p was observed to be downregulated in glioblastoma. Findings also indicated that HOXA-AS2 could negatively regulate miR-885-5p, thereby enhancing RBBP4 expression. CONCLUSION: Overall, HOXA-AS2 promoted the tumorigenesis of glioblastoma by targeting and regulating miR-885-5p to induce the expression of RBBP4.	NA	Cancer Cell Int. 2021 Jan 11;21(1):39. doi: 10.1186/s12935-020-01690-1.
4699	Circular RNA	hsa_circ_0075960	miR-361-3	SH2B1	EC cells	Endometrial Cancer	Homo sapiens (human)	qRT-PCR	33356989	Hsa_circ_0075960 Serves as a Sponge for miR-361-3p/SH2B1 in Endometrial Carcinoma.	Although the cases of endometrial carcinoma (EC) is gradually increasing across the world, its etiology and pathogenesis remain unknown. The present study is the first to define the role and biological function of circRNA hsa_circ_0075960 in the development and progression of EC. We first determined that hsa_circ_0075960 is aberrantly expressed in EC cells. Then, we uncovered that the downregulation of hsa_circ_0075960 suppressed cell proliferation and promoted cell apoptosis of EC cells, suggesting that hsa_circ_0075960 could inhibit the progression of EC in vitro. In addition, we identified that miR-361-3p was the direct target of hsa_circ_0075960. Further analysis revealed that hsa_circ_0075960 affected the development of EC via sponging miR-361-3p. Interestingly, we verified that the level of SH2B1 was controlled by the downregulation of hsa_circ_0075960 and that the negative effect caused by hsa_circ_0075960 could be reversed via miR-361-3p inhibition. Our cumulative results revealed that the novel tumor regulator hsa_circ_0075960 functioned as a sponge for miR-361-3p/SH2B1 in EC cells and regulated the progression of EC through the modulation of miR-361-3p.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820983079. doi: 10.1177/1533033820983079.
4700	LncRNA	KCNQ1OT1	miR-148a-3p	IGF1R	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33349156	Long Non-Coding RNA KCNQ1OT1 Promotes Progression of Hepatocellular Carcinoma by miR-148a-3p/IGF1R Axis.	Accumulating evidence have suggested that long non-coding RNAs (lncRNAs) act as a critical regulator in tumorgenesis. LncRNA KCNQ1OT1 (KCNQ1OT1) has been recently shown to be dysregulated in many cancers. This study was aimed to explore the biological role of KCNQ1OT1 in hepatocellular carcinoma (HCC). In our study, we first observed the expression level of KCNQ1OT1 was distinctly up-regulated in HCC tissues and cell lines compared with adjacent non-cancer tissues and normal liver cell line. And clinical results indicated that higher expression of KCNQ1OT1 was correlated with poor prognosis of patients with HCC. Next, functional studies revealed that knockdown of KCNQ1OT1 induced apoptosis and repressed proliferation, migration and invasion of HCC cells. In addition, knockdown of KCNQ1OT1 suppressed xenograft tumor growth in vivo. Mechanically, we found that KCNQ1OT1 can promote the expression of IGF1R by functioning as a competing endogenous RNA of miR-148a-3p. In conclusion, our results shown the oncogenic role of KCNQ1OT1 in HCC by regulating the miR-148a-3p/IGF1R axis and may provide a new insight and a potential therapeutic target for HCC.	NA	Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820980117. doi: 10.1177/1533033820980117.
4701	LncRNA	KCNQ1OT1	miR-211-5p	TCF4	osteoarthritis cells	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;MTT assay;RACE;Western blot;Luciferase reporter assay;MTT assay;	33747189	Knockdown of long non-coding RNA KCNQ1OT1 suppresses the progression of osteoarthritis by mediating the miR-211-5p/TCF4 axis in vitro.	Numerous studies have reported the critical roles of long non-coding RNAs (lncRNAs) in the regulation of osteoarthritis (OA) development. The present study aimed to assess the function and regulatory mechanism of a lncRNA, KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), in OA in vitro. C28/I2 cells were treated with lipopolysaccharide (LPS) to generate an in vitro OA model. The relative expression levels of KCNQ1OT1, microRNA (miR)-211-5p and transcription factor 4 (TCF4) were determined via reverse transcription-quantitative polymerase chain reaction. The associations between KCNQ1OT1, miR-211-5p and TCF4 were confirmed using a dual-luciferase reporter assay. Furthermore, cell viability was assessed using the MTT assay. Inflammatory cytokine levels were measured using ELISA. The protein expression levels of matrix metalloproteinase-3/13, collagen II/X and TCF4 were detected by western blotting. KCNQ1OT1 and TCF4 were highly expressed in the cartilage tissues of patients with OA and C28/I2 cells treated with LPS (OA cells), whereas miR-211-5p was downregulated concomitantly in OA tissues and cells. Knockdown of KCNQ1OT1 stimulated cell viability, and suppressed the inflammation and degradation of the extracellular matrix (ECM) in OA cells. In addition, overexpression of miR-211-5p stimulated cell viability, and inhibited inflammation and degradation of the ECM in OA cells. Notably, miR-211-5p was revealed to be the target of, and was negatively regulated by, KCNQ1OT1. TCF4 was targeted and negatively modulated by miR-211-5p. Transfection of cells with the miR-211-5p inhibitor or pcDNA-TCF4 reversed the suppressive effects of short hairpin RNA (sh)-KCNQ1OT1 on inflammation and ECM degradation, as well as the promotive effect of sh-KCNQ1OT1 on viability in OA in vitro. Therefore, KCNQ1OT1 may regulate the miR-211-5p/TCF4 axis to ameliorate OA in vitro.	NA	Exp Ther Med. 2021 May;21(5):455. doi: 10.3892/etm.2021.9886. Epub 2021 Mar 1.
4702	LncRNA	Kcnq1ot1	miR-486a-3p	NLRP3	Podocytes	Chronic Renal Diseases	Homo sapiens (human)	qRT-PCR	33296289	Long noncoding RNA Kcnq1ot1 promotes sC5b-9-induced podocyte pyroptosis by inhibiting miR-486a-3p and upregulating NLRP3.	Podocytes are epithelial cells adhering glomerular capillaries, which regulate the integrity of glomerular filtration barrier. Irreversible podocyte injury induces glomerular inflammation and causes chronic renal diseases. Kcnq1ot1, a long noncoding RNA, participates in the pathogenesis of diabetic retinopathy and cardiomyopathy. However, its function in podocyte injury is elusive. Pyroptosis of murine podocyte MPC5 was triggered by sublytic complement C5b-9 (sC5b-9) for subsequent in vitro functional and mechanistic investigation. Gain/loss-of-function analysis was conducted to examine the functional role of Kcnq1ot1 in podocyte pyroptosis. Meanwhile, the molecular mechanism of Kcnq1ot1's effect on podocyte injury was explored by identifying downstream molecules and their intermediate interactions. Kcnq1ot1 was upregulated in sC5b-9-induced podocytes, and silencing Kcnq1ot1 could inhibit sC5b-9's effect on podocyte pyroptosis. We also identified the interaction between Kcnq1ot1 and miR-486a-3p, through which Kcnq1ot1 mediated miR-486a-3p inhibition by sC5b-9. Furthermore, miR-486a-3p reduced the transcriptional activity of NLRP3, while the overexpression of NLRP3 enhanced sC5b-9's effect on podocyte pyroptosis through activating NLRP3 inflammasome. sC5b-9 induces pyroptosis in podocytes through modulating the Kcnq1ot1/miR-486a-3p/NLRP3 regulatory axis, and these uncovered key molecules might facilitate podocyte-targeted treatment for renal inflammatory diseases.	NA	Am J Physiol Cell Physiol. 2021 Mar 1;320(3):C355-C364. doi: 10.1152/ajpcell.00403.2020. Epub 2020 Dec 9.
4703	LncRNA	KCNQ1OT1	miR-124	SP1	retinoblastoma cells	Retinoblastoma	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33345272	KCNQ1OT1 regulates the retinoblastoma cell proliferation, migration and SIRT1/JNK signaling pathway by targeting miR-124/SP1 axis.	OBJECTIVE: Long non-coding RNA (lncRNA) KCNQ1OT1 was reported to be tightly associated with tumorigenesis and progression of multiple cancers. However, the expression and biological functions of KCNQ1OT1 in retinoblastoma (RB) are still unknown. We aim to elucidate the potential function and underlying mechanism of KCNQ1OT1 in regulating the progression of RB. METHODS: The levels of KCNQ1OT1 were assayed by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) analysis. The cell proliferation of RB cells (Y79 and WERI-Rb-1) were evaluated through Cell Counting Kit 8 (CCK-8) assay. Meanwhile, Y79 and WERI-Rb-1 cell apoptosis and cell cycle were assessed by Flow Cytometry analysis. Dual luciferase reporter assay were performed to illustrate the interaction between KCNQ1OT1, miR-124, and SP1. RESULTS: We found that KCNQ1OT1 was up-regulated and miR-124 was down-regulated in RB tissues and cells. Moreover, knockdown of KCNQ1OT1 reduced the proliferation, migration, and cell cycle, as well as promoted cell apoptosis of Y79 and WERI-Rb-1 cells. Western blot analysis consistently proved cell cycle and apoptosis related protein expression levels. More importantly, KCNQ1OT1 was a sponge of microRNA (miR)-124. MiR-124 inhibition strongly reversed the effect on cell proliferation, cycle arrest, and apoptosis by KCNQ1OT1 knockdown mediation. In addition, KCNQ1OT1 regulated expression of SP1, a direct target of miR-124 in RB. On the other hand, miR-124 inhibitor abrogated the active effect of KCNQ1OT1 silencing on silent information regulator 1 (SIRT1)/c-Jun N-terminal kinase (JNK) signaling pathway. The function of KCNQ1OT1 was verified in vivo. CONCLUSIONS: These findings implied that KCNQ1OT1 silencing inhibited RB progression and activated SIRT1/JNK signaling pathway partially by modulating the miR-124/SP1 axis.	NA	Biosci Rep. 2021 Jan 29;41(1):BSR20201626. doi: 10.1042/BSR20201626.
4704	LncRNA	KCNQ1OT1	miR-216b-5p	ZNF146	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	33394291	LncRNA KCNQ1OT1 acts as miR-216b-5p sponge to promote colorectal cancer progression via up-regulating ZNF146.	Long non-coding RNAs (lncRNAs) have shown to act as important regulators in cancer biology. The aim of this study was to investigate the role and mechanism of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in colorectal cancer (CRC) progression. The abundance of KCNQ1OT1, microRNA-216b-5p (miR-216b-5p) and zinc finger protein 146 (ZNF146) messenger RNA (mRNA) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell migration and invasion abilities were assessed by transwell assays. Western blot assay was performed for determination of protein levels. LncBase v.2 of DIANA Tool and StarBase software were used to predict the targets of KCNQ1OT1 and miR-216b-5p, respectively. Dual-luciferase reporter assay was implemented to confirm the target interaction between miR-216b-5p and KCNQ1OT1 or ZNF146. KCNQ1OT1 expression was higher in CRC tissues and cell lines. KCNQ1OT1 interference restrained the proliferation, migration and invasion of CRC cells. MiR-216b-5p was a target of KCNQ1OT1 in CRC cells, and KCNQ1OT1 knockdown-induced effects in CRC cells were partly overturned by miR-216b-5p silencing. MiR-216b-5p bound to the 3' untranslated region (3'UTR) of ZNF146, and ZNF146 overexpression partly attenuated miR-216b-5p overexpression-mediated influences in CRC cells. KCNQ1OT1 up-regulated the abundance of ZNF146 through sequestering miR-216b-5p in CRC cells. KCNQ1OT1 accelerated the proliferation and motility of CRC cells through elevating ZNF146 expression via sponging miR-216b-5p. KCNQ1OT1/miR-216b-5p/ZNF146 axis might be underlying target for the diagnosis and treatment of CRC patients.	NA	J Mol Histol. 2021 Jun;52(3):479-490. doi: 10.1007/s10735-020-09942-0. Epub 2021 Jan 4.
4705	LncRNA	KCNQ1OT1	miR-29a-3p	CBX3	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34008749	lncRNA KCNQ1OT1 reverses the effect of sevoflurane on hepatocellular carcinoma progression via regulating the miR-29a-3p/CBX3 axis.	Sevoflurane (SEVO) is widely applied as an anesthetic, which exerts antitumor capacity in various cancers, including hepatocellular carcinoma (HCC). Previous studies indicated that long non-coding RNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) was upregulated, while microRNA-29a-3p (miR-29a-3p) was downregulated in HCC. Thus, we aimed to explore the roles of KCNQ1OT1 and miR-29a-3p in HCC cells exposed to SEVO. Cell proliferation, apoptosis, migration, and invasion were assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, and transwell assays, respectively. The levels of genes were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Furthermore, the interaction between miR-29a-3p and KCNQ1OT1 or chromebox protein homolog 3 (CBX3) was predicted by Starbase or Targetscan, and then confirmed by dual-luciferase reporter assay. We found that the levels of KCNQ1OT1 and CBX3 were decreased, while miR-29a-3p was increased in SEVO-treated HCC cells. KCNQ1OT1 overexpression weakened the inhibitory effects of SEVO on HCC cell proliferation, apoptosis, migration, and invasion. Interestingly, KCNQ1OT1 bound to miR-29a-3p, and miR-29a-3p targeted CBX3. KCNQ1OT1 upregulated CBX3 level by repressing miR-29a-3p expression. Furthermore, KCNQ1OT1 exerted tumor promotion in HCC cells via suppressing miR-29a-3p to regulate CBX3 expression. Collectively, our findings demonstrated that KCNQ1OT1 regulated the antitumor effects of SEVO on HCC cells through modulating the miR-29a-3p/CBX3 axis, providing a theoretical basis for the treatment of HCC.	NA	Braz J Med Biol Res. 2021 May 17;54(7):e10213. doi: 10.1590/1414-431X2020e10213. eCollection 2021.
4706	LncRNA	LIFR-AS1	miR-4698	MTUS1	gastric carcinoma tissues and cells	Gastric Cancer	Homo sapiens (human)	Western blot;	33355363	lncRNA LIFR-AS1 inhibits gastric carcinoma cell proliferation, migration and invasion by sponging miR-4698.	The vital functions of long non-coding (lnc)RNAs have been verified in gastric carcinoma (GC). However, as a novel cancer-related lncRNA, the influence of leukemia inhibitory factor receptor antisense RNA 1 (LIFR-AS1) in GC cell biological behaviors remains unreported. The present study explored the biological effects of lncRNA LIFR-AS1 on GC progression. Reverse transcription-quantitative PCR was performed to examine lncRNA LIFR-AS1 expression in GC tissues and cells. Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine incorporation, cell wound healing and Transwell invasion assays were used to assess the functions of lncRNA LIFR-AS1 in GC cell proliferation, migration and invasion. Additionally, associations among lncRNA LIFR-AS1, microRNA (miR)-4698 and microtubule-associated tumor suppressor 1 (MTUS1) were investigated via bioinformatics software and a luciferase reporter system. In addition, western blotting was used to examine the expression of MEK and ERK. Decreased lncRNA LIFR-AS1 expression was observed in GC tissues and cells. Upregulated lncRNA LIFR-AS1 inhibited GC cell proliferation, migration and invasion. Upregulated miR-4698 and downregulated MTUS1 were identified in GC tissues and cells. The inhibitory interaction between lncRNA LIFR-AS1 and miR-4698 was confirmed. Additionally, MTUS1 was predicted as a target gene of miR-4698 positively regulated by lncRNA LIFR-AS1. The MEK/ERK pathway was inhibited by lncRNA LIFR-AS1 via regulating MTUS1. These findings revealed the inhibitory functions of lncRNA LIFR-AS1 in GC cell proliferation, migration and invasion. The process was mediated via miR-4698, MTUS1 and the MEK/ERK pathway.	NA	Mol Med Rep. 2021 Feb;23(2):153. doi: 10.3892/mmr.2020.11792. Epub 2020 Dec 23.
4707	LncRNA	LINC00052	miR-145-5p	TGFBR2	breast cancer cells	Breast Cancer	Homo sapiens (human)	Western blot;	33777194	LINC00052 promotes breast cancer cell progression and metastasis by sponging miR-145-5p to modulate TGFBR2 expression.	Long non-coding RNAs (lncRNAs) may participate in biological regulatory mechanisms of tumors. The aim of the present study was to uncover the molecular mechanism of the lncRNA LINC00052 in the tumorigenesis of breast cancer (BC). LINC00052 expression in BC tissues and cell lines was detected by reverse transcription-quantitative PCR analysis. The Cell Counting Kit-8, proliferation, Transwell and wound healing assays were employed to confirm the effect of LINC00052 on cell proliferation, migration and invasion. The cell localization of LINC00052 was estimated by cytoplasmic nuclear separation assay. Finally, the potential regulatory mechanism of LINC00052 in BC was detected by western blot analysis. The expression levels of LINC00052 were found to be significantly higher in BC tissues compared with those in the adjacent normal tissues. Downregulation of LINC00052 expression in vitro significantly suppressed the proliferation, migration and invasion of BC cells. LINC00052 was mainly expressed in the cytoplasm and was considered to bind with microRNA (miR)-145-5p based on various databases. Notably, the high expression levels of LINC00052 led to the low expression levels of miR-145-5p and high expression levels of TGF-β receptor II (TGFBR2). In conclusion, the findings of the present study demonstrated that LINC00052 may sponge miR-145-5p to upregulate TGFBR2 expression in order to promote the proliferation and metastasis of BC cells. Therefore, LINC00052 may be an effective potential target for the diagnosis and treatment of BC.	NA	Oncol Lett. 2021 May;21(5):368. doi: 10.3892/ol.2021.12629. Epub 2021 Mar 11.
4708	LncRNA	LINC00184	miR-145	ANGPT2	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	RT-PCR;Western blot;RNA sequencing;	33758610	LINC00184 involved in the regulatory network of ANGPT2 via ceRNA mediated miR-145 inhibition in gastric cancer.	Background: Disrupted gene levels are intimately correlated with the occurrence and prognosis of gastric cancer (GC). As genes do not function in isolation, we set out to investigate the possible relationship among mRNA and non-coding RNAs (ncRNAs). Materials and methods: RNA sequencing from 406 cases of GC was acquired through the TCGA database. R packages were utilized to assess differential RNA expression. The competing endogenous RNA (ceRNA) network was predicted using miRcode, miRDB, mirTarBase, Target Scan and constructed by Cytoscape 3.6.1. GO enrichment analysis, KEGG pathway analysis, GSEA, and WGCNA were applied for pathway analysis. The expression of select candidate molecules was confirmed using western blot and RT-PCR in GC cells and tissues. CCK-8, EdU staining, and Transwell assays were conducted to assess the influence of candidate molecules on proliferation and invasion. The gain and loss-of-function were achieved by co-culture with sh-lncRNA, mimics and sh-mRNA. Luciferase reporters were created using the psiCHECK2 vector, and the relative luciferase activity was calculated. Results: Using data from TCGA, we determined differentially expressed RNAs and created a ceRNA regulatory network. Interestingly, we identified a regulatory complex surrounding ANGPT2. We detected that ANGPT2 was highly expressed in GC, which correlated with a worse prognosis. Our findings indicated that ANGPT2 encourages growth, invasion, and epithelial-mesenchymal transition (EMT) in GC. Importantly, miR-145 inhibits ANGPT2 and abrogates its effects. Furthermore, LINC00184, a ceRNA, blocks miR-145, thereby improving ANGPT2-mediated carcinogenesis. Conclusions: Our findings indicate that the LINC00184/miR-145/ANGPT2 pathway has a crucial function in the development of GC and can act as a possible biomarker and targets for GC therapy.	NA	J Cancer. 2021 Feb 22;12(8):2336-2350. doi: 10.7150/jca.49138. eCollection 2021.
4709	LncRNA	LINC00240	miR-7-5p	EGFR	lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	microarray;qRT-PCR;	33422052	LncRNA LINC00240 suppresses invasion and migration in non-small cell lung cancer by sponging miR-7-5p.	BACKGROUND: lncRNAs have important roles in regulating cancer biology. Accumulating evidence has established a link between the dysregulation of lncRNAs and microRNA in cancer progression. In previous studies, miR-7-5p has been found to be significantly down-regulated in mesenchymal-like lung cancer cell lines and directly regulated EGFR. In this work, we investigated the lncRNA partner of miR-7-5p in the progression of lung cancer. METHODS: We investigated the expression of miR-7-5p and the lncRNA after transfection with an miR-7-5p mimics using a microarray. The microarray results were validated using quantitative real time-polymerase Chain Reaction (qRT-PCR). The regulatory effects of lncRNA on miR-7-5p and its target were evaluated by changes in the expression of miR-7-5p after transfection with siRNAs for lncRNA and the synthesis of full-length lncRNA. The effect of miR-7-5p on lncRNA and the miRNA target was evaluated after transfection with miRNA mimic and inhibitor. The role of lncRNA in cancer progression was determined using invasion and migration assays. The level of lncRNA and EGFR in lung cancer and normal lung tissue was analyzed using TCGA data. RESULTS: We found that LINC00240 was downregulated in lung cancer cell line after miR-7-5p transfection with an miR-7-5p mimic. Further investigations revealed that the knockdown of LINC00240 induced the overexpression of miR-7-5p. The overexpression of miR-7-5p diminished cancer invasion and migration. The EGFR expression was down regulated after siRNA treatment for LINC00240. Silencing LINC00240 suppressed the invasion and migration of lung cancer cells, whereas LINC00240 overexpression exerted the opposite effect. The lower expression of LINC00240 in squamous lung cancer was analyzed using TCGA data. CONCLUSIONS: Taken together, LINC00240 acted as a sponge for miR-7-5p and induced the overexpression of EGFR. LINC00240 may represent a potential target for the treatment of lung cancer.	NA	BMC Cancer. 2021 Jan 9;21(1):44. doi: 10.1186/s12885-020-07755-8.
4710	LncRNA	LINC00319	miR-200a-3p	caspase3	neuronal cells	Ischemic Stroke	Homo sapiens (human)	qRT-PCR	34149890	Upregulated LINC00319 aggravates neuronal injury induced by oxygen-glucose deprivation via modulating miR-200a-3p.	Ischemic stroke is one of the main causes of physical disability and mortality worldwide. Long non-coding RNAs (lncRNAs) are reported to be dysregulated in various biological progressions and serve important roles in pathological processes of cerebral ischemia. However, their biological actions and potential mechanisms in the progression of ischemic stroke remain unknown. The present study aimed to investigate the functions of LINC00319 on ischemic brain injury. It was identified that LINC00319 was significantly upregulated in the Gene Expression Omnibus profile of ischemic stroke. Furthermore, LINC00319 overexpression elevated caspase-3 activity and increased the apoptotic rate of neuronal cells, as well as decreased cell viability and glucose uptake. It was also demonstrated that LINC00319 participated in oxygen-glucose deprivation (OGD)-induced cerebral ischemic injury. LINC00319 could competitively bind with microRNA (miR)-200a-3p and decrease its expression. Moreover, miR-200a-3p could partly offset the negative effects of LINC00319 overexpression on neuronal injury caused by OGD. Collectively, the present results suggested that LINC00319 promoted apoptosis and aggravated neuronal injury induced by OGD by regulating miR-200a-3p, which may be important for ischemic stroke treatment.	NA	Exp Ther Med. 2021 Aug;22(2):844. doi: 10.3892/etm.2021.10276. Epub 2021 Jun 7.
4711	LncRNA	LINC00342	miR-19a-3p	NPEPL1	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	RT-PCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33588834	LncRNA LINC00342 contributes to the growth and metastasis of colorectal cancer via targeting miR-19a-3p/NPEPL1 axis.	BACKGROUND: Long intergenic non-protein coding RNA 00342 (LINC00342) has been identified as a novel oncogene. However, the functional role of LINC00342 in colorectal cancer (CRC) remains unclear. METHODS: The expression of LINC00342 is detected by real-time PCR (RT-PCR) analysis. Cell proliferation, migration and invasion and xenograft model are examined to analyze the biological functions of LINC00342 in vitro and in vivo using colony formation, would healing and transwell analyses. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays are used to identify the target interactions between LINC00342, miR-19a-3p and aminopeptidase like 1 (NPEPL1). RESULTS: LINC00342 was highly expressed in CRC. Down-regulation of LINC00342 inhibited cell proliferation and metastasis of CRC cells. Moreover, knocking down LINC00342 inhibited the tumor growth in vivo. Mechanistic investigation revealed that LINC00342 might sponge miR-19a-3p to regulate NPEPL1 expression. Further investigation indicated that the ontogenesis facilitated by LINC00342 was inhibited due to the depletion of NPEPL1. CONCLUSION: LINC00342 promotes CRC progression by competitively binding miR-19a-3p with NPEPL1.	NA	Cancer Cell Int. 2021 Feb 15;21(1):105. doi: 10.1186/s12935-020-01705-x.
4712	LncRNA	LINC00461	miR-518a-3p	WDR1	Non small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;	33233986	Long-noncoding RNA LINC00461 promotes proliferation and invasion of Non small cell lung cancer cells via targeting miR-518a-3p/WDR1 pathway.	Long noncoding RNAs (lncRNAs) are a class of RNAs participating in many biological processes such as imprinting, alternative splicing and RNA decay. Recently, lncRNAs have drawn a great deal of attention for their critical role in cancer progression. LINC00461, a newly identified lncRNA, has been reported to be significantly overexpressed in breast cancer and markedly expedited breast cancer progression. However, the specific role of LINC00461 in Non small cell lung cancer (NSCLC) remains unknown. In this study, we for the first time showed the biological functions of LINC00461 in NSCLC. Our results demonstrated that LINC00461 was significantly up-regulated in NSCLC tissues and cell lines. Furthermore, knockdown of LINC00461 inhibited NSCLC cell proliferation and invasion in vitro as well as suppressed tumor growth and metastasis in vivo. We also performed luciferase reporter assays and found that LINC00461 functioned as a sponge for miR-518a-3p and WDR1 was a target of miR-518a-3p. Taken together, we suggested an essential role of LINC00461/miR-518a-3p/WDR1 axis in NSCLC, which could be used as a potential therapeutic target for NSCLC treatment.	NA	J Recept Signal Transduct Res. 2020 Nov 24:1-8. doi: 10.1080/10799893.2020.1850786.
4713	LncRNA	LINC00466	miR-137	PPP1R14B	glioma cells	Glioma	Homo sapiens (human)	qRT-PCR;RIP assay;	33642868	LINC00466 Impacts Cell Proliferation, Metastasis and Sensitivity to Temozolomide of Glioma by Sponging miR-137 to Regulate PPP1R14B Expression.	PURPOSE: LINC00466 is a newfound long non-coding RNA (lncRNA) that has been rarely explored in cancers. However, the specific role and molecular mechanism of LINC00466 in glioma remain to be further elucidated. METHODS: Bioinformatic analysis was used to screen differentially expressed genes. Quantitative real-time PCR (qRT-PCR) was used to determine the expression of LINC00466, microRNA-137 (miR-137) and protein phosphatase 1 regulatory subunit 14B (PPP1R14B). Dual-luciferase reporter gene assay and RNA binding protein Immunoprecipitation (RIP) assays were employed to verify the binding relationship among LINC00466, miR-137 and PPP1R14B. The sensitivity of glioma cells to temozolomide (TMZ) was measured by cell counting kit-8 (CCK8) assay. The xenograft nude models were used to test the effects of LINC00466 on glioma tumor growth in vivo. RESULTS: Highly expressed LINC00466 and PPP1R14B and lowly expressed miR-137 were eventually revealed in glioma tissues. Overexpression of LINC00466 could promote proliferation, metastasis and drug sensitivity to TMZ of glioma cells. LINC00466 could bind to miR-137, and up-regulation of miR-137 could attenuate the enhancing effects caused by LINC00466 overexpression. We took a further step and found that miR-137 could bind to PPP1R14B. Besides, LINC00466 could function as a sponge to miR-137 to regulate PPP1R14B. In addition, overexpression of LINC00466 could promote tumor growth in vivo. CONCLUSION: These findings validate LINC00466 could restrain the miR-137 expression to up-regulate PPP1R14B and therefore promote proliferation, metastasis and resistance to TMZ of glioma.	NA	Onco Targets Ther. 2021 Feb 19;14:1147-1159. doi: 10.2147/OTT.S273264. eCollection 2021.
4714	LncRNA	LINC00466	miR-493	HMGA2	tongue squamous cell carcinoma cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)	qRT-PCR	33376400	Long Non-Coding RNA LINC00466 Knockdown Inhibits Tongue Squamous Cell Carcinoma Malignancy by Targeting microRNA-493/HMGA2.	PURPOSE: Long intergenic non-protein-coding RNA 00466 (LINC00466) promotes lung adenocarcinoma progression. Nonetheless, the expression and precise roles of LINC00466 in tongue squamous cell carcinoma (TSCC) remains uncertain and warrant further investigation. Hence, the present study aimed to examine the LINC00466 effects on the aggressive TSCC cell characteristics and to elucidate the potential underlying mechanisms. METHODS: First, LINC00466 expression in TSCC was determined by reverse transcription-quantitative PCR. Subsequently, cell proliferation, apoptosis, migration, and invasion in vitro, as well as tumor growth in vivo were assessed to examine the LINC00466 effects on TSCC cells. RESULTS: LINC00466 was upregulated in TSCC. This upregulation was notably associated with shorter overall TSCC patient survival. In vitro experiments indicated that LINC00466 depletion suppressed TSCC cell proliferation, migration and invasion, and promoted apoptosis. An in vivo experiment revealed that LINC00466 downregulation attenuated TSCC tumor growth in vivo. Mechanistic analysis revealed that LINC00466 functions as a microRNA-493 (miR-493) molecular sponge, a miRNA that targets high-mobility group AT-hook 2 (HMGA2) mRNA. LINC00466 upregulated HMGA2 in TSCC cells, and this phenomenon was regulated by the miR-493 sponge. Rescue experiments revealed a decrease in the miR-493/HMGA2 axis output, partially reversing the effects of LINC00466 downregulation on aggressive TSCC cell behavior. CONCLUSION: These findings demonstrate that LINC00466 promotes TSCC cell oncogenicity in vitro and in vivo by upregulating the miR-493/HMGA2 axis output. These results may provide a new perspective and new insight into the molecular mechanisms of TSCC.	NA	Cancer Manag Res. 2020 Dec 22;12:13071-13084. doi: 10.2147/CMAR.S282625. eCollection 2020.
4715	LncRNA	LINC00467	miR-217	KPNA4	Osteosarcoma tissues and cells	Osteosarcoma	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33537823	LINC00467 facilitates osteosarcoma progression by sponging miR-217 to regulate KPNA4 expression.	Osteosarcoma (OS) is a musculoskeletal malignancy that originates from interstitial cells. An increasing number of studies have verified that long non-coding RNAs (lncRNAs) participate in the progression of numerous types of cancer. It has been reported that LINC00467 is a cancer-promoting gene in some types of cancer; however, the regulatory mechanism of LINC00467 in OS remains unknown. In the present study, reverse transcription-quantitative PCR was used to determine LINC00467 expression in OS tissues and cells. Additionally, the impact of LINC00467-knockdown on OS cell proliferation, migration and invasion was analyzed using Cell Counting Kit-8, colony formation and Transwell assays, as well as western blot analysis. RNA pulldown and luciferase reporter assays were conducted to investigate the regulatory mechanism of LINC00467 in OS. The results delineated that LINC00467 expression was elevated in OS tissues and cells, and that high LINC00467 expression was associated with a poor prognosis in patients with OS. LINC00467 inhibition suppressed OS progression by inhibiting cell proliferation, migration, invasion and epithelial-mesenchymal transition. LINC00467 served as a molecular sponge for microRNA (miR)-217, while karyopherin subunit α4 (KPNA4) was a downstream target gene of miR-217. Moreover, the overexpression of KPNA4 reversed the inhibitory effects of LINC00467 inhibition on OS progression. Therefore, the present study elucidated the potential mechanism of LINC00467 in OS and indicated that LINC00467 exerted its carcinogenic effects on OS through the miR-217/KPNA4 axis, implying that LINC00467 may be a novel potential therapeutic target for OS.	NA	Int J Mol Med. 2021 Mar;47(3):26. doi: 10.3892/ijmm.2021.4859. Epub 2021 Feb 4.
4716	LncRNA	LINC00525	miR-31-5p	NA	spinal chordoma cells	Spinal Chordoma	Homo sapiens (human)	qRT-PCR;	33370717	Long non-coding RNA LINC00525 interacts with miR-31-5p and miR-125a-5p to act as an oncogenic molecule in spinal chordoma.	LINC00525 is a new-researched long non-coding RNA (lncRNA) in a few cancers. This study aims at researching the function of LINC00525 in spinal chordoma and the underlying mechanism of action. LINC00525, microRNA-31-5p (miR-31-5p) and microRNA-125a-5p (miR-125a-5p) detection was performed by quantitative real-time polymerase chain reaction (qRT-PCR). We found the high expression of LINC00525 but the low levels of miR-31-5p and miR-125a-5p in spinal chordoma tissues. After LINC00525 was downregulated in spinal chordoma cells, there were inhibitory effects on cell proliferation, migration, invasion and EMT but a promoting effect on cell apoptosis. MiR-31-5p and miR-125a-5p were the downstream targets of LINC00525. The function of LINC00525 knockdown in spinal chordoma cells were achieved by upregulating miR-31-5p and miR-125a-5p. Tumorigenesis of spinal chordoma in vivo was also inhibited by knockdown of LINC00525 via the promotion of miR-31-5p and miR-125a-5p. All these results suggested that LINC00525 targeted miR-31-5p and miR-125a-5p to promote the tumorigenesis and progression of spinal chordoma. LINC00525 can be a novel molecular target in spinal chordoma.	NA	Biochem Biophys Res Commun. 2021 Jan 15;536:80-87. doi: 10.1016/j.bbrc.2020.12.042. Epub 2020 Dec 25.
4717	LncRNA	LINC00525	miR-125a-5p	NA	spinal chordoma cells	Spinal Chordoma	Homo sapiens (human)	qRT-PCR;	33370717	Long non-coding RNA LINC00525 interacts with miR-31-5p and miR-125a-5p to act as an oncogenic molecule in spinal chordoma.	LINC00525 is a new-researched long non-coding RNA (lncRNA) in a few cancers. This study aims at researching the function of LINC00525 in spinal chordoma and the underlying mechanism of action. LINC00525, microRNA-31-5p (miR-31-5p) and microRNA-125a-5p (miR-125a-5p) detection was performed by quantitative real-time polymerase chain reaction (qRT-PCR). We found the high expression of LINC00525 but the low levels of miR-31-5p and miR-125a-5p in spinal chordoma tissues. After LINC00525 was downregulated in spinal chordoma cells, there were inhibitory effects on cell proliferation, migration, invasion and EMT but a promoting effect on cell apoptosis. MiR-31-5p and miR-125a-5p were the downstream targets of LINC00525. The function of LINC00525 knockdown in spinal chordoma cells were achieved by upregulating miR-31-5p and miR-125a-5p. Tumorigenesis of spinal chordoma in vivo was also inhibited by knockdown of LINC00525 via the promotion of miR-31-5p and miR-125a-5p. All these results suggested that LINC00525 targeted miR-31-5p and miR-125a-5p to promote the tumorigenesis and progression of spinal chordoma. LINC00525 can be a novel molecular target in spinal chordoma.	NA	Biochem Biophys Res Commun. 2021 Jan 15;536:80-87. doi: 10.1016/j.bbrc.2020.12.042. Epub 2020 Dec 25.
4718	LncRNA	LINC00526	miR-5581-3p	BEX1	glioma tissues and cells	Glioma	Homo sapiens (human)	qRT-PCR	33613672	Long Noncoding RNA LINC00526 Represses Glioma Progression via Regulating miR-5581-3p/BEX1.	The roles of long noncoding RNAs (lncRNAs) in regulating glioma progression have been widely recognized in recent years. This work was to investigate the roles and associated mechanisms of LINC00526 in glioma progression. LINC00526 expression in glioma tissues and cells and their normal counterparts was measured with quantitative real-time polymerase chain reaction method. Functions of LINC00526 in glioma were investigated with in vitro experiments. Moreover, competitive RNA (ceRNA) theory was employed to understand mechanisms of action of LINC00526 in glioma. LINC00526 was found to be decreased in glioma tissues and cell lines compared with their normal counterparts. Silencing the expression of LINC00526 promotes, while forcing its expression, inhibits glioma cell growth and invasion. Mechanism analyses showed LINC00526 functions as a sponge for microRNA-5581-3p (miR-5581-3p) to regulate brain-expressed X-linked 1 (BEX1) expression and, in the end, affects glioma progression. Collectively, our study indicated LINC00526 serves as a tumor-suppressive lncRNA and directly regulates miR-5581-3p/BEX1 axis in glioma.	NA	J Oncol. 2021 Feb 4;2021:8171250. doi: 10.1155/2021/8171250. eCollection 2021.
4719	LncRNA	LINC00607	miR-607	E2F6	endothelial cells	Osteosarcoma	Homo sapiens (human)	RNA pull-down assay;RNA pull-down;	33585204	Silencing of Long Non-Coding RNA LINC00607 Prevents Tumor Proliferation of Osteosarcoma by Acting as a Sponge of miR-607 to Downregulate E2F6.	Osteosarcoma (OS), a type of malignant bone tumor, is commonly found in children and adolescents. Although previous studies have identified that long non-coding RNAs (lncRNAs) regulate OS, it is unclear whether lncRNAs impact the progression of OS. Here, we identified LINC00607, a lncRNA that facilitates OS proliferation, migration, and invasion. Based on the RNA-sequencing results, LINC00607 expression was significantly upregulated in pulmonary metastasis within OS. Functional experiments revealed that LINC00607 promoted migration and invasion of endothelial cells to exacerbate epithelial-mesenchymal transition (EMT). Furthermore, the results of RNA pull-down assay and invasion assay suggested that the binding between LINC00607 and miR-607 promoted OS invasion. Bioinformatic analysis and rescue experiments demonstrated that E2F6, a transcriptional factor, functioned downstream of LINC00607/miR-607. Finally, we found that LINC00607 promoted OS progression in vivo. This work revealed that LINC00607 worked as an miR-607 sponge to upregulate E2F6 expression, which promoted tumor proliferation in OS. These results identified a novel therapeutic target for treating OS.	NA	Front Oncol. 2021 Jan 28;10:584452. doi: 10.3389/fonc.2020.584452. eCollection 2020.
4720	LncRNA	LINC00659	miR-342-3p	ANXA2	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Western blot;	33407563	Exosomal LncRNA LINC00659 transferred from cancer-associated fibroblasts promotes colorectal cancer cell progression via miR-342-3p/ANXA2 axis.	BACKGROUND: Cancer-associated fibroblasts (CAFs) play a pivotal role in regulating tumor progression by transferring exosomes to adjacent cells. Our aim was to clarify the role of LINC00659 encapsulated in CAFs-derived exosomes (CAFs-exo) in colorectal cancer (CRC). METHODS: CAFs and normal fibroblasts (NFs) were isolated and cultured. CAFs-exo and NFs-derived exosomes (NFs-exo) were characterized by transmission electron microscope and Western blot. The mRNA level of LINC00659 in CAFs-exo and NFs-exo were measured. Then we analyzed cell proliferation by CCK-8 and clone formation assay, cell migration by cell scratch, and cell invasion by Transwell. Epithelial mesenchymal transformation (EMT) related markers E-cadherin, N-cadherin, Vimentin and Snail-1 expressions were assessed by Western blot. The binding of LINC00659 and miR-342-3p, miR-342-3p and ANXA2 were analyzed by dual-luciferase reporter gene assay. RESULTS: CAFs and NFs showed a spindle-like morphology. CAFs-exo promoted CRC cell proliferation, migration, invasion and EMT progression. The expression of LINC00659 in CAF-derived exosomes was significantly increased, and fibroblasts could transfer exosomal LINC00659 to CRC cells. We further revealed that transfection of miR-342-3p mimic or sh-ANXA2 could obviously reverse the promotion effect of exosomal LINC00659 on CRC progression. Functional studies reveal that LINC00659 is transferred from CAFs to the cancer cells via exosomes, where it promotes CRC cell proliferation, invasion, migration and EMT progression in vitro. Mechanistically, LINC00659 interacts directly with miR-342-3p to increase ANXA2 expression in CRC cells. CONCLUSION: Collected evidence supported that CAFs-derived exosomal LINC00659 promotes CRC cell proliferation, invasion and migration via miR-342-3p/ANXA2axis.	NA	J Transl Med. 2021 Jan 6;19(1):8. doi: 10.1186/s12967-020-02648-7.
4721	LncRNA	LINC00665	miR-424-5p	BCL9L	cholangiocarcinoma cells	Cholangiocarcinoma	Homo sapiens (human)	microarray;	33436545	Long non-coding RNA LINC00665 promotes gemcitabine resistance of Cholangiocarcinoma cells via regulating EMT and stemness properties through miR-424-5p/BCL9L axis.	Gemcitabine is the first-line chemotherapy drug for cholangiocarcinoma (CCA), but acquired resistance has been frequently observed in CCA patients. To search for potential long noncoding RNAs (lncRNAs) involved in gemcitabine resistance, two gemcitabine resistant CCA cell lines were established and dysregulated lncRNAs were identified by lncRNA microarray. Long intergenic non-protein coding RNA 665 (LINC00665) were found to rank the top 10 upregulated lncRNAs in our study, and high LINC00665 expression was closely associated with poor prognosis and chemoresistance of CCA patients. Silencing LINC00665 in gemcitabine resistant CCA cells impaired gemcitabine tolerance, while enforced LINC00665 expression increased gemcitabine resistance of sensitive CCA cells. The gemcitabine resistant CCA cells showed increased EMT and stemness properties, and silencing LINC00665 suppressed sphere formation, migration, invasion and expression of EMT and stemness markers. In addition, Wnt/β-Catenin signaling was activated in gemcitabine resistant CCA cells, but LINC00665 knockdown suppressed Wnt/β-Catenin activation. B-cell CLL/lymphoma 9-like (BCL9L), the nucleus transcriptional regulators of Wnt/β-Catenin signaling, plays a key role in the nucleus translocation of β-Catenin and promotes β-Catenin-dependent transcription. In our study, we found that LINC00665 regulated BCL9L expression by acting as a molecular sponge for miR-424-5p. Moreover, silencing BCL9L or miR-424-5p overexpression suppressed gemcitabine resistance, EMT, stemness and Wnt/β-Catenin activation in resistant CCA cells. In conclusion, our results disclosed the important role of LINC00665 in gemcitabine resistance of CCA cells, and provided a new biomarker or therapeutic target for CCA treament.	NA	Cell Death Dis. 2021 Jan 12;12(1):72. doi: 10.1038/s41419-020-03346-4.
4722	LncRNA	LINC00689	miR-526b-3p	IGF2BP1	glioma	Glioma	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33389570	LncRNA LINC00689 Promotes the Tumorigenesis of Glioma via Mediation of miR-526b-3p/IGF2BP1 Axis.	Glioma ranks first among the aggressive brain tumors all over the world. LncRNA LINC00689 has been confirmed to play key roles in the progression of cancers, and LINC00689 was upregulated in glioma. However, the biological function of LINC00689 in glioma is unclear. qRT-PCR was applied to detect the expressions of LINC00689 and miR-526b-3p in glioma cells. Dual-luciferase report was performed to examine the relation among LINC00689, miR-526b-3p, and insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1). Then, the growth, migration, and invasion of glioma cells were detected by colony formation, flow cytometry, and transwell assay, respectively. The expressions of p21, cleaved caspase 3, and MAPK signaling-related proteins in glioma cells were tested by western blotting. Finally, xenograft mice model was established to detect the effect of LINC00689 on tumor growth of glioma in vivo. LINC00689 was upregulated in glioma cells, while miR-526b-3p was downregulated. In addition, LINC00689 bound to miR-526b-3p, and IGFBP1 was targeted by miR-526b-3p. Moreover, LINC00689 knockdown or upregulation of miR-526b-3p inhibited the proliferation of glioma cells and induced the apoptosis. Consistently, the migration and invasion of glioma cells were notably reduced by LINC00689 shRNA/miR-526-3p mimics. miR-526b-3p inhibitor or IGF2BP1 upregulation could reverse the effect of LINC00689 knockdown or miR-526b-3p mimics. Finally, knockdown of LINC00689 inhibited the tumor growth of glioma in vivo through regulating miR-526b-3p/IGF2BP1/MAPK axis. In conclusion, silencing of LINC00689 could inhibit the tumorigenesis of glioma via mediation of miR-526b-3p/IGF2BP1 axis. LINC00689 may serve as a new target for the treatment of glioma.	NA	Neuromolecular Med. 2021 Jan 3. doi: 10.1007/s12017-020-08635-x.
4723	LncRNA	LINC00691	miR-1256	ST5	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR	33380807	The lncRNA LINC00691Functions as a ceRNA for miRNA-1256 to Suppress Osteosarcoma by Regulating the Expression of ST5.	INTRODUCTION: Osteosarcoma is the most common primary malignant tumor in children and young patients. Although neoadjuvant chemotherapy and surgery could improve the prognosis of these patients, treatment outcomes are poor because of its low early diagnosis rate and high degree of malignancy as well as its tendency for early metastasis. In the field of osteosarcoma, lncRNAs have become a hot spot for studying the molecular mechanisms driving malignant biological characteristics and exploring effective treatment methods. An lncRNA is a long noncoding RNA lacking protein-encoding ability, and in its RNA form, it regulates various gene expression processes, such as epigenetic regulation, transcriptional regulation, and posttranscriptional regulation. LncRNAs play an important role in tumorigenesis and metastasis. METHODS: We used bioinformatics software to analyze the data in geo database. CCK-8 and Transwell were used to detect the effect of lncRNA LINC00691 on the proliferation and migration of osteosarcoma cells. The target gene of LINC00691 was detected by bioinformatics analysis and RNA pull down. RESULTS: In this study, we identified the lncRNA LINC00691 and confirmed its expression in osteosarcoma cells through GEO database analysis. Expression analysis showed that the levels of lncRNA LINC00691 in osteosarcoma cells were decreased compared to those of control cells. Overexpression of LINC00691 could inhibit the proliferation, migration, invasion, and induction of G1 cell cycle arrest in osteosarcoma cells, which was shown through in vitro and in vivo studies. Using bioinformatics analysis, RNA pull down experiments and luciferase reporter gene detection assays, we found that LINC00691 regulated ST5 expression by binding miR-1256. LINC00691 overexpression inhibited EMT by promoting the expression of E-cadherin and increasing the expression of ZEB1, Snail, and Fibronectin. CONCLUSION: These results suggested that overexpressed LINC00691 promoted the expression of ST5 by regulating the function of miR-1256 through a ceRNA mechanism. The LINC00691/miR-1256/ST5 pathway plays an important role in the progression and metastasis of osteosarcoma and represents a good therapeutic target.	NA	Onco Targets Ther. 2020 Dec 24;13:13171-13181. doi: 10.2147/OTT.S266435. eCollection 2020.
4724	LncRNA	LINC00941	miR-335-5p	ROCK1	pancreatic cancer tissues and cell lines	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR	33414429	Long noncoding RNA LINC00941 promotes pancreatic cancer progression by competitively binding miR-335-5p to regulate ROCK1-mediated LIMK1/Cofilin-1 signaling.	An accumulation of evidence indicates that long noncoding RNAs are involved in the tumorigenesis and progression of pancreatic cancer (PC). In this study, we investigated the functions and molecular mechanism of action of LINC00941 in PC. Quantitative PCR was used to examine the expression of LINC00941 and miR-335-5p in PC tissues and cell lines, and to investigate the correlation between LINC00941 expression and clinicopathological features. Plasmid vectors or lentiviruses were used to manipulate the expression of LINC00941, miR-335-5p, and ROCK1 in PC cell lines. Gain or loss-of-function assays and mechanistic assays were employed to verify the roles of LINC00941, miR-335-5p, and ROCK1 in PC cell growth and metastasis, both in vivo and in vitro. LINC00941 and ROCK1 were found to be highly expressed in PC, while miR-335-5p exhibited low expression. High LINC00941 expression was strongly associated with larger tumor size, lymph node metastasis, and poor prognosis. Functional experiments revealed that LINC00941 silencing significantly suppressed PC cell growth, metastasis and epithelial-mesenchymal transition. LINC00941 functioned as a molecular sponge for miR-335-5p, and a competitive endogenous RNA (ceRNA) for ROCK1, promoting ROCK1 upregulation, and LIMK1/Cofilin-1 pathway activation. Our observations lead us to conclude that LINC00941 functions as an oncogene in PC progression, behaving as a ceRNA for miR-335-5p binding. LINC00941 may therefore have potential utility as a diagnostic and treatment target in this disease.	NA	Cell Death Dis. 2021 Jan 4;12(1):36. doi: 10.1038/s41419-020-03316-w.
4725	LncRNA	LINC00943	miR-15b-5p	RAB3IP	MPP(+)-challenged SK-N-SH cells	Parkinsons Disease	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33208053	LINC00943 knockdown attenuates MPP(+)-induced neuronal damage via miR-15b-5p/RAB3IP axis in SK-N-SH cells.	OBJECTIVES: Parkinson's disease (PD) is a neurodegenerative problem correlated with neuronal damage. Long noncoding RNAs (lncRNAs) are implicated in neuronal damage in PD development. This research aims to analyze the function and mechanism of LINC00943 in 1-methyl-4-phenylpyridinium (MPP(+))-caused neuronal injury. METHODS: MPP(+)-challenged SK-N-SH cells served as a PD-like model of neuronal damage. LINC00943, microRNA-15b-5p (miR-15b-5p) and RAB3A interacting protein (RAB3IP) abundances were examined via quantitative reverse transcription polymerase chain reaction or western blot. MPP(+)-caused neuronal damage was assessed via cell viability, apoptosis, inflammatory injury and oxidative injury. The association between miR-15b-5p and LINC00943 or RAB3IP was determined via dual-luciferase reporter analysis and RNA immunoprecipitation. RESULTS: LINC00943 abundance was up-regulated in MPP(+)-challenged SK-N-SH cells. LINC00943 silence alleviated MPP(+)-caused decrease of cell viability and elevation of apoptosis, inflammatory injury and oxidative injury. miR-15b-5p was inhibited via LINC00943, and miR-15b-5p inhibition reversed knockdown of LINC00943-mediated suppression of MPP(+)-induced neuronal damage. RAB3IP was targeted via miR-15b-5p, and LINC00943 could regulate RAB3IP via miR-15b-5p. miR-15b-5p addition mitigated MPP(+)-induced neuronal damage through decreasing RAB3IP. CONCLUSION: LINC00943 inhibition alleviated MPP(+)-induced neuronal injury via miR-15b-5p/RAB3IP axis, indicating a potential target for treatment of PD.	NA	Neurol Res. 2021 Mar;43(3):181-190. doi: 10.1080/01616412.2020.1834290. Epub 2020 Nov 19.
4726	LncRNA	LINC01116	miR-93-5p	STAT3	lung cancer tissues	Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR	33535997	LncRNA LINC01116 sponges miR-93-5p to promote cell invasion and migration in small cell lung cancer.	BACKGROUND: LINC01116 is a recently identified oncogenic lncRNA in glioma. Differential expression analysis using the public gene expression analysis tool GEPIA revealed the upregulation of LINC01116 in lung cancer. We studied the functions of LINC01116 in small cell lung cancer (SCLC). METHODS: The expression of LINC01116 in several types of cancer tissue and the paired non-tumor tissues was evaluated by GEPIA. The effects of the overexpression of LINC01116 and miR-93-5p on the expression of STAT3 were evaluated. The effects of the overexpression of LINC01116, miR-93-5p and STAT3 on SHP-77 cell behaviors were evaluated by Transwell assays. RESULTS: LINC01116 was highly expressed in SCLC and predicted poor survival. In SCLC tissues, the expression of LINC01116 was positively correlated with STAT3. Bioinformatics analysis revealed that miR-93-5p may target LINC01116. Overexpression of LINC01116 increased STAT3 but did not affect the expression of miR-93-5p. Transwell assay showed that LINC01116 and STAT3 increased cell invasion and migration rates. MiR-93-5p played an suppressed cell behaviors and suppressed the role of LINC01116. CONCLUSION: Therefore, LINC01116 might upregulate STA3 by sponging miR-93-5p, thereby promoting cell invasion and migration in SCLC.	NA	BMC Pulm Med. 2021 Feb 3;21(1):50. doi: 10.1186/s12890-020-01369-3.
4727	LncRNA	LINC01194	miR-641	SETD7	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33372601	Long non-coding RNA LINC01194 promotes the proliferation, migration and invasion of lung adenocarcinoma cells by targeting miR-641/SETD7 axis.	BACKGROUND: It is increasingly evidenced that long non-coding RNAs (lncRNAs) play an important role in various diseases. LncRNA LINC01194 acts as an oncogene in several cancer types. Nevertheless, the role of LINC01194 in lung adenocarcinoma (LUAD) has not yet been revealed. METHODS: qRT-PCR was used to detect the expression of LINC01194, miR-641 and SETD7 mRNA, while western blot was exploited to examine SETD7 protein level. Cell proliferation was detected by colony formation and EdU assays. Transwell assays detected cell migration and invasion. TUNEL assay and flow cytometry analysis were used to detect cell apoptosis. RIP, RNA pull down and luciferase reporter assays detected the binding among LINC01194, miR-641 and SETD7. RESULTS: LINC01194 was significantly upregulated in LUAD tissues and cell lines. Knockdown of LINC01194 resulted in decreased cell proliferation, migration and invasion, and increased apoptosis. Mechanistic experiments unveiled that LINC01194 augmented SETD7 expression in LUAD cells by competitively interacting with miR-641. Rescue experiments showed that miR-641 inhibition and SETD7 overexpression rescued the repressing impacts on LUAD cell proliferation, migration and invasion caused by LINC01194 knockdown. CONCLUSION: LINC01194 promotes the progression of LUAD by enhancing miR-641-targeted SETD7. The LINC01194/miR-641/SETD7 axis might provide new molecular targets for treating LUAD.	NA	Cancer Cell Int. 2020 Dec 7;20(1):588. doi: 10.1186/s12935-020-01680-3.
4728	LncRNA	LINC01207	miR-1301-3p	PODXL	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	33495099	CTCF-induced upregulation of LINC01207 promotes gastric cancer progression via miR-1301-3p/PODXL axis.	BACKGROUND: Long non coding RNAs (lncRNAs) have been validated to be involved in the complicated biological processes during tumor progression. LINC01207 has been identified as an oncogene in several cancer types. However, the function of LINC01207 and its underlying molecular mechanism in gastric cancer (GC) are poorly understood. METHODS: The expression level of LINC01207, miR-1301-3p and PODXL mRNA was detected in GC tissues and cells by RT-qPCR. The level of PODXL protein was examined by western blot. Colony formation assay, EdU assay, TUNEL assay, caspase-3 activity test and transwell assays were carried out to analyze the effect of LINC01207 on GC cell proliferation, apoptosis, migration and invasion. The interaction between RNAs was confirmed by luciferase reporter assay, RNA pull-down assay and RIP assay. RESULTS: LINC01207 was expressed at high level in GC tissues and cells. Silencing of LINC01207 impaired GC cell proliferation, migration and invasion but promoted cell apoptosis. Mechanistically, LINC01207 acted as a ceRNA by sponging miR-1301-3p to upregulate PODXL. Besides, miR-1301-3p silencing or PODXL overexpression could abolish the inhibitory effect of LINC01207 knockdown on GC cell growth and migration. CCCTC-binding factor (CTCF) could transcriptionally activate LINC01207 in GC cells. CONCLUSIONS: CTCF-induced activation of LINC01207 contributes to GC progression through regulating miR-1301-3p/PODXL axis.	NA	Dig Liver Dis. 2021 Apr;53(4):486-495. doi: 10.1016/j.dld.2020.12.006. Epub 2021 Jan 22.
4729	LncRNA	LINC01278	miR-134-5p	KRAS	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR;RIP assay;Flow Cytometry assay;RNA pull-down;	33531816	LINC01278 is Highly Expressed in Osteosarcoma and Participates in the Development of Tumors by Mediating the miR-134-5p/KRAS Axis.	PURPOSE: There is increasing evidence that non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), produce a critical regulatory effect on osteosarcoma (OS). LINC01278, as a newly discovered lncRNA, is found to be highly expressed in OS, but its related mechanism remains unclear. This research, therefore, is designed to study the mechanism of LINC01278 in OS and to find potential targets for clinical use. METHODS: qRT-PCR was applied to determine the relative expression of LINC01278 and analyze its diagnostic value in OS. CCK-8, Transwell and flow cytometry were utilized for the determination of cell proliferation, migration/invasion, and apoptosis. RIP and RNA pull-down experiments were used to verify the targeted binding effect of miR-134-5p and LINC01278. The relationship between miR-134-5p and LINC01278 or KRAS was analyzed using dual luciferase reporter gene. The effects of LINC01278 on tumor growth in nude mice was analyzed by in vivo experiment. RESULTS: qRT-PCR showed that LINC01278 increased in OS tissues and serum, indicating poor prognosis. In addition, LINC01278 was also of high value for OS diagnosis. Functional experiments showed that LINC01278 inhibited KRAS-mediated OS cell proliferation and metastasis through miR-134-5p. Finally, the results of an in vivo animal model indicated that LINC01278 promoted OS growth. CONCLUSION: LINC01278 is expressed highly in OS, and patients with high LINC01278 expression have poor prognosis. Moreover, LINC01278 can suppress the proliferation and apoptosis of OS cells through mediating miR-134-5p/KRAS axis, which is expected to become a potential therapeutic target for OS.	NA	Onco Targets Ther. 2021 Jan 26;14:683-695. doi: 10.2147/OTT.S265591. eCollection 2021.
4730	LncRNA	LINC01410	miR-122-5p	NDRG3	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	luciferase assay;	33583123	The LINC01410/miR-122-5p/NDRG3 axis is involved in the proliferation and migration of osteosarcoma cells.	PURPOSE: It is generally accepted that long noncoding RNAs (lncRNAs) function as vital regulators of tumor development and progression. Long intergenic non-coding RNA 1410 (LINC01410) is a newly discovered lncRNA, and its role in osteosarcoma (OS) is yet to be determined. MATERIALS AND METHODS: The expression of LINC01410, microRNA-122-5p (miR-122-5p), and N-myc downstream-regulated gene 3 (NDRG3) in OS tissues was determined using reverse transcription-quantitative PCR. Interactions between LINC01410, miR-122-5p, and NDRG3 were predicted and verified using bioinformatics tools and luciferase assays. Cell proliferation, migration, and invasion were detected using cell counting Kit-8 and Transwell assays. RESULTS: LINC01410 was overexpressed in OS tissues. Furthermore, it was confirmed that LINC01410 facilitated OS cell proliferation and migration. Our studies also showed that LINC01410 binds to miR-122-5p, and miR-122-5p binds to NDRG3. Finally, we observed that LINC01410 knockdown inhibited the proliferation, invasion, and migration of OS cells. Knockdown of LINC01410 resulted in the upregulation of miR-122-5p and downregulation of NDRG3. CONCLUSION: Our results demonstrated that the LINC01410/miR-122-5p/NDRG3 axis is involved in the progression of OS.	NA	IUBMB Life. 2021 Apr;73(4):705-717. doi: 10.1002/iub.2452. Epub 2021 Mar 1.
4731	LncRNA	LINC01503	miR-335-5p	P4HA1	pancreatic cancer tissues	Pancreatic Cancer	Homo sapiens (human)	RACE;	33415167	Systematic Analysis of the Expression and Prognostic Significance of P4HA1 in Pancreatic Cancer and Construction of a lncRNA-miRNA-P4HA1 Regulatory Axis.	OBJECTIVES: Prolyl 4-hydroxylase subunit alpha 1 (P4HA1) plays a crucial role in modulating extracellular matrix component and promoting tumor progression by changing tumor adhesion, migration, and other biological behaviors in some cancers. However, its expression pattern, biological function, and underlying mechanism in pancreatic cancer remain largely unclear. MATERIALS AND METHODS: In this study, a set of bioinformatics tools were used to analyze the expression of P4HA1 and its prognostic value in pancreatic cancer. In addition, the mechanism through which P4HA1 promotes the progression of pancreatic cancer was explored by constructing a competing endogenous RNA (ceRNA) regulatory axis. RESULTS: It was found that the mRNA and protein expression of P4HA1 was significantly higher in pancreatic cancer tissues than in normal tissues. Its high P4HA1 expression correlated with poor clinicopathological features (T stage: P = 0.0078; N stage: P = 0.0124; TNM stage: P = 0.0013; pathological grade: P = 0.0108) and poor prognosis [OS: HR = 1, 95% CI (1-1.01), P = 0.00028; DSS: HR = 1, 95% CI (1-1.01), P = 0.00049; PFI: HR = 1.01, 95% CI (1.01-1.02), P = 0.0057; and DFI: HR = 1, 95% CI (1-1.01), P = 0.0034]. The LINC01503/miR-335-5p/P4HA1 axis might mediate the effects of P4HA1 in promoting the progression on pancreatic cancer. CONCLUSIONS: Collectively, our findings suggest that high expression of P4HA1 may be used as a promising prognostic biomarker and could be considered for the development of a novel therapeutic strategy for pancreatic cancer in the future.	NA	Biomed Res Int. 2020 Dec 19;2020:8877334. doi: 10.1155/2020/8877334. eCollection 2020.
4732	LncRNA	LINC01554	miR-3681-3p	NGFR	HCC cells	Melanoma	Homo sapiens (human)	qRT-PCR;	33378013	Long-chain non-coding RNA LINC01554 promotes NGFR expression and inhibits cell proliferation, migration, and invasion in hepatocellular carcinoma by binding to microRNA-3681-3p.	OBJECTIVE: The aim of this study was to analyze the role of LINC01554 in the pathogenesis of hepatocellular carcinoma (HCC) and explore the potential mechanism through which LINC01554 affects the migration and proliferation of HCC cells. PATIENTS AND METHODS: LINC01554 expression in HCC tissues and its link to the prognosis of patients were analyzed by The Cancer Genome Atlas (TCGA) database. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to examine LINC01554 levels in 60 cases of HCC clinical tissues and HCC cell lines. Then, LINC01554 overexpression model was constructed using lentivirus in HCC cell lines. HCC proliferation and invasive ability were evaluated through Cell Counting Kit (CCK-8) and transwell tests, respectively. Furthermore, the potential action mechanism of LINC01554 was explored using bioinformatics analysis and in vitro cell experiments. RESULTS: Analysis of the TCGA database revealed that LINC01554 was remarkably under-expressed in HCC tissues. Decreased expression of LINC01554 predicted a poor prognosis for patients. Besides, LINC01554 overexpression markedly blunted the proliferation and migratory capacities of HCC cells. LINC01554 competed with NGFR to bind to microRNA-3681-3p, thereby providing possible mechanisms by which LINC01554 could participate in the progression of HCC. CONCLUSIONS: This study shows for the first time that LINC01554 modulates NGFR expression by binding to microRNA-3681-3p, thereby participating in the progression of HCC.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12667-12674. doi: 10.26355/eurrev_202012_24164.
4733	LncRNA	LINC01857	miR-141-3p	MAP4K4	diffuse large B-cell lymphoma tissues and cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;Luciferase reporter assay;	33311569	LncRNA LINC01857 promotes cell growth and diminishes apoptosis via PI3K/mTOR pathway and EMT process by regulating miR-141-3p/MAP4K4 axis in diffuse large B-cell lymphoma.	LINC01857 has been proven to be involved in glioma and breast cancer. However, the biological function of LINC01857 in diffuse large B-cell lymphoma (DLBCL) is poorly investigated. By accessing to the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTE(X)), LINC01857 expression was found upregulated in both DLBCL tissues and cells. Cell proliferation and flow cytometry assays showed that LINC01857 promoted proliferation and cell cycle, but suppressed apoptosis in DLBCL cells. Bioinformatics analysis and luciferase reporter assay confirmed that LINC01857 may serve as a sponge for miR-141-3p and miR-141-3p may target MAP4K4. Mechanically, the regulatory action of miR-141-3p/MAP4K4 on DLBCL cellular behaviors was regulated by LINC01857. In addition, LINC01857 could increase the activity of PI3K/mTOR pathway and facilitate the EMT process in a miR-141-3p-mediated manner in DLBCL. Our data illustrated that the LINC01857/miR-141-3p/MAP4K4 might function as a promising therapeutic avenue for DLBCL treatment.	NA	Cancer Gene Ther. 2020 Dec 12. doi: 10.1038/s41417-020-00267-4.
4734	LncRNA	LINC01969	miR-144-5p	LARP1	SKOV3 cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;	33614632	Long Non-coding RNA LINC01969 Promotes Ovarian Cancer by Regulating the miR-144-5p/LARP1 Axis as a Competing Endogenous RNA.	Accumulating evidence has shown that long non-coding RNAs (lncRNAs) can be used as biological markers and treatment targets in cancer and play various roles in cancer-related biological processes. However, the lncRNA expression profiles and their roles and action mechanisms in ovarian cancer (OC) are largely unknown. Here, we assessed the lncRNA expression profiles in OC tissues from The Cancer Genome Atlas (TCGA) database, and one upregulated lncRNA, LINC01969, was selected for further study. LINC01969 expression levels in 41 patients were verified using quantitative real-time polymerase chain reaction (qRT-PCR). The in vitro effects of LINC01969 on OC cell migration, invasion, and proliferation were determined by the CCK-8, ethynyl-2-deoxyuridine (EdU), wound healing, and Transwell assays. Epithelial-mesenchymal transition (EMT) was evaluated using qRT-PCR and Western blotting. The molecular mechanisms of LINC01969 in OC were assessed through bioinformatics analysis, RNA-binding protein immunoprecipitation (RIP), dual luciferase reporter gene assays, and a rescue experiment. Finally, in vivo experiments were conducted to evaluate the functions of LINC01969. The results of the current study showed that LINC01969 was dramatically upregulated in OC, and patients with lower LINC01969 expression levels tended to have better overall survival. Further experiments demonstrated that LINC01969 promoted the migration, invasion, and proliferation of OC cells in vitro and sped up tumor growth in vivo. Additionally, LINC01969, which primarily exists in the cytoplasm, boosted LARP1 expression by sponging miR-144-5p and promoted the malignant phenotypes of OC cells. In conclusion, the LINC01969/miR-144-5p/LARP1 axis is a newly identified regulatory signaling pathway involved in OC progression.	NA	Front Cell Dev Biol. 2021 Feb 4;8:625730. doi: 10.3389/fcell.2020.625730. eCollection 2020.
4735	LncRNA	Linc-ROR	miR-138	SOX9	mesenchymal stem cells	Mesenchymal Stem Cell(Bmscs) Chondrogenesis	Homo sapiens (human)	Western blot;luciferase assay;	33485931	Linc-ROR promotes mesenchymal stem cells chondrogenesis and cartilage formation via regulating SOX9 expression.	OBJECTIVE: The present study is to characterize the role of long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) in bone marrow mesenchymal stem cell (BMSCs) chondrogenesis, cartilage formation and OA development. METHODS: Linc-ROR expression pattern in articular cartilage tissue sample from OA patients were studied by real-time PCR. Linc-ROR lentivirus mediated BMSCs were constructed. In vitro micromass cultured BMSCs chondrogenesis or in vivo MeHA hydrogel encapsulated BMSCs cartilage formation activity were studied. Linc-ROR associating miRNAs which repressed SOX9 expression were characterized by luciferase assay, real-time PCR and Western blot. Linc-ROR was co-transfected with miRNAs into BMSCs to study its rescue effect on SOX9 expression and chondrogenesis activity. RESULTS: Linc-ROR was down-regulated in articular cartilage tissue from OA patients and was positively correlated with the expression level of SOX9 (R(2) = 0.43). Linc-ROR expression was upregulated during BMSCs chondrogenesis. Linc-ROR ectopic expression significantly promoted in vitro BMSCs chondrogenesis and in vivo cartilage formation activities as revealed by safranin O, alcian blue and COL II staining. The mRNA expression level of chondrogenesis markers including COL II, SOX9 and ACAN were increased, and the hypertrophy markers MMP13 and COL X were decreased upon linc-ROR overexpression in BMSCs. Linc-ROR functioned as a miRNA sponge for miR-138 and miR-145. Both miR-138 and miR-145 suppressed BMSCs chondrogenesis activity and SOX9 expression, while co-expression of linc-ROR displayed a rescuing effect. CONCLUSIONS: Taken together, linc-ROR modulated BMSCs chondrogenesis differentiation and cartilage formation by acting as a competing endogenous RNA for miR-138 and miR-145 and activating SOX9 expression. Linc-ROR could be considered as a new diagnostic and therapeutic target for OA treatment.	NA	Osteoarthritis Cartilage. 2021 Apr;29(4):568-578. doi: 10.1016/j.joca.2020.12.020. Epub 2021 Jan 22.
4736	LncRNA	Linc-ROR	miR-145	SOX9	mesenchymal stem cells	Mesenchymal Stem Cell(Bmscs) Chondrogenesis	Homo sapiens (human)	Western blot;luciferase assay;	33485931	Linc-ROR promotes mesenchymal stem cells chondrogenesis and cartilage formation via regulating SOX9 expression.	OBJECTIVE: The present study is to characterize the role of long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) in bone marrow mesenchymal stem cell (BMSCs) chondrogenesis, cartilage formation and OA development. METHODS: Linc-ROR expression pattern in articular cartilage tissue sample from OA patients were studied by real-time PCR. Linc-ROR lentivirus mediated BMSCs were constructed. In vitro micromass cultured BMSCs chondrogenesis or in vivo MeHA hydrogel encapsulated BMSCs cartilage formation activity were studied. Linc-ROR associating miRNAs which repressed SOX9 expression were characterized by luciferase assay, real-time PCR and Western blot. Linc-ROR was co-transfected with miRNAs into BMSCs to study its rescue effect on SOX9 expression and chondrogenesis activity. RESULTS: Linc-ROR was down-regulated in articular cartilage tissue from OA patients and was positively correlated with the expression level of SOX9 (R(2) = 0.43). Linc-ROR expression was upregulated during BMSCs chondrogenesis. Linc-ROR ectopic expression significantly promoted in vitro BMSCs chondrogenesis and in vivo cartilage formation activities as revealed by safranin O, alcian blue and COL II staining. The mRNA expression level of chondrogenesis markers including COL II, SOX9 and ACAN were increased, and the hypertrophy markers MMP13 and COL X were decreased upon linc-ROR overexpression in BMSCs. Linc-ROR functioned as a miRNA sponge for miR-138 and miR-145. Both miR-138 and miR-145 suppressed BMSCs chondrogenesis activity and SOX9 expression, while co-expression of linc-ROR displayed a rescuing effect. CONCLUSIONS: Taken together, linc-ROR modulated BMSCs chondrogenesis differentiation and cartilage formation by acting as a competing endogenous RNA for miR-138 and miR-145 and activating SOX9 expression. Linc-ROR could be considered as a new diagnostic and therapeutic target for OA treatment.	NA	Osteoarthritis Cartilage. 2021 Apr;29(4):568-578. doi: 10.1016/j.joca.2020.12.020. Epub 2021 Jan 22.
4737	LncRNA	LncOGD-1006	miR-184-5p	CAAP1	brain microvascular endothelial cells	Ischemic Stroke	Homo sapiens (human)	qRT-PCR	33336752	LncRNA LncOGD-1006 alleviates OGD-induced ischemic brain injury regulating apoptosis through miR-184-5p/CAAP1 axis.	OBJECTIVE: This study aimed to explore the effect of long non-coding RNA (LncRNA) LncOGD-1006 to ischemic stroke and the possible mechanism. MATERIALS AND METHODS: The primary brain microvascular endothelial cells (bEnd.3) of oxygen-glucose deprivation (OGD) was used as a mimic of ischemic stroke in vitro. RESULTS: The results showed that LncOGD-1006 was upregulated in bEnd.3 after OGD-induced. CONCLUSIONS: LncOGD-1006 might act as a ceRNA to inhibit apoptosis in bEnd.3 cells by targeting miR-184-5p/CAAP1 pathway.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12324-12333. doi: 10.26355/eurrev_202012_24025.
4738	LncRNA	lncRNAS56464.1	miR-152-3p	Wnt	fibroblast-like synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;	33448322	lncRNAS56464.1 as a ceRNA promotes the proliferation of fibroblast-like synoviocytes in experimental arthritis via the Wnt signaling pathway and sponges miR-152-3p.	Rheumatoid arthritis (RA) is an autoimmune disease that occurs in approximately 1.0% of the general population. In RA patients, physical disability and joint damage are the major prognostic factors, which are associated with a reduction in the quality of life and early mortality. At present, the exact molecular mechanism of RA remains elusive. Long noncoding RNAs (lncRNAs) have been revealed to play a regulatory role in the pathogenesis of RA. To reveal the function of lncRNAs in rheumatoid arthritis, lncRNAS56464.1 was screened to verify its targeting of the microRNA (miR)-152-3p/Wnt pathway and its effect on the proliferation of fibroblast-like synoviocytes (FLS). In the present study, based on the competing endogenous RNA (ceRNA) theory, siRNA was designed for transfection into FLS to calculate the lncRNAS56464.1 interference efficiency and then the effect of lncRNAS56464.1 interference on FLS proliferation was detected by MTT assay. Then, lncRNAS56464.1 targeting of the miR-152-3p/Wnt pathway was detected by a dual-luciferase reporter assay. In addition, RT-qPCR, immunofluorescence and western blotting techniques were employed to detect the expression of lncRNAS56464.1, miR-152-3p and some key genes of the Wnt signaling pathway in FLS after lncRNAS56464.1 interference. The results revealed that lncRNAS56464.1 could combine with miR-152-3p and promoted the proliferation of FLS. In addition, lncRNAS56464.1 interference could not only decrease the proliferation of FLS and the expression of Wnt1, β-catenin, c-Myc, cyclin D1, and p-GSK-3β/GSK-3β, but it also increased the expression of SFRP4. The present data indicated that lncRNAS56464.1 could target the miR-152-3p/Wnt pathway to induce synovial cell proliferation and then participate in the pathogenesis of RA.	NA	Int J Mol Med. 2021 Mar;47(3):17. doi: 10.3892/ijmm.2021.4850. Epub 2021 Jan 15.
4739	LncRNA	LRCF	miR138-5p	caspase3	oligodendrocytes	Proliferation And Apoptosis Of Oligodendrocytes	Homo sapiens (human)	qRT-PCR	33411226	The Role of the lncRNA-LRCF in Propofol-Induced Oligodendrocyte Damage in Neonatal Mouse.	In this study, LRCF, a long noncoding RNA (lncRNA) related to cognitive function, which was first discovered and named by our group, was shown to be involved in the propofol-induced proliferation and apoptosis of oligodendrocytes (OLGs). Our systematic study showed that LRCF expression differs in OLGs of mice of different ages. We found that neonatal mice with a high level of LRCF typically showed greater propofol-induced injury of OLGs. Mechanistic research has shown that LRCF can block the HIF-1α/miR138-5p/Caspase-3 pathway by binding to miR138-5p to form a microRNA (miRNA) sponge and result in cell damage through HIF-1α/Caspase-3 pathway in propofol induced OLGs. This may be the intrinsic reason why neonatal animals with high levels of LRCF tend to develop learning disability and neuro-degeneration more frequently than adults' after exposure to general anesthesia. When LRCF is highly expressed, HIF-1α directly regulates the transcription of the Caspase-3 gene by binding to the transcription factor binding site (TFBS) in its promoter, which induces OLGs apoptosis. LRCF is crucial for the mutual activation of the HIF-1α/miR138-5p/Caspase-3 OLGs survival pathway and the HIF-1α/Caspase-3 OLGs damage pathway. This study is the first to report that up-regulation of HIF-1α in OLGs treated with Propofol can promote apoptosis through HIF-1α/caspase-3 pathway and resist apoptosis through HIF-1α/miR-138-5p/caspase-3 pathway. The effect of HIF-1α on Caspase-3 expression depends on LRCF expression, which provides important theoretical support for gene therapy targeting LRCF. The further significance of this study is points to an involvement of the genetic background with high LRCF expression may serve as an important marker for identifying patients with a high risk of OLGs injury by Propofol. Thus, caution should be taken when administrating propofol in these patients, especially pediatric patients with high level of LRCF.	NA	Neurochem Res. 2021 Apr;46(4):778-791. doi: 10.1007/s11064-020-03205-w. Epub 2021 Jan 7.
4740	LncRNA	LUCAT1	miR-199a-5p	ZEB1	renal tubular epithelial cells	Renal Fibrosis	Homo sapiens (human)	qRT-PCR	33426083	Knockdown of the Long Noncoding RNA LUCAT1 Inhibits High-Glucose-Induced Epithelial-Mesenchymal Transition through the miR-199a-5p-ZEB1 Axis in Human Renal Tubular Epithelial Cells.	Renal fibrosis, the leading cause of end-stage renal disease and in which epithelial-mesenchymal transition (EMT) plays a central role, has a complex pathogenesis that is not fully understood. Therefore, we investigated the role of the long noncoding RNA LUCAT1 in the EMT of renal tubular epithelial cells under high-glucose (HG) conditions and the underlying mechanism involved. In this study, we established HG and normal glucose groups of HK-2 cells by treating HK-2 cells 30.0 or 5.5 mmol/L glucose, respectively. To investigate the roles of LUCAT1 and miR-199a-5p in HG-induced EMT, we transfected the HG group with negative control small interfering RNA (siRNA), siRNA targeting LUCAT1, negative control microRNA, or an miR-199a-5p mimic. The results of the quantitative reverse transcription PCR indicated that the LUCAT1 level in the HG group was increased, whereas the miR-199a-5p level was decreased. The EMT in the cells was induced by treatment with HG but was weakened by LUCAT1 knockdown or miR-199a-5p overexpression, which both also inhibited the HG-induced phosphorylation of SMAD3. Moreover, LUCAT1 and ZEB1 mRNA comprised the same microRNA response elements of miR-199a-5p. LUCAT1 knockdown had no effect on the miR-199a-5p level but decreased the HG-induced upregulation of ZEB1. In conclusion, HG conditions induced the upregulation of LUCAT1, and LUCAT1 knockdown inhibited the EMT in HG-treated HK-2 cells. LUCAT1 likely promotes HG-induced EMT through ZEB1 by sponging miR-199a-5p.	NA	Biomed Res Int. 2020 Dec 28;2020:8895003. doi: 10.1155/2020/8895003. eCollection 2020.
4741	LncRNA	MAFG-AS1	miR-3196	OTX1	Hepatocellular carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;	33336731	Long noncoding RNA MAFG-AS1 facilitates the progression of hepatocellular carcinoma via targeting miR-3196/OTX1 axis.	OBJECTIVE: Hepatocellular carcinoma (HCC) is an invasive malignant tumor with high mortality rate. Long non-coding RNA (lncRNA) MAFG-AS1 has been showed to play an oncogenic role in several malignant tumors. Nonetheless, the exact role of MAFG-AS1 in the progression of HCC has not been fully elucidated. PATIENTS AND METHODS: Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot were used to detect the mRNA and protein expression of MAFG-AS1 in HCC tissues and cells. Cell counting kit-8 (CCK-8), transwell and tubule formation assays were applied to uncover the proliferation, migration, invasion and tumor angiogenesis of HCC cells, respectively. RNA binding protein immunoprecipitation (RIP) assay and Luciferase reporter gene assay were employed to explore the molecular mechanism. In addition, Xenograft assay was used to investigate the effect of MAFG-AS1 in vivo. RESULTS: MAFG-AS1 was highly expressed in HCC tissues and cells. Attenuation of MAFG-AS1 evidently suppressed the proliferation, migration, invasion and tumor angiogenesis of HCC cells, suggesting that MAFG-AS1 played an oncogenic role in HCC. MiR-3196 was sponged by MAFG-AS1, and OTX1 was a downstream target of miR-3196 in HCC. In addition, OTX1 expression was negatively associated with miR-3196 but positively associated with MAFG-AS1 in HCC tissues. Overexpression of OTX1 could abolish the repressive influence of MAFG-AS1 inhibition on the proliferation, migration, invasion and tumor angiogenesis of HCC cells. CONCLUSIONS: MAFG-AS1 facilitated the progression of HCC via targeting miR-3196/OTX1 axis, which might be used as a new insight for HCC treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12131-12143. doi: 10.26355/eurrev_202012_24002.
4742	LncRNA	MAFG-AS1	miR-125b-5p	SphK1	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase activity assay;	33400245	LncRNA MAFG-AS1 regulates miR-125b-5p/SphK1 axis to promote the proliferation, migration, and invasion of bladder cancer cells.	MAFG-AS1 is an oncogenic lncRNA in multiple types of cancer. However, its role in bladder cancer (BC) remains unclear. The present study aimed to investigate the function of MAFG-AS1 in BC. BC and paired non-tumor tissues were collected. Two BC cell lines HT01197 and HT-1376 were used. Dual luciferase activity assay, RT-qPCR, western blot, CCK-8, transwell invasion assay, and wound healing assay were performed. We found that MAFG-AS1 was significantly up-regulated in BC tissues and predicted a poor survival rate. MAFG-AS1 interacted with miR-125b-5p. However, the expression levels of MAFG-AS1 and miR-125b-5p were not obviously correlated in BC tissues, and MAFG-AS1 and miR-125b-5p did not regulate the expression of each other. Interestingly, we found that SphK1, a downstream target of miR-125b-5p, was negatively correlated with miR-125b-5p, while it was positively correlated with MAFG-AS1 across BC tissues. In addition, overexpression of MAFG-AS1 upregulated the expression of SphK1 in BC cells, and attenuated the inhibitory effects of miR-125b-5p on the expression of SphK1. Functional assays showed that overexpression of MAFG-AS1 promoted BC cell proliferation, migration, and invasion, while its effects were attenuated by overexpression of miR-125b-5p. Moreover, overexpression of miR-125b-5p inhibited BC cell proliferation, migration, and invasion, while its effects were alleviated by overexpression of SphK1. Taken together, our findings demonstrated that MAFG-AS1 has an oncogenic role in BC by regulating the miR-125b-5p/SphK1 axis. MAFG-AS1 might serve as a good diagnostic marker and a potential therapeutic target of BC.	NA	Hum Cell. 2021 Mar;34(2):588-597. doi: 10.1007/s13577-020-00470-3. Epub 2021 Jan 5.
4743	LncRNA	MAFG-AS1	miR-3196	NFIX	Pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Luciferase reporter assay;	33298078	MAFG-AS1 aggravates the progression of pancreatic cancer by sponging miR-3196 to boost NFIX.	BACKGROUND: A host of researches have demonstrated the regulation of long non-coding RNAs (lncRNAs) in the progression of Pancreatic cancer (PC). In this study, our main task was to analyze the function of MAF bZIP transcription factor G antisense RNA 1 (MAFG-AS1) in PC. METHODS: RT-qPCR measured gene expression. Functional experiments, including EdU assay, flow cytometry analysis, TUNEL assay and transwell assay, assessed the biological changes of PC cells. RNA pull down assay, luciferase reporter assay and RIP assay verified the interaction between RNAs. RESULTS: MAFG-AS1 was lowly expressed in normal pancreatic samples but up-regulated in PC tissues and cell lines. Besides, MAFG-AS1 silence suppressed cell proliferation and migration whereas promoted cell apoptosis in PC. Mechanism assays verified that miR-3196 could bind with MAFG-AS1. Moreover, miR-3196 was discovered to be lowly expressed in PC cell lines, and its overexpression inhibited PC cell growth and migration. Importantly, nuclear factor I X (NFIX), overexpressed in PC cell lines, was validated to be positively modulated by MAFG-AS1 through absorbing miR-3196. Moreover, overexpression of NFIX could countervail the restraining effects of MAFG-AS1 knockdown on the growth and migration of PC cells. CONCLUSION: MAFG-AS1 had an oncogenic function in the progression of PC via regulating miR-3196/NFIX pathway, and decreasing MAFG-AS1 expression could attenuate PC progression.	NA	Cancer Cell Int. 2020 Dec 9;20(1):591. doi: 10.1186/s12935-020-01669-y.
4744	LncRNA	MAGI2-AS3	miR-374b-5p	BACE1	SH-SY5Y and BV2 cells	Alzheimers Disease	Homo sapiens (human)	ELISA;MTT assay;Luciferase reporter assay;MTT assay;	33279663	Deregulated lncRNA MAGI2-AS3 in Alzheimer's disease attenuates amyloid-β induced neurotoxicity and neuroinflammation by sponging miR-374b-5p.	BACKGROUND: Alzheimer's disease (AD) is a common neurodegenerative disease, which is characterized by aberrant accumulation of amyloid-β (Aβ) and neuroinflammation. The purpose of this study was to explore the regulatory effects of long non-coding RNA (lncRNA) MAGI2-AS3 and microRNA-374b-5p (miR-374b-5p) on Aβ-induced neurotoxicity and neuroinflammation, as well as the relationship between MAGI2-AS3 and miR-374b-5p in AD patients. METHODS: A luciferase reporter assay was used to analyze the interaction between MAGI2-AS3 and miR-374b-5p and between miR-374b-5p and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1). SH-SY5Y and BV2 cells treated with Aβ25-35 were used to mimic neuronal injury and neuroinflammation in AD pathogenesis. Cell viability was evaluated using a MTT assay, and pro-inflammatory cytokine levels were measured using ELISA kits. MAGI2-AS3 and miR-374b-5p expression was examined using quantitative real-time PCR. RESULTS: BACE1 served as a target gene of miR-374b-5p, and MAGI2-AS3 could sponge miR-374b-5p. The expression of MAGI2-AS3 was increased, and miR-374b-5p was decreased in both SH-SY5Y and BV2 cells exposed to Aβ25-35. MAGI2-AS3 reduction enhanced neuronal viability and attenuated neuroinflammation in AD cell models, and miR-374b-5p overexpression led to same effects, but miR-374b-5p inhibition reversed these effects. Serum MAGI2-AS3 and miR-374b-5p levels in AD patients were negatively correlated and correlated with disease severity. CONCLUSION: The findings indicated that the MAGI2-AS3/miR-374b-5p axis regulates Aβ-induced neurotoxicity in SH-SY5Y cells and neuroinflammation in BV2 cells. The MAGI2-AS3/miR-374b-5p axis may provide novel biomarkers and therapeutic targets for AD.	NA	Exp Gerontol. 2021 Feb;144:111180. doi: 10.1016/j.exger.2020.111180. Epub 2020 Dec 3.
4745	LncRNA	MALAT1	miR-141-3p	H9C2	H9C2 cells	Diabetic Cardiomyopathy	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33576445	lncRNA-MALAT1 promotes high glucose-induced H9C2 cardiomyocyte pyroptosis by downregulating miR-141-3p expression.	Diabetic cardiomyopathy (DCM) is caused by diabetes and can result in heart failure. Long non-coding RNAs (lncRNAs) have been demonstrated to be closely associated with DCM development. The present study aimed to investigate whether lncRNA-metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) altered high glucose (HG)-induced H9C2 cardiomyocyte pyroptosis by targeting microRNA (miR)-141-3p. H9C2 cells were treated with normal glucose (NG) or HG. lncRNA-MALAT1 and miR-141-3p expression levels were determined via reverse transcription-quantitative PCR (RT-qPCR). MALAT1 and miR-141-3p knockdown and overexpression were established and confirmed via RT-qPCR. The association between MALAT1 expression and miR-141-3p expression, as well as the induction of pyroptosis and gasdermin D (GSDMD)-N expression were evaluated by performing dual luciferase reporter, TUNEL staining and immunofluorescence staining assays, respectively. Western blotting was conducted to measure the expression levels of pyroptosis-associated proteins, including apoptosis-associated speck-like protein, GSDMD-N, caspase-1, nucleotide oligomerization domain-like receptor protein 3 and GSDMD. MALAT1 mRNA expression levels were significantly increased, whereas miR-141-3p expression levels were significantly decreased in HG-treated H9C2 cells compared with the NG group. Compared with the HG group, MALAT1 overexpression significantly reduced miR-141-3p expression levels, increased the rate of TUNEL positive cells and upregulated the expression levels of pyroptosis-associated proteins. MALAT1 knockdown displayed the opposite effect on the rate of TUNEL positive cells and the expression levels of pyroptosis-associated proteins. Furthermore, the rate of TUNEL positive cells, and GSDMD-N and pyroptosis-associated protein expression levels were significantly reduced by miR-141-3p overexpression in MALAT1-overexpression H9C2 cells. The results indicated that compared with NG treatment, HG treatment increased MALAT1 expression levels and decreased miR-141-3p expression levels in H9C2 cells. Therefore, the present study suggested that lncRNA-MALAT1 targeted miR-141-3p to promote HG-induced H9C2 cardiomyocyte pyroptosis.	NA	Mol Med Rep. 2021 Apr;23(4):259. doi: 10.3892/mmr.2021.11898. Epub 2021 Feb 12.
4746	LncRNA	MALAT1	miR-206	NA	C57BL/6J mice and BEAS-2B cells	Neonatal Bronchopulmonary Dysplasia	Homo sapiens (human)	qRT-PCR	33594304	LncRNA-MALAT1, as a biomarker of neonatal BPD, exacerbates the pathogenesis of BPD by targeting miR-206.	Neonatal bronchopulmonary dysplasia (BPD) is one of the common causes of premature birth complications, which is caused by lung dysplasia. Long non-coding RNA (LncRNA) has been proved to be related to BPD and other disease processes, but the molecular mechanism of metastasis-related lung adenocarcinoma transcript 1 (MALAT1) in BPD has not been fully understood. This study focused on exploring the clinical and molecular mechanism of MALAT1 in neonatal BPD, aiming to provide new insights for the management of neonatal BPD. In our study, we first found that serum MALAT1 was up-regulated in neonatal BPD and severe BPD. Further, through receiver operating characteristic curve (ROC) analysis, it was found that the area under the curve of MALAT1 for differentiating neonatal BPD from severe BPD was 0.943 and 0.866, respectively. Then, we established BPD models in vivo and in vitro with C57BL/6J mice and BEAS-2B cells, and found that MALAT1 was also highly expressed in them and increased with the induction time of the models. Pathological evaluation confirmed that down-regulating MALAT1 or up-regulating miR-206 might improve the pathological condition of BPD. Obvious inflammatory response, oxidative stress and up-regulated apoptosis were observed in BPD models in vivo and in vitro. However, after MALAT1 knockdown treatment, the above abnormal phenomena were alleviated to varying degrees. Furthermore, we also found that MALAT1 has a targeted relationship with miR-206, and miR-206 is down-regulated in BPD in vivo and in vitro. Down-regulating miR-206 could also eliminate the anti-BPD effect after knocking down MALAT1. The above results indicated that MALAT1 has the potential as a blood biomarker of neonatal BPD, and MALAT1-miR-206 axis mediates BPD process, which may be a new target for neonatal BPD treatment.	NA	Am J Transl Res. 2021 Feb 15;13(2):462-479. eCollection 2021.
4747	LncRNA	MEG3	miR-9-5p	MDK	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33747202	Long non-coding RNA maternally expressed gene 3 affects cell proliferation, apoptosis and migration by targeting the microRNA-9-5p/midkine axis and activating the phosphoinositide-dependent kinase/AKT pathway in hepatocellular carcinoma.	Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) is a tumor suppressor in several cancers, such as glioma, prostate cancer and esophageal cancer. However, the role of MEG3 in hepatocellular carcinoma (HCC) and the related molecular mechanisms are not well understood. The present study aimed to determine the biological function of MEG3 in regulating HCC cell viability, apoptosis and migration. In addition, the interaction between MEG3, microRNA (miR)-9-5p and Midkine (MDK), and the activation of the phosphoinositide-dependent kinase (PDK)/AKT pathway in HCC cell line MHCC-97L were examined. Luciferase reporter assays, reverse transcription-quantitative PCR and western blotting were used to determine the interaction between MEG3, miR-9-5p and MDK and the activation of the PDK/AKT pathway. Cell viability was determined by the CCK8 assay and the cell cycle analysis using flow cytometry analysis. Cell apoptosis was examined by flow cytometry analysis and caspase 3/9 activity. Wound healing assays and western blotting were used to investigate cell migration. The present study demonstrated that MEG3 suppressed HCC cell viability and migration, and induced cell apoptosis. In addition, it was also found that MEG3 targets the miR-9-5p/MDK axis and modulates the PDK/AKT pathway in HCC. In conclusion, the findings of the present study demonstrated that lncRNA MEG3 affects HCC cell viability, apoptosis and migration through its targeting of miR-9-5p/MDK and regulation of the PDK/AKT pathway. The MEG3/miR-9-5p/MDK axis may be a potential therapeutic target in HCC.	NA	Oncol Lett. 2021 May;21(5):345. doi: 10.3892/ol.2021.12606. Epub 2021 Mar 3.
4748	LncRNA	MIAT	miR-147a	BCOR	laryngeal squamous cell carcinoma	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;	33419582	Long Noncoding RNA MIAT Regulates the Process of Laryngeal Squamous Cell Carcinoma Through Regulation of miR-147a/BCOR.	BACKGROUND: Myocardial infarction associated transcript (MIAT) is a long non-coding RNA (lncRNA) that can play oncogenic role in different kinds of cancers. However, its role in laryngeal squamous cell carcinoma (LSCC) remains unknown. AIM: The study aimed to explore the effect of MIAT/miR-147a/BCOR axis on LSCC progression. METHODS: The expression pattern of MIAT, miR-147a and BCOR in LSCC samples and cells was identified through qRT-PCR. The proliferation of LSCC cells was assessed by colony formation assay and CCK-8 assays. Transwell assays were implemented to test the migratory and invasive abilities of LSCC cells. Proteins associated with migration and epithelial-mesenchymal transition were probed in transfected LSCC cells by western blot. The interaction of miR-147a with MIAT or BCOR was analyzed by luciferase reporter assays, RNA pulls down assays and Ago2-RIP assays. RESULTS: High MIAT expression was closely correlated with unfavorable prognosis. MIAT knockdown inhibited cell proliferation, migration, invasion and EMT progress in LSCC. MIAT acted as a miR-147a sponge to increase the expression of BCOR. Silencing of MIAT suppressed LSCC progression through miR-147a/BCOR axis. CONCLUSION: MIAT acts as an oncogene by controlling miR-147a/BCOR axis in LSCC.	NA	Arch Med Res. 2021 May;52(4):371-379. doi: 10.1016/j.arcmed.2020.12.001. Epub 2021 Jan 5.
4749	LncRNA	MIR22HG	miR-2861	STAT3	endometrial cells	Adenomyosis	Homo sapiens (human)	Cell proliferation assay;qPCR;RT-qPCR;Luciferase report assay;	33624428	LncRNA MIR22HG is downregulated in adenomyosis and upregulates miR-2861 through demethylation to inhibit endometrial cell proliferation.	AIM: Endometrial cell proliferation plays a critical role in adenomyosis. It has been reported that MIR22HG and miR-2861 play similar roles in regulating endometrial cell proliferation, indicating their involvement in adenomyosis. This study aimed to investigate the potential involvement of MIR22HG and miR-2861 in adenomyosis. METHODS: Endometrial biopsy was collected from both adenomyosis (n = 45) and the healthy controls (n = 45). The expression of MIR22HG and miR-2861 in biopsies were determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR). The relationship between MIR22HG and miR-2861 in endometrial cells was analyzed by RT-qPCR. Methylation-specific PCR (MSP) was performed to analyze the effects of overexpression of MIR22HG on the expression of miR-2861. Western-blot assays were performed to illustrate the effect of MIR22HG, miR-2861, STAT3, and MMP2 on adenomyosis. Luciferase report assay was performed to analyze the interactions among miR-2861, STAT3, and MMP2. The role of MIR22HG and miR-2861 in regulating the proliferation of endometrial cells was analyzed by cell proliferation assay. RESULTS: The expression of MIR22HG and miR-2861 in adenomyosis did not change with menstrual cycle. MIR22HG and miR-2861 were significantly downregulated in adenomyosis and they were significantly and positively correlated with each other. In endometrial cells, overexpression of MIR22HG upregulated the expression of miR-2861 and decreased methylation of miR-2861 gene. MIR22HG and miR-2861 downregulated STAT3 and MMP2 to inhibit the proliferation of endometrial cells. In addition, overexpression of both MIR22HG and miR-2861 showed stronger effects. CONCLUSION: MIR22HG is downregulated in adenomyosis and upregulates miR-2861 through demethylation to inhibit endometrial cell proliferation.	NA	J Obstet Gynaecol Res. 2021 May;47(5):1837-1845. doi: 10.1111/jog.14665. Epub 2021 Feb 23.
4750	LncRNA	MIR22HG	miR-2861	MMP2	endometrial cells	Adenomyosis	Homo sapiens (human)	Cell proliferation assay;qPCR;RT-qPCR;Luciferase report assay;	33624428	LncRNA MIR22HG is downregulated in adenomyosis and upregulates miR-2861 through demethylation to inhibit endometrial cell proliferation.	AIM: Endometrial cell proliferation plays a critical role in adenomyosis. It has been reported that MIR22HG and miR-2861 play similar roles in regulating endometrial cell proliferation, indicating their involvement in adenomyosis. This study aimed to investigate the potential involvement of MIR22HG and miR-2861 in adenomyosis. METHODS: Endometrial biopsy was collected from both adenomyosis (n = 45) and the healthy controls (n = 45). The expression of MIR22HG and miR-2861 in biopsies were determined by quantitative reverse transcription polymerase chain reaction (RT-qPCR). The relationship between MIR22HG and miR-2861 in endometrial cells was analyzed by RT-qPCR. Methylation-specific PCR (MSP) was performed to analyze the effects of overexpression of MIR22HG on the expression of miR-2861. Western-blot assays were performed to illustrate the effect of MIR22HG, miR-2861, STAT3, and MMP2 on adenomyosis. Luciferase report assay was performed to analyze the interactions among miR-2861, STAT3, and MMP2. The role of MIR22HG and miR-2861 in regulating the proliferation of endometrial cells was analyzed by cell proliferation assay. RESULTS: The expression of MIR22HG and miR-2861 in adenomyosis did not change with menstrual cycle. MIR22HG and miR-2861 were significantly downregulated in adenomyosis and they were significantly and positively correlated with each other. In endometrial cells, overexpression of MIR22HG upregulated the expression of miR-2861 and decreased methylation of miR-2861 gene. MIR22HG and miR-2861 downregulated STAT3 and MMP2 to inhibit the proliferation of endometrial cells. In addition, overexpression of both MIR22HG and miR-2861 showed stronger effects. CONCLUSION: MIR22HG is downregulated in adenomyosis and upregulates miR-2861 through demethylation to inhibit endometrial cell proliferation.	NA	J Obstet Gynaecol Res. 2021 May;47(5):1837-1845. doi: 10.1111/jog.14665. Epub 2021 Feb 23.
4751	LncRNA	MRPL23-AS1	miR-30b	MYH9	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	FISH;FISH;RNA pull-down;	33356805	Long non-coding RNA (LncRNA) MRPL23-AS1 promotes tumor progression and carcinogenesis in osteosarcoma by activating Wnt/β-catenin signaling via inhibiting microRNA miR-30b and upregulating myosin heavy chain 9 (MYH9).	Long non-coding RNA (LncRNA) contributes to the occurrence and development of osteosarcoma (OS), although the underlying mechanism is not clear. In the present study, we showed that lncRNA MRPL23-AS1 was remarkably increased in OS tissues and cell lines. Stable knockdown of MRPL23-AS1 evidently attenuated cell viability and invasive ability, meanwhile inhibited in vivo tumor growth and dissemination. In terms of mechanism, luciferase reporter, RNA pull-down and fluorescence in situ hybridization (FISH) assays showed that MRPL23-AS1 competitively interacted with miR-30b, increasing myosin heavy chain 9 (MYH9) expression, a trans- activator of β-catenin, resulting in the activation of Wnt/β-catenin pathway, thereby promoting OS tumorigenesis and metastasis. Importantly, high MRPL23-AS1 was positively correlated with MYH9, while conversely correlated with miR-30b, suggesting that the regulatory axis of MRPL23-AS1/miR-30b/MYH9 does exist in OS. Clinically, OS patients with high MRPL23-AS1 had larger tumor size, higher stage and easier metastasis than those with low MRPL23-AS1, moreover, MRPL23-AS1 was identified as an adverse prognostic factor for OS survival. In conclusion, our results show that MRPL23-AS1 is a key oncogenic lncRNA in OS, targeting of MRPL23-AS1 may be a promising treatment for OS patients.	NA	Bioengineered. 2021 Dec;12(1):162-171. doi: 10.1080/21655979.2020.1863014.
4752	LncRNA	MSC-AS1	miR-142-5p	DDX5	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR	33819916	MSC-AS1 induced cell growth and inflammatory mediators secretion through sponging miR-142-5p/DDX5 in gastric carcinoma.	Emerging studies have noted that dysregulated lncRNAs are implicated in cancer progression and tumorigenesis. We first showed that MSC-AS1 was overexpressed in gastric cancer (GC) cells (HGC-27, MKN-45, SGC-7901 and MGC-803 cells) compared with GES cells. We observed that MSC-AS1 was upregulated in GC specimens compared with paired normal specimens. MSC-AS1 increased cell growth and cycle progression. Moreover, the overexpression of MSC-AS1 enhanced the secretion of the inflammatory mediators IL-1β, IL-6 and TNF-α. We found that the overexpression of MSC-AS1 inhibited the expression of miR-142-5p in HGC-27 cells. We noted that DDK5 was a target gene of miR-142-5p. The overexpression of miR-142-5p suppressed the luciferase activity of wild-type DDX5, but the luciferase activity of the mutant DDX5 was not changed. We showed that miR-142-5p was downregulated in GC specimens compared with paired normal specimens. MSC-AS1 expression was inversely correlated with miR-142-5p expression in GC specimens. MSC-AS1 induced cell growth, cell cycle progression and inflammatory mediator secretion by modulating DDX5. These results showed that MSC-AS1 functions as a key oncogene in the development of GC.	NA	Aging (Albany NY). 2021 Apr 4;13(7):10387-10395. doi: 10.18632/aging.202800. Epub 2021 Apr 4.
4753	LncRNA	NEAT1	miR-590-3p	MDM2	ESCC cells	Esophageal Squamous Cancer	Homo sapiens (human)	Western blot;	33680941	Long Noncoding RNA Nuclear Paraspeckle Assembly Transcript 1 Promotes Progression and Angiogenesis of Esophageal Squamous Cell Carcinoma Through miR-590-3p/MDM2 Axis.	Angiogenesis has been identified as one of the hallmarks of cancer and aggravates cancer development and progression. Accumulating evidence indicated that long noncoding RNAs (lncRNAs) are powerful factors in regulating various cancer behaviors. The aim of this study is to verify the function and potential mechanisms of lncRNA NEAT1 in progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). We found that NEAT1 was overexpressed in ESCC tissues and correlated with clinical characteristics of patients. Silence of NEAT1 inhibited proliferation, migration, invasion and angiogenesis of ESCC cells. High throughput sequencing and western blotting revealed that NEAT1 regulated MDM2/p53 pathway. Rescue of MDM2 restored the effect of NEAT1 on progression and angiogenesis of ESCC cells. Nude mice xenograft models further validated the role of NEAT1 in vivo. Importantly, NEAT1 functioned as a competing endogenous RNA for miR-590-3p to regulate MDM2 expression and miR-590-3p acted as a tumor suppressor in ESCC progression and angiogenesis. These findings suggested that NEAT1/miR-590-3p/MDM2 axis might serve as potential therapeutic targets for ESCC patients.	NA	Front Oncol. 2021 Feb 19;10:618930. doi: 10.3389/fonc.2020.618930. eCollection 2020.
4754	LncRNA	NEAT1	miR-222-3p	CDKN1B	mesangial cells	High Glucose-Induced Mesangial Cell Hypertrophy	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Chromatin immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33585566	LncRNA NEAT1 Promotes High Glucose-Induced Mesangial Cell Hypertrophy by Targeting miR-222-3p/CDKN1B Axis.	Glomerular hypertrophy is an early morphological alteration in diabetic nephropathy. Cyclin-Dependent Kinases have been shown to be required for high glucose (HG)-induced hypertrophy; however, the upstream regulators of CDKN1B in glomerular hypertrophy remain unclear. Herein we describe a novel pathway in which Long noncoding RNA (lncRNA) NEAT1 regulates the progression of mesangial cell hypertrophy via a competing endogenous RNA (ceRNA) mechanism. Real-time PCR was performed to detect the relative NEAT1 and miR-222-3p expressions and further confirmed the relationship between NEAT1 and miR-222-3p. Cell cycle was evaluated by flow cytometry. The related mechanisms were explored by Western blot, RNA immunoprecipitation and chromatin immunoprecipitation assay. We show that NEAT1 forms double stranded RNA (dsRNA) with miR-222-3p, thus limiting miR-222-3p's binding with CDKN1B. This release of CDKN1B mRNA leads to elevated CDKN1B protein expression, resulting in hypertrophy. In addition, we demonstrated that STAT3 which is activated by HG induces the transcription of NEAT1 by binding to its promoter. Our findings underscore an unexpected role of lncRNAs on gene regulation and introduce a new mode of proliferation regulation in mesangial cells.	NA	Front Mol Biosci. 2021 Jan 27;7:627827. doi: 10.3389/fmolb.2020.627827. eCollection 2020.
4755	LncRNA	NEAT1	miR-486-5p	NR4A1	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33337350	Upregulation lnc-NEAT1 contributes to colorectal cancer progression through sponging miR-486-5p and activating NR4A1/Wnt/β-catenin pathway.	Colorectal cancer is a major public health problem and fourth guiding cause of cancer-induced mortality worldwide. The five-year survival rate for patients with colorectal cancer remains poor, and almost half of colorectal cancer patients present recurrence and die within five years. The increasing studies showed that long non-coding RNA (lncRNA) was involved in colorectal cancer. Therefore, this study was used to explore molecular mechanisms of nuclear paraspeckle assembly transcript 1 (NEAT1) in colorectal cancer. The real-time quantitative polymerase chain reaction (RT-qPCR) was employed to estimate the expression levels of NEAT1, Nuclear receptor 4 A1 (NR4A1), and miR-486-5p in colorectal cancer tissues and cells. Kaplan-Meier curve was conducted to analyze relationship between survival time of colorectal cancer patients and level of NEAT1. The protein levels of NR4A1, β-catenin, c-Myc, and cyclinD1 were assessed with western blot assay. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and flow cytometry assays were performed to evaluate proliferation and apoptosis of colorectal cancer cells, respectively. The migration and invasion abilities of cells were examined by transwell assay. The relationship between miR-486-5p and NEAT1 or NR4A1 was confirmed by dual-luciferase reporter assay. We found NEAT1 and NR4A1 were highly expressed in colorectal cancer tissues and cell lines compared with controls. Loss-functional experiments revealed that knockdown of NEAT1 or NR4A1 repressed proliferation and motility, while inducing apoptosis of colorectal cancer cells. The gain of NR4A1 could abolish NEAT1 silencing-induced effects in colorectal cancer cells. In addition, NEAT1 contributed to colorectal cancer progression through mediating NR4A1/Wnt/β-catenin signaling pathway. In conclusion, NEAT1 stimulated colorectal cancer progression via acting as competing endogenous RNA to sponge miR-486-5p and regulate NR4A1/Wnt/β-catenin signaling pathway.	NA	Cancer Biomark. 2021;30(3):309-319. doi: 10.3233/CBM-201733.
4756	LncRNA	NEAT1	miR-455-3p	SMAD3	epithelial cells	Pulmonary Fibrosis	Homo sapiens (human)	Western blot;	33495816	Long non-coding RNA NEAT1 promotes pulmonary fibrosis by regulating the microRNA-455-3p/SMAD3 axis.	Pulmonary fibrosis is an excessive repair response to tissue damage, triggering hyperplasia of fibrotic connective tissues; however, there is no effective treatment in a clinical setting. The purpose of the present study was to investigate the roles of long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) and microRNA-455-3p (miR-455-3p) were investigated in pulmonary fibrosis. In this study, the mRNA expression levels of NEAT1, miR-455-3p and SMAD3 in the HPAEpiC alveolar and BEAS-2B bronchial epithelial cell lines were determined using reverse transcription-quantitative PCR, while the markers of epithelial-mesenchymal transformation (EMT) and collagen production were determined using western blot analysis. A wound healing assay was performed to evaluate the migratory ability of the HPAEpiC and BEAS-2B cell lines. The interactions between NEAT1 and miR-455-3p or SMAD3 and miR-455-3p were validated using a luciferase reporter gene assay. The results showed that the mRNA expression levels of NEAT1 and SMAD3 were upregulated in the TGF-β1-treated HPAEpiC and BEAS-2B cell lines, while the mRNA expression level of miR-455-3p was significantly decreased. In addition, silencing NEAT1 effectively alleviated the migratory ability, EMT and collagen generation of the epithelial cells. Following these experiments, NEAT1 was identified as a sponge for miR-455-3p, and SMAD3 was a target gene of miR-455-3p. NEAT1 downregulation or miR-455-3p mimic inhibited the migratory ability, EMT and collagen production of the epithelial cells; however, the effects were reversed by the overexpression of SMAD3. Furthermore, NEAT1 knockdown reduced the expression level of SMAD3 by increasing the expression level of miR-455-3p to further inhibit the migratory ability, EMT and collagen production of epithelial cells.	NA	Mol Med Rep. 2021 Mar;23(3):218. doi: 10.3892/mmr.2021.11857. Epub 2021 Jan 26.
4757	LncRNA	NEAT1	miR-186-5p	PTP4A1	cholangiocarcinoma cells	Cholangiocarcinoma	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33502823	LncRNA NEAT1 promotes cell proliferation, migration, and invasion via the miR-186-5p/PTP4A1 axis in cholangiocarcinoma.	Cholangiocarcinoma (CCA) is a highly aggressive and malignant tumor. In this study, the effect and molecular mechanism of nuclear enriched abundant transcript 1 (NEAT1) in CCA were elucidated. The expressions of NEAT1, microRNA-186-5p (miR-186-5p), and PTP4A1 were measured by quantitative real-time PCR. The protein levels were measured by Western blotting. Kaplan-Meier analysis was performed to create survival curves. The interactions between NEAT1, miR-186-5p, and PTP4A1 were assessed through the dual luciferase reporter assay. Additionally, the cell proliferation, apoptosis, migration, and invasion were measured by colony formation, flow cytometry, the Transwell assay, and the wound healing assay, respectively. NEAT1 and PTP4A1 were significantly upregulated in CCA tissues and cells, but miR-186-5p was downregulated. NEAT1 expression was negatively correlated with the survival of CCA patients and has remarkable correlation with serum CA199 levels and lymph node metastasis. Besides, NEAT1 could act as a molecular sponge for miR-186-5p to upregulate PTP4A1 expression. More importantly, the knockdown of NEAT1 or overexpression of miR-186-5p inhibited the proliferation, migration and invasion of CCA cells, and the inhibition of miR-186-5p reversed the effects of the knockdown of NEAT1. In addition, NEAT1 could also activate the PI3K/AKT signaling pathway and regulate the epithelial-mesenchymal transition (EMT) through the miR-186-5p/PTP4A1 axis. In conclusion, NEAT1 was involved in cell proliferation, migration and invasion in CCA, and the NEAT1/miR-186-5p/PTP4A1/PI3K/AKT axis indicated novel regulatory mechanisms and therapeutics for the treatment of CCA.	NA	Kaohsiung J Med Sci. 2021 May;37(5):379-391. doi: 10.1002/kjm2.12354. Epub 2021 Jan 27.
4758	LncRNA	NEAT1	miR-128-3p	AQP4	microglial cells	Neuropathic Pain	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;RT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33373887	LncRNA NEAT1/miR-128-3p/AQP4 axis regulating spinal cord injury-induced neuropathic pain progression.	BACKGROUND: Neuropathic pain (NP) is the comorbidity in spinal cord injury(SCI), which is the hardest to cure. Non-coding RNA dysregulations are related to the development of NP. NEAT1(nuclear paraspeckle assembly transcript 1) is a new type of lncRNA. This study explores the role and specific mechanism of NEAT1 in SCI-mediated NP. METHODS: Firstly, the NEAT1 expression in SCI rats and the control group was detected with RT-PCR to analyze the relationship between NEAT13 and NP symptoms. Then, SCI rats were intrathecally injected with NEAT13 overexpressing and knocking down lentiviruses. Afterward, ELISA was utilized to assess the expression of IL-6, IL-1β and TNFα in rats. Subsequently, immunohistochemistry was adopted to verify the activation of microglial cells. After that, bioinformatics analysis was employed to further predict the downstream target genes of NEAT1, while RT-PCR and Western blot were conducted to determine the relative expression of miR-128-3p and aquaporin-4(AQP4). Meanwhile, a dual-luciferase reporter assay was performed to further study the targeting relationship between NEAT1 and miR-128-3p, and miR-128-3p and AQP4. RESULTS: SCI rats showed distinctly higher NEAT1 expression compared with that of the control group. ELISA experiment confirmed that the over-expression of NEAT1 enhanced the expression of IL-6, IL-1β, and TNFα in SCI rats. Other related mechanism studies revealed that NEAT13 targeted and inhibited miR-128-3p as its competing endogenous RNA (ceRNA), and enhanced AQP4 expression, while miR-128-3p targeted AQP4 to regulate its expression. SUMMARY: NEAT1 affects AQP4 signaling pathway to alleviate the spinal cord injury-induced NP via promoting miR-128-3p expression.	NA	J Neuroimmunol. 2021 Feb 15;351:577457. doi: 10.1016/j.jneuroim.2020.577457. Epub 2020 Dec 9.
4759	LncRNA	NEAT1	miR-944	TRIM37	WI-38 cells	Acute Lung Injury	Homo sapiens (human)	Rescue assay;	33451755	LncRNA NEAT1 acts as a key regulator of cell apoptosis and inflammatory response by the miR-944/TRIM37 axis in acute lung injury.	Acute lung injury (ALI), a common complication of sepsis, is characterized by the impairment and injury of pulmonary function. The nuclear factor kappa-B (NF-κB) pathway is activated in ALI. Tripartite motif-containing 37 (TRIM37) can activate the NF-κB pathway and is closely associated with inflammation. The purpose of our study is to reveal the role of TRIM37 in ALI. The present study revealed that TRIM37 presented high levels in lung tissues of ALI mice, and knockdown of TRIM37 alleviated lipopolysaccharide (LPS)-induced lung injury, inflammatory response, and cell apoptosis in vivo. In addition, knockdown of TRIM37 inhibited the inflammatory response, and cell apoptosis of LPS-treated WI-38 cells. Mechanistically, miR-944 was identified to bind with and negatively regulate TRIM37. Furthermore, NEAT1 was indicated to act as a competitive endogenous RNA to promote TRIM37 expression by sequestering miR-944. Detailly, NEAT1 bound with miR-944, negatively modulated miR-944 expression, and positively modulated TRIM37 expression. The rescue assays suggested that overexpression of TRIM37 rescued the influence of NEAT1 knockdown on cell apoptosis and inflammatory response. Overall, NEAT1 facilitated cell apoptosis and inflammatory response of WI-38 cells by the miR-944/TRIM37 axis in sepsis-induced ALI, implying that NEAT1 may provide a novel insight for the treatment of sepsis-induced ALI.	NA	J Pharmacol Sci. 2021 Feb;145(2):202-212. doi: 10.1016/j.jphs.2020.11.009. Epub 2020 Nov 24.
4760	LncRNA	NEAT1	miR-29b-3p	Sp1	multiple myeloma cells	Multiple Myeloma	Homo sapiens (human)	MTT assay;Chromatin immunoprecipitation;Flow Cytometry assay;MTT assay;	33253679	Lnc NEAT1/miR-29b-3p/Sp1 form a positive feedback loop and modulate bortezomib resistance in human multiple myeloma cells.	The overall survival of multiple myeloma (MM) patients significantly improved with the use of proteasome inhibitor such as bortezomib. However, resistance to sorafenib limits its use. Bortezomib-resistant MM cells were generated and their bortezomib-resistant properties were confirmed by cell viability and apoptosis assays. To explore functions and underlying mechanisms of long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) on bortezomib resistance in MM, MTT assays, flow cytometry analyses, dual luciferase report gene assays, RNA pulldown assays and chromatin immunoprecipitation assays were carried out. NEAT1 and specific protein 1 (Sp1) was upregulated while miR-29b-3p was down regulated in bortezomib-resistant MM cells. NEAT1 promoted Sp1 expression by sponging miR-29b-3p and then enhanced the tolerance of MM cells to bortezomib. Sp1 targeted to NEAT1 promoter region promoting NEAT1 transcription and formed a positive feedback loop. NEAT1 and Sp1 levels were higher and miR-29b-3p was levels were lower in bortezomib-resistant MM patients. NEAT1/miR-29b-3p/Sp1 feedback loop enhanced the tolerance of MM cells to bortezomib. These results indicate potentially valuable targets for overcoming bortezomib resistance for MM.	NA	Eur J Pharmacol. 2021 Jan 15;891:173752. doi: 10.1016/j.ejphar.2020.173752. Epub 2020 Nov 28.
4761	LncRNA	NORAD	miR-211-5p	FOXD1	Hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Luciferase report assay;	33309645	LncRNA NORAD promotes proliferation, migration and angiogenesis of hepatocellular carcinoma cells through targeting miR-211-5p/FOXD1/VEGF-A axis.	INTRODUCTION AND OBJECTIVES: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death around the world. Despite improvement in the prevention and treatment of HCC, the clinical prognosis is still poor with increasing mortality. Non-coding RNAs play pivotal roles in HCC oncogenesis, but the detailed mechanism is poorly known. Therefore, the functions and interaction of lncRNA NORAD and miR-211-5p in HCC was investigated in this study. METHODS: Quantitative real-time PCR method was used to analyze the expression of NORAD and miR-211-5p in clinical HCC tissues and cultured cell lines. Knockdown of NORAD and overexpression of miR-211-5p were then carried in HCC cells. Moreover, bioinformatics analysis and luciferase report assays were further employed to analyze the interaction between miR-211-5p and NORAD or FOXD1. RESULTS: Increased lncRNA NORAD and decreased miR-211-5p expression were first detected in HCC compared with the peritumorial area. Further studies showed that knockdown of NORAD or overexpression of miR-211-5p impaired the proliferation, migration and angiogenesis of HCC cells. Mechanistically, we found that NORAD functions as a sponge for miR-211-5p. Moreover, it was revealed that decreased miR-211-5p induced the expression of FOXD1 as well as its downstream target VEGF-A, thereby contributes to enhanced angiogenesis of HCC. CONCLUSION: Elevated NORAD works as a sponge for miR-211-5p in HCC, thus release the inhibition effect of the latter on its downstream target FOXD1 and VEGF-A, which finally promotes angiogenesis. These results provide new insights into the interaction between NORAD and miR-211-5p in HCC and their potential usage as targets for the development of novel therapeutics against HCC.	NA	Microvasc Res. 2021 Mar;134:104120. doi: 10.1016/j.mvr.2020.104120. Epub 2020 Dec 11.
4762	LncRNA	NORAD	miR-211-5p	VEGF-A	Hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	Luciferase report assay;	33309645	LncRNA NORAD promotes proliferation, migration and angiogenesis of hepatocellular carcinoma cells through targeting miR-211-5p/FOXD1/VEGF-A axis.	INTRODUCTION AND OBJECTIVES: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death around the world. Despite improvement in the prevention and treatment of HCC, the clinical prognosis is still poor with increasing mortality. Non-coding RNAs play pivotal roles in HCC oncogenesis, but the detailed mechanism is poorly known. Therefore, the functions and interaction of lncRNA NORAD and miR-211-5p in HCC was investigated in this study. METHODS: Quantitative real-time PCR method was used to analyze the expression of NORAD and miR-211-5p in clinical HCC tissues and cultured cell lines. Knockdown of NORAD and overexpression of miR-211-5p were then carried in HCC cells. Moreover, bioinformatics analysis and luciferase report assays were further employed to analyze the interaction between miR-211-5p and NORAD or FOXD1. RESULTS: Increased lncRNA NORAD and decreased miR-211-5p expression were first detected in HCC compared with the peritumorial area. Further studies showed that knockdown of NORAD or overexpression of miR-211-5p impaired the proliferation, migration and angiogenesis of HCC cells. Mechanistically, we found that NORAD functions as a sponge for miR-211-5p. Moreover, it was revealed that decreased miR-211-5p induced the expression of FOXD1 as well as its downstream target VEGF-A, thereby contributes to enhanced angiogenesis of HCC. CONCLUSION: Elevated NORAD works as a sponge for miR-211-5p in HCC, thus release the inhibition effect of the latter on its downstream target FOXD1 and VEGF-A, which finally promotes angiogenesis. These results provide new insights into the interaction between NORAD and miR-211-5p in HCC and their potential usage as targets for the development of novel therapeutics against HCC.	NA	Microvasc Res. 2021 Mar;134:104120. doi: 10.1016/j.mvr.2020.104120. Epub 2020 Dec 11.
4763	LncRNA	NORAD	miR-30-5p	RAB11A	Prostate cancer cells	Prostate Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33292272	Long non-coding RNA NORAD contributes to the proliferation, invasion and EMT progression of prostate cancer via the miR-30a-5p/RAB11A/WNT/β-catenin pathway.	BACKGROUND: Prostate cancer (PC) is common male cancer with high mortality worldwide. Emerging evidence demonstrated that long noncoding RNAs (lncRNAs) play critical roles in various type of cancers including PC by serving as competing endogenous RNAs (ceRNAs) to modulate microRNAs (miRNAs). LncRNA activated by DNA damage (NORAD) was found to be upregulated in PC cells, while the detailed function and regulatory mechanism of NORAD in PC progression remains largely unclear. METHODS: Expression of NORAD in PC tissues and cell lines were detected by real-time quantitative PCR (qRT-PCR). NORAD was respectively overexpressed and knocked down by transfection with pcDNA-NORAD and NORAD siRNA into PC-3 and LNCap cells. Cell proliferation, invasion and apoptosis were determined by using CCK-8, Transwell and Flow cytometry assays, respectively. The target correlations between miR-30-5p and NORAD or RAB11A were confirmed by using dual luciferase reporter assay. Moreover, expression levels of RAB11A, the epithelial-mesenchymal transition (EMT) marker proteins and the Wnt pathway related proteins were measured by Western blotting. Tumor xenograft assay was used to study the effect of NORAD on tumor growth in vivo. RESULTS: NORAD was upregulated in PC tissues and cells. Overexpression of NORAD promoted cell proliferation, invasion, EMT, and inhibited cell apoptosis; while knockdown of NORAD had the opposite effect. NORAD was found to be functioned as a ceRNA to bind and downregulated miR-30a-5p that was downregulated in PC tumor tissues. Rescue experiments revealed that miR-30a-5p could weaken the NORAD-mediated promoting effects on cell proliferation, invasion and EMT. Furthermore, RAB11A that belongs to a member of RAS oncogene family was verified as a target of miR-30a-5p, and reintroduction of RAB11A attenuated the effects of miR-30a-5p overexpression on cell proliferation, invasion, EMT and apoptosis of PC cells. More importantly, silencing RAB11A partially reversed the promoting effects of NORAD overexpression on cell proliferation, invasion and EMT of PC cells via the WNT/β-catenin pathway. Lastly, tumorigenicity assay in vivo demonstrated that NORAD increased tumor volume and weight via miR-30a-5p /RAB11A pathway. CONCLUSION: Our results indicated a significant role of NORAD in mechanisms associated with PC progression. NORAD promoted cell proliferation, invasion and EMT via the miR-30a-5p/RAB11A/WNT/β-catenin pathway, thus inducing PC tumor growth.	NA	Cancer Cell Int. 2020 Nov 27;20(1):571. doi: 10.1186/s12935-020-01665-2.
4764	LncRNA	NORAD	miR-30-5p	WNT	Prostate cancer cells	Prostate Cancer	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33292272	Long non-coding RNA NORAD contributes to the proliferation, invasion and EMT progression of prostate cancer via the miR-30a-5p/RAB11A/WNT/β-catenin pathway.	BACKGROUND: Prostate cancer (PC) is common male cancer with high mortality worldwide. Emerging evidence demonstrated that long noncoding RNAs (lncRNAs) play critical roles in various type of cancers including PC by serving as competing endogenous RNAs (ceRNAs) to modulate microRNAs (miRNAs). LncRNA activated by DNA damage (NORAD) was found to be upregulated in PC cells, while the detailed function and regulatory mechanism of NORAD in PC progression remains largely unclear. METHODS: Expression of NORAD in PC tissues and cell lines were detected by real-time quantitative PCR (qRT-PCR). NORAD was respectively overexpressed and knocked down by transfection with pcDNA-NORAD and NORAD siRNA into PC-3 and LNCap cells. Cell proliferation, invasion and apoptosis were determined by using CCK-8, Transwell and Flow cytometry assays, respectively. The target correlations between miR-30-5p and NORAD or RAB11A were confirmed by using dual luciferase reporter assay. Moreover, expression levels of RAB11A, the epithelial-mesenchymal transition (EMT) marker proteins and the Wnt pathway related proteins were measured by Western blotting. Tumor xenograft assay was used to study the effect of NORAD on tumor growth in vivo. RESULTS: NORAD was upregulated in PC tissues and cells. Overexpression of NORAD promoted cell proliferation, invasion, EMT, and inhibited cell apoptosis; while knockdown of NORAD had the opposite effect. NORAD was found to be functioned as a ceRNA to bind and downregulated miR-30a-5p that was downregulated in PC tumor tissues. Rescue experiments revealed that miR-30a-5p could weaken the NORAD-mediated promoting effects on cell proliferation, invasion and EMT. Furthermore, RAB11A that belongs to a member of RAS oncogene family was verified as a target of miR-30a-5p, and reintroduction of RAB11A attenuated the effects of miR-30a-5p overexpression on cell proliferation, invasion, EMT and apoptosis of PC cells. More importantly, silencing RAB11A partially reversed the promoting effects of NORAD overexpression on cell proliferation, invasion and EMT of PC cells via the WNT/β-catenin pathway. Lastly, tumorigenicity assay in vivo demonstrated that NORAD increased tumor volume and weight via miR-30a-5p /RAB11A pathway. CONCLUSION: Our results indicated a significant role of NORAD in mechanisms associated with PC progression. NORAD promoted cell proliferation, invasion and EMT via the miR-30a-5p/RAB11A/WNT/β-catenin pathway, thus inducing PC tumor growth.	NA	Cancer Cell Int. 2020 Nov 27;20(1):571. doi: 10.1186/s12935-020-01665-2.
4765	LncRNA	NR2F1-AS1	miR-493-5p	TRIM2	NB cells	Neuroblastoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33378023	Long non-coding RNA NR2F1-AS1 promoted neuroblastoma progression through miR-493-5p/TRIM2 axis.	OBJECTIVE: Long noncoding RNA (lncRNA) plays a vital role in the progression of various cancers. However, the potential mechanisms of NR2F1-AS1 in the tumorigenesis of neuroblastoma (NB) have not been determined. PATIENTS AND METHODS: The expression levels of NR2F1-AS1, miR-493 and TRIM2 were detected by RT-qPCR. The downstream target genes of NR2F1-AS1 or miR-493 were predicted by bioinformatics analysis (http://starbase.sysu.edu.cn/), which was further indicated by Luciferase reporter and RNA immunoprecipitation (RIP) assays. CCK-8, transwell, and TUNEL assays were performed to determine the viability, migration, invasion and apoptosis of NB cells. RESULTS: NR2F1-AS1 was highly expressed and miR-493 was lowly expressed in NB tissues and cell lines. The high expression of NR2F1-AS1 was associated with poor prognosis in NB. NR2F1-AS1 knockdown inhibited proliferation, migration, and invasion, and accelerated apoptosis of NB cells. MiR-493 was a downstream target of NR2F1-AS1, and the silencing of miR-493 reversed NR2F1-AS1 knockdown-attenuated progression of NB. Moreover, TRIM2 was demonstrated to be directly targeted by miR-493, and the upregulation of TRIM2 could abolish the inhibitory effect of miR-493 overexpression on the progression of NB. Finally, it was found that NR2F1-AS1 regulated TRIM2 expression by sponging miR-493. CONCLUSIONS: The present study demonstrated that NR2F1-AS1 promoted the progression of NB through the miR-493/TRIM2 axis. This finding may provide new insight into the treatment of NB.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12748-12756. doi: 10.26355/eurrev_202012_24174.
4766	LncRNA	OIP5-AS1	miR-143-3p	NA	gallbladder cancer cell lines and gallbladder epithelial cells	Gallbladder Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down;	33364844	Long Non-Coding RNA OIP5-AS1 Contributes to Gallbladder Cancer Cell Invasion and Migration by miR-143-3p Suppression.	OBJECTIVE: This study was designed to investigate the effect of long non-coding RNA (lncRNA) OIP5-AS1 on cell migration and invasion of gallbladder cancer (GBC) and its specific mechanism. METHODS: The expressions of lncRNA OIP5-AS1 and miR-143-3p in GBC cell lines (GBC-SD, SGC996 and NOZ) and gallbladder epithelial cells (HGBE cells) were measured by qRT-PCR. After loss- and gain-of-function experiments for OIP5-AS1 and miR-143-3p in GBC-SD cells, CCK-8 was applied to examine cell viability, cell scratch assay to measure cell migration, and transwell chamber to inspect cell invasion capacity. The interaction between OIP5-AS1 and miR-143-3p was predicted by StarBase. Then, luciferase reporter gene assay and RNA pull-down were used to verify the targeting relationship between miR-143-3p and OIP5-AS1. RESULTS: OIP5-AS1 was highly expressed and miR-143-3p was downregulated in GBC cell lines, when compared with HGBE cells. Overexpression of OIP5-AS1 or downregulation of miR-143-3p facilitated GBC-SD cell invasion, proliferation and migration, while different expression patterns were found in GBC-SD cells in response to OIP5-AS1 suppression or miR-143-3p overexpression. OIP5-AS1 negatively mediated miR-143-3p. MiR-143-3p upregulation partially reversed the inhibitory effect of OIP5-AS1 knockdown on GBC-SD cell activities. CONCLUSION: LncRNA OIP5-AS1 accelerates the progression of GBC by suppressing miR-143-3p.	NA	Cancer Manag Res. 2020 Dec 17;12:12983-12992. doi: 10.2147/CMAR.S278719. eCollection 2020.
4767	LncRNA	OSER1-AS1	miR-612	FOXM1	lung adenocarcinoma	Lung Cancer	Homo sapiens (human)	qRT-PCR	33841662	LncRNA OSER1-AS1 interacts with miR-612/FOXM1 axis to modulate gefitinib resistance of lung adenocarcinoma.	Long noncoding RNAs (lncRNAs) play crucial roles in the acquired resistance to EGFR-directed therapies in lung cancer. LncRNA OSER1-AS1 has been reported to promote tumorigenesis of hepatocellular carcinoma. However, its functions and underlying molecular mechanisms remain unclear in the acquired gefitinib-resistance of lung cancer. Our study revealed that increased expression of OSER1-AS1 was correlated with gefitinib resistance in lung adenocarcinoma. Higher OSER1-AS1 expression predicted disease progression of lung adenocarcinoma patients. The in vitro assays indicated OSER1-AS1 contributed to gefitinib resistance of lung adenocarcinoma cells via inhibiting cell apoptosis and cell cycle arrest. In vivo experiments showed that the knockdown of OSER1-AS1 restored the sensitivity of lung cancer cells to gefitinib. Further studies showed that OSER1-AS1 functioned as a molecular sponge of miR-612. OSER1-AS1 down-regulated miR-612 to increase FOXM1 expression, suggesting that miR-612/FOXM1 axis was regulated by OSER1-AS1, which was partially responsible for gefitinib resistance of lung adenocarcinoma. In conclusion, OSER1-AS1 promoted gefitinib resistance of lung adenocarcinoma through the miR-612/FOXM1 axis.	NA	Am J Transl Res. 2021 Mar 15;13(3):1365-1376. eCollection 2021.
4768	LncRNA	PART1	miR-185-5p	Six1	lung squamous cell carcinoma cells	Lung Cancer	Homo sapiens (human)	qRT-PCR	33346098	Circular RNAs: Promising biomarkers for cancer diagnosis and prognosis.	Circular RNAs (circRNAs), a group of non-coding RNA characterized by the presence of covalent bonds linking 3' and 5' ends, act as miRNA sponges to participate in the tumorigenesis. Being stable, conserved and cell- or tissue-specific, circRNAs have shown their potentials as molecular markers for cancer. Convenient and noninvasive approaches may be developed based on the roles of circRNAs to diagnose or predict the prognosis of tumors. Although most of the potential mechanisms are not entirely clear, circRNAs have shown a universal and critical role in regulating cellular processes of cancers. This review summarized the classification, formation, characteristics, detection, and biological functions of circRNAs. We proposed the possibility of using circRNAs as biomarkers for cancer diagnosis, treatment and prognosis.	NA	Gene. 2021 Mar 1;771:145365. doi: 10.1016/j.gene.2020.145365. Epub 2020 Dec 18.
4769	LncRNA	PART1	miR-18a-5p	SOX6	esophageal squamous cell carcinoma cells	Esophageal Squamous Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33432363	lncRNA PART1, manipulated by transcriptional factor FOXP2, suppresses proliferation and invasion in ESCC by regulating the miR-18a-5p/SOX6 signaling axis.	An increasing number of studies have demonstrated that long non-coding (lnc)RNAs are associated with tumor invasion, metastasis and the prognosis of patients with a variety of different tumors. However, the roles of lncRNA prostate androgen regulated transcript 1 (PART1) in esophageal squamous cell carcinoma (ESCC) remain unknown. In the present study, reverse transcription-quantitative PCR was performed to investigate the levels of PART1, SRY-box transcription factor 6 (SOX6) and miR-18a-5p in ESCC tissues and cells. The functions of PART1 in ESCC were demonstrated using Cell Counting Kit-8 and Matrigel assays. Promoter activity and dual-luciferase reporter assays, RNA immunoprecipitation and western blot analyses were also used to determine the potential mechanisms of PART1 in ESCC cell lines. It was found that PART1 and SOX6 were both downregulated in ESCC tissues and cells, and their low expression levels were associated with TNM stage, lymph node metastasis and poor prognosis in patients with ESCC. Forkhead box protein P2 (FOXP2) exhibited low expression level in ESCC tissues, and its expression was positively correlated with PART1 expression level in ESCC tissues. FOXP2 was found to bind to the promoter region of PART1 to regulate its expression in ESCC cells. Functionally, PART1 overexpression suppressed cell proliferation and invasion, whereas PART1 downregulation promoted cell proliferation and invasion in the ESCC cell lines. Mechanistically, PART1 functions as a competing endogenous (ce)RNA by sponging miR-18a-5p, resulting in the upregulation of the downstream target gene, SOX6, coupled with the inactivation of the β-catenin/c-myc signaling axis, to suppress ESCC cell proliferation and invasion. In conclusion, data from the present study unveil a potential ceRNA regulatory pathway, in which PART1 affects SOX6 expression level by sponging miR-18a-5p, to ultimately suppress ESCC development and progression.	NA	Oncol Rep. 2021 Mar;45(3):1118-1132. doi: 10.3892/or.2021.7931. Epub 2021 Jan 11.
4770	LncRNA	PCAT6	miR-139-3p	BRD4	pituitary adenomas cells	Pituitary Adenoma	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33407504	LncRNA PCAT6 regulates the progression of pituitary adenomas by regulating the miR-139-3p/BRD4 axis.	BACKGROUND: Dysregulated lncRNA PCAT6 was discovered in many cancers excluding pituitary adenomas (PA). Therefore, we explored the role of PCAT6 in PA in this research. METHODS: Abnormally expressed miRNAs were analyzed by bioinformatics and RT-qPCR. The target and regulator of miR-139-3p were determined by bioinformatics, dual-luciferase reporter assay, or RIP. The correlation among PCAT6, miR-139-3p, and BRD4 was further analyzed. The viability, apoptosis, cell cycle distribution of PA cells, as well as their ability to invade, migrate, and proliferate, were tested after transfection through CCK-8, flow cytometry, transwell, wound healing, and colony formation assays. After construction of transplanted-tumor model in nude mice, cell apoptosis in the tumor was detected by TUNEL. The expressions of PCAT6, BRD4, miR-139-3p, and apoptosis-related factors in PA tissues, cells, or tumor tissues were detected by RT-qPCR, Western blot, or IHC. RESULTS: PCAT6 and BRD4 were high-expressed but miR-139-3p was low-expressed in PA. Both the 3'-untranslated regions of PCAT6 and BRD4 mRNAs were demonstrated to contain a potential binding site for miR-139-3p. PCAT6 was positively correlated to BRD4, and miR-139-3p was negatively correlated to PCAT6 and BRD4. MiR-139-3p mimic, shPCAT6 and siBRD4 inhibited the viability, migration, invasion, and proliferation of PA cells while inducing apoptosis. MiR-139-3p mimic and shPCAT6 inhibited the cell cycle progression of PA cells, decreased the weight and volume of the xenotransplanted tumor, and reduced the levels of Bcl-2 and BRD4 while enhancing the levels of Bax, miR-139-3p, and Cleaved caspase-3. MiR-139-3p inhibitor caused the opposite effect of miR-139-3p mimic and further reversed the effect of shPCAT6 on on PA cells. CONCLUSION: PCAT6 regulated the progression of PA via modulating the miR-139-3p/BRD4 axis, which might provide a novel biomarker for the prevention, diagnosis, and treatment of PA.	NA	Cancer Cell Int. 2021 Jan 6;21(1):14. doi: 10.1186/s12935-020-01698-7.
4771	LncRNA	PCGEM1	miR-539-5p	CDK6	glioma tissues and tumor cells	Glioma	Homo sapiens (human)	qRT-PCR;Luciferase reporter assay;	33589577	LncRNA PCGEM1 contributes to malignant behaviors of glioma by regulating miR-539-5p/CDK6 axis.	BACKGROUND: Glioma, one of the most prevalent and aggressive cancers, is regulated by long noncoding RNAs (lncRNAs). This study aims to research the functional mechanism of lncRNA PCGEM1 involved in glioma progression. METHODS: Expression levels of PCGEM1, miR-539-5p and CDK6 were analyzed by qRT-PCR in NHA, U251, U87, and LN229 cells or glioma tissues. shRNAs were used to knock down PCGEM1 in U251 and LN229 cells. Kaplan-Meier curve and log rank test were utilized to examine survival rate. CCK8 (Cell Counting Kit-8) assay, colony formation assay and EdU staining were conducted to detect cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Luciferase reporter assay was conducted to assess RNA interaction between PCGEM1 and miR-539-5p. Nude mice were used for tumor xenograft assay. RESULTS: LncRNA PCGEM1 was upregulated in glioma tissues and tumor cell lines. PCGEM1 upregulation predicted unsatisfactory prognosis. PCGEM1 knockdown inhibited proliferation, colony formation, migration and invasion. PCGEM1 knockdown delayed tumor growth in vivo. PCGEM1 played as a competing endogenous RNA (ceRNA) for miR-539-5p to promote CDK6 expression. MiR-539-5p mimics repressed glioma progression while CDK6 overexpression reversed the roles of PCGEM1 knockdown. CONCLUSION: PCGEM1 knockdown suppressed glioma progression through sponging miR-539-5p and regulating CDK6 expression, implying PCGEM1 as a potential therapeutic target.	NA	Aging (Albany NY). 2021 Feb 11;13(4):5475-5484. doi: 10.18632/aging.202476. Epub 2021 Feb 11.
4772	LncRNA	PGM5P4-AS1	miR-1275	LZTS3	lung cancer cells	Lung Cancer	Homo sapiens (human)	Cell cycle assay;	33315502	Long non-coding RNA (lncRNA) PGM5P4-AS1 inhibits lung cancer progression by up-regulating leucine zipper tumor suppressor (LZTS3) through sponging microRNA miR-1275.	It is necessary to explore new molecules for the improvement of precise diagnosis and antitumor therapies in lung cancer. LncRNAs (long non-coding RNAs) play an important role in the regulation of cancer cell malignant behavior and tumor development. In this work, we found that a newly discovered lncRNA, lncRNA PGM5P4-AS1, was lower expressed in lung cancer tissues than adjacent tissues. Then, the lncRNA PGM5P4-AS1 was overexpressed or knocked-down in different lung cancer cells, and its effects on the malignant phenotypes were measured by 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle assay, wound healing assay, and transwell assay. The results showed that the overexpression of PGM5P4-AS1 inhibited lung cancer cell proliferation, migration, and invasion activities, while these abilities were prominently promoted by the interference of PGM5P4-AS1. Further, the growth of lung cancer tumors in nude mice was also inhibited by PGM5P4-AS1 overexpression. In mechanism, PGM5P4-AS1 has the binding site of miR-1275 and could positively regulate the expression of LZTS3 via sponging miR-1275. In conclusion, PGM5P4-AS1 could be a potential precise diagnosis and therapeutic target biomarker of lung cancer.	NA	Bioengineered. 2021 Dec;12(1):196-207. doi: 10.1080/21655979.2020.1860492.
4773	Circular RNA	PIP5K1A	miR-515-5p	TCF12	glioma tissues and adjacent normal tissues	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33413401	CircRNA PIP5K1A promotes the progression of glioma through upregulation of the TCF12/PI3K/AKT pathway by sponging miR-515-5p.	BACKGROUND: Increasing studies have revealed that circular RNAs (CircRNAs) make great contributions to regulating tumor progression. Therefore, we intended to explore the expression characteristics, function, and related mechanisms of a novel type of circRNA, PIP5K1A, in glioma. METHODS: Firstly, reverse transcription-polymerase chain reaction (RT-PCR) was carried out to examine CircPIP5K1A expression in glioma tissues and adjacent normal tissues, and the correlation between CircPIP5K1A level and the clinical-pathological indicators of glioma was analyzed. Then, the CircPIP5K1A expression in various glioma cell lines was detected, and CircPIP5K1A overexpression and knockdown cell models were constructed. Subsequently, cell proliferation and viability were detected by the CCK8 method and BrdU staining. Cell apoptosis was detected by flow cytometry, and cell invasion was examined by Transwell assay. The expression of TCF12, PI3K/AKT pathway apoptotic related proteins (Caspase3, Bax, and Bcl2) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin, and N-cadherin) was determined by western blot or RT-PCR. RESULTS: The results manifested that CircPIP5K1A was upregulated in glioma tissues (compared with that in normal adjacent tissues), and overexpressed CircPIP5K1A was related to glioma volume and histopathological grade. Functionally, overexpressing CircPIP5K1A notably elevated glioma cell proliferation, invasion, and EMT and inhibited apoptosis both in vivo and in vitro. Besides, CircPIP5K1A upregulated TCF12 and PI3K/AKT activation. Bioinformatics analysis testified that miR-515-5p was a common target of CircPIP5K1A and TCF12, while the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) experiment further confirmed that CircPIP5K1A targeted miR-515-5p, which bound the 3'-untranslated region (UTR) of TCF12. CONCLUSIONS: Overall, the study illustrated that CircPIP5K1A is a potential prognostic marker in glioma and regulates glioma evolvement by modulating the miR-515-5p-mediated TCF12/PI3K/AKT axis.	NA	Cancer Cell Int. 2021 Jan 7;21(1):27. doi: 10.1186/s12935-020-01699-6.
4774	Circular RNA	PIP5K1A	miR-515-5p	PI3K	glioma tissues and adjacent normal tissues	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33413401	CircRNA PIP5K1A promotes the progression of glioma through upregulation of the TCF12/PI3K/AKT pathway by sponging miR-515-5p.	BACKGROUND: Increasing studies have revealed that circular RNAs (CircRNAs) make great contributions to regulating tumor progression. Therefore, we intended to explore the expression characteristics, function, and related mechanisms of a novel type of circRNA, PIP5K1A, in glioma. METHODS: Firstly, reverse transcription-polymerase chain reaction (RT-PCR) was carried out to examine CircPIP5K1A expression in glioma tissues and adjacent normal tissues, and the correlation between CircPIP5K1A level and the clinical-pathological indicators of glioma was analyzed. Then, the CircPIP5K1A expression in various glioma cell lines was detected, and CircPIP5K1A overexpression and knockdown cell models were constructed. Subsequently, cell proliferation and viability were detected by the CCK8 method and BrdU staining. Cell apoptosis was detected by flow cytometry, and cell invasion was examined by Transwell assay. The expression of TCF12, PI3K/AKT pathway apoptotic related proteins (Caspase3, Bax, and Bcl2) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin, and N-cadherin) was determined by western blot or RT-PCR. RESULTS: The results manifested that CircPIP5K1A was upregulated in glioma tissues (compared with that in normal adjacent tissues), and overexpressed CircPIP5K1A was related to glioma volume and histopathological grade. Functionally, overexpressing CircPIP5K1A notably elevated glioma cell proliferation, invasion, and EMT and inhibited apoptosis both in vivo and in vitro. Besides, CircPIP5K1A upregulated TCF12 and PI3K/AKT activation. Bioinformatics analysis testified that miR-515-5p was a common target of CircPIP5K1A and TCF12, while the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) experiment further confirmed that CircPIP5K1A targeted miR-515-5p, which bound the 3'-untranslated region (UTR) of TCF12. CONCLUSIONS: Overall, the study illustrated that CircPIP5K1A is a potential prognostic marker in glioma and regulates glioma evolvement by modulating the miR-515-5p-mediated TCF12/PI3K/AKT axis.	NA	Cancer Cell Int. 2021 Jan 7;21(1):27. doi: 10.1186/s12935-020-01699-6.
4775	Circular RNA	PIP5K1A	miR-515-5p	AKT	glioma tissues and adjacent normal tissues	Glioma	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33413401	CircRNA PIP5K1A promotes the progression of glioma through upregulation of the TCF12/PI3K/AKT pathway by sponging miR-515-5p.	BACKGROUND: Increasing studies have revealed that circular RNAs (CircRNAs) make great contributions to regulating tumor progression. Therefore, we intended to explore the expression characteristics, function, and related mechanisms of a novel type of circRNA, PIP5K1A, in glioma. METHODS: Firstly, reverse transcription-polymerase chain reaction (RT-PCR) was carried out to examine CircPIP5K1A expression in glioma tissues and adjacent normal tissues, and the correlation between CircPIP5K1A level and the clinical-pathological indicators of glioma was analyzed. Then, the CircPIP5K1A expression in various glioma cell lines was detected, and CircPIP5K1A overexpression and knockdown cell models were constructed. Subsequently, cell proliferation and viability were detected by the CCK8 method and BrdU staining. Cell apoptosis was detected by flow cytometry, and cell invasion was examined by Transwell assay. The expression of TCF12, PI3K/AKT pathway apoptotic related proteins (Caspase3, Bax, and Bcl2) and epithelial-mesenchymal transition (EMT) markers (E-cadherin, Vimentin, and N-cadherin) was determined by western blot or RT-PCR. RESULTS: The results manifested that CircPIP5K1A was upregulated in glioma tissues (compared with that in normal adjacent tissues), and overexpressed CircPIP5K1A was related to glioma volume and histopathological grade. Functionally, overexpressing CircPIP5K1A notably elevated glioma cell proliferation, invasion, and EMT and inhibited apoptosis both in vivo and in vitro. Besides, CircPIP5K1A upregulated TCF12 and PI3K/AKT activation. Bioinformatics analysis testified that miR-515-5p was a common target of CircPIP5K1A and TCF12, while the dual-luciferase reporter assay and RNA immunoprecipitation (RIP) experiment further confirmed that CircPIP5K1A targeted miR-515-5p, which bound the 3'-untranslated region (UTR) of TCF12. CONCLUSIONS: Overall, the study illustrated that CircPIP5K1A is a potential prognostic marker in glioma and regulates glioma evolvement by modulating the miR-515-5p-mediated TCF12/PI3K/AKT axis.	NA	Cancer Cell Int. 2021 Jan 7;21(1):27. doi: 10.1186/s12935-020-01699-6.
4776	LncRNA	PMS2L2	miR-24	Bax	plasma	Ulcerative Colitis	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	33238281	LncRNA PMS2L2 downregulates miR-24 through methylation to suppress cell apoptosis in ulcerative colitis.	BACKGROUND: Ulcerative colitis (UC) is an inflammatory bowel disease characterized by chronic inflammation of the colon. It has been reported that PMS2L2 plays protective roles in inflammatory injury. This study aimed to investigate the role of lncRNA PMS2L2 in UC. METHODS: 62 patients with UC as well as 62 age- and gender- matched healthy controls were enrolled. Expressions of PMS2L2 and miR-24 in plasma from UC patients and healthy controls were determined by RT-qPCR. The interaction between PMS2L2 and miR-24 was predicted by bioinformatics and confirmed by RNA immunoprecipitation (RIP) and RNA pull-down. The role of PMS2L2 in the regulation of miR-24 gene methylation was analyzed by methylation-specific PCR (MSP). The effects of PMS2L2 and miR-24 on the expressions of apoptosis-related proteins were detected by western blots. RESULTS: PMS2L2 was downregulated in the plasma of UC patients compared to that in age- and gender- matched healthy control. In HCnEpCs, PMS2L2 overexpression inhibited miR-24 expression via promoting the methylation of miR-24 gene. In contrast, miR-24 overexpression failed to affect PMS2L2. In the detection of cell apoptosis, PMS2L2 overexpression could promote the expression of Bcl-2 and inhibit Bax, cleaved-caspase-3 and cleaved-caspase-9 expressions stimulated by LPS. Flow cytometer revealed that PMS2L2 elevation suppressed the apoptosis of HCnEpCs induced by LPS, but miR-24 aggravated the apoptosis. PMS2L2 overexpression rescued the detrimental effect of miR-24 on cell apoptosis. CONCLUSION: PMS2L2 may downregulate miR-24 via methylation to suppress cell apoptosis in UC.	NA	Dig Dis. 2020 Nov 25. doi: 10.1159/000513330.
4777	LncRNA	PMS2L2	miR-24	caspase3	plasma	Ulcerative Colitis	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	33238281	LncRNA PMS2L2 downregulates miR-24 through methylation to suppress cell apoptosis in ulcerative colitis.	BACKGROUND: Ulcerative colitis (UC) is an inflammatory bowel disease characterized by chronic inflammation of the colon. It has been reported that PMS2L2 plays protective roles in inflammatory injury. This study aimed to investigate the role of lncRNA PMS2L2 in UC. METHODS: 62 patients with UC as well as 62 age- and gender- matched healthy controls were enrolled. Expressions of PMS2L2 and miR-24 in plasma from UC patients and healthy controls were determined by RT-qPCR. The interaction between PMS2L2 and miR-24 was predicted by bioinformatics and confirmed by RNA immunoprecipitation (RIP) and RNA pull-down. The role of PMS2L2 in the regulation of miR-24 gene methylation was analyzed by methylation-specific PCR (MSP). The effects of PMS2L2 and miR-24 on the expressions of apoptosis-related proteins were detected by western blots. RESULTS: PMS2L2 was downregulated in the plasma of UC patients compared to that in age- and gender- matched healthy control. In HCnEpCs, PMS2L2 overexpression inhibited miR-24 expression via promoting the methylation of miR-24 gene. In contrast, miR-24 overexpression failed to affect PMS2L2. In the detection of cell apoptosis, PMS2L2 overexpression could promote the expression of Bcl-2 and inhibit Bax, cleaved-caspase-3 and cleaved-caspase-9 expressions stimulated by LPS. Flow cytometer revealed that PMS2L2 elevation suppressed the apoptosis of HCnEpCs induced by LPS, but miR-24 aggravated the apoptosis. PMS2L2 overexpression rescued the detrimental effect of miR-24 on cell apoptosis. CONCLUSION: PMS2L2 may downregulate miR-24 via methylation to suppress cell apoptosis in UC.	NA	Dig Dis. 2020 Nov 25. doi: 10.1159/000513330.
4778	LncRNA	PMS2L2	miR-24	caspase9	plasma	Ulcerative Colitis	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	33238281	LncRNA PMS2L2 downregulates miR-24 through methylation to suppress cell apoptosis in ulcerative colitis.	BACKGROUND: Ulcerative colitis (UC) is an inflammatory bowel disease characterized by chronic inflammation of the colon. It has been reported that PMS2L2 plays protective roles in inflammatory injury. This study aimed to investigate the role of lncRNA PMS2L2 in UC. METHODS: 62 patients with UC as well as 62 age- and gender- matched healthy controls were enrolled. Expressions of PMS2L2 and miR-24 in plasma from UC patients and healthy controls were determined by RT-qPCR. The interaction between PMS2L2 and miR-24 was predicted by bioinformatics and confirmed by RNA immunoprecipitation (RIP) and RNA pull-down. The role of PMS2L2 in the regulation of miR-24 gene methylation was analyzed by methylation-specific PCR (MSP). The effects of PMS2L2 and miR-24 on the expressions of apoptosis-related proteins were detected by western blots. RESULTS: PMS2L2 was downregulated in the plasma of UC patients compared to that in age- and gender- matched healthy control. In HCnEpCs, PMS2L2 overexpression inhibited miR-24 expression via promoting the methylation of miR-24 gene. In contrast, miR-24 overexpression failed to affect PMS2L2. In the detection of cell apoptosis, PMS2L2 overexpression could promote the expression of Bcl-2 and inhibit Bax, cleaved-caspase-3 and cleaved-caspase-9 expressions stimulated by LPS. Flow cytometer revealed that PMS2L2 elevation suppressed the apoptosis of HCnEpCs induced by LPS, but miR-24 aggravated the apoptosis. PMS2L2 overexpression rescued the detrimental effect of miR-24 on cell apoptosis. CONCLUSION: PMS2L2 may downregulate miR-24 via methylation to suppress cell apoptosis in UC.	NA	Dig Dis. 2020 Nov 25. doi: 10.1159/000513330.
4779	LncRNA	PSMA3-AS1	miR-4429	NA	colorectal cancer tissues and cells	Colorectal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;luciferase assay;	33275226	LncRNA PSMA3-AS1 promotes colorectal cancer cell migration and invasion via regulating miR-4429.	OBJECTIVE: Many studies have revealed that long non-coding RNAs (lncRNAs) are related to various cancers, including colorectal cancer (CRC). This study aims to explore the biological function of lncRNA PSMA3-AS1 in CRC progression. MATERIALS AND METHODS: The expression levels of PSMA3-AS1 and miR-4429 were assessed by RT-qPCR. CRC progression was explored by cell viability, migration, and invasion using CCK-8 and transwell assays. The interaction between PSMA3-AS1 and miR-4429 was verified by bioinformatics analysis, Dual-Luciferase assay, and RIP assay. RESULTS: It was found that PSMA3-AS1 expression was increased and miR-4429 expression was decreased in CRC tissues and cells. In addition, PSMA3-AS1 interference markedly hindered the proliferation, migration, and invasion of CRC cells. MiR-4429 was a direct target of PSMA3-AS1, and the knockdown of PSMA3-AS1 significantly suppressed miR-4429 expression. The depletion of PSMA3-AS1 inhibited CRC progression, which was neutralized by miR-4429 inhibitor. CONCLUSIONS: PSMA3-AS1 accelerated CRC progression by regulating miR-4429 expression, which could be used as a potential therapeutic target for CRC patients.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11594-11601. doi: 10.26355/eurrev_202011_23802.
4780	LncRNA	PTTG3P	miR-146a-3p	PTTG1	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	qPCR;Western blot;luciferase assay;	33743960	The lncRNA PTTG3P promotes the progression of CRPC via upregulating PTTG1.	BACKGROUND: Overexpression of certain long non-coding RNAs (lncRNAs) promotes the progression of castration-resistant prostate cancer (CRPC). The significance and potential role of the lncRNA designated pituitary tumour-transforming 3, pseudogene (PTTG3P) in CRPC is unknown. METHODS: We detected PTTG3P expression by qPCR. Upregulated PTTG3P expression was performed to explore the role of PTTG3P in PCa cells resistant to ADT (androgen deprivation therapy). The relationship among PTTG3P, mir-146a-3p and PTTG1 were validated by qPCR, western blot and luciferase assay. RESULTS: PTTG3P levels were significantly increased in the androgen-independent PC cell lines, as well as in CRPC tissues compared with those of the androgen-dependent prostate cancer cell line LNCaP and tumour tissues of patients with hormone-naive prostate cancers. Enforced expression of PTTG3P in androgen-deprived LNCaP cells significantly enhanced survival, clonogenicity, and tumorigenicity. Further, PTTG3P acted as a competing endogenous RNA (ceRNA, natural miRNA sponge) to upregulate PTTG1 expression by competing for mir-146a-3p in the progression to CRPC. CONCLUSION: Our findings suggest that PTTG3P promotes the resistance of prostate cancer cells to androgen-deprivation therapy via upregulating PTTG1. PTTG3P may therefore represent a potential target for therapy of CRPC.	NA	Bull Cancer. 2021 Apr;108(4):359-368. doi: 10.1016/j.bulcan.2020.11.022. Epub 2021 Mar 18.
4781	LncRNA	PVT1	miR-20a-5p	NLRP3	HK-2 cells	Sepsis-Induced Acute Kidney Injury	Homo sapiens (human)	ELISA;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33576456	lncRNA PVT1 modulates NLRP3-mediated pyroptosis in septic acute kidney injury by targeting miR-20a-5p.	Acute kidney injury (AKI) is the most common complication of sepsis. The current incidence of sepsis is high (0.3% of total population) worldwide, and septic AKI may cause death in patients. Long non-coding (lnc)RNAs serve important roles in the pathogenesis of AKI. Therefore, the present study investigated the mechanism underlying lncRNA plasmacytoma variant translocation 1 (PVT1)-mediated regulation of pyroptosis in septic AKI. Septic kidney injury was induced in mice using the caecal ligation and puncture method, and lipopolysaccharide (LPS)-induced HK-2 cell models were also established. Haematoxylin-eosin staining was performed to assess pathological alterations of kidney tissues in the mice. The levels of IL-1β, IL-18 and lactate dehydrogenase were determined by conducting ELISAs. Reverse transcription-quantitative PCR was used to detect the expression levels of PVT1 and microRNA (miR)-20a-5p. To assess pyroptosis, the protein expression levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), IL-1β, IL-18, apoptosis-associated speck-like protein containing a CARD and cleaved caspase-1 were measured via western blotting. Flow cytometry was performed to assess the rate of cell pyroptosis. Dual luciferase reporter assays were used to assess the binding relationships of PVT1/miR-20a-5p and miR-20a-5p/NLRP3. PVT1 expression was significantly increased, whereas miR-20a-5p expression was significantly decreased in sepsis model mice and LPS-induced HK-2 cells compared with sham mice and control HK-2 cells, respectively. PVT1 knockdown significantly suppressed cell pyroptosis and downregulated the expression of inflammatory factors in LPS-induced HK-2 cells. The results also indicated that PVT1 served as a sponge of miR-20a-5p, and miR-20a-5p directly targeted NLRP3. miR-20a-5p knockdown significantly promoted LPS-induced cell pyroptosis. Moreover, PVT1 knockdown inhibited LPS-induced cell pyroptosis by targeting the miR-20a-5p/NLRP3 signalling pathway. The results of the present study suggested that PVT1 modulated NLRP3-mediated pyroptosis in septic AKI by targeting miR-20a-5p, which might suggest significant potential therapeutic targets for septic AKI.	NA	Mol Med Rep. 2021 Apr;23(4):271. doi: 10.3892/mmr.2021.11910. Epub 2021 Feb 12.
4782	LncRNA	PVT1	miR-1301-3p	TMBIM6	glioblastoma multiforme cells	Glioblastoma Multiforme	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;	33275233	Long non-coding RNA plasmacytoma variant translocation 1 (PVT1) promotes glioblastoma multiforme progression via regulating miR-1301-3p/TMBIM6 axis.	OBJECTIVE: To explore whether plasmacytoma variant translocation 1 (PVT1) could regulate glioblastoma multiforme (GBM) progression via microRNA-1301-3p (miR-1301-3p) and transmembrane BAX inhibitor motif containing 6 (TMBIM6) axis. MATERIALS AND METHODS: Expression patterns of PVT1 and RMBIM6 in GBM patients were analyzed using GEPIA, an online gene expression analysis tool. Levels of PVT1 in GBM cells and normal cells were analyzed with quantitative real-time PCR method. Cell Counting Kit-8 (CCK-8), transwell invasion assay, and flow cytometry assay were applied to detect cell viability and apoptosis. Connections of PVT1 or TMBIM6 with miR-1301-3p were validated with bioinformatic tool and luciferase activity reporter assay. RESULTS: PVT1 was significantly expressed in GBM tissues and cells. PVT1 promotes GBM cell proliferation and invasion but inhibits apoptosis in vitro. TMBIM6 was significantly expressed in GBM tissues. The knockdown of TMBIM6 reversed the stimulation effects of PVT1 on GBM cell malignancy behaviors with miR-1301-3p as a bridge. CONCLUSIONS: Collectively, we showed PVT1 elevated TMBIM6 expression mediated by miR-1301-3p and thus to promote GBM progression.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11658-11665. doi: 10.26355/eurrev_202011_23810.
4783	LncRNA	PVT1-214	miR-128	IRF-1	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	ChIP;qRT-PCR;Western blot;Chromatin immunoprecipitation;	33277837	IRF-1 mediated long non-coding RNA PVT1-214 promotes oxaliplatin resistance of colorectal cancer via miR-128 inhibition.	PURPOSE: Long non-coding RNA (lncRNA) plasmacytoma variant translocation 1-214 transcript (PVT1-214) is a notable lncRNA involved in gastric cancer and colorectal cancer (CRC) so far. Nowadays, the biological function of PVT1-214 on the response of CRC to chemotherapy is still unclear. We aimed to explore the molecular mechanism of PVT1-214 and its regulatory mechanism in advanced CRC. METHODS: The levels of PVT1-214, microRNA (miR)-128, and interferon regulatory factor-1 (IRF-1) in CRC tissues and cell lines were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Log-rank test was applied to evaluate the role of high PVT1-214 levels in shortening the overall survival of CRC patients. Chi-square test was to assess the relation between PVT1-214 expression and clinicopathological features of CRC patients. CCK8 assays tested the cell proliferation of oxaliplatin-resistant CRC cells (HCT116/Oxa and SW480/Oxa) with PVT1-214 knockdown. The underlying regulatory mechanism between PVT1-214 and miR-128 was predicted by bioinformatics and verified by RNA transfection, qRT-PCR and western blotting. Chromatin immunoprecipitation (ChIP) assay was done to examine the relationship between or IRF-1 and the PVT1-214 gene. RESULTS: High levels of PVT1-214 expression were more likely to be present in patients with late-stage (IV), chemotherapy resistance, and inferior overall survival. PVT1-214 was aberrantly elevated in oxaliplatin-resistant CRC tissues and cell lines (HCT116/Oxa and SW480/Oxa). PVT1-214 knockdown reduced cell proliferation, migration and invasion of oxaliplatin-resistant CRC cells in vitro. Moreover, IRF-1 was found to be a negative transcription regulator of PVT1-214 and decreased PVT1-214 levels in oxaliplatin-resistant CRC cells. Besides, PVT1-214 repressed miR-128 function by binding to the complementary sites of miR-128. CONCLUSIONS: IRF-1/PVT1-214 may markedly boost the oxaliplatin-resistance of CRC, resulting in the late TNM stage and poor survival. These findings suggest that the IRF-1/PVT1-214 axis may be a helpful target for intervention in CRC.	NA	J BUON. 2020 Sep-Oct;25(5):2205-2214.
4784	LncRNA	RACGAP1P	miR-345-5p	RACGAP1	breast cancer tissues	Breast Cancer	Homo sapiens (human)	microarray;qRT-PCR;	33252198	Long non-coding RNA RACGAP1P promotes breast cancer invasion and metastasis via miR-345-5p/RACGAP1-mediated mitochondrial fission.	Long non-coding RNAs (lncRNAs) are emerging as key molecules in various cancers, yet their potential roles in the pathogenesis of breast cancer are not fully understood. Herein, using microarray analysis, we revealed that the lncRNA RACGAP1P, the pseudogene of Rac GTPase activating protein 1 (RACGAP1), was up-regulated in breast cancer tissues. Its high expression was confirmed in 25 pairs of breast cancer tissues and 8 breast cell lines by qRT-PCR. Subsequently, we found that RACGAP1P expression was positively correlated with lymph node metastasis, distant metastasis, TNM stage, and shorter survival time in 102 breast cancer patients. Then, in vitro and in vivo experiments were designed to investigate the biological function and regulatory mechanism of RACGAP1P in breast cancer cell lines. Overexpression of RACGAP1P in MDA-MB-231 and MCF7 breast cell lines increased their invasive ability and enhanced their mitochondrial fission. Conversely, inhibition of mitochondrial fission by Mdivi-1 could reduce the invasive ability of RACGAP1P-overexpressing cell lines. Furthermore, the promotion of mitochondrial fission by RACGAP1P depended on its competitive binding with miR-345-5p against its parental gene RACGAP1, leading to the activation of dynamin-related protein 1 (Drp1). In conclusion, lncRNA RACGAP1P promotes breast cancer invasion and metastasis via miR-345-5p/RACGAP1 pathway-mediated mitochondrial fission.	NA	Mol Oncol. 2021 Feb;15(2):543-559. doi: 10.1002/1878-0261.12866. Epub 2020 Dec 16.
4785	LncRNA	RHPN1-AS1	miR-3133	JAK2	retinoblastoma cells	Retinoblastoma	Homo sapiens (human)	Flow cytometry assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33426053	lncRNA RHPN1-AS1 Serves as a Sponge for miR-3133 Modulating the Cell Proliferation of Retinoblastoma through JAK2.	PURPOSE: To investigate the effects of lncRNA RHPN1-AS1 on retinoblastoma (RB) and further explore its underlying molecular mechanisms. METHODS: The expression of RHPN1-AS1, miR-3133, (JAK2), and signal transducer and activator of transcription 3 (STAT3) was detected by qRT-PCR. CCK-8, EDU, and flow cytometry assays were conducted to assess the proliferation activity and apoptosis of RB cells. Double fluorescein and RNA immunoprecipitation assays were performed to detect the interaction between RHPN1-AS1 and miR-3133 or miR-3133 and JAK2. Western blotting was performed to detect the expression of apoptosis-related proteins. RESULTS: In RB cells, RHPN1-AS1 was upregulated. Silencing RHPN1-AS1 inhibited the activity of RB cells and promoted apoptosis. The expressions of proapoptotic factors (Bax and p53) were increased, while antiapoptotic factors (Bcl-2 and Survivin) were suppressed in siRHPN1-AS1 groups. Furthermore, we predicted and verified that RHPN1-AS1 regulated RB progression by targeting miR-3133/JAK2. In addition, siRHPN1-AS1 also inhibited oncogene STAT3 protein expression. CONCLUSION: lncRNA RHPN1-AS1 served as a sponge for miR-3133 to counteract miR-3133-mediated JAK2/STAT3 suppression, indicating that the lncRNA RHPN1-AS1 may be a potential therapeutic target for the treatment of RB.	NA	Biomed Res Int. 2020 Dec 22;2020:3502981. doi: 10.1155/2020/3502981. eCollection 2020.
4786	LncRNA	RMRP	miR-206	CDK9	chondrocytes	Osteoarthritis	Homo sapiens (human)	RIP assay;Flow Cytometry assay;Rescue assay;RNA pull-down;	33305725	LncRNA RMRP knockdown promotes proliferation and inhibits apoptosis in osteoarthritis chondrocytes by miR-206/CDK9 axis.	The etiology of osteoarthritis (OA) has been discussed widely, but the molecular mechanisms beneath OA aggravation have not yet been investigated in detail. This study focused on the role of lncRNA RMRP (RMRP) on OA progression. We found that the expression of RMRP was significantly increased in cartilage tissues of patients with OA. CCK-8 and colony formation assays showed that RMRP knockdown promoted proliferation of chondrocytes treated with IL-1β. Flow cytometry and caspase-3 activity analysis indicated that RMRP silence inhibited apoptosis of chondrocytes treated with IL-1β. Moreover, luciferase reporter, RNA pull-down and RIP assays showed that RMRP competing with miR-206. Additionally, CDK9 acted as a direct target of miR-206. Moreover, rescue assays indicated that miR-206 inhibitor or pcDNA-CDK9 reversed the effects of RMRP suppression on the proliferation and apoptosis of chondrocytes. Taken together, our results indicated that RMRP knockdown could promote proliferation and inhibit apoptosis in OA chondrocytes via the miR-206/CDK9 axis.	NA	Pharmazie. 2020 Oct 1;75(10):500-504. doi: 10.1691/ph.2020.0591.
4787	LncRNA	RMST	miR-377	SEMA3A	LncRNA	Ischemic Stroke	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33409855	Knockdown of RMST Impedes Neuronal Apoptosis and Oxidative Stress in OGD/R-Induced Ischemic Stroke Via Depending on the miR-377/SEMA3A Signal Network.	Long non-coding RNAs (lncRNAs) have pivotal roles in regulating ischemic stroke (IS), including lncRNA rhabdomyosarcoma 2-associated transcript (RMST). The purpose of this report is to discover the functional mechanism of RMST. The expression detection of RMST, microRNA-377 (miR-377) and Semaphorin 3A (SEMA3A) was performed by quantitative real-time polymerase chain reaction (qRT-PCR). Oxygen and glucose deprivation/reperfusion (OGD/R) in N2a cells was used to mimic IS environment in vitro. Cell Counting Kit-8 (CCK-8) and flow cytometry were implemented to assess cell viability and apoptosis. Oxidative stress was analyzed via assaying the associated indicators. Dual-luciferase reporter, RNA pull-down and RNA immunoprecipitation (RIP) assays were jointly administrated for binding analysis between targets. SEMA3A protein level was measured using western blot. We found in IS serum samples, RMST was upregulated while miR-377 was downregulated. After the establishment of OGD/R-induced IS model, we found that the decreased RMST abrogated the OGD/R-triggered apoptosis and oxidative stress. Through the target analysis, miR-377 was shown to be sponged by RMST and the effects of RMST knockdown on OGD/R-induced cell injuries were related to miR-377 upregulation. Besides, SEMA3A served as a target gene of miR-377 and the mitigation of miR-377 for ischemic brain damages was achieved by downregulating SEMA3A. What's more, RMST could regulate SEMA3A by playing the sponge action on miR-377. Collectively, all these findings clarified that RMST repression retarded IS progression in vitro via SEMA3A downregulation by targeting miR-377, which represented a different perspective in the pathological development of IS.	NA	Neurochem Res. 2021 Mar;46(3):584-594. doi: 10.1007/s11064-020-03194-w. Epub 2021 Jan 6.
4788	LncRNA	RNF185-AS1	miR-221-5p	IntegrinB5	hepatocellular carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;Rescue assay;	33358902	RNF185-AS1 promotes hepatocellular carcinoma progression through targeting miR-221-5p/integrin β5 axis.	AIMS: Recently, long noncoding RNAs (lncRNAs) have been reported to play important role in the pathogenesis of various cancers. However, the functions of RNF185-AS1 in hepatocellular carcinoma (HCC) remain unknown. MATERIALS AND METHODS: The RNF185-AS1 expression in HCC cells and tissues was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of RNF185-AS1 on tumor cell proliferation, migration and invasion were assessed by Cell Counting Kit-8 (CCK8) assay, colony formation assay, transwell assay. The luciferase reporter assay, RNA-binding protein immunoprecipitation assay, qRT-PCR and Western blot were performed to explore and confirm the interaction between RNF185-AS1 and miR-221-5p and integrin β5. The role of RNF185-AS1 in tumor progression was explored through in vivo experiments. KEY FINDINGS: RNF185-AS1 was highly expressed in HCC tissues and cell lines. High levels of RNF185-AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. RNF185-AS1 knockdown inhibited cell proliferation, migration and invasion. Additionally, RNF185-AS1 acted as a sponge for miR-221-5p and integrin β5 was identified as a target gene of miR-221-5p. Rescue assays showed that miR-221-5p inhibitor or integrin β5 overexpression rescued the function of RNF185-AS1 knockdown on cell proliferation, migration, and invasion. Moreover, we found that RNF185-AS1 knockdown inhibited tumor growth and metastasis. SIGNIFICANCE: Our study demonstrates that RNF185-AS1 is a new oncogenic lncRNA in HCC and suggests that the RNF185-AS1/miR-221-5p/integrin β5 axis might be a potential therapeutic target for HCC.	NA	Life Sci. 2021 Feb 15;267:118928. doi: 10.1016/j.lfs.2020.118928. Epub 2020 Dec 31.
4789	LncRNA	RP3-439F8.1	miR-139-5p	NR5A2	glioblastoma multiforme cells	Glioblastoma Multiforme	Homo sapiens (human)	Cell cycle assay;	33991848	The lncRNA RP3-439F8.1 promotes GBM cell proliferation and progression by sponging miR-139-5p to upregulate NR5A2.	BACKGROUND: Nuclear Receptor Subfamily 5 Group A Member 2 (NR5A2, LRH-1) is an oncogene in a wide range of cancer types. Bioinformatics analysis on glioblastoma multiforme (GBM) tumors has revealed that the miR-139-5p-NR5A2 axis may be putatively regulated by the long non-coding RNA (lncRNA) RP3-439F8.1. This led us to hypothesize the existence of a RP3-439F8.1-miR-139-5p-NR5A2 regulatory axis in GBM cells. METHODS: Gene expression analysis was performed in GBM tumor samples and normal controls from our hospital, the Cancer Genome Atlas Glioblastoma Multiforme (TCGA-GBM) cohort, and the Gene Expression Omnibus (GEO) database (GSE7696). Cell proliferation, apoptosis, Matrigel Transwell, colony formation, and cell cycle assays were performed in T98 G and U251 cells in vitro. An orthotopic U251 xenograft murine model was employed to test the effects of RP3-439F8.1 knockdown in vivo. RESULTS: NR5A2 was upregulated in the three independent GBM tumor cohorts. In vitro, NR5A2 overexpression enhanced GBM cell proliferation, colony formation, invasiveness, and G0-G1 cell cycle phase shift via co-activating β-catenin/TCF4 signaling, with no apparent effect upon apoptosis. In contrast, RP3-439F8.1 knockdown produced the opposite effects. RP3-439F8.1 knockdown reduced tumor progression in vivo, increasing overall survival in model mice. Further in vitro experiments revealed that RP3-439F8.1 acts as a competing endogenous RNA (ceRNA) to regulate NR5A2 by sponging the microRNA miR-139-5p. These findings were clinically validated by a positive correlation between RP3-439F8.1 and NR5A2 and a negative correlation between RP3-439F8.1 and miR-139-5p in GBM tumors. CONCLUSIONS: Our study supports a tumorigenic role for RP3-439F8.1 in GBM through the RP3-439F8.1/miR-139-5p/NR5A2 axis.	NA	Pathol Res Pract. 2021 Jul;223:153319. doi: 10.1016/j.prp.2020.153319. Epub 2021 Jan 2.
4790	LncRNA	RUNX1-IT1	miR-21	NA	endometrial cancer cells	Endometrial Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;RNA pull-down assay;Luciferase activity assay;RNA pull-down;	33408517	LncRNA RUNX1-IT1 is Downregulated in Endometrial Cancer and Binds to miR-21 Precursor to Suppress Its Maturation.	BACKGROUND: RUNX1-IT1 suppresses colorectal cancer and liver cancer, while its role in other cancers is unknown. This study was performed to investigate the role of RUNX1-IT1 in endometrial cancer (EC). METHODS: EC and paired non-tumor tissues were collected from 62 EC patients, and the expression of RUNX1-IT1, mature miR-21 and miR-21 precursor in these tissue samples were determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of RUNX1-IT1 was achieved in EC cells and the expression of mature miR-21 and miR-21 precursor were analyzed by RT-qPCR. CCK-8 assay was used for cell proliferation analysis. RESULTS: We found that RUNX1-IT1 was downregulated in EC and inversely correlated with mature miR-21 but not miR-21 precursor. RUNX1-IT1 was predicted to bind with miR-21 precursor. The interaction between them was verified by dual-luciferase activity assay and RNA pull-down assay. In EC cells, overexpression of RUNX1-IT1 downregulated mature miR-21, but not miR-21 precursor. Overexpression of RUNX1-IT1 suppressed the role of miR-21 in increasing cell proliferation. CONCLUSION: RUNX1-IT1 is downregulated in EC and inhibits cancer cell proliferation by suppressing the maturation of miR-21.	NA	Cancer Manag Res. 2020 Dec 30;12:13451-13459. doi: 10.2147/CMAR.S272165. eCollection 2020.
4791	LncRNA	SBF2-AS1	miR-338-3P	E2F1	ageal squamous cell	OEsophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR	33436941	The molecular mechanisms of the long noncoding RNA SBF2-AS1 in regulating the proliferation of oesophageal squamous cell carcinoma.	The long noncoding RNASBF2-AS1 can promote the occurrence and development of many kinds of tumours, but its role in oesophageal squamous cell carcinoma (ESCC) is unknown. We found that SBF2-AS1 was up-regulated in ESCC, and its expression was positively correlated with tumor size (P = 0.0001), but was not related to gender, age, TNM stage, histological grade, and lymphnode metastasis (P > 0.05). It was further found that the higher the expression of SBF2-AS1, the lower the survival rate. COX multivariate analysis showed that the expression of SBF2-AS1 was an independent prognostic factor. Functional experiments show that inhibition of SBF2-AS1 can inhibit the proliferation of ESCC through in vivo and in vitro, and overexpression of SBF2-AS1 can promote the proliferation of ESCC and inhibit its apoptosis. In mechanism, SBF2-AS1/miR-338-3P, miR-362-3P/E2F1 axis are involved in the regulation of ESCC growth. In general, SBF2-AS1 may be used as ceRNA to combine with miR-338-3P and miR-362-3P to up-regulate the expression ofE2F1, and ultimately play a role in promoting cancer. It may be used as a therapeutic target and a biomarker for prognosis.	NA	Sci Rep. 2021 Jan 12;11(1):805. doi: 10.1038/s41598-020-80817-w.
4792	LncRNA	SBF2-AS1	miR-494-3p	FGF	OCI-LY-3 cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	qRT-PCR	33519236	LncRNA SBF2-AS1 Promotes Diffuse Large B-Cell Lymphoma Growth by Regulating FGFR2 via Sponging miR-494-3p.	PURPOSE: Currently, there is no efficient and feasible method for diffuse large B-cell lymphoma (DLBCL) in clinical practice, and the main reason is the unclear pathogenesis of DLBCL, which leads to a high fatality rate of DLBCL. METHODS: Therefore, it is meaningful to explore the molecular mechanism of DLBCL and find a targeted therapeutic approach from the molecular level. RESULTS: Long non-coding RNA (lncRNA) SBF2-AS1 was highly expressed in DLBCL tissues and cell lines. Silencing of SBF2-AS1 inhibited the viability and growth of OCI-LY-3 cells. Furthermore, SBF2-AS1 acted as a sponge of miR-494-3p and inhibited its expression. And miR-494-3p directly targeted FGFR2. Functionally, forced expression of miR-494-3p or knockdown of FGFR2 removed the promoted effects of lncRNA SBF2-AS1 on DLBCL development. In vivo tumorigenesis experiments indicated SBF2-AS1 accelerated tumor growth via miR-494-3p/FGFR2 axis. CONCLUSION: Our study revealed that SBF2-AS1 promoted the growth of DLBCL, which were mediated by miR-494-3p/FGFR2 axis.	NA	Cancer Manag Res. 2021 Jan 22;13:571-578. doi: 10.2147/CMAR.S284258. eCollection 2021.
4793	LncRNA	SNHG1	miR-362-3p	Jak2	PC12 cells	Spinal Cord Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;Western blot;	33515352	Knockdown of SNHG1 alleviates autophagy and apoptosis by regulating miR-362-3p/Jak2/stat3 pathway in LPS-injured PC12 cells.	Spinal cord injury (SCI) is a serious neurological disease. Long non-coding RNA (lncRNA) small nucleolar RNA host gene (SNHG1) and microRNA-362-3p (miR-362-3p) were confirmed to be related to neurological disorders. However, it is unclear whether SNHG1 was involved in the development of SCI via regulating miR-362-3p. PC12 cells were treated with lipopolysaccharide (LPS) to imitate the in vitro cell model of SCI. Cell ciability and apoptosis rate were detected by cell counting kit-8 (CCK-8) assay and flow cytometry assay. The levels of SNHG1, miR-362-3p, and Janus kinase-2 (Jak2) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The dual-luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay were performed to verify the interaction between miR-362-3p and SNHG1 or Jak2. Besides, the levels of apoptosis- and autophagy- related proteins were detected by western blot assay. In present research, LPS suppressed cell viability, and induced apoptosis and autophagy in PC12 cells. SNHG1 knockdown could affect cell viability, and suppress cell apoptosis and autophagy in LPS-treated PC12 cells. Moreover, miR-362-3p was a target of SNHG1, miR-362-3p targeted Jak2 and negatively regulated Jak2/stat3 pathway. Our data also demonstrated that SNHG1 depletion inactivated Jak2/stat3 pathway to affect cell viability and confine apoptosis, autophagy in LPS-treated PC12 cells. Taken together, SNHG1 regulated cell viability, apoptosis and autophagy in LPS-treated PC12 cells by activating Jak2/stat3 pathway via sponging miR-362-3p.	NA	Neurochem Res. 2021 Apr;46(4):945-956. doi: 10.1007/s11064-020-03224-7. Epub 2021 Jan 30.
4794	LncRNA	SNHG1	miR-362-3p	stat3	PC12 cells	Spinal Cord Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;Western blot;	33515352	Knockdown of SNHG1 alleviates autophagy and apoptosis by regulating miR-362-3p/Jak2/stat3 pathway in LPS-injured PC12 cells.	Spinal cord injury (SCI) is a serious neurological disease. Long non-coding RNA (lncRNA) small nucleolar RNA host gene (SNHG1) and microRNA-362-3p (miR-362-3p) were confirmed to be related to neurological disorders. However, it is unclear whether SNHG1 was involved in the development of SCI via regulating miR-362-3p. PC12 cells were treated with lipopolysaccharide (LPS) to imitate the in vitro cell model of SCI. Cell ciability and apoptosis rate were detected by cell counting kit-8 (CCK-8) assay and flow cytometry assay. The levels of SNHG1, miR-362-3p, and Janus kinase-2 (Jak2) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The dual-luciferase reporter assay, RNA pull-down assay, and RNA immunoprecipitation (RIP) assay were performed to verify the interaction between miR-362-3p and SNHG1 or Jak2. Besides, the levels of apoptosis- and autophagy- related proteins were detected by western blot assay. In present research, LPS suppressed cell viability, and induced apoptosis and autophagy in PC12 cells. SNHG1 knockdown could affect cell viability, and suppress cell apoptosis and autophagy in LPS-treated PC12 cells. Moreover, miR-362-3p was a target of SNHG1, miR-362-3p targeted Jak2 and negatively regulated Jak2/stat3 pathway. Our data also demonstrated that SNHG1 depletion inactivated Jak2/stat3 pathway to affect cell viability and confine apoptosis, autophagy in LPS-treated PC12 cells. Taken together, SNHG1 regulated cell viability, apoptosis and autophagy in LPS-treated PC12 cells by activating Jak2/stat3 pathway via sponging miR-362-3p.	NA	Neurochem Res. 2021 Apr;46(4):945-956. doi: 10.1007/s11064-020-03224-7. Epub 2021 Jan 30.
4795	LncRNA	SNHG1	miR-216b-5p	NA	A2780/Taxol cells	Ovarian Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;Luciferase reporter assay;	33302997	Dysregulation of lnc-SNHG1 and miR-216b-5p correlate with chemoresistance and indicate poor prognosis of serous epithelial ovarian cancer.	AIM: This study aimed to explore whether the dysregulation of lnc-small nucleolar RNA host gene 1 (SNHG1) and miR-216b-5p correlated with chemoresistance and indicated poor prognosis of serous epithelial ovarian cancer (EOC). METHODS AND RESULTS: The expression of lnc-SNHG1 was upregulated, while miR-216b-5p showed low expression in patients with chemoresistant EOC compared with patients with chemosensitive EOC. The multivariate Cox regression analysis showed that the expression of miR-216b-5p and FIGO stage were independent prognostic factors for the overall survival (OS) of patients with serous EOC. Kaplan-Meier curves revealed a significant association of the increased expression level of lnc-SNHG1 with shorter OS and disease-free survival (DFS). Patients with a low expression level of miR-216b-5p also had shorter OS and DFS. The biological functions were tested using CCK-8 assay, colony formation assay, wound healing assay, and cell apoptosis. The knockdown of SNHG1 and the overexpression of miR-216b-5p stimulated paclitaxel sensitivity in A2780/Taxol cells through inhibiting cell growth and migration and promoting apoptosis. The inhibition of miR-216b-5p could rescue the effect of lnc-SNHG1 inhibition on the sensitivity of A2780/Taxol cells to paclitaxel. Luciferase reporter assay, RNA Binding Protein Immunoprecipitation Assay (RIP), and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) indicated that lnc-SNHG1 acted as a sponge of miR-216b-5p in A2780/Taxol cells. CONCLUSIONS: This study showed that the overexpression of lnc-SNHG1 and decreased expression level of miR-216b-5p correlated with the chemoresistance of patients with serous EOC and indicated shorter OS and DFS. Lnc-SNHG1 functioned as a ceRNA with miR-216b-5p, which was critical in modulating the paclitaxel sensitivity of ovarian cancer cells.	NA	J Ovarian Res. 2020 Dec 10;13(1):144. doi: 10.1186/s13048-020-00750-4.
4796	LncRNA	SNHG1	miR-181a-5p	CXCL12	neuroblastoma cells	Parkinsons Disease	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33389428	LncRNA SNHG1 promotes neuronal injury in Parkinson's disease cell model by miR-181a-5p/CXCL12 axis.	Small molecule RNA host gene 1 (SNHG1) has been found to be an important regulator in the neurotoxicity of Parkinson's disease (PD). However, the underlying molecular mechanisms of SNHG1 in PD remains elusive. The expression of SNHG1, microRNA (miR)-181a-5p, and C-X-C motif chemokine 12 (CXCL12) mRNA was detected using quantitative real-time polymerase chain reaction. Cell viability and apoptosis were analyzed by cell counting kit-8 and Flow cytometry, respectively. Western blot was utilized to determine the levels of B-cell lymphoma-2 (Bcl-2), CyclinD1, Cleaved-caspase-3, and CXCL12 protein. The interaction between miR-181a-5p and SNHG1 or CXCL12 was confirmed by the dual-luciferase reporter assay. We discovered that SNHG1 was significantly elevated, while miR-181a-5p was decreased in N-methyl-4-phenylpyridinium (MPP(+))-treated neuroblastoma cells in dose-dependent manners. MPP(+) induced cell viability inhibition and apoptosis promotion, while these effects were reversed by SNHG1 knockdown or miR-181a-5p re-expression. SNHG1 directly bound to miR-181a-5p, and miR-181a-5p inhibition could block the action of SNHG1 knockdown on MPP+-induced neurotoxicity in neuroblastoma cells. CXCL12 was identified as a downstream target of miR-181a-5p, and the impact of miR-181a-5p on MPP(+)-induced neuronal damage could be attenuated by CXCL12 overexpression. Besides, SNHG1 could indirectly regulate CXCL12 expression via miR-181a-5p. We demonstrated that SNHG1 promoted MPP(+) induced neuronal injury in neuroblastoma cells by regulating miR-181a-5p/CXCL12 axis, suggesting SNHG1 might contribute to the development of PD, which provided a novel insight into the pathogenesis and treatment of PD.	NA	J Mol Histol. 2021 Apr;52(2):153-163. doi: 10.1007/s10735-020-09931-3. Epub 2021 Jan 3.
4797	LncRNA	SNHG14	miR-124-3p	MMP2	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	ELISA;MTT assay;qRT-PCR;Western blot;MTT assay;	33490282	Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion-Induced Acute Kidney Injury by Regulating miR-124-3p/MMP2 Axis.	PURPOSE: Ample evidence has proved that lncRNAs are pivotal regulators in acute kidney injury (AKI). Here, we focus on the role and mechanism of lncRNA SNHG14 in ischemia/reperfusion- (I/R-) caused AKI. METHODS: I/R and hypoxia/reoxygenation (H/R) were applied to induce rats and HK-2 cells to establish AKI models in vivo and in vitro. Relative expression of SNHG14, miR-124-3p, and MMP2 was determined by qRT-PCR. HE staining was used to evaluate pathological changes in renal tissues, and acute tubular necrosis (ATN) score was calculated. Renal function was evaluated by measuring serum creatinine content and blood urea nitrogen content. Levels of IL-1β, IL-6, and TNF-α were measured by ELISA. Cell viability was examined by MTT assay. Oxidative stress was assessed by measuring SOD, MDA, and ROS levels. The target of SNHG14 or miR-124-3p was verified by DLR assay. Protein expression of MMP2 was examined by western blot. RESULTS: SNHG14 was boosted in renal tissues of I/R-stimulated rats and H/R-induced HK-2 cells, while miR-124-3p was diminished in H/R-stimulated HK-2 cells. Si-SNHG14 or miR-124-3p mimics repressed inflammation and oxidative stress and enhanced cell viability in H/R-stimulated HK-2 cells. Sh-SNHG14 mitigated I/R-induced AKI in rats. MiR-124-3p was targeted by SNHG14, and MMP2 was targeted by miR-124-3p. Inhibition of miR-124-3p or upregulation of MMP2 reversed inhibitory effects of SNHG14 silence on inflammation and oxidative stress as well as the promoting effect of SNHG14 silence on cell viability in H/R-induced HK-2 cells. CONCLUSION: Knockdown of SNHG14 alleviated I/R-induced AKI by miR-124-3p-mediated downregulation of MMP2.	NA	Biomed Res Int. 2021 Jan 4;2021:8884438. doi: 10.1155/2021/8884438. eCollection 2021.
4798	LncRNA	SNHG14	miR-181b-5p	LPS	PC-12 cells	Spinal Cord Injury	Homo sapiens (human)	ELISA;Western blot;Luciferase reporter assay;	33791006	Knockdown of lncRNA SNHG14 alleviates LPS-induced inflammation and apoptosis of PC12 cells by regulating miR-181b-5p.	Spinal cord injury (SCI) is a traumatic central nervous system disorder that leads to permanent functional loss, and unavailable treatment of this disease results in poor quality of life. However, the specific role of long non-coding RNA small nucleolar RNA host gene 14 (lncRNA SNHG14) in SCI has not been fully studied. The aim of the current study was to investigate the role of SNHG14 and its regulatory mechanism in lipopolysaccharide (LPS)-induced PC-12 cells. LPS was used to stimulate PC-12 cells to simulate inflammatory injury following SCI in vitro. Cell viability and apoptosis were respectively assessed by Cell Counting Kit-8 assay and TUNEL assay. Western blotting was performed to detect the expressions of apoptosis-related proteins. The mRNA levels of SNHG14 and microRNA (miR)-181b-5p were detected by reverse transcription-quantitative PCR. The target of SNGH14 was predicted by bioinformatics analysis and subsequently validated by a luciferase reporter assay. ELISA was then used to detect the levels of inflammatory factors. The results indicated that LPS induced inflammation, decreased cell viability and increased the apoptosis of PC-12 cells. Interference of SNHG14 alleviated this type of injury of PC-12 cells. Bioinformatics prediction and luciferase reporter assay demonstrated that miR-181b-5p could directly bind to SNHG14. Moreover, mechanistic investigations revealed that the miR-181b-5p inhibitor could reverse the inhibitory effects of SNHG14 silencing on cell viability, inflammation and apoptosis of PC-12 cells. To conclude, the present results showed that SNHG14 knockdown alleviated PC-12 cell inflammation and apoptosis induced by LPS via regulating miR-181b-5p, which might provide a novel insight into the treatment of SCI.	NA	Exp Ther Med. 2021 May;21(5):497. doi: 10.3892/etm.2021.9928. Epub 2021 Mar 17.
4799	LncRNA	SNHG15	miR-302a-3p	STAT1	HT22 cells	Ischemic Brain Injury	Homo sapiens (human)	qRT-PCR	33396557	Unpacking Pandora From Its Box: Deciphering the Molecular Basis of the SARS-CoV-2 Coronavirus.	An enigmatic localized pneumonia escalated into a worldwide COVID-19 pandemic from Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). This review aims to consolidate the extensive biological minutiae of SARS-CoV-2 which requires decipherment. Having one of the largest RNA viral genomes, the single strand contains the genes ORF1ab, S, E, M, N and ten open reading frames. Highlighting unique features such as stem-loop formation, slippery frameshifting sequences and ribosomal mimicry, SARS-CoV-2 represents a formidable cellular invader. Hijacking the hosts translational engine, it produces two polyprotein repositories (pp1a and pp1ab), armed with self-cleavage capacity for production of sixteen non-structural proteins. Novel glycosylation sites on the spike trimer reveal unique SARS-CoV-2 features for shielding and cellular internalization. Affording complexity for superior fitness and camouflage, SARS-CoV-2 challenges diagnosis and vaccine vigilance. This review serves the scientific community seeking in-depth molecular details when designing drugs to curb transmission of this biological armament.	NA	Int J Mol Sci. 2020 Dec 31;22(1):386. doi: 10.3390/ijms22010386.
4800	LncRNA	SNHG15	miR-302a-3p	NF-KB	HT22 cells	Ischemic Brain Injury	Homo sapiens (human)	qRT-PCR	33396557	Unpacking Pandora From Its Box: Deciphering the Molecular Basis of the SARS-CoV-2 Coronavirus.	An enigmatic localized pneumonia escalated into a worldwide COVID-19 pandemic from Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). This review aims to consolidate the extensive biological minutiae of SARS-CoV-2 which requires decipherment. Having one of the largest RNA viral genomes, the single strand contains the genes ORF1ab, S, E, M, N and ten open reading frames. Highlighting unique features such as stem-loop formation, slippery frameshifting sequences and ribosomal mimicry, SARS-CoV-2 represents a formidable cellular invader. Hijacking the hosts translational engine, it produces two polyprotein repositories (pp1a and pp1ab), armed with self-cleavage capacity for production of sixteen non-structural proteins. Novel glycosylation sites on the spike trimer reveal unique SARS-CoV-2 features for shielding and cellular internalization. Affording complexity for superior fitness and camouflage, SARS-CoV-2 challenges diagnosis and vaccine vigilance. This review serves the scientific community seeking in-depth molecular details when designing drugs to curb transmission of this biological armament.	NA	Int J Mol Sci. 2020 Dec 31;22(1):386. doi: 10.3390/ijms22010386.
4801	LncRNA	SNHG16	miR-302b-3p	SLC2A4	pancreatic adenocarcinoma tissues and cells	Pancreatic Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33435953	LncRNA SNHG16 contributes to tumor progression via the miR-302b-3p/SLC2A4 axis in pancreatic adenocarcinoma.	BACKGROUND: It has been reported that the lncRNA SNHG16 has significantly increased expression in pancreatic adenocarcinoma (PC). However, the functions and mechanisms of SNHG16 are not clear. The aim of this study was to explore the effects of SNHG16 on PC. METHODS: qRT-PCR analysis was applied to detect the expression levels of SNHG16, miR-302b-3p and SLC2A4 in PC tissues and cells. CCK8 and EdU assays were used to evaluate the proliferation of PC cells. Transwell assays were used to assess PC cell migration and invasion. Apoptosis was evaluated by flow cytometry, and the expression of apoptosis-related proteins (including Bax, Bcl-2, cleaved caspase-3 and cleaved caspase-9) was tested by western blotting. The interactions between miR-302b-3p and SNHG16 or miR-302b-3p and the 3'UTR of SLC2A4 mRNA were clarified by a dual luciferase reporter assay and RNA immunoprecipitation. RESULTS: SNHG16 expression was significantly elevated in PC tissues and cell lines and was associated with poor prognosis of PC patients. Knockdown of SNHG16 reduced PC cell proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. In addition, miR-302b-3p targeted SLC2A4 directly. CONCLUSIONS: SNHG16 promoted the progression of PC via the miR-302b-3p/SLC2A4 axis and was expected to be a potential target for the early diagnosis and treatment of PC.	NA	Cancer Cell Int. 2021 Jan 12;21(1):51. doi: 10.1186/s12935-020-01715-9.
4802	LncRNA	SNHG3	miR-340-5p	HOXA10	non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	qRT-PCR;Western blot;	33225676	lncRNA SNHG3 accelerates the proliferation and invasion of non-small cell lung cancer by downregulating miR-340-5p.	Small nucleolar RNA host genes (SNHGs) as a subset of long non-coding RNAs (lncRNAs) act critical roles in tumor progression. The present study aimed to elucidate the role and mechanisms of SNHG3 in non-small cell lung cancer (NSCLC). The correlation of SNHG3/miR-340-5p/HOXA10 with the clinicopathological features and outcomes in NSCLC was analyzed by TCGA cohort. In vitro and in vivo functional experiments were conducted to assess the role of SNHG3 in NSCLC cells. Bioinformatic analysis and luciferase gene reporter were used to estimate the interaction between miR-340-5p and SNHG3/HOXA10 3'UTR. The effects of SNHG3 and (or) miR-340-5p on HOXA10 expression were detected by qRT-PCR and Western blot analysis. As a consequence, the elevated expression of SNHG3 and HOXA10 or lowered expression of miR-340-5p was related to the lymph node infiltration, distant metastases and unfavorable prognosis in NSCLC. Ectopic expression of SNHG3 boosted the proliferation and invasion of NSCLC cells in vitro and in vivo, whereas downregulation of SNHG3 reversed these effects. Moreover, SNHG3 could bind with miR-340-5p and reduce its expression levels, and miR-340-5p attenuated SNHG3-induced tumor proliferation and HOXA10 expression in NSCLC cells. Our findings unveiled that SNHG3 might be an oncogenic factor in NSCLC by downregulating miR-340-5p.	NA	J Biol Regul Homeost Agents. 2020 Nov-Dec;34(6):2017-2027. doi: 10.23812/20-388-A.
4803	LncRNA	Snhg8	miR-425-5p	SIRT1	brain microvascular endothelial cells	Ischemic Stroke	Homo sapiens (human)	qRT-PCR	33491845	LncRNA Snhg8 attenuates microglial inflammation response and blood-brain barrier damage in ischemic stroke through regulating miR-425-5p mediated SIRT1/NF-κB signaling.	Increasing studies have indicated that abnormal expressed long noncoding RNAs (lncRNAs) play a vital role in ischemic stroke. Small nucleolar RNA host gene 8 (Snhg8), a member of lncRNAs, has been found to induce neuronal apoptosis in chronic cerebral ischemia models. Here, we aim to explore the function and molecular mechanism of Snhg8 in modulating microglial inflammation as well as brain microvascular endothelial cell (BMEC) damage following ischemic injury. Our data suggested that Snhg8 was low-expressed in the brain tissues of mice that underwent middle cerebral artery occlusion (MCAO) surgery and oxygen-glucose deprivation (OGD)-treated primary microglia and BMECs. Gain- or loss-of function approaches found that Snhg8 upregulation not only attenuated ischemic induced inflammatory response in microglia but also relieved BMECs injury both in vitro and in vivo. Furthermore, we conducted a bioinformatics analysis to explore the underlying mechanism of Snhg8. The results indicated that Snhg8 served as a competitive endogenous RNA by sponging miR-425-5p, which was proved to promote microglial inflammation and BMECs injury by targeting sirtuin1 (SIRT1)-mediated nuclear factor-κB (NF-κB) pathway. Overall, these results revealed that the Snhg8/miR-425-5p/SIRT1/NF-κB axis plays a critical role in the regulation of cerebral ischemia-induced microglial inflammation and brain-blood barrier damage.	NA	J Biochem Mol Toxicol. 2021 May;35(5):e22724. doi: 10.1002/jbt.22724. Epub 2021 Jan 25.
4804	LncRNA	Snhg8	miR-425-5p	NF-kB	brain microvascular endothelial cells	Ischemic Stroke	Homo sapiens (human)	qRT-PCR	33491845	LncRNA Snhg8 attenuates microglial inflammation response and blood-brain barrier damage in ischemic stroke through regulating miR-425-5p mediated SIRT1/NF-κB signaling.	Increasing studies have indicated that abnormal expressed long noncoding RNAs (lncRNAs) play a vital role in ischemic stroke. Small nucleolar RNA host gene 8 (Snhg8), a member of lncRNAs, has been found to induce neuronal apoptosis in chronic cerebral ischemia models. Here, we aim to explore the function and molecular mechanism of Snhg8 in modulating microglial inflammation as well as brain microvascular endothelial cell (BMEC) damage following ischemic injury. Our data suggested that Snhg8 was low-expressed in the brain tissues of mice that underwent middle cerebral artery occlusion (MCAO) surgery and oxygen-glucose deprivation (OGD)-treated primary microglia and BMECs. Gain- or loss-of function approaches found that Snhg8 upregulation not only attenuated ischemic induced inflammatory response in microglia but also relieved BMECs injury both in vitro and in vivo. Furthermore, we conducted a bioinformatics analysis to explore the underlying mechanism of Snhg8. The results indicated that Snhg8 served as a competitive endogenous RNA by sponging miR-425-5p, which was proved to promote microglial inflammation and BMECs injury by targeting sirtuin1 (SIRT1)-mediated nuclear factor-κB (NF-κB) pathway. Overall, these results revealed that the Snhg8/miR-425-5p/SIRT1/NF-κB axis plays a critical role in the regulation of cerebral ischemia-induced microglial inflammation and brain-blood barrier damage.	NA	J Biochem Mol Toxicol. 2021 May;35(5):e22724. doi: 10.1002/jbt.22724. Epub 2021 Jan 25.
4805	LncRNA	SNHG8	miR-634	ZBTB20	breast cancer cells	Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	33854372	LncRNA SNHG8 Serves as an Oncogene in Breast Cancer Through miR-634/ZBTB20 Axis.	BACKGROUND: Small nucleolus RNA Host Gene 8 (SNHG8) belongs to a subgroup with long non-coding RNAs. LncRNA SNHG8 presents up-regulated in miscellaneous cancers, like gastric cancer, liver cancer, and esophageal squamous cell cancer. Nevertheless, the expression pattern and the pathological function of lncRNA SNHG8 in breast cancer remain obscure. METHODS: We examined the expression levels of lncRNA SNHG8 in the tissue samples and cell lines from breast cancer via RT-qPCR in the present study. The functions of lncRNA SNHG8 on the progression of breast cancer cell were examined by CCK-8, EdU, Transwell chamber assays, and flow cytometry analyses. The expression of proteins was assessed using Western blot assay. RESULTS: We found that proliferation, migration, and invasion of breast cancer cells were significantly inhibited due to knockdown of lncRNA SNHG8, while inducing apoptosis of these cells. Mechanistically, SNHG8 functioned as an inhibitor of miR-634 in tumor tissues. CONCLUSION: LncRNA SNHG8 sponged the miR-634 to increase the expression level of ZBTB20, thus further aggravating the malignancy of breast cancer. Hence, the lncRNA SNHG8-miR-634-ZBTB20 axis may be a promising therapeutic target to treat breast cancers.	NA	Cancer Manag Res. 2021 Apr 7;13:3017-3028. doi: 10.2147/CMAR.S270128. eCollection 2021.
4806	LncRNA	SNHG8	miR-634	ZBTB20	breast cancer cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;	33275231	LncRNA SNHG8 promotes cell migration and invasion in breast cancer cell through miR-634/ZBTB20 axis.	OBJECTIVE: Small nucleolus RNA Host Gene 8 (SNHG8) belongs to a subgroup of long non-coding RNAs. SNHG8 is upregulated in many cancers, such as gastric cancer, liver cancer, and esophageal squamous cell cancer. However, whether SNHG8 is abnormally expressed in breast cancer and its biological functions remain unclear. Therefore, our research intended to determine the expression status of SNHG8 in breast cancer, explore the effects of SNHG8 on the development of breast cancer, and investigate the potential molecular mechanisms in cancer progression. PATIENTS AND METHODS: The expression levels of SNHG8 were detected in tissue samples and cell lines via qRT-PCR. The effects of SNHG8 on viability of breast cancer cells were detected via CCK-8, EdU, transwell, and flow cytometry analyses. RESULTS: qRT-PCR results showed that the expression level of SNHG8 was significantly upregulated in tumor tissues and cell lines. Gene functional studies showed that the downregulation of the expression level of SNHG8 significantly inhibited the breast cancer cells migration and invasion, and induced apoptosis. Meanwhile, we found that SNHG8 served as an inhibitor of miR-634 in tumor tissues. SNHG8 may participate in the malignancy of breast cancer by sponging the miR-634 to increase the expression level of ZBTB20. CONCLUSIONS: The SNHG8-miR-634-ZBTB20 pathway may be a potential target for the treatment of breast cancers.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(22):11639-11649. doi: 10.26355/eurrev_202011_23808.
4807	LncRNA	SNHG8	miR-384	HOXB7	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33450101	Long non-coding RNA SNHG8 promotes prostate cancer progression through repressing miR-384 and up-regulating HOXB7.	BACKGROUND: Multiple long non-coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression. METHODS: A quantitative real-time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA-384 (miR-384) and homeobox B7 (HOXB7) expression. Call-couting kit-8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual-luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR-384, SNHG8 and HOXB7. RESULTS: SNHG8 was up-regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR-384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR-384 inhibition. HOXB7 was confirmed to be a target gene of miR-384. SNHG8 knockdown repressed HOXB7 expression via targeting miR-384. CONCLUSIONS: SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR-384 and up-regulating HOXB7.	NA	J Gene Med. 2021 Mar;23(3):e3309. doi: 10.1002/jgm.3309. Epub 2021 Feb 23.
4808	LncRNA	SNHG8	miR-384	HOXB7	prostate cancer cells	Prostate Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33450101	Long non-coding RNA SNHG8 promotes prostate cancer progression through repressing miR-384 and up-regulating HOXB7.	BACKGROUND: Multiple long non-coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression. METHODS: A quantitative real-time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA-384 (miR-384) and homeobox B7 (HOXB7) expression. Call-couting kit-8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual-luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR-384, SNHG8 and HOXB7. RESULTS: SNHG8 was up-regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR-384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR-384 inhibition. HOXB7 was confirmed to be a target gene of miR-384. SNHG8 knockdown repressed HOXB7 expression via targeting miR-384. CONCLUSIONS: SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR-384 and up-regulating HOXB7.	NA	J Gene Med. 2021 Mar;23(3):e3309. doi: 10.1002/jgm.3309. Epub 2021 Feb 23.
4809	LncRNA	SOX2OT	miR-200a	DEK	pancreatic cancer cells	Pancreatic Cancer	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;	33336718	Long noncoding RNA SOX2OT maintains the stemness of pancreatic cancer cells by regulating DEK via interacting with miR-200a/141.	The article "Long noncoding RNA SOX2OT maintains the stemness of pancreatic cancer cells by regulating DEK via interacting with miR-200a/141, by C.-S. Liu, Q. Zhou, Y.-D. Zhang, Y. Fu, published in Eur Rev Med Pharmacol Sci 2020; 24 (5): 2368-2379-DOI: 10.26355/eurrev_202003_20504-PMID: 32196588" has been withdrawn from the authors stating that "to validate the effect of lncRNA-SOX2OT, we constructed SOX2OT overexpressed cells using lentiviral vector with -IRES2-EGFP to easily visualize the transfection efficiency. Therefore, the stably transfected cells were carrying the green fluorescence. However, during our Flow cytometry assay, we took PC cells (Control) with no fluorescence to standardize our equipment and measured the negative control (NC) and overexpressed-Sox2ot (oe-Sox2ot) according to the manufacturer's guidance, without removing the disturbance that the green fluorescence caused. This means that, despite having performed the standard assay, the results obtained in Figure 2D were wrong and unscientific". The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20504.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):11991. doi: 10.26355/eurrev_202012_23980.
4810	LncRNA	TapSAKI	miR-205	IRF3	HK-2 cells	Sepsis	Homo sapiens (human)	qRT-PCR	33869780	Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway.	Sepsis is a common and lethal syndrome. Long non-coding RNA (lncRNA) transcript predicting survival in AKI (TapSAKI) has recently been found to serve as an important regulator in sepsis. However, the underlying mechanism of TapSAKI in sepsis pathogenesis remains largely unknown. Our data demonstrated that lipopolysaccharide (LPS)-induced HK-2 cell injury by weakening cell viability and enhancing cell apoptosis and inflammation. TapSAKI was upregulated and miR-205 was downregulated in LPS-induced HK-2 cells. TapSAKI knockdown or miR-205 overexpression alleviated LPS-induced cytotoxicity in HK-2 cells. TapSAKI sequestered miR-205 via acting as a miR-205 sponge. Moreover, the mitigating effect of TapSAKI silencing on LPS-induced HK-2 cell injury was mediated by miR-205. Additionally, the interferon regulatory factor 3 (IRF3) signaling was involved in the regulation of the TapSAKI/miR-205 axis on LPS-induced HK-2 cell damage. Our current study suggested that TapSAKI silencing relieved LPS-induced injury in HK-2 cells at least in part by sponging miR-205 and regulating the IRF3 signaling pathway, highlighting a novel understanding for sepsis pathogenesis and a promising target for this disease treatment.	NA	Open Med (Wars). 2021 Apr 7;16(1):581-590. doi: 10.1515/med-2021-0204. eCollection 2021.
4811	LncRNA	TMPO-AS1	miR-320a	SOX4	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33488123	TMPO-AS1 Regulates the Aggressiveness-Associated Traits of Nasopharyngeal Carcinoma Cells Through Sponging miR-320a.	BACKGROUND: Previous evidence demonstrates that the long non-coding RNA (lncRNA) TMPO antisense RNA 1 (TMPO-AS1) is involved in the aggressiveness of several cancers. Nevertheless, its functions in nasopharyngeal carcinoma (NPC) are unclear. METHODS: qRT-PCR was used to evaluate the levels of TMPO-AS1 and miR-320a in NPC tissues. Furthermore, the growth and invasiveness of NPC cells were evaluated by colony formation and Transwell assays. The protein expression ofSRY-Box Transcription Factor 4 (SOX4) was observed by Western blotting and immunohistochemistry. Bioinformatic prediction and luciferase reporter assays were used to explore the interaction between miR-320a and TMPO-AS1. The transplanted model was employed to disclose the interference of TMPO-AS1 in the tumor growth of NPC cells in vivo. RESULTS: We found that TMPO-AS1 was distinctly upregulated in NPC. Downregulation of TMPO-AS1 restrained aggressiveness-associated traits in NPC cells. Nevertheless, upregulation of TMPO-AS1 yielded the opposite results. Further studies revealed that lncRNA TMPO-AS1 acts as a "sponge" for miR-320a, resulting in increased levels of SOX4 in NPC cells. Finally, TMPO-AS1 silencing suppressed tumor growth of NPC cells in vivo. CONCLUSION: Collectively, these results reveal the presence of a novel TMPO-AS1/miR-320a/SOX4 pathway associated with NPC progression, suggesting that lncRNA TMPO-AS1 may be a potential therapeutic target for NPC.	NA	Cancer Manag Res. 2021 Jan 15;13:415-425. doi: 10.2147/CMAR.S285113. eCollection 2021.
4812	LncRNA	TMPO-AS1	miR-383-5p	SOX11	pancreatic carcinoma tissues and cells	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33664819	Long non-coding RNA TMPO-AS1 serves as a tumor promoter in pancreatic carcinoma by regulating miR-383-5p/SOX11.	The dysregulation of lncRNA TMPO antisense RNA 1 (TMPO-AS1) has been detected in various malignant tumors. However, the role of lncRNA TMPO-AS1 remains unclear in pancreatic carcinoma. The present study aimed to elucidate the functional mechanism of TMPO-AS1 in pancreatic carcinoma. In the present study, RT-qPCR, western blotting, MTT, Transwell, luciferase reporter and xenograft assays were used to investigate the role of lncRNA TMPO-AS1 in pancreatic carcinoma. Upregulation of lncRNA TMPO-AS1 was revealed in pancreatic carcinoma tissues and cells. Furthermore, knockdown of TMPO-AS1 restrained cell proliferation and motility in pancreatic carcinoma. In addition, microRNA (miR)-383-5p acted as a 'sponge' for lncRNA TMPO-AS1. The expression levels of lncRNA TMPO-AS1 and miR-383-5p were mutually inhibited in pancreatic carcinoma. Moreover, miR-383-5p was revealed to directly target SRY-related high-mobility group box 11 (SOX11). Notably, SOX11 could promote the occurrence of pancreatic carcinoma by interacting with the lncRNA TMPO-AS1/miR-383-5p axis. In conclusion, upregulation of lncRNA TMPO-AS1 promoted tumor growth, cell migration and invasion in pancreatic carcinoma by downregulating miR-383-5p and upregulating SOX11.	NA	Oncol Lett. 2021 Apr;21(4):255. doi: 10.3892/ol.2021.12517. Epub 2021 Feb 4.
4813	LncRNA	TMPO-AS1	miR-126-5p	BRCC3	Gastric cancer tissues and cells	Gastric Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;Rescue assay;RNA pull-down;	33295056	Long noncoding RNA TMPO-AS1/miR-126-5p/BRCC3 axis accelerates gastric cancer progression and angiogenesis via activating PI3K/Akt/mTOR pathway.	BACKGROUND AND AIM: Gastric cancer (GC) is an aggressive tumor featured by uncontrolled cell proliferation and metastasis. In recent years, long noncoding RNAs (lncRNAs) act as crucial regulators and biological markers in multiple cancers. LncRNA TMPO-AS1 has been revealed to be an oncogene in some cancers. Nevertheless, there is little known about the biological role of TMPO-AS1 in GC. METHODS: Reverse transcription-quantitative polymerase chain reaction analysis was used to examine the expression level of TMPO-AS1 in GC tissues and cells. Cell Counting Kit-8, colony formation, wound healing assays, and western blot analysis were performed to determine the role of TMPO-AS1 in GC cells. RNA pull-down, luciferase reporter, and RNA immunoprecipitation assays were used to test the interaction among TMPO-AS1, miR-126-5p, and BRCC3. RESULTS: TMPO-AS1 was highly expressed in GC tissues and cells. Upregulated TMPO-AS1 was closely associated with adverse prognosis of GC patients. Functional assays showed that TMPO-AS1 promoted GC cell proliferation, migration, and angiogenesis. Furthermore, it was found that TMPO-AS1 acted as a competing endogenous RNA for miR-126-5p to upregulate BRCC3 expression. Rescue assays revealed that TMPO-AS1 facilitated cellular progression of GC by sponging miR-126-5p and upregulating BRCC3. In addition, we found that the effects of the TMPO-AS1/miR-126-5p/BRCC3 axis on GC cell progression were related to the PI3K/Akt/mTOR pathway. CONCLUSIONS: Our study demonstrated that the TMPO-AS1/miR-126-5p/BRCC3 axis was involved in GC progression via the regulation of PI3K/Akt/mTOR pathway, which might provide a potential therapeutic strategy for GC.	NA	J Gastroenterol Hepatol. 2020 Dec 8. doi: 10.1111/jgh.15362.
4814	LncRNA	TP73-AS1	miR-495	JAM-A	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Homo sapiens (human)	Cell migration assay;Dual-luciferase reporter assay;MTT assay;qRT-PCR;Western blot;Luciferase reporter assay;MTT assay;	33400379	LncRNA TP73-AS1 regulates miR-495 expression to promote migration and invasion of nasopharyngeal carcinoma cells through junctional adhesion molecule A.	The main obstacle to the treatment of nasopharyngeal carcinoma (NPC) is metastasis. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are highly involved in the progression of NPC. In this study, we aimed to explore the regulatory role of lncRNA P73 antisense RNA 1 T (TP73-AS1) and miR-495 in migration and invasion of NPC cells. The expression levels of TP73-AS1, miR-495, and junctional adhesion molecule A (JAM-A) in NPC tissue samples and cell lines were examined by quantitative real-time PCR (qRT-PCR) and/or Western blot. NPC cells were transfected with vectors overexpressing TP73-AS1, short hairpin RNA (shRNA) against TP73-AS1, shRNA against JAM-A, miR-495 mimics, miR-495 inhibitor, and their corresponding negative controls as designated. The MTT assay, cell migration assay, and transwell assay were performed to detect cell viability, migration, and invasion, respectively. Dual-luciferase reporter assay was performed to confirm the binding of TP73-AS1 and miR-495, and miR-495 and JAM-A. TP73-AS1 and JAM-A were significantly upregulated while miR-495 was markedly downregulated in NPC tissues and cell lines compared to normal controls. The overexpression of TP73-AS1 promoted migration and invasion of NPC cell line CNE-2. TP73-AS1 targeted miR-495 and negatively regulated its expression. TP73-AS1 upregulated the expression of JAM-A through miR-495. TP73-AS1 mediated migration and invasion of CNE-2 cells via upregulating JAM-A. LncRNA TP73-AS1, miR-495, and JAM-A are involved in migration and invasion of NPC cells. The TP73-AS1/miR-495/JAM-A axis may serve as a therapeutic target for the treatment of NPC.	NA	Kaohsiung J Med Sci. 2021 May;37(5):361-370. doi: 10.1002/kjm2.12338. Epub 2021 Jan 5.
4815	LncRNA	TRIM52-AS1	miR-218-5p	ROBO1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	33519234	Long Non-Coding RNA TRIM52-AS1 Promotes Growth and Metastasis via miR-218-5p/ROBO1 in Hepatocellular Carcinoma.	BACKGROUND: Hepatocellular carcinoma (HCC) is a malignant disease with a high mortality among primary HCC patients worldwide. Lots of studies have shown that lncRNAs are known as the biomarkers in diagnosis, treatment and prognosis of hepatocellular carcinoma. Therefore, clarifying the detailed function and mechanism of the lncRNA in the HCC progressing seems particularly important. METHODS: The TCGA and GEO database and RT-qPCR were used to analyse the expression of TRIM52-AS1 in HCC tissues and cell lines. Clinical data were collected to further analyze the correlation between indicators of clinical samples and the expression of TRIM52-AS1. CCK-8, plate clone and transwell assays were employed to evaluate the role of TRIM52-AS1 on cell proliferation, migration and invasion. Then, bioinformatics prediction, luciferase reporter, RNA immunoprecipitation (RIP), and RT-qPCR were employed to analyze the direct interaction among TRIM52-AS1, miR-218-5p and ROBO1. Additionally, the rescue function assays were used to verify that miR-218-5p/ROBO1 was the function downstream of TRIM52-AS1. RESULTS: TRIM52-AS1 was overexpressed in HCC according to the TCGA database and RT-qPCR assay. The expression of TRIM52-AS1 was higher in the metastatic foci compared with primary tumor according to the GEO database. Additionally, TRIM52-AS1 knockdown inhibited the proliferation and metastasis of HCC cells. TRIM52-AS1 could act as competitive endogenous RNA to regulate ROBO1 through miR-218-5p, then promoted the HCC cell progression. CONCLUSION: TRIM52-AS1 is overexpressed in HCC and can promote the proliferation and metastasis of HCC cells through miR-218-5p/ROBO1 axis, then drives the HCC cell progression.	NA	Cancer Manag Res. 2021 Jan 22;13:547-558. doi: 10.2147/CMAR.S286205. eCollection 2021.
4816	LncRNA	TRPM2-AS	miR-138-5p	SDC3	OvC cells	Ovarian Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA pull-down assay;Western blot;RNA pull-down;	33621194	LncRNA TRPM2-AS promotes ovarian cancer progression and cisplatin resistance by sponging miR-138-5p to release SDC3 mRNA.	The role of TRPM2-AS lncRNA in OvC has not been explored. This study aimed to investigate whether and how TRPM2-AS contributes to the progression of OvC. First, qRT-PCR was employed to measure the expression of TRPM2-AS, miR-138-5p and SDC3 in OvC samples. A xenograft formation assay was subsequently performed to detect the tumor growth in vivo. The cell viability, colony formation, cell migration, cell invasion and cell apoptosis were later evaluated using a series of experiments. The western blot assay was utilized to detect the SDC3 protein expression and cell-apoptosis markers. Luciferase reporter gene assay, RIP, and RNA pull-down assays were performed to identify the association between TRPM2-AS, miR-138-5p and SDC3. Findings indicated that the expression of TRPM2-AS and SDC3 was significantly upregulated in OvC tissues and cells, while miR-138-5p expression was significantly downregulated in OvC samples. Unlike miR-138-5p, TRPM2-AS and SDC3 were found to promote OvC development. It was also found that TRPM2-AS could sponge miR-138-5p to release SDC3, thus promoting OvC progression. Apart from that, we discovered that both sh-TRPM2-AS and cisplatin could enhance the apoptosis of OvC cells. Overall, our findings suggested that the TRPM2-AS/miR-138-5p/SDC3 axis was closely associated with OvC tumorigenesis and cisplatin resistance.	NA	Aging (Albany NY). 2021 Feb 17;13(5):6832-6848. doi: 10.18632/aging.202541. Epub 2021 Feb 17.
4817	LncRNA	TTN-AS1	miR-134	ITGB1	Hepatocellular carcinoma tissues and cells	Hepatocellular Carcinoma	Homo sapiens (human)	microarray;	33387127	Silencing of Long Non-coding RNA TTN-AS1 Inhibits Hepatocellular Carcinoma Progression by the MicroRNA-134/ITGB1 Axis.	BACKGROUND: Hepatocellular carcinoma (HCC) causes considerable mortality worldwide. Long non-coding RNA (lncRNA) TTN-AS1 has been recently identified as an oncogene in several cancers, but its role in HCC and the molecules remain largely unknown. AIMS: The study aims to probe the function of lncRNA TTN-AS1 in HCC progression and the molecules involved. METHODS: Differentially expressed lncRNAs between HCC and the adjacent normal tissues were analyzed using a microarray. TTN-AS1 expression in HCC and normal tissues and cells was determined. Targeting relationships between TTN-AS1 and miR-134 and between miR-134 and ITGB1 were validated. Artificial up-regulation or down-regulation of TTN-AS1, miR-134 and ITGB1 was introduced in HCC cells to probe their effects on the biological behaviors of HCC cells. Xenograft tumors were induced in nude mice for in vivo experiments. RESULTS: TTN-AS1 and ITGB1 were highly expressed, while miR-134 was poorly expressed in HCC tissues. TTN-AS1 enforced ITGB1 expression through sequestering miR-134. Silencing of TTN-AS1 or over-expression of miR-134 inhibited proliferation, invasion, migration, and resistance to death of Huh7 cells. Following miR-134 silencing, further down-regulation of ITGB1 suppressed the malignant behaviors of HUH7 cells. The similar results were reproduced in vivo. CONCLUSION: The current study provided evidence that TTN-AS1 might promote HCC progression through sponging miR-134 and the following ITGB1 up-regulation. TTN-AS1 may serve as a potential target for HCC treatment.	NA	Dig Dis Sci. 2021 Jan 2. doi: 10.1007/s10620-020-06737-x.
4818	LncRNA	TUG1	miR-381-3p	MDM2	cervical cancer tissues and cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR	33340525	Long non-coding RNA TUG1 sponges microRNA-381-3p to facilitate cell viability and attenuate apoptosis in cervical cancer by elevating MDM2 expression.	OBJECTIVE: Based on the theory that long non-coding RNAs (lncRNAs) sponge microRNAs (miRNAs) to engage in cervical cancer development, this work was set out to investigate the possible role of lncRNA taurine upregulated gene 1 (TUG1) and miR-381-3p in the development of cervical cancer. METHODS: TUG1, miR-381-3p and murine double minute 2 (MDM2) expression were measured in cervical cancer tissues and cells. The nexus between TUG1 and clinicopathological features of cervical cancer was discussed. The biological functions of TUG1, miR-381-3p and MDM2 on cervical cancer cell process were interpreted via gain- and loss-of-function experiments. Also, tumor xenograft in nude mice was conducted in vivo. The interactions between TUG1, miR-381-3p and MDM2 were identified. RESULTS: TUG1 and MDM2 raised while miR-381-3p reduced in cervical cancer. TUG1 expression was related to tumor size, differentiation, international federation of gynecology and obstetrics stage and lymph node metastasis of cervical cancer. Restored miR-381-3p, depleted TUG1 or reduced MDM2 decreased viability, colony-forming, migration and invasion abilities, and facilitated apoptosis of cervical cancer cells. Xenografted tumors grew slowly upon injection with restored miR-381-3p and depleted TUG1. TUG1 bound to miR-381-3p and miR-381-3p targeted MDM2. CONCLUSION: On all accounts, this present study provides evidence that silencing TUG1 depressed cervical cancer cell progression through miR-381-3p/MDM2 axis, highlighting a theoretical basis for cervical cancer treatment.	NA	Life Sci. 2021 Feb 15;267:118902. doi: 10.1016/j.lfs.2020.118902. Epub 2020 Dec 16.
4819	LncRNA	TUG1	miR-9-5p	eIF5A2	Breast cancer cells	Breast Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;luciferase assay;siRNA knockdown;	33380806	Interactions Between lncRNA TUG1 and miR-9-5p Modulate the Resistance of Breast Cancer Cells to Doxorubicin by Regulating eIF5A2.	PURPOSE: Breast cancer (BC) is one of the leading causes of cancer-related deaths. Chemoresistance of BC remains a major unmet clinical obstacle. TUG1 (taurine-upregulated gene 1), a long noncoding RNA (lncRNA), and microRNAs (miRNA) are implicated in therapeutic resistance. However, the interactions between TUG1 and miRNAs that regulate doxorubicin (Dox) resistance in BC remain elusive. MATERIALS AND METHODS: Expression of TUG1 and miR-9 was measured by real-time PCR. EIF5A2 (eukaryotic translation initiation factor 5A-2) was detected by Western blot. Transfection of siRNAs or miRNA inhibitors was applied to silence lncRNA TUG1, eIF5A2 or miR-9. Cell viability, proliferation, and apoptosis were determined by CCK-8 (cell counting kit-8), flow cytometry, and EdU (5-ethynyl-2'-deoxyuridine) assays, respectively. The regulatory relationship between TUG1 and miR-9 was determined by a luciferase assay. RESULTS: LncRNA TUG1 was highly expressed in BC tissues and positively associated with Dox resistance in BC cell lines. SiRNA knockdown of TUG1 reversed Dox resistance in MCF-7/ADR cells. Mechanistically, TUG1 acted as a "sponge" for miR-9 and downregulated miR-9. Treatment with a miR-9 inhibitor blocked the effect of TUG1 siRNA, and knockdown of TUG1 inhibited the effects of miR-9. Furthermore, TUG1 inhibition of apoptosis induced by Dox involved miR-9 targeting of eIF5A2. CONCLUSION: TUG1 modulates the susceptibility of BC cells to Dox by regulating the expression of eIF5A2 via interacting with miR-9. These results indicate that the lncRNA TUG1 may be a novel therapeutic target in breast cancer.	NA	Onco Targets Ther. 2020 Dec 23;13:13159-13170. doi: 10.2147/OTT.S255113. eCollection 2020.
4820	LncRNA	UBA6-AS1	miR-760	HOXA2	glioblastoma cells	Glioblastoma	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;Rescue assay;	33469379	Long Non-Coding RNA UBA6-AS1 Promotes the Malignant Properties of Glioblastoma by Competitively Binding to microRNA-760 and Enhancing Homeobox A2 Expression.	BACKGROUND: The dysregulation of long non-coding RNAs is a frequent finding in glioblastoma (GBM) and is considered as a crucial mechanism contributing to GBM oncogenesis and progression. The biological roles and underlying mechanisms of action of UBA6 antisense RNA 1 (UBA6-AS1) in GBM have been rarely investigated. Therefore, the aim of the present study was to investigate in detail the role of UBA6-AS1 in the modulation of the malignant properties of GBM and explore the possible underlying mechanism(s). METHODS: The expression of UBA6-AS1 in GBM was determined via reverse transcription-quantitative PCR. Cell Counting Kit-8 assay, flow cytometric analysis, Transwell migration and invasion assays, and in vivo tumorigenicity assay were applied to elucidate the biological effects of UBA6-AS1 on GBM cells. The possible biological events associated with UBA6-AS1 were investigated by luciferase reporter, RNA immunoprecipitation (RIP) and rescue assays. RESULTS: UBA6-AS1 was overexpressed in GBM, which was consistent with the data from The Cancer Genome Atlas database. In the case of UBA6-AS1 depletion, GBM cell proliferation, migration and invasion were notably decreased and cell apoptosis was enhanced in vitro. Additionally, knockdown of UBA6-AS1 suppressed the proliferation of GBM cells in vivo. Mechanistically, UBA6-AS1 functioned as a competing endogenous RNA by adsorbing miR-760 and, consequently, upregulating homeobox A2 (HOXA2) expression. Rescue experiments demonstrated that the UBA6-AS1 silencing-mediated regulatory effects on GBM cells were reversed by the decrease of miR-760 or restoration of HOXA2 expression. CONCLUSION: Therefore, the results of the present study revealed that UBA6-AS1 promoted the malignant progression of GBM via targeting the miR-760/HOXA2 axis, thereby representing a promising effective target for the treatment of GBM.	NA	Cancer Manag Res. 2021 Jan 14;13:379-392. doi: 10.2147/CMAR.S287676. eCollection 2021.
4821	LncRNA	UCA1	miR-582-5p	NA	hyperglycemic vascular smooth muscle cells	Repair Of Hyperglycemic Vascular Smooth Muscle	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33378036	LncRNA UCA1 stimulates the repair of hyperglycemic vascular smooth muscle cells through targeting miR-582-5p.	OBJECTIVE: The purpose of this study was to elucidate the role of long non-coding RNA (lncRNA) UCA1 in inducing the repair of hyperglycemic vascular smooth muscle cells (VSMCs) by targeting microRNA-582-5p (miR-582-5p), thus alleviating diabetic angiopathy. PATIENTS AND METHODS: Arterial vessels and serum exosomes were collected from 40 type 2 diabetes mellitus (T2DM) patients and 40 non-T2DM patients. Relative levels of UCA1 and miR-582-5p in collected samples were detected. Then, the interaction between UCA1 and miR-582-5p was assessed by Dual-Luciferase reporter assay. Moreover, the regulatory effects of UCA1 and miR-582-5p on VSMCs phenotypes were determined. RESULTS: Results showed that compared with non-T2DM patients, UCA1 was markedly downregulated, while miR-582-5p was upregulated in VSMCs and serum exosomes of T2DM patients. They exerted a negative expression correlation between each other. Besides, miR-582-5p was the direct target of UCA1. Under the induction of increased doses of glucose, UCA1 stimulated proliferative and invasive abilities in VSMCs. MiR-582-5p was responsible for the repairability of UCA1 in VSMCs under the hyperglycemia state. CONCLUSIONS: LncRNA UCA1 induces the repair of hyperglycemic VSMCs via negatively regulating miR-582-5p. UCA1 may be a novel target for T2DM diagnosis and treatment.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12859-12866. doi: 10.26355/eurrev_202012_24188.
4822	LncRNA	UCA1	miR-423-5p	KCTD20	SK-N-SH cells	Urothelial Carcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33464446	Silencing of UCA1 Protects Against MPP(+)-Induced Cytotoxicity in SK-N-SH Cells via Modulating KCTD20 Expression by Sponging miR-423-5p.	Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder. Long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) has been implicated in PD development. Nevertheless, little insight has been gained on the mechanisms of UCA1 in PD pathogenesis. The levels of UCA1, miR-423-5p and potassium channel tetramerization domain containing 20 (KCTD20) were assessed by qRT-PCR and western blot. Cell viability was gauged by the CCK-8 assay, and cell apoptosis was detected by flow cytometry. Targeted relationships among UCA1, miR-423-5p and KCTD20 were verified by dual-luciferase reporter and RNA immunoprecipitation assays. Our data showed that MPP(+) induced UCA1 expression in SK-N-SH cells. UCA1 silencing protected against MPP(+)-evoked cytotoxicity in SK-N-SH cells. UCA1 functioned as a miR-423-5p sponge, and the protective impact of UCA1 silencing on MPP(+)-evoked cytotoxicity was mediated by miR-423-5p. KCTD20 was a direct target of miR-423-5p, and miR-423-5p overexpression mitigated MPP(+)-triggered cell injury by down-regulating KCTD20. Furthermore, UCA1 regulated KCTD20 expression by acting as a sponge of miR-423-5p in SK-N-SH cells. Our study first identified that the silencing of UCA1 protected SK-N-SH cells from MPP(+)-evoked cytotoxicity at least in part by targeting the miR-423-5p/KCTD20 axis.	NA	Neurochem Res. 2021 Apr;46(4):878-887. doi: 10.1007/s11064-020-03214-9. Epub 2021 Jan 19.
4823	LncRNA	UCA1	miR-499b-5p	TLR4	LPS-injured WI-38 cells	Pneumonia	Homo sapiens (human)	qRT-PCR	33368965	LncRNA UCA1 remits LPS-engendered inflammatory damage through deactivation of miR-499b-5p/TLR4 axis.	Neonatal pneumonia is a high neonatal mortality disease. The current research was designed to elucidate the modulatory function and feasible molecular mechanism of UCA1 in LPS-induced injury in pneumonia. Herein, LPS was applied to induce WI-38 cell inflammatory damage. We displayed that UCA1 was elevated in LPS-injured WI-38 cells. In the functional aspect, intervention of UCA1 evidently aggrandized cell viability in LPS-triggered WI-38 cells. In the meanwhile, elimination of UCA1 distinctly assuaged cell apoptosis concomitant with declined levels of proapoptotic proteins Bax and C-caspase-3, and ascended the expression of antiapoptotic protein Bcl-2. Subsequently, disruption of UCA1 manifestly restrained inflammatory damage as characterized by declination of multiple pro-inflammatory factors IL-1β, IL-6, and TNF-α in WI-38 cells under LPS circumstance. More importantly, we predicted and verified that UCA1 functioned as a ceRNA by efficaciously binding to miR-499b-5p thereby inversely adjusting miR-499b-5p expression. Interesting, TLR4 was identified as direct target of miR-499b-5p, and positively regulated by UCA1 through sponging miR-499b-5p. Mechanistically, absence of miR-499b-5p or restoration of TLR4 impeded the beneficial effects of UCA1 ablation on LPS-stimulated apoptosis and inflammatory response. Collectively, these observations illuminated that UCA1 inhibition protected WI-38 cells against LPS-managed inflammatory injury and apoptosis process via miR-499b-5p/TLR4 crosstalk, which ultimately influencing the development of pneumonia.	NA	IUBMB Life. 2021 Feb;73(2):463-473. doi: 10.1002/iub.2443. Epub 2020 Dec 31.
4824	LncRNA	UCA1	miR-375	SFRP1	neural progenitors in vitro	Temporal Lobe Epileps	Homo sapiens (human)	luciferase assay;	33829718	LncRNA UCA1 alleviates aberrant hippocampal neurogenesis through regulating miR-375/SFRP1-mediated WNT/β-catenin pathway in kainic acid-induced epilepsy.	Temporal lobe epilepsy (TLE) is a chronic disease of the nervous system, associated with increased proliferation in the hippocampus. Urothcarcinoma associated 1 (UCA1) is a long long non-coding RNA that was shown to regulate proliferation and differentiation of neural progenitors in vitro. We hypothesised that TLE-associated abnormal proliferation is a consequence of the downregulation of UCA1. This hypothesis was tested in mice with kainic acid (KA)-induced seizures, and then the potential mechanism was explored in vitro and in vivo. Result showed that the expression of UCA1 and Secreted Frizzled Related Protein 1 (SFRP1) were significantly reduced in hippocampal tissues of epileptic mice, while miR-375 was increased compared with the control group. Pearson correlation analysis showed that UCA1 was positively correlated with SFRP1, while miR-375 was negatively correlated with UCA1 and SFRP1. Besides, UCA1 was overexpressed in mice and the overexpression of UCA1 significantly reversed the abnormal proliferation of hippocampal neurons in epilepsy mice. In vitro Luciferase assay showed that UCA1 and Sfrp1 are both the targets of miR-375, and UCA1 promotes the expression of Sfrp1 by competitively adsorbing miR-375, thereby inhibiting the activation of the WNT/β-catenin pathway. The inactivation of the WNT/β-catenin pathway prevented the abnormal proliferation of neural progenitors in the epileptic hippocampus. In conclusion, our findings provide a theoretical basis for the clinical application of UCA1.	NA	Acta Biochim Pol. 2021 Apr 8;68(2):159-167. doi: 10.18388/abp.2020_5448.
4825	LncRNA	UCA1	miR-125a-A20	NF-kB	psoriasis cells	Psoriasis	Homo sapiens (human)	ELISA;	33554442	LncRNA UCA1 negatively regulates NF-kB activity in psoriatic keratinocytes through the miR125a-A20 axis.	Psoriasis is one of the most common chronic inflammatory skin diseases that affects approximately 3% of the world's population. Hyper proliferation, infiltration of inflammatory cells and aberrant differentiation of keratinocytes are the three most important characteristics of psoriasis. Previous reports showed that NF-κBis the crucial mediator linking psoriatic keratinocytes and immune cell states through its effects on chemokine and cytokine production. To identify the role of NF-κB in psoriasis, we conducted ELISA assay to detect the activity of NF-κB in lesional skin and nonlesional skin of patients with psoriasis. Mounting evidence suggests that the interaction between long noncoding RNAs (lncRNAs) and microRNAs plays important role in the regulation of the initiation and development of various diseases. In this article, we identified that lncRNA UCA1 was down-regulated in lesional skin of patients with psoriasis. Further studies showed that lncRNA UCA1 could promote the expression of A20 by inhibitingmiR125a, and up-regulated A20 decreased the activity of NF-κB through its ubiquitin editing function. Taken together, we identified and demonstrated that lncRNA UCA1 negatively regulated NF-κB activity in psoriasis through the miR125a-A20 axis.	NA	Kaohsiung J Med Sci. 2021 Mar;37(3):172-180. doi: 10.1002/kjm2.12363. Epub 2021 Feb 8.
4826	LncRNA	VPS9D1-AS1	miR-491-5p	SEC61A	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33627127	Long non-coding RNA VPS9D1-AS1 facilitates cell proliferation, migration and stemness in hepatocellular carcinoma.	BACKGROUND: Hepatocellular carcinoma (HCC) is a common cancer leading to high morbidity and mortality in worldwide. Previous studies revealed that SEC61 translocon alpha 1 subunit1 (SEC61A) can act as an oncogene in colon adenocarcinoma. However, the functions and molecular mechanism associated with HCC progression remain to be explored. This study aimed at exploring the role of SEC61A1 in HCC progression. METHODS: EdU assay and colony formation assay were applied to assess cell proliferation. The migratory ability of transfected HCC cells was evaluated by transwell migration assay. Sphere formation assay was used to detect the stemneess of HCC cells. Bioinformatics analysis tools and mechanism experiments were used to predict and analyze the potential molecular mechanism associated with the upregulation of SEC61A1 in HCC cells. RESULTS: Up-regulated SEC61A1 facilitated cell proliferation, migration and stemness in HCC cells. MiR-491-5p negatively regulated SEC61A1 and inhibited HCC cell proliferation and migration by targeting SEC61A1. VPS9D1 antisense RNA 1 (VPS9D1-AS1) could up-regulate SEC61A1 through sponging miR-491-5p. Early growth response 1 (EGR1) was identified as the upstream transcriptional activator for both SEC61A1 and VPS9D1-AS1. CONCLUSIONS: Our study unveiled a novel molecular pathway facilitating HCC cell proliferation, migration and stemness, which may shed new insight into HCC treatment.	NA	Cancer Cell Int. 2021 Feb 24;21(1):131. doi: 10.1186/s12935-020-01741-7.
4827	LncRNA	WT1-AS	miR-494-3p	PTEN	Non-Small Cell Lung Cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33603394	LncRNA WT1-AS/miR-494-3p Regulates Cell Proliferation, Apoptosis, Migration and Invasion via PTEN/PI3K/AKT Signaling Pathway in Non-Small Cell Lung Cancer.	BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the most common malignancies with the highest morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting NSCLC. However, the biological functions and regulatory mechanism of lncRNA WT1-AS in NSCLC progression still stay uninvestigated. METHODS: WT1-AS and miR-494-3p levels in NSCLC cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). In the current study, the regulatory effects of WT1-AS/miR-494-3p axis on cellular behaviors of NSCLC cell lines (A549 and NCI-H1975) were evaluated by a variety of methods. Cell counting kit-8 (CCK-8) and EDU assays were adopted to assess NSCLC cell proliferation. Tunnel staining and flow cytometry assay were applied to determine cell apoptosis and cell cycle distribution. Besides, cell migration and invasion abilities were analyzed by performing wound healing and transwell assays. Meanwhile, the levels of key proteins related to NSCLC cell apoptosis and PTEN/PI3K/AKT pathway were examined using Western blot assay. In addition, luciferase reporter assays were used to determine the interaction between WT1-AS and miR-494-3p or miR-494-3p and PTEN. RESULTS: Visibly downregulated WT1-AS in NSCLC cell lines was obtained from Broad Institute Cancer Cell Line Encyclopedia (CCLE) database and further verified by performing RT-qPCR. Besides, miR-494-3p was the downstream target gene of WT1-AS and obviously upregulated miR-494-3p in NSCLC cell lines was confirmed. WT1-AS overexpression suppressed cell proliferation, migration and invasion abilities while enhanced cell apoptosis of A549 and NCI-H1975 cells. Furthermore, upregulation of miR-494-3p distinctly reversed these inhibitory effects of WT1-AS overexpression on the tumorigenesis and progression of NSCLC. In addition, WT1-AS promoted PTEN expression and thereby inhibited activation of PI3K/AKT pathway by sponging miR-494-3p. CONCLUSION: To conclude, lncRNA WT1-AS impeded cell proliferation, migration, invasion but accelerated cell apoptosis via negatively regulating miR-494-3p to mediate PTEN/PI3K/AKT pathway in NSCLC.	NA	Onco Targets Ther. 2021 Feb 9;14:891-904. doi: 10.2147/OTT.S278233. eCollection 2021.
4828	LncRNA	WT1-AS	miR-494-3p	PI3K	Non-Small Cell Lung Cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33603394	LncRNA WT1-AS/miR-494-3p Regulates Cell Proliferation, Apoptosis, Migration and Invasion via PTEN/PI3K/AKT Signaling Pathway in Non-Small Cell Lung Cancer.	BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the most common malignancies with the highest morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting NSCLC. However, the biological functions and regulatory mechanism of lncRNA WT1-AS in NSCLC progression still stay uninvestigated. METHODS: WT1-AS and miR-494-3p levels in NSCLC cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). In the current study, the regulatory effects of WT1-AS/miR-494-3p axis on cellular behaviors of NSCLC cell lines (A549 and NCI-H1975) were evaluated by a variety of methods. Cell counting kit-8 (CCK-8) and EDU assays were adopted to assess NSCLC cell proliferation. Tunnel staining and flow cytometry assay were applied to determine cell apoptosis and cell cycle distribution. Besides, cell migration and invasion abilities were analyzed by performing wound healing and transwell assays. Meanwhile, the levels of key proteins related to NSCLC cell apoptosis and PTEN/PI3K/AKT pathway were examined using Western blot assay. In addition, luciferase reporter assays were used to determine the interaction between WT1-AS and miR-494-3p or miR-494-3p and PTEN. RESULTS: Visibly downregulated WT1-AS in NSCLC cell lines was obtained from Broad Institute Cancer Cell Line Encyclopedia (CCLE) database and further verified by performing RT-qPCR. Besides, miR-494-3p was the downstream target gene of WT1-AS and obviously upregulated miR-494-3p in NSCLC cell lines was confirmed. WT1-AS overexpression suppressed cell proliferation, migration and invasion abilities while enhanced cell apoptosis of A549 and NCI-H1975 cells. Furthermore, upregulation of miR-494-3p distinctly reversed these inhibitory effects of WT1-AS overexpression on the tumorigenesis and progression of NSCLC. In addition, WT1-AS promoted PTEN expression and thereby inhibited activation of PI3K/AKT pathway by sponging miR-494-3p. CONCLUSION: To conclude, lncRNA WT1-AS impeded cell proliferation, migration, invasion but accelerated cell apoptosis via negatively regulating miR-494-3p to mediate PTEN/PI3K/AKT pathway in NSCLC.	NA	Onco Targets Ther. 2021 Feb 9;14:891-904. doi: 10.2147/OTT.S278233. eCollection 2021.
4829	LncRNA	WT1-AS	miR-494-3p	AKT	Non-Small Cell Lung Cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33603394	LncRNA WT1-AS/miR-494-3p Regulates Cell Proliferation, Apoptosis, Migration and Invasion via PTEN/PI3K/AKT Signaling Pathway in Non-Small Cell Lung Cancer.	BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the most common malignancies with the highest morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting NSCLC. However, the biological functions and regulatory mechanism of lncRNA WT1-AS in NSCLC progression still stay uninvestigated. METHODS: WT1-AS and miR-494-3p levels in NSCLC cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). In the current study, the regulatory effects of WT1-AS/miR-494-3p axis on cellular behaviors of NSCLC cell lines (A549 and NCI-H1975) were evaluated by a variety of methods. Cell counting kit-8 (CCK-8) and EDU assays were adopted to assess NSCLC cell proliferation. Tunnel staining and flow cytometry assay were applied to determine cell apoptosis and cell cycle distribution. Besides, cell migration and invasion abilities were analyzed by performing wound healing and transwell assays. Meanwhile, the levels of key proteins related to NSCLC cell apoptosis and PTEN/PI3K/AKT pathway were examined using Western blot assay. In addition, luciferase reporter assays were used to determine the interaction between WT1-AS and miR-494-3p or miR-494-3p and PTEN. RESULTS: Visibly downregulated WT1-AS in NSCLC cell lines was obtained from Broad Institute Cancer Cell Line Encyclopedia (CCLE) database and further verified by performing RT-qPCR. Besides, miR-494-3p was the downstream target gene of WT1-AS and obviously upregulated miR-494-3p in NSCLC cell lines was confirmed. WT1-AS overexpression suppressed cell proliferation, migration and invasion abilities while enhanced cell apoptosis of A549 and NCI-H1975 cells. Furthermore, upregulation of miR-494-3p distinctly reversed these inhibitory effects of WT1-AS overexpression on the tumorigenesis and progression of NSCLC. In addition, WT1-AS promoted PTEN expression and thereby inhibited activation of PI3K/AKT pathway by sponging miR-494-3p. CONCLUSION: To conclude, lncRNA WT1-AS impeded cell proliferation, migration, invasion but accelerated cell apoptosis via negatively regulating miR-494-3p to mediate PTEN/PI3K/AKT pathway in NSCLC.	NA	Onco Targets Ther. 2021 Feb 9;14:891-904. doi: 10.2147/OTT.S278233. eCollection 2021.
4830	LncRNA	XIST	miR-873-5p	MCL1	H9c2 cells	Cardiomyocyte Apoptosis	Homo sapiens (human)	qRT-PCR;Western blot;	33378038	Long noncoding RNA XIST regulates cardiomyocyte apoptosis by targeting miR-873-5p/MCL1 axis.	OBJECTIVE: The purpose of this study was to investigate the expression of miR-873-5p and long non-coding RNA X-inactive specific transcript (lncRNA-XIST) in myocardial infarction (MI), the interaction mechanism and the effect of target gene MCL1 on apoptosis in H9c2 cells. MATERIALS AND METHODS: quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect and compare the expressions of miR-873-5p and lncRNA XIST in 8 myocardial infarction rats and 8 normal rats tissues, respectively, and the correlation between the expressions of miR-873-5p and lncRNA XIST in the myocardial tissues was explored. Next, qRT-PCR and Western blot were used to detect the effects of upregulation of miR-873-5p and downregulation of lncRNA XIST, as well as the impacts of their interactions on the expression level of MCL1 in H9c2 cells and the apoptosis of cells. RESULTS: It was found that the downregulation of miR-873-5p protected the heart against apoptosis after AMI, and lncRNA XIST inhibited apoptosis in H9c2 cells after hypoxia. Besides, inhibiting lncRNA XIST could upregulate miR-873-5p and downregulate MCL1, thus increasing apoptosis in the H9c2 cells after hypoxia. CONCLUSIONS: LncRNA XIST can regulate cardiomyocyte apoptosis by targeting miR-873-5p.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12878-12886. doi: 10.26355/eurrev_202012_24191.
4831	LncRNA	XIST	miR-125b-2-3p	Wee1	CRC cells	Colorectal Cancer	Homo sapiens (human)	RT-PCR;Western blot;Luciferase reporter assay;	33666372	The lncRNA XIST/miR-125b-2-3p axis modulates cell proliferation and chemotherapeutic sensitivity via targeting Wee1 in colorectal cancer.	BACKGROUND: Numerous reports on microRNAs have illustrated their role in tumor growth and metastasis. Recently, a new prognostic factor, miR-125b-2-3p, has been identified for predicting chemotherapeutic sensitivity in advanced colorectal cancer (CRC). However, the specific mechanisms and biological functions of miR-125b-2-3p in advanced CRC under chemotherapy have yet to be elucidated. METHODS: MiR-125b-2-3p expression was detected by real-time PCR (RT-PCR) in CRC tissues. The effects of miR-125b-2-3p on the growth, metastasis, and drug sensitivity of CRC cells were tested in vitro and in vivo. Based on multiple databases, the upstream competitive endogenous RNAs (ceRNAs) and the downstream genes for miR-125b-2-3p were predicted by bioinformatic analysis, followed by the experiments including luciferase reporter assays, western blot assays, and so on. RESULTS: MiR-125b-2-3p was significantly lowly expressed in the tissues and cell lines of CRC. Higher expression of miR-125b-2-3p was associated with relatively lower proliferation rates and fewer metastases. Moreover, overexpressed miR-125b-2-3p remarkably improved chemotherapeutic sensitivity of CRC in vivo and in vitro. Mechanistically, miR-125b-2-3p was absorbed by long noncoding RNA (lncRNA) XIST regulating WEE1 G2 checkpoint kinase (WEE1) expression. The upregulation of miR-125b-2-3p inhibited the proliferation and epithelial-mesenchymal transition (EMT) of CRC induced by lncRNA XIST. CONCLUSIONS: Lower miR-125b-2-3p expression resulted in lower sensitivity of CRC to chemotherapy and was correlated with poorer survival of CRC patients. LncRNA XIST promoted CRC metastasis acting as a ceRNA for miR-125b-2-3p to mediate WEE1 expression. LncRNA XIST-miR-125b-2-3p-WEE1 axis not only regulated CRC growth and metastasis but also contributed to chemotherapeutic resistance to CRC.	NA	Cancer Med. 2021 Apr;10(7):2423-2441. doi: 10.1002/cam4.3777. Epub 2021 Mar 5.
4832	LncRNA	XIST	miR-30	AVEN	viable cells of podocyte under HG treatment	Diabetic Nephropathy	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33332155	LncRNA XIST protects podocyte from high glucose-induced cell injury in diabetic nephropathy by sponging miR-30 and regulating AVEN expression.	Diabetic nephropathy (DN) is one of the most important complications of diabetes mellitus. Thus, it is urgent to develop a novel diagnosis or therapeutic strategy that could suspend DN progression. Moreover, there is increasing evidence demonstrating that long non-coding RNA (lncRNA) acts as critical players in regulating autophagy and are involved in DN. We demonstrated that lncRNA X-inactive specific transcript (XIST) was downregulated in high glucose (HG) treated podocytes, accompanied by increased apoptosis of podocytes. Overexpression of XIST significantly reduced the apoptosis and promoted the number of viable cells of podocyte under HG treatment. Prediction by Targets can and dual-luciferase reporter assay revealed the interaction between miR-30 and XIST and AVEN. Further WB (Western Blot), MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), and flow cytometry confirmed that XIST could reverse the expression of AVEN and ameliorate HG-induced apoptosis. In conclusion, our research revealed that XIST plays a protective effect on podocyte injury induced by HG through miR-30/AVEN axis.	NA	Arch Physiol Biochem. 2020 Dec 17:1-8. doi: 10.1080/13813455.2020.1854307.
4833	LncRNA	XIST	miR-448	ROCK1	glioblastoma cells	Glioblastoma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33325210	LncRNA XIST regulates cell proliferation, migration and invasion of glioblastoma via regulating miR-448 and ROCK1.	Long non-coding ribonucleic acids (lncRNAs) have been recognized as markers in several cancers and play important roles in glioblastoma (GBM). But the role of lncRNA X inactive-specific transcript (XIST) in GBM and its possible mechanisms are rarely studied in depth. This study was conducted to explore the detailed roles of XIST in cell proliferation, migration, and invasion of GBM. Expressions of XIST, miR-448, and ρ associated coiled coil containing protein kinase 1 (ROCK1) were detected by qRT-PCR or Western blot in A172 and U251 cells. The interactions among XIST, miR-448 and ROCK1 were verified through luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell Counting Kit-8 (CCK-8) assay and Transwell assay were introduced to detect how XIST knockdown, miR-448 overexpression, or along with ROCK1 overexpression affect cellular malignancy of GBM cells. XIST and ROCK1 were up-regulated while miR-448 expression was decreased in GBM cells. XIST knockdown or miR-448 overexpression could dramatically inhibit GBM cell proliferation, migration, and invasion. Moreover, XIST negatively regulated miR-448 expression through the function as competing endogenous RNA (ceRNA), thus leading to the up-regulation of ROCK1, one miR-448 target gene. Moreover, ROCK1 overexpression could reverse the suppression of XIST knockdown or miR-448 upregulation on cellular malignancy. In brief, the effects of XIST may promote cellular malignancy of GBM through miR-448/ROCK1 axis, which will provide new understanding of GBM pathogenesis and progression.	NA	J Biol Regul Homeost Agents. 2020 Nov-Dec;34(6):2049-2058. doi: 10.23812/20-558-L.
4834	LncRNA	XIST	miR-30b	RECK	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Homo sapiens (human)	qPCR;Western blot;	33664820	lncRNA XIST regulates cell proliferation, migration and invasion via regulating miR-30b and RECK in nasopharyngeal carcinoma.	Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) plays an essential role in the development and progress of nasopharyngeal carcinoma (NPC). MicroRNA-30b (miR-30b) has been confirmed to play an inhibitory role in various types of cancer. The molecular mechanisms underlying the lncRNA XIST-mediated regulation of the metastasis of NPC cells by miR-30b is not clear. qPCR and western blot analysis were used to detect the expression of XIST, miR-30b, and reversion inducing cysteine rich protein with kazal motifs (RECK) in NPC tissues and cell lines. The detection of luciferase reporter gene confirmed the relationship between lncRNA XIST, miR-30b and RECK. CCK-8 and Transwell assays were performed in order to detect the proliferation, migration and invasion of the NPC cells. The results of qPCR and western blotting indicated that the expression levels of lncRNA XIST and RECK were higher in the NPC tissues and cell lines than that of the control group, while the expression of miR-30b was lower. Knockdown of lncRNA XIST significantly inhibited cell proliferation, migration and invasion in the NPC cell lines. In addition, lncRNA XIST was found to negatively regulate the expression of miR-30b, resulting in the upregulation of RECK. Overexpression of RECK was found to reverse the inhibitory effect of lncRNA XIST knockdown or miR-30b on NPC cell metastasis. Our results showed that cell migration and invasion were inhibited by knockdown of lncRNA XIST, suggesting that the lncRNA XIST/miR-30b/RECK axis is involved in the development of NPC.	NA	Oncol Lett. 2021 Apr;21(4):256. doi: 10.3892/ol.2021.12513. Epub 2021 Feb 4.
4835	LncRNA	XIST	miR-326	HNRNPA1	Multiple sclerosis tissues	Multiple Sclerosis	Homo sapiens (human)	qRT-PCR	33507382	Identification of hub lncRNA ceRNAs in multiple sclerosis based on ceRNA mechanisms.	Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, and the pathogenesis is influenced by genetic susceptibility. Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) play essential roles in complex diseases, including acting as competing endogenous RNAs (ceRNAs). However, the functional roles and regulatory mechanisms of lncRNAs acting as ceRNAs in MS are still unclear. In this study, we identified hub lncRNA ceRNAs in MS based on ceRNA mechanisms and annotated their functions. The lncRNA-associated ceRNA network (LACN) was constructed by integrating the expression profiles of lncRNA/mRNA and miRNA in MS and normal samples, and the experimentally validated interactions of lncRNA-miRNA and mRNA-miRNA. We found three hub lncRNA ceRNAs (XIST, OIP5-AS1, and CTB-89H12.4) using the network analysis and obtained 96 lncRNA-mediated competing triplets (LCTs, lncRNA-miRNA-mRNA) with the hub lncRNA ceRNAs, which constituted 3 hub ceRNA modules. The functional analysis identified 12 pathways enriched by the 3 hub lncRNA ceRNAs, of which 6 were confirmed to be related to MS. For example, XIST was enriched in the 'spliceosome' and 'RNA transport' related to the typing of MS, and CTB-89H12.4 was enriched in the 'mTOR signaling pathway,' a potential therapeutic target for MS. We dissected the expression patterns of the 96 LCTs in MS individually. LCT XIST-miR-326-HNRNPA1, for which the expression pattern in MS revealed that XIST and HNRNPA1 were up-regulated and miR-326 was down-regulated, consisted of risk RNAs for MS that were validated by other research. Therefore, XIST-miR-326-HNRNPA1 might play a central role in the pathogenesis of MS. These results will contribute to the discovery of novel biomarkers and the development of new therapeutic methods for MS.	NA	Mol Genet Genomics. 2021 Mar;296(2):423-435. doi: 10.1007/s00438-020-01750-1. Epub 2021 Jan 28.
4836	LncRNA	XIST	miR-106a	NA	Ovarian cancer tissues and cells	Ovarian Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;RNA pull-down assay;Flow Cytometry assay;RNA pull-down;	33400246	Upregulation of long noncoding RNA XIST has anticancer effects on ovarian cancer through sponging miR-106a.	Ovarian cancer (OC) is a highly malignant tumor. X inactive specific transcript (XIST) was identified as a cancer-related gene, while its therapeutic effect in OC was poorly defined. The present study was designed to investigate the effectual corollary of the lncRNA XIST in OC. RT-qPCR was used to detect the XIST and miR-106a expression levels of OC tissues and cell lines. OC cell apoptosis and proliferation were detected by flow cytometry, colony formation, and CCK-8 assays. Moreover, bioinformatics analysis was used to predict the targeted miRNA of XIST. The dual-luciferase reporter and RNA pull-down assays were then used to verify the interaction between miR-106a and XIST. OC xenograft nude mice were raised to measure tumor growth. Notably, OC tissues and cells exhibited low XIST levels and high miR-106a levels. The XIST upregulation decreased the OVCAR3 and CAOV3 cell proliferation and inversely promoted cell apoptosis. miR-106a targeted the XIST. Also, the miR-106a overexpression reversed the inhibitory effects of XIST on OC cell proliferation and apoptosis. Our in vivo results suggested that XIST was involved in tumor growth deceleration, while the miR-106a reversed the effect. To conclusion, the present study demonstrated that XIST suppressed OC development via sponging miR-106a both in vitro and in vivo.	NA	Hum Cell. 2021 Mar;34(2):579-587. doi: 10.1007/s13577-020-00469-w. Epub 2021 Jan 5.
4837	LncRNA	XIST	miR-23a-3p	GINS2	A375 cells	Melanoma	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	33389496	GINS2 was regulated by lncRNA XIST/miR-23a-3p to mediate proliferation and apoptosis in A375 cells.	Melanoma ranks second in aggressive tumors, and the occurrence of metastasis in melanoma results in a persistent drop in the survival rate of patients. Therefore, it is very necessary to find a novel therapeutic method for treating melanoma. It has been reported that lncRNA XIST could promote the tumorigenesis of melanoma. However, the mechanism by which lncRNA XIST regulates the progression of melanoma remains unclear. The proliferation of A375 cells was measured by clonal formation. Cell viability was detected by MTT assay. Flow cytometry was performed to detect cell apoptosis and cycle. The level of GINS2, miR-23a-3p, and lncRNA XIST was investigated by qRT-PCR. Protein level was detected by Western blot, and the correctness of prediction results was confirmed by Dual luciferase. In present study, GINS2 and lncRNA XIST were overexpressed in melanoma, while miR-23a-3p was downregulated. Silencing of GINS2 or overexpression of miR-23a-3p reversed cell growth and promoted apoptosis in A375 cells. Mechanically, miR-23a-3p directly targeted GINS2, and XIST regulated GINS2 level though mediated miR-23a-3p. Moreover, XIST exerted its function on cell proliferation, cell viability, and promoted the cell apoptosis of A375 cells though miR-23a-3p/GINS2 axis. LncRNA XIST significantly promoted the tumorigenesis of melanoma via sponging miR-23a-3p and indirectly targeting GINS2, which can be a potential new target for treating melanoma.	NA	Mol Cell Biochem. 2021 Mar;476(3):1455-1465. doi: 10.1007/s11010-020-04007-y. Epub 2021 Jan 3.
4838	LncRNA	ZEB2-AS1	miR-107	SALL4	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;Luciferase reporter assay;	33841645	Long non-coding RNA ZEB2-AS1 regulates osteosarcoma progression by acting as a molecular sponge of miR-107 to modulate SALL4 expression.	Increasing evidence has confirmed long non-coding RNAs (lncRNAs) as important regulators involved in several pathophysiological processes in many diseases. The aim of this study was to investigate the roles of lncRNA ZEB2-AS1 (ZEB2-AS1) in osteosarcoma (OS). The levels of ZEB2-AS1 in OS tissues and cells were detected using RT-PCR. The clinical significance of ZEB2-AS1 expressions in OS patients was statistically analyzed. The functional effects of ZEB2-AS1 on the proliferation, apoptosis, invasion, and metastasis of OS cells was determined by a series of cellular experiments. Bioinformatic analysis, dual-luciferase reporter assays and pull-down assays were carried out for the confirmation of the molecular binding. We found that ZEB2-AS1 expression was distinctly upregulated in OS specimens and cell lines. Higher levels of ZEB2-AS1 in OS patients were associated with clinical stage, distant metastasis and unfavorable survivals. A multivariate Cox model revealed that ZEB2-AS1 expression was an independent prognostic factor for OS patients. Cellular experiments revealed that knockdown of ZEB2-AS1 inhibited proliferation and metastasis, and induced apoptosis in vitro. Mechanistic investigation revealed that ZEB2-AS1 acted as a sponge for miR-107 and blocked the inhibition of spalt like transcription factor 4 (SALL4) via miR-107 in OS cells. Rescue experiments suggested that up-regulation of ZEB2-AS1 could partly attenuate the miR-107 mediated inhibition of SALL4 expression in OS cells. To sum up, our data revealed that ZEB2-AS1 played an oncogenic role in OS progression, and could serve as a novel molecular target for treating this tumor.	NA	Am J Transl Res. 2021 Mar 15;13(3):1140-1154. eCollection 2021.
4839	LncRNA	ZFAS1	miR-7-5p	ENO2	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR;	33342344	IncRNA ZFAS1 contributes to the radioresistance of nasopharyngeal carcinoma cells by sponging hsa-miR-7-5p to upregulate ENO2.	Previous research revealed that lncRNA ZFAS1 could promote nasopharyngeal carcinoma (NPC) by inhibiting its downstream target axis. However, the association between ZFAS1 and radioresistant NPC cells is unclear. This study aimed to explore the roles of ZFAS1 in the radioresistance of NPC. Bioinformatics analysis was conducted to identify the significant factors (ENO2 and miR-7-5p) that contributed to the radioresistance of NPC cells. After performing qRT-PCR analysis, we found that the expression of ZFAS1 and ENO2 was upregulated in NPC cells but that the miR-7-5p expression was downregulated in the same samples. Apart from that, we noticed that ZFAS1 inhibition enhanced the sensitivity of NPC cells to radiation therapy by repressing cell proliferation and promoting cell apoptosis. Subsequently, we found that ZFAS1 could sponge miR-7-5p to upregulate ENO2, which was the target of miR-7-5p. Experimental results also indicated that the suppression of miR-7-5p inhibited the sensitivity of NPC cells to radiation therapy, thereby suppressing ENO2 expression. Overall, our findings suggested that ZFAS1 contributed to the radioresistance of NPC cells by regulating the miR-7-5p/ENO2 axis and that ZFAS1 might be a potential therapeutic target for addressing the radioresistance of NPC cells.	NA	Cell Cycle. 2021 Jan;20(1):126-141. doi: 10.1080/15384101.2020.1864128. Epub 2020 Dec 20.
4840	LncRNA	ZFAS1	miR-302d-3p	SMAD2	chondrocyte	Osteoarthritis	Homo sapiens (human)	qRT-PCR	33686420	Long noncoding RNA ZFAS1 suppresses chondrocytes apoptosis via miR-302d-3p/SMAD2 in osteoarthritis.	Osteoarthritis (OA) seriously affects people's quality of life due to joint pain, stiffness, disability, and dyskinesia worldwide. Long noncoding RNA zinc finger antisense 1 (ZFAS1) is downregulated and tightly associated with proliferation, migration, apoptosis, and matrix synthesis of chondrocyte in OA. However, the molecular mechanisms of ZFAS1 in OA remain unknown. The expression correlation between ZFAS1, miR-302d-3p, and SMAD2 in OA tissues was analyzed by Pearson correlation analysis. ZFAS1 was a lower expression, and expedited proliferation and repressed apoptosis of chondrocytes. MiR-302d-3p was a direct target of ZFAS1. MiR-302d-3p hindered proliferation and facilitated apoptosis of chondrocytes. MiR-302d-3p partially reversed the effect of ZFAS1 on proliferation and apoptosis of chondrocytes. SMAD2 was positively regulated by the ZFAS1/miR-302d-3p. MiR-302d-3p-mediated proliferation and apoptosis were partly abrogated by targeting SMAD2. ZFAS1 promoted chondrocytes proliferation and repressed apoptosis possibly by regulating miR-302d-3p/SMAD2 axis, providing a potential target for OA treatment.	NA	Biosci Biotechnol Biochem. 2021 Mar 24;85(4):842-850. doi: 10.1093/bbb/zbab008.
4841	LncRNA	ZFAS1	miR-150-5p	Notch3	atherosclerosis model of mice	Atherosclerosis	Homo sapiens (human)	RT-PCR;Western blot;Luciferase reporter assay;	33278458	lncRNA ZFAS1 promotes ox-LDL induced EndMT through miR-150-5p/Notch3 signaling axis.	EndMT is an active contributor to atherosclerosis pathology, and lncRNAs is widely involved in the occurrence and development of atherosclerosis. The purpose of this study was to investigate the regulatory mechanisms of ZFAS1 in EndMT of atherosclerosis. Here, the ApoE(-/-) mice were feed with high-fat diet to establish the atherosclerosis model, and HUVECs was stimulated with ox-LDL to induce EndMT. RT-PCR and western blot were used to detect the mRNA and protein expression, respectively. The expression of EndMT markers were detected by immune-fluorescence. The relationships among ZFAS1, miR-150-5p and Notch3 were evaluated by luciferase reporter assay. The role of ZFAS1 in EndMT and its dependence on miR-150-5p/Notch3 axis was further detected by knocking down or over-expressing ZFAS1. We found that ZFAS1 and Notch3 were upregulated while miR-150-5p was downregulated in atherosclerosis mice and ox-LDL-treated HUVECs. The expression of CD31 and vWF were significant decreased, while the α-SMA and vimentin were significant increased in ox-LDL-treated HUVECs, and overexpression of ZFAS1 enhanced the effect of ox-LDL on HUVECs. Further, ZFAS1 functions as a ceRNA to increase Notch3 expression through sponging miR-150-5p, and miR-150-5p mimic or si-Notch3 could reverse LV-ZFAS1-mediated EndMT. In summary, lncRNA ZFAS1 promotes ox-LDL induced HUVECs EndMT through regulating miR-150-5p/Notch3 axis.	NA	Microvasc Res. 2021 Mar;134:104118. doi: 10.1016/j.mvr.2020.104118. Epub 2020 Dec 2.
4842	LncRNA	ZFPM2-AS1	miR-650	NOTCH1	malignant melanoma cells	Melanoma	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	33406278	ZFPM2-AS1 facilitates cell proliferation and migration in cutaneous malignant melanoma through modulating miR-650/NOTCH1 signaling.	Aberrant expression of long non-coding RNA (lncRNA) zinc finger protein, FOG family member 2 antisense RNA 1 (ZFPM2-AS1) has been identified in many tumors, but its role in cutaneous malignant melanoma remains largely obscure. Our present study was intended to unveil the role and potential mechanism of ZFPM2-AS1 in cutaneous malignant melanoma. RT-qPCR was utilized to analyze ZFPM2-AS1 expression in cutaneous malignant melanoma cells. Cell counting kit-8 (CCK-8), colony formation, flow cytometry, and transwell analyses were utilized to assess ZFPM2-AS1 function on cell proliferation, apoptosis, and migration. Luciferase reporter, RNA immunoprecipitation, and RNA-pull down assays were applied to probe the regulatory mechanism of ZFPM2-AS1 in cutaneous malignant melanoma cells. Up-regulation of ZFPM2-AS1 was discovered in cutaneous malignant melanoma cells. ZFPM2-AS1 deletion restrained cell proliferation, migration, and elevated cell apoptosis in cutaneous malignant melanoma. ZFPM2-AS1 regulated notch receptor 1 (NOTCH1) to activate the NOTCH pathway. ZFPM2-AS1 acted as a competing endogenous RNA (ceRNA) to affect NOTCH1 expression via sponging miR-650. Collectively, ZFPM2-AS1 exerted an oncogenic role in cutaneous malignant melanoma progression via targeting miR-650/NOTCH1 signaling. Our study might offer a novel sight for cutaneous malignant melanoma treatment.	NA	Dermatol Ther. 2021 Mar;34(2):e14751. doi: 10.1111/dth.14751. Epub 2021 Jan 23.
4843	Circular RNA	ZFR	miR-1270	WNT5A	Bladder Cancer cells	Bladder Cancer	Homo sapiens (human)	qRT-PCR;luciferase assay;	33928018	Circ-ZFR Promotes Progression of Bladder Cancer by Upregulating WNT5A Via Sponging miR-545 and miR-1270.	BACKGROUND: Bladder cancer is one of the most common cancers all over the world. CircZFR is a circular RNA and has been implicated in tumor generation and invasion. However, the exact role of circZFR in the development of bladder cancer (BCa) remains unknown. This study aimed to investigate the function of circZFR in BCa, and further to probe into the association between circ-ZFR, miR-545/miR-1270 and WNT5A. METHODS: The expression of circZFR in BCa was quantified by qRT-PCR and was positively correlated with the prognosis of BCa patients. Next, the stable knockdown of circZFR BCa cell lines was established and the resulting capacities of proliferation, migration and invasion were measured. The association of circZFR with miR-1270/miR-545 was predicted by circinteractome prediction, and was confirmed by luciferase assay as well as RNA pull down assay. Furthermore, miRNA inhibitors, WNT5A overexpression and Pearson correlation analysis were used to examine the relationship between circZFR, miR-1270/miR-545 and WNT5A. RESULTS: The expression of CircZFR was up-regulated both in BCa tissues and in BCa cell lines, and was positively correlated with patient survival rates. Blocking of circZFR's expression by RNA inhibitors suppressed the proliferation, migration and invasion of BCa cells both in vitro and in vivo. On the other hand, overexpression of target miRNA supported that circZFR directly interact with miR-545 and miR-1270. Moreover, we demonstrated that circZFR promotes the progression of BCa by upregulating WNT5A's expression via sponging miR-545 and miR-1270. CONCLUSIONS: CircZFR promotes the proliferation, migration and invasion of BCa cells by upregulating WNT5A signaling pathway via sponging miR-545 and miR-1270. These results provide new insights into the molecular mechanism of circZFR in BCa progression, and more important, a novel target for BCa clinical treatment.	NA	Front Oncol. 2021 Apr 13;10:596623. doi: 10.3389/fonc.2020.596623. eCollection 2020.
4844	LncRNA	ZNF667-AS1	miR-206	AKAP13	bone tissues	Acute Myeloid Leukemia	Homo sapiens (human)	FISH;microarray;FISH;	33380835	Long Non-Coding RNA ZNF667-AS1 Knockdown Curbs Liver Metastasis in Acute Myeloid Leukemia by Regulating the microRNA-206/AKAP13 Axis.	BACKGROUND: Zinc finger protein 667-antisense RNA 1 (ZNF667-AS1), a long non-coding RNA (lncRNA), plays important parts in tumorigenesis and development of esophageal squamous cell carcinoma, but its function in acute myeloid leukemia (AML) is unknown. Our goal here was to probe the functional mechanism of ZNF667-AS1 in AML by mediating microRNA-206 (miR-206)/A-kinase anchoring protein 13 (AKAP13) axis. MATERIALS AND METHODS: The bone marrow samples from AML patients and controls were selected for microarray analysis to select significantly upregulated lncRNAs. Next, effects of ZNF667-AS1 on cell aggressiveness of AML were assessed after delivery of cells with siRNA against ZNF667-AS1. Subcellular fractionation location assay and FISH experiments were used to determine ZNF667-AS1 localization in cells. Dual-luciferase experiments detect the targeting relationships among ZNF667-AS1, miR-206 and AKAP13. Finally, tumor growth and metastasis were evaluated in vivo to determine the relevance of ZNF667-AS1/miR-206/AKAP13 axis. RESULTS: The expression of ZNF667-AS1 was upregulated in AML patients, which predicted poor prognosis. Downregulation of ZNF667-AS1 reduced cell proliferation, invasion, tumorigenesis and metastasis. miR-206 inhibitor reversed the repressive role of ZNF667-AS1 knockdown in cell proliferation, invasion and tumorigenesis, while AKAP13 silencing flattened the stimulative role of miR-206 inhibitor in AML malignant aggressiveness. Mechanistically, we demonstrated that ZNF667-AS1 functioned as a molecular sponge for miR-206. In addition, we observed that Wnt/β-catenin pathway was suppressed by ZNF667-AS1 knockdown. CONCLUSION: ZNF667-AS1 potentiated AML progression by targeting the miR-206/AKAP13 axis. This indicates ZNF667-AS 1 inhibition may act as a prospective therapeutic option for the treatment of AML.	NA	Cancer Manag Res. 2020 Dec 23;12:13285-13300. doi: 10.2147/CMAR.S269258. eCollection 2020.
4845	LncRNA	AFAP1-AS1	miR-545-3p	HDGF	lung cancer tissues and cells	Lung Cancer	Homo sapiens (human)	Western blot;Flow Cytometry assay;Luciferase reporter assay;	33290312	The knockdown of LncRNA AFAP1-AS1 suppressed cell proliferation, migration, and invasion, and promoted apoptosis by regulating miR-545-3p/hepatoma-derived growth factor axis in lung cancer.	Lung cancer is one of the most common human cancers. Long noncoding RNA AFAP1-AS1 (LncRNA AFAP1-AS1) and microRNA-545-3p (miR-545-3p) were reported to play important roles in lung cancer development. This study aimed to elucidate the functional mechanisms of AFAP1-AS1 and miR-545-3p in lung cancer. Quantitative real time polymerase chain reaction was carried out to determine the levels of AFAP1-AS1, miR-545-3p and hepatoma-derived growth factor (HDGF). Cell proliferation, apoptosis, migration and invasion were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry, and transwell migration and invasion assays, respectively. Furthermore, the interaction between miR-545-3p and AFAP1-AS1 or HDGF was predicted by bioinformatics analysis software starbase and confirmed by the dual luciferase reporter assay. Western blot assay was used to detect the protein level of HDGF. Besides, murine xenograft model was conducted through injecting A549 cells transfected with sh-AFAP1-AS1. The expression levels of AFAP1-AS1 and HDGF were increased, while miR-545-3p was decreased in lung cancer tissues and cells. AFAP1-AS1 knockdown suppressed lung cancer cell proliferation, migration, and invasion and induced apoptosis. Furthermore, AFAP1-AS1 mediated cell progression through regulating miR-545-3p expression. In addition, miR-545-3p negatively regulated the expression level of HDGF via binding 3'-untranslated region of HDGF. As expected, AFAP1-AS1 knockdown inhibited lung cancer progression via affecting miR-545-3p/HDGF axis. Besides, AFAP1-AS1 knockdown suppressed lung cancer tumor growth in vivo. Collectively, our results suggested that AFAP1-AS1 promoted the development of lung cancer via regulating miR-545-3p/HDGF axis, providing a potential target for the treatment of lung cancer.	NA	Anticancer Drugs. 2021 Jan 1;32(1):11-21. doi: 10.1097/CAD.0000000000001003.
4846	Circular RNA	CCS	miR-383	E2F7	lung cancer cells	Lung Cancer	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Immunohistochemistry;RNA immunoprecipitation;	33359669	Circ-CCS is identified as a cancer-promoting circRNA in lung cancer partly by regulating the miR-383/E2F7 axis.	BACKGROUND: Increasing biomolecules have been found to be involved in the lung cancer development. This study will perform the function and mechanism analyses of a novel circular RNA copper chaperone for superoxide dismutase (circ-CCS) in lung cancer. METHODS: Circ-CCS, microRNA-383 (miR-383) and E2F transcription factor 7 (E2F7) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was detected using Cell Counting Kit-8 (CCK-8). Clonal ability was measured by colony formation assay. Cell apoptosis was determined via flow cytometry. Cell migration and invasion were assessed by transwell assay. Detection of protein was completed using western blot. Xenograft assay was used for the functional analysis of circ-CCS in vivo. The binding between targets was proved by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. E2F7 protein level was also examined by Immunohistochemistry (IHC) analysis in human tissues. RESULTS: Circ-CCS was upregulated in lung cancer and could predict poor prognosis. Downregulation of circ-CCS inhibited lung cancer cell growth and metastasis while promoted apoptosis in vitro, and suppressed tumorigenesis of lung cancer in vivo. Circ-CCS had sponge effect on miR-383 and the function of si-circ-CCS was achieved by upregulating miR-383. E2F7 was a target gene of miR-383 and its downregulation was responsible for the anti-cancerous role of miR-383 in lung cancer. Circ-CCS could elevate E2F7 expression via interacting with miR-383. CONCLUSION: Circ-CCS was shown to facilitate lung cancer progression via the miR-383/E2F7 axis, exhibiting the pivotal value of circ-CCS in diagnosis and treatment of lung cancer.	NA	Life Sci. 2021 Feb 15;267:118955. doi: 10.1016/j.lfs.2020.118955. Epub 2020 Dec 24.
4847	LncRNA	CDKN2B-AS1	miR-143-3p	CDKN2B	smooth muscle cells	In-Stent Restenosis	Homo sapiens (human)	Luciferase reporter assay;	33603842	Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense ribonucleic acid 1 is associated with in-stent restenosis and promotes human carotid artery smooth muscle cell proliferation and migration by sponging miR-143-3p.	Carotid angioplasty and stenting (CAS) is an efficient therapeutic approach for carotid stenosis. However, in-stent restenosis (ISR) frequently occurs and seriously affects the therapeutic efficacy of CAS. Certain non-coding (nc)RNAs serve potential roles in ISR development and progression. Thus, the goals of the present study were to investigate novel biomarkers for ISR development and to further uncover the mechanisms underlying the progression of ISR. The expression of long ncRNA cyclin-dependent kinase inhibitor (CDKN)2B-antisense 1 (AS1) and microRNA (miR)-143-3p in patients with ISR and human carotid artery smooth muscle cells (hHCtASMCs) was analyzed using reverse transcription-quantitative PCR. A luciferase reporter assay was performed to examine the interaction between CDKN2B-AS1 and miR-143-3p. The effects of the CDKN2B/miR-143-3p axis on hHCtASMC proliferation and migration were assessed using Cell Counting Kit-8 and Transwell assays. The results indicated that serum CDKN2B-AS1 was increased and miR-143-3p was decreased in patients with ISR as compared with that in patients with no ISR (all P<0.001). CDKN2B-AS1 and miR-143-3p were identified as risk factors for ISR onset (all P<0.05) and knockdown of CDKN2B-AS1 in hHCtASMCs led to inhibited cell proliferation and migration. Furthermore, the luciferase reporter assay and expression analysis indicated that miR-143-3p is a target of CDKN2B-AS1 and may mediate the effects of CDKN2B-AS1 on hHCtASMC proliferation and migration. In conclusion, dysregulation of CDKN2B-AS1 and miR-143-3p may represent risk factors for the occurrence of ISR. The in vitro results suggested that the CDKN2B-AS1/miR-143-3p axis may regulate the proliferation and migration of hHCtASMCs, indicating its potential to be developed as a target for preventative measures and therapies for ISR.	NA	Exp Ther Med. 2021 Mar;21(3):234. doi: 10.3892/etm.2021.9665. Epub 2021 Jan 21.
4848	LncRNA	CDKN2B-AS1	miR-15b-5p	WNT2B	human mesangial cells	Diabetic Nephropathy	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33298110	Long non-coding RNA CDKN2B-AS1 regulates high glucose-induced human mesangial cell injury via regulating the miR-15b-5p/WNT2B axis.	BACKGROUND: Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) has been reported to be related to diabetic nephropathy (DN) progression. However, the regulatory mechanisms of CDKN2B-AS1 in DN are unclear. METHODS: High glucose (HG) was used to induce human mesangial cells (HMCs) for establishing the DN model. Expression levels of CDKN2B-AS1, microRNA (miR)-15b-5p, wingless-Type family member 2B (WNT2B) mRNA in serum and HMCs were detected through quantitative real-time polymerase chain reaction (qRT-PCR). The viability and cell cycle progression of HMCs were determined with Cell Counting Kit-8 (CCK-8) or flow cytometry assays. The levels of several proteins and inflammatory factors in HMCs were analyzed by western blotting or enzyme-linked immunosorbent assay (ELISA). The relationship between CDKN2B-AS1 or WNT2B and miR-15b-5p was verified with dual-luciferase reporter assay. RESULTS: CDKN2B-AS1 and WNT2B were upregulated while miR-15b-5p was downregulated in serum of DN patients and HG-treated HMCs. CDKN2B-AS1 inhibition reduced HG-induced viability, cell cycle progression, ECM accumulation, and inflammation response in HMCs. CDKN2B-AS1 regulated WNT2B expression via competitively binding to miR-15b-5p. MiR-15b-5p inhibitor reversed CDKN2B-AS1 knockdown-mediated influence on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs. The repressive effect of miR-15b-5p mimic on viability, cell cycle progression, ECM accumulation, and inflammation response of HG-treated HMCs was abolished by WNT2B overexpression. CONCLUSION: CDKN2B-AS1 regulated HG-induced HMC viability, cell cycle progression, ECM accumulation, and inflammation response via regulating the miR-15b-5p/WNT2B axis, provided a new mechanism for understanding the development of DN.	NA	Diabetol Metab Syndr. 2020 Dec 9;12(1):109. doi: 10.1186/s13098-020-00618-z.
4849	Circular RNA	Circ_0020095	miR-487a-3p	SOX9	Colon cancer tissues and cells	Colon Cancer	Homo sapiens (human)	qRT-PCR	33520987	Hsa_circ_0020095 Promotes Oncogenesis and Cisplatin Resistance in Colon Cancer by Sponging miR-487a-3p and Modulating SOX9.	OBJECTIVES: Colon cancer (CC) currently ranks as the third most common human cancer worldwide with an increasing incidence and a poor prognosis. Recently, circular RNAs have been reported to regulate the progression of diverse human cancers. However, the role of circRNA hsa_circ_0020095 in CC remains largely unclear. METHODS: Expression levels of the related circRNAs, microRNAs and mRNA in CC tissues and cells were determined. The impacts of circ_0020095 or miR-487a-3p on CC cells were examined at the indicated times after transfection. Meanwhile, a luciferase-reporter experiment was employed to validate the interplay between miR-487a-3p and circ_002009695 or SOX9. Moreover, the in vivo tumor growth assay was applied to further evaluate the effects of circ_0020095 knockdown on CC progression. RESULTS: We demonstrated that circ_0020095 was highly expressed in CC tissues and cells. The proliferation, migration, invasion, and cisplatin resistance of CC were suppressed by silencing circ_0020095 in vitro and in vivo or by ectopic expression of miR-487a-3p in vitro. Mechanistically, circ_0020095 could directly bind to miR-487a-3p and subsequently act as a miR-487a-3p sponge to modulate the activity by targeting the 3'-UTR of SOX9. Interestingly, overexpression of circ_0020095 dramatically reversed the suppressive effects of miR-487a-3p mimics on CC cells. CONCLUSION: Circ_0020095 functions as an oncogene to accelerate CC cell proliferation, invasion, migration and cisplatin resistance through the miR-487a-3p/SOX9 axis, which could be a promising target for CC treatment.	NA	Front Cell Dev Biol. 2021 Jan 15;8:604869. doi: 10.3389/fcell.2020.604869. eCollection 2020.
4850	Circular RNA	Circ_0068	miR-21-5p	LPS	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR	33429194	Circular RNA circ_0068,888 protects against lipopolysaccharide-induced HK-2 cell injury via sponging microRNA-21-5p.	Our previous findings revealed that hsa_circ_0068,888 was markedly down-regulated in the plasma of patients with sepsis-associated acute kidney injury (AKI). However, its molecular mechanism in AKI remains unclear. Herein, we explored the role of hsa_circ_0068,888 in AKI. Human renal proximal tubular cell line HK-2 was stimulated with lipopolysaccharide (LPS) to mimic AKI in vitro. Decreased hsa_circ_0068,888 expression was observed in AKI cell model. The overexpression of hsa_circ_0068,888 significantly increased the viability of LPS-stimulated HK-2 cells, whereas hsa_circ_0068,888 downregulation showed the opposite effect. Furthermore, LPS triggered inflammatory response and oxidative stress, which was inhibited by hsa_circ_0068,888 overexpression and enhanced by hsa_circ_0068,888 down-regulation. Hsa_circ_0068,888 overexpression suppressed the activation of nuclear factor-κB (NF-κB) pathway triggered by LPS as evidenced by decreased p-p65 protein level and nuclear translocation of p65 in hsa_circ_0068,888 overexpressed cells. Additionally, we proved that hsa_circ_0068,888 targeted microRNA-21-5p (miR-21-5p). The expression of miR-21-5p was markedly increased and was negatively regulated by hsa_circ_0068,888 in LPS-stimulated HK-2 cells. Furthermore, we demonstrated that miR-21-5p overexpression reversed the effects on cell viability, inflammatory response, oxidative stress, and NF-κB pathway induced by hsa_circ_0068,888 overexpression in LPS-stimulated HK-2 cells. Overall, these results implied that hsa_circ_0068,888 shows a protective effect on AKI by sponging miR-21-5p. Hence, up-regulation of hsa_circ_0068,888 might be a potential strategy in treatment for AKI.	NA	Biochem Biophys Res Commun. 2021 Feb 12;540:1-7. doi: 10.1016/j.bbrc.2020.12.018. Epub 2021 Jan 8.
4851	Circular RNA	Circ_888	miR-21-5p	LPS	HK-2 cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR	33429194	Circular RNA circ_0068,888 protects against lipopolysaccharide-induced HK-2 cell injury via sponging microRNA-21-5p.	Our previous findings revealed that hsa_circ_0068,888 was markedly down-regulated in the plasma of patients with sepsis-associated acute kidney injury (AKI). However, its molecular mechanism in AKI remains unclear. Herein, we explored the role of hsa_circ_0068,888 in AKI. Human renal proximal tubular cell line HK-2 was stimulated with lipopolysaccharide (LPS) to mimic AKI in vitro. Decreased hsa_circ_0068,888 expression was observed in AKI cell model. The overexpression of hsa_circ_0068,888 significantly increased the viability of LPS-stimulated HK-2 cells, whereas hsa_circ_0068,888 downregulation showed the opposite effect. Furthermore, LPS triggered inflammatory response and oxidative stress, which was inhibited by hsa_circ_0068,888 overexpression and enhanced by hsa_circ_0068,888 down-regulation. Hsa_circ_0068,888 overexpression suppressed the activation of nuclear factor-κB (NF-κB) pathway triggered by LPS as evidenced by decreased p-p65 protein level and nuclear translocation of p65 in hsa_circ_0068,888 overexpressed cells. Additionally, we proved that hsa_circ_0068,888 targeted microRNA-21-5p (miR-21-5p). The expression of miR-21-5p was markedly increased and was negatively regulated by hsa_circ_0068,888 in LPS-stimulated HK-2 cells. Furthermore, we demonstrated that miR-21-5p overexpression reversed the effects on cell viability, inflammatory response, oxidative stress, and NF-κB pathway induced by hsa_circ_0068,888 overexpression in LPS-stimulated HK-2 cells. Overall, these results implied that hsa_circ_0068,888 shows a protective effect on AKI by sponging miR-21-5p. Hence, up-regulation of hsa_circ_0068,888 might be a potential strategy in treatment for AKI.	NA	Biochem Biophys Res Commun. 2021 Feb 12;540:1-7. doi: 10.1016/j.bbrc.2020.12.018. Epub 2021 Jan 8.
4852	Circular RNA	Circ_0107593	miR-20a-5p	NA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33585208	Hsa_circ_0107593 Suppresses the Progression of Cervical Cancer via Sponging hsa-miR-20a-5p/93-5p/106b-5p.	Circular RNAs (circRNAs) are a new class of single-stranded RNAs that form a continuous loop with crucial role in regulation of gene expression. Because their circular conformation conforms numerous properties, circRNAs have been investigated recently to demonstrate their important role in the development and progression of various cancers. However, the function of circRNAs and their regulatory outcomes in cervical cancer (CC) have rarely been explored. In this study, the role and molecular mechanism of hsa_circ_0107593 in cervical cancer are demonstrated. Quantitative polymerase chain reaction (qRT-PCR) was used to determine the expression of hsa_circ_0107593 and three miRNAs (hsa-miR-20a-5p, 93-5p, and 106b-5p) in paired CC tissues (tumor tissue vs. adjacent normal cervical tissue), CC cell lines, and human normal cervical epithelial immortalized cell line. A series of functional experiments were conducted to assess the function of hsa_circ_0107593 in CC development. The Receiver Operating Characteristic (ROC) curve was plotted to estimate the diagnostic value of hsa_circ_0107593 in CC. The dual-luciferase reporter assay was used to explore the interaction between hsa_circ_0107593 and hsa-miR-20a-5p/93-5p/106b-5p. Bioinformatic analysis was conducted to predict the target mRNAs, pathways, and functional enrichment. The results revealed that hsa_circ_0107593 has low expression in CC tissues and CC cell lines. Moreover, negative correlations of hsa_circ_0107593 expression were found against tumor diameter, FIGO stage, and myometrial invasion. Also, hsa_circ_0107593 impedes CC cell proliferation, migration, and invasion. Based on ROC curve analysis, hsa_circ_0107593 could serve as a diagnostic biomarker. Its low expression may indicate increased patient's risk to developing cervical cancer. Mechanistically, hsa_circ_0107593 serves as a sponge of hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p. Collectively, our study implies that hsa_circ_0107593 has tumor-suppressing activity in CC by physically binding with hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p.	NA	Front Oncol. 2021 Jan 15;10:590627. doi: 10.3389/fonc.2020.590627. eCollection 2020.
4853	Circular RNA	Circ_0107593	miR-93-5p	NA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33585208	Hsa_circ_0107593 Suppresses the Progression of Cervical Cancer via Sponging hsa-miR-20a-5p/93-5p/106b-5p.	Circular RNAs (circRNAs) are a new class of single-stranded RNAs that form a continuous loop with crucial role in regulation of gene expression. Because their circular conformation conforms numerous properties, circRNAs have been investigated recently to demonstrate their important role in the development and progression of various cancers. However, the function of circRNAs and their regulatory outcomes in cervical cancer (CC) have rarely been explored. In this study, the role and molecular mechanism of hsa_circ_0107593 in cervical cancer are demonstrated. Quantitative polymerase chain reaction (qRT-PCR) was used to determine the expression of hsa_circ_0107593 and three miRNAs (hsa-miR-20a-5p, 93-5p, and 106b-5p) in paired CC tissues (tumor tissue vs. adjacent normal cervical tissue), CC cell lines, and human normal cervical epithelial immortalized cell line. A series of functional experiments were conducted to assess the function of hsa_circ_0107593 in CC development. The Receiver Operating Characteristic (ROC) curve was plotted to estimate the diagnostic value of hsa_circ_0107593 in CC. The dual-luciferase reporter assay was used to explore the interaction between hsa_circ_0107593 and hsa-miR-20a-5p/93-5p/106b-5p. Bioinformatic analysis was conducted to predict the target mRNAs, pathways, and functional enrichment. The results revealed that hsa_circ_0107593 has low expression in CC tissues and CC cell lines. Moreover, negative correlations of hsa_circ_0107593 expression were found against tumor diameter, FIGO stage, and myometrial invasion. Also, hsa_circ_0107593 impedes CC cell proliferation, migration, and invasion. Based on ROC curve analysis, hsa_circ_0107593 could serve as a diagnostic biomarker. Its low expression may indicate increased patient's risk to developing cervical cancer. Mechanistically, hsa_circ_0107593 serves as a sponge of hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p. Collectively, our study implies that hsa_circ_0107593 has tumor-suppressing activity in CC by physically binding with hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p.	NA	Front Oncol. 2021 Jan 15;10:590627. doi: 10.3389/fonc.2020.590627. eCollection 2020.
4854	Circular RNA	Circ_0107593	miR-106b-5p	NA	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33585208	Hsa_circ_0107593 Suppresses the Progression of Cervical Cancer via Sponging hsa-miR-20a-5p/93-5p/106b-5p.	Circular RNAs (circRNAs) are a new class of single-stranded RNAs that form a continuous loop with crucial role in regulation of gene expression. Because their circular conformation conforms numerous properties, circRNAs have been investigated recently to demonstrate their important role in the development and progression of various cancers. However, the function of circRNAs and their regulatory outcomes in cervical cancer (CC) have rarely been explored. In this study, the role and molecular mechanism of hsa_circ_0107593 in cervical cancer are demonstrated. Quantitative polymerase chain reaction (qRT-PCR) was used to determine the expression of hsa_circ_0107593 and three miRNAs (hsa-miR-20a-5p, 93-5p, and 106b-5p) in paired CC tissues (tumor tissue vs. adjacent normal cervical tissue), CC cell lines, and human normal cervical epithelial immortalized cell line. A series of functional experiments were conducted to assess the function of hsa_circ_0107593 in CC development. The Receiver Operating Characteristic (ROC) curve was plotted to estimate the diagnostic value of hsa_circ_0107593 in CC. The dual-luciferase reporter assay was used to explore the interaction between hsa_circ_0107593 and hsa-miR-20a-5p/93-5p/106b-5p. Bioinformatic analysis was conducted to predict the target mRNAs, pathways, and functional enrichment. The results revealed that hsa_circ_0107593 has low expression in CC tissues and CC cell lines. Moreover, negative correlations of hsa_circ_0107593 expression were found against tumor diameter, FIGO stage, and myometrial invasion. Also, hsa_circ_0107593 impedes CC cell proliferation, migration, and invasion. Based on ROC curve analysis, hsa_circ_0107593 could serve as a diagnostic biomarker. Its low expression may indicate increased patient's risk to developing cervical cancer. Mechanistically, hsa_circ_0107593 serves as a sponge of hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p. Collectively, our study implies that hsa_circ_0107593 has tumor-suppressing activity in CC by physically binding with hsa-miR-20a-5p, hsa-miR-93-5p, and hsa-miR-106b-5p.	NA	Front Oncol. 2021 Jan 15;10:590627. doi: 10.3389/fonc.2020.590627. eCollection 2020.
4855	Circular RNA	Circ_102049	miR-455-3p	CD80	pancreatic ductal adenocarcinoma cells	Pancreatic Cancer	Homo sapiens (human)	RT-PCR;Western blot;luciferase assay;	33505218	circRNA circ_102049 Implicates in Pancreatic Ductal Adenocarcinoma Progression through Activating CD80 by Targeting miR-455-3p.	Emerging evidence has shown that circular RNAs (circRNAs) and DNA methylation play important roles in the causation and progression of cancers. However, the roles of circRNAs and abnormal methylation genes in the tumorigenesis of pancreatic ductal adenocarcinoma (PDAC) are still largely unknown. Expression profiles of circRNA, gene methylation, and mRNA were downloaded from the GEO database, and differentially expressed genes were obtained via GEO2R, and a ceRNA network was constructed based on circRNA-miRNA pairs and miRNA-mRNA pairs. Inflammation-associated genes were collected from the GeneCards database. Then, functional enrichment analysis and protein-protein interaction (PPI) networks of inflammation-associated methylated expressed genes were investigated using Metascape and STRING databases, respectively, and visualized in Cytoscape. Hub genes of PPI networks were identified using the NetworkAnalyzer plugin. Also, we analyzed the methylation, protein expression levels, and prognostic value of hub genes in PDAC patients through the UALCAN, Human Protein Atlas (HPA), and Kaplan-Meier plotter databases, respectively. The circRNA_102049/miR-455-3p/CD80 axis was identified by the ceRNA network and hub genes. In vitro and in vivo experiments were performed to evaluate the functions of circRNA_102049. The regulatory mechanisms of circRNA_102049 and miR-455-3p were explored by RT-PCR, western blot, and dual-luciferase assays. In the present study, twelve hub genes (STAT1, CCND1, KRAS, CD80, ICAM1, ESR1, RAF1, RPS6KA2, KDM6B, TNRC6A, FOSB, and DNM1) were determined from the PPI networks. Additionally, the circRNA_102049 was upregulated in PDAC cell lines. Functionally, the knockdown of circRNA_102049 by siRNAs inhibited cell growth, inflammatory factors, and migratory and invasive potential and promoted cell apoptosis. Mechanistically, circRNA_102049 functioned as a sponge of miR-455-3p and partially reversed the effect of miR-455-3p and consequently upregulated CD80 expression. Our findings showed that circRNA_102049 and methylated hub genes play an important role in the proliferation, apoptosis, migration, invasion, and inflammatory response of PDAC, which might be selected as a promising prognostic marker and therapeutic target for PDAC.	NA	Mediators Inflamm. 2021 Jan 7;2021:8819990. doi: 10.1155/2021/8819990. eCollection 2021.
4856	Circular RNA	CircAKT3	miR-206	CX43	osteogenesis of stem cells	Mesenchymal Stem Cell (Mscs) For Bone Tissue Regeneration	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Immunohistochemistry;Luciferase reporter assay;RNA sequencing;	33298186	circAKT3 positively regulates osteogenic differentiation of human dental pulp stromal cells via miR-206/CX43 axis.	BACKGROUND: Human dental pulp stromal cells (hDPSCs) are promising sources of mesenchymal stem cells (MSCs) for bone tissue regeneration. Circular RNAs (circRNAs) have been demonstrated to play critical roles in stem cell osteogenic differentiation. Herein, we aimed to investigate the role of circAKT3 during osteogenesis of hDPSCs and the underlying mechanisms of its function. METHODS: We performed circRNA sequencing to investigate the expression profiles of circular RNAs during osteogenesis of hDPSCs. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to detect the expression pattern of circAKT3 and miR-206 in hDPSCs during osteogenesis. We knocked down circAKT3 and interfered the expression of miR-206 to verify their regulatory role in hDPSC osteogenesis. We detected hDPSCs mineralization by alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining and used dual-luciferase reporter assay to validate the direct binding between circAKT3 and miR-206. To investigate in vivo mineralization, we performed subcutaneous transplantation in nude mice and used hematoxylin and eosin, Masson's trichrome, and immunohistochemistry staining. RESULTS: Totally, 86 circRNAs were differentially expressed during hDPSC osteogenesis, in which 29 were downregulated while 57 were upregulated. circAKT3 was upregulated while miR-206 was downregulated during hDPSC osteogenesis. Knockdown of circAKT3 inhibited ALP/ARS staining and expression levels of osteogenic genes. circAKT3 directly interacted with miR-206, and the latter one suppressed osteogenesis of hDPSCs. Silencing miR-206 partially reversed the inhibitory effect of circAKT3 knockdown on osteogenesis. Connexin 43 (CX43), which positively regulates osteogenesis of stem cells, was predicted as a target of miR-206, and overexpression or knockdown of miR-206 could correspondingly decrease and increase the expression of CX43. In vivo study showed knockdown of circAKT3 suppressed the formation of mineralized nodules and expression of osteogenic proteins. CONCLUSION: During osteogenesis of hDPSCs, circAKT3 could function as a positive regulator by directly sponging miR-206 and arresting the inhibitive effect of miR-206 on CX43 expression.	NA	Stem Cell Res Ther. 2020 Dec 9;11(1):531. doi: 10.1186/s13287-020-02058-y.
4857	Circular RNA	Circ-LDLRAD3	miR-224-5p	NRP2	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Rescue assay;	33389349	Circ-LDLRAD3 Enhances Cell Growth, Migration, and Invasion and Inhibits Apoptosis by Regulating MiR-224-5p/NRP2 Axis in Gastric Cancer.	BACKGROUND: Emerging as a newly discovered type of noncoding RNAs, circular RNAs have been manifested as a crucial regulator in tumorigenesis of human malignancies, including gastric cancer (GC). Although circ-LDLRAD3 has been revealed as an oncogene in pancreatic cancer, the underlying role of circ-LDLRAD3 in GC remains poorly understood. AIMS: Exploring the underlying function of circ-LDLRAD3 on GC progression. METHODS: Circ-LDLRAD3 expression was detected through RT-qPCR. EdU, colony formation, TUNEL, and transwell assays were performed to analyze the function of circ-LDLRAD3 on GC progression. Luciferase reporter and RIP assays were applied to testify the interaction between circ-LDLRAD, miR-224-5p, and NRP2 in GC. RESULTS: We detected preliminarily the expression of circ-LDLRAD3 and observed a markedly high expression of circ-LDLRAD3 in GC cells. Besides, circ-LDLRAD3 was featured with loop structure. Biological function assays testified that silenced circ-LDLRAD3 inhibited cell proliferation, migration, and invasion capacity but facilitated apoptosis of GC cells. Molecular mechanism assays uncovered that circ-LDLRAD3 combined with miR-224-5p in GC. Moreover, rescue assays delineated that inhibited expression of miR-224-5p could restore the inhibitive influence of circ-LDLRAD3 knockdown on the progression of GC. Moreover, neuropilin 2 (NRP2) was a downstream target of miR-224-5p. Additionally, circ-LDLRAD3 regulated NRP2 expression by sponging miR-224-5p in GC. Furthermore, circ-LDLRAD3 depletion-mediated effect on GC progression could be reversed by overexpressing NRP2. CONCLUSIONS: Circ-LDLRAD3 facilitates GC progression by regulating miR-224-5p/NRP2 axis, providing new insights for the researches of GC treatment.	NA	Dig Dis Sci. 2021 Jan 2. doi: 10.1007/s10620-020-06733-1.
4858	Circular RNA	CircPARP4	miR-125a-5p	FUT4	glioma tissues	Glioma	Homo sapiens (human)	qRT-PCR	33520365	CircularRNA circPARP4 promotes glioblastoma progression through sponging miR-125a-5p and regulating FUT4.	Circular RNA (circRNA) is a widely expressed non-coding RNA element characterized by a covalently closed continuous loop. Emerging evidence suggests important roles of circRNAs in the pathogenesis of human cancers. However, the functions and underlying mechanisms of circRNAs in glioma remain largely unclear. Previously, our studies uncovered a batch of abnormally expressed circRNAs in glioma tissue, among which circPARP4 was significantly upregulated with the top fold change. Here, we focused on the functional investigation toward circPARP4 in glioblastoma progression and looked for insight into its underlying mechanisms. The results confirmed the elevated expression of circPARP4 in glioma and found its association with glioma pathological grade. Gain- and loss-of-function strategies showed that circPARP4 could obviously promote glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Mechanistically, in vivo and in vitro studies demonstrated that circPARP4, as a miRNA sponge, directly interacted with miR-125a-5p, which then regulated FUT4 to exert the oncogenic effect on glioma behavior. Our findings illustrate functions of circPARP4 in modulating glioma progression through miR-125a-5p/FUT4 pathway, which provides a novel and potential target for glioma therapy.	NA	Am J Cancer Res. 2021 Jan 1;11(1):138-156. eCollection 2021.
4859	LncRNA	DANCR	miR-125b-5p	MAPK	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33597534	The regulation of protein translation and its implications for cancer.	In addition to the deregulation of gene transcriptions and post-translational protein modifications, the aberrant translation from mRNAs to proteins plays an important role in the pathogenesis of various cancers. Targeting mRNA translation are expected to become potential approaches for anticancer treatments. Protein translation is affected by many factors including translation initiation factors and RNA-binding proteins. Recently, modifications of mRNAs mainly N6-methyladenine (m(6)A) modification and noncoding RNAs, such as microRNAs and long noncoding RNAs are involved. In this review, we generally summarized the recent advances on the regulation of protein translation by the interplay between mRNA modifications and ncRNAs. By doing so, we hope this review could offer some hints for the development of novel approaches in precision therapy of human cancers.	NA	Signal Transduct Target Ther. 2021 Feb 18;6(1):68. doi: 10.1038/s41392-020-00444-9.
4860	LncRNA	DLEU2L	miR-100-5p	TAOK1	Hepatocellular carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33575116	Comprehensive analysis to identify DLEU2L/TAOK1 axis as a prognostic biomarker in hepatocellular carcinoma.	Hepatocellular carcinoma (HCC) is one of the deadliest malignant tumors that are harmful to human health. Increasing evidence has underscored the critical role of the competitive endogenous RNA (ceRNA) regulatory networks among various human cancers. However, the complexity and behavior characteristics of the ceRNA network in HCC were still unclear. In this study, we aimed to clarify a phosphatase and tensin homolog (PTEN)-related ceRNA regulatory network and identify potential prognostic markers associated with HCC. The expression profiles of three RNAs (long non-coding RNAs [lncRNAs], microRNAs [miRNAs], and mRNAs) were extracted from The Cancer Genome Atlas (TCGA) database. The DLEU2L-hsa-miR-100-5p/ hsa-miR-99a-5p-TAOK1 ceRNA network related to the prognosis of HCC was obtained by performing bioinformatics analysis. Importantly, we identified the DLEU2L/TAOK1 axis in the ceRNA by using correlation analysis, and it appeared to become a clinical prognostic model by Cox regression analysis. Furthermore, methylation analyses suggested that the abnormal upregulation of the DLEU2L/TAOK1 axis likely resulted from hypomethylation, and immune infiltration analysis showed that the DLEU2L/TAOK1 axis may have an impact on the changes in the tumor immune microenvironment and the development of HCC. In summary, the current study constructing a ceRNA-based DLEU2L/TAOK1 axis might be a novel important prognostic factor associated with the diagnosis and prognosis of HCC.	NA	Mol Ther Nucleic Acids. 2021 Jan 1;23:702-718. doi: 10.1016/j.omtn.2020.12.016. eCollection 2021 Mar 5.
4861	LncRNA	DLEU2L	miR-99a-5p	TAOK1	Hepatocellular carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR	33575116	Comprehensive analysis to identify DLEU2L/TAOK1 axis as a prognostic biomarker in hepatocellular carcinoma.	Hepatocellular carcinoma (HCC) is one of the deadliest malignant tumors that are harmful to human health. Increasing evidence has underscored the critical role of the competitive endogenous RNA (ceRNA) regulatory networks among various human cancers. However, the complexity and behavior characteristics of the ceRNA network in HCC were still unclear. In this study, we aimed to clarify a phosphatase and tensin homolog (PTEN)-related ceRNA regulatory network and identify potential prognostic markers associated with HCC. The expression profiles of three RNAs (long non-coding RNAs [lncRNAs], microRNAs [miRNAs], and mRNAs) were extracted from The Cancer Genome Atlas (TCGA) database. The DLEU2L-hsa-miR-100-5p/ hsa-miR-99a-5p-TAOK1 ceRNA network related to the prognosis of HCC was obtained by performing bioinformatics analysis. Importantly, we identified the DLEU2L/TAOK1 axis in the ceRNA by using correlation analysis, and it appeared to become a clinical prognostic model by Cox regression analysis. Furthermore, methylation analyses suggested that the abnormal upregulation of the DLEU2L/TAOK1 axis likely resulted from hypomethylation, and immune infiltration analysis showed that the DLEU2L/TAOK1 axis may have an impact on the changes in the tumor immune microenvironment and the development of HCC. In summary, the current study constructing a ceRNA-based DLEU2L/TAOK1 axis might be a novel important prognostic factor associated with the diagnosis and prognosis of HCC.	NA	Mol Ther Nucleic Acids. 2021 Jan 1;23:702-718. doi: 10.1016/j.omtn.2020.12.016. eCollection 2021 Mar 5.
4862	LncRNA	FER1L4	miR-133a-5p	Prx1	SCC-9 and HN4 cells	Oral Squamous Cell Cancer 	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33568918	LncRNA FER1L4 Promotes Oral Squamous Cell Carcinoma Progression via Targeting miR-133a-5p/Prx1 Axis.	BACKGROUND: Oral squamous cell carcinoma (OSCC) is a common cancer especially young people in the world. The long non-coding RNA Fer-1-like protein 4 (FER1L4) has been reported to be closely associated with the progression of various human cancers. However, the role of FER1L4 in OSCC remains unclear. METHODS: The expression level of FER1L4 in OSCC tissues and cancer cell lines was detected by using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was evaluated by cell counting kit-8 (CCK-8) assay and EdU staining assay. Cell invasion and migration were evaluated by Transwell assay. Cell apoptosis was detected by flow cytometry. Luciferase reporter assay was performed to determine the targeting relationship between FER1L4, miR-133a-5p and Prx1. The protein expression of Prx1 was detected by Western blot. In addition, a xenograft tumor model in vivo was constructed to confirm the function of FER1L4. RESULTS: FERIL4 was significantly upregulated in OSCC tissues and cancer cell lines. Moreover, high level of FER1L4 predicted a poor prognosis of OSCC patients. Silencing of FER1L4 not only significantly inhibited cell growth, invasion, migration and induced apoptosis in SCC-9 and HN4 cells in vitro, but also effectively suppressed the tumorigenesis of OSCC cells in vivo. Knockdown of FER1L4 significantly enhanced the expression of miR-133a-5p by sponging it, and then downregulated Prx1 expression. CONCLUSION: Our study elucidated a new mechanism of lncRNA FER1L4 that promoting OSCC progression by directly targeting miR-133a-5p/Prx1 axis and provided novel therapeutic targets for OSCC.	NA	Onco Targets Ther. 2021 Feb 4;14:795-806. doi: 10.2147/OTT.S277351. eCollection 2021.
4863	LncRNA	FERRE	miR-19a-5p	EZH2	breast cancer cells	Breast Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;luciferase assay;	33215433	Upregulation of long noncoding RNA FERRE promoted growth and invasion of breast cancer through modulating miR-19a-5p/EZH2 axis.	OBJECTIVE: It has been demonstrated that long non-coding RNA (LncRNA) plays an important regulatory role in a series of diseases. The purpose of this study is to investigate the expression of long non-coding RNA (LncRNA) FERRE and its facilitating effects on proliferation and invasion of breast cancer by regulating oncogene EZH2 through sponging with miR-19a-5p. PATIENTS AND METHODS: qRT-PCR was performed to detect the expressions of FERRE and EZH2 in human breast cancer tissues and cells. CCK-8 assay was performed to evaluate the MCF-7 cells proliferation and transwell assay was performed to evaluate the MCF-7 cells migration. Correlation analysis between FERRE and miR-19a-5p was detected by statistical analysis. Bioinformatics prediction was made to detect the binding site of FERRE and miR-19a-5p and Luciferase activity was conducted to investigate the interaction between EZH2 and miR-19a-5p. Furthermore, we cloned the mice EZH2 3'-UTR into the Luciferase reporter vector and constructed miR-19a-5p binding mutants to validate the inhibited modulation of miR-19a-5p to the EZH2 expression. RESULTS: Results showed that expression of FERRE and EZH2 were upregulated in human breast cancer tissues and cells. qRT-PCR and CCK-8 assay showed that FERRE expression is associated with the proliferation of breast cancer cells, upregulated FERRE contributed to cell proliferation of MCF-7. Transwell assay showed that FERRE was associated with the migration ability of tumor cells, increased expression of FERRE promoted the migration and invasion of breast cancer cells. The bioinformatics prediction and Luciferase assay demonstrated that by sponging with miR-19a-5p, FERRE can serve as a molecular sponge to further regulate the expression of EZH2. CONCLUSIONS: We found that lncRNA-FERRE was upregulated in human breast cancer patients, which could accelerate tumor proliferation, migration and invasion as a molecular sponge by modulating the inhibitory effect of miR-19a-5p on oncogene EZH2.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):11154-11164. doi: 10.26355/eurrev_202011_23603.
4864	LncRNA	H19	miR-148b-3p	ELF5	umbilical vein endothelial cells	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33510936	Icariin attenuates endothelial-mesenchymal transition via H19/miR-148b-3p/ELF5 in ox-LDL-stimulated HUVECs.	Atherosclerosis is the main cause of cardio-cerebrovascular diseases. Endothelial-mesenchymal transition plays an important role in atherosclerosis. Icariin has a protective effect on atherosclerosis; however, the underlying mechanism remains unclear. In this study, we explored the molecular mechanism underlying the protective function of icariin in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells. H19, a long non-coding RNA, was identified to be downregulated in the background of the oxidized low-density lipoprotein-induced endothelial-mesenchymal transition in human umbilical vein endothelial cells. Icariin upregulated H19 expression and inhibited the transformation of endothelial cells into interstitial cells. Overexpression of H19 affected endothelial-mesenchymal transition in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas H19 knockdown reversed endothelial protective effects of icariin and reduced human umbilical vein endothelial cell migration. Knockdown of H19 significantly downregulated oxidized low-density lipoprotein-induced E74-like factor 5 and upregulated miR-148b-3p, which was reversed by icariin. Thus, icariin may play a protective role in atherosclerosis, and H19 may be a potential therapeutic target.	NA	Mol Ther Nucleic Acids. 2020 Dec 3;23:464-475. doi: 10.1016/j.omtn.2020.11.021. eCollection 2021 Mar 5.
4865	LncRNA	HCG11	miR-579	MMP13	osteosarcoma cells	Osteosarcoma	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	33408506	Long Non-Coding RNA HCG11 Aggravates Osteosarcoma Carcinogenesis via Regulating the microRNA-579/MMP13 Axis.	BACKGROUND: Previous studies have suggested that long non-coding RNAs (lncRNAs) were involved in tumorigenesis of various human carcinomas, including osteosarcoma (OS). However, the expression and specific role of lncRNA HLA complex group 11 (HCG11) in OS remain unknown. The current study aimed at revealing the role of lncRNA HCG11 and its related mechanism in OS. METHODS: lncRNA HCG11 expression was verified with RT-qPCR followed by sub-localization determination. LncRNA-microRNA (miRNA) and miRNA-mRNA interactions were predicted by online bioinformatics websites. Validation was performed using dual-luciferase reporter gene assays, and gain- and loss-of-function experiments. The effects of lncRNA HCG11, miR-579 and matrix metalloproteinase 13 (MMP13) on the proliferation, migration and invasion, epithelial-mesenchymal transition (EMT) of OS cells were detected using cell counting kit-8 (CCK-8), Transwell assays and Western blot analysis. RESULTS: LncRNA HCG11 overexpression was observed in OS tissues and cell lines. Downregulation of lncRNA HCG11/MMP13 or overexpression of miR-579 blocked the progression of OS cells. LncRNA HCG11, which is located in the cytoplasm, promoted MMP13 expression through sponging miR-579. CONCLUSION: LncRNA HCG11 might be beneficial for OS aggravation via sponging miR-579 and facilitating MMP13 expression, which represents a candidate biomarker and target for OS therapy.	NA	Int J Gen Med. 2020 Dec 31;13:1685-1695. doi: 10.2147/IJGM.S274641. eCollection 2020.
4866	LncRNA	HCG11	miR-144-3p	PBX3	SKOV3 cells	Ovarian Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;	33215418	Knockdown of lncRNA HCG11 suppresses cell progression in ovarian cancer by modulating miR-144-3p/PBX3.	OBJECTIVE: LncRNA HCG11 has been confirmed to act as a crucial role in several human cancers. Nevertheless, to our knowledge, the function of HCG11 on the progression of ovarian cancer (OC) has not been studied. This article is designed to explore the mechanism and role of HCG11 in the tumorigenesis and development of OC. PATIENTS AND METHODS: RT-qPCR analysis was applied to detect the expression of HCG11, miR-144-3p and PBX3 in OC tissues and cell lines. MTT assay and transwell assay were opted to measure the cell viability of OC cells. The protein expression level of PBX3 was measured by Western blot assay. Dual-Luciferase reporter assay was carried out to assess the correlation between HCG11, miR-144-3p and PBX3. RESULTS: The upregulated of HCG11 was observed in OC tissues and OC cell lines. Moreover, miR-144-3p was down expressed in OC tissues and cell lines. Functionally, the knockdown of HCG11 prevented cell viability of SKOV3 cells, while miR-144-3p inhibitor abrogated the suppressor on cell progression. Furthermore, PBX3 was verified to be a target gene of miR-144-3p. In addition, PBX3 knockdown prevented the cell progression of SKOV3 cells. CONCLUSIONS: These data displayed that the knockdown of HCG11 prevented cell progression in OC by sponging miR-144-3p and downregulating PBX3. All results revealed that HCG11 can be a potential therapeutic target for OC therapy.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):11032-11040. doi: 10.26355/eurrev_202011_23588.
4867	LncRNA	LINC00520	miR-1252-5p	FOXR2	lung adenocarcinoma cells	Lung Cancer	Homo sapiens (human)	RIP assay;Luciferase reporter assay;	33464477	Long noncoding RNA LINC00520 accelerates lung adenocarcinoma progression via miR-1252-5p/FOXR2 pathway.	It has been corroborated that long noncoding RNA (lncRNA) played fundamental function in various human malignancies development including lung adenocarcinoma (lung ADC). In our study, LINC00520 roles in lung ADC tumorigenesis were explored. We found that LINC00520 level was elevated in lung ADC tissues and cell lines. Besides, the LINC00520 expression had a negative connection with miR-1252-5p level in lung ADC tissues. Additionally, our results demonstrated the reciprocal repression influence between LINC00520 and miR-1252-5p. Moreover, luciferase reporter assays, RIP (RNA-binding protein immunoprecipitation) and pull down assays revealed that miR-1252-5p regulated LINC00520 in RISC-dependent. Furthermore, knockdown of LINC00520 inhibited lung ADC cells proliferation, migration and invasion, while co-transfection with a miR-1252-5p inhibitor inverted these influences. Additionally, the findings also demonstrated that FOXR2 was a target of miR-1252-5p; thus, LINC00520 could regulate FOXR2 level. Moreover, LINC00520 silencing suppressed the tumor growth of lung ADC in vivo. In summary, our data indicated that LINC00520 may act as a ceRNA to modulated FOXR2 level by sponging miR-1252-5p, which might bring a potential and effective biomarker to lung ADC treatment.	NA	Hum Cell. 2021 Mar;34(2):478-490. doi: 10.1007/s13577-020-00478-9. Epub 2021 Jan 19.
4868	LncRNA	Linc00887	miR-454-3	FRMD6	cervical epithelial cells	Cervical Cancer	Homo sapiens (human)	qPCR;RT-qPCR;	33413358	Linc00887 suppresses tumorigenesis of cervical cancer through regulating the miR-454-3p/FRMD6-Hippo axis.	BACKGROUND: Emerging evidence suggested that long intergenic noncoding RNA (lincRNA) 00887 (NR_024480) reduced the invasion and metastasis of non-small cell lung cancer by sponging miRNAs degradation. However, the role and regulatory mechanism of linc00887 in the progression of cervical cancer remain largely unknown. METHODS: In vivo or vitro, RT-qPCR assay was used to detect the expression of linc00887 in human normal (N = 30), cervical cancer tissues (N = 30), human normal cervical epithelial cells (Ect1/E6E7) and cervical cancer cell lines (HeLa, C33A). Then, CCK-8 and Transwell assays were used to examine cell proliferation and invasion when linc00887 was overexpressed or knocked down. In addition, bioinformatics, luciferase reporter gene and pull-down assays were used to predict and validate the relationship between linc00887 and miR-454-3p. Moreover, we detected the expression of miR-454-3p in Ect1/E6E7, HeLa and C33A cells when linc00887 was overexpressed or knocked down. Cell proliferation and invasion were also measured when pcDNA-linc00887 and miR-454-3p were transfected alone or together. Next, miR-454-3p target gene was predicted and validated by bioinformatics and luciferase reporter gene assays. Gain- and loss-of-function experiments were performed in HeLa cells to evaluate the effect of miR-454-3p or linc00887 on the expression of FERM domain containing protein 6 (FRMD6) protein and several key proteins in the FRMD6-Hippo signaling pathway. RESULTS: Linc00887 was downregulated in cervical cancer tissues or human cervical cancer cell lines (Hela, C33A) compared with normal tissues or cell lines. Overexpression of linc00887 inhibited proliferation and invasion HeLa and C33A cells, while linc00887 knockdown had the opposite effect. Linc00887 bound with miR-454-3p, and overexpression of miR-454-3p rescued linc00887-induced inhibition proliferation and invasion of HeLa cells. MiR-454-3p targeted and suppressed the expression of FRMD6, and linc00887 suppressed tumorigenesis of cervical cancer through activating the FRMD6-Hippo signaling pathway. CONCLUSIONS: Linc00887, sponging miR-454-3p, inhibited the progression of cervical cancer by activating the FRMD6-Hippo signaling pathway.	NA	Cancer Cell Int. 2021 Jan 7;21(1):33. doi: 10.1186/s12935-020-01730-w.
4869	LncRNA	LINC00958	miR-378a-3p	YY1	breast cancer tissues and cells	Breast Cancer	Homo sapiens (human)	qRT-PCR	33531456	m(6)A-induced LINC00958 promotes breast cancer tumorigenesis via the miR-378a-3p/YY1 axis.	Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N(6)-methyladenosine (m(6)A) regulate BC tumorigenesis are still unclear. In the present research, LINC00958 was markedly overexpressed in BC tissue and cells, and LINC00958 upregulation promoted the tumor progression of BC cells. Mechanistically, m(6)A methyltransferase-like 3 (METTL3) gave rise to the upregulation of LINC00958 by promoting its RNA transcript stability. Moreover, LINC00958 acted as a competitive endogenous RNA for miR-378a-3p to promote YY1. Overall, these data provide novel insight into how m(6)A-mediated LINC00958 regulates BC tumorigenesis.	NA	Cell Death Discov. 2021 Feb 2;7(1):27. doi: 10.1038/s41420-020-00382-z.
4870	LncRNA	LINC00963	miR-612	CDC5L	Gastric cancer cells	Gastric Cancer	Homo sapiens (human)	Western blot;	33376349	Long Noncoding RNA LINC00963 Promotes CDC5L-Mediated Malignant Progression in Gastric Cancer.	BACKGROUND: Gastric cancer (GC) is a common cancer with high incidence and mortality worldwide. In recent years, accumulating evidence has shown that long noncoding RNAs (lncRNAs) exert critical roles in the development and progression of cancer by acting as a tumor initiator or suppressor. LINC00963 is a newly reported lncRNA related to cancer, and its role in GC remains unclear. MATERIALS AND METHODS: The expression levels of LINC00963, miR-612, and cell division cycle 5-like protein (CDC5L) were measured using quantitative real-time PCR or Western blot. The biological functions of LINC00963, miR-612, and CDC5L in GC cells were analyzed by transwell and proliferation experiments. The expression of CDC5L in patients with GC was evaluated using the Oncomine database. Bone marrow-derived dendritic cells (DCs) were derived from C57BL/6 mice. RESULTS: LINC00963 expression was higher in GC tissues than in adjacent normal tissues. Similar results were found in GC cell lines and normal human gastric epithelial cells. Upregulation of LINC00963 was related to the poor prognosis of patients with GC. Knockdown of LINC00963 inhibited the proliferation, invasion, and metastasis but promoted the apoptosis of GC cells. Furthermore, silencing of LINC00963 in GC cells significantly suppressed the tumor growth of GC. Bioinformatics analysis indicated that LINC00963 could target miR-612 by functioning as a competing endogenous RNA. The expression of miR-612 decreased in GC tissues and cell lines. Meanwhile, LINC00963 expression was negatively associated with miR-612. CDC5L was a direct target of miR-612. miR-612 suppressed the expression of CDC5L in GC tissues and cells. Moreover, LINC00963 inhibited the differentiation and maturation of DCs by regulating miR-612 expression in DCs. CONCLUSION: LINC00963 promoted the progression of GC by competitively binding to miR-612 to regulate the expression of CDC5L and mediated DC-related anti-tumor immune response. Thus, targeting LINC00963 may be a promising therapeutic strategy for GC.	NA	Onco Targets Ther. 2020 Dec 22;13:12999-13013. doi: 10.2147/OTT.S274708. eCollection 2020.
4871	LncRNA	LINC01224	miR-2467	NA	CRC cells	Colorectal Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;Luciferase reporter assay;	33542656	LINC01224 Promotes Colorectal Cancer Progression by Sponging miR-2467.	INTRODUCTION: Colorectal cancer (CRC) is one of the most common human cancers and a leading cause of cancer-related death. Accumulating evidence has confirmed that long non-coding RNA (lncRNA) plays crucial roles in CRC development. METHODS: qRT-PCR was performed to examine the expressions of LINC01224 and miR-2467. CCK-8 assay, colony formation assay and transwell invasion assay were used to examine the progression of breast cancer cells. Luciferase and RNA-binding protein immunoprecipitation (RIP) assay were applied to verify the binding site. Correlation analysis of miR-2467 and LINC01224 expression in lung cancer tissues was shown. Pancreatic cancer cells growth in vivo was evaluated using xenograft tumor assay. RESULTS: LINC01224 expression was observed to be up-regulated in CRC tissues and cell lines. Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. Luciferase reporter assays illustrated that LINC01224 regulated miR-2467 directly, and RNA-binding protein immunoprecipitation (RIP) further confirmed that the suppression of LINC01224 by miR-2467 was in an RISC-dependent manner. Finally, LINC01224 silence inhibited the growth CRC cells in vivo. CONCLUSION: In conclusion, our findings showed that LINC01224 promoted CRC progression through sponging miR-2467. LINC01224 may serve as a potential diagnostic biomarker and therapeutic target for CRC patients.	NA	Cancer Manag Res. 2021 Jan 26;13:733-742. doi: 10.2147/CMAR.S281625. eCollection 2021.
4872	LncRNA	LINC01303	miR-200c	TIMP2	laryngeal squamous cell carcinoma tissues and cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;	33841686	LINC01303 promotes the proliferation and migration of laryngeal carcinoma by regulating miR-200c/TIMP2 axis.	BACKGROUND: It is reported that long non-coding RNA is crucial in many cancer progressions. But the function and regulatory mechanism of LINC01303 in human laryngeal squamous cell carcinoma (LSCC) remains unclear. Hence, this research aims at investigating the biological function and potential mechanism of LINC01303 in LSCC. METHODS: Real-time quantitative PCR (qRT-PCR) was applied for the determination of LINC01303, miR-200c and TIMP metallopeptidase inhibitor 2 (TIMP2) expression in LSCC tissues and cell lines. Corresponding experiments were carried out to determine the impacts of LINC01303 on LSCC cell proliferation, apoptosis, migration and invasion. The interaction between LINC01303 and miR-200c was analyzed with bioinformatics analysis and luciferase activity analysis. RESULTS: LINC01303 expression in LSCC tissues was notably higher than that in adjacent normal tissues. High LINC01303 expression was bound up with lymphatic metastasis and advanced clinical stage. In addition, inhibition of LINC01303 by siRNA could evidently block LSCC cell proliferation, induce apoptosis, and inhibit invasion and migration. Mechanically, LINC01303 acted as carcinogenic lncRNA in LSCC by regulating miR-200c/TIMP2 axis. CONCLUSION: LINC01303 plays a carcinogenic part in LSCC carcinogenesis through regulating miR-200c/TIMP2 axis, which may become a promising target of LSCC therapy.	NA	Am J Transl Res. 2021 Mar 15;13(3):1643-1656. eCollection 2021.
4873	LncRNA	Linc-SCRG1	miR-26a	SKP2	HCC cells	Hepatocellular Carcinoma	Homo sapiens (human)	qPCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33422101	Linc-SCRG1 accelerates progression of hepatocellular carcinoma as a ceRNA of miR26a to derepress SKP2.	BACKGROUND: Increasing evidence has demonstrated that long noncoding RNAs (lncRNAs) have regulatory functions in hepatocellular carcinoma (HCC). The link between lincSCRG1 and HCC remains unclear. METHODS: To explore the lincSCRG1 regulation axis, bioinformatics, RIP and luciferase reporter assay were performed. The expressions of lincSCRG1-miR26a-SKP2 were detected in HCC tissues and cell lines through qPCR and western blot. The functions of HCC cells were investigated through in vitro assays (MTT, colony formation, transwell and flow cytometry) and the inner effect of lincSCRG1-miR26a in vivo was evaluated by xenografts and liver metatstatic nude mice models. RESULTS: LincSCRG1 was found to be strongly elevated in human HCC tissues and cell lines. MiR26a and S phase kinase-related protein 2 (SKP2) were predicted as the target miRNA for lincSCRG1 and the target gene for miR26a with direct binding sites, respectively. LincSCRG1 was verified as a competing endogenous RNA (ceRNA) via negative regulation of miR26a and derepression of SKP2 in HCC cells. Both overexpression of lincSCRG1 (ov-lincSCRG1) and inhibition of miR26a (in-miR26a) obviously stimulated cellular viability, colony formation, migration and proliferation of S phase cells and also significantly increased the protein levels of cyclinD1, CDK4, MMP2/3/9, Vimentin, and N-cadherin or inhibited the protein level of E-cadherin of HCC cells, while knockdown of lincSCRG1 (sh-lincSCRG1) and upregulation of miR26a (mi-miR26a) had the opposite effects on HCC cells. Cotransfection of in-miR26a or overexpression of SKP2 (ov-SKP2) with sh-lincSCRG1 could rescue the anticancer functions of sh-lincSCRG1, including suppressing proliferation and migration of HCC cells. Additionally, sh-lincSCRG1 could effectively inhibit the growth of subcutaneous xenograft tumours and lung metastasis, while the anticancer effect of sh-lincSCRG1 could be reversed by cotransfection of in-miR26a. CONCLUSIONS: LincSCRG1 acts as a ceRNA of miR26a to restrict its ability to derepress SKP2, thereby inducing the proliferation and migration of HCC cells in vitro and in vivo. Depletion of lincSCRG1 could be used as a potential therapeutic approach in HCC.	NA	J Exp Clin Cancer Res. 2021 Jan 9;40(1):26. doi: 10.1186/s13046-020-01825-2.
4874	LncRNA	MALAT1	miR-204-5p	Smad4	lens epithelial cells	Posterior Capsular Opacification	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;qPCR;RT-qPCR;Western blot;FISH;Luciferase reporter assay;	33327804	LncRNA-MALAT1/miRNA-204-5p/Smad4 Axis Regulates Epithelial-Mesenchymal Transition, Proliferation and Migration of Lens Epithelial Cells.	Purpose: Posterior capsular opacification (PCO), a common complication after cataract surgery, primarily originated from the epithelial-mesenchymal transition (EMT), proliferation, and migration of human lens epithelial cells (LECs). This study aimed to explore whether the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/miR-204-5p/Smad4 axis are involved in EMT of LECs.Materials and methods: LECs were cultured and induced with TGF-β2 (10 ng/mL). SiRNA against MALAT1 (Si-MALAT1) was transfected into LECs to knockdown the expression of MALAT1. To overexpress or knockdown miR-204-5p, miR-204-5p mimics (miR-204-5p mimics) and anti-miR-204-5p (miR-204-5p inhibitor) were transfected into LECs. We used RNA FISH to identify the location of MALAT1. RNA levels of MALAT1 and miR-204-5p were analyzed by RT-qPCR. Additionally, target protein levels of Smad4, epithelial differentiation and mesenchymal markers were analyzed with Western blot. We employed EdU Labeling to measured cell proliferation and performed Transwell Assay to analyze the cell migration. Dual-luciferase reporter assays in LECs were conducted to verify whether miRNA-204-5p was negatively regulated by MALAT1 and Smad4 was a direct target of miR-204-5p.Results: The expression of MALAT1 was upregulated in PCO specimens. MALAT1 was overexpressed in TGF-β2 induced LECs, and the knockdown of MALAT1 could attenuate TGF-β2 induced EMT. Besides, the upregulation of MALAT1 was correlated with the downregulation of miR-204-5p and upregulation of Smad4. Importantly, MALAT1 was revealed to be located in the cytoplasm of LECs. Furthermore, luciferase reporter assays confirmed that MALAT1 could negatively regulate the expression of miR-204-5p and then regulate its direct target Smad4. Finally, the knockdown of MALAT1 could inhibit the EMT, proliferation, and migration of LECs; however, those can be reversed by anti-miR-204-5p.Conclusions: Our findings reveal that MALAT1 may regulate EMT, proliferation, and migration of LECs as a ceRNA by "sponging" miR-204-5p and targeting Smad4, and serve as a promising therapeutic target in preventing PCO.	NA	Curr Eye Res. 2020 Dec 17:1-11. doi: 10.1080/02713683.2020.1857778.
4875	LncRNA	MALAT1	miR-320a-5p	Runx2	renal interstitial fibroblasts	Randalls Plaques	Homo sapiens (human)	RACE;RNA immunoprecipitation;luciferase assay;RNA immunoprecipitation;	33505960	Osteogenic Differentiation of Renal Interstitial Fibroblasts Promoted by lncRNA MALAT1 May Partially Contribute to Randall's Plaque Formation.	BACKGROUND: The current belief is that Randall's plaques (RP) constitute a nidus for the formation of idiopathic calcium oxalate stones, but the upstream events in RP formation remain unclear. The present study aimed to investigate whether RP formation shares similarities with biomineralization and to illustrate the potential role played by the lncRNA MALAT1 in osteogenic differentiation of human renal interstitial fibroblasts (hRIFs). MATERIALS AND METHODS: Biomineralization and MALAT1 expression were assessed in RP, and hRIFs were isolated and induced under osteogenic conditions for further experiments. The transcription initiation and termination sites in MALAT1 were identified by 5' and 3' RACE. RNA immunoprecipitation assays and luciferase assays were used to validate the interactions among MALAT1, Runx2 and miRNAs. RESULTS: Upregulated expression of osteogenic markers and MALAT1 was observed in RP and hRIFs induced with osteogenic medium. Biomineralization in RP and calcium phosphate (CaP) deposits in induced hRIFs were further verified by electron microscopy. Furthermore, overexpression of MALAT1 promoted the osteogenic phenotype of hRIFs, while treatment with a miR-320a-5p mimic and knockdown of Runx2 significantly suppressed the osteogenic phenotype. Further analysis showed that MALAT1 functioned as a competing endogenous RNA to sponge miR-320a-5p, leading to upregulation of Runx2 and thus promoting osteogenic differentiation of hRIFs. CONCLUSION: Ectopic calcification and MALAT1 partially contributed to the formation of RP, in which MALAT1 might promote Runx2 expression to regulate osteogenic differentiation of hRIFs by sponging miRNA-320a-5p. The current study sheds new light on the lncRNA-directed mechanism of RP formation via a process driven by osteogenic-like cells.	NA	Front Cell Dev Biol. 2021 Jan 11;8:596363. doi: 10.3389/fcell.2020.596363. eCollection 2020.
4876	LncRNA	MALAT1	miR-150-5p	ZBTB4	peripheral blood mononuclear cells	Systemic Juvenile Idiopathic Arthritis	Homo sapiens (human)	Rescue assay;	33341002	Suppression of lncRNA MALAT1 reduces pro-inflammatory cytokines production by regulating miR-150-5p/ZBTB4 axis through JAK/STAT signal pathway in systemic juvenile idiopathic arthritis.	Systemic juvenile idiopathic arthritis (sJIA) is a common chronic disease occurring in children. Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of diverse human diseases. This study aimed to explore the role of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and its mechanism in sJIA. We found that the expression of MALAT1, the plasma level of pro-inflammatory cytokines (IL-6, IL-17, IL-1β, and TNF-α) as well as MMP-8 and MMP-9 production were significantly elevated in sJIA patients. Moreover, we observed that the production of these cytokines in peripheral blood mononuclear cells (PBMCs) from sJIA patients were reduced after MALAT1 knockdown. Furthermore, bioinformatics analysis predicted that MALAT1 might bind to miR-150-5p and ZBTB4 was a downstream target gene of miR-150-5p. Besides, rescue assays revealed that MALAT1 knockdown-mediated suppressive effects on cytokine production could be reversed by ZBTB4 overexpression. In addition, MALAT1 activated the JAK/STAT signaling by upregulating ZBTB4 expression. In summary, our findings demonstrated that MALAT1 promoted pro-inflammatory cytokine and MMP production by targeting the miR-150-5p/ZBTB4 axis through JAK/STAT signaling pathway in sJIA, suggesting that MALAT1 may have a potential diagnostic biomarker for the pathogenesis and therapy of sJIA.	NA	Cytokine. 2021 Feb;138:155397. doi: 10.1016/j.cyto.2020.155397. Epub 2020 Dec 16.
4877	LncRNA	MAPKAPK5-AS1	miR-519e-5p	YWHAH	thyroid cancer cells	Thyroid Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Rescue assay;	33272009	IncRNA MAPKAPK5-AS1 promotes proliferation and migration of thyroid cancer cell lines by targeting miR-519e-5p/YWHAH.	Thyroid cancer is a common malignant tumour of the endocrine system and ranks ninth in cancer incidence worldwide. An extensive body of evidence has demonstrated that lncRNAs play a critical role in the progression of thyroid cancer. The lncRNA MAPKAPK5-AS1 has been reported to be abnormally expressed and to play a role in the development of various human cancers. However, MAPKAPK5-AS1's potential role in thyroid cancer progression remains unknown. The objective of our study was to explore the role and mechanism of MAPKAPK5-AS1 in thyroid cancer cells and provide a potential target for its biological diagnosis and treatment. We transfected sh-MAPKAPK5-AS1 and sh-NC into BCPAP and TPC-1 cells for loss-of-function assays. Results of RT-qPCR analysis demonstrated that MAPKAPK5-AS1 was more highly expressed in thyroid cancer cells compared to normal cells. Functional assays demonstrated that interfering with the expression of MAPKAPK5-AS1 notably repressed proliferation and invasion and accelerated apoptosis of BCPAP and TPC-1 cells. Mechanistically, we found that miR-519e-5p was negatively regulated by MAPKAPK5-AS1 and that tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta (YWHAH) was a target of miR-519e-5p. Additionally, rescue assays demonstrated that downregulation of MAPKAPK5-AS1 expression inhibited cell proliferation, migration, and invasion and promoted apoptosis by sponging miR-519e-5p, thereby increasing YWHAH expression. Ultimately, our study revealed that MAPKAPK5-AS1 promotes proliferation and migration of thyroid cancer cells by targeting the miR-519e-5p/YWHAH axis, which provides novel insight into the development and progression of thyroid cancer.	NA	Eur J Histochem. 2020 Dec 3;64(4):3177. doi: 10.4081/ejh.2020.3177.
4878	LncRNA	MCM3AP-AS1	miR-138	FOXC1	gastric cancer cells	Gastric Cancer	Homo sapiens (human)	Western blot;	33510812	MCM3AP-AS1 promotes cisplatin resistance in gastric cancer cells via the miR-138/FOXC1 axis.	The dysregulation of long non-coding RNAs (lncRNAs) serves a pivotal role in the pathogenesis and development of multiple types of human cancer, including gastric cancer (GC). MCM3AP-antisense 1 (MCM3AP-AS1) has been reported to function as a tumor promoter in various types of cancer. However, the biological function of MCM3AP-AS1 in the resistance of GC cells to cisplatin (CDDP) remains to be elucidated. The present study aimed to elucidate the mechanisms of MCM3AP-AS1 in the resistance of GC cells to CDDP. The expression levels of MCM3AP-AS1, miR-138 and FOXC1 were measured via reverse transcription-quantitative PCR. In addition, cell viability, migration and invasion were assessed via the Cell Counting Kit-8, wound healing and transwell assays, respectively. The interaction between genes was confirmed via the dual-luciferase reporter and pull-down assays. Western blot analysis was performed to detect FOXC1 protein expression. In the present study, it was demonstrated that MCM3AP-AS1 expression was upregulated in CDDP-resistant GC cells and that MCM3AP-AS1-knockdown suppressed CDDP resistance in GC cells. Moreover, the examination of the molecular mechanism indicated that MCM3AP-AS1 upregulated FOXC1 expression by sponging microRNA (miR)-138. Additionally, it was identified that the overexpression of FOXC1 abolished MCM3AP-AS1-knockdown- or miR-138 mimic-mediated inhibitory effects on CDDP resistance in GC cells. In conclusion, the present findings suggested that MCM3AP-AS1 enhanced CDDP resistance by sponging miR-138 to upregulate FOXC1 expression, indicating that MCM3AP-AS1 may be a novel promising biomarker for the diagnosis and treatment of patients with GC.	NA	Oncol Lett. 2021 Mar;21(3):211. doi: 10.3892/ol.2021.12472. Epub 2021 Jan 18.
4879	LncRNA	MCM3AP-AS1	miR-19a-3p	FOXF2	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33450091	lncRNA MCM3AP-AS1 inhibits the progression of colorectal cancer via the miR-19a-3p/FOXF2 axis.	BACKGROUND: Long non-coding RNA MCM3AP antisense RNA 1 (lncRNA MCM3AP-AS1) has a regulatory role in the development of diverse malignancies, whereas its role and mechanism in colorectal cancer (CRC) is not yet clear. METHODS: The relative expression of MCM3AP-AS1, miR-19a-3p and forkhead box F2 (FOXF2) mRNA in 53 cases of CRC and its adjacent normal tissues, human normal colonic mucosal cells (FHC cells) and CRC cell lines was examined by a quantitative real-time polymerase chain reaction, and the changes of cell multiplication and migration were examined by the cell counting kit-8 method, EdU test, and scratch-healing test, respectively. Bioinformatics, dual-luciferase reporter gene assay and a RNA immunoprecipitation experiment were adopted to predict and verify the relationship between MCM3AP-AS1 and miR-19a-3p; bioinformatics and dual-luciferase reporter gene assay were adopted to predict and verify the relationship between miR-19a-3p and FOXF2. Western blotting was executed to examine the effects of MCM3AP-AS1 overexpression or knockdown on FOXF2 protein expression. RESULTS: MCM3AP-AS1 expression was down-modulated in CRC, and its dysregulation was linked to unfavorable pathological characteristics. MCM3AP-AS1 significantly impeded the multiplication and migration of CRC cells. MCM3AP-AS1 was recognized as a molecular sponge to suppress miR-19a-3p expression, and FOXF2 was a target gene of miR-19a-3p. MCM3AP-AS1 positively modulated FOXF2 expression, and its biological effect was dependent the on miR-19a-3p/FOXF2 axis. CONCLUSIONS: MCM3AP-AS1 can inhibit CRC promoting by modulating the miR-19a-3p/FOXF2 axis.	NA	J Gene Med. 2021 Mar;23(3):e3306. doi: 10.1002/jgm.3306. Epub 2021 Jan 19.
4880	LncRNA	MIAT	miR-613	NA	laryngeal squamous cell carcinoma tissues cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33603840	Long non-coding RNA MIAT promotes the proliferation and invasion of laryngeal squamous cell carcinoma cells by sponging microRNA-613.	Accumulating evidence indicates that the long non-coding RNA myocardial infarction associated transcript (lncRNA MIAT) serves an important role in the progression of a number of cancer types. However, the precise molecular mechanism of MIAT in laryngeal squamous cell carcinoma (LSCC) progression remain elusive. The aim of the current study was to assess the effects and to clarify the molecular mechanism of MIAT on the proliferation and invasion of LSCC cells. The expression of MIAT was detected in LSCC tissues and cells using reverse transcription-quantitative PCR. MTT and colony formation assays were performed to examine the effects of MIAT on the proliferation of LSCC cells. Additionally, wound healing and Transwell experiments were employed to examine cellular migration and invasion. Luciferase reporter gene assay was also used to confirm the direct binding between MIAT and microRNA (miR)-613 in LSCC cells. An RNA immunoprecipitation assay was performed to verify the interaction between MIAT and miR-613. In the present study, it was found that the expression of MIAT in LSCC tissues was markedly higher compared with that in adjacent non-tumor tissues. In addition, MIAT expression was also increased in the human LSCC cell lines TU686, TU-177 and AMC-HN-8 compared with that in normal human keratinocytes (HaCaT). Knocking down MIAT expression significantly reduced LSCC cell proliferation and inhibited colony formation, a shown by MTT and colony formation assays, respectively. MIAT knockdown also substantially inhibited the migratory and invasive abilities of LSCC cells, as shown by wound healing and Transwell invasion assays, respectively. Subsequently, luciferase reporter assays verified that MIAT could bind to miR-613, where a negative correlation was observed between the expression of MIAT and miR-613 in LSCC tissues. Suppression of miR-613 partially reversed the inhibitory effects of MIAT knockdown on the proliferation, migration and invasion of LSCC cells. Taken together, the present study identified that MIAT may function as an oncogenic lncRNA to promote LSCC progression, which provides a potential therapeutic target or as a novel diagnostic biomarker for LSCC.	NA	Exp Ther Med. 2021 Mar;21(3):232. doi: 10.3892/etm.2021.9663. Epub 2021 Jan 21.
4881	LncRNA	MIR205HG	miR-214	SOX4	Esophageal squamous cell carcinoma tissues and cell lines	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;Rescue assay;	33376358	LncRNA MIR205HG Drives Esophageal Squamous Cell Carcinoma Progression by Regulating miR-214/SOX4 Axis.	BACKGROUND: Esophageal squamous cell carcinoma (ESCC) is a common and fatal malignancy, which has posed a great challenge to public health, especially in China. Dysregulation of long non-coding RNAs is involved in the occurrence, development, invasion, and metastasis of multiple cancers including ESCC. However, little is known about the function of MIR205HG in ESCC. METHODS: We used qRT-PCR to detect the expression level of MIR205HG, miR-214, and SOX4 in human ESCC tissues and cell lines. Loss-of-functional assays were performed to test the impact of MIR205HG on cell proliferation, metastasis, and apoptosis process via CCK-8, transwell, and flow cell cytometry assays. Additionally, the downstream molecular mechanism of MIR205HG in ESCC was explored. RESULTS: Here, we found MIR205HG was substantially up-regulated in ESCC, and there was a positive correlation between MIR205HG expression and tumor size and lymphatic metastasis of ESCC patients. Inhibition of MIR205HG attenuated cell proliferation, migration, and invasion. Silencing MIR205HG increased G1 phase cell counts and decreased S phase cell counts, along with increased apoptotic cell populations. Notably, the rescue assays indicated that miR-214 could partly reverse the influence of MIR205HG on ESCC cell migration. We also found that SOX4 was a direct target mRNA of miR-214, and MIR205HG could act as a molecular sponge to regulate SOX4 expression in ESCC. CONCLUSION: Taken together, our findings demonstrate that MIR205HG promotes ESCC progression by regulating the miR-214/SOX4 axis. MIR205HG may be a novel candidate target for ESCC diagnosis and therapy.	NA	Onco Targets Ther. 2020 Dec 22;13:13097-13109. doi: 10.2147/OTT.S286627. eCollection 2020.
4882	LncRNA	MNX1-AS1	miR-744-5p	NA	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	Western blot;Luciferase report assay;	33590038	Long noncoding RNA MNX1-AS1 functions as a competing endogenous RNA to regulate epithelial-mesenchymal transition by sponging MiR-744-5p in colorectal cancer.	Colorectal cancer (CRC) is the fourth most deadly cancer globally. Long noncoding RNA MNX1-AS1 has been proven to play a regulatory role in various human cancers. The present research aimed to explore the MNX1-AS1 function in CRC and the corresponding mechanism. A series of experiments were conducted to detect the effects of MNX1-AS1 and miR-744-5p on the biological function of CRC cells, including quantitative reverse transcription-polymerase chain reaction, CCK-8, transwell, wound healing assay, Western blot, and dual-luciferase report assay. MNX1-AS1 was elevated in CRC tissues and cell lines. Si-MNX1-AS1 inhibited cell viability, invasion, migration, and the protein expressions of N-cadherin and Vimentin but promoted the protein expression of E-cadherin. MiR-744-5p bound to MNX1-AS1. MiR-744-5p inhibitor had the opposite effect of si-MNX1-AS1. Cotransfection of miR-744-5p inhibitor and si-MNX1-AS1 recovered the effects mentioned above. In conclusion, MNX1-AS1/miR-744-5p axis plays a pivotal role in the viability, invasion, migration, and epithelial-mesenchymal transition of colorectal cancer cells.	NA	Biosci Biotechnol Biochem. 2021 Feb 24;85(3):568-578. doi: 10.1093/bbb/zbaa096.
4883	LncRNA	NEAT1	miR-98-5p	BZW1	glioma cells	Glioma	Homo sapiens (human)	Western blot;luciferase assay;Luciferase reporter assay;	33393590	LncRNA NEAT1 promotes glioma cancer progression via regulation of miR-98-5p/BZW1.	BACKGROUND: Glioma is the most common malignant tumor in the human central nervous system. Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes oncogenesis in various tumors. In the present study, we aimed to examine the role of NEAT1 in altering the properties of gliomas. METHODS: Quantitative real-time PCR technology was used to determine the expression levels of relevant genes in tumor tissues and cell lines. The protein expression levels were validated by Western blotting. CCK-8 and colony formation assays were used to test the cell proliferation ability. A luciferase reporter assay was used to determine the interactions of the genes. Tumor xenografts were used to detect the role of NEAT1 in gliomas in vivo. RESULTS: We demonstrated that NEAT1 was upregulated glioma cells and negatively correlated with miR-98-5p in glioma tissues. A potential binding region between NEAT1 and miR-98-5p was confirmed by dual-luciferase assays. NEAT1 knockdown inhibited glioma cell proliferation. The inhibition of miR-98-5p rescued the knockdown of NEAT1 in glioma cells. BZW1 was identified as a direct target of miR-98-5p. We also identified that BZW1 was positively correlated with NEAT1 in glioma tissues. NEAT1 knockdown inhibited glioma cell proliferation in vivo via miR-98-5p/BZW1. CONCLUSION: Our results suggest that NEAT1 plays an oncogenic function in glioma progression. Targeting NEAT1/miR-98-5p/BZW1 may be a novel therapeutic treatment approach for glioma patients.	NA	Biosci Rep. 2021 Jan 4:BSR20200767. doi: 10.1042/BSR20200767.
4884	LncRNA	NORAD	miR-150-5p	ZEB1	HG-induced AC16 cells	Diabetic Cardiomyopathy	Homo sapiens (human)	qRT-PCR;	33215445	NORAD regulates proliferation and apoptosis in cardiomyocytes under high-glucose treatment through miRNA-150-5p/ZEB1 axis.	OBJECTIVE: The purpose of this study was to uncover the potential role of non-coding RNA activated by DNA damage (lncRNA NORAD) in the disease progression of diabetic cardiomyopathy (DCM) and the underlying mechanism. MATERIALS AND METHODS: Cell viability, 5-Ethynyl-2'-deoxyuridine (EdU)-positive ratio and apoptotic rate in human cardiomyocyte cell line AC16 undergoing treatment of normal-level (NG) or high-level glucose (HG) were assessed at first. NORAD level in HG-induced AC16 cells at different time points was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Subsequently, cell viability, EdU-positive ratio, and apoptotic rate in HG-induced AC16 cells overexpressing NORAD were evaluated. Next, subcellular distribution of NORAD was examined, and Dual-Luciferase reporter gene assay was performed to clarify the interaction among NORAD, miRNA-150-5p, and ZEB1. At last, rescue experiments were conducted to clarify the role of NORAD/miRNA-150-5p/ZEB1 axis in influencing the proliferation and apoptosis in HG-induced AC16 cells. RESULTS: Results revealed that HG treatment suppressed the proliferative ability and stimulated apoptosis in AC16 cells. Besides, NORAD was time-dependently downregulated in HG-induced AC16 cells, and it was mainly distributed in cytoplasm. In addition, the overexpression of NORAD enhanced proliferative ability, attenuated apoptosis, and increased Bcl-2/Bax ratio in HG-induced AC16 cells. Finally, NORAD/miRNA-150-5p/ZEB1 axis was verified to protect the malignant progression of DCM. CONCLUSIONS: NORAD is upregulated under high-level glucose treatment. Overexpression of NORAD protects DCM development via miRNA-150-5p/ZEB1 axis.	NA	Eur Rev Med Pharmacol Sci. 2020 Nov;24(21):11259-11265. doi: 10.26355/eurrev_202011_23615.
4885	LncRNA	OIP5-AS1	miR-186-5p	CTRP3	injury and microglial cells	Neuron Injury	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Luciferase report assay;RNA immunoprecipitation;	33516048	Up-regulating lncRNA OIP5-AS1 protects neuron injury against cerebral hypoxia-ischemia induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	BACKGROUND: Inflammation and oxidative stress is closely associated with the development of ischemic brain stroke. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long non-coding RNA (lncRNA), has been suggested to play an important role in the development of many types of human cancers. However, the functional involvement of OIP5-AS1 in ischemic stroke is still unknown. METHODS: Quantitative real-time polymerase chain reaction and /or western blot were conducted to determine the expression profiles of OIP5-AS1, C1q/TNF-related protein 3 (CTRP3) and miR-186-5p in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and microglial cells treated with oxygen glucose deprivation/re-oxygenation (OGD/R). Upon selective regulation of OIP5-AS1 and miR-186-5p, the inflammation and oxidative stress responses in microglia/macrophage as well as neurologic functions in MCAO/R rats were detected. Furthermore, the interactions between OIP5-AS1 and miR-186-5p, miR-186-5p and CTRP3 were investigated by RNA immunoprecipitation (RIP) assay, luciferase report assay and bioinformation anaylsis. RESULTS: We observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis. CONCLUSION: Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	NA	Int Immunopharmacol. 2021 Mar;92:107339. doi: 10.1016/j.intimp.2020.107339. Epub 2021 Jan 27.
4886	LncRNA	OIP5-AS1	miR-186-5p	CTRP3	injury and microglial cells	Cerebral Hypoxia-Ischemia Induced Inflammation	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Luciferase report assay;RNA immunoprecipitation;	33516048	Up-regulating lncRNA OIP5-AS1 protects neuron injury against cerebral hypoxia-ischemia induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	BACKGROUND: Inflammation and oxidative stress is closely associated with the development of ischemic brain stroke. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long non-coding RNA (lncRNA), has been suggested to play an important role in the development of many types of human cancers. However, the functional involvement of OIP5-AS1 in ischemic stroke is still unknown. METHODS: Quantitative real-time polymerase chain reaction and /or western blot were conducted to determine the expression profiles of OIP5-AS1, C1q/TNF-related protein 3 (CTRP3) and miR-186-5p in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and microglial cells treated with oxygen glucose deprivation/re-oxygenation (OGD/R). Upon selective regulation of OIP5-AS1 and miR-186-5p, the inflammation and oxidative stress responses in microglia/macrophage as well as neurologic functions in MCAO/R rats were detected. Furthermore, the interactions between OIP5-AS1 and miR-186-5p, miR-186-5p and CTRP3 were investigated by RNA immunoprecipitation (RIP) assay, luciferase report assay and bioinformation anaylsis. RESULTS: We observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis. CONCLUSION: Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	NA	Int Immunopharmacol. 2021 Mar;92:107339. doi: 10.1016/j.intimp.2020.107339. Epub 2021 Jan 27.
4887	LncRNA	OIP5-AS1	miR-186-5p	CTRP3	injury and microglial cells	Oxidative Stress	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;Western blot;Luciferase report assay;RNA immunoprecipitation;	33516048	Up-regulating lncRNA OIP5-AS1 protects neuron injury against cerebral hypoxia-ischemia induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	BACKGROUND: Inflammation and oxidative stress is closely associated with the development of ischemic brain stroke. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1), a novel identified long non-coding RNA (lncRNA), has been suggested to play an important role in the development of many types of human cancers. However, the functional involvement of OIP5-AS1 in ischemic stroke is still unknown. METHODS: Quantitative real-time polymerase chain reaction and /or western blot were conducted to determine the expression profiles of OIP5-AS1, C1q/TNF-related protein 3 (CTRP3) and miR-186-5p in the serum of stroke patients, as well as in the ischemic penumbra of rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury and microglial cells treated with oxygen glucose deprivation/re-oxygenation (OGD/R). Upon selective regulation of OIP5-AS1 and miR-186-5p, the inflammation and oxidative stress responses in microglia/macrophage as well as neurologic functions in MCAO/R rats were detected. Furthermore, the interactions between OIP5-AS1 and miR-186-5p, miR-186-5p and CTRP3 were investigated by RNA immunoprecipitation (RIP) assay, luciferase report assay and bioinformation anaylsis. RESULTS: We observed markedly increased infarct volume, neuronal apoptosis, inflammation and oxidative stress responses in the infarcted lesions of MCAO/R rats, in line with down-regulated levels of OIP5-AS1 and CTRP3 while up-regulated miR-186-5p. Functional studies demonstrated that up-regulation of OIP5-AS1 attenuated infarct volume, neuronal apoptosis, microglia/macrophage inflammation and oxidative stress responses induced by MCAO/R or OGD/R. In terms of mechanism, we revealed that OIP5-AS1-miR-186-5p-CTRP3 axis played a vital role in modulating microglia/macrophage activation and neuronal apoptosis. CONCLUSION: Up-regulating lncRNA OIP5-AS1 protects neuron injury against MCAO/R induced inflammation and oxidative stress in microglia/macrophage through activating CTRP3 via sponging miR-186-5p.	NA	Int Immunopharmacol. 2021 Mar;92:107339. doi: 10.1016/j.intimp.2020.107339. Epub 2021 Jan 27.
4888	LncRNA	PAICC	miR-141-3p	YAP1	Intrahepatic cholangiocarcinoma cells	Intrahepatic Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR	33552968	Long Non-Coding RNA-PAICC Promotes the Tumorigenesis of Human Intrahepatic Cholangiocarcinoma by Increasing YAP1 Transcription.	Intrahepatic cholangiocarcinoma (ICC) is a heterogeneous hepatobiliary tumor with poor prognosis, and it lacks reliable prognostic biomarkers and effective therapeutic targets. Long non-coding RNAs (lncRNAs) have been documented to be involved in the progression of various cancers. However, the role of lncRNAs in ICC remains largely unknown. In the present work, we used bioinformatics analysis to identify the differentially expressed lncRNAs in human ICC tissues, among which lncRNA-PAICC was found to be an independent prognostic marker in ICC. Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-3p. The competitive binding property was essential for lncRNA-PAICC to promote tumor growth and metastasis through activating the Hippo pathway. In summary, our results highlighted the important role of the lncRNA-PAICC-miR-141-3p/27a-3p-Yap1 axis in ICC, which offers a novel perspective on the molecular pathogenesis and may serve as a potential target for antimetastatic molecular therapies of ICC.	NA	Front Oncol. 2021 Jan 8;10:595533. doi: 10.3389/fonc.2020.595533. eCollection 2020.
4889	LncRNA	PAICC	miR-27a-3p	YAP1	Intrahepatic cholangiocarcinoma cells	Intrahepatic Cholangiocarcinoma	Homo sapiens (human)	qRT-PCR	33552968	Long Non-Coding RNA-PAICC Promotes the Tumorigenesis of Human Intrahepatic Cholangiocarcinoma by Increasing YAP1 Transcription.	Intrahepatic cholangiocarcinoma (ICC) is a heterogeneous hepatobiliary tumor with poor prognosis, and it lacks reliable prognostic biomarkers and effective therapeutic targets. Long non-coding RNAs (lncRNAs) have been documented to be involved in the progression of various cancers. However, the role of lncRNAs in ICC remains largely unknown. In the present work, we used bioinformatics analysis to identify the differentially expressed lncRNAs in human ICC tissues, among which lncRNA-PAICC was found to be an independent prognostic marker in ICC. Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-3p. The competitive binding property was essential for lncRNA-PAICC to promote tumor growth and metastasis through activating the Hippo pathway. In summary, our results highlighted the important role of the lncRNA-PAICC-miR-141-3p/27a-3p-Yap1 axis in ICC, which offers a novel perspective on the molecular pathogenesis and may serve as a potential target for antimetastatic molecular therapies of ICC.	NA	Front Oncol. 2021 Jan 8;10:595533. doi: 10.3389/fonc.2020.595533. eCollection 2020.
4890	LncRNA	RAD51-AS1	miR-29b-3p	NDRG2	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33314669	LncRNA RAD51-AS1/miR-29b/c-3p/NDRG2 crosstalk repressed proliferation, invasion and glycolysis of colorectal cancer.	LncRNAs are recently increasingly emerging as molecules that take its part in human carcinogenesis. A large body of literature has identified the functional roles of lncRNAs in the pathophysiology of CRC. The current study was intended to provide new ideas and perspectives for the functional role of lncRNA RAD51-AS1 in regulating CRC progression. Herein, a survey of RAD51-AS1 expression profile in The Cancer Genome Atlas (TCGA)-colon adenocarcinoma (COAD) dataset revealed that RAD51-AS1 was downregulated in COAD specimens. Consistently, RAD51-AS1 expression was observed to be lower in CRC cell lines compared with normal cell line (NCM460). In the meanwhile, both the levels of miR-29b-3p and miR-29c-3p were prominently elevated in CRC cells. Functionally, administration of RAD51-AS1 refrained growth, invasion and migration of CRC cells. Additionally, accumulation of RAD51-AS1 hampered glucose consumption and lactate production, as well as the restraint of hexokinase 2 (HK2) and glucose transporter 1 (GLUT1) levels. More important, RAD51-AS1 functioned as a competing endogenous RNA (ceRNA) for sponging miR-29b-3p and miR-29c-3p, leading to enhancement of their common target N-myc downstream-regulated gene 2 (NDRG2). Mechanistically, the delivery of miR-29b/c-3p mimics or ablation of NDRG2 effectively blunted the salutary effects of RAD51-AS1 on CRC cell behaviors. Moreover, augmentation of RAD51-AS1 inhibited the tumorigenesis of CRC cells in vivo. Collectively, these findings provide comprehensive evidence that RAD51-AS1 repressed cell proliferation, migration, invasion and glycolysis process, ultimately contributing to the progression of CRC by repressing the miR-29b/c-3p/NDRG2 signaling axis, insinuating the putative potential of RAD51-AS1/miR-29b/c-3p/NDRG2 interaction network in unraveling CRC pathology and hopefully contributed to the treatment of CRC patients.	NA	IUBMB Life. 2021 Jan;73(1):286-298. doi: 10.1002/iub.2427. Epub 2020 Dec 12.
4891	LncRNA	RAD51-AS1	miR-29c-3p	NDRG2	colorectal cancer cells	Colorectal Cancer	Homo sapiens (human)	qRT-PCR	33314669	LncRNA RAD51-AS1/miR-29b/c-3p/NDRG2 crosstalk repressed proliferation, invasion and glycolysis of colorectal cancer.	LncRNAs are recently increasingly emerging as molecules that take its part in human carcinogenesis. A large body of literature has identified the functional roles of lncRNAs in the pathophysiology of CRC. The current study was intended to provide new ideas and perspectives for the functional role of lncRNA RAD51-AS1 in regulating CRC progression. Herein, a survey of RAD51-AS1 expression profile in The Cancer Genome Atlas (TCGA)-colon adenocarcinoma (COAD) dataset revealed that RAD51-AS1 was downregulated in COAD specimens. Consistently, RAD51-AS1 expression was observed to be lower in CRC cell lines compared with normal cell line (NCM460). In the meanwhile, both the levels of miR-29b-3p and miR-29c-3p were prominently elevated in CRC cells. Functionally, administration of RAD51-AS1 refrained growth, invasion and migration of CRC cells. Additionally, accumulation of RAD51-AS1 hampered glucose consumption and lactate production, as well as the restraint of hexokinase 2 (HK2) and glucose transporter 1 (GLUT1) levels. More important, RAD51-AS1 functioned as a competing endogenous RNA (ceRNA) for sponging miR-29b-3p and miR-29c-3p, leading to enhancement of their common target N-myc downstream-regulated gene 2 (NDRG2). Mechanistically, the delivery of miR-29b/c-3p mimics or ablation of NDRG2 effectively blunted the salutary effects of RAD51-AS1 on CRC cell behaviors. Moreover, augmentation of RAD51-AS1 inhibited the tumorigenesis of CRC cells in vivo. Collectively, these findings provide comprehensive evidence that RAD51-AS1 repressed cell proliferation, migration, invasion and glycolysis process, ultimately contributing to the progression of CRC by repressing the miR-29b/c-3p/NDRG2 signaling axis, insinuating the putative potential of RAD51-AS1/miR-29b/c-3p/NDRG2 interaction network in unraveling CRC pathology and hopefully contributed to the treatment of CRC patients.	NA	IUBMB Life. 2021 Jan;73(1):286-298. doi: 10.1002/iub.2427. Epub 2020 Dec 12.
4892	LncRNA	MALAT1	miR-375	PDE4D	PC-12 cells	Cerebral Ischemic-Reperfusion Injury	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33519668	Long Non-coding RNAMALAT1 Knockdown Alleviates Cerebral Ischemia/Reperfusion Injury of Rats Through Regulating the miR-375/PDE4D Axis.	Objectives: Cerebral ischemic/reperfusion injury (CI/RI) is the clinical manifestation of cerebral ischemic stroke, which severely affects the health and life of the patients. We aimed to investigate the regulatory mechanism of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on CI/RI in this study. Methods: The expression of lncRNA MALAT1 and miR-375 was detected by qRT-PCR. MTT was utilized to measure the viability of PC-12 cells. The levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and reactive oxygen species (ROS) were detected by LDH assay, SOD assay, and ROS assay, respectively. The apoptosis rate of PC-12 cells was measured by flow cytometry analysis. Through enzyme-linked immunosorbent assay, the levels of NF-α, IL-1β, and IL-6 were determined. The interactions between miR-375 and MALAT1/PDE4D were predicted by Starbase/Targetscan software and verified by the dual-luciferase reporter assay. Western blot assay was performed to determine the protein expression of Bcl-2, Caspase-3, and PDE4D. Results: LncRNA MALAT1 expression was highly upregulated in the middle cerebral artery occlusion (MCAO)/reperfusion (R) model of rats. Both MALAT1 downregulation and miR-375 upregulation reversed the inhibitory effect of oxygen and glucose deprivation (OGD)/R on cell viability and the promoting effects on LDH level, cell apoptosis, and inflammatory factors levels. MALAT1 targeted miR-375, whereas miR-375 targeted PDE4D. Overexpression of miR-375 attenuated OGD/R-induced injury in PC-12 cells by targeting PDE4D. Both the low expression of miR-375 and high expression of PDE4D reversed the promoting effect of MALAT1 knockdown on SOD level and the inhibitory effects on ROS level, inflammatory factor levels, and cell apoptosis. Conclusion: Suppression of MALAT1 alleviates CI/RI of rats through regulating the miR-375/PDE4D axis. This study provides a possible therapeutic strategy for human CI/RI in clinic.	NA	Front Neurol. 2021 Jan 14;11:578765. doi: 10.3389/fneur.2020.578765. eCollection 2020.
4893	LncRNA	SNHG15	miR-455-3p	TP53INP1	P12 cells	Ogd/R-Induced Injury	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	33528807	LncRNA SNHG15 Knockdown Protects Against OGD/R-Induced Neuron Injury by Downregulating TP53INP1 Expression via Binding to miR-455-3p.	Cerebral ischemia-reperfusion (I/R) injury is the common symptom of ischemic stroke, which poses a heavy burden to human health. Long non-coding RNA (lncRNA) is indicated to be a critical regulator in cerebral ischemia. This study aims to reveal the effects of lncRNA small nucleolar RNA host gene 15 (SNHG15) on oxygen-glucose deprivation and reoxygenation (OGD/R)-induced neuron injury and underlying mechanism. The expression levels of SNHG15, microRNA-455-3p (miR-455-3p) and tumour protein p53 inducible nuclear protein 1 (TP53INP1) mRNA were determined by quantitative real time polymerase chain reaction in P12 cells. The protein levels of TP53INP1, cleaved caspase-3, caspase-3, B-cell lymphoma-2 and BCL2-associated x protein (Bax) were detected by western blot in P12 cells. Cell viability and apoptosis were revealed by cell counting kit-8 assay and flow cytometry analysis, respectively, in P12 cells. Caspase-3 activity, the levels of tumor necrosis factor-α and interleukin-1β and the production of reactive oxygen species (ROS) were severally determined by caspase-3 activity assay, Enzyme-linked immunosorbent assay and ROS detection assay in P12 cells. The binding relationship between miR-455-3p and SNHG15 or TP53INP1 was predicted by starbase online database, and identified by dual-luciferase reporter, RNA pull-down or RNA immunoprecipitation assay. SNHG15 expression and the mRNA and protein levels of TP53INP1 were dramatically upregulated, while miR-455-3p expression was apparently downregulated in OGD/R-induced PC12 cells. SNHG15 silencing hindered the effects of OGD/R treatment on cell viability, apoptosis, inflammation and oxidative in PC12 cells; however, these impacts were restored after miR-455-3p inhibitor transfection. Additionally, SNHG15 acted as a sponge of miR-455-3p and miR-455-3p bound to TP53INP1. SNHG15 contributed to OGD/R-induced neuron injury by regulating miR-455-3p/TP53INP1 axis, which provided a novel insight to study lncRNA-directed therapy in ischemia stoke.	NA	Neurochem Res. 2021 Apr;46(4):1019-1030. doi: 10.1007/s11064-020-03222-9. Epub 2021 Feb 2.
4894	LncRNA	SNHG16	miR-195	mfn2	retinal microvascular endothelial cells	Diabetic Retinopathy	Homo sapiens (human)	RIP assay;Luciferase reporter assay;	33530902	Decreased lncRNA SNHG16 Accelerates Oxidative Stress Induced Pathological Angiogenesis in Human Retinal Microvascular Endothelial Cells by Regulating miR-195/mfn2 Axis.	BACKGROUND: This study was performed to identify the alterations of Long non-coding RNAs (lncRNAs) induced by oxidative stress and investigate the functional roles of SNHG16 in the pathological angiogenesis by human retinal microvascular endothelial cells (HMRECs). METHODS: The expression profiles of lncRNAs and mRNAs induced by oxidative stress were identified by RNA-Seq, and the dysregulation of 16 lncRNAs including SNHG16 were verified in H2O2-treated human umbilical vein endothelial cells (HUVECs). Luciferase reporter assay and RIP analysis were used to investigate the binding relationship of SNHG16 to miR-195. RESULTS: We confirmed that over-expression of SNGH16 attenuated H2O2-induced angiogenesis by HMRECs. In addition, SNHG16 was significantly decreased whereas miR-195, a predictive target of SNHG16, was upregulated in H2O2, HG, and AGE-treated HMRECs. The binding relationship of SNHG16 to miR-195 was subsequently verified by luciferase reporter assay and RIP analysis. SNHG16 cotransfection abolished miR-195-mediated repression on mitofusin 2 (mfn2) protein level and counteracted the inductive effect of miR-195 on angiogenesis by HMRECs. CONCLUSION: These results indicated that decreased SNHG16 accelerates oxidative stress induced pathological angiogenesis in HMRECs by regulating miR-195/mfn2 axis, providing a potential target for diabetic retinopathy (DR) therapy.	NA	Curr Pharm Des. 2021 Feb 2. doi: 10.2174/1381612827666210202141541.
4895	LncRNA	SNHG17	miR-942	NA	pancreatic carcinoma cells	Pancreatic Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	33841638	lncRNA SNHG17 promotes pancreatic carcinoma progression via cross-talking with miR-942.	OBJECTIVE: Long non-coding RNA (lncRNA) SNHG17 has been shown to modulate the biological behavior of multiple cancers (e.g., colorectal and lung cancers). However, its involvement in pancreatic cancer (PC) has not been explored; therefore, in the present study, we sought to examine this involvement. METHODS: First, the mRNA expression levels of various genes were quantified in PC tissues and cell lines using quantitative reverse-transcription PCR (qRT-PCR). The interaction between SNHG17 and miR-942 was explored by bioinformatics prediction as well as a dual luciferase reporter assay. The proliferation and viability of pancreatic carcinoma cells were examined using cell counting kit-8 and MTT assays, respectively. Cellular migratory and invasive properties were evaluated using transwell migration and wound healing assays. Cell death was measured using flow cytometry. Protein expression was quantified by western blotting. RESULTS: SNHG17 expression was markedly higher in human PC specimens and cell lines than in normal healthy tissues and pancreatic epithelial cells. MiR-942 expression displayed the opposite trend. Bioinformatics prediction and a dual luciferase reporter assay confirmed that SNHG17 serves as a sponge for miR-942. Loss-of-function assay revealed that SNHG17 silencing reduced the proliferation and viability of PC cells, impaired their migratory and invasive capacities, and led to their apoptosis. All these changes could be reversed by miR-942 inhibition. Further mechanical studies showed that SNHG17 silencing decreased the expression of several tumor modulators, including XXX, and this decrease was countered by miR-942 inhibition. CONCLUSION: Our study provides experimental evidence for an interaction between SNHG17 and miR-942, which may unveil a new approach for PC pharmacotherapy.	NA	Am J Transl Res. 2021 Mar 15;13(3):1037-1050. eCollection 2021.
4896	LncRNA	SNHG17	miR-3180-3p	RFX1	Hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	CCK-8 assay;qRT-PCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	33519911	Long Non-coding RNA SNHG17 Upregulates RFX1 by Sponging miR-3180-3p and Promotes Cellular Function in Hepatocellular Carcinoma.	BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common types of cancer that is associated with poor quality of life in patients and a global health burden. The mechanisms involved in the development and progression of HCC remain poorly understood. METHODS: Hepatocellular carcinoma human samples and cell lines were subjected to qRT-PCR for expression assessment. CCK-8 assay, Transwell migration and invasion assay, were applied for cell function detection. Animal experiment was used to measure the function of SNHG17 on cell growth in vivo. Western blot was conducted to evaluate the level of EMT in cells. RIP, RNA pull-down and luciferase reporter assays were performed to assess the correlation between SNHG17, miR-3180-3p and RFX1. RESULTS: Our study demonstrated that SNHG17 was upregulated in HCC human samples and involved cell proliferation, migration, invasion progress. SNHG17 promoted HCC cell growth and metastasis in vivo. Furthermore, we investigated the downstream factor of SNHG17, SNHG17 acted as a molecular sponge for miR-3180-3p, and SNHG17 regulated RFX1 expression via miR-3180-3p. SNHG17 promotes tumor-like behavior in HCC cells via miR-3180-3p/RFX1. CONCLUSION: We determined RFX1 as the target of miR-3810-3p; SNHG17 enhanced the progression of HCC via the miR-3180-3p/RFX1 axis. Taken together, our findings may provide insight into the molecular mechanism involved in the progression of HCC and develop SNHG17 as a novel therapeutic target against HCC.	NA	Front Genet. 2021 Jan 15;11:607636. doi: 10.3389/fgene.2020.607636. eCollection 2020.
4897	LncRNA	SNHG4	miR-let-7e	KDM3A	non-small cell lung cancer cells	Lung Cancer	Homo sapiens (human)	Flow Cytometry assay;	33816782	The long non-coding RNA SNHG4/microRNA-let-7e/KDM3A/p21 pathway is involved in the development of non-small cell lung cancer.	Non-small cell lung cancer (NSCLC) is a foremost cause of malignancy-associated mortality globally. Recent studies have emphasized long non-coding RNAs (lncRNAs) as important biomarkers with diagnostic and therapeutic potential in regard to NSCLC. This study aimed to elucidate the functional role of lncRNA small nucleolar RNA host gene 4 (SNHG4) in NSCLC. Initially, 50 paired cancerous and noncancerous tissues were obtained from NSCLC patients. Human NSCLC H1299 cells were assayed to evaluate viability, colony formation, invasion, migration, cycle arrest, and apoptosis via Cell Counting Kit-8 (CCK-8), plate clone formation, and transwell invasion assays, as well as a scratch test and flow cytometry. A dual-luciferase reporter gene assay was used to examine lncRNA SNHG4 binding with miR-let-7e and miR-let-7e binding with lysine demethylase 3A (KDM3A). H1299 cells were xenografted into nude mice. lncRNAs SNHG4 and KDM3A were both upregulated in NSCLC tissues. The knockdown of lncRNA SNHG4 or KDM3A inhibited H1299 cell viability, colony formation, invasion, migration, and cycle progression while inducing apoptosis. lncRNA SNHG4 was found to bind to miR-let-7e that negatively targeted KDM3A. KDM3A inhibited p53-K372me1, thus reducing p21 expression. The NSCLC development was inhibited by downregulating lncRNA SNHG4 in nude mice. Taken together, the key findings of the current study demonstrate a novel lncRNA SNHG4/let-7e/KDM3A/p21 axis in NSCLC, highlighting a promising therapeutic target for NSCLC.	NA	Mol Ther Oncolytics. 2020 Dec 25;20:634-645. doi: 10.1016/j.omto.2020.12.010. eCollection 2021 Mar 26.
4898	LncRNA	TDRG1	miR-214-5p	SEMA4C	cervical cancer tissues and cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	33394293	Long non-coding RNA TDRG1 promotes hypoxia-induced glycolysis by targeting the miR-214-5p/SEMA4C axis in cervical cancer cells.	Long non-coding RNA (lncRNA) has been demonstrated as vital regulator in human cancer. However, the precise role of lnc-TDRG1 in cervical cancer (CC) remains unclear, so this study was aimed to clarify the role and underlying molecular mechanism of lnc-TDRG1 in CC. The real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to assess the expression levels of lnc-TDRG1, miR-214-5p and Semaphorin 4C (SEMA4C). Under hypoxia condition, the biological behaviors of CC cell, including invasion and glycolysis were determined by transwell assay and Glucose Assay Kit and Lactate Assay Kit, respectively. The Western blot assay was employed to test the expression level of SEMA4C and hexokinase 2 (HK2) expression. The interaction relationship between miR-214-5p and lnc-TDRG1 or SEMA4C was analyzed bioinformatics database and confirmed by dual-luciferase reporter assay, respectively. A xenograft experiment in nude mice was established to clarify the functional role of lnc-TDRG1 in vivo. We found Lnc-TDRG1 was highly expressed in CC tissues and cells and it was upregulated in response to hypoxia. Loss-of-functional experiment suggested that knockdown of lnc-TDRG1 impede invasion, hypoxia-induced glycolysis in vitro and tumor growth in vivo, which was abolished by knockdown of miR-214-5p or overexpression of SEMA4C. Moreover, we confirmed that miR-214-5p specifically bound to SEMA4C and negatively correlated with SEMA4C expression. Collectively, lnc-TDRG1 regulated SEMA4C expression by sponging miR-214-5p in CC. Collectively, mechanistically, lnc-TDRG1 could act as a sponge of miR-214-5p to regulate the expression of SEMA4C, and further regulate invasion and hypoxia-glycolysis in CC cells.	NA	J Mol Histol. 2021 Apr;52(2):245-256. doi: 10.1007/s10735-020-09944-y. Epub 2021 Jan 4.
4899	LncRNA	TUG1	miR-140	TNF	AML12 cells	Hepatitis	Homo sapiens (human)	microarray;qRT-PCR;	33644034	Silencing lncRNA TUG1 Alleviates LPS-Induced Mouse Hepatocyte Inflammation by Targeting miR-140/TNF.	Hepatitis is a major public health problem that increases the risk of liver cirrhosis and liver cancer. Numerous studies have revealed that long non-coding RNAs (lncRNAs) exert essential function in the inflammatory response of multiple organs. Herein, we aimed to explore the effect of lncRNA TUG1 in LPS-induced hepatocyte inflammation response and further illuminate the underlying mechanisms. Mice were intraperitoneally injected with LPS, and the liver inflammation was evaluated. Microarray showed that lncRNA TUG1 was upregulated in LPS-induced hepatocyte inflammation. qRT-PCR and immunofluorescence assay indicated a significant increase of TUG1 in mice with LPS injection. Functional analysis showed that si-TUG1 inhibited LPS-induced inflammation response in mice liver, inhibited apoptosis level, and protected liver function. Then, we knock down TUG1 in normal human hepatocyte AML12. Consistent with in vivo results, si-TUG1 removed the injury of LPS on AML12 cells. Furthermore, TUG1 acted as a sponge of miR-140, and miR-140 directly targeted TNFα (TNF). MiR-140 or si-TNF remitted the beneficial effects of TUG1 on LPS-induced hepatocyte inflammation response both in vitro and in vivo. Our data revealed that deletion of TUG1 protected against LPS-induced hepatocyte inflammation via regulating miR-140/TNF, which might provide new insight for hepatitis treatment.	NA	Front Cell Dev Biol. 2021 Feb 11;8:616416. doi: 10.3389/fcell.2020.616416. eCollection 2020.
4900	LncRNA	UCID	miR-122	Snail	hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;luciferase assay;	33536764	LncRNA UCID Promotes Hepatocellular Carcinoma Metastasis via Stabilization of Snail.	BACKGROUND: LncRNAs are functional regulators in tumor progression which act by regulating mRNAs in multiple types of cancer. However, the effect of lnc-UCID on hepatocellular carcinoma (HCC) metastasisremains unclear. METHODS: Lnc-UCID expression was quantified in HCC tissues and HCC cell lines by qRT-PCR. HCC cell lines with lnc-UCID knockdown were established by lentivirus transduction. The migration and invasion abilities of HCC cells were analyzed by Transwell and wound-healing assays. Protein expression of epithelial-mesenchymal transition (EMT)-related factors was examined by Western blot assay. Dual-luciferase assays and actinomycin D treatment were conducted to explore the relationship between lnc-UCID and Snail mRNA. The direct interaction between lnc-UCID and Snail mRNA was subjected to quantification analysis by biotinylated lnc-UCID pulldown assays. Pearson's correlation coefficient was used to analyze correlations between lnc-UCID and Snail expression level in clinical samples. Rescue experiments were performed to uncover the role of Snail in the HCC metastasis process. RESULTS: Lnc-UCID was upregulated in human HCC tissues and HCC cell lines. Lnc-UCID promoted the cells' mobility and invasiveness by enhancing the EMT process of HCC cells. The expression of Snail positively correlated with lnc-UCID abundance, and the interaction between lnc-UCID and Snail mRNA prevented miR-122, miR-203, miR-30b, miR-34a or miR-153 binding to the 3'-UTR of Snail. Transfection of Snail greatly rescued the migration and invasion of HCC cells. CONCLUSION: Lnc-UCID was upregulated in clinical HCC samples and directly interacted with Snail mRNA to enhance the stability of Snail mRNA, thus promoting the EMT process to accelerate HCC metastasis.	NA	Onco Targets Ther. 2021 Jan 28;14:725-736. doi: 10.2147/OTT.S277951. eCollection 2021.
4901	LncRNA	XIST	miR-101-3p	CEBPa	tumor-associated macrophages	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;	33510942	lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration.	The phenotypic switch in tumor-associated macrophages (TAMs) mediates immunity escape of cancer. However, the underlying mechanisms in the TAM phenotypic switch have not been systematically elucidated. In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)α, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1). Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPα and KLF6 expression. Furthermore, miR-101 could combine with both Xist and C/EBPα and KLF6 through the same microRNA response element (MRE) predicted by bioinformatics and verified by luciferase reporter assays. Moreover, we found that miR-101 knockdown restored the decreased M1 marker and the increased M2 marker expression and also reversed the promotion of proliferation and migration of human breast cancer cells (MCF-7) and human ovarian cancer (OV) cells caused by silencing Xist. Generally, the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPα and KLF6 expression. The promotion of Xist expression in M1 macrophages and inhibition of miR-101 expression in M2 macrophages might play an important role in inhibiting breast and ovarian tumor proliferation and migration abilities.	NA	Mol Ther Nucleic Acids. 2020 Dec 10;23:536-551. doi: 10.1016/j.omtn.2020.12.005. eCollection 2021 Mar 5.
4902	LncRNA	XIST	miR-101-3p	KLF6	tumor-associated macrophages	Ovarian Cancer	Homo sapiens (human)	Luciferase reporter assay;	33510942	lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration.	The phenotypic switch in tumor-associated macrophages (TAMs) mediates immunity escape of cancer. However, the underlying mechanisms in the TAM phenotypic switch have not been systematically elucidated. In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)α, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1). Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPα and KLF6 expression. Furthermore, miR-101 could combine with both Xist and C/EBPα and KLF6 through the same microRNA response element (MRE) predicted by bioinformatics and verified by luciferase reporter assays. Moreover, we found that miR-101 knockdown restored the decreased M1 marker and the increased M2 marker expression and also reversed the promotion of proliferation and migration of human breast cancer cells (MCF-7) and human ovarian cancer (OV) cells caused by silencing Xist. Generally, the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPα and KLF6 expression. The promotion of Xist expression in M1 macrophages and inhibition of miR-101 expression in M2 macrophages might play an important role in inhibiting breast and ovarian tumor proliferation and migration abilities.	NA	Mol Ther Nucleic Acids. 2020 Dec 10;23:536-551. doi: 10.1016/j.omtn.2020.12.005. eCollection 2021 Mar 5.
4903	LncRNA	XIST	miR-101-3p	CEBPa	tumor-associated macrophages	Breast Cancer	Homo sapiens (human)	Luciferase reporter assay;	33510942	lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration.	The phenotypic switch in tumor-associated macrophages (TAMs) mediates immunity escape of cancer. However, the underlying mechanisms in the TAM phenotypic switch have not been systematically elucidated. In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)α, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1). Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPα and KLF6 expression. Furthermore, miR-101 could combine with both Xist and C/EBPα and KLF6 through the same microRNA response element (MRE) predicted by bioinformatics and verified by luciferase reporter assays. Moreover, we found that miR-101 knockdown restored the decreased M1 marker and the increased M2 marker expression and also reversed the promotion of proliferation and migration of human breast cancer cells (MCF-7) and human ovarian cancer (OV) cells caused by silencing Xist. Generally, the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPα and KLF6 expression. The promotion of Xist expression in M1 macrophages and inhibition of miR-101 expression in M2 macrophages might play an important role in inhibiting breast and ovarian tumor proliferation and migration abilities.	NA	Mol Ther Nucleic Acids. 2020 Dec 10;23:536-551. doi: 10.1016/j.omtn.2020.12.005. eCollection 2021 Mar 5.
4904	LncRNA	XIST	miR-101-3p	KLF6	tumor-associated macrophages	Ovarian Cancer	Homo sapiens (human)	Luciferase reporter assay;	33510942	lncRNA-Xist/miR-101-3p/KLF6/C/EBPα axis promotes TAM polarization to regulate cancer cell proliferation and migration.	The phenotypic switch in tumor-associated macrophages (TAMs) mediates immunity escape of cancer. However, the underlying mechanisms in the TAM phenotypic switch have not been systematically elucidated. In this study, long noncoding RNA (lncRNA)-Xist, CCAAT/enhancer-binding protein (C/EBP)α, and Kruppel-like factor 6 (KLF6) were upregulated, whereas microRNA (miR)-101 was downregulated in M1 macrophages-type (M1). Knockdown of Xist or overexpression of miR-101 in M1 could induce M1-to-M2 macrophage-type (M2) conversion to promote cell proliferation and migration of breast and ovarian cancer by inhibiting C/EBPα and KLF6 expression. Furthermore, miR-101 could combine with both Xist and C/EBPα and KLF6 through the same microRNA response element (MRE) predicted by bioinformatics and verified by luciferase reporter assays. Moreover, we found that miR-101 knockdown restored the decreased M1 marker and the increased M2 marker expression and also reversed the promotion of proliferation and migration of human breast cancer cells (MCF-7) and human ovarian cancer (OV) cells caused by silencing Xist. Generally, the present study indicates that Xist could mediate macrophage polarization to affect cell proliferation and migration of breast and ovarian cancer by competing with miR-101 to regulate C/EBPα and KLF6 expression. The promotion of Xist expression in M1 macrophages and inhibition of miR-101 expression in M2 macrophages might play an important role in inhibiting breast and ovarian tumor proliferation and migration abilities.	NA	Mol Ther Nucleic Acids. 2020 Dec 10;23:536-551. doi: 10.1016/j.omtn.2020.12.005. eCollection 2021 Mar 5.
4905	LncRNA	XIST	miR-599	TLR4	vascular smooth muscle cells	Atherosclerosis	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;Luciferase reporter assay;	33566259	LncRNA XIST Promotes Atherosclerosis by Regulating miR-599/TLR4 Axis.	Long noncoding RNAs (lncRNAs) have been reported to be implicated in various biological and pathological processes. However, the function and mechanism of XIST in vascular smooth muscle cells (VSMCs) remains unknown. The levels of XIST, miR-599, and TLR4 were tested by RT-qPCR. VSMCs and human mononuclear cells (U937) treated with ox-LDL were used as atherosclerosis (AS) cell models. The CCK-8 assay was adopted to detect cell viability. Cell apoptosis was examined by the TUNEL assay. A dual-luciferase reporter assay was employed to investigate the interaction between miR-599 and XIST or TLR4. In this research, we uncovered that the XIST level was elevated in the serum of AS patients and ox-LDL-treated AS cell models. Functional analysis revealed that XIST depletion restrained cell proliferation, while induced the apoptosis in AS cell models. Besides, miR-599 was verified to be a direct downstream target of XIST and miR-599 inhibitor reversed the effects of XIST knockdown on AS progression. Finally, we demonstrated that XIST increased TLR4 expression by serving as a ceRNA of miR-599. All these findings manifested the role of the XIST/miR-599/TLR4 axis in AS development.	NA	Inflammation. 2021 Jun;44(3):965-973. doi: 10.1007/s10753-020-01391-x. Epub 2021 Feb 10.
4906	LncRNA	XIST	miR-27b-3p	CDDP	oral squamous cell carcinoma cells	Oral Squamous Cell Cancer	Homo sapiens (human)	Flow cytometry assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33191714	LncRNA XIST promotes proliferation and cisplatin resistance of oral squamous cell carcinoma by downregulating miR-27b-3p.	Chemotherapy resistance has become a major obstacle to effective treatment of human cancer. This study aimed to investigate the effect of lncRNA XIST on cell proliferation and cisplatin (CDDP) of oral squamous cell carcinoma (OSCC). RT-qPCR and Western blot analysis were used to detect mRNA and protein expression. CCK-8 and flow cytometry assays were explored to evaluate CDDP sensitivity in OSCC cells. The relationship between lncRNA XIST and miR-27b-3p was confirmed by luciferase reporter assay. The results showed that lncRNA XIST was upregulated in OSCC tissues, cell lines, and CDDP-resistant OSCC cells. Functionally, upregulation of lncRNA XIST promoted cell proliferation, enhanced CDDP resistance, and inhibited apoptosis in OSCC cells. In addition, lncRNA XIST acts as a molecular sponge for miR-27b-3p in OSCC. Downregulation of miR-27b-3p partially reversed the tumor suppression effect and CDDP chemosensitivity of XIST knockdown in CDDP-resistant OSCC cells. In conclusion, lncRNA XIST promotes cell proliferation and enhances resistance to CDDP in OSCC by downregulating miR-27b-3p.	NA	J Biol Regul Homeost Agents. 2020 Nov-Dec;34(6):1993-2001. doi: 10.23812/20-222-A.
4907	LncRNA	ZEB1-AS1	miR-590-5p	ETS1	umbilical vein endothelial cells	Atherosclerosis	Homo sapiens (human)	ELISA;MTT assay;Western blot;Flow Cytometry assay;MTT assay;	33818551	Exosomes-Mediated LncRNA ZEB1-AS1 Facilitates Cell Injuries by miR-590-5p/ETS1 Axis Through the TGF-β/Smad Pathway in Oxidized Low-density Lipoprotein-induced Human Umbilical Vein Endothelial Cells.	Atherosclerosis is a chronic lipid-induced inflammation of the vessel wall. Oxidized low-density lipoprotein was confirmed to drive the onset of atherogenesis. Zinc finger e-box-binding homeobox 1 antisense 1 (ZEB1-AS1) is a long noncoding RNA that is involved in human diseases, including atherosclerosis. In this study, the role of exosomes-mediated ZEB1-AS1 and its underlying mechanisms in atherosclerosis were explored in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs). Exosomes were extracted from HUVECs. Quantitative real-time polymerase chain reaction was conducted to measure the expression of ZEB1-AS1, microRNA-590-5p (miR-590-5p), or erythroblastosis virus E26 oncogene homolog 1 (ETS1) in cells or exosomes. Cell proliferation and apoptosis were assessed by MTT assay and flow cytometry analysis, respectively. Western blot was performed to detect apoptosis-related factors, ETS1, and TGF-β/Smad pathway protein levels. The secretion of inflammatory factors in supernatant was detected by ELISA assay. Oxidative stress damage indicators were used to assess cellular damage. Relationship between miR-590-5p and ZEB1-AS1 or ETS1 was analyzed. Our data indicated that ox-LDL-induced exosomes-mediated ZEB1-AS1 in HUVECs. Ox-LDL treatment resulted in limited proliferation, proapoptosis, inflammation, and oxidative stress damage, whereas knockdown of ZEB1-AS1 could reverse these effects. Mechanically, ZEB1-AS1 sponged miR-590-5p to regulate ETS1 expression. MiR-590-5p knockdown inverted effects above of si-ZEB1-AS1 on HUVECs under ox-LDL exposure. Moreover, ETS1 reversed miR-590-5p-induced effects and activated the TGF-β/Smad pathway in ox-LDL-treated HUVECs. Taken together, our findings demonstrated that exosomes-mediated ZEB1-AS1 enhanced cell injuries by miR-590-5p/ETS1 axis through the TGF-β/Smad pathway in ox-LDL-induced HUVECs, suggesting that inhibiting ZEB1-AS1 might be an effective way for atherosclerosis treatment.	NA	J Cardiovasc Pharmacol. 2021 Apr 1;77(4):480-490. doi: 10.1097/FJC.0000000000000974.
4908	Circular RNA	Circ0083429	miR-346	SMAD3	Osteoarthritis cells	Osteoarthritis	Homo sapiens (human)	qRT-PCR;RACE;Western blot;Luciferase reporter assay;	33520980	Circ0083429 Regulates Osteoarthritis Progression via the Mir-346/SMAD3 Axis.	Osteoarthritis (OA) is a degenerative joint disease. Currently, apart from symptomatic treatment or joint replacement, no other effective treatments for OA exist. The mechanisms underlying OA remain elusive and require further research. Circular RNAs (circRNAs) are known to be involved in many diseases; however, their function in OA is not yet fully understood. Here, we identified a novel circRNA, Circ0083429. The role of Circ0083429 in OA was confirmed via western blot (WB), quantitative real-time PCR (qRT-PCR), and immunofluorescence (IF) through knockdown and overexpression experiments. The binding of Circ0083429 to downstream miR-346 and its target gene SMAD3 was predicted via bioinformatics analysis and verified using a luciferase reporter assay and RNA pulldown experiments. Finally, the function of Circ0083429 was evaluated in mouse OA models. In our study, we found that Circ0083429 regulates the homeostasis of the extracellular matrix (ECM) in human chondrocytes. Mechanistically, Circ0083429 affects OA by regulating the mRNA level of SMAD3 through the sponging of microRNA (miRNA)-346. Injecting adeno-associated virus Circ0083429 into the intra-junction of the mouse knee alleviated OA. In conclusion, Circ0083429 regulates the ECM via the regulation of the downstream miRNA-346/SMAD3 in human chondrocytes, which provides a new therapeutic strategy for OA.	NA	Front Cell Dev Biol. 2021 Jan 15;8:579945. doi: 10.3389/fcell.2020.579945. eCollection 2020.
4909	Circular RNA	Circ0083429	miR-346	SMAD3	Osteoarthritis cells	Osteoarthritis	Mus musculus (mouse)	qRT-PCR;RACE;Western blot;Luciferase reporter assay;	33520980	Circ0083429 Regulates Osteoarthritis Progression via the Mir-346/SMAD3 Axis.	Osteoarthritis (OA) is a degenerative joint disease. Currently, apart from symptomatic treatment or joint replacement, no other effective treatments for OA exist. The mechanisms underlying OA remain elusive and require further research. Circular RNAs (circRNAs) are known to be involved in many diseases; however, their function in OA is not yet fully understood. Here, we identified a novel circRNA, Circ0083429. The role of Circ0083429 in OA was confirmed via western blot (WB), quantitative real-time PCR (qRT-PCR), and immunofluorescence (IF) through knockdown and overexpression experiments. The binding of Circ0083429 to downstream miR-346 and its target gene SMAD3 was predicted via bioinformatics analysis and verified using a luciferase reporter assay and RNA pulldown experiments. Finally, the function of Circ0083429 was evaluated in mouse OA models. In our study, we found that Circ0083429 regulates the homeostasis of the extracellular matrix (ECM) in human chondrocytes. Mechanistically, Circ0083429 affects OA by regulating the mRNA level of SMAD3 through the sponging of microRNA (miRNA)-346. Injecting adeno-associated virus Circ0083429 into the intra-junction of the mouse knee alleviated OA. In conclusion, Circ0083429 regulates the ECM via the regulation of the downstream miRNA-346/SMAD3 in human chondrocytes, which provides a new therapeutic strategy for OA.	NA	Front Cell Dev Biol. 2021 Jan 15;8:579945. doi: 10.3389/fcell.2020.579945. eCollection 2020.
4910	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Intimal Hyperplasia	Homo sapiens (human)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4911	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Restenosis	Homo sapiens (human)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4912	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Atherosclerosis	Homo sapiens (human)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4913	LncRNA	H19	miR-193b-3p	MMP-2	aortic smooth muscle cells	Thoracic Aorta Pathological Damage	Homo sapiens (human)	RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;luciferase assay;RNA immunoprecipitation;RNA pull-down;	33403385	LncRNA H19 regulates smooth muscle cell functions and participates in the development of aortic dissection through sponging miR-193b-3p.	BACKGROUND: Multiple studies showed that long-chain noncoding RNA H19 (LncRNA H19) is high-expressed in human and mouse abdominal aortic aneurysms (AAAs). We speculated that it plays an important role in arterial disease, and therefore studied the role and mechanism of H19 in aortic dissection (AD). METHODS: The expressions of related genes in human aortic smooth muscle cells (HASMCs) induced by platelet-derived growth factor BB (PDGF-BB) or in the aortic tissue of AD patients/mice were identified by Western blot and quantitative real-time polymerase chain reaction. The targeting relationship between H19 and miR-193b-3p was predicted and verified by bioinformatics analysis, dual luciferase assay, RNA pull-down assay, RNA immunoprecipitation (RIP), and Pearson correlation coefficient. The H19 and miR-193b-3p effects on the biological functions of tissues and cells were examined by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, thiazolyl blue tetrazolium bromide) assay, wound-healing assay, and Hematoxylin-Eosin (HE) staining. RESULTS: LncRNA H19 was abnormally high-expressed in thoracic aorta tissues of AD patients, and it could competitively bind to and inhibit miR-193b-3p. In the PDGF-BB group, the expressions of H19, matrix metallopeptidase (MMP) 2 (MMP-2) and MMP-9 were up-regulated and the expressions of miR-193b-3p, α-SMA, and SM22α were down-regulated; moreover, the proliferation and migration rate of HASMCs were increased. However, H19 silencing reversed the regulation of PDGF-BB on HASMCs. More interestingly, miR-193b-3p inhibitor could partially reverse the effect of H19 silencing. In addition, the above results were verified by animal experiments, showing that shH19 and up-regulated miR-193b-3p could significantly reduce the thoracic aorta pathological damage in AD mice. CONCLUSION: LncRNA H19 regulated smooth muscle cell function by sponging miR-193b-3p and it participated in the development of AD.	NA	Biosci Rep. 2021 Jan 29;41(1):BSR20202298. doi: 10.1042/BSR20202298.
4914	LncRNA	Linc-ROR	miR-212-3p	FGF7	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;Luciferase reporter assay;	33564265	Upregulation of Linc-ROR Promotes the Proliferation, Migration, and Invasion of Gastric Cancer Cells Through miR-212-3p/FGF7 Axis.	BACKGROUND: Linc-ROR is a long non-coding RNA, that is found aberrantly expressed in various human cancers. We aim here to unveil the role of Linc-ROR in gastric cancer (GC) progression. METHODS: qPCR was used to determine gene expression. Cell viability was measured by CCK-8 assay. Transwell assays were performed to evaluate the GC cells' migratory and invasive abilities. Xenograft mouse model was conducted to measure tumor growth. RESULTS: We found that Linc-ROR were overexpressed in GC tissues compared to the adjacent tissues. High Linc-ROR predicts poor prognosis of GC patients. The prediction of bioinformatics online revealed that Linc-ROR could bind to miR-212-3p. Further, dual-luciferase reporter assay confirmed a direct interaction between Linc-ROR and miR-212-3p. Overexpression of miR-212-3p facilitated GC cells' migration and invasion, while the silencing of miR-212-3p attenuated GC cell migratory and invasive abilities. Moreover, Linc-ROR knockdown significantly suppressed the proliferation, migration, and invasion of GC cells, whereas miR-212-3p antagomir partially reversed Linc-ROR knockdown-induced phenotypes. Fibroblast growth factor 7 (FGF7), a downstream molecule of miR-212-3p, was overexpressed in GC cells. The recovery of FGF7 expression partially reversed the phenotypes caused by Linc-ROR silencing. Mechanistically, silencing of Linc-ROR contributed to the downregulation of CDK4, CDK6, Cyclin D1, N-Cadherin, Vimentin, MMP-9, MMP-2, but caused the upregulation of P21, P27, E-Cadherin, CK-19 in MGC-803 cells; however, FGF7 treatment could reverse the results induced by Linc-ROR silencing. Results in vivo further suggested that Linc-ROR knockdown repressed GC tumor growth, where the expression of miR-212-3p was up-regulated and FGF7 expression was downregulated in tumor tissues of mice. CONCLUSION: These findings indicated that Linc-ROR/miR-212-3p/FGF7 axis played an important role in gastric cancer progression. Linc-ROR expression level was associated with the prognosis of GC patients.	NA	Cancer Manag Res. 2021 Feb 2;13:899-912. doi: 10.2147/CMAR.S287775. eCollection 2021.
4915	LncRNA	XIST	miR-129-5p	CCND1	esophageal squamous cell carcinoma cells	Esophageal Squamous Cancer	Homo sapiens (human)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33345719	Long non-coding RNA XIST promotes the progression of esophageal squamous cell carcinoma through sponging miR-129-5p and upregulating CCND1 expression.	Long non-coding RNA (lncRNA) X inactive specific transcript (XIST) has been identified as an oncogenic lncRNA in a series of human cancers, including esophageal squamous cell carcinoma (ESCC). In this study, we aimed to further explore the underlying mechanism of XIST on ESCC progression. qRT-PCR assay was used to determine the levels of XIST and miR-129-5p. Western blot analysis was performed to assess cyclin D1 (CCND1) expression. Bioinformatic analysis was performed using starBase v2.0 software. Dual-luciferase reporter and RNA immunoprecipitation assays were employed to confirm the interaction between XIST and miR-129-5p or miR-129-5p and CCND1. Cell cycle progression and apoptosis were measured by flow cytometric analysis, and cell migration and invasion were detected by transwell assay. Mouse studies were used to observe the effect of XIST silencing on tumor growth in vivo. Our results indicated that XIST was upregulated and miR-129-5p was downregulated in ESCC. XIST silencing or miR-129-5p overexpression repressed cell cycle progression, proliferation, migration, invasion, and promoted the apoptosis in ESCC cells. Moreover, XIST directly interacted with miR-129-5p and repressed miR-129-5p expression. MiR-129-5p mediated the regulatory effect of XIST on ESCC cell progression in vitro, and XIST promoted CCND1 expression by sponging miR-129-5p. Additionally, XIST silencing inhibited tumor growth in vivo. Our findings suggested that XIST silencing repressed the progression of ESCC at least partly through regulating the miR-129-5p/CCND1 axis. Targeting XIST might be a potential therapeutic strategy for ESCC treatment.	NA	Cell Cycle. 2021 Jan;20(1):39-53. doi: 10.1080/15384101.2020.1856497. Epub 2020 Dec 19.
4916	LncRNA	XIST	miR-137	Notch1	pancreatic cancer tissues and cells	Pancreatic Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33336734	Long non-coding RNA XIST promotes cell proliferation of pancreatic cancer through miR-137 and Notch1 pathway.	OBJECTIVE: Long non-coding ribonucleic acids X-inactive specific transcript (lncRNA XIST) is one lncRNAs which involved in multiple human cancers. However, the functions and potential molecular regulatory mechanisms of XIST/microRNA-137 (miR-137) in pancreatic cancer (PC) still need to explore. PATIENTS AND METHODS: PC tissues and cell lines were analyzed for XIST, miR-137 and Notch1 expressions through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Nude mouse xenograft tumor assay was used to detect XIST effects on pancreatic tumorigenesis in vivo. Cell Counting Kit (CCK-8) assay was performed to detect PC cell proliferation. Dual-Luciferase reporter assay, qRT-PCR, RNA immunoprecipitation (RIP) and Western blot assays were applied to validate the target relationship of XIST, miR-137 and Notch1. RESULTS: Results demonstrated that XIST expression was increased in PC tissues and cells. XIST knockdown inhibited PC cell proliferation in vitro and also repressed the tumor growth in vivo. XIST directly interacted with miR-137 and negatively regulated its expression. Notch1 was identified as a target gene of miR-137 and XIST acted as a competitive endogenous RNA (ceRNA) to positively regulate Notch1 expression by suppressing miR-137. In addition, we detected miR-137 was negatively correlated with XIST and Notch1 respectively, and a positive correlation between Notch1 and XIST expression in PC tissues. Furthermore, Notch1 overexpression could offset the suppressing effect of XIST knockdown or miR-137 overexpression on cell proliferation. Therefore, XIST may play an important role in promoting cell proliferation through miR-137 and Notch1 pathway in PC. CONCLUSIONS: To sum up, these results proposed that XIST functioned as an endogenous sponge in promoting PC cell proliferation through competing for miR-137 to regulate Notch1 expression, and may provide more therapeutic targets for the patients with PC.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12161-12170. doi: 10.26355/eurrev_202012_24005.
4917	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Intimal Hyperplasia	Mus musculus (mouse)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4918	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Restenosis	Mus musculus (mouse)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4919	Circular RNA	CircMAP3K5	miR-22-3p	TET2	smooth muscle cells	Atherosclerosis	Mus musculus (mouse)	Luciferase reporter assay;RNA pull-down;RNA sequencing;	33207953	Circular RNA CircMAP3K5 Acts as a MicroRNA-22-3p Sponge to Promote Resolution of Intimal Hyperplasia Via TET2-Mediated Smooth Muscle Cell Differentiation.	BACKGROUND: Aberrant expression of circular RNA contributes to human diseases. Circular RNAs regulate gene expression by sequestering specific microRNAs. In this study, we investigated whether circMAP3K5 (circular mitogen-activated protein kinase 5) could act as a competing endogenous microRNA-22-3p (miR-22-3p) sponge and regulate neointimal hyperplasia. METHODS: Circular RNA profiling from genome-wide RNA sequencing data was compared between human coronary artery smooth muscle cells (SMCs) treated with or without platelet-derived growth factor. Expression levels of circMAP3K5 were assessed in human coronary arteries from autopsies on patients with dilated cardiomyopathy or coronary heart disease. The role of circMAP3K5 in intimal hyperplasia was further investigated in mice with adeno-associated virus 9-mediated circMAP3K5 transfection. SMC-specific Tet2 (ten-eleven translocation-2) knockout mice and global miR-22-3p knockout mice were used to delineate the mechanism by which circMAP3K5 attenuated neointimal hyperplasia using the femoral arterial wire injury model. RESULTS: RNA sequencing demonstrated that treatment with platelet-derived growth factor-BB significantly reduced expression of circMAP3K5 in human coronary artery SMCs. Wire-injured mouse femoral arteries and diseased arteries from patients with coronary heart disease (where platelet-derived growth factor-BB is increased) confirmed in vivo downregulation of circMAP3K5 associated with injury and disease. Lentivirus-mediated overexpression of circMAP3K5 inhibited the proliferation of human coronary artery SMCs. In vivo adeno-associated virus 9-mediated transfection of circMap3k5 (mouse circular Map3k5) specifically inhibited SMC proliferation in the wire-injured mouse arteries, resulting in reduced neointima formation. Using a luciferase reporter assay and RNA pull-down, circMAP3K5 (human circular MAP3K5) was found to sequester miR-22-3p, which, in turn, inhibited the expression of TET2. Both in vitro and in vivo results demonstrate that the loss of miR-22-3p recapitulated the antiproliferative effect of circMap3k5 on vascular SMCs. In SMC-specific Tet2 knockout mice, loss of Tet2 abolished the circMap3k5-mediated antiproliferative effect on vascular SMCs. CONCLUSIONS: We identify circMAP3K5 as a master regulator of TET2-mediated vascular SMC differentiation. Targeting the circMAP3K5/miR-22-3p/TET2 axis may provide a potential therapeutic strategy for diseases associated with intimal hyperplasia, including restenosis and atherosclerosis.	NA	Circulation. 2021 Jan 26;143(4):354-371. doi: 10.1161/CIRCULATIONAHA.120.049715. Epub 2020 Nov 19.
4920	LncRNA	H19	miR-193b-3p	MMP-2	aortic smooth muscle cells	Thoracic Aorta Pathological Damage	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;luciferase assay;RNA immunoprecipitation;RNA pull-down;	33403385	LncRNA H19 regulates smooth muscle cell functions and participates in the development of aortic dissection through sponging miR-193b-3p.	BACKGROUND: Multiple studies showed that long-chain noncoding RNA H19 (LncRNA H19) is high-expressed in human and mouse abdominal aortic aneurysms (AAAs). We speculated that it plays an important role in arterial disease, and therefore studied the role and mechanism of H19 in aortic dissection (AD). METHODS: The expressions of related genes in human aortic smooth muscle cells (HASMCs) induced by platelet-derived growth factor BB (PDGF-BB) or in the aortic tissue of AD patients/mice were identified by Western blot and quantitative real-time polymerase chain reaction. The targeting relationship between H19 and miR-193b-3p was predicted and verified by bioinformatics analysis, dual luciferase assay, RNA pull-down assay, RNA immunoprecipitation (RIP), and Pearson correlation coefficient. The H19 and miR-193b-3p effects on the biological functions of tissues and cells were examined by MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, thiazolyl blue tetrazolium bromide) assay, wound-healing assay, and Hematoxylin-Eosin (HE) staining. RESULTS: LncRNA H19 was abnormally high-expressed in thoracic aorta tissues of AD patients, and it could competitively bind to and inhibit miR-193b-3p. In the PDGF-BB group, the expressions of H19, matrix metallopeptidase (MMP) 2 (MMP-2) and MMP-9 were up-regulated and the expressions of miR-193b-3p, α-SMA, and SM22α were down-regulated; moreover, the proliferation and migration rate of HASMCs were increased. However, H19 silencing reversed the regulation of PDGF-BB on HASMCs. More interestingly, miR-193b-3p inhibitor could partially reverse the effect of H19 silencing. In addition, the above results were verified by animal experiments, showing that shH19 and up-regulated miR-193b-3p could significantly reduce the thoracic aorta pathological damage in AD mice. CONCLUSION: LncRNA H19 regulated smooth muscle cell function by sponging miR-193b-3p and it participated in the development of AD.	NA	Biosci Rep. 2021 Jan 29;41(1):BSR20202298. doi: 10.1042/BSR20202298.
4921	LncRNA	Linc-ROR	miR-212-3p	FGF7	Gastric Cancer Cells	Gastric Cancer	Mus musculus (mouse)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;Luciferase reporter assay;	33564265	Upregulation of Linc-ROR Promotes the Proliferation, Migration, and Invasion of Gastric Cancer Cells Through miR-212-3p/FGF7 Axis.	BACKGROUND: Linc-ROR is a long non-coding RNA, that is found aberrantly expressed in various human cancers. We aim here to unveil the role of Linc-ROR in gastric cancer (GC) progression. METHODS: qPCR was used to determine gene expression. Cell viability was measured by CCK-8 assay. Transwell assays were performed to evaluate the GC cells' migratory and invasive abilities. Xenograft mouse model was conducted to measure tumor growth. RESULTS: We found that Linc-ROR were overexpressed in GC tissues compared to the adjacent tissues. High Linc-ROR predicts poor prognosis of GC patients. The prediction of bioinformatics online revealed that Linc-ROR could bind to miR-212-3p. Further, dual-luciferase reporter assay confirmed a direct interaction between Linc-ROR and miR-212-3p. Overexpression of miR-212-3p facilitated GC cells' migration and invasion, while the silencing of miR-212-3p attenuated GC cell migratory and invasive abilities. Moreover, Linc-ROR knockdown significantly suppressed the proliferation, migration, and invasion of GC cells, whereas miR-212-3p antagomir partially reversed Linc-ROR knockdown-induced phenotypes. Fibroblast growth factor 7 (FGF7), a downstream molecule of miR-212-3p, was overexpressed in GC cells. The recovery of FGF7 expression partially reversed the phenotypes caused by Linc-ROR silencing. Mechanistically, silencing of Linc-ROR contributed to the downregulation of CDK4, CDK6, Cyclin D1, N-Cadherin, Vimentin, MMP-9, MMP-2, but caused the upregulation of P21, P27, E-Cadherin, CK-19 in MGC-803 cells; however, FGF7 treatment could reverse the results induced by Linc-ROR silencing. Results in vivo further suggested that Linc-ROR knockdown repressed GC tumor growth, where the expression of miR-212-3p was up-regulated and FGF7 expression was downregulated in tumor tissues of mice. CONCLUSION: These findings indicated that Linc-ROR/miR-212-3p/FGF7 axis played an important role in gastric cancer progression. Linc-ROR expression level was associated with the prognosis of GC patients.	NA	Cancer Manag Res. 2021 Feb 2;13:899-912. doi: 10.2147/CMAR.S287775. eCollection 2021.
4922	LncRNA	XIST	miR-129-5p	CCND1	esophageal squamous cell carcinoma cells	Esophageal Squamous Cancer	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	33345719	Long non-coding RNA XIST promotes the progression of esophageal squamous cell carcinoma through sponging miR-129-5p and upregulating CCND1 expression.	Long non-coding RNA (lncRNA) X inactive specific transcript (XIST) has been identified as an oncogenic lncRNA in a series of human cancers, including esophageal squamous cell carcinoma (ESCC). In this study, we aimed to further explore the underlying mechanism of XIST on ESCC progression. qRT-PCR assay was used to determine the levels of XIST and miR-129-5p. Western blot analysis was performed to assess cyclin D1 (CCND1) expression. Bioinformatic analysis was performed using starBase v2.0 software. Dual-luciferase reporter and RNA immunoprecipitation assays were employed to confirm the interaction between XIST and miR-129-5p or miR-129-5p and CCND1. Cell cycle progression and apoptosis were measured by flow cytometric analysis, and cell migration and invasion were detected by transwell assay. Mouse studies were used to observe the effect of XIST silencing on tumor growth in vivo. Our results indicated that XIST was upregulated and miR-129-5p was downregulated in ESCC. XIST silencing or miR-129-5p overexpression repressed cell cycle progression, proliferation, migration, invasion, and promoted the apoptosis in ESCC cells. Moreover, XIST directly interacted with miR-129-5p and repressed miR-129-5p expression. MiR-129-5p mediated the regulatory effect of XIST on ESCC cell progression in vitro, and XIST promoted CCND1 expression by sponging miR-129-5p. Additionally, XIST silencing inhibited tumor growth in vivo. Our findings suggested that XIST silencing repressed the progression of ESCC at least partly through regulating the miR-129-5p/CCND1 axis. Targeting XIST might be a potential therapeutic strategy for ESCC treatment.	NA	Cell Cycle. 2021 Jan;20(1):39-53. doi: 10.1080/15384101.2020.1856497. Epub 2020 Dec 19.
4923	LncRNA	XIST	miR-137	Notch1	pancreatic cancer tissues and cells	Pancreatic Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	33336734	Long non-coding RNA XIST promotes cell proliferation of pancreatic cancer through miR-137 and Notch1 pathway.	OBJECTIVE: Long non-coding ribonucleic acids X-inactive specific transcript (lncRNA XIST) is one lncRNAs which involved in multiple human cancers. However, the functions and potential molecular regulatory mechanisms of XIST/microRNA-137 (miR-137) in pancreatic cancer (PC) still need to explore. PATIENTS AND METHODS: PC tissues and cell lines were analyzed for XIST, miR-137 and Notch1 expressions through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Nude mouse xenograft tumor assay was used to detect XIST effects on pancreatic tumorigenesis in vivo. Cell Counting Kit (CCK-8) assay was performed to detect PC cell proliferation. Dual-Luciferase reporter assay, qRT-PCR, RNA immunoprecipitation (RIP) and Western blot assays were applied to validate the target relationship of XIST, miR-137 and Notch1. RESULTS: Results demonstrated that XIST expression was increased in PC tissues and cells. XIST knockdown inhibited PC cell proliferation in vitro and also repressed the tumor growth in vivo. XIST directly interacted with miR-137 and negatively regulated its expression. Notch1 was identified as a target gene of miR-137 and XIST acted as a competitive endogenous RNA (ceRNA) to positively regulate Notch1 expression by suppressing miR-137. In addition, we detected miR-137 was negatively correlated with XIST and Notch1 respectively, and a positive correlation between Notch1 and XIST expression in PC tissues. Furthermore, Notch1 overexpression could offset the suppressing effect of XIST knockdown or miR-137 overexpression on cell proliferation. Therefore, XIST may play an important role in promoting cell proliferation through miR-137 and Notch1 pathway in PC. CONCLUSIONS: To sum up, these results proposed that XIST functioned as an endogenous sponge in promoting PC cell proliferation through competing for miR-137 to regulate Notch1 expression, and may provide more therapeutic targets for the patients with PC.	NA	Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12161-12170. doi: 10.26355/eurrev_202012_24005.
4924	LncRNA	MALAT1	miR-181a-5p	Fas	human pulmonary microvascular endothelial cells	Acute Lung Injury	Homo sapiens (human)	qRT-PCR	33407436	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Res. 2021 Jan 6;22(1):1. doi: 10.1186/s12931-020-01578-8.
4925	LncRNA	MALAT1	miR-181a-5p	Fas	human pulmonary microvascular endothelial cells	Acute Respiratory Distress Syndrome	Homo sapiens (human)	qRT-PCR	33407436	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Res. 2021 Jan 6;22(1):1. doi: 10.1186/s12931-020-01578-8.
4926	LncRNA	Xist	miR-29b-3p	Eln	smooth muscle cells	Thoracic Aortic Aneurysm	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33761588	LncRNA Xist induces arterial smooth muscle cell apoptosis in thoracic aortic aneurysm through miR-29b-3p/Eln pathway.	BACKGROUND: Thoracic aortic aneurysm (TAA) is a serious disease usually happening in elder people and with high death rate. Accumulating studies have reported that long non-coding RNAs (lncRNAs) are implicated in the progression of various human diseases, including TAA. AIM: In our study, we intended to explore the function of elastin (Eln) and its upstream mechanism in TAA. METHODS: RT-qPCR determined gene expressions and western blot tested changes in protein levels. Ang Ⅱ treatment was implemented to induce cell apoptosis. Flow cytometry analysis, TUNEL assay and JC-1 assay were exploited to measure cell apoptosis. Meanwhile, mechanistic assays such as RIP, RNA pull down and luciferase reporter assays were employed to identify the interplay between RNAs. RESULTS: Eln inhibition was identified to protect rat arterial smooth muscle cells from apoptosis. Also, miR-29b-3p was identified to bind to Eln, and X inactive specific transcript (Xist) could boost Eln expression through absorbing miR-29b-3p. Meanwhile, Eln overexpression counteracted the suppression of silenced Xist on the apoptosis of rat arterial smooth muscle cells. More importantly, such ceRNA network was proved to aggravate the apoptosis of human aortic smooth muscle cells. CONCLUSION: LncRNA Xist contributes to arterial smooth muscle cell apoptosis through miR-29b-3p/Eln pathway, providing new potential roads for treating TAA.	NA	Biomed Pharmacother. 2021 May;137:111163. doi: 10.1016/j.biopha.2020.111163. Epub 2021 Feb 22.
4927	LncRNA	MALAT1	miR-181a-5p	Fas	human pulmonary microvascular endothelial cells	Acute Lung Injury	Rattus (rat)	qRT-PCR	33407436	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Res. 2021 Jan 6;22(1):1. doi: 10.1186/s12931-020-01578-8.
4928	LncRNA	MALAT1	miR-181a-5p	Fas	human pulmonary microvascular endothelial cells	Acute Respiratory Distress Syndrome	Rattus (rat)	qRT-PCR	33407436	Targeting MALAT1 and miRNA-181a-5p for the intervention of acute lung injury/acute respiratory distress syndrome.	BACKGROUND: ALI/ARDS is a severe lung injury leading to refractory respiratory failure, accounting for high morbidity and mortality. However, therapeutic approaches are rather limited. Targeting long non-coding RNA MALAT1 and microRNA miR-181a-5p might be potential option for ALI/ARDS intervention. OBJECTIVE: We aimed to investigate the role of MALAT and miR-181a-5p in the pathogenesis of ALI/ARDS, and test the therapeutic effects of targeting MALAT and miR-181a-5p for ALI/ARDS intervention in vitro. METHODS: MALAT1 and miR-181a-5p levels were measured in plasma from ALI/ARDS patients. In vitro human pulmonary microvascular endothelial cell (HPMEC) injury was induced by LPS treatment, and molecular targets of MALAT1 and miR-181a-5p were explored by molecular biology approaches, mainly focusing on cell apoptosis and vascular inflammation. Interaction between MALAT1 and miR-181a-5p was also detected. Finally, the effects of targeting MALAT1 and miR-181a-5p for ALI/ARDS intervention were validated in a rat ALI/ARDS model. RESULTS: MALAT1 upregulation and miR-181a-5p downregulation were observed in ALI/ARDS patients. Transfection of mimic miR-181a-5p into HPMECs revealed decreased Fas and apoptosis, along with reduced inflammatory factors. Fas was proved to be a direct target of miR-181a-5p. Similar effects were also present upon MALAT1 knockdown. As for the interaction between MALAT1 and miR-181a-5p, MALAT1 knockdown increased miR-181a-5p expression. Knocking down of MALAT1 and miR-181a-5p could both improve the outcome in ALI/ARDS rats. CONCLUSION: MALAT1 antagonism or miR-181a-5p could both be potential therapeutic strategies for ALI/ARDS. Mechanistically, miR-181a-5p directly inhibits Fas and apoptosis, along with reduced inflammation. MALAT1 negatively regulates miR-181a-5p.	NA	Respir Res. 2021 Jan 6;22(1):1. doi: 10.1186/s12931-020-01578-8.
4929	LncRNA	Xist	miR-29b-3p	Eln	smooth muscle cells	Thoracic Aortic Aneurysm	Rattus (rat)	qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33761588	LncRNA Xist induces arterial smooth muscle cell apoptosis in thoracic aortic aneurysm through miR-29b-3p/Eln pathway.	BACKGROUND: Thoracic aortic aneurysm (TAA) is a serious disease usually happening in elder people and with high death rate. Accumulating studies have reported that long non-coding RNAs (lncRNAs) are implicated in the progression of various human diseases, including TAA. AIM: In our study, we intended to explore the function of elastin (Eln) and its upstream mechanism in TAA. METHODS: RT-qPCR determined gene expressions and western blot tested changes in protein levels. Ang Ⅱ treatment was implemented to induce cell apoptosis. Flow cytometry analysis, TUNEL assay and JC-1 assay were exploited to measure cell apoptosis. Meanwhile, mechanistic assays such as RIP, RNA pull down and luciferase reporter assays were employed to identify the interplay between RNAs. RESULTS: Eln inhibition was identified to protect rat arterial smooth muscle cells from apoptosis. Also, miR-29b-3p was identified to bind to Eln, and X inactive specific transcript (Xist) could boost Eln expression through absorbing miR-29b-3p. Meanwhile, Eln overexpression counteracted the suppression of silenced Xist on the apoptosis of rat arterial smooth muscle cells. More importantly, such ceRNA network was proved to aggravate the apoptosis of human aortic smooth muscle cells. CONCLUSION: LncRNA Xist contributes to arterial smooth muscle cell apoptosis through miR-29b-3p/Eln pathway, providing new potential roads for treating TAA.	NA	Biomed Pharmacother. 2021 May;137:111163. doi: 10.1016/j.biopha.2020.111163. Epub 2021 Feb 22.
4930	LncRNA	AK148321	miR-1199-5p	HSPA5	LPS-stimulated BV2 cells	Neuroinflammation	Mus musculus (mouse)	ELISA;qPCR;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33301806	LncRNA AK148321 alleviates neuroinflammation in LPS-stimulated BV2 microglial cell through regulating microRNA-1199-5p/HSPA5 axis.	AIMS: Dysregulated long non-coding RNA (lncRNA) expression is closely related to neuroinflammation, leading to multiple neurodegenerative diseases. In this study, we investigated the function and regulation of lncRNA AK148321 in neuroinflammation using an in vitro lipopolysaccharide (LPS)-stimulated BV2 microglial cell system. METHODS: Expression of AK148321 was analyzed by qPCR. Inflammatory cytokine expression levels were determined by ELISA assay. The interaction between AK148321, microRNA (miRNA), and its target gene was validated by luciferase reporter assay and RNA immunoprecipitation (RIP). Cell apoptosis was analyzed by Annexin V/PI staining. RESULTS: LPS treatment suppressed AK148321 expression in BV2 cells. Overexpression of AK148321 inhibited LPS-induced BV2 microglial cell activation and decreased the expression of inflammatory cytokine TNF-α and IL-1β. AK148321 function as a competing endogenous RNA (ceRNA) by sponging microRNA-1199-5p (MiR-1199-5p). In LPS-stimulated BV2 cells, AK148321 exerted its inhibitory function via negatively modulating miR-1199-5p expression. Moreover, we identified that Heat Shock Protein Family A Member 5 (HSPA5) was a direct target of miR-1199-5p. RIP assay using the anti-Ago2 antibody further validated the relationship among AK148321, miR-1199-5p and HSPA5. The AK148321/miR-1199-5p/HSPA5 axis regulated the neuroinflammation in LPS-induced BV2 microglial cells. Microglial cell culture supernatant from LPS-stimulated, AK148321-overexpressing BV2 cells suppressed the cell apoptosis of mouse hippocampal neuronal cell HT22, while HSPA5 knockdown abrogated the suppression effect. CONCLUSION: Our findings suggest that AK148321 alleviates neuroinflammation in LPS-stimulated BV2 microglial cells through miR-1199-5p/HSPA5 axis.	NA	Life Sci. 2021 Feb 1;266:118863. doi: 10.1016/j.lfs.2020.118863. Epub 2020 Dec 7.
4931	Circular RNA	AKT3	miR-17-5p	RHOC	esophageal cancer cells	Esophageal Cancer	Mus musculus (mouse)	Luciferase reporter assay;	33519139	Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p.	BACKGROUND: Recent studies have demonstrated that circular RNA AKT3 (circAKT3) plays a crucial role in regulating the malignant phenotypes of tumor cells. However, the potential effects of circAKT3 on esophageal cancer have not been investigated. AIM: To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism. METHODS: Clinical samples were collected to detect the expression of circAKT3. The role of circAKT3 in proliferation, migration, invasion, and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8, wound healing assays, Transwell assays, and fluorescence analysis, respectively. The target of circAKT3 was screened and identified using an online database and luciferase reporter assay. A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo. RESULTS: In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer. CONCLUSION: CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.	NA	World J Gastroenterol. 2021 Jan 21;27(3):240-254. doi: 10.3748/wjg.v27.i3.240.
4932	Circular RNA	AKT3	miR-17-5p	STAT3	esophageal cancer cells	Esophageal Cancer	Mus musculus (mouse)	Luciferase reporter assay;	33519139	Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p.	BACKGROUND: Recent studies have demonstrated that circular RNA AKT3 (circAKT3) plays a crucial role in regulating the malignant phenotypes of tumor cells. However, the potential effects of circAKT3 on esophageal cancer have not been investigated. AIM: To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism. METHODS: Clinical samples were collected to detect the expression of circAKT3. The role of circAKT3 in proliferation, migration, invasion, and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8, wound healing assays, Transwell assays, and fluorescence analysis, respectively. The target of circAKT3 was screened and identified using an online database and luciferase reporter assay. A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo. RESULTS: In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer. CONCLUSION: CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.	NA	World J Gastroenterol. 2021 Jan 21;27(3):240-254. doi: 10.3748/wjg.v27.i3.240.
4933	Circular RNA	Circ_002631	miR-181a-5p	Creb1	kidney tissues	Cardiorenal Syndrome	Mus musculus (mouse)	qRT-PCR	33494070	RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome.	Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4215-4241. doi: 10.18632/aging.202385. Epub 2021 Jan 20.
4934	Circular RNA	Circ_002631	mmiR-33-y	Kpan6	kidney tissues	Cardiorenal Syndrome	Mus musculus (mouse)	qRT-PCR	33494070	RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome.	Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4215-4241. doi: 10.18632/aging.202385. Epub 2021 Jan 20.
4935	Circular RNA	CircEPSTI1	miR-375	SLC7A11	cervical cancer cells	Cervical Cancer	Mus musculus (mouse)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4936	Circular RNA	CircEPSTI1	miR-409-3p	SLC7A11	cervical cancer cells	Cervical Cancer	Mus musculus (mouse)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4937	Circular RNA	CircEPSTI1	miR-515-5p	SLC7A11	cervical cancer cells	Cervical Cancer	Mus musculus (mouse)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4938	Circular RNA	CircLMO7	miR-30a-3p	WNT2	Gastric cancer cells	Gastric Cancer	Mus musculus (mouse)	Western blot;Luciferase reporter assay;RNA pull-down;RNA sequencing;	33397440	Circular RNA circLMO7 acts as a microRNA-30a-3p sponge to promote gastric cancer progression via the WNT2/β-catenin pathway.	BACKGROUND: Gastric cancer (GC) is one of the most common malignant tumors worldwide. Currently, the overall survival rate of GC is still unsatisfactory despite progress in diagnosis and treatment. Therefore, studying the molecular mechanisms involved in GC is vital for diagnosis and treatment. CircRNAs, a type of noncoding RNA, have been proven to act as miRNA sponges that can widely regulate various cancers. By this mechanism, circRNA can regulate tumors at the genetic level by releasing miRNA from inhibiting its target genes. The WNT2/β-Catenin regulatory pathway is one of the canonical signaling pathways in tumors. It can not only promote the development of tumors but also provide energy for tumor growth through cell metabolism (such as glutamine metabolism). METHODS: Through RNA sequencing, we found that hsa_circ_0008259 (circLMO7) was highly expressed in GC tissues. After verifying the circular characteristics of circLMO7, we determined the downstream miRNA (miR-30a-3p) of circLMO7 by RNA pull-down and luciferase reporter assays. We verified the effect of circLMO7 and miR-30a-3p on GC cells through a series of functional experiments, including colony formation, 5-ethynyl-2'-deoxyuridine and Transwell assays. Through Western blot and immunofluorescence analyses, we found that WNT2 was the downstream target gene of miR-30a-3p and further confirmed that the circLMO7-miR-30a-3p-WNT2 axis could promote the development of GC. In addition, measurement of related metabolites confirmed that this axis could also provide energy for the growth of GC cells through glutamine metabolism. We found that circLMO7 could promote the growth and metastasis of GC in vivo by the establishment of nude mouse models. Finally, we also demonstrated that HNRNPL could bind to the flanking introns of the circLMO7 exons to promote circLMO7 cyclization. RESULTS: CircLMO7 acted as a miR-30a-3p sponge affecting the WNT2/β-Catenin pathway to promote the proliferation, migration and invasion of GC cells. Moreover, animal results also showed that circLMO7 could promote GC growth and metastasis in vivo. CircLMO7 could also affect the glutamine metabolism of GC cells through the WNT2/β-Catenin pathway to promote its malignant biological function. In addition, we proved that HNRNPL could promote the self-cyclization of circLMO7. CONCLUSIONS: CircLMO7 promotes the development of GC by releasing the inhibitory effect of miR-30a-3p on its target gene WNT2.	NA	J Exp Clin Cancer Res. 2021 Jan 5;40(1):6. doi: 10.1186/s13046-020-01791-9.
4939	Circular RNA	CircPVT1	miR-423-5p	HK2	Osteosarcoma cells	Bone Cancer	Mus musculus (mouse)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4940	Circular RNA	CircPVT1	miR-423-5p	PKM2	Osteosarcoma cells	Bone Cancer	Mus musculus (mouse)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4941	Circular RNA	CircPVT1	miR-423-5p	GLUT1	Osteosarcoma cells	Bone Cancer	Mus musculus (mouse)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4942	Circular RNA	CircPVT1	miR-423-5p	LDHA	Osteosarcoma cells	Bone Cancer	Mus musculus (mouse)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4943	Circular RNA	CircRNA_0005529	miR-527	Sp1	gastric cancer tissues and cells	Gastric Cancer	Mus musculus (mouse)	FISH;qRT-PCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	33472586	circRNA_0005529 facilitates growth and metastasis of gastric cancer via regulating miR-527/Sp1 axis.	BACKGROUND: Circular RNAs (circRNAs) are endogenous non-coding RNAs, which are associated with various biological processes, including microRNA (miRNA) interaction, protein binding and regulatory splicing. circRNA_0005529 (circ_0005529) is derived from vacuolar protein sorting 33 homologue B (VPS33B), and its biological role in gastric cancer (GC) has not been examined. In this study, the expression and location of circ_0005529 and microRNA-527 (miR-527) were determined by qRT-PCR and fluorescence in situ hybridization (FISH). Cell proliferation and cell migration were determined by MTT, EdU incorporation, colony formation, wound scratch and transwell assays. In addition, immunohistochemistry and western blotting were performed to determine the expressions of specificity protein 1 (Sp1), PCNA, c-myc, E-cadherin and N-cadherin. Western blotting and luciferase reporter assay were performed to study the interaction between circ_0005529 and miR-527 or miR-527 and Sp1. The functional effects of circ_0005529 on GC through regulating Sp1 were further evaluated using xenograft and metastatic mouse models in vivo. RESULTS: Our results showed that circ_0005529 was upregulated in GC tissues and cells, and had promoting effects on cell proliferation and cell migration. Mechanism analysis suggested that circ_0005529 could bind to microRNA-527 (miR-527) and reduce its expression. The interaction between miR-527 and Sp1 in GC was systematically studied. In addition, the results indicated that Sp1 upregulation could rescue the effects on cell proliferation and migration caused by circ_0005529. Moreover, the inhibitory effects of circ_0005529 downregulation on GC growth and metastasis were evaluated in mouse models. These findings suggested that the axis of circ_0005529/miR-527/Sp1 may serve as a promising treatment target for GC diagnosis and treatment. CONCLUSIONS: These findings suggested that the signal axis of circ_0005529/miR-527/Sp1 may has the potential to be explored as a novel therapeutic target for GC diagnosis and treatment. Mechanism diagram: During GC development, overexpressed circ_0005529 sponged miR-527 and then upregulated the expression of Sp1. Subsequently, epithelial-mesenchymal transition (EMT), cell proliferation and cell migration were promoted, which ultimately facilitated the tumor metastasis.	NA	BMC Mol Cell Biol. 2021 Jan 20;22(1):6. doi: 10.1186/s12860-020-00340-8.
4944	Circular RNA	CircSND1	miR-125a-3p	FUT6	HeLa cells	Cervical Cancer	Mus musculus (mouse)	qRT-PCR;Western blot;Fluorescent reporter;luciferase assay;	33469369	CircSND1 Regulated by TNF-α Promotes the Migration and Invasion of Cervical Cancer Cells.	AIM: To explore the role and potential mechanism of circSND1 in cervical cancer (CC). MAIN METHODS: qRT-PCR was used to determine the expression of circSND1 in tumor necrosis factor-α (TNF-α)-treated HeLa cells. CircSND1 overexpression and knockdown were performed to indicate the functional role of circSND1 in vitro and in vivo. Luciferase assay was used to analyze promoter activity. The expression and regulation of circSND1, miR-125a-3p and FUT6 were evaluated using EGFP fluorescent reporter assay and rescue experiments. Immunofluorescence and Western blot assays were used to analyze the activation of nuclear factor-κB (NF-κB). RESULTS: In HeLa cells, TNF-α up-regulated the expression of circSND1 by activating the NF-κB signaling pathway. Overexpression of circSND1 significantly increased the migration and invasion and the epithelial-mesenchymal transition (EMT) process of CC cells, and promoted tumor metastasis in xenograft nude mouse model, whereas down-regulation of circSND1 exerted opposite effects. Furthermore, circSND1 enhanced the expression of FUT6 via sponging miR-125a-3p, and FUT6 activated NF-κB signaling pathway. CONCLUSION: We found that circSND1 promoted the expression of FUT6 and the malignant behavior of cervical cancer through the ceRNA mechanism, and there was a TNF-α/NF-κB/circSND1/miR-125a-3p/FUT6/NF-κB positive feedback pathway between them, which suggests that circSND1 can be a promising prognostic marker and therapeutical target for cervical cancer.	NA	Cancer Manag Res. 2021 Jan 12;13:259-275. doi: 10.2147/CMAR.S289032. eCollection 2021.
4945	LncRNA	HIF1A-AS1	miR-138	NF-kB	myocardium and primary cardiomyocytes	Cardiomyocyte Apoptosis	Mus musculus (mouse)	Flow Cytometry assay;	33224748	The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.	BACKGROUND: Cardiomyocyte apoptosis and inflammation induced by Coxsackievirus B3 (CVB3) are key pathogenetic mechanisms in viral myocarditis. Alterations in microRNAs and lncRNAs are associated with cardiac remodeling. However, whether the microRNA and lncRNA interact to regulate cardiomyocyte apoptosis and inflammation is unknown. METHODS: BALB/c mice were infected with CVB3 to generate acute viral myocarditis model. The expression levels of lncRNA HIF1A-AS1 and miR-138 were examined in mouse myocardium and primary cardiomyocytes with CVB3 infection. We then knocked down HIF1A-AS1 by siRNA and upregulated miR-138 by microRNA mimics in cardiomyocytes. RESULTS: The expression of lncRNA HIF1A-AS1was significantly increased in CVB3-induced myocardium and cardiomyocytes. As documented by flow cytometry, silencing of HIF1A-AS1 alleviated late apoptosis (5.1%±2.8% vs. 17.2%±4.2%, P<0.01) and ROS production (68.73%±2.78% vs. 90.40%±2.86%, P<0.01) compared to their levels in cardiomyocytes transfected with control siRNA. The content of proinflammatory cytokines was substantially decreased by HIF1A-AS1 siRNA. Furthermore, we identified that HIF1A-AS1 bound to miR-138 and significantly suppressed miR-138 expression. Blocking HIF1A-AS1 attenuated IκBα phosphorylation and NF-κB activity, while cotransfection with miR-138 mimics markedly reversed its effect. CONCLUSIONS: In conclusion, lncRNA HIF1A-AS1 promotes NF-κB signaling and subsequently aggravates cardiomyocyte apoptosis and inflammation via targeting miR-138.	NA	Cardiovasc Diagn Ther. 2020 Oct;10(5):1245-1255. doi: 10.21037/cdt-20-545.
4946	LncRNA	HIF1A-AS1	miR-138	NF-kB	myocardium and primary cardiomyocytes	Cardiomyocyte Inflammation	Mus musculus (mouse)	Flow Cytometry assay;	33224748	The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.	BACKGROUND: Cardiomyocyte apoptosis and inflammation induced by Coxsackievirus B3 (CVB3) are key pathogenetic mechanisms in viral myocarditis. Alterations in microRNAs and lncRNAs are associated with cardiac remodeling. However, whether the microRNA and lncRNA interact to regulate cardiomyocyte apoptosis and inflammation is unknown. METHODS: BALB/c mice were infected with CVB3 to generate acute viral myocarditis model. The expression levels of lncRNA HIF1A-AS1 and miR-138 were examined in mouse myocardium and primary cardiomyocytes with CVB3 infection. We then knocked down HIF1A-AS1 by siRNA and upregulated miR-138 by microRNA mimics in cardiomyocytes. RESULTS: The expression of lncRNA HIF1A-AS1was significantly increased in CVB3-induced myocardium and cardiomyocytes. As documented by flow cytometry, silencing of HIF1A-AS1 alleviated late apoptosis (5.1%±2.8% vs. 17.2%±4.2%, P<0.01) and ROS production (68.73%±2.78% vs. 90.40%±2.86%, P<0.01) compared to their levels in cardiomyocytes transfected with control siRNA. The content of proinflammatory cytokines was substantially decreased by HIF1A-AS1 siRNA. Furthermore, we identified that HIF1A-AS1 bound to miR-138 and significantly suppressed miR-138 expression. Blocking HIF1A-AS1 attenuated IκBα phosphorylation and NF-κB activity, while cotransfection with miR-138 mimics markedly reversed its effect. CONCLUSIONS: In conclusion, lncRNA HIF1A-AS1 promotes NF-κB signaling and subsequently aggravates cardiomyocyte apoptosis and inflammation via targeting miR-138.	NA	Cardiovasc Diagn Ther. 2020 Oct;10(5):1245-1255. doi: 10.21037/cdt-20-545.
4947	LncRNA	HOXA-AS3	miR-455-5p	Notch1	bladder cancer cells	Bladder Cancer	Mus musculus (mouse)	CCK-8 assay;Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33643896	Reduction of Bladder Cancer Chemosensitivity Induced by the Effect of HOXA-AS3 as a ceRNA for miR-455-5p That Upregulates Notch1.	Chemoresistance is one of the main causes of recurrence in bladder cancer patients and leads to poor prognosis. Recently, long non-coding RNAs, like HOXA-AS3, have been reported to regulate chemoresistance in several types of cancer. In this study, we aimed to determine whether HOXA-AS3 can mediate cisplatin resistance in bladder cancer, and its potential mechanism of action. We determined the viability, proliferation, and apoptosis of bladder cancer cells using a CCK-8 assay, EdU staining, and flow cytometry, respectively. We used western blot analysis to assess the expression of markers of epithelial-mesenchymal transition (EMT) and Notch1. We then confirmed expression of these EMT-related markers by immunofluorescence analysis. We found that hypoxia promoted resistance to cisplatin and upregulated the level of HOXA-AS3 in BC cells. Inhibition of HOXA-AS3 enhanced hypoxia-induced cisplatin sensitivity by regulating EMT and Notch1 in BC cells. A dual-luciferase reporter assay confirmed that HOXA-AS3 directly targets miR-455-5p and that Notch1 was a potential target of miRNA-455-5p. We also found that the positive effect of HOXA-AS3 inhibition on cisplatin resistance and tumorigenesis was alleviated when BC cells were transfected with miR-455-5p. Finally, we showed combining HOXA-AS3 small interfering RNA (siRNA) with cisplatin treatment inhibited tumorigenesis in a BALB/c nu/nu mouse model. Our findings indicate that HOXA-AS3 may function as a competing endogenous RNA (ceRNA) of miR-455-5p to regulate Notch1 and play an important role in regulating chemotherapeutic drug sensitivity in BC cells. Therefore, HOXA-AS3 may be a novel therapeutic target for treating bladder cancer.	NA	Front Oncol. 2021 Feb 12;10:572672. doi: 10.3389/fonc.2020.572672. eCollection 2020.
4948	LncRNA	kcnq1ot1	miR-452-3p	HDAC3	mouse aorta with atherosclerosis and lipid-loaded macrophages	Atherosclerosis	Mus musculus (mouse)	qRT-PCR	33293505	LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.	Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE(-/-) mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE(-/-) mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.	NA	Cell Death Dis. 2020 Dec 9;11(12):1043. doi: 10.1038/s41419-020-03263-6.
4949	LncRNA	kcnq1ot1	miR-452-3p	ABCA1	mouse aorta with atherosclerosis and lipid-loaded macrophages	Atherosclerosis	Mus musculus (mouse)	qRT-PCR	33293505	LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.	Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE(-/-) mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE(-/-) mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.	NA	Cell Death Dis. 2020 Dec 9;11(12):1043. doi: 10.1038/s41419-020-03263-6.
4950	LncRNA	LINC00242	miR-1-3p	G6PD	gastric cancer tissues and cells	Gastric Cancer	Mus musculus (mouse)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	33514309	LINC00242/miR-1-3p/G6PD axis regulates Warburg effect and affects gastric cancer proliferation and apoptosis.	BACKGROUND: Reprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark of cancer. Long non-coding RNAs (lncRNAs) have been certified to play a crucial role in tumor progression. The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer. METHOD: LINC00242, miR-1-3p and G6PD expression levels in gastric cancer tissues and cells were determined by qRT-PCR. Cell apoptosis or viability were examined by Flow cytometry or MTT assay. Western blot was utilized to investigate G6PD protein expression levels. Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining were used for histopathological detection. The targeted relationship between LINC00242 or G6PD and miR-1-3p was verified by luciferase reporter gene assay. Nude mouse xenograft was utilized to detect tumor formation in vivo. RESULT: LINC00242 and G6PD was high-expressed in gastric cancer tissues and cells, and LINC00242 is positively correlated with G6PD. Silencing of LINC00242 or G6PD within gastric cancer cells prominently inhibited cell proliferation and aerobic glycolysis in vitro and relieved the tumorigenesis of gastric cancer in vivo. miR-1-3p was predicted to directly target both LINC00242 and G6PD. Overexpression of miR-1-3p suppressed gastric cancer cells proliferation and aerobic glycolysis. LINC00242 competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression on G6PD. CONCLUSION: LINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ G6PD axis, therefore affecting gastric cancer cell proliferation.	NA	Mol Med. 2021 Jan 29;27(1):9. doi: 10.1186/s10020-020-00259-y.
4951	LncRNA	LINC00667	miR-4319	FOXQ1	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Mus musculus (mouse)	qRT-PCR	33569351	LINC00667 Sponges miR-4319 to Promote the Development of Nasopharyngeal Carcinoma by Increasing FOXQ1 Expression.	Accumulating evidence has indicated that lncRNAs regulate various biological and pathological processes in diverse malignant tumors. The roles of LINC00667 in cancer development have been explored in glioma, hepatocellular carcinoma and non-small cell lung cancer, but not in nasopharyngeal carcinoma (NPC). In the present study, we characterize the role and molecular mechanism of LINC00667 in NPC progression. It was found that LINC00667 was overexpressed in NPC cells compared to normal cells. Silencing LINC00667 suppressed the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) in NPC cells. In addition, bioinformatics analysis revealed that LINC00667 acted as a ceRNA to absorb miR-4319. Further investigations illustrated that miR-4319 had low expression in NPC cells and functioned as a tumor suppressor in the progression of NPC. Mechanistic study identified forkhead box Q1 (FOXQ1) as a functional target of miR-4319. The effect of LINC00667 in NPC development was mediated by the miR-4319/FOXQ1 axis. Analysis on tumorxenograft mouse model demonstrated that knockdown of LINC00667 repressed NPC tumor growth in vivo and confirmed the in vitro results. Our present study suggested that LINC00667 promoted the malignant phenotypes of NPC cells by competitively binding to miR-4319 to up-regulate FOXQ1 expression. Our results reveled that LINC00667 could be a diagnostic and therapeutic target for NPC patients.	NA	Front Oncol. 2021 Jan 25;10:632813. doi: 10.3389/fonc.2020.632813. eCollection 2020.
4952	LncRNA	lincRNA-p21	miR-181a	NA	mononuclear and urine cells	Lupus Nephritis	Mus musculus (mouse)	qRT-PCR	33396699	Up-Regulated Expression of Pro-Apoptotic Long Noncoding RNA lincRNA-p21 with Enhanced Cell Apoptosis in Lupus Nephritis.	Accelerated cell apoptosis with dysregulated long noncoding RNAs is the crucial pathogenesis in lupus nephritis (LN). Pro-apoptotic lincRNA-p21 was studied in LN patients, cell lines with lentivirus-mediated overexpression and CRISPR interference (CRISPRi)-conducted repression, and a mouse model. Clinical samples were from patients and age/sex-matched controls. Expression of lincRNA-p21 and endogenous RNA target miR-181a, were examined in mononuclear and urine cells. Guide RNA sequences targeting lincRNA-p21 were cloned into CRISPRi with dCas9/ Krüppel-associated box (KRAB) domain. LincRNA-p21-silened transfectants were investigated for apoptosis and miR-181a expression. LincRNA-p21-overexpressed cells were evaluated for apoptosis and p53-related down-stream molecules. Balb/C mice were injected with pristane to induce LN and examined for apoptosis and lincRNA-p21. Higher lincRNA-p21 levels were found in LN mononuclear and urine cells, positively correlated with activity. There were lower miR-181a levels in LN mononuclear cells, negatively correlated with activity. Doxorubicin-induced apoptotic cells had up-regulated lincRNA-p21 levels. CRISPRi with dCas9/KARA domain showed efficient repression ability on transcription initiation/elongation. CRISPRi-conducted lincRNA-p21-silenced transfectants displayed reduced apoptosis with up-regulated miR-181a levels, whereas lentivirus-mediated lincRNA-p21-overexpressed cells revealed enhanced apoptosis with up-regulated downstream PUMA/Bax expression. LN mice had glomerular apoptosis with progressive increased lincRNA-p21 levels. Our results demonstrate up-regulated lincRNA-p21 expression in LN, implicating a potential diagnostic marker and therapeutic target.	NA	Int J Mol Sci. 2020 Dec 30;22(1):301. doi: 10.3390/ijms22010301.
4953	LncRNA	loc339803	miR-30a-5p	SNAIL1	Hepatocellular carcinoma cells	Hepatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR;Western blot;Luciferase reporter assay;	33442404	LncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells.	Background: Hepatocellular carcinoma (HCC), a most common malignant tumor, has an unfavorable clinical outcome. Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) play an important role in the carcinogenesis and progression of HCC. However, the clinical significances and the biological roles of most lncRNAs in HCC remain poorly understood. Methods: The expression levels of lncRNA loc339803 in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR) assay. The cellular sublocalization of loc339803 was determined by fluorescence in situ hybridization and nuclear and cytoplasmic RNA isolation assay. Western blot, CCK-8, Edu, colony formation, migration and invasion assays were used to investigate the roles of loc339803 in HCC progression in vitro. A mouse model for lung metastasis was constructed to evaluate the role of loc339803 in HCC development in vivo. The correlations among loc339803, miR-30a-5p and SNAIL1 were validated by qRT-PCR and a dual- luciferase reporter assay. Results: The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. Loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro. Further studies demonstrated that loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of SNAIL1, a target gene of miR-30a-5p. Moreover, miR-30a-5p upregulation blocked the enhanced migration and invasion of HCC cells induced by loc339803 overexpression. Conclusions: Loc339803 may be oncogenic in HCC and associated with poor clinical outcomes. LncRNA loc339803 might promote the invasion and migration of HCC cells through regulating miR-30a-5p/ SNAIL1 axis.	NA	J Cancer. 2021 Jan 1;12(4):1061-1072. doi: 10.7150/jca.52413. eCollection 2021.
4954	LncRNA	MEG3	miR-107-5p	PABPC4	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4955	LncRNA	MEG3	miR-149-3p	PABPC4	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4956	LncRNA	MEG3	miR-346-3	PABPC4	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4957	LncRNA	MEG3	miR-107-5p	CEP131	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4958	LncRNA	MEG3	miR-149-3p	CEP131	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4959	LncRNA	MEG3	miR-346-3	CEP131	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4960	LncRNA	MEG3	miR-107-5p	NUMB1	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4961	LncRNA	MEG3	miR-149-3p	NUMB1	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4962	LncRNA	MEG3	miR-346-3	NUMB1	mouse model	Cholesterol Gallstone	Mus musculus (mouse)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
4963	LncRNA	Peg13	miR-128-3p	Sox13	neural stem cells	Sevoflurane Exposure-Related Neurotoxicity Against Neural Stem Cells	Mus musculus (mouse)	Flow cytometry assay;Flow Cytometry assay;Luciferase reporter assay;	33296418	Long non-coding RNA Peg13 attenuates the sevoflurane toxicity against neural stem cells by sponging microRNA-128-3p to preserve Sox13 expression.	BACKGROUND: Exposure to anesthetics during brain development may impair neurological function, however, the mechanisms underlying anesthetic neurotoxicity are unclear. Recent studies indicate that long non-coding RNAs (lncRNAs) are crucial for regulating the functional brain development during neurogenesis. This study aimed to determine the regulatory effects and potential mechanisms of lncRNA Peg13 (Peg13) on sevoflurane exposure-related neurotoxicity against neural stem cells (NSCs). METHODS: Mouse embryotic NSCs were isolated and their self-renewal and differentiation were characterized by immunofluorescence. NSCs were exposed to 4.1% sevoflurane 2 h daily for three consecutive days. The potential toxicities of sevoflurane against NSCs were evaluated by neurosphere formation, 5-ethynyl-2'-deoxyuridine (EdU) incorporation and flow cytometry assays. The Peg13, miR-128-3p and Sox13 expression in NSCs were quantified. The potential interactions among Peg13, miR-128-3p and Sox13 were analyzed by luciferase reporter assay. The effects of Peg13 and/or miR-128-3p over-expression on the sevoflurane-related neurotoxicity and Sox13 expression were determined in NSCs. RESULTS: The isolated mouse embryotic NSCs displayed potent self-renewal ability and differentiated into neurons, astrocytes and oligodendrocytes in vitro, which were significantly inhibited by sevoflurane exposure. Sevoflurane exposure significantly down-regulated Peg13 and Sox13, but enhanced miR-128-3p expression in NSCs. Transfection with miR-128-3p mimics, but not the control, significantly mitigated the Peg13 or Sox13-regulated luciferase expression in 293T cells. Peg13 over-expression significantly reduced the sevoflurane-related neurotoxicity and increased Sox13 expression in NSCs, which were mitigated by miR-128-3p transfection. CONCLUSION: Such data indicated that Peg13 mitigated the sevoflurane-related neurotoxicity by sponging miR-128-3p to preserve Sox13 expression in NSCs.	NA	PLoS One. 2020 Dec 9;15(12):e0243644. doi: 10.1371/journal.pone.0243644. eCollection 2020.
4964	LncRNA	PVT1	miR-146a	SMAD4	Articular tissues	Diabetic Osteoarthritis	Mus musculus (mouse)	Western blot;Luciferase reporter assay;	33569722	LncPVT1 promotes cartilage degradation in diabetic OA mice by downregulating miR-146a and activating TGF-β/SMAD4 signaling.	INTRODUCTION: To investigate the role of LncRNA PVT1 (plasmacytoma variant translocation 1) in hyperglycemia-triggered cartilage damage using the diabetic osteoarthritis (OA) mice model. MATERIALS AND METHODS: Streptozotocin (STZ) was used to induce mouse diabetes. Knee OA model was induced through transection of anterior cruciate ligament (ACLT). Severity of arthritis was assessed histologically by Safranin O-Fast Green Staining using Mankin Scores. LncRNA PVT1 and miR-146a were detected by real-time polymerase chain reaction (PCR) in cartilage tissue. Moreover, the interaction among PVT1, miR-146a, and SMAD4 was examined by luciferase reporter assays. Mice were injected intra-articularly with ad-siRNA-PVT1 and ad-siRNA scramble control. Articular concentrations of TNF-α, IL-1, IL-6 and TGF-β1 were determined using enzyme-linked immunosorbent assay. Levels of type II Collagen (COL2A1), TGF-β1, p-SMAD2, SMAD2, p-SMAD3, SMAD3, SMAD4 and nuclear SMAD4 were detected by western blot analysis. RESULTS: PVT1 expression was significantly increased, whereas miR-146a was markedly decreased in diabetic OA mice than in non-diabetic OA and control. Increased PVT1 expression in diabetic OA mice was significantly associated with Mankin score and reduced miR-146a as well as Collagen alpha-1(II) (COL2A1) expressions. In vivo, intra-articular injection of ad-siRNA-PVT1 efficiently increased miR-146a and COL2A1 expressions, alleviated joint inflammation, decreased the expression of pro-inflammatory mediators, and suppressed TGF-β/SMAD4 pathway in diabetic OA mice. CONCLUSIONS: Our results demonstrate LncRNA PVT1 is involved in cartilage degradation in diabetic OA and correlated with disease severity. Efficiency of ad-siRNA-PVT1 in controlling joint inflammation in diabetic OA mice is associated with the suppression of the expression of miR-146a, pro-inflammatory cytokines and activation of TGF-β/SMAD4 pathway.	NA	J Bone Miner Metab. 2021 Feb 10. doi: 10.1007/s00774-020-01199-7.
4965	LncRNA	RAET1K	miR-503-5p	INPP4B	HL-60 and THP-1 cells	Acute Myeloid Leukemia	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33500628	lncRNA RAET1K Promotes the Progression of Acute Myeloid Leukemia by Targeting miR-503-5p/INPP4B Axis.	BACKGROUND: Although long non-coding RNA (lncRNA) RAET1K has been observed to be abnormally expressed in patients with various cancers, its role and molecular mechanism in acute myeloid leukemia (AML) remain unclear. METHODS: The expression of RAET1K and miR-503-5p in bone marrow tissues and cell lines was detected by qRT-PCR. Cell proliferation was evaluated by cell counting kit-8 and 5-ethynyl-20-deoxyuridine (EdU) staining assay. Cell invasion and migration were detected by transwell assay. Cell apoptosis was evaluated by flow cytometry. The relationship between RAET1K and miR-503-5p, as well as miR-503-5p and INPP4B, was determined by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. In addition, the tumorigenesis of leukemia cells was evaluated by using a xenograft mouse model in vivo. RESULTS: RAET1K was significantly upregulated and miR-503-5p was markedly downregulated in bone marrow tissues and cell lines (HL-60 and THP-1). Silencing of RAET1K (si-RAET1K) and overexpression of miR-503-5p inhibited cell proliferation, migration, and invasion but promoted apoptosis of HL-60 and THP-1 cells. RAET1K functioned as a sponge of miR-503-5p, and miR-503-5p inhibitor obviously attenuated the effect of si-RAET1K on AML progression in vitro. INPP4B was identified as a target of miR-503-5p, and INPP4B overexpression obviously reversed the effect of miR-503-5p mimics on cell proliferation, migration, invasion, and apoptosis of HL-60 and THP-1 cells in vitro. Knockdown of RAET1K effectively inhibited the tumorigenesis of leukemia cells in vivo. CONCLUSION: Our results demonstrated that RAET1K/miR-503-5p/INPP4B axis contributed to AML progression, suggesting that RAET1K might be a potential target for the treatment of AML.	NA	Onco Targets Ther. 2021 Jan 18;14:531-544. doi: 10.2147/OTT.S291123. eCollection 2021.
4966	LncRNA	TRPM2-AS	miR-138-5p	EGFR	non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;Luciferase reporter assay;	33209893	Long non-coding RNA TRPM2-AS sponges microRNA-138-5p to activate epidermal growth factor receptor and PI3K/AKT signaling in non-small cell lung cancer.	BACKGROUND: Long non-coding RNAs (lncRNAs) can play pivotal roles in tumor progression by acting as microRNA (miRNA) sponges. This study aimed to investigate the association of a novel lncRNA, TRPM2-AS, with the miR-138-5p/EGFR axis in the development of non-small cell lung cancer (NSCLC). METHODS: Sixty NSCLC tissues and paired adjacent non-tumor tissues were analyzed. The relative expression levels of TRPM2-AS, miR138-5p, and epidermal growth factor receptor (EGFR) and the interactions between them were analyzed. The NSCLC cell lines NCI-H1299 and A549 were transfected with TRPM2-AS shRNA/pcDNA, and miR-138-5p mimics. Cell proliferation, migration, invasion, and apoptosis were examined in response to different transfection conditions. Dual-luciferase reporter assay was performed to identify the target interactions between TRPM2-AS, miR-138-5p, and EGFR. A549 cells stably transfected with shRNA were injected into BALB/c null nude mice to establish a tumor xenograft model. RESULTS: TRPM2-AS was up-regulated in NSCLC tumors and cell lines. Cell proliferation, migration, and invasion were inhibited in NSCLC cells treated with sh-TRPM2-AS, while apoptosis was induced. The targeting of TRPM2-AS by miR138-5p and miR138-5p by EGFR were validated with dual-luciferase reporter assay. TRPM2-AS was found to be negatively correlated with miR138-5p but positively correlated with EGFR. PI3K/AKT/mTOR was activated by pcDNA-EGFR but inactivated by miR-138-5p mimics. In the tumor xenograft mouse model, sh-TRPM2-AS suppressed tumor formation, reduced the expression of EGFR and Ki67, and promoted tumor cell apoptosis. CONCLUSIONS: Our results suggested that TRPM2-AS can increase the levels of EGFR via sponging miR-138-3p; this promoted NSCLC cell proliferation, migration, and invasion in vitro, and exacerbated tumors in vivo. These findings highlight TRPM2-AS/miR-138-5p as a potential target for reducing drug resistance in patients with NSCLC.	NA	Ann Transl Med. 2020 Oct;8(20):1313. doi: 10.21037/atm-20-6331.
4967	LncRNA	TTTY15	miR-374a-5p	FOXO1	H9c2 and HL-1 cells	Myocardial Ischamia Reperfusion Injury Injury	Mus musculus (mouse)	qRT-PCR	33296140	Knockdown of lncRNA TTTY15 alleviates myocardial ischemia-reperfusion injury through the miR-374a-5p/FOXO1 axis.	Myocardial ischemia/reperfusion (I/R) injury greatly contributes to myocardial tissue damage in patients with coronary disease, which eventually leads to heart failure. Long noncoding RNAs (lncRNAs) have an emerging role in the process of myocardial I/R injury. Our previous work revealed the protective role of miR-374a-5p against myocardial I/R injury. In this study, we explored the role of lncRNA TTTY15 and its potential interaction mechanisms with miR-374a-5p in myocardial I/R injury. The expression of TTTY15 was increased both in vitro and in vivo after myocardial I/R injury models according to quantitative real-time polymerase chain reaction. Various assays were conducted to evaluate the regulatory relationship among TTTY15, miR-374a-5p, FOXO1, and autophagy in H9c2 and HL-1 cells. The results showed that TTTY15 suppresses autophagy and myocardial I/R injury by targeting miR-374a-5p. We found that TTTY15 regulates miR-374a-5p, thus affecting FOXO1 expression and autophagy in myocytes during I/R. Furthermore, in an in vivo mouse model of myocardial I/R injury, suppression of TTTY15 successfully alleviated myocardial I/R injury. Our results reveal a novel feedback mechanism in which TTTY15 regulates miRNA processing and a potential target in myocardial I/R injury. TTTY15 is a promising therapeutic target for treating myocardial I/R injury.	NA	IUBMB Life. 2021 Jan;73(1):273-285. doi: 10.1002/iub.2428. Epub 2020 Dec 9.
4968	LncRNA	XIST	miR-758-3p	caspase3	osteoblast	Postmenopausal Osteoporosis	Mus musculus (mouse)	ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33336851	Iron accumulation regulates osteoblast apoptosis through lncRNA XIST/miR-758-3p/caspase 3 axis leading to osteoporosis.	Postmenopausal osteoporosis (PMOP) is mainly caused by multiple factors. Recent studies have suggested that iron accumulation (IA) was closely related to PMOP. However, the detailed molecular mechanisms have not been well demonstrated. We constructed the IA mouse model by intraperitoneal injections of ferric ammonium citrate (FAC) and cell model by culturing with the medium containing FAC. Osteoporosis was confirmed in mouse bone tissues using H&E staining, and the level of serum ferritin, alkaline phosphatase (ALP), procollagen-1 N-terminal peptide (P1NP), and osteocalcin in mice was examined by ELISA. The expressions of XIST and miR-758-3p were detected by qRT-PCR. Cell proliferation and apoptosis were measured by CCK-8, TUNEL, and flow cytometry. The expression levels of apoptotic-related proteins were evaluated by western blot. Dual luciferase reporter assay was used to examine the molecular interaction. The expressions of ALP, P1NP, and osteocalcin, and the H&E staining of bone tissues in mice were analyzed to confirm the biological function of XIST and miR-758-3p in vivo. XIST was up-regulated while miR-758-3p was down-regulated in IA mouse and cell models. XIST knockdown significantly reduced FAC-induced osteoblast apoptosis, which was mimicked by transfection with miR-758-3p mimics. XIST acted as a sponge of miR-758-3p, which targeted caspase 3. IA led to the high expression of XIST and promoted osteoblast apoptosis through miR-758-3p/caspase 3. Transfection with shXIST or miR-758-3p mimics alleviated IA-induced mouse osteoporosis. IA regulated osteoblast apoptosis through XIST/miR-758-3p/caspase 3 axis, which might provide alternative targets for the treatment of osteoporosis.	NA	IUBMB Life. 2021 Feb;73(2):432-443. doi: 10.1002/iub.2440.
4969	LncRNA	H19	miR-29b-3p	FoxO3	umbilical cord mesenchymal stem cells	Osteochondral Regeneration	Rattus (rat)	Dual-luciferase reporter assay;FISH;RIP assay;RNA immunoprecipitation;FISH;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33463060	The umbilical cord mesenchymal stem cell-derived exosomal lncRNA H19 improves osteochondral activity through miR-29b-3p/FoxO3 axis.	BACKGROUND: Our previous study revealed that the exosomal lncRNA H19 derived from umbilical cord mesenchymal stem cells (UMSCs) plays a pivotal role in osteochondral regeneration. In this study, we investigated whether the exosomal lncRNA H19 could act as a competing endogenous RNA (ceRNA) to potentiate osteochondral activity in chondrocytes. METHODS: Dual-luciferase reporter assay, RNA pull-down, RNA immunoprecipitation (RIP), and fluorescence in situ hybridization (FISH) were carried to verify the interaction between miR-29b-3p and both lncRNA H19 and the target mRNA FoxO3. Chondrocytes were treated with UMSC-derived exosomes, which highly expressing lncRNA H19 expression, followed by apoptosis, migration, senescence, and matrix secretion assessments. An in vivo SD rat cartilage defect model was carried out to explore the role and mechanism of lncRNA H19/miR-29b-3p. RESULTS: UMSCs were successfully identified, and exosomes were successfully extracted. Exosomes exhibited the ability to transfer lncRNA H19 to chondrocytes. Mechanistically, exosomal lncRNA H19 potentiated osteochondral activity by acting as a competing endogenous sponge of miR-29b-3p, and miR-29b-3p directly targeted FoxO3. Intra-articular injection of exosomes overexpressing lncRNA H19 could promote sustained cartilage repair; however, this effect could be undermined by miR-29b-3p agomir. CONCLUSIONS: Our study revealed a significant role in the development of strategies against cartilage defects for UMSC-derived exosomes that overexpress lncRNA H19. Exosomal H19 was found to promote chondrocyte migration, matrix secretion, apoptosis suppression, as well as senescence suppression, both in vitro and in vivo. The specific mechanism lies in the fact that exosomal H19 acts as a ceRNA against miR-29b-3p to upregulate FoxO3 in chondrocytes.	NA	Clin Transl Med. 2021 Jan;11(1):e255. doi: 10.1002/ctm2.255.
4970	LncRNA	MEG3	miR-98-5p	IL-10	Ulcerative colitis tissues	Ulcerative Colitis	Rattus (rat)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33394187	Long Non-coding RNA MEG3 Alleviated Ulcerative Colitis Through Upregulating miR-98-5p-Sponged IL-10.	Ulcerative colitis (UC) is a refractory chronic colitis disease with the particularly complex cause. Recently, long noncoding RNAs (lncRNAs) have been reported to be related to the development of UC. LncRNA MEG3 has been proved to play an anti-inflammatory role in a variety of inflammatory diseases, which share similar pathogenesis with UC, indicating the potential involvement of lncRNA MEG3 in UC. This study aims to investigate the functional role and underlying mechanism of lncRNA MEG3 in UC. Gradient concentration of H(2)O(2) (0, 20, 50, 100, and 200 μM) was used to induce Caco-2 damage models in vitro. Cell viability was detected by cell counting kit-8 (CCK-8) assay. LncRNA MEG3, miR-98-5p, and IL-10 levels in H(2)O(2-)treated Caco-2 cells were assessed by performing real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the binding relationship between lncRNA MEG3 and miR-98-5p, as well as the binding relationship between miR-98-5p and IL-10, was validated using dual-luciferase reporter assay. 2, 4, 6-Trinitrobenzenesulfonic acid solution (TNBS) was applied to induce ulcerative colitis in young rats. The body weight, disease activity index (DAI), length and weight of the colons, pathological scores of UC rats, reactive oxygen species (ROS), and inflammatory cytokines were determined to evaluate the effects of lncRNA MEG3 on the progression of UC. Besides, hematoxylin-eosin (HE) staining was exploited to observe histological changes of UC rat colons. In addition, western blotting analysis was also performed to evaluate the apoptosis and pyroptosis-related protein levels. Moreover, lncRNA MEG3, miR-98-5p, and IL-10 levels in UC rat colons were further assessed by RT-qPCR. Meanwhile, IL-10 expression was determined using immunohistochemistry. LncRNA MEG3 and IL-10 levels were distinctly decreased while miR-98-5p was increased in Caco-2 damage models and UC rats. Bioinformatics analysis predicted the binding sites of lncRNA MEG3 to miR-98-5p and miR-98-5p to IL-10. Besides, dual-luciferase reporter assay validated the negative correlation between lncRNA MEG3 and miR-98-5p, miR-98-5p, and IL-10. Overexpressed lncRNA MEG3 reduced. DAI scores and colon weight/length ratio improved UC ulceration. In addition, upregulation of lncRNA MEG3 relieved oxidative stress, inflammatory response, apoptosis, and pyroptosis of UC rat colons. LncRNA MEG3 overexpression alleviates the serve ulceration of UC rat colons by upregulating IL-10 expression via sponging miR-98-5p. To sum up, this study reveals the protective role of lncRNA MEG3 in the development of UC and may provide potential therapeutic targets for UC.	NA	Inflammation. 2021 Jun;44(3):1049-1059. doi: 10.1007/s10753-020-01400-z. Epub 2021 Jan 4.
4971	LncRNA	SOX2OT	miR-331-3p	Neurod1	PC-12 cells	Spinal Cord Injury	Rattus (rat)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33340723	LncRNA SOX2OT Knockdown Alleviates Lipopolysaccharide-Induced Damage of PC12 Cells by Regulating miR-331-3p/Neurod1 Axis.	BACKGROUND: Long noncoding RNAs (lncRNAs) serve as crucial regulators in the pathogenesis of spinal cord injury (SCI). However, the role of lncRNA SOX2 overlapping transcript (SOX2OT) in SCI remains to be well revealed. METHODS: An SCI rat model was established and assessed by the Basso-Beattie-Bresnahan (BBB) method. An SCI PC12 cell model was established through lipopolysaccharide (LPS) treatment. Quantitative real-time polymerase chain reaction assay was used for SOX2OT, miR-331-3p, and neurogenic differentiation 1 (Neurod1) mRNA levels. Cell counting kit-8 assay and flow cytometry analysis were performed for cell viability and apoptosis, respectively. Enzyme-linked immunosorbent assay was performed for the levels of inflammatory cytokines. The production of superoxide dismutase and malondialdehyde was determined with relevant kits. Dual-luciferase reporter and RNA immunoprecipitation assays were conducted for the relationships among SOX2OT, miR-331-3p, and Neurod1. Western blot assay was employed for protein levels. RESULTS: SOX2OT was elevated in SCI rat and cell models. SOX2OT knockdown relieved the injury of SCI in SCI rat model. Moreover, the suppressive role in PC12 cell viability and the promotional roles in apoptosis, inflammation, and oxidative stress mediated by LPS were all restored by silencing SOX2OT. For mechanism analysis, SOX2OT was identified as a sponge of miR-331-3p to positively regulate Neurod1 expression. Inhibition of miR-331-3p reversed the effect of SOX2OT knockdown on LPS-induced PC12 damage. Overexpression of miR-331-3p protected PC12 cells from LPS-induced damage by binding to Neurod1. In addition, SOX2OT knockdown relieved PC12 cell injury by inactivation of Janus kinase-signal transducer and activator of transcription pathway. CONCLUSIONS: SOX2OT promoted PC12 cell injury through modulating miR-331-3p/Neurod1 axis and activating Janus kinase-signal transducer and activator of transcription pathway.	NA	World Neurosurg. 2021 Mar;147:e293-e305. doi: 10.1016/j.wneu.2020.12.049. Epub 2020 Dec 16.
4972	LncRNA	SOX2-OT	miR-942-5p	DP5	cardiomyocyte	Cardiomyocyte Apoptosis	Rattus (rat)	qRT-PCR;Immunoblotting;Luciferase reporter assay;	33603338	Long Noncoding RNA SOX2-OT Aggravates Doxorubicin-Induced Apoptosis of Cardiomyocyte by Targeting miR-942-5p/DP5.	BACKGROUND: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis. METHODS: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography. RESULTS: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo. CONCLUSION: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.	NA	Drug Des Devel Ther. 2021 Feb 11;15:481-492. doi: 10.2147/DDDT.S267474. eCollection 2021.
4973	LncRNA	TUG1	miR-29b-1-5p	MTDH	rat model of spinal cord IR	Ischemia Reperfusion Injury	Rattus (rat)	Dual-luciferase reporter assay;Luciferase reporter assay;	33225366	Downregulation of Long Noncoding RNA TUG1 Attenuates MTDH-Mediated Inflammatory Damage via Targeting miR-29b-1-5p After Spinal Cord Ischemia Reperfusion.	Long noncoding RNAs and microRNAs (miRNAs) play a vital role in spinal cord ischemia reperfusion (IR) injury. The aim of this study was to identify the potential interactions between taurine upregulated gene 1 (TUG1) and miRNA-29b-1-5p in a rat model of spinal cord IR. The IR injury was established by 14-minute occlusion of aortic arch. TUG1 and metadherin (MTDH) knockdown were induced by respective siRNAs, and miR-29b-1-5p expression was modulated using specific inhibitor or mimics. The interactions between TUG1, miR-29b-1-5p, and the target genes were determined using the dual-luciferase reporter assay. We found that IR respectively downregulated and upregulated miR-29b-1-5p and TUG1, and significantly increased MTDH expression. MTDH was predicted as a target of miR-29b-1-5p and its knockdown downregulated NF-κB and IL-1β levels. A direct interaction was observed between TUG1 and miR-29b-1-5p, and knocking down TUG1 upregulated the latter. Furthermore, overexpression of miR-29b-1-5p or knockdown of TUG1 alleviated blood-spinal cord barrier leakage and improved hind-limb motor function by suppressing MTDH and its downstream pro-inflammatory cytokines. Knocking down TUG1 also alleviated MTDH/NF-κB/IL-1β pathway-mediated inflammatory damage after IR by targeting miR-29b-1-5p, whereas blocking the latter reversed the neuroprotective effect of TUG1 knockdown and restored MTDH/NF-κB/IL-1β levels.	NA	J Neuropathol Exp Neurol. 2021 Feb 22;80(3):254-264. doi: 10.1093/jnen/nlaa138.
4974	LncRNA	AK148321	miR-1199-5p	HSPA5	LPS-stimulated BV2 cells	Neuroinflammation	Homo sapiens (human)	ELISA;qPCR;RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	33301806	LncRNA AK148321 alleviates neuroinflammation in LPS-stimulated BV2 microglial cell through regulating microRNA-1199-5p/HSPA5 axis.	AIMS: Dysregulated long non-coding RNA (lncRNA) expression is closely related to neuroinflammation, leading to multiple neurodegenerative diseases. In this study, we investigated the function and regulation of lncRNA AK148321 in neuroinflammation using an in vitro lipopolysaccharide (LPS)-stimulated BV2 microglial cell system. METHODS: Expression of AK148321 was analyzed by qPCR. Inflammatory cytokine expression levels were determined by ELISA assay. The interaction between AK148321, microRNA (miRNA), and its target gene was validated by luciferase reporter assay and RNA immunoprecipitation (RIP). Cell apoptosis was analyzed by Annexin V/PI staining. RESULTS: LPS treatment suppressed AK148321 expression in BV2 cells. Overexpression of AK148321 inhibited LPS-induced BV2 microglial cell activation and decreased the expression of inflammatory cytokine TNF-α and IL-1β. AK148321 function as a competing endogenous RNA (ceRNA) by sponging microRNA-1199-5p (MiR-1199-5p). In LPS-stimulated BV2 cells, AK148321 exerted its inhibitory function via negatively modulating miR-1199-5p expression. Moreover, we identified that Heat Shock Protein Family A Member 5 (HSPA5) was a direct target of miR-1199-5p. RIP assay using the anti-Ago2 antibody further validated the relationship among AK148321, miR-1199-5p and HSPA5. The AK148321/miR-1199-5p/HSPA5 axis regulated the neuroinflammation in LPS-induced BV2 microglial cells. Microglial cell culture supernatant from LPS-stimulated, AK148321-overexpressing BV2 cells suppressed the cell apoptosis of mouse hippocampal neuronal cell HT22, while HSPA5 knockdown abrogated the suppression effect. CONCLUSION: Our findings suggest that AK148321 alleviates neuroinflammation in LPS-stimulated BV2 microglial cells through miR-1199-5p/HSPA5 axis.	NA	Life Sci. 2021 Feb 1;266:118863. doi: 10.1016/j.lfs.2020.118863. Epub 2020 Dec 7.
4975	Circular RNA	AKT3	miR-17-5p	RHOC	esophageal cancer cells	Esophageal Cancer	Homo sapiens (human)	Luciferase reporter assay;	33519139	Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p.	BACKGROUND: Recent studies have demonstrated that circular RNA AKT3 (circAKT3) plays a crucial role in regulating the malignant phenotypes of tumor cells. However, the potential effects of circAKT3 on esophageal cancer have not been investigated. AIM: To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism. METHODS: Clinical samples were collected to detect the expression of circAKT3. The role of circAKT3 in proliferation, migration, invasion, and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8, wound healing assays, Transwell assays, and fluorescence analysis, respectively. The target of circAKT3 was screened and identified using an online database and luciferase reporter assay. A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo. RESULTS: In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer. CONCLUSION: CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.	NA	World J Gastroenterol. 2021 Jan 21;27(3):240-254. doi: 10.3748/wjg.v27.i3.240.
4976	Circular RNA	AKT3	miR-17-5p	STAT3	esophageal cancer cells	Esophageal Cancer	Homo sapiens (human)	Luciferase reporter assay;	33519139	Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p.	BACKGROUND: Recent studies have demonstrated that circular RNA AKT3 (circAKT3) plays a crucial role in regulating the malignant phenotypes of tumor cells. However, the potential effects of circAKT3 on esophageal cancer have not been investigated. AIM: To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism. METHODS: Clinical samples were collected to detect the expression of circAKT3. The role of circAKT3 in proliferation, migration, invasion, and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8, wound healing assays, Transwell assays, and fluorescence analysis, respectively. The target of circAKT3 was screened and identified using an online database and luciferase reporter assay. A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo. RESULTS: In vitro assays showed that proliferative, migratory, and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression. Furthermore, miR-17-5p was screened as the target of circAKT3, and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells. Moreover, we identified RHOC and STAT3 as the direct target molecules of miR-17-5p, and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p. In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer. CONCLUSION: CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.	NA	World J Gastroenterol. 2021 Jan 21;27(3):240-254. doi: 10.3748/wjg.v27.i3.240.
4977	Circular RNA	ARID1A	miR-6368	Tlr4	skeletal muscle tissues	Skeletal Muscle Cell Development And Regeneration	Homo sapiens (human)	ChIP;	33421208	CircARID1A regulates mouse skeletal muscle regeneration by functioning as a sponge of miR-6368.	The noncoding RNAs play important role in growth and development of mammalian skeletal muscle. Recent work has shown that circRNAs are abundant in skeletal muscle tissue, with significant changes in their expression patterns during muscle development and aging. We identified a novel circRNA called circARID1A that is highly expressed in mice skeletal muscle compare to its linear transcript. Experiments shown that circARID1A significantly inhibited the process of C2C12 cell proliferation and promoted its differentiation. Interactions between circRNA and miRNA were screened by miRNA gene chip sequencing. The results indicated that circARID1A can sponge miR-6368, which was further verified by miRNA sensor and other experiments. Besides, miR-6368 is a commonly expressed miRNA that regulates the expression of several target genes including Tlr4. A mouse model of skeletal muscle injury was successfully established to explore the role of circARID1A in skeletal muscle development and regeneration in vivo. Moreover, we found the overexpression of circARID1A significantly promoted the regeneration of skeletal muscle. The results of our study suggest that circARID1A may regulate skeletal muscle cell development and regeneration by sponging miR-6368.	NA	FASEB J. 2021 Feb;35(2):e21324. doi: 10.1096/fj.202001992R.
4978	Circular RNA	Circ_002631	miR-181a-5p	Creb1	kidney tissues	Cardiorenal Syndrome	Homo sapiens (human)	qRT-PCR	33494070	RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome.	Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4215-4241. doi: 10.18632/aging.202385. Epub 2021 Jan 20.
4979	Circular RNA	Circ_002631	mmiR-33-y	Kpan6	kidney tissues	Cardiorenal Syndrome	Homo sapiens (human)	qRT-PCR	33494070	RNA interactions in right ventricular dysfunction induced type II cardiorenal syndrome.	Right ventricular (RV) dysfunction induced type II cardiorenal syndrome (CRS) has a high mortality rate, but little attention has been paid to this disease, and its unique molecular characteristics remain unclear. This study aims to investigate the transcriptomic expression profile in this disease and identify key RNA pairs that regulate related molecular signaling networks. We established an RV dysfunction-induced type II CRS mouse model by pulmonary artery constriction (PAC). PAC mice developed severe RV hypertrophy and fibrosis; renal atrophy and dysfunction with elevated creatinine were subsequently observed. Expression profiles in RV and kidney tissues were obtained by whole transcriptome sequencing, revealing a total of 741 and 86 differentially expressed (DE) mRNAs, 159 and 29 DEmiRNAs and 233 and 104 DEcircRNAs between RV and kidney tissue, respectively. Competing endogenous RNA (ceRNA) networks were established. A significant alteration in proliferative, fibrotic and metabolic pathways was found based on GO and KEGG analyses, and the network revealed key ceRNA pairs, such as novel_circ_002631/miR-181a-5p/Creb1 and novel_circ_002631/miR-33-y/Kpan6. These findings indicate that significantly dysregulated pathways in RV dysfunction induced type II CRS include Ras, PI3K/Akt, cGMP-PKG pathways, and thyroid metabolic pathways. These ceRNA pairs can be considered potential targets for the treatment of type II CRS.	NA	Aging (Albany NY). 2021 Jan 20;13(3):4215-4241. doi: 10.18632/aging.202385. Epub 2021 Jan 20.
4980	Circular RNA	CircEPSTI1	miR-375	SLC7A11	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4981	Circular RNA	CircEPSTI1	miR-409-3p	SLC7A11	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4982	Circular RNA	CircEPSTI1	miR-515-5p	SLC7A11	cervical cancer cells	Cervical Cancer	Homo sapiens (human)	RACE;RIP assay;Luciferase reporter assay;	33534779	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis.	BACKGROUND: Circular RNAs (circRNAs) is one kind of non-coding RNAs (ncRNAs) and exert crucial functions in biological processes and intracellular gene expression modulation. However, the biological roles and expression status of the majority of circRNAs still remain unknown in cervical cancer. RESULTS: In this study, circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay. CONCLUSIONS: circEPSTI1-miR-375/409-3P/515-5p-SLC7A11 axis affected the proliferation of cervical cancer via the competing endogenous RNAs (ceRNA) mechanism and was relative to ferroptosis. Our findings provided experimental evidences which revealed that circEPSTI1 might act as a new and useful biomarker for monitoring and treatment target for cervical cancer. METHODS: The expression of circEPSTI1 was examined in cervical cancer cells. Then, we observed the impact of circEPSTI1 expression on the proliferation of cervical cancer by loss-of-function assays both in vivo and vitro. RIP and luciferase reporter assay revealed that circEPSTI1 sponges miR-375, miR-409-3p and miR-515-5p to upregulate SLC7A11 expression. We applied mouse xenograft experiments in mice to validate our results.	NA	Aging (Albany NY). 2021 Feb 2;13(3):4663-4673. doi: 10.18632/aging.202518. Epub 2021 Feb 2.
4983	Circular RNA	CircLMO7	miR-30a-3p	WNT2	Gastric cancer cells	Gastric Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;RNA pull-down;RNA sequencing;	33397440	Circular RNA circLMO7 acts as a microRNA-30a-3p sponge to promote gastric cancer progression via the WNT2/β-catenin pathway.	BACKGROUND: Gastric cancer (GC) is one of the most common malignant tumors worldwide. Currently, the overall survival rate of GC is still unsatisfactory despite progress in diagnosis and treatment. Therefore, studying the molecular mechanisms involved in GC is vital for diagnosis and treatment. CircRNAs, a type of noncoding RNA, have been proven to act as miRNA sponges that can widely regulate various cancers. By this mechanism, circRNA can regulate tumors at the genetic level by releasing miRNA from inhibiting its target genes. The WNT2/β-Catenin regulatory pathway is one of the canonical signaling pathways in tumors. It can not only promote the development of tumors but also provide energy for tumor growth through cell metabolism (such as glutamine metabolism). METHODS: Through RNA sequencing, we found that hsa_circ_0008259 (circLMO7) was highly expressed in GC tissues. After verifying the circular characteristics of circLMO7, we determined the downstream miRNA (miR-30a-3p) of circLMO7 by RNA pull-down and luciferase reporter assays. We verified the effect of circLMO7 and miR-30a-3p on GC cells through a series of functional experiments, including colony formation, 5-ethynyl-2'-deoxyuridine and Transwell assays. Through Western blot and immunofluorescence analyses, we found that WNT2 was the downstream target gene of miR-30a-3p and further confirmed that the circLMO7-miR-30a-3p-WNT2 axis could promote the development of GC. In addition, measurement of related metabolites confirmed that this axis could also provide energy for the growth of GC cells through glutamine metabolism. We found that circLMO7 could promote the growth and metastasis of GC in vivo by the establishment of nude mouse models. Finally, we also demonstrated that HNRNPL could bind to the flanking introns of the circLMO7 exons to promote circLMO7 cyclization. RESULTS: CircLMO7 acted as a miR-30a-3p sponge affecting the WNT2/β-Catenin pathway to promote the proliferation, migration and invasion of GC cells. Moreover, animal results also showed that circLMO7 could promote GC growth and metastasis in vivo. CircLMO7 could also affect the glutamine metabolism of GC cells through the WNT2/β-Catenin pathway to promote its malignant biological function. In addition, we proved that HNRNPL could promote the self-cyclization of circLMO7. CONCLUSIONS: CircLMO7 promotes the development of GC by releasing the inhibitory effect of miR-30a-3p on its target gene WNT2.	NA	J Exp Clin Cancer Res. 2021 Jan 5;40(1):6. doi: 10.1186/s13046-020-01791-9.
4984	Circular RNA	CircPVT1	miR-423-5p	HK2	Osteosarcoma cells	Bone Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4985	Circular RNA	CircPVT1	miR-423-5p	PKM2	Osteosarcoma cells	Bone Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4986	Circular RNA	CircPVT1	miR-423-5p	GLUT1	Osteosarcoma cells	Bone Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4987	Circular RNA	CircPVT1	miR-423-5p	LDHA	Osteosarcoma cells	Bone Cancer	Homo sapiens (human)	qRT-PCR;RT-PCR;RIP assay;Western blot;luciferase assay;	33369809	circPVT1 promotes osteosarcoma glycolysis and metastasis by sponging miR-423-5p to activate Wnt5a/Ror2 signaling.	Osteosarcoma (OS) is the most prevalent form of bone cancer. It has a high metastatic potential and progresses rapidly. The molecular mechanisms of OS remain unclear and this study aims to examine the functional role of circPVT1 and miR-423-5p in OS. Quantitative RT-PCR (qRT-PCR) and western blotting were used to examine levels of miR-423-5p, circPVT1, Wnt5a, Ror2, and glycolysis-related proteins, including HK2, PKM2, GLUT1, and LDHA. Colony formation and transwell assays were used to test the roles of miR-423-5p, circPVT1, and Wnt5a/Ror2 in OS cell proliferation, migration, and invasion. Dual luciferase assay and Ago2-RIP were used to validate the interactions of miR-423-5p/Wnt5a, miR-423-5p/Ror2, and circPVT1/miR-423-5p. Glucose uptake assay and measurement of lactate production were performed to assess the glycolysis process. A nude mouse xenograft model was used to evaluate the effects of sh-circPVT1 and miR-423-5p mimics on tumor growth and metastasis in vivo. miR-423-5p was reduced in both OS tissues and OS cell lines, while Wnt5a/Ror2 and circPVT1 were elevated. miR-423-5p bound to 3'-UTR of Wnt5a and Ror2 mRNA, and inhibited glycolysis and OS cell proliferation, migration, and invasion by targeting Wnt5a and Ror2. circPVT1 interacted with miR-423-5p and activated Wnt5a/Ror2 signaling by sponging miR-423-5p. Knockdown of circPVT1 or overexpression of miR-423-5p suppressed OS tumor growth and metastasis in vivo. miR-423-5p inhibited OS glycolysis, proliferation, migration, and metastasis by targeting and suppressing Wnt5a/Ror2 signaling pathway, while circPVT1 promoted those processes by acting as a sponge of miR-423-5p.	NA	Cancer Sci. 2021 May;112(5):1707-1722. doi: 10.1111/cas.14787. Epub 2021 Mar 10.
4988	Circular RNA	CircRNA_0005529	miR-527	Sp1	gastric cancer tissues and cells	Gastric Cancer	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	33472586	circRNA_0005529 facilitates growth and metastasis of gastric cancer via regulating miR-527/Sp1 axis.	BACKGROUND: Circular RNAs (circRNAs) are endogenous non-coding RNAs, which are associated with various biological processes, including microRNA (miRNA) interaction, protein binding and regulatory splicing. circRNA_0005529 (circ_0005529) is derived from vacuolar protein sorting 33 homologue B (VPS33B), and its biological role in gastric cancer (GC) has not been examined. In this study, the expression and location of circ_0005529 and microRNA-527 (miR-527) were determined by qRT-PCR and fluorescence in situ hybridization (FISH). Cell proliferation and cell migration were determined by MTT, EdU incorporation, colony formation, wound scratch and transwell assays. In addition, immunohistochemistry and western blotting were performed to determine the expressions of specificity protein 1 (Sp1), PCNA, c-myc, E-cadherin and N-cadherin. Western blotting and luciferase reporter assay were performed to study the interaction between circ_0005529 and miR-527 or miR-527 and Sp1. The functional effects of circ_0005529 on GC through regulating Sp1 were further evaluated using xenograft and metastatic mouse models in vivo. RESULTS: Our results showed that circ_0005529 was upregulated in GC tissues and cells, and had promoting effects on cell proliferation and cell migration. Mechanism analysis suggested that circ_0005529 could bind to microRNA-527 (miR-527) and reduce its expression. The interaction between miR-527 and Sp1 in GC was systematically studied. In addition, the results indicated that Sp1 upregulation could rescue the effects on cell proliferation and migration caused by circ_0005529. Moreover, the inhibitory effects of circ_0005529 downregulation on GC growth and metastasis were evaluated in mouse models. These findings suggested that the axis of circ_0005529/miR-527/Sp1 may serve as a promising treatment target for GC diagnosis and treatment. CONCLUSIONS: These findings suggested that the signal axis of circ_0005529/miR-527/Sp1 may has the potential to be explored as a novel therapeutic target for GC diagnosis and treatment. Mechanism diagram: During GC development, overexpressed circ_0005529 sponged miR-527 and then upregulated the expression of Sp1. Subsequently, epithelial-mesenchymal transition (EMT), cell proliferation and cell migration were promoted, which ultimately facilitated the tumor metastasis.	NA	BMC Mol Cell Biol. 2021 Jan 20;22(1):6. doi: 10.1186/s12860-020-00340-8.
4989	Circular RNA	CircSND1	miR-125a-3p	FUT6	HeLa cells	Cervical Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Fluorescent reporter;luciferase assay;	33469369	CircSND1 Regulated by TNF-α Promotes the Migration and Invasion of Cervical Cancer Cells.	AIM: To explore the role and potential mechanism of circSND1 in cervical cancer (CC). MAIN METHODS: qRT-PCR was used to determine the expression of circSND1 in tumor necrosis factor-α (TNF-α)-treated HeLa cells. CircSND1 overexpression and knockdown were performed to indicate the functional role of circSND1 in vitro and in vivo. Luciferase assay was used to analyze promoter activity. The expression and regulation of circSND1, miR-125a-3p and FUT6 were evaluated using EGFP fluorescent reporter assay and rescue experiments. Immunofluorescence and Western blot assays were used to analyze the activation of nuclear factor-κB (NF-κB). RESULTS: In HeLa cells, TNF-α up-regulated the expression of circSND1 by activating the NF-κB signaling pathway. Overexpression of circSND1 significantly increased the migration and invasion and the epithelial-mesenchymal transition (EMT) process of CC cells, and promoted tumor metastasis in xenograft nude mouse model, whereas down-regulation of circSND1 exerted opposite effects. Furthermore, circSND1 enhanced the expression of FUT6 via sponging miR-125a-3p, and FUT6 activated NF-κB signaling pathway. CONCLUSION: We found that circSND1 promoted the expression of FUT6 and the malignant behavior of cervical cancer through the ceRNA mechanism, and there was a TNF-α/NF-κB/circSND1/miR-125a-3p/FUT6/NF-κB positive feedback pathway between them, which suggests that circSND1 can be a promising prognostic marker and therapeutical target for cervical cancer.	NA	Cancer Manag Res. 2021 Jan 12;13:259-275. doi: 10.2147/CMAR.S289032. eCollection 2021.
4990	LncRNA	HIF1A-AS1	miR-138	NF-kB	myocardium and primary cardiomyocytes	Cardiomyocyte Apoptosis	Homo sapiens (human)	Flow Cytometry assay;	33224748	The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.	BACKGROUND: Cardiomyocyte apoptosis and inflammation induced by Coxsackievirus B3 (CVB3) are key pathogenetic mechanisms in viral myocarditis. Alterations in microRNAs and lncRNAs are associated with cardiac remodeling. However, whether the microRNA and lncRNA interact to regulate cardiomyocyte apoptosis and inflammation is unknown. METHODS: BALB/c mice were infected with CVB3 to generate acute viral myocarditis model. The expression levels of lncRNA HIF1A-AS1 and miR-138 were examined in mouse myocardium and primary cardiomyocytes with CVB3 infection. We then knocked down HIF1A-AS1 by siRNA and upregulated miR-138 by microRNA mimics in cardiomyocytes. RESULTS: The expression of lncRNA HIF1A-AS1was significantly increased in CVB3-induced myocardium and cardiomyocytes. As documented by flow cytometry, silencing of HIF1A-AS1 alleviated late apoptosis (5.1%±2.8% vs. 17.2%±4.2%, P<0.01) and ROS production (68.73%±2.78% vs. 90.40%±2.86%, P<0.01) compared to their levels in cardiomyocytes transfected with control siRNA. The content of proinflammatory cytokines was substantially decreased by HIF1A-AS1 siRNA. Furthermore, we identified that HIF1A-AS1 bound to miR-138 and significantly suppressed miR-138 expression. Blocking HIF1A-AS1 attenuated IκBα phosphorylation and NF-κB activity, while cotransfection with miR-138 mimics markedly reversed its effect. CONCLUSIONS: In conclusion, lncRNA HIF1A-AS1 promotes NF-κB signaling and subsequently aggravates cardiomyocyte apoptosis and inflammation via targeting miR-138.	NA	Cardiovasc Diagn Ther. 2020 Oct;10(5):1245-1255. doi: 10.21037/cdt-20-545.
4991	LncRNA	HIF1A-AS1	miR-138	NF-kB	myocardium and primary cardiomyocytes	Cardiomyocyte Inflammation	Homo sapiens (human)	Flow Cytometry assay;	33224748	The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.	BACKGROUND: Cardiomyocyte apoptosis and inflammation induced by Coxsackievirus B3 (CVB3) are key pathogenetic mechanisms in viral myocarditis. Alterations in microRNAs and lncRNAs are associated with cardiac remodeling. However, whether the microRNA and lncRNA interact to regulate cardiomyocyte apoptosis and inflammation is unknown. METHODS: BALB/c mice were infected with CVB3 to generate acute viral myocarditis model. The expression levels of lncRNA HIF1A-AS1 and miR-138 were examined in mouse myocardium and primary cardiomyocytes with CVB3 infection. We then knocked down HIF1A-AS1 by siRNA and upregulated miR-138 by microRNA mimics in cardiomyocytes. RESULTS: The expression of lncRNA HIF1A-AS1was significantly increased in CVB3-induced myocardium and cardiomyocytes. As documented by flow cytometry, silencing of HIF1A-AS1 alleviated late apoptosis (5.1%±2.8% vs. 17.2%±4.2%, P<0.01) and ROS production (68.73%±2.78% vs. 90.40%±2.86%, P<0.01) compared to their levels in cardiomyocytes transfected with control siRNA. The content of proinflammatory cytokines was substantially decreased by HIF1A-AS1 siRNA. Furthermore, we identified that HIF1A-AS1 bound to miR-138 and significantly suppressed miR-138 expression. Blocking HIF1A-AS1 attenuated IκBα phosphorylation and NF-κB activity, while cotransfection with miR-138 mimics markedly reversed its effect. CONCLUSIONS: In conclusion, lncRNA HIF1A-AS1 promotes NF-κB signaling and subsequently aggravates cardiomyocyte apoptosis and inflammation via targeting miR-138.	NA	Cardiovasc Diagn Ther. 2020 Oct;10(5):1245-1255. doi: 10.21037/cdt-20-545.
4992	LncRNA	HOXA-AS3	miR-455-5p	Notch1	bladder cancer cells	Bladder Cancer	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33643896	Reduction of Bladder Cancer Chemosensitivity Induced by the Effect of HOXA-AS3 as a ceRNA for miR-455-5p That Upregulates Notch1.	Chemoresistance is one of the main causes of recurrence in bladder cancer patients and leads to poor prognosis. Recently, long non-coding RNAs, like HOXA-AS3, have been reported to regulate chemoresistance in several types of cancer. In this study, we aimed to determine whether HOXA-AS3 can mediate cisplatin resistance in bladder cancer, and its potential mechanism of action. We determined the viability, proliferation, and apoptosis of bladder cancer cells using a CCK-8 assay, EdU staining, and flow cytometry, respectively. We used western blot analysis to assess the expression of markers of epithelial-mesenchymal transition (EMT) and Notch1. We then confirmed expression of these EMT-related markers by immunofluorescence analysis. We found that hypoxia promoted resistance to cisplatin and upregulated the level of HOXA-AS3 in BC cells. Inhibition of HOXA-AS3 enhanced hypoxia-induced cisplatin sensitivity by regulating EMT and Notch1 in BC cells. A dual-luciferase reporter assay confirmed that HOXA-AS3 directly targets miR-455-5p and that Notch1 was a potential target of miRNA-455-5p. We also found that the positive effect of HOXA-AS3 inhibition on cisplatin resistance and tumorigenesis was alleviated when BC cells were transfected with miR-455-5p. Finally, we showed combining HOXA-AS3 small interfering RNA (siRNA) with cisplatin treatment inhibited tumorigenesis in a BALB/c nu/nu mouse model. Our findings indicate that HOXA-AS3 may function as a competing endogenous RNA (ceRNA) of miR-455-5p to regulate Notch1 and play an important role in regulating chemotherapeutic drug sensitivity in BC cells. Therefore, HOXA-AS3 may be a novel therapeutic target for treating bladder cancer.	NA	Front Oncol. 2021 Feb 12;10:572672. doi: 10.3389/fonc.2020.572672. eCollection 2020.
4993	LncRNA	kcnq1ot1	miR-452-3p	HDAC3	mouse aorta with atherosclerosis and lipid-loaded macrophages	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33293505	LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.	Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE(-/-) mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE(-/-) mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.	NA	Cell Death Dis. 2020 Dec 9;11(12):1043. doi: 10.1038/s41419-020-03263-6.
4994	LncRNA	kcnq1ot1	miR-452-3p	ABCA1	mouse aorta with atherosclerosis and lipid-loaded macrophages	Atherosclerosis	Homo sapiens (human)	qRT-PCR	33293505	LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.	Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE(-/-) mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE(-/-) mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.	NA	Cell Death Dis. 2020 Dec 9;11(12):1043. doi: 10.1038/s41419-020-03263-6.
4995	LncRNA	LINC00242	miR-1-3p	G6PD	gastric cancer tissues and cells	Gastric Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	33514309	LINC00242/miR-1-3p/G6PD axis regulates Warburg effect and affects gastric cancer proliferation and apoptosis.	BACKGROUND: Reprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark of cancer. Long non-coding RNAs (lncRNAs) have been certified to play a crucial role in tumor progression. The current study aims to inquire into the potential regulatory mechanism of long intergenic non-protein coding RNA 242 (LINC00242) on aerobic glycolysis in gastric cancer. METHOD: LINC00242, miR-1-3p and G6PD expression levels in gastric cancer tissues and cells were determined by qRT-PCR. Cell apoptosis or viability were examined by Flow cytometry or MTT assay. Western blot was utilized to investigate G6PD protein expression levels. Immunohistochemical (IHC) and hematoxylin and eosin (H&E) staining were used for histopathological detection. The targeted relationship between LINC00242 or G6PD and miR-1-3p was verified by luciferase reporter gene assay. Nude mouse xenograft was utilized to detect tumor formation in vivo. RESULT: LINC00242 and G6PD was high-expressed in gastric cancer tissues and cells, and LINC00242 is positively correlated with G6PD. Silencing of LINC00242 or G6PD within gastric cancer cells prominently inhibited cell proliferation and aerobic glycolysis in vitro and relieved the tumorigenesis of gastric cancer in vivo. miR-1-3p was predicted to directly target both LINC00242 and G6PD. Overexpression of miR-1-3p suppressed gastric cancer cells proliferation and aerobic glycolysis. LINC00242 competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression on G6PD. CONCLUSION: LINC00242 plays a stimulative role in gastric cancer aerobic glycolysis via regulation of miR-1-3p/ G6PD axis, therefore affecting gastric cancer cell proliferation.	NA	Mol Med. 2021 Jan 29;27(1):9. doi: 10.1186/s10020-020-00259-y.
4996	LncRNA	LINC00667	miR-4319	FOXQ1	nasopharyngeal carcinoma cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR	33569351	LINC00667 Sponges miR-4319 to Promote the Development of Nasopharyngeal Carcinoma by Increasing FOXQ1 Expression.	Accumulating evidence has indicated that lncRNAs regulate various biological and pathological processes in diverse malignant tumors. The roles of LINC00667 in cancer development have been explored in glioma, hepatocellular carcinoma and non-small cell lung cancer, but not in nasopharyngeal carcinoma (NPC). In the present study, we characterize the role and molecular mechanism of LINC00667 in NPC progression. It was found that LINC00667 was overexpressed in NPC cells compared to normal cells. Silencing LINC00667 suppressed the proliferation, migration, invasion and epithelial mesenchymal transition (EMT) in NPC cells. In addition, bioinformatics analysis revealed that LINC00667 acted as a ceRNA to absorb miR-4319. Further investigations illustrated that miR-4319 had low expression in NPC cells and functioned as a tumor suppressor in the progression of NPC. Mechanistic study identified forkhead box Q1 (FOXQ1) as a functional target of miR-4319. The effect of LINC00667 in NPC development was mediated by the miR-4319/FOXQ1 axis. Analysis on tumorxenograft mouse model demonstrated that knockdown of LINC00667 repressed NPC tumor growth in vivo and confirmed the in vitro results. Our present study suggested that LINC00667 promoted the malignant phenotypes of NPC cells by competitively binding to miR-4319 to up-regulate FOXQ1 expression. Our results reveled that LINC00667 could be a diagnostic and therapeutic target for NPC patients.	NA	Front Oncol. 2021 Jan 25;10:632813. doi: 10.3389/fonc.2020.632813. eCollection 2020.
4997	LncRNA	lincRNA-p21	miR-181a	NA	mononuclear and urine cells	Lupus Nephritis	Homo sapiens (human)	qRT-PCR	33396699	Up-Regulated Expression of Pro-Apoptotic Long Noncoding RNA lincRNA-p21 with Enhanced Cell Apoptosis in Lupus Nephritis.	Accelerated cell apoptosis with dysregulated long noncoding RNAs is the crucial pathogenesis in lupus nephritis (LN). Pro-apoptotic lincRNA-p21 was studied in LN patients, cell lines with lentivirus-mediated overexpression and CRISPR interference (CRISPRi)-conducted repression, and a mouse model. Clinical samples were from patients and age/sex-matched controls. Expression of lincRNA-p21 and endogenous RNA target miR-181a, were examined in mononuclear and urine cells. Guide RNA sequences targeting lincRNA-p21 were cloned into CRISPRi with dCas9/ Krüppel-associated box (KRAB) domain. LincRNA-p21-silened transfectants were investigated for apoptosis and miR-181a expression. LincRNA-p21-overexpressed cells were evaluated for apoptosis and p53-related down-stream molecules. Balb/C mice were injected with pristane to induce LN and examined for apoptosis and lincRNA-p21. Higher lincRNA-p21 levels were found in LN mononuclear and urine cells, positively correlated with activity. There were lower miR-181a levels in LN mononuclear cells, negatively correlated with activity. Doxorubicin-induced apoptotic cells had up-regulated lincRNA-p21 levels. CRISPRi with dCas9/KARA domain showed efficient repression ability on transcription initiation/elongation. CRISPRi-conducted lincRNA-p21-silenced transfectants displayed reduced apoptosis with up-regulated miR-181a levels, whereas lentivirus-mediated lincRNA-p21-overexpressed cells revealed enhanced apoptosis with up-regulated downstream PUMA/Bax expression. LN mice had glomerular apoptosis with progressive increased lincRNA-p21 levels. Our results demonstrate up-regulated lincRNA-p21 expression in LN, implicating a potential diagnostic marker and therapeutic target.	NA	Int J Mol Sci. 2020 Dec 30;22(1):301. doi: 10.3390/ijms22010301.
4998	LncRNA	loc339803	miR-30a-5p	SNAIL1	Hepatocellular carcinoma cells	Hepatocellular Carcinoma	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	33442404	LncRNA loc339803 acts as CeRNA of miR-30a-5p to promote the migration and invasion of hepatocellular carcinoma cells.	Background: Hepatocellular carcinoma (HCC), a most common malignant tumor, has an unfavorable clinical outcome. Emerging evidence has demonstrated that long noncoding RNAs (lncRNAs) play an important role in the carcinogenesis and progression of HCC. However, the clinical significances and the biological roles of most lncRNAs in HCC remain poorly understood. Methods: The expression levels of lncRNA loc339803 in HCC tissues and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR) assay. The cellular sublocalization of loc339803 was determined by fluorescence in situ hybridization and nuclear and cytoplasmic RNA isolation assay. Western blot, CCK-8, Edu, colony formation, migration and invasion assays were used to investigate the roles of loc339803 in HCC progression in vitro. A mouse model for lung metastasis was constructed to evaluate the role of loc339803 in HCC development in vivo. The correlations among loc339803, miR-30a-5p and SNAIL1 were validated by qRT-PCR and a dual- luciferase reporter assay. Results: The expression of loc339803 was upregulated in HCC tissues and cell lines, and positively correlated with tumor size, advanced tumor stage, higher serum AFP level and poor prognosis of HCC patients. Loc339803 can promote the migration and invasion of HCC cells in vivo and in vitro. Further studies demonstrated that loc339803 functioned as a competing endogenous RNA (ceRNA) by directly binding to miR-30a-5p, thus up-regulating the expression of SNAIL1, a target gene of miR-30a-5p. Moreover, miR-30a-5p upregulation blocked the enhanced migration and invasion of HCC cells induced by loc339803 overexpression. Conclusions: Loc339803 may be oncogenic in HCC and associated with poor clinical outcomes. LncRNA loc339803 might promote the invasion and migration of HCC cells through regulating miR-30a-5p/ SNAIL1 axis.	NA	J Cancer. 2021 Jan 1;12(4):1061-1072. doi: 10.7150/jca.52413. eCollection 2021.
4999	LncRNA	MEG3	miR-107-5p	PABPC4	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5000	LncRNA	MEG3	miR-149-3p	PABPC4	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5001	LncRNA	MEG3	miR-346-3	PABPC4	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5002	LncRNA	MEG3	miR-107-5p	CEP131	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5003	LncRNA	MEG3	miR-149-3p	CEP131	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5004	LncRNA	MEG3	miR-346-3	CEP131	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5005	LncRNA	MEG3	miR-107-5p	NUMB1	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5006	LncRNA	MEG3	miR-149-3p	NUMB1	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5007	LncRNA	MEG3	miR-346-3	NUMB1	mouse model	Cholesterol Gallstone	Homo sapiens (human)	qRT-PCR;	33665015	The long non-coding RNA MEG3 plays critical roles in the pathogenesis of cholesterol gallstone.	BACKGROUND: Cholesterol gallstone (CG) is the most common gallstone disease, which is induced by biliary cholesterol supersaturation. The purpose of this study is to investigate the pathogenesis of CG. METHODS: Sixteen mice were equally and randomly divided into model group and normal control group. The model group was fed with lithogenic diets to induce CG, and then gallbladder bile lipid analysis was performed. After RNA-seq library was constructed, differentially expressed mRNAs (DE-mRNAs) and differentially expressed lncRNAs (DE-lncRNAs) between model group and normal control group were analyzed by DESeq2 package. Using the cluster Profiler package, enrichment analysis for the DE-mRNAs was carried out. Based on Cytoscape software, the protein-protein interaction (PPI) network and competing endogenous RNA (ceRNA) network were built. Using quantitative real-time reverse transcription-PCR (qRT-PCR) analysis, the key RNAs were validated. RESULTS: The mouse model of CG was suc cessfully established, and then 181 DE-mRNAs and 33 DE-lncRNAs between model and normal groups were obtained. Moreover, KDM4A was selected as a hub node in the PPI network, and lncRNA MEG3 was considered as a key lncRNA in the regulatory network. Additionally, the miR-107-5p/miR-149-3p/miR-346-3-MEG3 regulatory pairs and MEG3-PABPC4/CEP131/NUMB1 co-expression pairs existed in the regulatory network. The qRT-PCR analysis showed that KDM4A expression was increased, and the expressions of MEG3, PABPC4, CEP131, and NUMB1 were downregulated. CONCLUSION: These RNAs might be related to the pathogenesis of CG.	NA	PeerJ. 2021 Feb 23;9:e10803. doi: 10.7717/peerj.10803. eCollection 2021.
5008	LncRNA	Peg13	miR-128-3p	Sox13	neural stem cells	Sevoflurane Exposure-Related Neurotoxicity Against Neural Stem Cells	Homo sapiens (human)	Flow cytometry assay;Flow Cytometry assay;Luciferase reporter assay;	33296418	Long non-coding RNA Peg13 attenuates the sevoflurane toxicity against neural stem cells by sponging microRNA-128-3p to preserve Sox13 expression.	BACKGROUND: Exposure to anesthetics during brain development may impair neurological function, however, the mechanisms underlying anesthetic neurotoxicity are unclear. Recent studies indicate that long non-coding RNAs (lncRNAs) are crucial for regulating the functional brain development during neurogenesis. This study aimed to determine the regulatory effects and potential mechanisms of lncRNA Peg13 (Peg13) on sevoflurane exposure-related neurotoxicity against neural stem cells (NSCs). METHODS: Mouse embryotic NSCs were isolated and their self-renewal and differentiation were characterized by immunofluorescence. NSCs were exposed to 4.1% sevoflurane 2 h daily for three consecutive days. The potential toxicities of sevoflurane against NSCs were evaluated by neurosphere formation, 5-ethynyl-2'-deoxyuridine (EdU) incorporation and flow cytometry assays. The Peg13, miR-128-3p and Sox13 expression in NSCs were quantified. The potential interactions among Peg13, miR-128-3p and Sox13 were analyzed by luciferase reporter assay. The effects of Peg13 and/or miR-128-3p over-expression on the sevoflurane-related neurotoxicity and Sox13 expression were determined in NSCs. RESULTS: The isolated mouse embryotic NSCs displayed potent self-renewal ability and differentiated into neurons, astrocytes and oligodendrocytes in vitro, which were significantly inhibited by sevoflurane exposure. Sevoflurane exposure significantly down-regulated Peg13 and Sox13, but enhanced miR-128-3p expression in NSCs. Transfection with miR-128-3p mimics, but not the control, significantly mitigated the Peg13 or Sox13-regulated luciferase expression in 293T cells. Peg13 over-expression significantly reduced the sevoflurane-related neurotoxicity and increased Sox13 expression in NSCs, which were mitigated by miR-128-3p transfection. CONCLUSION: Such data indicated that Peg13 mitigated the sevoflurane-related neurotoxicity by sponging miR-128-3p to preserve Sox13 expression in NSCs.	NA	PLoS One. 2020 Dec 9;15(12):e0243644. doi: 10.1371/journal.pone.0243644. eCollection 2020.
5009	LncRNA	PVT1	miR-146a	SMAD4	Articular tissues	Diabetic Osteoarthritis	Homo sapiens (human)	Western blot;Luciferase reporter assay;	33569722	LncPVT1 promotes cartilage degradation in diabetic OA mice by downregulating miR-146a and activating TGF-β/SMAD4 signaling.	INTRODUCTION: To investigate the role of LncRNA PVT1 (plasmacytoma variant translocation 1) in hyperglycemia-triggered cartilage damage using the diabetic osteoarthritis (OA) mice model. MATERIALS AND METHODS: Streptozotocin (STZ) was used to induce mouse diabetes. Knee OA model was induced through transection of anterior cruciate ligament (ACLT). Severity of arthritis was assessed histologically by Safranin O-Fast Green Staining using Mankin Scores. LncRNA PVT1 and miR-146a were detected by real-time polymerase chain reaction (PCR) in cartilage tissue. Moreover, the interaction among PVT1, miR-146a, and SMAD4 was examined by luciferase reporter assays. Mice were injected intra-articularly with ad-siRNA-PVT1 and ad-siRNA scramble control. Articular concentrations of TNF-α, IL-1, IL-6 and TGF-β1 were determined using enzyme-linked immunosorbent assay. Levels of type II Collagen (COL2A1), TGF-β1, p-SMAD2, SMAD2, p-SMAD3, SMAD3, SMAD4 and nuclear SMAD4 were detected by western blot analysis. RESULTS: PVT1 expression was significantly increased, whereas miR-146a was markedly decreased in diabetic OA mice than in non-diabetic OA and control. Increased PVT1 expression in diabetic OA mice was significantly associated with Mankin score and reduced miR-146a as well as Collagen alpha-1(II) (COL2A1) expressions. In vivo, intra-articular injection of ad-siRNA-PVT1 efficiently increased miR-146a and COL2A1 expressions, alleviated joint inflammation, decreased the expression of pro-inflammatory mediators, and suppressed TGF-β/SMAD4 pathway in diabetic OA mice. CONCLUSIONS: Our results demonstrate LncRNA PVT1 is involved in cartilage degradation in diabetic OA and correlated with disease severity. Efficiency of ad-siRNA-PVT1 in controlling joint inflammation in diabetic OA mice is associated with the suppression of the expression of miR-146a, pro-inflammatory cytokines and activation of TGF-β/SMAD4 pathway.	NA	J Bone Miner Metab. 2021 Feb 10. doi: 10.1007/s00774-020-01199-7.
5010	LncRNA	RAET1K	miR-503-5p	INPP4B	HL-60 and THP-1 cells	Acute Myeloid Leukemia	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	33500628	lncRNA RAET1K Promotes the Progression of Acute Myeloid Leukemia by Targeting miR-503-5p/INPP4B Axis.	BACKGROUND: Although long non-coding RNA (lncRNA) RAET1K has been observed to be abnormally expressed in patients with various cancers, its role and molecular mechanism in acute myeloid leukemia (AML) remain unclear. METHODS: The expression of RAET1K and miR-503-5p in bone marrow tissues and cell lines was detected by qRT-PCR. Cell proliferation was evaluated by cell counting kit-8 and 5-ethynyl-20-deoxyuridine (EdU) staining assay. Cell invasion and migration were detected by transwell assay. Cell apoptosis was evaluated by flow cytometry. The relationship between RAET1K and miR-503-5p, as well as miR-503-5p and INPP4B, was determined by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. In addition, the tumorigenesis of leukemia cells was evaluated by using a xenograft mouse model in vivo. RESULTS: RAET1K was significantly upregulated and miR-503-5p was markedly downregulated in bone marrow tissues and cell lines (HL-60 and THP-1). Silencing of RAET1K (si-RAET1K) and overexpression of miR-503-5p inhibited cell proliferation, migration, and invasion but promoted apoptosis of HL-60 and THP-1 cells. RAET1K functioned as a sponge of miR-503-5p, and miR-503-5p inhibitor obviously attenuated the effect of si-RAET1K on AML progression in vitro. INPP4B was identified as a target of miR-503-5p, and INPP4B overexpression obviously reversed the effect of miR-503-5p mimics on cell proliferation, migration, invasion, and apoptosis of HL-60 and THP-1 cells in vitro. Knockdown of RAET1K effectively inhibited the tumorigenesis of leukemia cells in vivo. CONCLUSION: Our results demonstrated that RAET1K/miR-503-5p/INPP4B axis contributed to AML progression, suggesting that RAET1K might be a potential target for the treatment of AML.	NA	Onco Targets Ther. 2021 Jan 18;14:531-544. doi: 10.2147/OTT.S291123. eCollection 2021.
5011	LncRNA	TRPM2-AS	miR-138-5p	EGFR	non-small cell lung cancer cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33209893	Long non-coding RNA TRPM2-AS sponges microRNA-138-5p to activate epidermal growth factor receptor and PI3K/AKT signaling in non-small cell lung cancer.	BACKGROUND: Long non-coding RNAs (lncRNAs) can play pivotal roles in tumor progression by acting as microRNA (miRNA) sponges. This study aimed to investigate the association of a novel lncRNA, TRPM2-AS, with the miR-138-5p/EGFR axis in the development of non-small cell lung cancer (NSCLC). METHODS: Sixty NSCLC tissues and paired adjacent non-tumor tissues were analyzed. The relative expression levels of TRPM2-AS, miR138-5p, and epidermal growth factor receptor (EGFR) and the interactions between them were analyzed. The NSCLC cell lines NCI-H1299 and A549 were transfected with TRPM2-AS shRNA/pcDNA, and miR-138-5p mimics. Cell proliferation, migration, invasion, and apoptosis were examined in response to different transfection conditions. Dual-luciferase reporter assay was performed to identify the target interactions between TRPM2-AS, miR-138-5p, and EGFR. A549 cells stably transfected with shRNA were injected into BALB/c null nude mice to establish a tumor xenograft model. RESULTS: TRPM2-AS was up-regulated in NSCLC tumors and cell lines. Cell proliferation, migration, and invasion were inhibited in NSCLC cells treated with sh-TRPM2-AS, while apoptosis was induced. The targeting of TRPM2-AS by miR138-5p and miR138-5p by EGFR were validated with dual-luciferase reporter assay. TRPM2-AS was found to be negatively correlated with miR138-5p but positively correlated with EGFR. PI3K/AKT/mTOR was activated by pcDNA-EGFR but inactivated by miR-138-5p mimics. In the tumor xenograft mouse model, sh-TRPM2-AS suppressed tumor formation, reduced the expression of EGFR and Ki67, and promoted tumor cell apoptosis. CONCLUSIONS: Our results suggested that TRPM2-AS can increase the levels of EGFR via sponging miR-138-3p; this promoted NSCLC cell proliferation, migration, and invasion in vitro, and exacerbated tumors in vivo. These findings highlight TRPM2-AS/miR-138-5p as a potential target for reducing drug resistance in patients with NSCLC.	NA	Ann Transl Med. 2020 Oct;8(20):1313. doi: 10.21037/atm-20-6331.
5012	LncRNA	TTTY15	miR-374a-5p	FOXO1	H9c2 and HL-1 cells	Myocardial Ischamia Reperfusion Injury Injury	Homo sapiens (human)	qRT-PCR	33296140	Knockdown of lncRNA TTTY15 alleviates myocardial ischemia-reperfusion injury through the miR-374a-5p/FOXO1 axis.	Myocardial ischemia/reperfusion (I/R) injury greatly contributes to myocardial tissue damage in patients with coronary disease, which eventually leads to heart failure. Long noncoding RNAs (lncRNAs) have an emerging role in the process of myocardial I/R injury. Our previous work revealed the protective role of miR-374a-5p against myocardial I/R injury. In this study, we explored the role of lncRNA TTTY15 and its potential interaction mechanisms with miR-374a-5p in myocardial I/R injury. The expression of TTTY15 was increased both in vitro and in vivo after myocardial I/R injury models according to quantitative real-time polymerase chain reaction. Various assays were conducted to evaluate the regulatory relationship among TTTY15, miR-374a-5p, FOXO1, and autophagy in H9c2 and HL-1 cells. The results showed that TTTY15 suppresses autophagy and myocardial I/R injury by targeting miR-374a-5p. We found that TTTY15 regulates miR-374a-5p, thus affecting FOXO1 expression and autophagy in myocytes during I/R. Furthermore, in an in vivo mouse model of myocardial I/R injury, suppression of TTTY15 successfully alleviated myocardial I/R injury. Our results reveal a novel feedback mechanism in which TTTY15 regulates miRNA processing and a potential target in myocardial I/R injury. TTTY15 is a promising therapeutic target for treating myocardial I/R injury.	NA	IUBMB Life. 2021 Jan;73(1):273-285. doi: 10.1002/iub.2428. Epub 2020 Dec 9.
5013	LncRNA	XIST	miR-758-3p	caspase3	osteoblast	Postmenopausal Osteoporosis	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33336851	Iron accumulation regulates osteoblast apoptosis through lncRNA XIST/miR-758-3p/caspase 3 axis leading to osteoporosis.	Postmenopausal osteoporosis (PMOP) is mainly caused by multiple factors. Recent studies have suggested that iron accumulation (IA) was closely related to PMOP. However, the detailed molecular mechanisms have not been well demonstrated. We constructed the IA mouse model by intraperitoneal injections of ferric ammonium citrate (FAC) and cell model by culturing with the medium containing FAC. Osteoporosis was confirmed in mouse bone tissues using H&E staining, and the level of serum ferritin, alkaline phosphatase (ALP), procollagen-1 N-terminal peptide (P1NP), and osteocalcin in mice was examined by ELISA. The expressions of XIST and miR-758-3p were detected by qRT-PCR. Cell proliferation and apoptosis were measured by CCK-8, TUNEL, and flow cytometry. The expression levels of apoptotic-related proteins were evaluated by western blot. Dual luciferase reporter assay was used to examine the molecular interaction. The expressions of ALP, P1NP, and osteocalcin, and the H&E staining of bone tissues in mice were analyzed to confirm the biological function of XIST and miR-758-3p in vivo. XIST was up-regulated while miR-758-3p was down-regulated in IA mouse and cell models. XIST knockdown significantly reduced FAC-induced osteoblast apoptosis, which was mimicked by transfection with miR-758-3p mimics. XIST acted as a sponge of miR-758-3p, which targeted caspase 3. IA led to the high expression of XIST and promoted osteoblast apoptosis through miR-758-3p/caspase 3. Transfection with shXIST or miR-758-3p mimics alleviated IA-induced mouse osteoporosis. IA regulated osteoblast apoptosis through XIST/miR-758-3p/caspase 3 axis, which might provide alternative targets for the treatment of osteoporosis.	NA	IUBMB Life. 2021 Feb;73(2):432-443. doi: 10.1002/iub.2440.
5014	LncRNA	H19	miR-29b-3p	FoxO3	umbilical cord mesenchymal stem cells	Osteochondral Regeneration	Homo sapiens (human)	Dual-luciferase reporter assay;FISH;RIP assay;RNA immunoprecipitation;FISH;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33463060	The umbilical cord mesenchymal stem cell-derived exosomal lncRNA H19 improves osteochondral activity through miR-29b-3p/FoxO3 axis.	BACKGROUND: Our previous study revealed that the exosomal lncRNA H19 derived from umbilical cord mesenchymal stem cells (UMSCs) plays a pivotal role in osteochondral regeneration. In this study, we investigated whether the exosomal lncRNA H19 could act as a competing endogenous RNA (ceRNA) to potentiate osteochondral activity in chondrocytes. METHODS: Dual-luciferase reporter assay, RNA pull-down, RNA immunoprecipitation (RIP), and fluorescence in situ hybridization (FISH) were carried to verify the interaction between miR-29b-3p and both lncRNA H19 and the target mRNA FoxO3. Chondrocytes were treated with UMSC-derived exosomes, which highly expressing lncRNA H19 expression, followed by apoptosis, migration, senescence, and matrix secretion assessments. An in vivo SD rat cartilage defect model was carried out to explore the role and mechanism of lncRNA H19/miR-29b-3p. RESULTS: UMSCs were successfully identified, and exosomes were successfully extracted. Exosomes exhibited the ability to transfer lncRNA H19 to chondrocytes. Mechanistically, exosomal lncRNA H19 potentiated osteochondral activity by acting as a competing endogenous sponge of miR-29b-3p, and miR-29b-3p directly targeted FoxO3. Intra-articular injection of exosomes overexpressing lncRNA H19 could promote sustained cartilage repair; however, this effect could be undermined by miR-29b-3p agomir. CONCLUSIONS: Our study revealed a significant role in the development of strategies against cartilage defects for UMSC-derived exosomes that overexpress lncRNA H19. Exosomal H19 was found to promote chondrocyte migration, matrix secretion, apoptosis suppression, as well as senescence suppression, both in vitro and in vivo. The specific mechanism lies in the fact that exosomal H19 acts as a ceRNA against miR-29b-3p to upregulate FoxO3 in chondrocytes.	NA	Clin Transl Med. 2021 Jan;11(1):e255. doi: 10.1002/ctm2.255.
5015	LncRNA	MEG3	miR-98-5p	IL-10	Ulcerative colitis tissues	Ulcerative Colitis	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Immunohistochemistry;Luciferase reporter assay;	33394187	Long Non-coding RNA MEG3 Alleviated Ulcerative Colitis Through Upregulating miR-98-5p-Sponged IL-10.	Ulcerative colitis (UC) is a refractory chronic colitis disease with the particularly complex cause. Recently, long noncoding RNAs (lncRNAs) have been reported to be related to the development of UC. LncRNA MEG3 has been proved to play an anti-inflammatory role in a variety of inflammatory diseases, which share similar pathogenesis with UC, indicating the potential involvement of lncRNA MEG3 in UC. This study aims to investigate the functional role and underlying mechanism of lncRNA MEG3 in UC. Gradient concentration of H(2)O(2) (0, 20, 50, 100, and 200 μM) was used to induce Caco-2 damage models in vitro. Cell viability was detected by cell counting kit-8 (CCK-8) assay. LncRNA MEG3, miR-98-5p, and IL-10 levels in H(2)O(2-)treated Caco-2 cells were assessed by performing real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the binding relationship between lncRNA MEG3 and miR-98-5p, as well as the binding relationship between miR-98-5p and IL-10, was validated using dual-luciferase reporter assay. 2, 4, 6-Trinitrobenzenesulfonic acid solution (TNBS) was applied to induce ulcerative colitis in young rats. The body weight, disease activity index (DAI), length and weight of the colons, pathological scores of UC rats, reactive oxygen species (ROS), and inflammatory cytokines were determined to evaluate the effects of lncRNA MEG3 on the progression of UC. Besides, hematoxylin-eosin (HE) staining was exploited to observe histological changes of UC rat colons. In addition, western blotting analysis was also performed to evaluate the apoptosis and pyroptosis-related protein levels. Moreover, lncRNA MEG3, miR-98-5p, and IL-10 levels in UC rat colons were further assessed by RT-qPCR. Meanwhile, IL-10 expression was determined using immunohistochemistry. LncRNA MEG3 and IL-10 levels were distinctly decreased while miR-98-5p was increased in Caco-2 damage models and UC rats. Bioinformatics analysis predicted the binding sites of lncRNA MEG3 to miR-98-5p and miR-98-5p to IL-10. Besides, dual-luciferase reporter assay validated the negative correlation between lncRNA MEG3 and miR-98-5p, miR-98-5p, and IL-10. Overexpressed lncRNA MEG3 reduced. DAI scores and colon weight/length ratio improved UC ulceration. In addition, upregulation of lncRNA MEG3 relieved oxidative stress, inflammatory response, apoptosis, and pyroptosis of UC rat colons. LncRNA MEG3 overexpression alleviates the serve ulceration of UC rat colons by upregulating IL-10 expression via sponging miR-98-5p. To sum up, this study reveals the protective role of lncRNA MEG3 in the development of UC and may provide potential therapeutic targets for UC.	NA	Inflammation. 2021 Jun;44(3):1049-1059. doi: 10.1007/s10753-020-01400-z. Epub 2021 Jan 4.
5016	LncRNA	SOX2OT	miR-331-3p	Neurod1	PC-12 cells	Spinal Cord Injury	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	33340723	LncRNA SOX2OT Knockdown Alleviates Lipopolysaccharide-Induced Damage of PC12 Cells by Regulating miR-331-3p/Neurod1 Axis.	BACKGROUND: Long noncoding RNAs (lncRNAs) serve as crucial regulators in the pathogenesis of spinal cord injury (SCI). However, the role of lncRNA SOX2 overlapping transcript (SOX2OT) in SCI remains to be well revealed. METHODS: An SCI rat model was established and assessed by the Basso-Beattie-Bresnahan (BBB) method. An SCI PC12 cell model was established through lipopolysaccharide (LPS) treatment. Quantitative real-time polymerase chain reaction assay was used for SOX2OT, miR-331-3p, and neurogenic differentiation 1 (Neurod1) mRNA levels. Cell counting kit-8 assay and flow cytometry analysis were performed for cell viability and apoptosis, respectively. Enzyme-linked immunosorbent assay was performed for the levels of inflammatory cytokines. The production of superoxide dismutase and malondialdehyde was determined with relevant kits. Dual-luciferase reporter and RNA immunoprecipitation assays were conducted for the relationships among SOX2OT, miR-331-3p, and Neurod1. Western blot assay was employed for protein levels. RESULTS: SOX2OT was elevated in SCI rat and cell models. SOX2OT knockdown relieved the injury of SCI in SCI rat model. Moreover, the suppressive role in PC12 cell viability and the promotional roles in apoptosis, inflammation, and oxidative stress mediated by LPS were all restored by silencing SOX2OT. For mechanism analysis, SOX2OT was identified as a sponge of miR-331-3p to positively regulate Neurod1 expression. Inhibition of miR-331-3p reversed the effect of SOX2OT knockdown on LPS-induced PC12 damage. Overexpression of miR-331-3p protected PC12 cells from LPS-induced damage by binding to Neurod1. In addition, SOX2OT knockdown relieved PC12 cell injury by inactivation of Janus kinase-signal transducer and activator of transcription pathway. CONCLUSIONS: SOX2OT promoted PC12 cell injury through modulating miR-331-3p/Neurod1 axis and activating Janus kinase-signal transducer and activator of transcription pathway.	NA	World Neurosurg. 2021 Mar;147:e293-e305. doi: 10.1016/j.wneu.2020.12.049. Epub 2020 Dec 16.
5017	LncRNA	SOX2-OT	miR-942-5p	DP5	cardiomyocyte	Cardiomyocyte Apoptosis	Homo sapiens (human)	qRT-PCR;Immunoblotting;Luciferase reporter assay;	33603338	Long Noncoding RNA SOX2-OT Aggravates Doxorubicin-Induced Apoptosis of Cardiomyocyte by Targeting miR-942-5p/DP5.	BACKGROUND: Long non-coding RNAs (LncRNAs) play important roles in doxorubicin (DOX)-induced apoptosis of cardiomyocytes. However, the function of lncRNA SOX2-OT is unclear. This study was carried out to investigate the function of SOX2-OT in doxorubicin-induced cardiomyocyte apoptosis. METHODS: qRT-PCR and immunoblotting were used to detect the expression levels of SOX2-OT, miR-942-5p and death protein-5 (DP5) in DOX-treated primary cardiomyocytes and rat models. The relationship among miR-942-5p, SOX2-OT, and DP5 was explored by luciferase reporter assay. The effects of SOX2-OT, miR-942-5p and DP5 on doxorubicin-induced cardiomyocyte apoptosis were evaluated by Annexin V-FITC/PI method and caspase-3 activity assay. The effect of SOX2-OT on cardiomyocyte apoptosis was analyzed by TUNEL staining and echocardiography. RESULTS: SOX2-OT and DP5 were highly expressed, while miR-942-5p was down-regulated in DOX-treated primary cardiomyocytes and rat model. SOX2-OT can upregulate DP5 as a sponge of miR-942-5p, which was a direct target of miR-942-5p. In addition, miR-942-5p reversed the protective effect of knockdown of SOX2-OT on cardiomyocytes by inhibiting the expression of DP5 in vitro and in vivo. CONCLUSION: Knockdown of SOX2-OT down-regulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis of primary cardiomyocytes.	NA	Drug Des Devel Ther. 2021 Feb 11;15:481-492. doi: 10.2147/DDDT.S267474. eCollection 2021.
5018	LncRNA	TUG1	miR-29b-1-5p	MTDH	rat model of spinal cord IR	Ischemia Reperfusion Injury	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	33225366	Downregulation of Long Noncoding RNA TUG1 Attenuates MTDH-Mediated Inflammatory Damage via Targeting miR-29b-1-5p After Spinal Cord Ischemia Reperfusion.	Long noncoding RNAs and microRNAs (miRNAs) play a vital role in spinal cord ischemia reperfusion (IR) injury. The aim of this study was to identify the potential interactions between taurine upregulated gene 1 (TUG1) and miRNA-29b-1-5p in a rat model of spinal cord IR. The IR injury was established by 14-minute occlusion of aortic arch. TUG1 and metadherin (MTDH) knockdown were induced by respective siRNAs, and miR-29b-1-5p expression was modulated using specific inhibitor or mimics. The interactions between TUG1, miR-29b-1-5p, and the target genes were determined using the dual-luciferase reporter assay. We found that IR respectively downregulated and upregulated miR-29b-1-5p and TUG1, and significantly increased MTDH expression. MTDH was predicted as a target of miR-29b-1-5p and its knockdown downregulated NF-κB and IL-1β levels. A direct interaction was observed between TUG1 and miR-29b-1-5p, and knocking down TUG1 upregulated the latter. Furthermore, overexpression of miR-29b-1-5p or knockdown of TUG1 alleviated blood-spinal cord barrier leakage and improved hind-limb motor function by suppressing MTDH and its downstream pro-inflammatory cytokines. Knocking down TUG1 also alleviated MTDH/NF-κB/IL-1β pathway-mediated inflammatory damage after IR by targeting miR-29b-1-5p, whereas blocking the latter reversed the neuroprotective effect of TUG1 knockdown and restored MTDH/NF-κB/IL-1β levels.	NA	J Neuropathol Exp Neurol. 2021 Feb 22;80(3):254-264. doi: 10.1093/jnen/nlaa138.
5019	Circular RNA	circ_RPPH1	miR-146b-3p	E2F2	Breast Carcinoma Cells	Breast Cancer	Homo sapiens (human)  	qRT-PCR;RNA immunoprecipitation;RNA immunoprecipitation;RNA pull-down;	34433131	Mediation of circ_RPPH1 on miR-146b-3p/E2F2 pathway to hinder the growth and metastasis of breast carcinoma cells.	BACKGROUND: Nova Circular RNA (circRNA) of non-coding RNA has gradually become an important regulatory factor, and it has made people attach great concern over the occurrence and development of many diseases, particularly carcinomas. circ_RPPH1 is a newly discovered circRNA. Gene Expression Omnibus (GEO) analysis showed that there are high contents of circ_RPPH1 in breast cancer (BC), but the mechanism of circRNA in BC remains unclear. METHODS: Real-time quantitative PCR (qRT-PCR) was applied to test the role of circ_RPPH1 in BC patients, and functional experiments were applied to test the role of circ_RPPH1 on BC tumor. Fluorescence in situ hybridization, double luciferase reporter gene analysis, RNA pull-down and RNA immunoprecipitation experiments were performed to explore the correlation of circ_RPPH1 with miR-146b-3p/E2F2 in BC. RESULTS: circ_RPPH1 was evidently enhanced in BC, and its content was related to the clinical stage and pathological grade. circ_RPPH1 can accelerate the proliferation, migration and invasion, and promote tumorigenesis and metastasis. Mechanism exploration indicated that circ_RPPH1 acted as ceRNA (competing endogenous RNA) of miR-146b-3p, so as to reduce the inhibitory role of miR-146b-3p on its target E2F2. CONCLUSION: Circ_RPPH1/miR-146b-3p/E2F2 axis can promote the progression of BC, and it might be a latent therapeutic target for clinical BC.		Aging (Albany NY). 2021 Aug 25;13(undefined). doi: 10.18632/aging.203439.
5020	Circular RNA	circVRK1	miR-337-3p	ZNF652	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	Northern blot;qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	34424826	Circular RNA circVRK1 suppresses the proliferation, migration and invasion of osteosarcoma cells by regulating zinc finger protein ZNF652 expression via microRNA miR-337-3p.	Circular RNA is an innovative kind of endogenous non-coding RNA, which could take part in tumorigenesis. Nonetheless, the potential molecular mechanisms of circVRK1 in the progression of osteosarcoma remain unresolved. In the current study, we initially investigated circVRK1 levels in osteosarcoma clinical samples and cell lines by qRT-PCR analysis and northern blot assay. RNase R treatments, RNA stability assay and nucleoplasmic separation assay were conducted to identify the characteristics of circVRK1. We adopted CCK-8, colony formation, wound-healing, and transwell assays to assess the biological effects of circVRK1 on the proliferation, migration, and invasiveness of osteosarcoma cells in vitro. We then constructed a xenograft model in nude mice to confirm the suppressive role of circVRK1 in vivo. Moreover, dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays were utilized to elucidate the underlying molecular mechanisms mediated by circVRK1. We demonstrated that circVRK1 was a stable circular transcript localized in the cytoplasm of osteosarcoma cells, and the down-regulation of circVRK1 in osteosarcoma tissues was related to poor outcome of patients. Meanwhile, over-expressed circVRK1 obviously restrained the growth, migration, and invasion of osteosarcoma in vitro and in vivo. Mechanistically, circVRK1 was assumed to be a microRNA sponge for miR-337-3p, and ZNF652 was the downstream gene of miR-337-3p. CircVRK1 overexpression or miR-337-3p knockdown accelerated ZNF652 expression, and up-regulated miR-337-3p efficiently abolished the promotion of ZNF652 induced by circVRK1. Moreover, rescue experiments have proved that circVRK1 inhibits the progression of osteosarcoma by modulating the miR-337-3p/ZNF652 axis. Therefore, we conclude that circVRK1 promotes ZNF652 expression by sponging miR-337-3p. CircVRK1 serves as a molecule sponge for miR-337-3p and mediates the ceRNA network to promote the expression of ZNF652, thus suppresses osteosarcoma proliferation, migration and invasion.		Bioengineered. 2021 Dec;12(1):5411-5427. doi: 10.1080/21655979.2021.1965695.
5021	Circular RNA	circGLI3	miR-339-5p	VEGFA	Ipec-J2 Cells	Oxidative Stress	Homo sapiens (human)  	FISH;Western blot;FISH;Luciferase reporter assay;	34423029	circGLI3 Inhibits Oxidative Stress by Regulating the miR-339-5p/VEGFA Axis in IPEC-J2 Cells.	As a new type of noncoding RNA, circular RNA (circRNA) is stable in cells and not easily degraded. This type of RNA can also competitively bind miRNAs to regulate the expression of their target genes. The role of circRNA in the mechanism of intestinal oxidative stress (OS) in weaned piglets is still unclear. In our research, diquat (DQ) was used to induce OS in small intestinal epithelial cells (IPEC-J2) to construct an OS cell model. Mechanistically, dual luciferase reporter assays, fluorescence in situ hybridization (FISH), and western blotting were performed to confirm that circGLI3 directly sponged miR-339-5p and regulated the expression of VEGFA. Overexpression of circGLI3 promoted IPEC-J2 cell proliferation, increased the proportion of S-phase cells (P < 0.01), and reduced reactive oxygen species (ROS) generation when IPEC-J2 cells were subjected to OS. circGLI3 can increase the activity of glutathione peroxidase (GSH-Px) and the total antioxidant capacity (T-AOC) in IPEC-J2 cells and reduce the malondialdehyde (MDA) content and levels of inflammatory factors. Therefore, overexpression of circGLI3 reduced oxidative damage, whereas miR-339-5p mimic counteracted these effects. We identified a regulatory network composed of circGLI3, miR-339-5p, and VEGFA and verified that circGLI3 regulates VEGFA by directly binding miR-339-5p. The expression of VEGFA affects IPEC-J2 cell proliferation, cell cycle progression, and ROS content and changes the levels of antioxidant enzymes and inflammatory factors. This study reveals the molecular mechanism by which circGLI3 inhibits OS in the intestine of piglets and provides a theoretical basis for further research on the effect of OS on intestinal function.		Biomed Res Int. 2021 Aug 11;2021:1086206. doi: 10.1155/2021/1086206. eCollection 2021.
5022	Circular RNA	circ-PDCD11	miR-432-5p	LDHA	Triple-Negative Breast Cance Cells	Triple Negative Breast Cancer	Homo sapiens (human)  	RACE;	34420029	CircRNA circ-PDCD11 promotes triple-negative breast cancer progression via enhancing aerobic glycolysis.	Well-described evidence has demonstrated the critical roles of aerobic glycolysis in triple-negative breast cancer (TNBC) oncotherapy. Moreover, next-generation high-throughput sequencing indicates the potential regulation of energy metabolism by circular RNAs (circRNAs) in TNBC. However, circRNA modulation of TNBC aerobic glycolysis is still unclear. Here, the present research aimed to investigate the function and underlying mechanisms of novel circPDCD11 (hsa_circ_0019853) in TNBC aerobic glycolysis. The results revealed that circPDCD11 expression was significantly upregulated in TNBC tissues and cells. Clinical data demonstrated that the high expression of circPDCD11 was closely correlated with a poor prognosis and acted as an independent risk factor for TNBC prognosis. Functionally, in vitro gain- and loss-of-function experiments revealed that circPDCD11 accelerated glucose uptake, lactate production, ATP generation, and the extracellular acidification rate in TNBC cells. In vivo, circPDCD11 silencing repressed tumor growth. Mechanistically, circPDCD11 acted as a miRNA sponge to enhance LDHA expression by sponging miR-432-5p. In conclusion, these combined results demonstrated that circPDCD11 acts as an oncogene for TNBC, providing a promising prognostic biomarker for TNBC.		Cell Death Discov. 2021 Aug 21;7(1):218. doi: 10.1038/s41420-021-00604-y.
5023	Circular RNA	CircEYA3	miR-1294	c-Myc	Pancreatic Ductal Adenocarcinoma Tissues And Cells	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)	FISH;qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;FISH;RNA immunoprecipitation;RNA pull-down;	34419070	Circular RNA CircEYA3 induces energy production to promote pancreatic ductal adenocarcinoma progression through the miR-1294/c-Myc axis.	BACKGROUND: Extensive studies have demonstrated the pivotal roles of circular RNAs (circRNAs) in the occurrence and development of different human cancers. However, the expression and regulatory roles of circRNAs in pancreatic ductal adenocarcinoma (PDAC) are unclear. METHODS: CircEYA3 was explored based on Gene Expression Omnibus (GEO) dataset analysis. qRT-PCR was applied to determine the expression of circRNAs, miRNAs and mRNAs in PDAC cells and tissues. The biological roles of circEYA3 in vitro and in vivo were determined by performing a series of functional experiments. Further, dual luciferase reporter, fluorescence in situ hybridization (FISH), RNA pull-down assays, and RNA immunoprecipitation (RIP) assays were used to confirm the interaction of circEYA3 with miR-1294. RESULTS: CircEYA3 was elevated in PDAC tissues and cells, and a higher level of circEYA3 was significantly associated with a poorer prognosis in patients with PDAC. Functionally, circEYA3 increased energy production via ATP synthesis to promote PDAC progression in vitro and in vivo. Mechanistically, circEYA3 functions as an endogenous miR-1294 sponge to elevate c-Myc expression, thus exerting its oncogenic functions. CONCLUSION: CircEYA3 promotes the progression of PDAC through the miR-1294/c-Myc signalling axis, and circEYA3 may be an efficient molecular therapeutic target in PDAC.		Mol Cancer. 2021 Aug 21;20(1):106. doi: 10.1186/s12943-021-01400-z.
5024	Circular RNA	circRNA_0001859	miR-29b-3p	Ctnnb1	Hl-1 Cells	Cardiac Hypertrophy	Homo sapiens (human)  	qRT-PCR 	34418850	Potential molecular mechanism of cardiac hypertrophy in mice induced by exposure to ambient PM(2.5).	Cardiac hypertrophy could be induced by ambient fine particulate matter (PM(2.5)) exposure. Since cardiac hypertrophy represents an early event leading to heart dysfunction, it is necessary to explore the molecular mechanisms, which are largely unknown. In the present study, an ambient particulate matter exposure mice model was established to explore its adverse effects related to the heart and the potential mechanisms. Forty-eight male C57BL/6 mice were randomly subjected to three groups: filtered air group, unfiltered air group and concentrated air group, and were exposed for 8 and 16 weeks, 6 h/day, respectively. In vitro experiments, the cardiac muscle cell line (HL-1) was treated with PM(2.5) (0, 25, 50 and 100 μg/mL) for 24 h. In the present study, cardiac hypertrophy was occurred in vivo and vitro after exposure to PM(2.5). Mechanistically, circ_0001859 could sponge miR-29b-3p, which could interact with 3'UTRs of Ctnnb1 (gene name of b-catenin). And Ctnnb1 expression was transcriptionally inhibited by si-circ_0001859 or miR-29b-3p mimic in HL-1 cells. Additionally, miR-29b-3p inhibitor could also make a reversion about the inhibition effect of circ_0001859 silencing on Ctnnb1 mRNA level in HL-1 cells. Functionally, knockout of circ_0001859 or overexpression of miR-29b-3p could inhibit LEF1/IGF-2R pathway and alleviate the progress of hypertrophy induced by PM(2.5) in HL-1 cells. And miR-29b-3p inhibitor could reverse the inhibition effect of circ_0001859 silencing on hypertrophic response induced by PM(2.5) in HL-1 cells. Consequently, the data demonstrated that circRNA_0001859 promoted the process of cardiac hypertrophy through suppressing miR-29b-3p leading to enhance Ctnnb1 level, and activated downstream pathway molecules LEF1/IGF-2R.		Ecotoxicol Environ Saf. 2021 Aug 19;224:112659. doi: 10.1016/j.ecoenv.2021.112659.
5025	Circular RNA	circRHOBTB3	miR-600	NACC1	Panc-1 And Miapaca-2 Cells	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)  	RIP assay;Western blot;Luciferase reporter assay;	34416910	FUS-induced circRHOBTB3 facilitates cell proliferation via miR-600/NACC1 mediated autophagy response in pancreatic ductal adenocarcinoma.	BACKGROUND: Circular RNAs (circRNAs) are becoming a unique member of non-coding RNAs (ncRNAs) with emerging evidence of their regulatory roles in various cancers. However, with regards to pancreatic ductal adenocarcinoma (PDAC), circRNAs biological functions remain largely unknown and worth investigation for potential therapeutic innovation. METHODS: In our previous study, next-generation sequencing was used to identify differentially expressed circRNAs in 3 pairs of PDAC and adjacent normal tissues. Further validation of circRHOBTB3 expression in PDAC tissues and cell lines and gain-and-loss function experiments verified the oncogenic role of circRHOBTB3. The mechanism of circRHOBTB3 regulatory role was validated by pull-down assays, RIP, luciferase reporter assays. The autophagy response of PANC-1 and MiaPaca-2 cells were detected by mCherry-GFP-LC3B labeling and confocal microscopy, transmission electron microscopy and protein levels of LC3B or p62 via Western blot. RESULTS: circRHOBTB3 is highly expressed in PDAC cell lines and tissues, which also promotes PDAC autophagy and then progression in vitro and in vivo. Mechanistically, circRHOBTB3 directly binds to miR-600 and subsequently acts as a miRNA-sponge to maintain the expression level of miR-600-targeted gene NACC1, which facilitates the autophagy response of PDAC cells for adaptation of proliferation via Akt/mTOR pathway. Moreover, the RNA-binding protein FUS (FUS) directly binds to pre-RHOBTB3 mRNA to mediate the biogenesis of circRHOBTB3. Clinically, circRHOBTB3, miR-600 and NACC1 expression levels are correlated with the prognosis of PDAC patients and serve as independent risk factors for PDAC patients. CONCLUSIONS: FUS-mediated circRHOBTB3 functions as a tumor activator to promote PDAC cell proliferation by modulating miR-600/NACC1/Akt/mTOR axis regulated autophagy.		J Exp Clin Cancer Res. 2021 Aug 20;40(1):261. doi: 10.1186/s13046-021-02063-w.
5026	Circular RNA	CircUBAP2	miR-582-5p	FOXO1	Colon Cancer Tissues And Cell Lines	Colon Cancer	Homo sapiens (human)  	qRT-PCR 	34416339	CircUBAP2 enhances autophagy and promotes colon cancer progression and metastasis via miR-582-5p/FOXO1 signaling.	Numerous circular RNAs (circRNAs) have been identified as vital regulators in various cancers. The newly reported circular RNA ubiquitin-associated protein 2 (circUBAP2) is a critical player in cell growth and metastasis in various types of cancers, although its role in colon cancer (CRC), has yet to be fully elucidated. We find that circUBAP2 is upregulated in CRC tissues and cell lines to induce autophagy both in vitro and in vivo. The effects of circUBAP2 on migration, invasion and proliferation may be partially related to autophagy. Mechanistically, we uncover that circUBAP2 can directly interact with miR-582-5p, and subsequently act as a miRNA sponge to regulate the expression of the miR-582-5p target gene forkhead box protein O1 (FOXO1) and downstream signaling molecules, which collectively advance the progression and metastasis of CRC. These results suggest that circUBAP2 acts as an oncogene via a novel circUBAP2/miR-582-5p/FOXO1 axis, providing a potential biomarker and therapeutic target for CRC management.		J Genet Genomics. 2021 Aug 17:S1673-8527(21)00260-5. doi: 10.1016/j.jgg.2021.07.017.
5027	Circular RNA	circ_0005909	miRNA-338-3p	SOX4	Non-Small-Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RT-PCR;Luciferase reporter assay;	34413915	circRNA hsa_circ_0005909 Predicts Poor Prognosis and Promotes the Growth, Metastasis, and Drug Resistance of Non-Small-Cell Lung Cancer via the miRNA-338-3p/SOX4 Pathway.	BACKGROUND: Circular RNAs (circRNAs) are powerful factors in regulating various cancer behaviors. It has been manifested in previous researches that circular RNA hsa_circ_0005909 (circ_0005909) exhibits a regulatory function in osteosarcoma. However, there are no other studies on whether circ_0005909 displays potential functions on the progression of non-small-cell lung cancer (NSCLC). METHODS: RT-PCR was applied to examine the expression of circ_0005909 in NSCLC. To study the specific behaviors of NSCLC cells after circ_0005909 knockdown, cell counting kit-8 (CCK-8) assays, colony formation assays, Transwell assays, and xenograft tumor model assays were conducted. Bioinformatics and luciferase reporter assays were employed to study the association among circ_0005909, miRNA-338-3p, and SOX4. RESULTS: In this research, our group firstly showed that circ_0005909 expressions were distinctly increased in NSCLC specimens and cell lines. Clinical studies revealed that high circ_0005909 expressions were associated with poor prognosis of NSCLC patients. Functionally, knockdown of circ_0005909 was observed to suppress the proliferation, metastasis, and drug resistance of NSCLC cells. In the terms of mechanism, circ_0005909 could act as a sponge of miRNA-338-3p, and miRNA-338-3p could target SOX4. In addition, miRNA-338-3p inhibitors reversed the suppressor ability of circ_0005909 silence on NSCLC behaviors. CONCLUSIONS: circ_0005909 promoted the progression of NSCLC via the modulation of the miRNA-338-3p/SOX4 axis, which may be a therapeutic target for NSCLC.		Dis Markers. 2021 Aug 6;2021:8388512. doi: 10.1155/2021/8388512. eCollection 2021.
5028	Circular RNA	circ_0099999	miR-330-5p	FSCN1	Pancreatic Cancer Tissues And Cells	Pancreatic Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34409897	A novel circ_0099999/miR-330-5p/FSCN1 ceRNA crosstalk in pancreatic cancer.	BACKGROUND: Pancreatic cancer is a lethal malignancy in both sexes throughout the world. Circular RNAs (circRNAs) have been implicated in the development of pancreatic cancer by operating as competing endogenous RNAs (ceRNAs). Here, we explored circ_0099999-mediated ceRNA activity in regulating pancreatic tumorigenesis. METHODS: Ribonuclease R (RNase R) and subcellular localization assays were utilized to characterize circ_0099999. The levels of circ_0099999, microRNA (miR)-330-5p, and fascin actin-bundling protein 1 (FSCN1) were gauged by quantitative real-time PCR (qRT-PCR) and western blot. Cell proliferation, colony formation, apoptosis, migration, and invasion were evaluated by the Cell Counting Kit-8 (CCK-8), colony formation, flow cytometry, and transwell assays, respectively. The levels of glucose consumption and lactate production were determined using the assay kits. A direct relationship between miR-330-5p and circ_0099999 or FSCN1 was validated by dual-luciferase reporter assay. Tumour xenograft assays were used to analyse the role of circ_0099999 in vivo. RESULTS: Circ_0099999 was highly up-regulated in pancreatic cancer tissues and cells. Knockdown of circ_0099999 impeded cell proliferation, migration, invasion, glycolysis, and promoted apoptosis in vitro, as well as diminished tumour growth in vivo. Circ_0099999 targeted miR-330-5p, and miR-330-5p was a downstream mediator of circ_0099999 function. FSCN1 was a direct and functional target of miR-330-5p. Furthermore, circ_0099999 operated as a ceRNA for miR-330-5p to modulate FSCN1 expression. CONCLUSIONS: Our findings established a novel causal mechanism, circ_0099999/miR-330-5p/FSCN1 ceRNA crosstalk, in regulating pancreatic carcinogenesis and provided that inhibition of circ_0099999 might have therapeutic benefits in pancreatic cancer.		Autoimmunity. 2021 Aug 19:1-12. doi: 10.1080/08916934.2021.1963958.
5029	Circular RNA	circCDYL	MiR-92b-3p	NA	Breast Cancer Tissues Or Cell Lines	Breast Cancer	Homo sapiens (human)  	qRT-PCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34395434	MiR-92b-3p Inhibits Proliferation of HER2-Positive Breast Cancer Cell by Targeting circCDYL.	OBJECTIVES: Circular RNA (circRNA) is a novel class of RNA, which exhibits powerful biological function in regulating cellular fate of various tumors. Previously, we had demonstrated that over-expression of circRNA circCDYL promoted progression of HER2-negative (HER2(-)) breast cancer via miR-1275-ULK1/ATG7-autophagic axis. However, the role of circCDYL in HER2-positive (HER2(+)) breast cancer, in particular its role in modulating cell proliferation, one of the most important characteristics of cellular fate, is unclear. MATERIALS AND METHODS: qRT-PCR and in situ hybridization analyses were performed to examine the expression of circCDYL and miR-92b-3p in breast cancer tissues or cell lines. The biological function of circCDYL and miR-92b-3p were assessed by plate colony formation and cell viability assays and orthotopic animal models. In mechanistic study, circRNAs pull-down, RNA immunoprecipitation, dual luciferase report, western blot, immunohistochemical and immunofluorescence staining assays were performed. RESULTS: CircCDYL was high-expressed in HER2(+) breast cancer tissue, similar with that in HER2(-) breast cancer tissue. Silencing HER2 gene had no effect on expression of circCDYL in HER2(+) breast cancer cells. Over-expression of circCDYL promoted proliferation of HER2(+) breast cancer cells but not through miR-1275-ULK1/ATG7-autophagic axis. CircRNA pull down and miRNA deep-sequencing demonstrated the binding of miR-92b-3p and circCDYL. Interestingly, circCDYL did not act as miR-92b-3p sponge, but was degraded in miR-92b-3p-dependent silencing manner. Clinically, expression of circCDYL and miR-92b-3p was associated with clinical outcome of HER2(+) breast cancer patients. CONCLUSION: MiR-92b-3p-dependent cleavage of circCDYL was an essential mechanism in regulating cell proliferation of HER2(+) breast cancer cells. CircCDYL was proved to be a potential therapeutic target for HER2(+) breast cancer, and both circCDYL and miR-92b-3p might be potential biomarkers in predicting clinical outcome of HER2(+) breast cancer patients.		Front Cell Dev Biol. 2021 Jul 29;9:707049. doi: 10.3389/fcell.2021.707049. eCollection 2021.
5030	Circular RNA	CircGNG4	miR-223	EYA3	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR 	34395419	CircGNG4 Promotes the Progression of Prostate Cancer by Sponging miR-223 to Enhance EYA3/c-myc Expression.	Patients diagnosed with prostate cancer often have a poor prognosis and limited treatment options, as the specific pathogenesis remains to be elucidated. Circular RNA (circRNA) is a type of non-coding RNA that interacts with microRNA (miRNA/miR) and transcription factors to regulate gene expression. However, little is known about specific circRNAs that serve roles in the pathogenesis of prostate cancer. Findings of the present study confirmed that circRNA G protein subunit γ 4 (circGNG4) was upregulated in prostate cancer tissues and cell lines. Knockdown of circGNG4 inhibited the malignant behavior of prostate cancer cells. Furthermore, bioinformatics were used to predict targeting interactions between circGNG4 or miR-223 and EYA transcriptional coactivator and phosphatase 3 (EYA3)/c-Myc mRNA. miR-223 inhibited the malignant behavior of prostate cancer cells, while EYA3/c-Myc had the opposite effect. circGNG4 enhanced the expression of EYA3/c-Myc by sponging miR-223 to promote the growth of prostate cancer tumors in vivo. In conclusion, the circGNG4/miR-223/EYA3/c-Myc regulatory pathway promoted the malignant progression of prostate cancer. The results of the present study may provide potential new targets for the diagnosis or treatment of prostate cancer.		Front Cell Dev Biol. 2021 Jul 28;9:684125. doi: 10.3389/fcell.2021.684125. eCollection 2021.
5031	Circular RNA	CircGNG4	miR-223	c-myc	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR 	34395419	CircGNG4 Promotes the Progression of Prostate Cancer by Sponging miR-223 to Enhance EYA3/c-myc Expression.	Patients diagnosed with prostate cancer often have a poor prognosis and limited treatment options, as the specific pathogenesis remains to be elucidated. Circular RNA (circRNA) is a type of non-coding RNA that interacts with microRNA (miRNA/miR) and transcription factors to regulate gene expression. However, little is known about specific circRNAs that serve roles in the pathogenesis of prostate cancer. Findings of the present study confirmed that circRNA G protein subunit γ 4 (circGNG4) was upregulated in prostate cancer tissues and cell lines. Knockdown of circGNG4 inhibited the malignant behavior of prostate cancer cells. Furthermore, bioinformatics were used to predict targeting interactions between circGNG4 or miR-223 and EYA transcriptional coactivator and phosphatase 3 (EYA3)/c-Myc mRNA. miR-223 inhibited the malignant behavior of prostate cancer cells, while EYA3/c-Myc had the opposite effect. circGNG4 enhanced the expression of EYA3/c-Myc by sponging miR-223 to promote the growth of prostate cancer tumors in vivo. In conclusion, the circGNG4/miR-223/EYA3/c-Myc regulatory pathway promoted the malignant progression of prostate cancer. The results of the present study may provide potential new targets for the diagnosis or treatment of prostate cancer.		Front Cell Dev Biol. 2021 Jul 28;9:684125. doi: 10.3389/fcell.2021.684125. eCollection 2021.
5032	Circular RNA	circ-SFMBT2	miR-885-3p	CHD7	Gastric Cancer Tissues And Cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Flow cytometry assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34387601	Downregulation of circ-SFMBT2 blocks the development of gastric cancer by targeting the miR-885-3p/CHD7 pathway.	Accumulating evidence insists that circular RNAs (circRNAs) play important roles in the development of human cancers, including gastric cancer. This study aimed to investigate the role of circ-SFMBT2 and provide a potential mechanism to explain its function. The expression of circ-SFMBT2, miR-885-3p and chromodomain-helicase-DNA-binding protein 7 (CHD7) mRNA was determined by quantitative real-time PCR (qRT-PCR), and the protein level of CHD7 was determined by western blot. To investigate the function of circ-SFMBT2 in vitro, the effects of circ-SFMBT2 on cell viability, colony formation, apoptosis, migration and invasion were assessed using cell counting kit-8 assay, colony formation assay, flow cytometry assay, wounding healing assay and transwell assay, respectively. The indicators of oxidative stress were assessed using matched kits. Besides, the function of circ-SFMBT2 was also investigated in animal models. The relationship between miR-885-3p and circ-SFMBT2 or CHD7 was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Circ-SFMBT2 and CHD7 were upregulated, whereas miR-885-3p was downregulated in gastric cancer tissues and cells. In functional assay, circ-SFMBT2 knockdown suppressed gastric cancer cell viability, colony formation ability, migration, invasion and oxidative stress but induced apoptosis, and circ-SFMBT2 downregulation also blocked tumor growth in vivo. In mechanism analysis, circ-SFMBT2 regulated CHD7 expression by sponging its target miRNA, miR-885-3p. Rescue experiments manifested that miR-885-3p inhibition reversed the effects of circ-SFMBT2 knockdown, and CHD7 overexpression abolished the antitumor role of miR-885-3p overexpression. Moreover, circ-SFMBT2 knockdown inactivated the Wnt/b-catenin signaling pathway. Circ-SFMBT2 downregulation repressed the development of gastric cancer partially by controlling the miR-885-3p/CHD7 axis, which might be a novel strategy to inhibit gastric cancer progression.		Anticancer Drugs. 2021 Aug 11. doi: 10.1097/CAD.0000000000001195.
5033	Circular RNA	circXPO1	miR-23a	NA	Pancreatic Cells	Prostate Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Cell Invasion Assay;Luciferase reporter assay;	34386427	The Circular RNA circXPO1 Promotes Tumor Growth via Sponging MicroRNA-23a in Prostate Carcinoma.	It has been shown that circular RNA XPO1 (circXPO1) is involved in cancer (e.g., lung adenocarcinoma and osteosarcoma) progression by sponging microRNAs. Nevertheless, the role of circXPO1 and its interaction with microRNAs in prostate cancer remains unknown. In this study, the results of quantitative real-time PCR showed that circXPO1 levels were dramatically increased in human prostate cancer tissue and cell lines compared with those in normal tissue and cell line. Furthermore, cell proliferation, colony formation, and cell invasion assays showed that circXPO1 promoted the malignant behavior of pancreatic cells in vitro. Mechanistically, bioinformatics prediction, a dual-luciferase reporter assay, and pull-down assay suggested that circXPO1 physically targets miR-23a and negatively regulates its expression in pancreatic cancer cells. miR-23a mimics and inhibitors effectively reversed the effects of circXPO1 on the malignant behavior of prostate cancer cells in vitro. Consistent results were observed in the xenograft tumor model. In conclusion, circXPO1 promotes prostate cancer progression via targeting miR-23a, thus suggesting the circXPO1/miR-23a axis can be used as a potential therapeutic target for prostate cancer treatment.		Front Oncol. 2021 Jul 27;11:712145. doi: 10.3389/fonc.2021.712145. eCollection 2021.
5034	Circular RNA	circCD151	miR-30d-5p	GLI2	A549 And Nci-H292 Cells	Lung Cancer	Homo sapiens (human)	Luciferase reporter assay;	34368867	circCD151 promotes GLI2 expression by regulating miR-30d-5p and enhancing proliferation, invasion and stemness of lung cancer.	To investigate the changes of circular (circ)RNA circCD151 expression in lung cancer tissues and cells and its effects on proliferation, migration and invasion of lung cancer cells. The relative expression levels of circCD151 in lung cancer tissues and lung cancer cells (A549 and NCI-H292) were determined by reverse transcription-quantitative PCR. The effects of silencing or upregulation of circCD151 on the activity and clonal forming ability of A549 and NCI-H292 cells were detected by CCK-8 and cloning formation experiments. Transwell invasion assay detected the effects of silencing or upregulation of circCD151 on the migration and invasion ability of A549 and NCI-H292 cells. The regulatory effect of circCD151 on miR-30d-5p was detected by dual luciferase reporter gene. The relative expression level of circCD151 in lung cancer tissues was significantly higher compared with that in adjacent tissues. The relative expression level of circCD151 in A549 and NCI-H292 cells was significantly higher compared with that in human lung epithelial cells. In A549 and NCI-H292 cells, silencing circCD151 decreased cell activity and clonal formation ability and invasion ability was also significantly decreased. circCD151 was upregulated in A549 and NCI-H292 cells and the activity and clonal formation ability of A549 and NCI-H292 cells were significantly increased and the invasion ability was also significantly increased. Double luciferase reporter assay confirmed the ceRNA regulatory mechanism of circCD151/miR-30d-5p/GLI2. In the present study, in vivo and in vitro functional studies demonstrated that circCD151 may promote the proliferation, invasion and cell stemness of lung cancer cells. Further molecular mechanism studies demonstrated that circCD151 could promote the malignant proliferation of lung adenocarcinoma by targeting miR-30d-5p and upregulating GLI2 expression. From the perspective of circRNA, the present study will provide new clues to the pathogenesis and prognostic judgment of lung adenocarcinoma and provide a new target for clinical treatment.		Mol Med Rep. 2021 Oct;24(4):699. doi: 10.3892/mmr.2021.12338. Epub 2021 Aug 9.
5035	Circular RNA	circEVI5	miR-4793-3p	FOXO1	Gastric Cancer Tissues And Cells	Gastric Cancer	Mus musculus (mouse)	CCK-8 assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Cell cycle assay;luciferase assay;RNA immunoprecipitation;	34354043	circEVI5 acts as a miR-4793-3p sponge to suppress the proliferation of gastric cancer.	Circular RNAs (circRNAs) are a novel class of endogenous noncoding RNAs (ncRNAs) with a covalently closed loop structure. Accumulating evidence shows that circRNAs play vital roles in the growth, metastasis, treatment and prognosis of various cancers. However, the detailed functions and underlying mechanisms of circEVI5 (hsa_circ_0013162) in gastric cancer (GC) remain undocumented. In this study, the expression levels and prognostic value of circEVI5 were validated in GC tissue samples by using qRT-PCR. circEVI5 was significantly downregulated in GC tissues and cells, and low circEVI5 expression was correlated with poor prognosis. Next, in vitro CCK-8 assay, EdU incorporation assay, PI staining cell cycle assay, and in vivo xenograft mouse models were conducted to assess the functions of circEVI5. Gain of function experiments indicated that circEVI5 could inhibit GC cell proliferation and retard the cell cycle. Moreover, bioinformatics prediction showed that circEVI5 binds to miR-4793-3p, while FOXO1 may be a target of miR-4793-3p. Pull-down assays, RNA immunoprecipitation (RIP) assays, luciferase assays, and western blot were used to confirm the interactions between circEVI5, miR-4793-3p, and FOXO1. Functional assays demonstrated that circEVI5 suppressed the proliferation of GC by sponging miR-4793-3p and increasing FOXO1 expression levels. In conclusion, our study demonstrated that circEVI5 can bind miR-4793-3p as a ceRNA to eliminate the negative regulation of FOXO1, therefore suppressing GC proliferation.		Cell Death Dis. 2021 Aug 5;12(8):774. doi: 10.1038/s41419-021-04061-4.
5036	Circular RNA	circ_VMA21	miR-409-3p	KLF4	Wi-38 Cells	Pneumonia	Homo sapiens (human)  	Dual-luciferase reporter assay;ELISA;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	34350833	circ_VMA21 protects WI-38 cells against LPS-induced apoptotic and inflammatory injury by acting on the miR-409-3p/KLF4 axis.	Pneumonia is a common inflammatory lung disease. Circular RNA (circRNA) vacuolar ATPase assembly factor (circ_VMA21) has been reported to mitigate the inflammatory injury in WI-38 cells. This study was to investigate the functional mechanism of circ_VMA21. Cell model was established by lipopolysaccharide (LPS) treatment in WI-38 cells. Cell cycle and apoptosis were analyzed by flow cytometry. Cell proliferation was assessed by colony formation and MTT assays. The expression quantification of circ_VMA21, microRNA-409-3p (miR-409-3p) and Kruppel-like transcription factor 4 (KLF4) was performed by qRT-PCR method. The expression of relative protein was detected by Western blot. Inflammatory response was evaluated by ELISA. The target binding was validated by dual-luciferase reporter assay. Cellular analysis indicated that LPS repressed cell cycle and proliferation but induced apoptosis. circ_VMA21 was downregulated in pneumonia samples and LPS-treated WI-38 cells. Functionally, circ_VMA21 assuaged the LPS-induced apoptotic and inflammatory damages. In addition, circ_VMA21 directly targeted miR-409-3p and its function was dependent on the sponge effect on miR-409-3p. Also, KLF4 was a target of miR-409-3p and miR-409-3p inhibitor attenuated LPS-induced cell injury by upregulating KLF4. Moreover, KLF4 was upregulated by circ_VMA21/miR-409-3p axis. These findings suggested that circ_VMA21 relieved the LPS-induced apoptotic and inflammatory injury by the regulation of miR-409-3p/KLF4 axis.		Gen Physiol Biophys. 2021 Jul;40(4):275-287. doi: 10.4149/gpb_2021011.
5037	Circular RNA	circ_0014130	miR-545-3p	YAP1	Non-Small-Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;MTT assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;MTT assay;	34349347	Blocking circ_0014130 suppressed drug resistance and malignant behaviors of docetaxel resistance-acquired NSCLC cells via regulating miR-545-3p-YAP1 axis.	Recent evidences have claimed that circular RNAs are deregulated in docetaxel (DTX) resistance in malignant tumors, including non-small-cell lung cancer (NSCLC). Hsa_circ_0014130 (circ_0014130) is a new biomarker in NSCLC. However, its role in DTX-resistant NSCLC remained to be annotated. In this study, real-time PCR was used to measure expression of circ_0014130, and circ_0014130 was upregulated in NSCLC tumors and DTX-resistant NSCLC cells (NCI-H1299/DTX and A549/DTX). MTT assay analyzed the half inhibitory concentration (IC50) of DTX, and it was lowered by circ_0014130 interference in DTX-resistant NSCLC cells. Moreover, colony formation assay, flow cytometry, transwell assays, and xenograft tumor model revealed that silencing circ_0014130 facilitated apoptosis rate of DTX-resistant NSCLC cells, suppressed the colony formation, migration and invasion, and retarded xenograft tumor growth in nude mice. Dual-luciferase reporter assay and RNA immunoprecipitation confirmed that circ_0014130 was one competing endogenous RNA (ceRNA) for miRNA (miR)-545-3p, and circ_0014130 modulated expression of yes-associated protein 1 (YAP1), a target gene for miR-545-3p. YAP1 upregulation and miR-545-3p downregulation were allied with circ_0014130 upregulation in NSCLC tumors and DTX-resistant NSCLC cells. Functionally, downregulating miR-545-3p could abate the effects of circ_0014130 knockdown in DTX-resistant NSCLC cells in vitro, whereas its overexpression exerted similar effects of circ_0014130 knockdown. Either, restoring YAP1 partially reversed miR-545-3p effects in DTX-resistant NSCLC cells. Collectively, there might be a novel circ_0014130-miR-545-3p-YAP1 ceRNA pathway in regulation of chemoresistance and malignant behaviors of DTX-resistant NSCLC cells, suggesting a potential therapeutic approach for DTX resistance.		Cytotechnology. 2021 Aug;73(4):571-584. doi: 10.1007/s10616-021-00478-z. Epub 2021 May 25.
5038	Circular RNA	circ_CDK14	miR-520a-3p	GAB1	Osteosarcoma Tissues And Cells	Osteosarcoma	Homo sapiens (human)  	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34348465	Depletion of circRNA circ_CDK14 inhibits osteosarcoma progression by regulating the miR-520a-3p/GAB1 axis.	Osteosarcoma (OS) is a lethal bone malignancy. Circular RNAs (circRNAs) have emerged as important regulators of OS development. CircRNA cyclin dependent kinase 14 (circ_CDK14) was reported to be a potential oncogene in OS. However, the mechanistic pathway by which circ_CDK14 functions in OS is largely unknown. The relative expression of circ_CDK14, microRNA (miR)-520a-3p, and GRB2 Associated Binding Protein 1 (GAB1) was evaluated by quantitative real-time PCR and western blot assays. Flow cytometry was employed to monitor cell cycle distribution and apoptosis. Methyl thiazolyl tetrazolium (MTT) and colony formation assays were performed to assess cell viability and colony formation ability, respectively. Western blot assay was also used to detect the expression of apoptosis-related proteins. Transwell assay was carried out to monitor cell migration and invasion. Additionally, the target association between miR-520a-3p and circ_CDK14 or GAB1 was confirmed by a dual-luciferase reporter assay. Xenograft assay was applied to investigate the role of circ_CDK14 in vivo. Circ_CDK14 and GAB1 expression was upregulated, while miR-520a-3p was downregulated in OS tissues and cells. Circ_CDK14 depletion hindered OS cell proliferation, metastasis, and tumorigenesis while facilitated apoptosis, which were all ameliorated by miR-520a-3p inhibition. Circ_CDK14 could sponge miR-520a-3p. miR-520a-3p targeted GAB1 to repress OS cell proliferation and metastasis. Circ_CDK14 knockdown blocked OS tumor growth in vivo. Circ_CDK14 might positively affect OS development by modulating the miR-520a-3p/GAB1 axis.		Neoplasma. 2021 Jul;68(4):798-809. doi: 10.4149/neo_2021_201206N1319. Epub 2021 Jun 17.
5039	Circular RNA	circ_0001883	miR-125-5p	NA	Laryngeal Squamous Cell Carcinoma Tissues And Cells	Laryngeal Squamous Cell Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34345289	Knockdown of circ_0001883 may inhibit epithelial-mesenchymal transition in laryngeal squamous cell carcinoma via the miR-125-5p/PI3K/AKT axis.	Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor with increasing incidence and poor prognosis. Circular RNAs (circRNAs) are known to modulate tumorigenesis and cancer development that may function through microRNAs (miRs). The aim of the present study was to investigate the functional roles of circ_0001883 in LSCC and the underlying molecular mechanism. The expression of circ_0001883 was upregulated and measured using reverse transcription-quantitative PCR (RT-qPCR) and RNase R. miR-125b-5p expression was downregulated in LSCC tissues and cells as determined using RT-qPCR. Subsequently, knockdown of circ_0001883 inhibited LSCC cell migration, invasion and epithelial-mesenchymal transition (EMT), which were tested by wound healing assays, Transwell assays and western blotting, respectively. Bioinformatics analysis predicted that circ_0001883 was a sponge of miR-125b-5p, which was verified using a dual-luciferase reporter assay. Knockdown of circ_0001883 played a functional role by sponging miR-125b-5p. Additionally, circ_0001883 and miR-125b-5p influenced phosphorylation of PI3K and AKT, detected via western blotting. In an in vivo study, knockdown of circ_0001883 reduced tumor volume and weight in mice, along with enhanced miR-125b-5p and E-cadherin expression levels, and decreased N-cadherin, phosphorylated (p)-PI3K/PI3K and p-AKT/AKT ratios. In conclusion, knockdown of circ_0001883 inhibited cell migration, invasion and EMT of LSCC by sponging miR-125b-5p. This is hypothesized to be via the PI3K/AKT signaling pathway, which suggested that circ_0001883 has potential for LSCC therapy.		Exp Ther Med. 2021 Sep;22(3):1007. doi: 10.3892/etm.2021.10440. Epub 2021 Jul 15.
5040	Circular RNA	circ_SEC24A	miR-26b-5p	DNMT3A	Osteoarthritic Cartilage Tissues	Osteoarthritis	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RACE;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34325283	CircRNA circ_SEC24A upregulates DNMT3A expression by sponging miR-26b-5p to aggravate osteoarthritis progression.	BACKGROUND: Osteoarthritis (OA) is a chronic degenerative disease characterized by degeneration and injury of articular cartilage. Circular RNA_SEC24A (circ_SEC24A; circBase ID: hsa_circ_0005105) is upregulated and promotes multiple tumor processes. However, its role in OA progression remained mostly unknown. METHODS: Quantitative real-time PCR (qRT-PCR) was used to detect the RNA expression of circ_SEC24A, miR-26b-5p and DNA methyltransferase 3 alpha (DNMT3A). Cell proliferation was verified by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) and 5-ethynyl-2'-deoxyuridine (EdU) assays. Flow cytometry was used to detect apoptosis. Western blot was used to detect protein expression of DNMT3A, proliferating cell nuclear antigen (PCNA), extracellular matrix (ECM) proteins (Collagen II and Aggrecan), and ECM degrading enzymes (matrix metalloproteinase-13 [MMP13] and metallopeptidase with thrombospondin type 1 motif 5 [ADAMTS5]). The target relationship between miR-26b-5p and circ_SEC24A or DNMT3A was predicted by Statbase3.0 or TargetScan and confirmed by dual-luciferase reporter assay, RNA pull-down assay and RNA immunoprecipitation. RESULTS: Circ_SEC24A was upregulated in osteoarthritic cartilage tissues and IL-1b-induced chondrocytes, accompanying with miR-26b-5p downregulation and DNMT3A upregulation. Circ_SEC24A expression was resistant to RNase R digestion and mainly expressed in the cytoplasm. Interfering circ_SEC24A abolished IL-1b-induced effects on proliferation inhibition, apoptosis, and ECM degradation in chondrocytes, but overexpressing circ_SEC24A had the opposite effects. Inhibiting miR-26b-5p counteracted but upregulating miR-26a-5p mimicked the functions of circ_SEC24A silencing. Reinforcing DNMT3A reversed miR-26b-5p overexpression's role in IL-1b-induced chondrocytes. Mechanically, circ_SEC24A and DNMT3A were competitive endogenous RNAs (ceRNAs) for miR-26b-5p. CONCLUSION: Circ_SEC24A was a promoting factor for IL-1b-induced OA progression via circ_SEC24A/miR-26b-5p/DNMT3A ceRNA axis.		Int Immunopharmacol. 2021 Jul 26;99:107957. doi: 10.1016/j.intimp.2021.107957.
5041	Circular RNA	circZFR	miR-16	MAPK1	Thyroid Cancer Cells	Thyroid Cancer	Homo sapiens (human)	qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34323000	circZFR regulates thyroid cancer progression by the miR-16/MAPK1 axis.	Previous studies have identified the dysregulation of various circRNAs in many types of human cancers including thyroid cancer (TC). Circular RNA ZFR (circZFR) serves as an oncogenic circRNA in TC. However, the detailed molecular mechanism of circZFR in TC progression remains to be further explored. CircZFR and miR-16 expressions in TC cells were analyzed through qRT-PCR. Cell viability, invasion, and apoptosis were detected using CCK-8, transwell invasion assay, and flow cytometry analysis, respectively. The relationship between circZFR and miR-16 was explored using luciferase reporter assay, RNA pull-down assay, and qRT-PCR. The relationship between miR-16 and mitogen-activated protein kinase 1 (MAPK1) was explored using luciferase reporter assay and western blot analysis. Results showed that circZFR was upregulated and miR-16 was downregulated in TC cells. CircZFR knockdown inhibited the viability and invasion and induced apoptosis in TC cells. CircZFR inhibited miR-16 expression by sponging miR-16 and miR-16 repressed MAPK1 expression by targeting MAPK1. Moreover, circZFR positively regulated MAPK1 expression in TC cells by serving as a ceRNA of miR-16. Mechanistically, circZFR knockdown-induced inhibition of cell viability and invasion and promotion of apoptosis were overturned after miR-16 downregulation and promotion of MAPK1. Collectively, circZFR knockdown retarded TC progression by sponging miR-16 and modulating MAPK1 expression.		Environ Toxicol. 2021 Jul 28. doi: 10.1002/tox.23337.
5042	Circular RNA	circ_0002062	miR-942-5p	CDK6	Pulmonary Artery Smooth Muscle Cells	Hypoxia-Induced Pulmonary Hypertension	Homo sapiens (human)  	RIP assay;luciferase assay;RNA pull-down;	34322152	Hsa_circ_0002062 Promotes the Proliferation of Pulmonary Artery Smooth Muscle Cells by Regulating the Hsa-miR-942-5p/CDK6 Signaling Pathway.	Currently, new strategies for the diagnosis and treatment of hypoxia-induced pulmonary hypertension (HPH) are urgently required. The unique features of circRNAs have unveiled a novel perspective for understanding the biological mechanisms underlying HPH and the possibility for innovative strategies for treatment of HPH. CircRNAs function as competing endogenous RNAs (CeRNA) to sequester miRNAs and regulate the expression of target genes. This study aimed to explore the roles of hsa_circ_0002062 on the biological behaviors of pulmonary artery smooth muscle cells (PASMCs) in hypoxic conditions. A number of in vitro assays, such as RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and dual-luciferase assays were performed to evaluate the interrelationship between hsa_circ_0002062, hsa-miR-942-5P, and CDK6. The potential physiological functions of hsa_circ_0002062, hsa-miR-942-5P, and CDK6 in hypoxic PASMCs were investigated through expression modulation. Our experiments demonstrated that hsa_circ_0002062 functions as a ceRNA, acts as a sponge for hsa-miR-942-5P, and consequently activates CDK6, which further promotes pulmonary vascular remodeling. Therefore, we speculate that hsa_circ_0002062 could serve as a candidate diagnostic biomarker and potential therapeutic target for HPH.		Front Genet. 2021 Jul 12;12:673229. doi: 10.3389/fgene.2021.673229. eCollection 2021.
5043	Circular RNA	circ_0051488	mir-6717-5p	SATB2	Lung Cancer Cell	Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34320692	Benzo[a]pyrene diol epoxide-induced transformed cells identify the significance of hsa_circ_0051488, a ERCC1-derived circular RNA in pulmonary squamous cell carcinoma.	ERCC1 is a gene for repairing DNA damage whose function is related to carcinogenic-induced tumorigenesis and the effectiveness of platinum therapies. Circular RNAs (circRNAs) are products of posttranscriptional regulation with pleiotropic effects on the pathogenesis of lung cancer. We aim to identify that specific circRNAs derived from ERCC1 can regulate key biological processes involved in the development of lung cancer. We performed bioinformatics analysis, in vitro experiments, and analyzed clinical samples, to determine the biological features of a certain ERCC1-derived circRNA termed as hsa_circ_0051488 in benzo[a]pyrene diol epoxide-induced malignant transformed cell and lung cancer cell. The well-established model of transformed cells provided an ideal platform for analyzing the molecular characteristics of this circRNA in the malignant transformation of lung epithelial cell, which supports that hsa_circ_0051488 functions in the onset and growth of lung squamous cell carcinoma (LUSC). Further analysis indicates that the absence of hsa_circ_0051488 promoted the proliferation of cells with the malignant phenotype. Extensive experiments confirm that hsa_circ_0051488 is present in the cytoplasm and functioned as a competing endogenous RNA. In particular, hsa_circ_0051488 binds to mir-6717-5p, thereby modulating the expression of SATB2 gene, a lung cancer suppressor. Furthermore, our in silico experiments indicate that SATB2 can inhibit multiple tumor pathways and its expression positively correlated with the tumor suppressor gene CRMP1. These findings suggest a possible regulatory mechanism of hsa_circ_0051488 in LUSC, and that the newly discovered hsa_circ_0051488/miR-6717-5p/SATB2 axis may be a potential route for therapeutic intervention of LUSC.		Mol Carcinog. 2021 Jul 28. doi: 10.1002/mc.23335.
5044	Circular RNA	circEGFR	miR-106a-5p	DDX5	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34320120	Circular RNA circEGFR regulates tumor progression via the miR-106a-5p/DDX5 axis in colorectal cancer.	Recently, an increasing number of studies have reported that dysregulation of circular RNA (circRNA) expression plays critical roles in the progression of several cancers, including colorectal cancer (CRC). However, the detailed molecular mechanisms of circRNAs involvement in CRC remain largely unknown. Here, we confirmed that the level of circEGFR was significantly increased in CRC tissues compared to matched adjacent non-tumor tissues, and a high level of circEGFR was correlated with poor clinicopathological characteristics and poor prognosis in patients with CRC. Moreover, increased circEGFR expression promoted CRC cell proliferation, migration, and invasion in vitro. Mechanistically, circEGFR acted as a ceRNA for miR-106a-5p to relieve the repressive effect of miR-106a-5p on DDX5 mRNA. Moreover, circEGFR enhanced DDX5 expression, thereby upregulating p-AKT levels. Together, these findings showed that circEGFR promoted CRC cell proliferation, migration, and invasion through the miR-106a-5p/DDX5/AKT axis, and may serve as a promising diagnostic marker and therapeutic target for CRC patients.		Braz J Med Biol Res. 2021 Jul 23;54(8):e10940. doi: 10.1590/1414-431X2020e10940. eCollection 2021.
5045	Circular RNA	UBAP2	miR-1294	c-Myc	Hcc And Healthy Tissue	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;luciferase assay;RNA pull-down;	34314478	CircRNA UBAP2 serves as a sponge of miR-1294 to increase tumorigenesis in hepatocellular carcinoma through regulating c-Myc expression.	Circular RNAs (circRNAs) are a class of regulatory RNAs with complex roles in healthy and diseased tissues. However, the oncogenic role of circRNAs in hepatocellular carcinoma (HCC) remains poorly understood, including the mechanisms by which the circular ubiquitin binding associated protein 2 (circUBAP2) contributes to tumorigenesis. We analyzed the expression of circUBAP2 in 20 paired samples of HCC and healthy tissue as well as in seven HCC cell lines via quantitative real-time polymerase chain reaction (qRT-PCR). Functional experiments, such as CCK8 viability assays, colony formation assays, wound healing, transwell assays, and flow cytometry, were conducted to assess the effects of circUBAP2 in vitro. To further elucidate the mechanisms by which circUBAP2 acts, we conducted dual-luciferase assays, western blots, RNA pull-down assays, and rescue experiments. CircUBAP2 was highly upregulated in most HCC tissues and was associated with poor prognosis. HCC patients with high circUBAP2 expression had greater vascular invasion and worse differentiation. Functionally, circUBAP2 overexpression enhanced HCC cell proliferation, migration, and invasion and inhibited apoptosis. Furthermore, we found that circUBAP2 upregulated c-Myc expression by sponging miR-1294, thus contributing to hepatocarcinogenesis. Inhibiting circUBAP2 expression in HCC attenuated the oncogenic effects of c-Myc. These findings suggest that circUBAP2 promotes HCC growth and metastasis. CircUBAP2 may have value as an independent prognostic biomarker or as a new target for the treatment of HCC.		Carcinogenesis. 2021 Jul 27:bgab068. doi: 10.1093/carcin/bgab068.
5046	Circular RNA	circSP3	miR-198	CDK4	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	Luciferase reporter assay;	34314379	Circular RNA circSP3 promotes hepatocellular carcinoma growth by sponging microRNA-198 and upregulating cyclin-dependent kinase 4.	As a new class of endogenous noncoding RNAs, circular RNAs (circRNAs), have been found to influence cell development and function by sponging microRNAs. MicroRNA (miR)-198 is downregulated in various cancers, including hepatocellular carcinoma (HCC). We therefore searched for dysregulated circRNAs that could sponge miR-198 in HCC. By analyzing relevant circRNA databases (circBase, TargetScan and CircInteractome), we found that the miR-198-binding circRNA hsa_circSP3 is upregulated in HCC. CircSP3 expression correlated negatively with miR-198 expression in HCC tissues. Dual luciferase reporter assays indicated that circSP3 bound to miR-198. CircSP3 overexpression in HCC cells induced expression of cyclin-dependent kinase 4, a target gene of miR-198. Silencing circSP3 inhibited HCC cell proliferation and migration by downregulating cyclin-dependent kinase 4, whereas inhibiting miR-198 reversed those effects. In vivo experiments confirmed that circSP3 promoted xenograft tumor growth. These data suggest that circSP3 may be a novel biomarker for HCC.		Aging (Albany NY). 2021 Jul 27;13(14):18586-18605. doi: 10.18632/aging.203303. Epub 2021 Jul 27.
5047	Circular RNA	circ_WHSC1	miR-296-3p	AKT3	Non-Small Cell Lung Cancer Tissues And Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR;RNA pull-down;	34313353	CircRNA WHSC1 promotes non-small cell lung cancer progression via sponging microRNA-296-3p and up-regulating expression of AKT serine/threonine kinase 3.	BACKGROUND: Lung cancer is the most commonly diagnosed cancer and leading cause of cancer death, with 80%-85% of non-small cell lung cancer (NSCLC). Circular RNAs (circRNAs) have been shown to be promising early diagnostic and therapeutic molecular biomarkers for NSCLC. However, biological role and regulatory mechanism of circRNA WHSC1 (circWHSC1) in NSCLC are unknown. Therefore, we aim to explore the function and mechanism of circWHSC1 in NSCLC oncogenesis and progression. METHODS: qRT-PCR was used for circWHSC1 level evaluation; Kaplan-Meier was used for survival analysis; bioinformatics, dual-luciferase activity, and RNA pull-down were used for evaluating competing endogenous RNA (ceRNA) network; cell viability, colony formation, apoptosis, migration, and invasion were used for cell function analysis; function gain and loss with rescue experiments were used for exploring mechanism of circWHSC1 in NSCLC development. RESULTS: Significantly up-regulated circWHSC1 and down-regulated microRNA-296-3p (miR-296-3p) were identified in NSCLC tissues and cells. Up-regulated circWHSC1 was associated with poor prognosis in NSCLC patients. MiR-296-3p was sponged by circWHSC1, and AKT serine/threonine kinase 3 (AKT3) was target of miR-296-3p; meanwhile, miR-296-3p over-expression significantly down-regulated AKT3 expression, and co-transfecting anti-miR-296-3p rescued circWHSC1 silence caused AKT3 down-regulation. CircWHSC1 silence significantly inhibited colony formation, viability, invasion, and migration, while increased NSCLC cell apoptosis, which were partially rescued by anti-miR-296-3p. CONCLUSION: CircWHSC1 is an independent indicator of poor prognosis in NSCLC patients, and functions as a ceRNA of miR-296-3p to up-regulate AKT3, consequently promotes NSCLC cell growth and metastasis. Targeting circWHSC1 might be a prospective strategy for diagnosis, therapeutics, and prognosis of NSCLC.		J Clin Lab Anal. 2021 Aug;35(8):e23865. doi: 10.1002/jcla.23865. Epub 2021 Jul 27.
5048	Circular RNA	circ_0089823	miR-507	SOX4	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34311177	Circ_0089823 reinforces malignant behaviors of non-small cell lung cancer by acting as a sponge for microRNAs targeting SOX4().	In recent years, increasing evidence indicates the significant roles of circRNAs in carcinogenesis. However, their roles in lung cancer remain largely unclear. We profiled the circRNA expression in 10 paired non-small cell lung cancer (NSCLC) and adjacent non-cancer tissues using high-throughput sequencing. A total of 183 up-regulated and 428 down-regulated circRNAs were identified in the NSCLC tissues (fold change ≥ 2, P < 0.05). Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history. Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3'-untranslated region, which was later confirmed by luciferase reporter assay. Interestingly, silencing SOX4 countervailed the effects of circ_0089823 over-expression on NSCLC cells. Here, we revealed that circ_0089823 might act as a sponge of microRNAs targeting SOX4, thus increasing the expression of SOX4, thereby reinforcing the malignant behaviors of NSCLC cells. This study indicates that circ_0089823 has the potential to become a candidate target for NSCLC treatment.		Neoplasia. 2021 Jul 23;23(9):887-897. doi: 10.1016/j.neo.2021.06.011.
5049	Circular RNA	circ_0089823	miR-557	SOX4	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34311177	Circ_0089823 reinforces malignant behaviors of non-small cell lung cancer by acting as a sponge for microRNAs targeting SOX4().	In recent years, increasing evidence indicates the significant roles of circRNAs in carcinogenesis. However, their roles in lung cancer remain largely unclear. We profiled the circRNA expression in 10 paired non-small cell lung cancer (NSCLC) and adjacent non-cancer tissues using high-throughput sequencing. A total of 183 up-regulated and 428 down-regulated circRNAs were identified in the NSCLC tissues (fold change ≥ 2, P < 0.05). Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history. Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3'-untranslated region, which was later confirmed by luciferase reporter assay. Interestingly, silencing SOX4 countervailed the effects of circ_0089823 over-expression on NSCLC cells. Here, we revealed that circ_0089823 might act as a sponge of microRNAs targeting SOX4, thus increasing the expression of SOX4, thereby reinforcing the malignant behaviors of NSCLC cells. This study indicates that circ_0089823 has the potential to become a candidate target for NSCLC treatment.		Neoplasia. 2021 Jul 23;23(9):887-897. doi: 10.1016/j.neo.2021.06.011.
5050	Circular RNA	circ_0089823	miR-579-3p	SOX4	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34311177	Circ_0089823 reinforces malignant behaviors of non-small cell lung cancer by acting as a sponge for microRNAs targeting SOX4().	In recent years, increasing evidence indicates the significant roles of circRNAs in carcinogenesis. However, their roles in lung cancer remain largely unclear. We profiled the circRNA expression in 10 paired non-small cell lung cancer (NSCLC) and adjacent non-cancer tissues using high-throughput sequencing. A total of 183 up-regulated and 428 down-regulated circRNAs were identified in the NSCLC tissues (fold change ≥ 2, P < 0.05). Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history. Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3'-untranslated region, which was later confirmed by luciferase reporter assay. Interestingly, silencing SOX4 countervailed the effects of circ_0089823 over-expression on NSCLC cells. Here, we revealed that circ_0089823 might act as a sponge of microRNAs targeting SOX4, thus increasing the expression of SOX4, thereby reinforcing the malignant behaviors of NSCLC cells. This study indicates that circ_0089823 has the potential to become a candidate target for NSCLC treatment.		Neoplasia. 2021 Jul 23;23(9):887-897. doi: 10.1016/j.neo.2021.06.011.
5051	Circular RNA	circ_0089823	miR-1287-5p	SOX4	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34311177	Circ_0089823 reinforces malignant behaviors of non-small cell lung cancer by acting as a sponge for microRNAs targeting SOX4().	In recent years, increasing evidence indicates the significant roles of circRNAs in carcinogenesis. However, their roles in lung cancer remain largely unclear. We profiled the circRNA expression in 10 paired non-small cell lung cancer (NSCLC) and adjacent non-cancer tissues using high-throughput sequencing. A total of 183 up-regulated and 428 down-regulated circRNAs were identified in the NSCLC tissues (fold change ≥ 2, P < 0.05). Circ_0089823, an up-regulated circRNA (5.4-fold, P = 0.0017), was further investigated through loss-of-function and gain-of-function. The circ_0089823 level in NSCLC samples was related to the gender, tumor size, pathological type, TNM stage and smoking history. Knockdown of circ_0089823 suppressed cell proliferation, induced cell cycle arrest and apoptosis of NSCLC cells in vitro. Additionally, circ_0089823-silenced xenografts grew much slowly. On the contrary, its over-expression promoted the malignant behaviors of NSCLC cells. Furthermore, SOX4, a tumor-promoting transcription factor, was highly expressed in NSCLC tissues and positively regulated by circ_0089823. Bioinformatic analysis revealed several potential binding sites for miR-507, miR-557, miR-579-3p and miR-1287-5p in circ_0089823 and SOX4 3'-untranslated region, which was later confirmed by luciferase reporter assay. Interestingly, silencing SOX4 countervailed the effects of circ_0089823 over-expression on NSCLC cells. Here, we revealed that circ_0089823 might act as a sponge of microRNAs targeting SOX4, thus increasing the expression of SOX4, thereby reinforcing the malignant behaviors of NSCLC cells. This study indicates that circ_0089823 has the potential to become a candidate target for NSCLC treatment.		Neoplasia. 2021 Jul 23;23(9):887-897. doi: 10.1016/j.neo.2021.06.011.
5052	Circular RNA	circPTK2	miR-182-5p	JAZF1	Adipose Tissues	Cachexia	Homo sapiens (human)  	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA sequencing;	34311131	Novel noncoding RNA CircPTK2 regulates lipolysis and adipogenesis in cachexia.	OBJECTIVE: Cancer-associated cachexia is a devastating pathological disorder characterized by skeletal muscle wasting and fat storage depletion. Circular RNA, a newly discovered class of noncoding RNAs with important roles in regulating lipid metabolism, has not been fully understood in the pathology of cachexia. We aimed to identify circular RNAs that are upregulated in adipose tissues from cachectic patients and explore their function and mechanism in lipid metabolism. METHODS: Whole transcriptome RNA sequencing was used to screen for differentially expressed circRNAs. Quantitative reverse transcription PCR was applied to detect the expression level of circPTK2 in adipose tissues. The diagnostic value of circPTK2 was evaluated in adipose tissues from patients with and without cachexia. Then, function experiments in vitro and in vivo were performed to evaluate the effects of circPTK2 on lipolysis and adipogenesis. Mechanistically, luciferase reporter assay, RNA immunoprecipitation, and fluorescent in situ hybridization were performed to confirm the interaction between circPTK2 and miR-182-5p in adipocytes. RESULTS: We detected 66 differentially expressed circular RNA candidates and proved that circPTK2 was upregulated in adipose tissues from cachectic patients. Then we identified that circPTK2 was closely related to the pathological process of cachexia and could be used as a diagnostic marker. Mechanistically, circPTK2 bound competitively to miR-182-5p and abrogated the suppression on its target gene JAZF1, which finally led to promotion of lipolysis and inhibition of adipogenesis. In vivo experiments demonstrated that overexpression of circPTK2 inhibited adipogenesis and enhanced lipolysis. CONCLUSIONS: Our findings reveal the novel role of circPTK2 in promoting lipolysis and reducing adipogenesis via a ceRNA mechanism and provide a potential diagnostic biomarker and therapeutic target for cancer-associated cachexia.		Mol Metab. 2021 Jul 23;53:101310. doi: 10.1016/j.molmet.2021.101310.
5053	Circular RNA	circ_ABCA1	miR-30d-3p	TP53RK	Mouse Aortic Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;RT-PCR;Western blot;Immunohistochemistry;	34307490	Differentially Expressed Circular Non-coding RNAs in Atherosclerotic Aortic Vessels and Their Potential Functions in Endothelial Injury.	Background: Circular non-coding RNA (circRNA) has a variety of biological functions. However, the expression profile and potential effects of circRNA on atherosclerosis (AS) and vascular endothelial injury have not been fully elucidated. This study aims to identify the differentially expressed circRNAs in atherosclerotic aortic vessels and predict their potential functions in endothelial injury. Method: ApoE-/- mice were fed with high-fat diet for 12 weeks to induce AS. Atherosclerotic plaques were evaluated by H&E and Masson staining and immunohistochemistry; differentially expressed circRNAs were detected by Arraystar Circular RNA Microarray and verified by RT-PCR; the potential target mircoRNAs of circRNAs were predicted by miRanda, Tarbase, Targetscan and their expression changes were verified by RT-PCR; the potential target genes of mircoRNAs were predicted by Targetscan and verified by Western blot; the signaling pathways that they might annotate or regulate and their potential functions in vascular endothelial injury were predicted by gene enrichment analysis. Results: Fifty two circRNAs were up-regulated more than twice and 47 circRNAs were down-regulated more than 1.5 times in AS aortic vessels. Mmmu_circRNA_36781 and 37699 were up-regulated both in AS aortic vessels and H(2)O(2)-treated mouse aortic endothelial cells (MAECs). The expression of miR-30d-3p and miR-140-3p, the target microRNA of circRNA_37699 and circRNA_36781, were downregulated both in AS vessels and H(2)O(2)-treated MAECs. On the contrary, MKK6 and TP53RK, the potential target gene of miR-140-3p and miR-30d-3p, were upregulated both in AS aortic roots and H(2)O(2)-treated MAECs. Besides, gene enrichment analysis showed that MAPK and PI3K-AKT signaling pathway were the most potential signaling pathways regulated by the differentially expressed circRNAs in atherosclerosis. Conclusions: Mmu_circRNA_36781 (circRNA ABCA1) and 37699 (circRNA KHDRBS1) were significantly up-regulated in AS aortic vessels and H(2)O(2)-treated MAECs. They have potential regulatory effects on atherosclerosis and vascular endothelial injury by targeting miR-30d-3p-TP53RK and miR-140-3p-MKK6 axis and their downstream signaling pathways.		Front Cardiovasc Med. 2021 Jul 7;8:657544. doi: 10.3389/fcvm.2021.657544. eCollection 2021.
5054	Circular RNA	circ_ABCA1	miR-140-3p	MKK6	Mouse Aortic Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;RT-PCR;Western blot;Immunohistochemistry;	34307490	Differentially Expressed Circular Non-coding RNAs in Atherosclerotic Aortic Vessels and Their Potential Functions in Endothelial Injury.	Background: Circular non-coding RNA (circRNA) has a variety of biological functions. However, the expression profile and potential effects of circRNA on atherosclerosis (AS) and vascular endothelial injury have not been fully elucidated. This study aims to identify the differentially expressed circRNAs in atherosclerotic aortic vessels and predict their potential functions in endothelial injury. Method: ApoE-/- mice were fed with high-fat diet for 12 weeks to induce AS. Atherosclerotic plaques were evaluated by H&E and Masson staining and immunohistochemistry; differentially expressed circRNAs were detected by Arraystar Circular RNA Microarray and verified by RT-PCR; the potential target mircoRNAs of circRNAs were predicted by miRanda, Tarbase, Targetscan and their expression changes were verified by RT-PCR; the potential target genes of mircoRNAs were predicted by Targetscan and verified by Western blot; the signaling pathways that they might annotate or regulate and their potential functions in vascular endothelial injury were predicted by gene enrichment analysis. Results: Fifty two circRNAs were up-regulated more than twice and 47 circRNAs were down-regulated more than 1.5 times in AS aortic vessels. Mmmu_circRNA_36781 and 37699 were up-regulated both in AS aortic vessels and H(2)O(2)-treated mouse aortic endothelial cells (MAECs). The expression of miR-30d-3p and miR-140-3p, the target microRNA of circRNA_37699 and circRNA_36781, were downregulated both in AS vessels and H(2)O(2)-treated MAECs. On the contrary, MKK6 and TP53RK, the potential target gene of miR-140-3p and miR-30d-3p, were upregulated both in AS aortic roots and H(2)O(2)-treated MAECs. Besides, gene enrichment analysis showed that MAPK and PI3K-AKT signaling pathway were the most potential signaling pathways regulated by the differentially expressed circRNAs in atherosclerosis. Conclusions: Mmu_circRNA_36781 (circRNA ABCA1) and 37699 (circRNA KHDRBS1) were significantly up-regulated in AS aortic vessels and H(2)O(2)-treated MAECs. They have potential regulatory effects on atherosclerosis and vascular endothelial injury by targeting miR-30d-3p-TP53RK and miR-140-3p-MKK6 axis and their downstream signaling pathways.		Front Cardiovasc Med. 2021 Jul 7;8:657544. doi: 10.3389/fcvm.2021.657544. eCollection 2021.
5055	Circular RNA	circ_KHDRBS1	miR-30d-3p	TP53RK	Mouse Aortic Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;RT-PCR;Western blot;Immunohistochemistry;	34307490	Differentially Expressed Circular Non-coding RNAs in Atherosclerotic Aortic Vessels and Their Potential Functions in Endothelial Injury.	Background: Circular non-coding RNA (circRNA) has a variety of biological functions. However, the expression profile and potential effects of circRNA on atherosclerosis (AS) and vascular endothelial injury have not been fully elucidated. This study aims to identify the differentially expressed circRNAs in atherosclerotic aortic vessels and predict their potential functions in endothelial injury. Method: ApoE-/- mice were fed with high-fat diet for 12 weeks to induce AS. Atherosclerotic plaques were evaluated by H&E and Masson staining and immunohistochemistry; differentially expressed circRNAs were detected by Arraystar Circular RNA Microarray and verified by RT-PCR; the potential target mircoRNAs of circRNAs were predicted by miRanda, Tarbase, Targetscan and their expression changes were verified by RT-PCR; the potential target genes of mircoRNAs were predicted by Targetscan and verified by Western blot; the signaling pathways that they might annotate or regulate and their potential functions in vascular endothelial injury were predicted by gene enrichment analysis. Results: Fifty two circRNAs were up-regulated more than twice and 47 circRNAs were down-regulated more than 1.5 times in AS aortic vessels. Mmmu_circRNA_36781 and 37699 were up-regulated both in AS aortic vessels and H(2)O(2)-treated mouse aortic endothelial cells (MAECs). The expression of miR-30d-3p and miR-140-3p, the target microRNA of circRNA_37699 and circRNA_36781, were downregulated both in AS vessels and H(2)O(2)-treated MAECs. On the contrary, MKK6 and TP53RK, the potential target gene of miR-140-3p and miR-30d-3p, were upregulated both in AS aortic roots and H(2)O(2)-treated MAECs. Besides, gene enrichment analysis showed that MAPK and PI3K-AKT signaling pathway were the most potential signaling pathways regulated by the differentially expressed circRNAs in atherosclerosis. Conclusions: Mmu_circRNA_36781 (circRNA ABCA1) and 37699 (circRNA KHDRBS1) were significantly up-regulated in AS aortic vessels and H(2)O(2)-treated MAECs. They have potential regulatory effects on atherosclerosis and vascular endothelial injury by targeting miR-30d-3p-TP53RK and miR-140-3p-MKK6 axis and their downstream signaling pathways.		Front Cardiovasc Med. 2021 Jul 7;8:657544. doi: 10.3389/fcvm.2021.657544. eCollection 2021.
5056	Circular RNA	circ_KHDRBS1	miR-140-3p	MKK6	Mouse Aortic Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;RT-PCR;Western blot;Immunohistochemistry;	34307490	Differentially Expressed Circular Non-coding RNAs in Atherosclerotic Aortic Vessels and Their Potential Functions in Endothelial Injury.	Background: Circular non-coding RNA (circRNA) has a variety of biological functions. However, the expression profile and potential effects of circRNA on atherosclerosis (AS) and vascular endothelial injury have not been fully elucidated. This study aims to identify the differentially expressed circRNAs in atherosclerotic aortic vessels and predict their potential functions in endothelial injury. Method: ApoE-/- mice were fed with high-fat diet for 12 weeks to induce AS. Atherosclerotic plaques were evaluated by H&E and Masson staining and immunohistochemistry; differentially expressed circRNAs were detected by Arraystar Circular RNA Microarray and verified by RT-PCR; the potential target mircoRNAs of circRNAs were predicted by miRanda, Tarbase, Targetscan and their expression changes were verified by RT-PCR; the potential target genes of mircoRNAs were predicted by Targetscan and verified by Western blot; the signaling pathways that they might annotate or regulate and their potential functions in vascular endothelial injury were predicted by gene enrichment analysis. Results: Fifty two circRNAs were up-regulated more than twice and 47 circRNAs were down-regulated more than 1.5 times in AS aortic vessels. Mmmu_circRNA_36781 and 37699 were up-regulated both in AS aortic vessels and H(2)O(2)-treated mouse aortic endothelial cells (MAECs). The expression of miR-30d-3p and miR-140-3p, the target microRNA of circRNA_37699 and circRNA_36781, were downregulated both in AS vessels and H(2)O(2)-treated MAECs. On the contrary, MKK6 and TP53RK, the potential target gene of miR-140-3p and miR-30d-3p, were upregulated both in AS aortic roots and H(2)O(2)-treated MAECs. Besides, gene enrichment analysis showed that MAPK and PI3K-AKT signaling pathway were the most potential signaling pathways regulated by the differentially expressed circRNAs in atherosclerosis. Conclusions: Mmu_circRNA_36781 (circRNA ABCA1) and 37699 (circRNA KHDRBS1) were significantly up-regulated in AS aortic vessels and H(2)O(2)-treated MAECs. They have potential regulatory effects on atherosclerosis and vascular endothelial injury by targeting miR-30d-3p-TP53RK and miR-140-3p-MKK6 axis and their downstream signaling pathways.		Front Cardiovasc Med. 2021 Jul 7;8:657544. doi: 10.3389/fcvm.2021.657544. eCollection 2021.
5057	Circular RNA	circ_0057452	miR-145-5p	TGF-b2	Hypertrophic Scar Fibroblast	Hypertrophic Scar	Homo sapiens (human)  	Dual-luciferase reporter assay;ELISA;qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	34306359	Circ_0057452 functions as a ceRNA in hypertrophic scar fibroblast proliferation and VEGF expression by regulating TGF-b2 expression and adsorbing miR-145-5p.	OBJECTIVE: To explore the mechanism by which circ_0057452/miR-145-5p/TGF-b2 axis regulates fibroblast proliferation as well as VEGF expression in hypertrophic scars (HS). METHODS: The expression of circ_0057452, miR-145-5p and TGF-b2 in HS tissues and fibroblasts was measured by quantitative real-time Polymerase Chain Reaction (qRT-PCR). The targeting relations between circ_0057452 and miR-145-5p, miR-145-5p and TGF-b2 were identified using dual-luciferase reporter assay. The expression of circ_0057452, miR-145-5p and TGF-b2 in fibroblasts was interfered with and cells were grouped. In each group, changes in cell proliferation were detected using CCK8 assay, apoptosis was measured by flow cytometry, and VEGF secreted in cell culture supernatant was tested by ELISA kit. RESULTS: Compared with normal tissues and fibroblasts, the expressions of circ_0057452 and TGF-b2 were increased and miR-145-5p decreased in HS tissues and cells (all P<0.05). Compared with the si-NC group, cell proliferation and VEGF expressions were decreased and the apoptotic rate increased in the si_circ_0057452 group (all P<0.05). Compared with the oe-NC group, cell proliferation and VEGF expression were increased and the apoptotic rate decreased in the oe-circ_0057452 group (all P<0.05). Compared with the oe-circ_0057452 + miR-NC group, the number of apoptotic cells was increased, and cell proliferation, as well as VEGF expression were decreased in the oe-circ_0057452 + miR-145-5p mimic group (all P<0.05). Compared with the miR-NC group, cell proliferation and VEGF expression were reduced and the apoptotic rate was increased in the miR-145-5p mimic group (all P<0.05). Compared with the miR-145-5p mimic + vector group, cell proliferation and VEGF expression were elevated, and apoptosis was inhibited in the miR-145-5p mimic + TGF-b2 group (all P<0.05). CONCLUSION: circ_0057452 can competitively bind miR-145-5p to induce the expression of TGF-b2, and then promote the proliferation of HS fibroblasts and secretion of VEGF, which is expected to be effective in the treatment of HS.		Am J Transl Res. 2021 Jun 15;13(6):6200-6210. eCollection 2021.
5058	Circular RNA	circNEURL4	miR-1278	LATS1	Ptc Samples	Papillary Thyroid Cancer	Homo sapiens (human)  	microarray;qRT-PCR;	34306334	Circular RNA circNEURL4 inhibits cell proliferation and invasion of papillary thyroid carcinoma by sponging miR-1278 and regulating LATS1 expression.	Circular RNAs (circRNA) are found to be closely associated with cancers as their possibility as "sponges" to miRNAs, thus liberating the downstream target mRNA. However, deep research is still needed to study the function of circRNA in papillary thyroid carcinoma (PTC). Here, we sought to explore new circRNA which could play an important role in the development of PTC. We filtered candidate circRNAs based on microarray data from public database and verified the result using qRT-PCR. We performed CCK8 assay, colony formation assay, apoptosis assay, transwell assays, and xenograft experiments to explore the function of selected circRNA on PTC. We predicted the miRNA targets of the circRNA and the target gene of miRNA through bioinformatic analysis and validated the target by mutant experiments. And by the use of overexpression experiments, knockdown experiments, and the functional assays mentioned above, we figured out the pathway behind the selected circRNA. Based on our data, we found that circNEURL4 was significantly decreased in the PTC samples and lower expression of circNEURL4 was closely associated with a poor prognosis of patients with PTC. Then, we proved that circNEURL4 could inhibit cell proliferation and invasion of PTC in vivo and in vitro. Furthermore, we demonstrated that circNEURL4 may binding to miR-1278 and thus indirectly improving the expression of LATS1. Our findings revealed that circNEURL4 may probably serve as a diagnostic marker to predict PTC patients' prognosis and a possible therapeutic target to PTC via miR-1278/LATS1 axis.		Am J Transl Res. 2021 Jun 15;13(6):5911-5927. eCollection 2021.
5059	Circular RNA	CircRtn4	miR-24-3p	CHD5	Neurite	NA	Mus musculus (mouse)	Dual-luciferase reporter assay;Luciferase reporter assay;	34305525	CircRtn4 Acts as the Sponge of miR-24-3p to Promote Neurite Growth by Regulating CHD5.	Circular RNAs (circRNAs) are covalently closed single-stranded RNA molecules. After derived from precursor mRNA back-splicing, circRNAs play important roles in many biological processes. Recently, it was shown that several circRNAs were enriched in the mammalian brain with unclear functions. The expression of circRtn4 in the mouse brain was increased with the differentiation of primary neurons. In our study, knockdown of circRtn4 inhibited neurite growth, while overexpression of circRtn4 significantly increased neurite length. By dual-luciferase reporter assay and RNA antisense purification assay, circRtn4 was identified as a miRNA sponge for miR-24-3p. Moreover, knockdown of miR-24-3p increased neurite length, while overexpression of miR-24-3p significantly inhibited neurite growth. Furthermore, CHD5 was confirmed to be a downstream target gene of miR-24-3p. And CHD5 silence counteracted the positive effect of circRtn4 overexpression on neurite growth. In conclusion, circRtn4 may act as the sponge for miR-24-3p to promote neurite growth by regulating CHD5.		Front Mol Neurosci. 2021 Jul 7;14:660429. doi: 10.3389/fnmol.2021.660429. eCollection 2021.
5060	Circular RNA	Circ-RBMS1	miR-197-3p	FBXO11	16Hbe Cells	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)	RIP assay;Western blot;Flow Cytometry assay;	34295155	Circ-RBMS1 Knockdown Alleviates CSE-Induced Apoptosis, Inflammation and Oxidative Stress via Up-Regulating FBXO11 Through miR-197-3p in 16HBE Cells.	BACKGROUND: Emerging evidence has reported that circular RNAs (circRNAs) are aberrantly expressed and act as significant regulators in pathological processes of chronic obstructive pulmonary disease (COPD). Here, the purpose of this article was to evaluate and clarify the biological functions and mechanism of circRNA single stranded interacting protein 1 (circ-RBMS1) in cigarette smoke (CS)-induced COPD. METHODS: Human bronchial epithelial cells 16HBE treated with or without cigarette smoke extract (CSE) were used in the experimental group in vitro. Levels of circ-RBMS1, microRNA (miR)-197-3p, and F-box only protein 11 (FBXO11) were detected using quantitative real-time polymerase chain reaction and Western blot. The present study used cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EDU), flow cytometry and Western blot assays to determine the survival of 16HBE cells. The activity of interleukin (IL)-1b, tumor necrosis factor (TNF-a), malondialdehyde (MDA) and superoxide dismutase (SOD) was evaluated using the relative commercial kits. Dual-luciferase activity and RIP assays were used to identify the target relationship between miR-197-3p and circ-RBMS1 or FBXO11. RESULTS: Circ-RBMS1 was highly expressed in COPD patients, and CSE induced an increased expression of circ-RBMS1 in a dose-dependent manner. Functionally, knockdown of circ-RBMS1 attenuated CSE-induced apoptosis, inflammation and oxidative stress in 16HBE cells. Circ-RBMS1 directly targeted miR-197-3p, and miR-197-3p inhibition reversed the effects of circ-RBMS1 knockdown on CSE-induced 16HBE cells. FBXO11 was a target of miR-197-3p. MiR-197-3p overexpression or FBXO11 silencing reduced the apoptosis, inflammation and oxidative stress in CSE-induced 16HBE cells. Moreover, miR-197-3p exerted its effects by targeting FBXO11. Additionally, circ-RBMS1 acted as a sponge for miR-197-3p to positively regulate FBXO11 expression in 16HBE cells. CONCLUSION: Circ-RBMS1 knockdown alleviated CSE-induced apoptosis, inflammation and oxidative stress in 16HBE cells via miR-197-3p/FBXO11 axis, suggesting a new insight into the pathogenesis of CS-induced COPD.		Int J Chron Obstruct Pulmon Dis. 2021 Jul 16;16:2105-2118. doi: 10.2147/COPD.S311222. eCollection 2021.
5061	Circular RNA	CircRIP2	miR-671-5p	FOXM1	Non-Small Cell Lung Cancer Tissues And Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RIP assay;Luciferase reporter assay;	34291441	CircRIP2 promotes NSCLC progression by sponging for miR-671-5p to regulate FOXM1 expression.	Lot of attention had been paid to the role of circular RNAs (circRNAs) in carcinogenesis recently. However, knowledge about circRNAs in NSCLC development is far from satisfactory. In this study, we aimed to provide a novel insight into the circRIP2 in NSCLC development. We used NSCLC tissues, as well as cell lines to elucidate the expression and location of circRIP2 in NSCLC. We also established the circRIP2 overexpression cells A549-circRIP2 and repression cells HCC827-shcircRIP2 for further functional and mechanism studies. The pro-tumorigenic role of circRIP2 was tested by using CCK-8, BrdU and transwell assays. The interaction between circRIP2 and miR-671-5p were validated by luciferase reporter assay, RIP assay, as well as RNA pull down assay. We showed circRIP2 is differentially expressed NSCLC, and acted as a predictor for overall survival (OS) and disease-free survival (DFS). CircRIP2 promoted NSCLC progression by acting as a miRNA sponge for miR-671-5p, thus facilitating its target gene FOXM1 expression. Targeting circRIP2 could be potentially beneficial for NSCLC patients in the future.		Histol Histopathol. 2021 Jul 22:18360. doi: 10.14670/HH-18-360.
5062	Circular RNA	circRNA_0082835	miRNA-429	EZH2	Melanoma Cells	Primary Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	34288815	Circular RNA circRNA_0082835 promotes progression and lymphatic metastasis of primary melanoma by sponging microRNA miRNA-429.	To identify how circular RNA circRNA_0082835 impacts melanoma cells and lymphatic metastasis to observe whether it exerts effects through its action mechanism of sponging microRNA miR-429. Clinical baseline information was collected, and clinical samples were used for detection on circRNA_0082835 and EZH2. The expression of circRNA_0082835, EZH2, and miR-429 was detected by quantitative real-time PCR (RT-qPCR). Cell proliferation was tested with cell counting kit-8 (CCK-8). Flow cytometry was applied to examination of cell cycle levels. Cell invasion and migration were observed by transwell and wound healing. The expression of Wnt/b-catenin pathway, cell cycle and epithelial-mesenchymal transition (EMT) marker proteins was analyzed by western blot. Dual-luciferase determined the binding of miR-429 and circ_0082835. As a result, the expression of circRNA_0082835 was increased and that of miR-429 was decreased with the increase in lymphatic metastasis level. CircRNA_0082835 expression was downregulated by circ_0082835 interference, upregulated by EZH2 interference and also downregulated after transfection of both shRNA-circ_0082835 and shRNA-EZH2. Inhibiting circ_0082835 and EZH2 suppressed the proliferation, invasion and migration, regulated the cell cycle levels, inhibited Wnt/b-catenin and attenuated EMT in melanoma cells. Inhibition of circ_0082835 and/or EZH2 elevated miR-429 expression. The binding among miR-429 and circ_0082835 was verified. MiR-429 inhibitor reversed the effect of circ_0082835 interference while having no significant impact on EZH2. In conclusion, circRNA_0082835 sponges miR-429 to affect the anti-tumor effect of miR-429 in primary melanoma and lymphatic metastasis.		Bioengineered. 2021 Dec;12(1):4159-4173. doi: 10.1080/21655979.2021.1953822.
5063	Circular RNA	circDHTKD1	miR-326	GAB1	Oral Squamous Cell Carcinoma Tissues And Cells	Oral Squamous Cell Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34287578	Oncogenic circDHTKD1 promotes tumor growth and metastasis of oral squamous cell carcinoma in vitro and in vivo via upregulating miR-326-mediated GAB1.	Circular RNAs (circRNAs) have been extensively elucidated with regard to their significant implications in oral squamous cell carcinoma (OSCC). This study performed the functional investigation of circRNA dehydrogenase E1 and transketolase domain containing 1 (circDHTKD1) in OSCC. RNA expression levels of different molecules were measured via quantitative real-time polymerase chain reaction (qRT-PCR). Cellular behaviors were detected by 3-(4, 5-dimethylthiazol-2-y1)-2,5-diphenyl tetrazolium bromide (MTT) for cell viability, colony formation assay for clonal capacity, flow cytometry for cell apoptosis, wound healing assay for migration, and transwell assay for migration/invasion. Western blot was used for analyzing protein expression. RNA pull-down and dual-luciferase reporter assays were applied to assess the binding between targets. A xenograft tumor model was established in nude mice for in vivo experiments. Our expression analysis revealed that circDHTKD1 was upregulated in OSCC tissues and cells. circDHTKD1 knockdown was shown to impede OSCC cell growth and metastasis but motivate apoptosis. Additionally, circDHTKD1 served as a microRNA-326 (miR-326) sponge and the function of circDHTKD1 was achieved by sponging miR-326 in OSCC cells. Also, miR-326 inhibited OSCC development via targeting GRB2-associated-binding protein 1 (GAB1). circDHTKD1 could sponge miR-326 to alter GAB1 expression. Furthermore, circDHTKD1 contributed to OSCC progression in vivo via the miR-326/GAB1 axis. These data disclosed a specific circDHTKD1/miR-326/GAB1 signal axis in governing the malignant progression of OSCC, showing the considerable possibility of circDHTKD1 as a predictive and therapeutic target for clinical diagnosis and treatment of OSCC.		Braz J Med Biol Res. 2021 Jul 16;54(10):e10837. doi: 10.1590/1414-431X2020e10837. eCollection 2021.
5064	Circular RNA	circUBE2K	miR-516b-5p	ARHGAP5	Bc Tissues	Bladder Cancer	Homo sapiens (human)  	FISH;qPCR;RT-qPCR;FISH;	34285193	High-throughput sequencing identified circular RNA circUBE2K mediating RhoA associated bladder cancer phenotype via regulation of miR-516b-5p/ARHGAP5 axis.	Bladder cancer (BC) is known as a common and lethal urinary malignancy worldwide. Circular RNAs (circRNAs), an emerging non-coding RNA, participate in carcinogenesis process of several cancers including BC. In this study, high-throughput sequencing and RT-qPCR were applied to discover and validate abnormal high expression of circUBE2K in BC tissues. Fluorescence in situ hybridization (FISH) was used to detect hsa_circ_0009154 (circUBE2K) expression and subcellular localization in BC tissues. High circUBE2K predicted unfavorable prognoses in BCs, as well as correlated with clinical features. CCK8, transwell, EdU and wound healing assays demonstrated down-regulating circUBE2K decreased BC cell phenotype as proliferation, invasion, and migration, respectively. Further studies showed that circUBE2K promoted BC progression via sponging miR-516b-5p and enhancing ARHGAP5 expression through regulating RhoA activity. Dual-luciferase reporter, FISH and RNA pulldown assays were employed to verify the relationships among circUBE2K/miR-516b-5p/ARHGAP5/RhoA axis. Down-regulating miR-516b-5p or overexpressing ARHGAP5 restored RhoA activity mediated BC cell properties after silencing circUBE2K. Subcutaneous xenograft and metastasis model identified circUBE2K significantly increased BC cell metastasis and proliferation in-vivo. Taken together, we found that circUBE2K is a tumor-promoting circRNA in BC that functions as a ceRNA to regulate ARHGAP5 expression via sponging miR-516b-5p.		Cell Death Dis. 2021 Jul 20;12(8):719. doi: 10.1038/s41419-021-03977-1.
5065	Circular RNA	CircSNHG5	Mir-495-3p	CITED2	Degenerative Cartilage Endplate Tissues	Intervertebral Disc Degeneration	Homo sapiens (human)	FISH;microarray;qRT-PCR;RT-PCR;RACE;Western blot;FISH;luciferase assay;	34277611	CircSNHG5 Sponges Mir-495-3p and Modulates CITED2 to Protect Cartilage Endplate From Degradation.	BACKGROUND: Intervertebral disc degeneration (IDD) is a highly prevalent degenerating disease that produces tremendous amount of low back and neck pain. The cartilage endplate (CEP) is vitally important to intervertebral discs in both physiological and pathological conditions. In addition, circular RNAs (circRNAs) have been shown to be involved in the regulation of various diseases, including IDD. However, the particular role of circRNAs in cervical vertebral CEP degeneration remains unclear. Here, we examined the unique role of circRNAs in CEP of patients with cervical fracture and degenerative cervical myelopathy (DCM). METHODS: Human competitive endogenous RNA (ceRNA) microarray was performed by previous research. Western blot (WB), immunofluorescence (IF), quantitative RT-PCR (qRT-PCR), luciferase assay, and fluorescence in situ hybridization (FISH) were employed to analyze the function of circSNHG5 and its downstream effectors, miR-495-3p, and CITED2. RESULTS: We demonstrated that circSNHG5 expression was substantially low in degenerative CEP tissues. Knockdown of circSNHG5 in chondrocytes resulted in a loss of cell proliferation and followed by degradation of extracellular matrix (ECM). In addition, circSNHG5 was shown to sponge miR-495-3p and modulate the expression of the downstream gene CITED2. This mechanism of action was further validated via overexpression and knockdown of CITED2. CONCLUSION: Our findings identified a novel circSNHG5-miR-495-3p axis responsible for IDD progression. Future investigations into IDD therapy may benefit from targeting this axis.		Front Cell Dev Biol. 2021 Jul 1;9:668715. doi: 10.3389/fcell.2021.668715. eCollection 2021.
5066	Circular RNA	circDPP4	miR-195	cyclin D1	Pca Cells	Prostate Cancer	Homo sapiens (human)	microarray;	34271919	Circular RNA-DPP4 serves an oncogenic role in prostate cancer progression through regulating miR-195/cyclin D1 axis.	BACKGROUND: Recently, more and more studies have highlighted the critical regulatory roles of circular RNAs (circRNAs), a class of non-coding RNAs, in the progression of many human cancers, including prostate cancer (PCa). circRNA microarray analysis was performed to identify circRNAs that are differentially expressed in PCa tissues. METHODS: 104 pairs of PCa tissues and matched adjacent normal prostate tissues (at least 2 cm distal to the tumor margin) were obtained. circRNA microarray analysis was performed on four pairs of PCa tissues and matched adjacent normal prostate tissues to investigate the potential involvement of circRNAs in PCa. Flow cytometric analysis was performed to investigate whether the effect of circDPP4 on PCa cell proliferation was associated with the alteration in cell cycle progression. The role of circDPP4 in PCa tumor growth was further explored in vivo. RESULTS: We found that circDPP4 was overexpressed in PCa tissues and cell lines, and its expression was closely associated with Gleason score and clinical stage of PCa patients. In vitro loss- and gain-of-function experiments demonstrated that circDPP4 knockdown inhibited, whereas circDPP4 overexpression promoted the proliferation, migration, invasion and cell cycle progression of PCa cells. Knockdown of circDPP4 also suppressed PCa tumor growth in vivo. We further found that circDPP4 functioned as a competing endogenous RNA (ceRNA) for miR-195 in PCa cells, and miR-195 negatively regulated the expression of oncogenic cyclin D1. Rescue experiments suggested that restoration of miR-195 blocked the oncogenic role of circDPP4 in PCa cells. CONCLUSIONS: Taken together, our findings revealed a novel regulatory mechanism between circDPP4 and miR-195/cyclin D1 axis, and offered novel strategies for the treatment of PCa.		Cancer Cell Int. 2021 Jul 16;21(1):379. doi: 10.1186/s12935-021-02062-z.
5067	Circular RNA	circCLSPN	miR-370-3p	USP39	Gbm Tumor Tissues And Cells	Glioblastoma Multiforme	Homo sapiens (human)	CCK-8 assay;Dual-luciferase reporter assay;qPCR;RT-qPCR;RNA pull-down assay;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34269180	circRNA derived from CLSPN (circCLSPN) is an oncogene in human glioblastoma multiforme by regulating cell growth, migration and invasion via ceRNA pathway.	Glioblastoma multiforme (GBM) is the most aggressive and prevalent brain tumor in adults. The circRNA derived from CLSPN (hsa_circ_0011591, circCLSPN) is remarkably upregulated in GBM; however its functional role was uncovered yet. First, we examined expression of circCLSPN using GSE109569 database and RT-qPCR, and circCLSPN level was upregulated in human GBM tumor tissues and cells (A172 and LN18); moreover, circCLSPN showed a stable structure stability. Then, a series of loss-of-functional experiments were performed using CCK-8 assay, colony formation assay, flow cytometry, scratch wound assay, and transwell assay. Consequently, circCLSPN silencing suppressed cell viability, colony formation ability, cell cycle progression, migration, and invasion of A172 and LN18 cells in vitro, and promoted apoptosis rate. Allied with those were decreased B cell lymphoma-2 (Bcl-2), matrix metalloproteinase-2 (MMP2) and MMP9 expression, and elevated Bcl-2-associated X protein (Bax) level. According to dual-luciferase reporter assay and RNA pull-down assay, miR-370-3p was identified to be targeted and sponged by circCLSPN, and further targeted and negatively regulated USP39. Functionally, overexpressing miR-370-3p could mimic in vitro effects of circCLSPN interference. Rescue experiments revealed that blocking miR-370-3p could partially reverse the suppression of circCLSPN knockdown on cell growth, migration and invasion, and role of miR- 370-3p overexpression was abrogated by restoring USP39. In vivo, circCLSPN knockdown hindered tumor growth of LN18 cells by affecting miR-370-3p, USP39, MMP2 and MMP9 expression. In conclusion, circCLSPN elicited an oncogenic role in tumorigenesis and malignant progression of human GBM cells through circCLSPN-miR-370-3p-USP39 pathway.		J Biosci. 2021;46:66.
5068	Circular RNA	circ_0080229	miR-1827	MDM2	Glioma Tissues And Cell Lines	Glioma	Homo sapiens (human)  	FISH;ISH;qRT-PCR;Western blot;FISH;	34268375	Hsa_circ_0080229 upregulates the expression of murine double minute-2 (MDM2) and promotes glioma tumorigenesis and invasion via the miR-1827 sponging mechanism.	BACKGROUND: Glioma is the most common and fatal primary cranial tumor. The epidermal growth factor receptor (EGFR) plays an important role in the occurrence and treatment of glioma, which might function through a circular ribonucleic acid (circRNA)-related mechanism. Hsa_circ_0080229 (circ_0080229) has been identified as a circRNA arising from an EGFR gene in gliomas; however, little is known about its molecular mechanism to date. METHODS: To address this question, a series of experiments were conducted to confirm the effect of circ_0080229 in gliomas and identify the downstream mechanism. A quantitative real-time polymerase chain reaction (qRT-PCR) analysis and in-situ hybridization/fluorescence in-situ hybridization (ISH/FISH) testing were performed to identify the expression of circ_0080229 in patient samples. Bioinformatic analysis was carried out to explore the possible mechanism. Next, a series of in-vitro functional assays and in-vivo assays with a xenograft subcutaneous glioma model was carried out to confirm the effect of circ_0080229. Finally, qRT-PCR analysis and a Western Blot analysis were performed to verify the related mechanism. RESULTS: The expression of circ_0080229 was upregulated in both glioma tissues and cell lines related to unfavorable clinicopathologic characteristics. The expression of circ_0080229 was found to be inversely correlated with miR-1827, a micro-ribonucleic acid (miRNA) targeting murine double minute-2 (MDM2). The downregulation of circ_0080229 inhibited gliomas in vivo and suppressed U87 and U251 cell lines in vitro, which the transfection of the miR-1827 inhibitor could reverse. Concerning the mechanism, a block of circ_0080229 decreased MDM2 expression, while the inhibition of miR-1827 reversed this effect. Thus, circ_0080229 appears to target the downstream miR-1827/MDM2 signaling pathway. CONCLUSIONS: Our results showed that the silencing of circ_0080229 upregulates the expression of miR-1827, which in turn resulted in the suppression of MDM2, and the mediation of the downstream P53 signaling pathway. Circ_0080229 exerted an effect in mediating tumor progression through the MDM2 signaling pathway by sponging miR-1827. Its importance as a potential prognostic biomarker in gliomas has thus been established.		Ann Transl Med. 2021 May;9(9):762. doi: 10.21037/atm-20-7123.
5069	Circular RNA	circ_0000020	miR-142-5p	BMP2	Primary Bmscs	Osteogenic Differentiation	Homo sapiens (human)  	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;luciferase assay;RNA immunoprecipitation;	34266353	Circular RNA circ_0000020 promotes osteogenic differentiation to reduce osteoporosis via sponging microRNA miR-142-5p to up-regulate Bone Morphogenetic Protein BMP2.	This study was designed to study functions of Circ_0000020 during osteogenic differentiation. First, we used RT-qPCR to detect the expression of Circ_0000020, miR-142-5p and osteogenesis-related genes, whereas western blot analysis detected the expression of osteogenesis markers after the osteogenic differentiation of primary BMSCs isolated from rats. Alkaline phosphatase (ALP) activity and alizarin red Sstaining validated osteoblast phenotypes. Flow cytometry was used to detect cell apoptosis. Sh-Circ_0000020 was used to study the function of Circ_0000020 in osteogenic differentiation of BMSCs. Luciferase assay and RNA immunoprecipitation were used to validate the interaction between Circ_0000020 and miR-142-5p, and BMP2 and miR-142-5p. Co-transfection of miR-142-5p and sh-Circ_0000020 was used to verify the downstream signaling pathway. Circ_0000020 expression was up-regulated during osteogenic differentiation, whereas miR-142-5p expression was significantly decreased. Silencing Circ_0000020 inhibited osteogenic differentiation and promoted apoptosis, and inhibited ALP activity and mineralization ability. Moreover, Circ_0000020 interacts directly with miR-142-5p which binds to the BMP2 3'UTR and inhibits its expression. Additionally, co-transfection of miR-142-5p inhibitors and sh-Circ_0000020 rescued down-regulated BMP2, increased the expression osteogenesis-related gene expressions, and thereby rescued the inhibition of osteogenic differentiation induced by Circ_0000020 silencing. Furthermore, co-transfection of miR-142-5p inhibitors and sh-Circ_0000020 reversed Circ_0000020 silencing-induced downregulation of p-Smad1/5/8, Runx2, and Osterix protein levels. Circ_0000020 regulates BMP2 expression through sponging miR-142-5p as ceRNA, thereby positively regulating BMSCs osteogenic differentiation through Circ_0000020/miR-142-5p/BMP2/SMAD-dependent signaling pathway.		Bioengineered. 2021 Dec;12(1):3824-3836. doi: 10.1080/21655979.2021.1949514.
5070	Circular RNA	circRNA_016194	miR-449a-5p	Atg4b	Rats	Testicular Injuries	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;	34265366	Rno_circRNA_016194 might be involved in the testicular injury induced by long-term formaldehyde exposure via rno-miR-449a-5p mediated Atg4b activation.	Although circular RNAs (circRNAs) can function as microRNAs (miRNAs) sponges to participate in spermatogenesis, little is known about the functions of circRNAs in testis exposed to formaldehyde. In this study, twenty-four male SD rats (6-8 weeks) were randomly assigned to four groups, including a control group, 0.5, 2.46, and 5 mg/m(3) formaldehyde exposure groups, inhaling formaldehyde for eight consecutive weeks. The RT-qPCR was used to detect the expression of rno_circRNA_016194; the testicular injuries were observed by testicular histopathology. Our study illustrated up-regulated rno_circRNA_016194 was dose-dependent with formaldehyde. Simultaneously, the testicular histopathology showed an obvious damages in the 2.46 and 5 mg/m(3) formaldehyde exposure rats. Combined with bioinformatics analysis, the rno-miR-449a-5p was predicted and verified that its expression decreased in the testis exposed to formaldehyde. Meanwhile, the testicular morphometry changes were contrary to the expression of rno_circRNA_016194 and consistent with rno-miR-449a-5p. Moreover, bioinformatics analysis also prompted the potential downstream target gene for rno_circRNA_016194/rno-miR-449a-5p was Atg4b, and Atg4b expression was up-regulated in rats exposed to formaldehyde verifying by Western blot. Collectively, the rno_circRNA_016194 might be involved in formaldehyde-induced male reproductive toxicity and become potential therapeutic targets for male occupational exposure to formaldehyde.		Food Chem Toxicol. 2021 Sep;155:112409. doi: 10.1016/j.fct.2021.112409. Epub 2021 Jul 12.
5071	Circular RNA	circSLC6A6	miR-497-5p	PI4KB	Ec Tissues And Cells	Endometrial Cancer	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34258297	circSLC6A6 Sponges miR-497-5p to Promote Endometrial Cancer Progression via the PI4KB/Hedgehog Axis.	BACKGROUND: As a new kind of noncoding RNAs, circular RNAs (circRNAs) have been substantiated to be involved in multiple biological processes. Accumulating studies indicate that circular RNAs (circRNAs) regulate the development of cancers by acting as miRNA sponges. However, the role of circRNAs in endometrial cancer (EC) is rarely reported. This study was aimed at investigating the functional roles of circSLC6A6 in EC. METHODS: The qRT-PCR assay was performed to detect the circSLC6A6 expression in EC tissues and cell lines. The luciferase reporter assay was performed to explore the connection between circSLC6A6 and miR-497-5p as well as the connection between miR-497-5p and PI4KB. The colony formation assay, EdU assay, wound healing assay, and transwell assay were performed to examine the proliferation, migration, and invasion of EC cells. The in vivo assay was performed to reveal the function of circSLC6A6 in tumorigenesis. RESULTS: We found that circSLC6A6 was highly expressed in both EC tissues and cells. And circSLC6A6 promoted the proliferation, migration, and invasion of EC cells in vitro. In vivo, circSLC6A6 promoted tumor growth. Besides, a mechanistic study demonstrated that circSLC6A6 could regulate tumor-associated signaling PI4KB/hedgehog pathway by sponging miR-497-5p. CONCLUSION: This study illustrates that circSLC6A6 plays a role in promoting EC progression via the miR-497-5p-mediated PI4KB/hedgehog pathway. Our study may provide a potential novel biomarker for EC diagnosis or treatment.		J Immunol Res. 2021 Jun 22;2021:5512391. doi: 10.1155/2021/5512391. eCollection 2021.
5072	Circular RNA	Circ_0044516	miR-136	MAT2A	Lung Cancer Tissues And Cells	Lung Cancer	Homo sapiens (human)  	Rescue assay;	34258296	Circ_0044516 Regulates miR-136/MAT2A Pathway to Facilitate Lung Cancer Development.	Circular RNA (circRNA) is a type of noncoding RNA that can interact with miRNAs to regulate gene expression. However, little is known concerning circRNA, which is crucial in the pathogenesis of lung cancer. To date, limited studies have explored the role of circ_0044516 in lung cancer progression. Recently, we observed that circ_0044516 expression levels were obviously elevated in lung cancer tissues and cells. A549 and SPCA1 cells were transfected with circ_0044516 siRNA. We observed that knockdown of circ_0044516 dramatically repressed cell proliferation, increased cell apoptosis, and repressed the cell cycle. Moreover, A549 and SPCA1 cell migration and invasion abilities were greatly repressed by circ_0044516 siRNA. Due to accumulating evidence demonstrating the vital role of cancer stem cells, their mechanism of involvement has drawn increasing attention in tumor progression and metastasis research. We also found that cancer stem cell properties were restrained by silencing circ_0044516 in A549 and SPC-A1 cells. Moreover, in vivo xenograft experiments showed that circ_0044516 downregulation reduced tumor growth. Mechanistically, in lung cancer and using bioinformatics, we demonstrated that circ_0044516 sponges miR-136 targeting MAT2A. Furthermore, rescue assays were carried out to identify that circ_0044516 modulates cell proliferation, invasion, and stemness by regulating miR-136 and MAT2A in lung cancer. In summary, our study revealed that the circ_0044516/miR-136/MAT2A axis is involved in lung cancer progression. Our findings may provide novel targets for diagnosis and therapeutic intervention in lung cancer patients.		J Immunol Res. 2021 Jun 24;2021:5510869. doi: 10.1155/2021/5510869. eCollection 2021.
5073	Circular RNA	circFAT1	miR-30e-5p	ITGA6	Hct116 And Rko Cells	Colorectal Cancer	Homo sapiens (human)  	CCK-8 assay;qRT-PCR;Luciferase reporter assay;Rescue assay;	34257702	Circular RNA circFAT1(e2) Promotes Colorectal Cancer Tumorigenesis via the miR-30e-5p/ITGA6 Axis.	circRNAs (circular RNAs) are a family of noncoding RNAs and have diverse physiological and pathological functions. However, the functions and mechanisms of circRNAs in the development and progression of colorectal cancer (CRC) remain largely unknown. Here, we aimed to explore the functions and roles of circFAT1(e2) in CRC. qRT-PCR revealed that circFAT1(e2) in CRC tumor tissues was upregulated compared with that in adjacent normal tissues and was also upregulated in CRC cell lines. Small interfering RNAs (siRNAs) against circFAT1(e2) were used to decrease the expression of circFAT1(e2) in HCT116 and RKO cells in vitro. The roles of circFAT1(e2) in CRC cell metastasis and proliferation were then determined by transwell and CCK-8 assays. The results showed that circFAT1(e2) silencing markedly suppressed CRC growth. Moreover, we identified circFAT1(e2) as a promoter of CRC metastasis. Knockdown of circFAT1(e2) evidently reduced HCT116 and RKO cell migration and invasion. Furthermore, the regulatory relationship between circFAT1(e2) and its target miRNAs was verified by a luciferase reporter assay. We demonstrated that circFAT1(e2) could sponge miR-30e-5p, which regulated the expression level of integrin a6 (ITGA6), the downstream target gene of miR-30e-5p. Rescue assays demonstrated that knockdown of miR-30e-5p enhanced CRC proliferation and migration via ITGA6. Taken together, our results reveal the novel oncogenic roles of circFAT1(e2) in CRC through the miR-30e-5p/ITGA6 axis.		Comput Math Methods Med. 2021 Jun 26;2021:9980459. doi: 10.1155/2021/9980459. eCollection 2021.
5074	Circular RNA	Hsa_circ_0043265	miR-1243	SALL1	Scc25 And Cal27 Cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)  	qRT-PCR;Western blot;luciferase assay;RNA pull-down;	34257535	Hsa_circ_0043265 Restrains Cell Proliferation, Migration and Invasion of Tongue Squamous Cell Carcinoma via Targeting the miR-1243/SALL1 Axis.	Increasing evidence has displayed critical roles of circular RNAs (circRNAs) in tongue squamous cell carcinoma (TSCC). Hsa_circ_0043265 (circ_0043265) has been identified as a tumor suppressor in various tumors. Nevertheless, the critical roles of circ_0043265 in the initiation and progression of TSCC are yet to be fully elucidated. In our study, RNA and protein expressions were detected via qRT-PCR and Western blot. Cell proliferation, migration and invasion were evaluated via CCK-8 and transwell assays. The interactions between circ_0043265, miR-1243 and SALL1 were analyzed via bioinformatics analyses, RNA pull-down and luciferase assays, respectively. The current study demonstrated that circ_0043265 expression was downmodulated in TSCC tissues and cell lines (SCC25, SCC15, SCC9 and Cal27). Functionally, circ_0043265 overexpression led to an attenuation of cell proliferation, migration and invasion of SCC25 and Cal27 cells. Mechanistically, circ_0043265 acted as a competing endogenous RNA (ceRNA) via competitively sponging miR-1243, and restoration of miR-1243 rescued the inhibitory effects of circ_0043265 on cell proliferation, migration and invasion of SCC25 and Cal27 cells. Finally, it was observed that spalt like transcription factor 1 (SALL1), a potential target of miR-1243, was positively modulated via circ_0043265 in SCC25 and Cal27 cells, and SALL1 knockdown reversed the inhibitory effects of circ_0043265 on SCC25 and Cal27 cells. Collectively, the current study demonstrated that circ_0043265 was downmodulated in TSCC and was identified as a ceRNA that restrained the cell proliferation, migration and invasion of SCC25 and Cal27 cells via modulating the miR-1243/SALL1 axis.		Pathol Oncol Res. 2021 Feb 3;27:587130. doi: 10.3389/pore.2021.587130. eCollection 2021.
5075	Circular RNA	circRNA_0001236	miR-3677-3p	Sox9	Human Bone Marrow-Derived Mscs	Osteoarthritis	Homo sapiens (human)	Luciferase reporter assay;	34256841	Exosome-transported circRNA_0001236 enhances chondrogenesis and suppress cartilage degradation via the miR-3677-3p/Sox9 axis.	OBJECTIVES: Aberrations in exosomal circular RNA (circRNA) expression have been identified in various human diseases. In this study, we investigated whether exosomal circRNAs could act as competing endogenous RNAs (ceRNAs) to regulate the pathological process of osteoarthritis (OA). This study aimed to elucidate the specific MSC-derived exosomal circRNAs responsible for MSC-mediated chondrogenic differentiation using human bone marrow-derived MSCs (hMSCs) and a destabilization of the medial meniscus (DMM) mouse model of OA. METHODS: Exosomal circRNA deep sequencing was performed to evaluate the expression of circRNAs in human bone marrow-derived MSCs (hMSCs) induced to undergo chondrogenesis from day 0 to day 21. The regulatory and functional roles of exosomal circRNA_0001236 were examined on day 21 after inducing chondrogenesis in hMSCs and were validated in vitro and in vivo. The downstream target of circRNA_0001236 was also explored in vitro and in vivo using bioinformatics analyses. A luciferase reporter assay was used to evaluate the interaction between circRNA_0001236 and miR-3677-3p as well as the target gene sex-determining region Y-box 9 (Sox9). The function and mechanism of exosomal circRNA_0001236 in OA were explored in the DMM mouse model. RESULTS: Upregulation of exosomal circRNA_0001236 enhanced the expression of Col2a1 and Sox9 but inhibited that of MMP13 in hMSCs induced to undergo chondrogenesis. Moreover, circRNA_0001236 acted as an miR-3677-3p sponge and functioned in human chondrocytes via targeting miR-3677-3p and Sox9. Intra-articular injection of exosomal circRNA_0001236 attenuated OA in the DMM mouse model. CONCLUSIONS: Our results reveal an important role for a novel exosomal circRNA_0001236 in chondrogenic differentiation. Overexpression of exosomal circRNA_0001236 promoted cartilage-specific gene and protein expression through the miR-3677-3p/Sox9 axis. Thus, circRNA_0001236-overexpressing exosomes may alleviate cartilage degradation, suppressing OA progression and enhancing cartilage repair. Our findings provide a potentially effective therapeutic strategy for treating OA.		Stem Cell Res Ther. 2021 Jul 13;12(1):389. doi: 10.1186/s13287-021-02431-5.
5076	Circular RNA	circRNA_0001236	miR-3677-3p	Sox9	Human Bone Marrow-Derived Mscs	Osteoarthritis	Mus musculus (mouse)	Luciferase reporter assay;	34256841	Exosome-transported circRNA_0001236 enhances chondrogenesis and suppress cartilage degradation via the miR-3677-3p/Sox9 axis.	OBJECTIVES: Aberrations in exosomal circular RNA (circRNA) expression have been identified in various human diseases. In this study, we investigated whether exosomal circRNAs could act as competing endogenous RNAs (ceRNAs) to regulate the pathological process of osteoarthritis (OA). This study aimed to elucidate the specific MSC-derived exosomal circRNAs responsible for MSC-mediated chondrogenic differentiation using human bone marrow-derived MSCs (hMSCs) and a destabilization of the medial meniscus (DMM) mouse model of OA. METHODS: Exosomal circRNA deep sequencing was performed to evaluate the expression of circRNAs in human bone marrow-derived MSCs (hMSCs) induced to undergo chondrogenesis from day 0 to day 21. The regulatory and functional roles of exosomal circRNA_0001236 were examined on day 21 after inducing chondrogenesis in hMSCs and were validated in vitro and in vivo. The downstream target of circRNA_0001236 was also explored in vitro and in vivo using bioinformatics analyses. A luciferase reporter assay was used to evaluate the interaction between circRNA_0001236 and miR-3677-3p as well as the target gene sex-determining region Y-box 9 (Sox9). The function and mechanism of exosomal circRNA_0001236 in OA were explored in the DMM mouse model. RESULTS: Upregulation of exosomal circRNA_0001236 enhanced the expression of Col2a1 and Sox9 but inhibited that of MMP13 in hMSCs induced to undergo chondrogenesis. Moreover, circRNA_0001236 acted as an miR-3677-3p sponge and functioned in human chondrocytes via targeting miR-3677-3p and Sox9. Intra-articular injection of exosomal circRNA_0001236 attenuated OA in the DMM mouse model. CONCLUSIONS: Our results reveal an important role for a novel exosomal circRNA_0001236 in chondrogenic differentiation. Overexpression of exosomal circRNA_0001236 promoted cartilage-specific gene and protein expression through the miR-3677-3p/Sox9 axis. Thus, circRNA_0001236-overexpressing exosomes may alleviate cartilage degradation, suppressing OA progression and enhancing cartilage repair. Our findings provide a potentially effective therapeutic strategy for treating OA.		Stem Cell Res Ther. 2021 Jul 13;12(1):389. doi: 10.1186/s13287-021-02431-5.
5077	Circular RNA	hsa_circ_0026337	miR-197-3p	NA	Nsclc Tissue And Compared To Adjacent Healthy Tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)  	microarray;	34254931	Bioinformatics Analysis Predicts hsa_circ_0026337/miR-197-3p as a Potential Oncogenic ceRNA Network for Non-small Cell Lung Cancers.	BACKGROUND: Circular RNAs (circRNAs) play an essential role in developing tumors, but their role in non-small cell lung cancer (NSCLC) is unclear. Thus, the present study explored the possible molecular mechanism of circRNAs in NSCLC. METHODS: Three circular RNA (circRNA) microarray datasets were downloaded from the Gene Expression Omnibus (GEO) database. Differential expressions of circRNAs (DECs) were identified in NSCLC tissue and compared to adjacent healthy tissue. The online cancer-specific circRNA database (CSCD) was used for the analysis of the DECs function. Protein-protein interaction (PPI) network, Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Ontology (GO), Cytoscape, and UALCAN were used to predict the critical nodes and perform patient survival analysis, respectively. The interaction between the DECs, the predicted miRNAs, and hub genes was also determined. Finally, the circRNA-miRNA-mRNA network was established. RESULTS: The expression of hsa_circ_0049271, hsa_circ_0026337, hsa_circ_0043256, and hsa_circ_0008234 was decreased in NSCLC tissues. The Encyclopedia of RNA Interactomes (ENCORI) and CSCD database results showed that hsa_circ_0026337 was found to sponge with miR-1193, miR-197-3p, miR-3605-5p, miR-433-3p, and miR-652-3p, and hsa_circ_0043256 to sponge with miR-1252-5p, miR-494-3p, and miR-558, respectively. Subsequently, 100 mRNAs were predicted to bind with these seven miRNA response elements (MREs). The GO analysis and KEGG pathway revealed that these 100 MREs might be involved in "histone deacetylase binding" and "cellular senescence". PPI network and Cytoscape identified the top ten hub genes. Survival analysis data showed that the low expression of hsa_circ_0026337 was significantly associated with shortened survival time in NSCLC (P=0.037), which increased the expression level of hsa-miR-197-3p, thereby inhibiting the translation of specific proteins. CONCLUSION: This study examined the circRNA-miRNA-mRNA regulatory network associated with NSCLC and explored the potential functions of DECs in the network to elucidate the mechanisms underlying disease progression in NSCLC.		Anticancer Agents Med Chem. 2021 Jul 11. doi: 10.2174/1871520621666210712090721.
5078	Circular RNA	circCCDC66	miR-320a	FOXM1	Glioma Cells	Glioma	Homo sapiens (human)  	qRT-PCR;	34252882	Circular RNA circCCDC66 promotes glioma proliferation by acting as a ceRNA for miR-320a to regulate FOXM1 expression.	BACKGROUND: In this study, we determine the potential roles and uncover the regulatory mechanisms of circCCDC66 in regulating cell growth and cell metastasis of glioma. METHODS: qRT-PCR was used to detect the expressions of circCCDC66 in gliomas and tissues. The biological function of circCCDC66 in glioma cell lines was elucidated by functional experiments. Cell counting kit-8 and transwell were used to detect the effect of circCCDC66 on the proliferation, migration and invasion of glioma cells. Bioinformatics analysis was applied to reveal the targets of circCCDC66. RESULTS: The results showed circCCDC66 was overexpressed in glioma and acted as an oncogene. CircCCDC66 knockdown suppressed the proliferation, migration, and invasion of glioma cells. We constructed a circCCDC66 regulating miRNA network and revealed miR-320a was a potential target of circCCDC66, which was down-regulated in high-grade gliomas compared to low-grade gliomas. Bioinformatics analysis showed circCCDC66-miR-320a/b axis was involved in regulating multiple cancer-related pathways. Furthermore, we identified FOXM1 as a key target of circCCDC66, which was involved in regulating DNA damage response pathways. In mechanism study, circCCDC66 could sponge miR-320a, thereby increasing the expression of FOXM1. CONCLUSIONS: CircCCDC66 could facilitate glioma cells proliferation, invasion and migration by down-regulating miR-320a and up-regulating FOXM1.		Aging (Albany NY). 2021 Jul 12;13(13):17673-17689. doi: 10.18632/aging.203258. Epub 2021 Jul 12.
5079	Circular RNA	Circ_0124644	miR-590-3p	SOX4	Ami Patients And Hypoxia-Induced Cardiomyocytes	Acute Myocardial Infarction	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34249089	Circ_0124644 Serves as a ceRNA for miR-590-3p to Promote Hypoxia-Induced Cardiomyocytes Injury via Regulating SOX4.	Circular RNA (circRNA) is an important factor for regulating the progression of many cardiovascular diseases, including acute myocardial infarction (AMI). However, the role of circ_0124644 in AMI progression remains unclear. Hypoxia was used to induce cardiomyocytes injury. The expression of circ_0124644, microRNA (miR)-590-3p, and SRY-box transcription factor 4 (SOX4) mRNA was measured by qRT-PCR. Cell counting kit 8 (CCK8) assay and flow cytometry were utilized to detect cell viability, cell cycle progression, and apoptosis. The protein levels of apoptosis markers and SOX4 were determined by western blot (WB) analysis, and the levels of oxidative stress markers were assessed using commercial Assay Kits. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were employed to confirm the interaction between miR-590-3p and circ_0124644 or SOX4. Circ_0124644 was upregulated in AMI patients and hypoxia-induced cardiomyocytes. Hypoxia could inhibit cardiomyocytes viability, cell cycle process, and promote apoptosis and oxidative stress, while silencing circ_0124644 could alleviate hypoxia-induced cardiomyocytes injury. In terms of mechanism, circ_0124644 could target miR-590-3p. MiR-590-3p overexpression could relieve hypoxia-induced cardiomyocytes injury. Also, the suppressive effect of circ_0124644 knockdown on hypoxia-induced cardiomyocytes injury could be reversed by miR-590-3p inhibitor. Moreover, SOX4 was found to be a target of miR-590-3p, and its overexpression also could reverse the regulation of miR-590-3p on hypoxia-induced cardiomyocytes injury. Circ_0124644 silencing could alleviate hypoxia-induced cardiomyocytes injury by regulating the miR-590-3p/SOX4 axis, suggesting that it might be a target for alleviating AMI.		Front Genet. 2021 Jun 25;12:667724. doi: 10.3389/fgene.2021.667724. eCollection 2021.
5080	Circular RNA	CircUBAP2	miR-194-3p	MMP9	Hcc And Adjacent Non-Tumor Tissues	Hepatocellular Carcinoma	Mus musculus (mouse)	Dual-luciferase reporter assay;FISH;qPCR;RT-qPCR;FISH;Luciferase reporter assay;	34239873	CircUBAP2 Promotes MMP9-Mediated Oncogenic Effect via Sponging miR-194-3p in Hepatocellular Carcinoma.	BACKGROUND: The physiological regulatory functions of circRNAs have become a topic of intensive research in recent years. Increasing evidence supports a significant role of circRNAs during cancer initiation and progression, including hepatocellular carcinoma (HCC). MATERIALS AND METHODS: A bioinformatics analysis from three independent Gene Expression Omnibus (GEO) databases was performed to profile and screen the dysregulated circRNAs in HCC. RT-qPCR was used to examine the expression level of circUBAP2 in HCC and adjacent non-tumor tissues. Then, proliferation assays (CCK8 and colony formation) and migration assays (transwell and wound healing) were performed to examine effect of circUBAP2 in vitro. Immunoprecipitation, RNA pulldown, FISH, and dual-luciferase reporter assay was conducted to explore the circUBAP2-related mechanism for regulating HCC progression. Moreover, a mouse xenograft model and a mouse lung metastasis model confirmed the effect of circUBAP2 in vivo. RESULTS: In this study, we found a novel circRNA: circUBAP2, which was identified by bioinformatics analysis. Among 91 HCC patients, circUBAP2 was significantly upregulated in HCC tissues, and negatively correlated with aggressive clinical characteristics and prognosis. Functional assays demonstrated that circUBAP2 promoted cell proliferation, colony formation, migration, and invasion in vitro. Moreover, circUBAP2 enhanced tumor growth and pulmonary metastasis in vivo. Mechanistically, circUBAP2 acts as a competing endogenous RNA (ceRNA) for miR-194-3p, a tumor suppressor in HCC. We confirmed that MMP9 was direct target for miR-194-3p, which was regulated by circUBAP2. CONCLUSION: CircUBAP2 plays a significant role in promoting HCC via the miR-194-3p/MMP9 pathway and could serve as a promising prognostic biomarker and novel therapeutic target for HCC patients.		Front Cell Dev Biol. 2021 Jun 22;9:675043. doi: 10.3389/fcell.2021.675043. eCollection 2021.
5081	Circular RNA	CircHIPK3	miR-30a-3p	FOXK2	Fibroblasts	Pulmonary Fibrosis	Homo sapiens (human)  	ChIP;RACE;RIP assay;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	34239356	CircHIPK3 regulates pulmonary fibrosis by facilitating glycolysis in miR-30a-3p/FOXK2-dependent manner.	Pulmonary fibrosis develops when myofibroblasts and extracellular matrix excessively accumulate in the injured lung, but what drives fibrosis is not fully understood. Glycolysis has been linked to cell growth and proliferation, and several studies have shown enhanced glycolysis promotes pulmonary fibrosis. However, detailed studies describing this switch remain limited. Here, we identified that TGF-b1 effectively increased the expression of circHIPK3 in lung fibroblasts, and circHIPK3 inhibition attenuated the activation, proliferation, and glycolysis of fibroblasts in vitro. Dual-luciferase reporter gene assays, RNA immunoprecipitation (RIP), and RNA pull-down assays showed that circHIPK3 could function as a sponge of miR-30a-3p and inhibit its expression. Furthermore, FOXK2, a driver transcription factor of glycolysis, was identified to be a direct target of miR-30a-3p. Mechanistically, circHIPK3 could enhance the expression of FOXK2 via sponging miR-30a-3p, thereby facilitating fibroblast glycolysis and activation. Besides, miR-30a-3p overexpression or FOXK2 knockdown blocked fibroblast activation induced by TGF-b1 and abrogated the profibrotic effects of circHIPK3. Moreover, circHIPK3 and miR-30a-3p were also dysregulated in fibrotic murine lung tissues induced by silica. Adeno-associated virus (AAV)-mediated circHIPK3 silence or miR-30a-3p overexpression alleviated silica-induced pulmonary fibrosis in vivo. In conclusion, our results identified circHIPK3/miR-30a-3p/FOXK2 regulatory pathway as an important glycolysis cascade in pulmonary fibrosis.		Int J Biol Sci. 2021 Jun 4;17(9):2294-2307. doi: 10.7150/ijbs.57915. eCollection 2021.
5082	Circular RNA	CircMTO1	miR-182-5p	RASA1	Vascular Smooth Muscle Cell	Atherosclerosis	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34238206	CircMTO1 inhibits ox-LDL-stimulated vascular smooth muscle cell proliferation and migration via regulating the miR-182-5p/RASA1 axis.	BACKGROUND: Circular RNAs (circRNAs) play critical roles in the development of atherosclerosis (AS). This study investigated the role of circMTO1 in the progression of AS. METHODS: Serum samples from AS patients and healthy volunteers and vascular smooth muscle cells (VSMCs) were used as the study materials. The expressions of circMTO1 and miR-182-5p were measured by RT-qPCR. The effects of circMTO1, miR-182-5p, and RASA1 on VSMC proliferation and apoptosis were examined by MTT and BrdU assays and wound healing and flow cytometric analyses, respectively. Downstream target genes of circMTO1 and miR-182-5p were predicted using target gene prediction and screening and confirmed using a luciferase reporter assay. RASA1 expression was detected by RT-qPCR and Western blot. RESULTS: circMTO1 expression was decreased, while miR-182-5p expression was increased in human AS sera and oxidized low-density lipoprotein (ox-LDL)-stimulated VSMCs. CircMTO1 overexpression inhibited the proliferation and promoted the apoptosis of ox-LDL-stimulated VSMCs. CircMTO1 was found to be served as a sponge of miR-182-5p and RASA1 as a target of miR-182-5p. Moreover, circMTO1 acted as a ceRNA of miR-182-5p to enhance RASA1 expression. Furthermore, miR-182-5p overexpression and RASA1 knockdown reversed the effects of circMTO1 overexpression on the proliferation, migration, and apoptosis of ox-LDL-stimulated VSMCs. CONCLUSION: CircMTO1 inhibited the proliferation and promoted the apoptosis of ox-LDL-stimulated VSMCs by regulating miR-182-5p/RASA1 axis. These results suggest that circMTO1 has potential in AS treatment.		Mol Med. 2021 Jul 8;27(1):73. doi: 10.1186/s10020-021-00330-2.
5083	Circular RNA	circPVT1	miR-30e	DLL4	Bone Marrows And Cell Lines Of T-All	T Cell Acute Lymphoblastic Leukemia	Homo sapiens (human)  	qRT-PCR 	34237615	Up-regulation of circPVT1 in T cell acute lymphoblastic leukemia promoted cell proliferation via miR-30e/DLL4 induced activating NOTCH signaling.	T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic cancer with dismal prognosis. Recent studies disclosed that circPVT1 played an oncogene role in various cancers. But its role in T-ALL is still unclear. In this study, we found the expression levels of circPVT1 in bone marrows and cell lines of T-ALL were significantly up regulated and knock-down of circPVT1 in T-ALL cell lines could inhibit the cell proliferation and increase the cell apoptosis. Further analysis showed that circPVT1 could bind directly to miR-30e and contributed to the activate the Notch signaling by regulating miR-30e/DLL4 pathway. The levels of circPVT1 were obviously related to cumulative relapse rate and 5-year survival rate. In conclusion, our study reveals that circPVT1 participates in the progression of T-ALL through the miR-30e/DLL4 pathway and might represent a potential therapeutic target for T-ALL treatment.		Pathol Res Pract. 2021 Aug;224:153536. doi: 10.1016/j.prp.2021.153536. Epub 2021 Jun 23.
5084	Circular RNA	hsa_circ_0008274	miR-578	HMGA2	Luad Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qRT-PCR;Western blot;	34236145	Overexpression of hsa_circ_0008274 inhibited the progression of lung adenocarcinoma by regulating HMGA2 via sponging miR-578.	BACKGROUND: Circular RNAs (circRNAs) had been identified as a non-coding RNA associated with many types of cancer in recent years. However, the involvement of hsa_circ_0008274 in lung adenocarcinoma (LUAD) has not been explored. The aim of our research is to explore the biological mechanism and function of hsa_circ_0008274 in LUAD. METHODS: The hsa_circ_0008274, miR-578, and high mobility group AT-Hook 2 (HMGA2) mRNA expression levels were detected via qRT-PCR. Cell Counting Kit-8 (CCK-8) Transwell assay and wound healing assay were performed to measure the cell proliferation, invasion, and migration ability. Luciferase reporter and Western blotting experiments were performed to characterize the competing endogenous RNA (ceRNA) mechanism of hsa_circ_0008274. RESULTS: Our findings determined that the expression of hsa_circ_0008274 in LUAD was significantly decreased. Cell experiments showed that overexpressed hsa_circ_0008274 could reduce the proliferation and invasion ability of LUAD cells. Moreover, miRNA-578 could identify as a miRNA sponge of hsa_circ_0008274. Overexpressed hsa_circ_0008274 reduced the proliferation and invasion of LUAD cells caused by miR-578 mimics. Increasing the expression of miR-578 can aggravate the proliferation and invasion of LUAD cells and block the inhibition of proliferation and invasion of LUAD cells mediated by overexpressed hsa_circ_0008274. Subsequent data indicate that HMGA2 of the tumor-promoting gene is the target gene of miR-578. The upregulation of HMGA2 partially reversed the tumor inhibitory effect of LUAD cells induced by overexpressed hsa_circ_0008274 or miR-578 mimics. CONCLUSIONS: In summary, our data show that the overexpression of hsa_circ_0008274 repressed the proliferation and invasion of LUAD through downregulating miR-578 and activating HMGA2.		Thorac Cancer. 2021 Aug;12(16):2258-2264. doi: 10.1111/1759-7714.14059. Epub 2021 Jul 8.
5085	Circular RNA	circARL15	miR-431-5p	DISC1	Idd Tissues	Intervertebral Disc Degeneration	Homo sapiens (human)  	microarray;Western blot;Immunohistochemistry;	34234811	circARL15 Plays a Critical Role in Intervertebral Disc Degeneration by Modulating miR-431-5p/DISC1.	BACKGROUND: Intervertebral disk degeneration (IDD) is a serious public health problem associated with genetic and environmental factors. However, the pathogenic factors involved and the pathological mechanism of this disease still remain enigmatic. METHODS: The associated microarray was downloaded and further analyzed using statistical software R. The competing endogenous RNA (ceRNA) co-expression network was constructed to measure the meaningful correlated expression of differentially expressed genes. We further measured the expression of circARL15/miR-431-5p/DISC1 in IDD tissues. Cell proliferation and apoptosis were detected in NP cells transfected with a circARL15 overexpression plasmid and miR-431-5p mimics. The expression of DISC1 was detected by immunohistochemistry and Western blot analysis. RESULTS: Within the ceRNA network, circARL15 is the most differentially expressed circular RNA. circARL15 was down-regulated in IDD and was negatively correlated with miR-431-5p and positively associated with DISC1. miR-431-5p was found to bind directly to circARL15 and DISC1. circARL15 inhibited nucleus pulposus cell apoptosis but promoted nucleus pulposus cell proliferation by targeting the miR-431-5p/DISC1 signaling pathway. CONCLUSION: circARL15/miR-431-5p/DISC1 is involved in the pathogenesis of IDD, which might be helpful in determining the diagnostic biomarkers and providing potential therapeutic targets for patients with IDD.		Front Genet. 2021 Jun 21;12:669598. doi: 10.3389/fgene.2021.669598. eCollection 2021.
5086	Circular RNA	CircCA12	miR-1184	NRAS	Ubc Cells	Bladder Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;	34234808	CircCA12 Promotes Malignant Process via Sponging miR-1184 and Upregulating RAS Family in Bladder Cancer.	Circular RNAs (circRNAs) are a panel of non-coding RNAs that mediate the regulation of gene expression, as well as pathological responses. Nonetheless, the function and expression pattern of circRNAs in urinary bladder cancer (UBC) remain unclear. Herein, we examined the function of circCA12 in UBC development. qRT-PCR results demonstrated remarkable circCA12 upregulation in UBC cell lines, as well as tissues. CCK-8, colony formation, and xenograft assays were employed to determine the effect of circCA12 on UBC. Our data illustrated silencing circCA12 repressed the proliferation along with the colony-formation capability of UBC cells. The migration and metastasis potential of UBC cells were remarkably abated in vivo, as well as in vitro after transfection with si-cirCA12 or sh-circCA12. Moreover, luciferase reporter and RIP assays indicated that circCA12 binds to miRNA-1184 through sponging miRNA, thereby up-regulating the expression of RAS family genes (NRAS, KRAS, and HRAS). In conclusion, the circCA12/miRNA-1184/RAS family was identified as a regulatory axis in UBC progression.		Front Genet. 2021 Jun 21;12:663982. doi: 10.3389/fgene.2021.663982. eCollection 2021.
5087	Circular RNA	CircCA12	miR-1184	KRAS	Ubc Cells	Bladder Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;	34234808	CircCA12 Promotes Malignant Process via Sponging miR-1184 and Upregulating RAS Family in Bladder Cancer.	Circular RNAs (circRNAs) are a panel of non-coding RNAs that mediate the regulation of gene expression, as well as pathological responses. Nonetheless, the function and expression pattern of circRNAs in urinary bladder cancer (UBC) remain unclear. Herein, we examined the function of circCA12 in UBC development. qRT-PCR results demonstrated remarkable circCA12 upregulation in UBC cell lines, as well as tissues. CCK-8, colony formation, and xenograft assays were employed to determine the effect of circCA12 on UBC. Our data illustrated silencing circCA12 repressed the proliferation along with the colony-formation capability of UBC cells. The migration and metastasis potential of UBC cells were remarkably abated in vivo, as well as in vitro after transfection with si-cirCA12 or sh-circCA12. Moreover, luciferase reporter and RIP assays indicated that circCA12 binds to miRNA-1184 through sponging miRNA, thereby up-regulating the expression of RAS family genes (NRAS, KRAS, and HRAS). In conclusion, the circCA12/miRNA-1184/RAS family was identified as a regulatory axis in UBC progression.		Front Genet. 2021 Jun 21;12:663982. doi: 10.3389/fgene.2021.663982. eCollection 2021.
5088	Circular RNA	CircCA12	miR-1184	HRAS	Ubc Cells	Bladder Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;	34234808	CircCA12 Promotes Malignant Process via Sponging miR-1184 and Upregulating RAS Family in Bladder Cancer.	Circular RNAs (circRNAs) are a panel of non-coding RNAs that mediate the regulation of gene expression, as well as pathological responses. Nonetheless, the function and expression pattern of circRNAs in urinary bladder cancer (UBC) remain unclear. Herein, we examined the function of circCA12 in UBC development. qRT-PCR results demonstrated remarkable circCA12 upregulation in UBC cell lines, as well as tissues. CCK-8, colony formation, and xenograft assays were employed to determine the effect of circCA12 on UBC. Our data illustrated silencing circCA12 repressed the proliferation along with the colony-formation capability of UBC cells. The migration and metastasis potential of UBC cells were remarkably abated in vivo, as well as in vitro after transfection with si-cirCA12 or sh-circCA12. Moreover, luciferase reporter and RIP assays indicated that circCA12 binds to miRNA-1184 through sponging miRNA, thereby up-regulating the expression of RAS family genes (NRAS, KRAS, and HRAS). In conclusion, the circCA12/miRNA-1184/RAS family was identified as a regulatory axis in UBC progression.		Front Genet. 2021 Jun 21;12:663982. doi: 10.3389/fgene.2021.663982. eCollection 2021.
5089	Circular RNA	CircASXL1	miR-206	HIF-1a	Nsclc Tissues, Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34234552	CircASXL1 Knockdown Restrains Hypoxia-Induced DDP Resistance and NSCLC Progression by Sponging miR-206.	BACKGROUND: Non-small cell lung carcinoma (NSCLC) is a primary prevalent type of cancer in people worldwide. Cisplatin (DDP) has been widely used to treat NSCLC; however, its curative effect was restrained under hypoxia. In this study, the effects of hypoxia treatment on DDP resistance and NSCLC progression and underneath mechanism were revealed. METHODS: The expression of circular RNA ASXL1 (circASXL1) and microRNA-206 (miR-206) in NSCLC tissues, cells and hypoxia-mediated NSCLC cells was determined by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of proliferation, metastasis and apoptosis-related proteins, drug resistance-related protein and hypoxia-inducible factor-1alpha (HIF-1a) protein was detected by Western blot. The effects of circASXL1 knockdown on hypoxia-induced DDP resistance and NSCLC progression were revealed by cell counting kit-8 proliferation (CCK-8), cell colony formation, transwell and flow apoptosis assays. RNA immunoprecipitation (RIP) assay was performed to determine whether circASXL1 could form silence-inducing complexes with miRNA. The associated relationship between circASXL1 and miR-206 was predicted by circBank online database, and identified by RNA pull-down and dual-luciferase reporter assays. The effects between circASXL1 knockdown and miR-206 downregulation on tumor growth in vivo were investigated by in vivo tumor formation assay. RESULTS: CircASXL1 expression was dramatically upregulated, whereas miR-206 was significantly down-regulated in NSCLC tissues, cells and hypoxia-mediated NSCLC cells as compared to control groups. CircASXL1 knockdown reversed hypoxia-mediated promotion effects on DDP resistance, cell proliferation, migration, and invasion, and inhibition impact on cell apoptosis, whereas these effects were restored by miR-206 inhibitor. Additionally, circASXL1 was found to form silence-inducing complexes with miRNA and act as a sponge of miR-206. CircASXL1 silencing downregulated HIF-1a expression by controlling miR-206 expression. Furthermore, circASXL1 silencing repressed tumor growth in vivo by sponging miR-206. CONCLUSION: CircASXL1 knockdown inhibited DDP resistance, cell proliferation, migration and invasion, whereas induced cell apoptosis under hypoxia by associating with miR-206 in NSCLC. This study provides a new sight in treating NSCLC with DDP under hypoxia.		Cancer Manag Res. 2021 Jun 28;13:5077-5089. doi: 10.2147/CMAR.S276964. eCollection 2021.
5090	Circular RNA	Circ_001209	miR-15b-5p	COL12A1	Human Retinal Vascular Endothelial Cells	Diabetic Retinopathy	Homo sapiens (human)	FISH;qRT-PCR;Western blot;FISH;	34233716	Circ_001209 aggravates diabetic retinal vascular dysfunction through regulating miR-15b-5p/COL12A1.	OBJECTIVE: Diabetic retinopathy, a common complication of diabetes mellitus and a major cause of blindness. circRNAs spongs target miRNA and thus influencing mRNA expression in DR. We investigated the mechanism of circ_001209 in regulating diabetic retinal vascular dysfunction. METHODS: QRT-PCR analysis was performed to detect the expression of miR-15b-5p, COL12A1 and circ_001209 in human retinal vascular endothelial cells (HRVECs) under high glucose conditions. Western blot assay, wound healing assay, transwell assay and tube formation were used to explore the roles of circ_001209/miR-15b-5p/COL12A1 in retinal vascular dysfunction. Bioinformatics analysis and luciferase reporter, RNA-FISH, and overexpression assays were performed to reveal the mechanisms of the circ_001209/miR-15b-5p/COL12A1 interaction. TUNEL staining and H&E staining were used to evaluate the pathological changes in streptozotocin (STZ)-induced DR in rats. RESULTS: Downregulation of miR-15b-5p under HG conditions promoted proliferation, migration, and tube formation of HRVECs. QRT-PCR and western blot results revealed that miR-15b-5p affected the HRVECs function through targeting COL12A1. Under HG conditions, circ_001209, which acts as a sponge of miR-15b-5p, is upregulated. Besides, overexpression of circ_001209 can affect HRVEC function and aggravate retinal injury in diabetic rats. CONCLUSION: Upregulation of circ_001209 contributes to vascular dysfunction in diabetic retinas through regulating miR-15b-5p and COL12A1, providing a potential treatment strategy for diabetic retinopathy.		J Transl Med. 2021 Jul 7;19(1):294. doi: 10.1186/s12967-021-02949-5.
5091	Circular RNA	Circ-DENND4C	miR-195-5p	TCF4	Hepatocellular Carcinoma Cell	Hepatocellular Carcinoma	Homo sapiens (human)  	FISH;qRT-PCR;RIP assay;Western blot;FISH;Luciferase reporter assay;Rescue assay;	34233663	Circ-DENND4C up-regulates TCF4 expression to modulate hepatocellular carcinoma cell proliferation and apoptosis via activating Wnt/b-catenin signal pathway.	BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignant tumor in China. Advanced treatment like transcatheter hepatic arterial chemoembolization (TACE) has prolonged the lives of many HCC patients. However, the prognosis of most HCC patients remains unsatisfactory. Recently, circular RNAs (circRNAs) have been gradually unveiled to exert considerable functions in cancer. Promising circRNAs in HCC remains to be further elucidated. METHODS: Gene expression was assessed by qRT-PCR and western blot. The function of circ-DENND4C in HCC was estimated by both in vitro and in vivo experiments. The location of circ-DENND4C in HCC cells was determined by subcellular fractionation and FISH assays. The association among molecules were analyzed through RNA pull down, RIP and luciferase reporter assays. RESULTS: circ-DENND4C (DENN domain containing 4C), an oncogene identified in breast cancer, was overexpressed in HCC cells. Also, circ-DENND4C exerted pro-tumor functions in HCC through activating Wnt/b-catenin pathway. Importantly, circ-DENND4C could augment transcription factor 4 (TCF4) expression to activate Wnt/b-catenin signaling via sequestering miR-195-5p. Moreover, following rescue assays disclosed that circ-DENND4C mediated malignant phenotypes in HCC cells via up-regulating TCF4 through sponging miR-195-5p. CONCLUSION: circ-DENND4C boosted TCF4 expression to modulate malignant behaviors of HCC cells via activating Wnt/b-catenin pathway, which might offer a promising target for HCC treatment.		Cancer Cell Int. 2020 Jul 8;20(1):295. doi: 10.1186/s12935-020-01346-0.
5092	Circular RNA	circPUS7	miR-770	KRAS	T-Beas-2B Cells	Cadmium Induced Transformation	Homo sapiens (human)	qRT-PCR 	34232319	A novel circular RNA, circPUS7 promotes cadmium-induced transformation of human bronchial epithelial cells by regulating Kirsten rat sarcoma viral oncogene homolog expression via sponging miR-770.	Cadmium is a human carcinogen, which induces cancers by mechanisms that are not fully understood. Induction of oxidative stress, apoptosis resistance, genotoxic effects, and epigenetic modulations have been indicated to regulate cadmium-induced carcinogenesis. Circular RNAs are epigenetic regulators that have been recognized to play essential roles in carcinogenesis. Yet, the involvement of circular RNAs in cadmium carcinogenesis remains unclear. In this study, a novel circular RNA, circPUS7, was identified and described for the first time. CircPUS7 was significantly upregulated at week 12, 16, and 20 during the cadmium-induced transformation of human bronchial epithelial BEAS-2B cells. Knockdown of circPUS7 in cadmium-transformed BEAS-2B (T-BEAS-2B) cells significantly attenuated transformation markers including cell proliferation, migration, invasion, and anchorage-independent growth. Moreover, circPUS7 promoted malignant phenotypes by competitively binding with miR-770. Overexpression of miR-770 significantly inhibited the transformation properties of T-BEAS-2B cells while inhibition of miR-770 potently reversed the inhibitory effects of circPUS7 knockdown in proliferation, migration, invasion, and anchorage-independent growth of the T-BEAS-2B cells. Kirsten rat sarcoma viral oncogene homolog (KRAS), which was increased synchronically with circPUS7 during cadmium-induced cell transformation, was regulated by circPUS7 through sponging miR-770. In summary, our findings demonstrate that circPUS7 promotes cadmium-induced cell transformation through sponging miR-770 to regulate KRAS expression, providing a new perspective with the involvement of circular RNAs to further understand the mechanisms of cadmium carcinogenesis.		Metallomics. 2021 Jul 24;13(7):mfab043. doi: 10.1093/mtomcs/mfab043.
5093	Circular RNA	circPUS7	miR-770	KRAS	T-Beas-2B Cells	Cadmium Induced Transformation	Rattus (rat)	qRT-PCR 	34232319	A novel circular RNA, circPUS7 promotes cadmium-induced transformation of human bronchial epithelial cells by regulating Kirsten rat sarcoma viral oncogene homolog expression via sponging miR-770.	Cadmium is a human carcinogen, which induces cancers by mechanisms that are not fully understood. Induction of oxidative stress, apoptosis resistance, genotoxic effects, and epigenetic modulations have been indicated to regulate cadmium-induced carcinogenesis. Circular RNAs are epigenetic regulators that have been recognized to play essential roles in carcinogenesis. Yet, the involvement of circular RNAs in cadmium carcinogenesis remains unclear. In this study, a novel circular RNA, circPUS7, was identified and described for the first time. CircPUS7 was significantly upregulated at week 12, 16, and 20 during the cadmium-induced transformation of human bronchial epithelial BEAS-2B cells. Knockdown of circPUS7 in cadmium-transformed BEAS-2B (T-BEAS-2B) cells significantly attenuated transformation markers including cell proliferation, migration, invasion, and anchorage-independent growth. Moreover, circPUS7 promoted malignant phenotypes by competitively binding with miR-770. Overexpression of miR-770 significantly inhibited the transformation properties of T-BEAS-2B cells while inhibition of miR-770 potently reversed the inhibitory effects of circPUS7 knockdown in proliferation, migration, invasion, and anchorage-independent growth of the T-BEAS-2B cells. Kirsten rat sarcoma viral oncogene homolog (KRAS), which was increased synchronically with circPUS7 during cadmium-induced cell transformation, was regulated by circPUS7 through sponging miR-770. In summary, our findings demonstrate that circPUS7 promotes cadmium-induced cell transformation through sponging miR-770 to regulate KRAS expression, providing a new perspective with the involvement of circular RNAs to further understand the mechanisms of cadmium carcinogenesis.		Metallomics. 2021 Jul 24;13(7):mfab043. doi: 10.1093/mtomcs/mfab043.
5094	Circular RNA	hsa_circ_0000277	miR-4766-5p	LAMA1	Escc Cells	Esophageal Squamous Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34226522	Circular RNA hsa_circ_0000277 sequesters miR-4766-5p to upregulate LAMA1 and promote esophageal carcinoma progression.	Growing evidence has indicated that circular RNAs (circRNAs) play a pivotal role as functional RNAs in diverse cancers. However, most circRNAs involved in esophageal squamous cell carcinoma (ESCC) remain undefined, and the underlying molecular mechanisms mediated by circRNAs are largely unclear. Here, we screened human circRNA expression profiles in ESCC tissues and found significantly increased expression of hsa_circ_0000277 (termed circPDE3B) in ESCC tissues and cell lines compared to the normal controls. Moreover, higher circPDE3B expression in patients with ESCC was correlated with advanced tumor-node-metastasis (TNM) stage and dismal prognosis. Functional experiments demonstrated that circPDE3B promoted the tumorigenesis and metastasis of ESCC cells in vitro and in vivo. Mechanistically, bioinformatics analysis, a dual-luciferase reporter assay, and anti-AGO2 RNA immunoprecipitation showed that circPDE3B could act as a competing endogenous RNA (ceRNA) by harboring miR-4766-5p to eliminate the inhibitory effect on the target gene laminin a1 (LAMA1). In addition, LAMA1 was significantly upregulated in ESCC tissues and was positively associated with the aggressive oncogenic phenotype. More importantly, rescue experiments revealed that the oncogenic role of circPDE3B in ESCC is partly dependent on the miR-4766-5p/LAMA1 axis. Furthermore, bioinformatics analysis combined with validation experiments showed that epithelial-mesenchymal transition (EMT) activation was involved in the oncogenic functions of the circPDE3B-miR-4766-5p/LAMA1 axis in ESCC. Taken together, we demonstrate for the first time that the circPDE3B/miR-4766-5p/LAMA1 axis functions as an oncogenic factor in promoting ESCC cell proliferation, migration, and invasion by inducing EMT, implying its potential prognostic and therapeutic significance in ESCC.		Cell Death Dis. 2021 Jul 5;12(7):676. doi: 10.1038/s41419-021-03911-5.
5095	Circular RNA	Hsa_circ_0008360	miR-186-5p	CCND2	Human Umbilical Vascular Endothelium Cells	Vascular Endothelial Dysfunction	Homo sapiens (human)	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;RNA pull-down;	34223793	Hsa_circ_0008360 sponges miR-186-5p to target CCND2 to modulate high glucose-induced vascular endothelial dysfunction.	Vascular endothelial dysfunction is associated with the progress of many diseases. Circular RNAs (circRNAs) take part in the dysfunction of vascular endothelium. CircRNA hsa_circ_0008360 (circ_0008360) is dysregulated in high glucose-treated vascular endothelium, while the role and mechanism of circ_0008360 in high glucose-induced dysfunction remain unknown. Human umbilical vascular endothelium cells (HUVEC) were stimulated via high glucose. The abundances of circ_0008360, miR-186-5p and cyclin D2 (CCND2) were examined via quantitative real-time polymerase chain reaction or western blot. Vascular endothelial dysfunction was assessed via cell viability, apoptosis, migration and tube formation. The target relationship between miR-186-5p and circ_0008360 or CCND2 was analyzed via dual-luciferase reporter, RNA pull-down and RNA immunoprecipitation analyses. Circ_0008360 expression was enhanced in high-glucose-treated HUVEC. Circ_0008360 silence mitigated high glucose-induced suppression of viability, migration, tube formation, and increase in apoptosis in HUVEC. MiR-186-5p was sponged by circ_0008360, and miR-186-5p inhibition reversed the effect of circ_0008360 silence on high glucose-induced vascular endothelial dysfunction. MiR-186-5p alleviated high glucose-induced vascular endothelial dysfunction via targeting CCND2. CCND2 interference abolished the aggravated effect of circ_0008360 on high glucose-induced vascular endothelial dysfunction. Circ_0008360 knockdown attenuated high glucose-induced vascular endothelial dysfunction via regulating miR-186-5p and CCND2, indicating circ_0008360 might act as a target for the treatment of vascular endothelial dysfunction.Abbreviations: circRNAs, circular RNAs; HUVEC, human umbilical vascular endothelium cells; CCND2, cyclin D2; XPNPEP3, X-prolyl aminopeptidase 3; ceRNAs, competing endogenous RNAs; miRNAs, microRNAs; qRT-PCR, quantitative real-time polymerase chain reaction; RIP, RNA immunoprecipitation; HIF-1a, hypoxia inducible factor 1 alpha; TLR3, toll-like receptor 3; AKAP12, A-Kinase Anchoring Protein 12; ox-LDL, oxidized low-density lipoprotein; HG, high glucose; NG, normal glucose.		Cell Cycle. 2021 Jul;20(14):1389-1401. doi: 10.1080/15384101.2021.1918877. Epub 2021 Jul 5.
5096	Circular RNA	CDR1as	miR-876-5p	GNG7	Gc Cells	Gastric Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;	34221006	Circular RNA CDR1as Inhibits the Metastasis of Gastric Cancer through Targeting miR-876-5p/GNG7 Axis.	Circular RNA CDR1as has been demonstrated to participate in various cancer progressions as miRNA sponges. The exact underlying mechanisms of CDR1as on gastric cancer (GC) metastasis remain unknown. Here, we found that CDR1as knockdown facilitated GC cell migration and invasion while its overexpression inhibited the migration and invasion abilities of GC cells in vitro and in vivo. Moreover, epithelial-mesenchymal transition- (EMT-) associated proteins and MMP2 and MMP9 were downregulated by CDR1as. Bioinformatics analysis combined with dual-luciferase reporter gene assays, western blot, RT-qPCR analysis, and functional rescue experiments demonstrated that CDR1as served as a miR-876-5p sponge and upregulated the target gene GNG7 expression to suppress GC metastasis. In summary, our findings indicate that CDR1as suppresses GC metastasis through the CDR1as/miR-876-5p/GNG7 axis.		Gastroenterol Res Pract. 2021 Jun 16;2021:5583029. doi: 10.1155/2021/5583029. eCollection 2021.
5097	Circular RNA	circGPC3	miR-378a-3p	APSM	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34199580	Clinicopathological-Associated Regulatory Network of Deregulated circRNAs in Hepatocellular Carcinoma.	Hepatocellular carcinoma (HCC) is one of the most common and lethal cancers worldwide. Here, we present a novel strategy to identify key circRNA signatures of clinically relevant co-expressed circRNA-mRNA networks in pertinent cancer-pathways that modulate prognosis of HCC patients, by integrating clinic-pathological features, circRNA and mRNA expression profiles. Through further integration with miRNA expression profiles, clinically relevant competing-endogenous-RNA (ceRNA) networks of circRNA-miRNA-mRNAs were constructed. At least five clinically relevant nodal-circRNAs, co-expressed with numerous genes, were identified from the circRNA-mRNA networks. These nodal circRNAs upregulated proliferation (except circRaly) and transformation in cells. The most upregulated nodal-circRNA, circGPC3, associated with higher-grade tumors and co-expressed with 33 genes, competes with 11 mRNAs for two shared miRNAs. circGPC3 was experimentally demonstrated to upregulate cell-cycle and migration/invasion in both transformed and non-transformed liver cell-lines. circGPC3 was further shown to act as a sponge of miR-378a-3p to regulate APSM (Abnormal spindle-like microcephaly associated) expression and modulate cell transformation. This study identifies 5 key nodal master circRNAs in a clinically relevant circRNA-centric network that are significantly associated with poorer prognosis of HCC patients and promotes tumorigenesis in cell-lines. The identification and characterization of these key circRNAs in clinically relevant circRNA-mRNA and ceRNA networks may facilitate the design of novel strategies targeting these important regulators for better HCC prognosis.		Cancers (Basel). 2021 Jun 2;13(11):2772. doi: 10.3390/cancers13112772.
5098	Circular RNA	circPTPN22	miR-3074-5p	NA	Peripheral Blood Mononuclear Cells	Rheumatoid Arthritis	Homo sapiens (human)  	RNA sequencing;	34184082	circPTPN22 as a novel biomarker and ceRNA in peripheral blood mononuclear cells of rheumatoid arthritis.	The role of circular RNAs (circRNAs) in rheumatoid arthritis (RA) remains to be elucidated. To determine the expression of circRNAs in peripheral blood mononuclear cells (PBMCs) and to identify novel biomarkers for RA and explore their potential effects in RA, the present study conducted high-throughput RNA sequencing to analyze circRNA expression profiles in PBMCs from 4 RA patients and 3 healthy controls (HCs). Reverse transcription-quantitative PCR was used to verify the expression of circPTPN22 in 42 RA patients, 44 HCs and 45 systemic lupus erythematosus (SLE) patients. In addition, bioinformatics analysis and Pearson's correlation test were conducted to assess the correlation of the relationships between circPTPN22 and RA progression. A receiver operating characteristic curve was calculated to evaluate the diagnostic value. Multilevel integrated analysis identified 41 upregulated and 30 downregulated circRNAs in RA patients compared with HCs. circPTPN22 was confirmed to be a common differentially expressed gene in RA and SLE compared with HCs. Area under the curve analysis suggested the diagnostic value of circPTPN22 expression to distinguish RA patients from both HCs and SLE patients. In addition, circPTPN22 levels in RA PBMCs were correlated with RA-IgG, RA-IgM, RA-IgA, anti-cyclic citrullinated peptide (anti-CCP), rheumatoid factor and C reactive protein levels. A total of four putative microRNAs (miRNAs or miRs), namely, hsa-miR-3074-5p, hsa-miR-373-3p, hsa-miR-766-3p and hsa-miR-34c-5p, were screened to be sponged by circPTPN22 via bioinformatics analysis and then experimentally verified to be upregulated in RA PBMCs compared with controls. The data suggested that circPTPN22 might be a novel biomarker for the diagnosis of RA and participate in RA pathogenesis through a sponge mechanism.		Mol Med Rep. 2021 Aug;24(2):617. doi: 10.3892/mmr.2021.12256. Epub 2021 Jun 29.
5099	Circular RNA	circPTPN22	miR-373-3p	NA	Peripheral Blood Mononuclear Cells	Rheumatoid Arthritis	Homo sapiens (human)  	RNA sequencing;	34184082	circPTPN22 as a novel biomarker and ceRNA in peripheral blood mononuclear cells of rheumatoid arthritis.	The role of circular RNAs (circRNAs) in rheumatoid arthritis (RA) remains to be elucidated. To determine the expression of circRNAs in peripheral blood mononuclear cells (PBMCs) and to identify novel biomarkers for RA and explore their potential effects in RA, the present study conducted high-throughput RNA sequencing to analyze circRNA expression profiles in PBMCs from 4 RA patients and 3 healthy controls (HCs). Reverse transcription-quantitative PCR was used to verify the expression of circPTPN22 in 42 RA patients, 44 HCs and 45 systemic lupus erythematosus (SLE) patients. In addition, bioinformatics analysis and Pearson's correlation test were conducted to assess the correlation of the relationships between circPTPN22 and RA progression. A receiver operating characteristic curve was calculated to evaluate the diagnostic value. Multilevel integrated analysis identified 41 upregulated and 30 downregulated circRNAs in RA patients compared with HCs. circPTPN22 was confirmed to be a common differentially expressed gene in RA and SLE compared with HCs. Area under the curve analysis suggested the diagnostic value of circPTPN22 expression to distinguish RA patients from both HCs and SLE patients. In addition, circPTPN22 levels in RA PBMCs were correlated with RA-IgG, RA-IgM, RA-IgA, anti-cyclic citrullinated peptide (anti-CCP), rheumatoid factor and C reactive protein levels. A total of four putative microRNAs (miRNAs or miRs), namely, hsa-miR-3074-5p, hsa-miR-373-3p, hsa-miR-766-3p and hsa-miR-34c-5p, were screened to be sponged by circPTPN22 via bioinformatics analysis and then experimentally verified to be upregulated in RA PBMCs compared with controls. The data suggested that circPTPN22 might be a novel biomarker for the diagnosis of RA and participate in RA pathogenesis through a sponge mechanism.		Mol Med Rep. 2021 Aug;24(2):617. doi: 10.3892/mmr.2021.12256. Epub 2021 Jun 29.
5100	Circular RNA	circPTPN22	miR-766-3p	NA	Peripheral Blood Mononuclear Cells	Rheumatoid Arthritis	Homo sapiens (human)  	RNA sequencing;	34184082	circPTPN22 as a novel biomarker and ceRNA in peripheral blood mononuclear cells of rheumatoid arthritis.	The role of circular RNAs (circRNAs) in rheumatoid arthritis (RA) remains to be elucidated. To determine the expression of circRNAs in peripheral blood mononuclear cells (PBMCs) and to identify novel biomarkers for RA and explore their potential effects in RA, the present study conducted high-throughput RNA sequencing to analyze circRNA expression profiles in PBMCs from 4 RA patients and 3 healthy controls (HCs). Reverse transcription-quantitative PCR was used to verify the expression of circPTPN22 in 42 RA patients, 44 HCs and 45 systemic lupus erythematosus (SLE) patients. In addition, bioinformatics analysis and Pearson's correlation test were conducted to assess the correlation of the relationships between circPTPN22 and RA progression. A receiver operating characteristic curve was calculated to evaluate the diagnostic value. Multilevel integrated analysis identified 41 upregulated and 30 downregulated circRNAs in RA patients compared with HCs. circPTPN22 was confirmed to be a common differentially expressed gene in RA and SLE compared with HCs. Area under the curve analysis suggested the diagnostic value of circPTPN22 expression to distinguish RA patients from both HCs and SLE patients. In addition, circPTPN22 levels in RA PBMCs were correlated with RA-IgG, RA-IgM, RA-IgA, anti-cyclic citrullinated peptide (anti-CCP), rheumatoid factor and C reactive protein levels. A total of four putative microRNAs (miRNAs or miRs), namely, hsa-miR-3074-5p, hsa-miR-373-3p, hsa-miR-766-3p and hsa-miR-34c-5p, were screened to be sponged by circPTPN22 via bioinformatics analysis and then experimentally verified to be upregulated in RA PBMCs compared with controls. The data suggested that circPTPN22 might be a novel biomarker for the diagnosis of RA and participate in RA pathogenesis through a sponge mechanism.		Mol Med Rep. 2021 Aug;24(2):617. doi: 10.3892/mmr.2021.12256. Epub 2021 Jun 29.
5101	Circular RNA	circPTPN22	miR-34c-5p	NA	Peripheral Blood Mononuclear Cells	Rheumatoid Arthritis	Homo sapiens (human)  	RNA sequencing;	34184082	circPTPN22 as a novel biomarker and ceRNA in peripheral blood mononuclear cells of rheumatoid arthritis.	The role of circular RNAs (circRNAs) in rheumatoid arthritis (RA) remains to be elucidated. To determine the expression of circRNAs in peripheral blood mononuclear cells (PBMCs) and to identify novel biomarkers for RA and explore their potential effects in RA, the present study conducted high-throughput RNA sequencing to analyze circRNA expression profiles in PBMCs from 4 RA patients and 3 healthy controls (HCs). Reverse transcription-quantitative PCR was used to verify the expression of circPTPN22 in 42 RA patients, 44 HCs and 45 systemic lupus erythematosus (SLE) patients. In addition, bioinformatics analysis and Pearson's correlation test were conducted to assess the correlation of the relationships between circPTPN22 and RA progression. A receiver operating characteristic curve was calculated to evaluate the diagnostic value. Multilevel integrated analysis identified 41 upregulated and 30 downregulated circRNAs in RA patients compared with HCs. circPTPN22 was confirmed to be a common differentially expressed gene in RA and SLE compared with HCs. Area under the curve analysis suggested the diagnostic value of circPTPN22 expression to distinguish RA patients from both HCs and SLE patients. In addition, circPTPN22 levels in RA PBMCs were correlated with RA-IgG, RA-IgM, RA-IgA, anti-cyclic citrullinated peptide (anti-CCP), rheumatoid factor and C reactive protein levels. A total of four putative microRNAs (miRNAs or miRs), namely, hsa-miR-3074-5p, hsa-miR-373-3p, hsa-miR-766-3p and hsa-miR-34c-5p, were screened to be sponged by circPTPN22 via bioinformatics analysis and then experimentally verified to be upregulated in RA PBMCs compared with controls. The data suggested that circPTPN22 might be a novel biomarker for the diagnosis of RA and participate in RA pathogenesis through a sponge mechanism.		Mol Med Rep. 2021 Aug;24(2):617. doi: 10.3892/mmr.2021.12256. Epub 2021 Jun 29.
5102	Circular RNA	circ-0005105	miR-20a-3p	COL11A1	Pdac Tissues And Cell Lines	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)  	qRT-PCR;RNA immunoprecipitation;RNA immunoprecipitation;	34183642	Circ-0005105 activates COL11A1 by targeting miR-20a-3p to promote pancreatic ductal adenocarcinoma progression.	Growing evidence indicates that circular RNAs (circRNAs) are closely involved in tumorigenesis, but the association between circRNAs and pancreatic ductal adenocarcinoma (PDAC) is far from clear. Here, we focused on the functional investigation of circ-0005105, a newly identified circRNA, in PDAC progression. In the present study, we assessed circ-0005105 expression in PDAC tissues and cell lines with quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The biological functions of circ-0005105 in cellular proliferation and invasion were identified through gain- and loss-of-function experiments in vitro and in vivo. The interaction between circ-0005105 and the microRNA (miR)-20a-3p-COL11A1 (collagen type XI alpha 1) axis was examined using luciferase reporter and RNA immunoprecipitation assays. We found that circ-0005105 expression was upregulated in both PDAC tissues and cell lines. Higher circ-0005105 expression correlated positively with the malignant clinical phenotype and poor prognosis of patients with PDAC. Gain- and loss-of-function analysis showed that circ-0005105 facilitated both in vitro and in vivo cellular proliferation and invasion. Mechanistically, circ-000510 served as a competing endogenous RNA (ceRNA) of miR-20a-3p and indirectly modulated COL11A1 expression, leading to activation of epithelial-mesenchymal transition (EMT). Rescue experiments suggested that the oncogenic activity of circ-0005105 was dependent on the modulation of the miR-20a-3p-COL11A1 axis. More importantly, COL11A1 overexpression was significantly associated with poor prognosis in PDAC, and silencing COL11A1 reduced PDAC cell tumorigenicity and metastasis. Taken together, our findings confirm for the first time that circ-0005105 has critical functions by regulating the miR-20a-3p-COL11A1 axis. In the clinic, circ-0005105 can act as a potential prognostic marker and therapeutic target in PDAC.		Cell Death Dis. 2021 Jun 28;12(7):656. doi: 10.1038/s41419-021-03938-8.
5103	Circular RNA	circ_0030586	miR-665	NR4A3	Bca Tissues And Cells	Bladder Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;RACE;Western blot;Luciferase reporter assay;	34175686	Circ_0030586 inhibits cell proliferation and stemness in bladder cancer by inactivating the ERK signaling via miR-665/NR4A3 axis.	Increasing evidence reveals that circular RNAs (circRNAs) serve as oncogenes or tumor suppressors in the development of various tumors including bladder cancer (BCa). In this study, we explored the function and mechanism of circ_0030586 (also named circABCC4, ATP binding cassette subfamily C member 4) in BCa. The expression of circ_0030586 was significantly decreased in BCa tissues and cells, as suggested by RT-qPCR. The circular characteristics of circ_0030586 were verified by agarose gel electrophoresis and RNase R treatment. Colony formation, 5-Ethynyl-2'-deoxyuridine and sphere formation assays revealed that overexpression of circ_0030586 suppressed BCa cell proliferation and stemness in vitro. According to xenograft experiment, circ_0030586 overexpression suppressed tumor growth in vivo. Mechanistically, RNA pulldown and luciferase reporter assays were carried out to explore the interaction between genes. Circ_0030586 served as a competing endogenous RNA (ceRNA) for hsa-miR-665 to upregulate the expression of nuclear receptor subfamily 4 group A member 3 (NR4A3) which is a downstream target gene of miR-665 in BCa. MiR-665 exhibited high expression in BCa tissues and cells while NR4A3 expression was downregulated in BCa. MiR-665 overexpression or NR4A3 silencing reversed the suppressive effect of circ_0030586 overexpression on BCa cell proliferation and stemness. Moreover, western blot analysis revealed that circ_0030586 inactivated the extracellular signal-regulated kinase (ERK) pathway by upregulating NR4A3 expression. In conclusion, circ_0030586 inhibits BCa cell proliferation and stemness by serving as a ceRNA for miR-665 to upregulate NR4A3 expression and thus inactivate the ERK signaling.		Acta Histochem. 2021 Jul;123(5):151745. doi: 10.1016/j.acthis.2021.151745. Epub 2021 Jun 25.
5104	Circular RNA	circSLIT2	miR-510-5p	c-Myc	Pdac Tissues And Cells	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)	qRT-PCR 	34168116	Novel circular RNA circSLIT2 facilitates the aerobic glycolysis of pancreatic ductal adenocarcinoma via miR-510-5p/c-Myc/LDHA axis.	Increasing evidence has indicated the great diagnostic and therapeutic potentials of circular RNAs (circRNAs) in human cancers. Although the biological roles of circRNAs in pancreatic ductal adenocarcinoma (PDAC) have been partially annotated, the potential regulatory mechanism of circRNAs in PDAC tumorigenesis remains poorly understood. Here, our study found that the novel circRNA circSLIT2 was significantly upregulated in PDAC tissues and cells. Clinically, ectopic high-expression of circSLIT2 was correlated with unfavorable prognosis of PDAC patients. Functional experiments demonstrated that circSLIT2 promoted the aerobic glycolysis and proliferation of PDAC cells in vitro, and circSLIT2 knockdown inhibited tumor growth in vivo. Mechanistically, circSLIT2 acted as miRNA sponge to target miR-510-5p/c-Myc axis. Furthermore, c-Myc bound with the promoter region of lactate dehydrogenase A (LDHA) to activate the transcription. Collectively, present findings reveal that circSLIT2/miR-510-5p/c-Myc/LDHA axis participates in the aerobic glycolysis and carcinogenesis of PDAC, and may act as a promising therapeutic target.		Cell Death Dis. 2021 Jun 24;12(7):645. doi: 10.1038/s41419-021-03918-y.
5105	Circular RNA	circSLIT2	miR-510-5p	LDHA	Pdac Tissues And Cells	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)	qRT-PCR 	34168116	Novel circular RNA circSLIT2 facilitates the aerobic glycolysis of pancreatic ductal adenocarcinoma via miR-510-5p/c-Myc/LDHA axis.	Increasing evidence has indicated the great diagnostic and therapeutic potentials of circular RNAs (circRNAs) in human cancers. Although the biological roles of circRNAs in pancreatic ductal adenocarcinoma (PDAC) have been partially annotated, the potential regulatory mechanism of circRNAs in PDAC tumorigenesis remains poorly understood. Here, our study found that the novel circRNA circSLIT2 was significantly upregulated in PDAC tissues and cells. Clinically, ectopic high-expression of circSLIT2 was correlated with unfavorable prognosis of PDAC patients. Functional experiments demonstrated that circSLIT2 promoted the aerobic glycolysis and proliferation of PDAC cells in vitro, and circSLIT2 knockdown inhibited tumor growth in vivo. Mechanistically, circSLIT2 acted as miRNA sponge to target miR-510-5p/c-Myc axis. Furthermore, c-Myc bound with the promoter region of lactate dehydrogenase A (LDHA) to activate the transcription. Collectively, present findings reveal that circSLIT2/miR-510-5p/c-Myc/LDHA axis participates in the aerobic glycolysis and carcinogenesis of PDAC, and may act as a promising therapeutic target.		Cell Death Dis. 2021 Jun 24;12(7):645. doi: 10.1038/s41419-021-03918-y.
5106	Circular RNA	hsa_circ_0005526	miR-498	NA	Serum	Osteoarthritis	Homo sapiens (human)  	qRT-PCR 	34165827	The role of circRNA derived from RUNX2 in the serum of osteoarthritis and its clinical value.	BACKGROUND: Circular RNA (circRNA) has been shown to affect the pathological process of osteoarthritis (OA) and is expected to become a potential marker for disease diagnosis. This study aimed to investigate the association between circRNA derived from the gene of runt-related transcription factor 2 (RUNX2) and OA risk. METHODS: The expression profile of RUNX2-derived circRNAs in serum of OA patients was detected. Then, the cytological localization of screened differential circRNAs was studied. Luciferase (LUC) reporter assay was used to identify the microRNA (miRNA) sponge capacity of the circRNAs. Bioinformatics analysis was used to construct the functional pathway of this circRNA-miRNAs network. And then, the diagnostic value of RUNX2-derived circRNAs in OA was evaluated. RESULTS: RUNX2-derived hsa_circ_0005526 (circ_RUNX2) is significantly highly expressed in OA serum and mainly located in the cytoplasm within the cartilage cell by sponging multiple miRNAs (miR-498, miR-924, miR-361-3p, and miR-665). Bioinformatics analysis showed ECM-receptor interaction pathway ranked the most significant pathway of circ_RUNX2-miRNAs regulatory network in KEGG database. The ROC curve showed that there may be good diagnostic value of serum circ_RUNX2 in OA. CONCLUSION: RUNX2-derived circ_RUNX2 may be involved in OA development via ECM-receptor interaction pathways and may be used as potential clinical indicator of OA.		J Clin Lab Anal. 2021 Jul;35(7):e23858. doi: 10.1002/jcla.23858. Epub 2021 Jun 24.
5107	Circular RNA	hsa_circ_0005526	miR-924	NA	Serum	Osteoarthritis	Homo sapiens (human)  	qRT-PCR 	34165827	The role of circRNA derived from RUNX2 in the serum of osteoarthritis and its clinical value.	BACKGROUND: Circular RNA (circRNA) has been shown to affect the pathological process of osteoarthritis (OA) and is expected to become a potential marker for disease diagnosis. This study aimed to investigate the association between circRNA derived from the gene of runt-related transcription factor 2 (RUNX2) and OA risk. METHODS: The expression profile of RUNX2-derived circRNAs in serum of OA patients was detected. Then, the cytological localization of screened differential circRNAs was studied. Luciferase (LUC) reporter assay was used to identify the microRNA (miRNA) sponge capacity of the circRNAs. Bioinformatics analysis was used to construct the functional pathway of this circRNA-miRNAs network. And then, the diagnostic value of RUNX2-derived circRNAs in OA was evaluated. RESULTS: RUNX2-derived hsa_circ_0005526 (circ_RUNX2) is significantly highly expressed in OA serum and mainly located in the cytoplasm within the cartilage cell by sponging multiple miRNAs (miR-498, miR-924, miR-361-3p, and miR-665). Bioinformatics analysis showed ECM-receptor interaction pathway ranked the most significant pathway of circ_RUNX2-miRNAs regulatory network in KEGG database. The ROC curve showed that there may be good diagnostic value of serum circ_RUNX2 in OA. CONCLUSION: RUNX2-derived circ_RUNX2 may be involved in OA development via ECM-receptor interaction pathways and may be used as potential clinical indicator of OA.		J Clin Lab Anal. 2021 Jul;35(7):e23858. doi: 10.1002/jcla.23858. Epub 2021 Jun 24.
5108	Circular RNA	hsa_circ_0005526	miR-361-3p	NA	Serum	Osteoarthritis	Homo sapiens (human)  	qRT-PCR 	34165827	The role of circRNA derived from RUNX2 in the serum of osteoarthritis and its clinical value.	BACKGROUND: Circular RNA (circRNA) has been shown to affect the pathological process of osteoarthritis (OA) and is expected to become a potential marker for disease diagnosis. This study aimed to investigate the association between circRNA derived from the gene of runt-related transcription factor 2 (RUNX2) and OA risk. METHODS: The expression profile of RUNX2-derived circRNAs in serum of OA patients was detected. Then, the cytological localization of screened differential circRNAs was studied. Luciferase (LUC) reporter assay was used to identify the microRNA (miRNA) sponge capacity of the circRNAs. Bioinformatics analysis was used to construct the functional pathway of this circRNA-miRNAs network. And then, the diagnostic value of RUNX2-derived circRNAs in OA was evaluated. RESULTS: RUNX2-derived hsa_circ_0005526 (circ_RUNX2) is significantly highly expressed in OA serum and mainly located in the cytoplasm within the cartilage cell by sponging multiple miRNAs (miR-498, miR-924, miR-361-3p, and miR-665). Bioinformatics analysis showed ECM-receptor interaction pathway ranked the most significant pathway of circ_RUNX2-miRNAs regulatory network in KEGG database. The ROC curve showed that there may be good diagnostic value of serum circ_RUNX2 in OA. CONCLUSION: RUNX2-derived circ_RUNX2 may be involved in OA development via ECM-receptor interaction pathways and may be used as potential clinical indicator of OA.		J Clin Lab Anal. 2021 Jul;35(7):e23858. doi: 10.1002/jcla.23858. Epub 2021 Jun 24.
5109	Circular RNA	hsa_circ_0005526	miR-665	NA	Serum	Osteoarthritis	Homo sapiens (human)  	qRT-PCR 	34165827	The role of circRNA derived from RUNX2 in the serum of osteoarthritis and its clinical value.	BACKGROUND: Circular RNA (circRNA) has been shown to affect the pathological process of osteoarthritis (OA) and is expected to become a potential marker for disease diagnosis. This study aimed to investigate the association between circRNA derived from the gene of runt-related transcription factor 2 (RUNX2) and OA risk. METHODS: The expression profile of RUNX2-derived circRNAs in serum of OA patients was detected. Then, the cytological localization of screened differential circRNAs was studied. Luciferase (LUC) reporter assay was used to identify the microRNA (miRNA) sponge capacity of the circRNAs. Bioinformatics analysis was used to construct the functional pathway of this circRNA-miRNAs network. And then, the diagnostic value of RUNX2-derived circRNAs in OA was evaluated. RESULTS: RUNX2-derived hsa_circ_0005526 (circ_RUNX2) is significantly highly expressed in OA serum and mainly located in the cytoplasm within the cartilage cell by sponging multiple miRNAs (miR-498, miR-924, miR-361-3p, and miR-665). Bioinformatics analysis showed ECM-receptor interaction pathway ranked the most significant pathway of circ_RUNX2-miRNAs regulatory network in KEGG database. The ROC curve showed that there may be good diagnostic value of serum circ_RUNX2 in OA. CONCLUSION: RUNX2-derived circ_RUNX2 may be involved in OA development via ECM-receptor interaction pathways and may be used as potential clinical indicator of OA.		J Clin Lab Anal. 2021 Jul;35(7):e23858. doi: 10.1002/jcla.23858. Epub 2021 Jun 24.
5110	Circular RNA	hsa_circ_IPCEF1	miR-3619-5p	CASR	Ptc Tumors And Matching Adjacent Normal Tissues	Papillary Thyroid Cancer	Homo sapiens (human)  	microarray;	34165176	Circular RNA profiling reveals a potential role of hsa_circ_IPCEF1 in papillary thyroid carcinoma.	Circular RNAs (circRNAs) are a novel type of non-coding RNAs that are expressed across species and are implicated in cellular biological processes, displaying dysregulated expression in various tumorigeneses. Therefore, circRNA deregulation could be a crucial event in thyroid carcinoma. The present study identified circRNA signatures in several patients with papillary thyroid carcinoma (PTC) to complement the understanding of PTC pathogenesis. Using microarray technology, the circRNA profiles in three pairs of PTC tumors and matching adjacent normal tissues were screened. Differentially expressed circRNAs were further validated by reverse transcription-quantitative PCR in whole blood from 57 pairs of subjects. Bioinformatics data analyses including miRNA response element prediction, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway, competing endogenous RNA and KEGG Orthology-Based Annotation System analyses were performed to predict circRNA associations with cancer-related putative downstream miRNAs and target genes. Receiver operating characteristic curves and the area under the curve (AUC) values were acquired to assess the performance of validated circRNAs in predicting potential associations with PTC. In total, 158 dysregulated circRNAs were identified in PTC tumors relative to adjacent normal tissues. Notably, one downregulated circRNA (hsa_circ_IPCEF1) showed the preferable predictive power (AUC=0.8010, P<0.0001) and interactions with four cancer-related genes (CASR, CDC25B, NFkB1 and SHOC2). From these analyses, one PTC-related miRNA (hsa-miR-3619-5p) was identified as a potential target for hsa_circ_IPCEF1 sponging, indicating the hsa_circ_IPCEF1/hsa-miR-3619-5p axis in pathogenesis.		Mol Med Rep. 2021 Aug;24(2):603. doi: 10.3892/mmr.2021.12241. Epub 2021 Jun 24.
5111	Circular RNA	hsa_circ_IPCEF1	miR-3619-5p	CDC25B	Ptc Tumors And Matching Adjacent Normal Tissues	Papillary Thyroid Cancer	Homo sapiens (human)  	microarray;	34165176	Circular RNA profiling reveals a potential role of hsa_circ_IPCEF1 in papillary thyroid carcinoma.	Circular RNAs (circRNAs) are a novel type of non-coding RNAs that are expressed across species and are implicated in cellular biological processes, displaying dysregulated expression in various tumorigeneses. Therefore, circRNA deregulation could be a crucial event in thyroid carcinoma. The present study identified circRNA signatures in several patients with papillary thyroid carcinoma (PTC) to complement the understanding of PTC pathogenesis. Using microarray technology, the circRNA profiles in three pairs of PTC tumors and matching adjacent normal tissues were screened. Differentially expressed circRNAs were further validated by reverse transcription-quantitative PCR in whole blood from 57 pairs of subjects. Bioinformatics data analyses including miRNA response element prediction, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway, competing endogenous RNA and KEGG Orthology-Based Annotation System analyses were performed to predict circRNA associations with cancer-related putative downstream miRNAs and target genes. Receiver operating characteristic curves and the area under the curve (AUC) values were acquired to assess the performance of validated circRNAs in predicting potential associations with PTC. In total, 158 dysregulated circRNAs were identified in PTC tumors relative to adjacent normal tissues. Notably, one downregulated circRNA (hsa_circ_IPCEF1) showed the preferable predictive power (AUC=0.8010, P<0.0001) and interactions with four cancer-related genes (CASR, CDC25B, NFkB1 and SHOC2). From these analyses, one PTC-related miRNA (hsa-miR-3619-5p) was identified as a potential target for hsa_circ_IPCEF1 sponging, indicating the hsa_circ_IPCEF1/hsa-miR-3619-5p axis in pathogenesis.		Mol Med Rep. 2021 Aug;24(2):603. doi: 10.3892/mmr.2021.12241. Epub 2021 Jun 24.
5112	Circular RNA	hsa_circ_IPCEF1	miR-3619-5p	NFkB1	Ptc Tumors And Matching Adjacent Normal Tissues	Papillary Thyroid Cancer	Homo sapiens (human)  	microarray;	34165176	Circular RNA profiling reveals a potential role of hsa_circ_IPCEF1 in papillary thyroid carcinoma.	Circular RNAs (circRNAs) are a novel type of non-coding RNAs that are expressed across species and are implicated in cellular biological processes, displaying dysregulated expression in various tumorigeneses. Therefore, circRNA deregulation could be a crucial event in thyroid carcinoma. The present study identified circRNA signatures in several patients with papillary thyroid carcinoma (PTC) to complement the understanding of PTC pathogenesis. Using microarray technology, the circRNA profiles in three pairs of PTC tumors and matching adjacent normal tissues were screened. Differentially expressed circRNAs were further validated by reverse transcription-quantitative PCR in whole blood from 57 pairs of subjects. Bioinformatics data analyses including miRNA response element prediction, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway, competing endogenous RNA and KEGG Orthology-Based Annotation System analyses were performed to predict circRNA associations with cancer-related putative downstream miRNAs and target genes. Receiver operating characteristic curves and the area under the curve (AUC) values were acquired to assess the performance of validated circRNAs in predicting potential associations with PTC. In total, 158 dysregulated circRNAs were identified in PTC tumors relative to adjacent normal tissues. Notably, one downregulated circRNA (hsa_circ_IPCEF1) showed the preferable predictive power (AUC=0.8010, P<0.0001) and interactions with four cancer-related genes (CASR, CDC25B, NFkB1 and SHOC2). From these analyses, one PTC-related miRNA (hsa-miR-3619-5p) was identified as a potential target for hsa_circ_IPCEF1 sponging, indicating the hsa_circ_IPCEF1/hsa-miR-3619-5p axis in pathogenesis.		Mol Med Rep. 2021 Aug;24(2):603. doi: 10.3892/mmr.2021.12241. Epub 2021 Jun 24.
5113	Circular RNA	hsa_circ_IPCEF1	miR-3619-5p	SHOC2	Ptc Tumors And Matching Adjacent Normal Tissues	Papillary Thyroid Cancer	Homo sapiens (human)  	microarray;	34165176	Circular RNA profiling reveals a potential role of hsa_circ_IPCEF1 in papillary thyroid carcinoma.	Circular RNAs (circRNAs) are a novel type of non-coding RNAs that are expressed across species and are implicated in cellular biological processes, displaying dysregulated expression in various tumorigeneses. Therefore, circRNA deregulation could be a crucial event in thyroid carcinoma. The present study identified circRNA signatures in several patients with papillary thyroid carcinoma (PTC) to complement the understanding of PTC pathogenesis. Using microarray technology, the circRNA profiles in three pairs of PTC tumors and matching adjacent normal tissues were screened. Differentially expressed circRNAs were further validated by reverse transcription-quantitative PCR in whole blood from 57 pairs of subjects. Bioinformatics data analyses including miRNA response element prediction, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway, competing endogenous RNA and KEGG Orthology-Based Annotation System analyses were performed to predict circRNA associations with cancer-related putative downstream miRNAs and target genes. Receiver operating characteristic curves and the area under the curve (AUC) values were acquired to assess the performance of validated circRNAs in predicting potential associations with PTC. In total, 158 dysregulated circRNAs were identified in PTC tumors relative to adjacent normal tissues. Notably, one downregulated circRNA (hsa_circ_IPCEF1) showed the preferable predictive power (AUC=0.8010, P<0.0001) and interactions with four cancer-related genes (CASR, CDC25B, NFkB1 and SHOC2). From these analyses, one PTC-related miRNA (hsa-miR-3619-5p) was identified as a potential target for hsa_circ_IPCEF1 sponging, indicating the hsa_circ_IPCEF1/hsa-miR-3619-5p axis in pathogenesis.		Mol Med Rep. 2021 Aug;24(2):603. doi: 10.3892/mmr.2021.12241. Epub 2021 Jun 24.
5114	Circular RNA	circ-CHI3L1.2	miR-340-5p	LPAATb	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34164774	Circular RNA circ-CHI3L1.2 modulates cisplatin resistance of osteosarcoma cells via the miR-340-5p/LPAATb axis.	Resistance to chemotherapy drugs is a major factor affecting the surgical outcome and prognosis of osteosarcoma patients. Circular RNAs (circRNAs) play an important role in tumor resistance to chemotherapy. In the present study, we aimed to investigate the role and mechanism of circRNA circ-chitinase 3-like 1.2 (CHI3L1.2) in resistance to cisplatin chemotherapy in osteosarcoma. We found that circ-CHI3L1.2 levels were higher in cisplatin-resistant cells than in their parent cells. circ-CHI3L1.2 knockdown decreased the half-maximal inhibitory concentration (IC(50)) of cisplatin and the expression levels of P-glycoprotein (P-gp), multidrug-resistance protein 1 (MRP1), and glutathione-S-transferase Pi1 (GSTP1), and promoted apoptosis of cisplatin-resistant osteosarcoma cells. In addition, circ-CHI3L1.2 knockdown induced mesenchymal to epithelial transition (MET) and suppressed cell migration and invasion. The competitive endogenous RNA (ceRNA) mechanism indicated that circ-CHI3L1.2 targets the micro-RNA (miR)-340-5p-lysophosphatidic acid acyltransferase b (LPAATb) axis, and inhibition of miR-340-5p alleviates the effect of circ-CHI3L1.2 knockdown. In conclusion, circ-CHI3L1.2 levels were increased in cisplatin-resistant osteosarcoma cells and circ-CHI3L1.2 knockdown sensitized cisplatin-resistant osteosarcoma cells to cisplatin through the miR-340-5p-LPAATb axis.		Hum Cell. 2021 Sep;34(5):1558-1568. doi: 10.1007/s13577-021-00564-6. Epub 2021 Jun 23.
5115	Circular RNA	hsa_circ_0001681	miR-942-5p	TWIST1	Tc Cells	Thyroid Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34164767	Downregulation of hsa_circ_0001681 suppresses epithelial-mesenchymal transition in thyroid carcinoma via targeting to miR-942-5p/TWIST1 signaling pathway.	Thyroid carcinoma (TC) seriously threatens the health and safety of patients, and the treatment target of it still is poor. RT-qPCR and Western blot were carried out to detect the expression of genes and proteins, respectively. Cell proliferation was confirmed using colony formation assay. Transwell assay were performed to measure the cell migration and invasion. Besides, luciferase reporter assay was accomplished to ensure the target relationship between miR-942-5p and TWIST1 mRNA as well as hsa_circ_0001681. Here, we proved that hsa_circ_0001681 was increased in TC, and located majorly in the cytoplasm of TC cells. However,  miR-942-5p was decreased in TC, and was negatively correlated with hsa_circ_0001681 expression. Knockdown of hsa_circ_0001681 significantly repressed the proliferation, migration, invasion and EMT of TC cells. We also found that the process of hsa_circ_0001681 silencing limited EMT, which was obstructed by TWIST1 increasing. Moreover, hsa_circ_0001681 acted as a miRNA sponge and completed with TWIST1 mRNA for binding to miR-942-5p, thus downregulation of hsa_circ_0001681 repressed EMT and subsequent malignant phenotype of TC cells through targeting miR-942-5p/TWIST1 signaling pathway. Finally, the studies in vivo showed that decreasing of hsa_circ_0001681 effectively inhibited the growth of tumor via repressing EMT by regulating miR-942-5p/TWIST1 signaling pathway. Overall, silencing of hsa_circ_0001681 significantly suppressed TC progression through inhibiting EMT via acting as a miR-942-5p sponge to facilitate the expression of TWIST1. Our data provided a reliable evidence for hsa_circ_0001681 is a potential treatment target in TC.		J Bioenerg Biomembr. 2021 Jun 23. doi: 10.1007/s10863-021-09907-2.
5116	Circular RNA	HIPK3	miR-637	NUPR1	Oscc Cells	Oral Squamous Cell Cancer	Homo sapiens (human)  	ChIP;qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;	34164494	CircRNA HIPK3 promotes the progression of oral squamous cell carcinoma through upregulation of the NUPR1/PI3K/AKT pathway by sponging miR-637.	BACKGROUND: To investigate the expression, function, and related mechanisms of circHIPK3 in oral squamous cell carcinoma (OSCC). METHODS: CircHIPK3 expression was determined by quantitative reverse transcription polymerized chain reaction (QRT-PCR) in OSCC and adjacent tissues, and the correlation between the circHIPK3 level and clinicopathological indexes of OSCC was analyzed. CircHIPK3 expressions in different OSCC cell lines were detected, cell counting kit-8 (CCK-8) and 5-bromodeoxyuridine (BrdU) assays were utilized to monitor cell proliferation and activity. Flow cytometry was adopted to detect apoptosis and transwell assay was used to detect cell invasion. The expressions of nuclear protein 1 (NUPR1), phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) (PI3K/AKT) pathway proteins, and E-cadherin, Vimentin, and N-cadherin markers of epithelial-mesenchymal transformation (EMT) were detected by Western blot or Quantitative Real-time PCR (QRT-PCR). RESULTS: Upregulated circHIPK3 was noted in OSCC tissues (compared with adjacent tissues), and its overexpression was related to OSCC size and histopathological grade. Functionally, overexpressed circHIPK3 can significantly promote EMT, proliferation, and invasion of OSCC cells and can inhibit cell apoptosis in vivo and in vitro. In addition, CircHIPK3 upregulated the activation of NUPR1 and PI3K/AKT. Bioinformatics analyses showed that miR-637 was the common target of circHIPK3 and NUPR1, while a dual luciferase reporting assay and RIP assay further demonstrated that circHIPK3 targeted miR-637 and bound to 3' UTR of NUPR1. CONCLUSIONS: CircHIPK3 demonstrates potential as a prognostic marker of OSCC and mediates OSCC progression via the miR-637-mediated NUPR1/PI3K/AKT axis.		Ann Transl Med. 2021 May;9(10):860. doi: 10.21037/atm-21-1908.
5117	Circular RNA	CircRNA_103801	miR-338-3p	HIF-1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34157832	CircRNA_103801 accelerates proliferation of osteosarcoma cells by sponging miR-338-3p and regulating HIF-1/Rap1/PI3K-Akt pathway.	This study aimed to investigate the roles of hsa_circRNA_103801 in the progression of osteosarcoma (OS) cells. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the expression level of circRNA_103801 in OS cells. Cell count kit-8 and Transwell migration and invasion assays were employed to detect the proliferation, migration, and invasion abilities of OS cells. The effects of circRNA_103801 on the apoptosis of OS cells were identified by flow cytometry. The binding relationship between circRNA_103801 and miR-338-3p was verified by bioinformatics analysis. MiR-338-3p level in OS cell lines was detected by RT-qPCR. Additionally, Western blotting was utilized to detect the expression levels of HIF-1, Rap1, PI3K, and Akt in OS cells. The results showed that the expression level of circRNA_103801 was significantly up-regulated in OS patients' tissues. Inhibiting the expression level of circRNA_103801 could attenuate the proliferation, migration, and invasion abilities of OS cells. In addition, the down-regulated expression level of circRNA_103801 could induce cell apoptosis. The results of the luciferase reporter assay suggested that circRNA_103801 could be combined with miR-338-3p, and the RT-qPCR revealed that the miR-338-3p level in OS cells after knockdown of circRNA_103801 was elevated compared with the control group. The results of Western blotting suggested that the expression levels of HIF-1, Rap1, PI3K, and Akt were elevated in OS cells. In conclusion, the circRNA_103801-miR-3388-3p-HIF-1/Rap1/PI3K-Akt pathway could be a therapeutic target of OS.		J Biol Regul Homeost Agents. 2021 May-Jun;35(3):1021-1028. doi: 10.23812/20-725-A.
5118	Circular RNA	CircRNA_103801	miR-338-3p	Rap1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34157832	CircRNA_103801 accelerates proliferation of osteosarcoma cells by sponging miR-338-3p and regulating HIF-1/Rap1/PI3K-Akt pathway.	This study aimed to investigate the roles of hsa_circRNA_103801 in the progression of osteosarcoma (OS) cells. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the expression level of circRNA_103801 in OS cells. Cell count kit-8 and Transwell migration and invasion assays were employed to detect the proliferation, migration, and invasion abilities of OS cells. The effects of circRNA_103801 on the apoptosis of OS cells were identified by flow cytometry. The binding relationship between circRNA_103801 and miR-338-3p was verified by bioinformatics analysis. MiR-338-3p level in OS cell lines was detected by RT-qPCR. Additionally, Western blotting was utilized to detect the expression levels of HIF-1, Rap1, PI3K, and Akt in OS cells. The results showed that the expression level of circRNA_103801 was significantly up-regulated in OS patients' tissues. Inhibiting the expression level of circRNA_103801 could attenuate the proliferation, migration, and invasion abilities of OS cells. In addition, the down-regulated expression level of circRNA_103801 could induce cell apoptosis. The results of the luciferase reporter assay suggested that circRNA_103801 could be combined with miR-338-3p, and the RT-qPCR revealed that the miR-338-3p level in OS cells after knockdown of circRNA_103801 was elevated compared with the control group. The results of Western blotting suggested that the expression levels of HIF-1, Rap1, PI3K, and Akt were elevated in OS cells. In conclusion, the circRNA_103801-miR-3388-3p-HIF-1/Rap1/PI3K-Akt pathway could be a therapeutic target of OS.		J Biol Regul Homeost Agents. 2021 May-Jun;35(3):1021-1028. doi: 10.23812/20-725-A.
5119	Circular RNA	CircRNA_103801	miR-338-3p	PI3K	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34157832	CircRNA_103801 accelerates proliferation of osteosarcoma cells by sponging miR-338-3p and regulating HIF-1/Rap1/PI3K-Akt pathway.	This study aimed to investigate the roles of hsa_circRNA_103801 in the progression of osteosarcoma (OS) cells. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the expression level of circRNA_103801 in OS cells. Cell count kit-8 and Transwell migration and invasion assays were employed to detect the proliferation, migration, and invasion abilities of OS cells. The effects of circRNA_103801 on the apoptosis of OS cells were identified by flow cytometry. The binding relationship between circRNA_103801 and miR-338-3p was verified by bioinformatics analysis. MiR-338-3p level in OS cell lines was detected by RT-qPCR. Additionally, Western blotting was utilized to detect the expression levels of HIF-1, Rap1, PI3K, and Akt in OS cells. The results showed that the expression level of circRNA_103801 was significantly up-regulated in OS patients' tissues. Inhibiting the expression level of circRNA_103801 could attenuate the proliferation, migration, and invasion abilities of OS cells. In addition, the down-regulated expression level of circRNA_103801 could induce cell apoptosis. The results of the luciferase reporter assay suggested that circRNA_103801 could be combined with miR-338-3p, and the RT-qPCR revealed that the miR-338-3p level in OS cells after knockdown of circRNA_103801 was elevated compared with the control group. The results of Western blotting suggested that the expression levels of HIF-1, Rap1, PI3K, and Akt were elevated in OS cells. In conclusion, the circRNA_103801-miR-3388-3p-HIF-1/Rap1/PI3K-Akt pathway could be a therapeutic target of OS.		J Biol Regul Homeost Agents. 2021 May-Jun;35(3):1021-1028. doi: 10.23812/20-725-A.
5120	Circular RNA	CircRNA_103801	miR-338-3p	Akt	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34157832	CircRNA_103801 accelerates proliferation of osteosarcoma cells by sponging miR-338-3p and regulating HIF-1/Rap1/PI3K-Akt pathway.	This study aimed to investigate the roles of hsa_circRNA_103801 in the progression of osteosarcoma (OS) cells. Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the expression level of circRNA_103801 in OS cells. Cell count kit-8 and Transwell migration and invasion assays were employed to detect the proliferation, migration, and invasion abilities of OS cells. The effects of circRNA_103801 on the apoptosis of OS cells were identified by flow cytometry. The binding relationship between circRNA_103801 and miR-338-3p was verified by bioinformatics analysis. MiR-338-3p level in OS cell lines was detected by RT-qPCR. Additionally, Western blotting was utilized to detect the expression levels of HIF-1, Rap1, PI3K, and Akt in OS cells. The results showed that the expression level of circRNA_103801 was significantly up-regulated in OS patients' tissues. Inhibiting the expression level of circRNA_103801 could attenuate the proliferation, migration, and invasion abilities of OS cells. In addition, the down-regulated expression level of circRNA_103801 could induce cell apoptosis. The results of the luciferase reporter assay suggested that circRNA_103801 could be combined with miR-338-3p, and the RT-qPCR revealed that the miR-338-3p level in OS cells after knockdown of circRNA_103801 was elevated compared with the control group. The results of Western blotting suggested that the expression levels of HIF-1, Rap1, PI3K, and Akt were elevated in OS cells. In conclusion, the circRNA_103801-miR-3388-3p-HIF-1/Rap1/PI3K-Akt pathway could be a therapeutic target of OS.		J Biol Regul Homeost Agents. 2021 May-Jun;35(3):1021-1028. doi: 10.23812/20-725-A.
5121	LncRNA	PART1	miR-185-5p	RUNX3	Bone Marrow Mesenchymal Stem Cells	Osteogenic Differentiation	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Western blot;Rescue assay;	34431433	LncRNA PART1/miR-185-5p/RUNX3 feedback loop modulates osteogenic differentiation of bone marrow mesenchymal stem cells.	BACKGROUND: Osteogenic differentiation of human bone marrow-derived mesenchymal stem cells (hBMSCs) is essential for bone formation, and its dysfunction is reported to be associated with osteoporosis (OP). Recent researches have determined that lncRNA PART1 participates in the pathogenesis of multiple diseases. However, its role in modulating osteogenic differentiation of hBMSCs is unclear. METHODS: PART1, miR-185-5p, and RUNX3 levels were assessed via RT-qPCR. The protein levels of OCN, OSN, and COL1A1 were measured by western blotting. The osteoblastic phenotype was evaluated via ALP activity and ARS staining. The relationship between miR-185-5p and PART1 or RUNX3 was validated by luciferase reporter, RIP assays. RESULTS: PART1 and RUNX3 expression were enhanced during hBMSC osteogenic differentiation. PART1 deletion decreased OCN, OSN, and COL1A1 levels and weakened ALP activity, but promoted the apoptosis of hBMSCs. Moreover, PART1 served as a ceRNA to influence the RUNX3 level via targeting miR-185-5p. In addition, RUNX3 was verified to activate the transcription of PART1 in hBMSCs. Finally, rescue assays indicated that suppression of miR-185-5p or addition of RUNX3 partially abolished the effects of PART1 knockdown on the levels of OCN, OSX, and COL1A1 levels, ALP activity, and apoptosis. CONCLUSION: Our study elaborated that PART1/miR-185-5p/RUNX3 feedback contributed to osteogenic differentiation and inhibited the hBMSCs apoptosis, suggesting that PART1 might be a novel target for OP treatment.		Autoimmunity. 2021 Aug 25:1-8. doi: 10.1080/08916934.2021.1966771.
5122	LncRNA	HAGLR	miR-130a-3p	MeCP2	Sh-Sy5Y Cells	Parkinsons Disease	Homo sapiens (human)	microarray;Western blot;luciferase assay;	34430707	HAGLR promotes neuron differentiation through the miR-130a-3p-MeCP2 axis.	Parkinson's disease (PD) is a prevalent neurodegenerative disease. Currently, the molecular mechanisms underlying the progressions of PD are not fully understood. The human neuroblastoma cell line SH-SY5Y has been widely used as an in vitro model for PD. This study aims to investigate the molecular mechanisms of the non-coding RNA-mediated SH-SY5Y differentiation induced by retinoic acid (RA). By microArray analysis, lncRNA HAGLR was observed to be significantly upregulated during the RA-induced SH-SY5Y differentiation. Silencing HAGLR blocked the RA-induced SH-SY5Y differentiation. Moreover, bioinformatical analysis illustrated that miR-130a-3p contains binding sites for HAGLR. The RNA-pull down assay and luciferase assay demonstrated that HAGLR functioned as a ceRNA of miR-130a-3p in SH-SY5Y cells. Overexpression of miR-130a-3p effectively inhibited SH-SY5Y differentiation. We identified MeCP2, a vital molecule in neuronal diseases, to be a direct target of miR-130a-3p in SH-SY5Y cells by western blot and luciferase assays. The rescue experiments verified that recovery of miR-130a-3p in HAGLR-overexpressing SH-SY5Y cells could successfully overcome the RA-induced SH-SY5Y differentiation by targeting MeCP2. In summary, this study reveals a potential molecular mechanism for the lncRNA-HAGLR-promoted in vitro neuron differentiation by targeting the miR-130a-3p-MeCP2 axis, contributing to the understanding of the pathogenesis and progression of PD.		Open Med (Wars). 2021 Aug 5;16(1):1121-1131. doi: 10.1515/med-2021-0301. eCollection 2021.
5123	LncRNA	LINC00460	miR-149-5p	NA	Ccrcc Cells	Clear Cell Renal Cancer	Homo sapiens (human)  	qRT-PCR;	34429655	Aberration of lncRNA LINC00460 is a Promising Prognosis Factor and Associated with Progression of Clear Cell Renal Cell Carcinoma.	PURPOSE: Long noncoding RNAs have been studied more and more as potential prognostic markers. However, the prognostic of LINC00460 in clear cell renal cell carcinoma (ccRCC) has not been explored. In this study, the potential role of LINC00460 was investigated in ccRCC. PATIENTS AND METHODS: One hundred thirteen pairs of ccRCC tissues and para-normal tissues were collected. The expressions of LINC00460 in these tissues and ccRCC cells were evaluated via qRT-PCR. The prognostic value of LINC00460 was accessed with the use of Kaplan-Meier analysis and Cox proportional hazards model analysis. The influence of LINC00460 on ccRCC cell proliferation, migration, and invasion was determined via cell counting kit-8 (CCK-8) and Transwell assays. RESULTS: The results revealed that LINC00460 was significantly enhanced in ccRCC tissues, as well as in ccRCC cell lines. The overexpression of LINC00460 was significantly associated with lymph node metastasis and TNM stage, and lead to poor overall survival. Knockdown of LINC00460 reduces the cell ability of proliferation, migration, and invasion. LINC00460 could sponge to miR-149-5p. CONCLUSION: LINC00460 may be developed as a prognostic biomarker and molecular therapy target for ccRCC.		Cancer Manag Res. 2021 Aug 16;13:6489-6497. doi: 10.2147/CMAR.S322747. eCollection 2021.
5124	LncRNA	SNHG17	miR-338-3p	SOX4	Escc Cells	Esophageal Squamous Cancer	Homo sapiens (human)  	qRT-PCR 	34429400	LncRNA SNHG17 regulates cell proliferation and invasion by targeting miR-338-3p/SOX4 axis in esophageal squamous cell carcinoma.	Small nucleolar RNA host gene 17 (SNHG17), a novel functional long noncoding RNA, has been demonstrated to play an essential role in the oncogenesis of several tumors. However, for esophageal squamous cell carcinoma (ESCC) the expression pattern and detailed function of SNHG17 are largely unknown. Hence, we conducted this study to explore potential roles and underlying oncogenic mechanisms for SNHG17 in ESCC progression. Results demonstrated SNHG17 to be markedly upregulated in ESCC. Knockdown of SNHG17 significantly suppressed ESCC cell proliferation, invasion, and epithelial-mesenchymal transition in vitro and tumor growth in vivo. Online database software analysis found miR-338-3p to interact with SNHG17 with the level of miR-338-3p negatively correlated with SNHG17 levels in ESCC samples. Further, miR-338-3p was found to directly target SRY-box transcription factor 4 (SOX4) in ESCC cells. Mechanistic analysis suggested that SNHG17 acts as an endogenous "sponge" competing with miR-338-3p to regulate SOX4, thereby promoting tumor progression. These results suggest that these molecular interactions may be potential therapeutic targets for ESCC.		Cell Death Dis. 2021 Aug 24;12(9):806. doi: 10.1038/s41419-021-04093-w.
5125	LncRNA	ZBED3-AS1	miR-513a-5p	KLF6	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	34427978	Long noncoding RNA ZBED3-AS1 restrains breast cancer progression by targeting the microRNA-513a-5p/KLF6 axis.	Breast cancer (BC) is the most commonly occurring malignancy in women. This study aimed to investigate the functions of the long noncoding RNA ZBED3-AS1 (ZBED3-AS1) in BC and its molecular mechanisms. qRT-PCR was conducted to access the expression of ZBED3-AS1, microRNA-513a-5p (miR-513a-5p), and Kruppel like factor 6 (KLF6) in BC. Additionally, BC cell viability and proliferative capacity were measured by MTT and 5-Ethynyl-20-deoxyuridine (EdU) assays. A transwell assay was used for evaluating BC cell migration and invasion. The interactions among ZBED3-AS1, miR-513a-5p, and KLF6 in BC were confirmed by dual-luciferase reporter assay. Furthermore, feedback approaches were performed to determine whether ZBED3-AS1 influences BC cell behaviors by regulating the miR-513a-5p/KLF6 axis. The murine xenograft model was established to assess the effect of ZBED3-AS1 on tumor growth. The expression of ZBED3-AS1 and KLF6 was reduced, while miR-513a-5p expression was elevated in BC. ZBED3-AS1 elevation attenuated the malignant behaviors of BC cells, including viability, proliferative capacity, migration, and invasion. Mechanical experiments revealed that ZBED3-AS1 targeted miR-513a-5p, and miR-513a-5p targeted KLF6 in BC. Feedback approaches validated that miR-513a-5p overexpression or KLF6 depletion reversed the inhibitory effects of ZBED3-AS1 upregulation on viability, proliferative capacity, migration, and invasion of BC cells. Furthermore, ZBED3-AS1 elevation attenuated the tumor growth in the murine xenograft model. ZBED3-AS1 hindered the malignant development of BC cells by regulating the miR-513a-5p/KLF6 axis, providing a novel therapeutic target in BC.		Thorac Cancer. 2021 Aug 24. doi: 10.1111/1759-7714.14111.
5126	LncRNA	LINC00511	miR-195-5p	SOX4	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qRT-PCR 	34427967	LINC00511 promotes gastric cancer progression by regulating SOX4 and epigenetically repressing PTEN to activate PI3K/AKT pathway.	Gastric cancer (GC) serves as a common malignancy. Long non-coding RNAs (lncRNAs) have been proven to regulate many cancers, including GC. Long intergenic non-protein-coding RNA 511 (LINC00511) has been poorly studied in GC, but its detailed regulatory mechanism has not been identified. Here, LINC00511 was detected to be highly expressed in GC cells. Functional assays were conducted and uncovered that LINC00511 boosted cell proliferation, migration, stemness and EMT process while inhibiting the apoptosis of GC cells. From a series of mechanism experiments, it was found that at the transcriptional level, LINC00511 recruited EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit) to the promoter of PTEN (phosphatase and tensin homolog) and facilitated methylation of PTEN promoter. LINC00511 epigenetically repressed PTEN to activate the PI3K/AKT pathway. Moreover, SRY-box transcription factor 4 (SOX4) activated the transcription of LINC00511. At the post-transcriptional level, LINC00511 sponged miR-195-5p to elevate SOX4 expression in GC cells. On the whole, the present study disclosed that SOX4-induced LINC00511 activated SOX4 via competing endogenous RNA (ceRNA) pattern and epigenetically repressed PTEN to activate PI3K/AKT pathway by recruiting EZH2, thus facilitating GC cell proliferation, migration and stemness while inhibiting GC cell apoptosis.		J Cell Mol Med. 2021 Aug 24. doi: 10.1111/jcmm.16656.
5127	LncRNA	LINC00943	miR-142-5p	KPNA4	Sk-N-Sh Cells	Neuronal Injury	Mus musculus (mouse)	ELISA;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34427876	Berberine Attenuates MPP(+)-Induced Neuronal Injury by Regulating LINC00943/miR-142-5p/KPNA4/NF-kB Pathway in SK-N-SH Cells.	Berberine plays a neuro-protective role in neurodegenerative diseases, including Parkinson's disease (PD). Long non-coding RNAs (lncRNAs) play critical roles in PD pathogenesis. The purpose of this study was to investigate whether LINC00943 was involved in the role of berberine in PD. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) or 1-methyl-4-phenyl pyridine (MPP(+)) were used to construct PD mouse and cell models, respectively. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (Edu) assays. Inflammation and cell apoptosis were assessed by enzyme-linked immunosorbent assay (ELISA) and flow cytometry, respectively. Quantitative real-time PCR (qRT-PCR) was employed to test the expression of LINC00943, microRNA (miR)-142-5p, and karyopherin subunit alpha 4 (KPNA4) mRNA. The protein levels of NF-kB pathway-related markers and KPNA4 were measured by western blot. Oxidative stress level was assessed by corresponding kits. The interaction between miR-142-5p and LINC00943 or KPNA4 was determined via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Berberine inhibited MPP(+)-induced injury in SK-N-SH cells by promoting cell proliferation and suppressing inflammation, apoptosis, and oxidative injury. LINC00943 and KPNA4 were upregulated and miR-142-5p was downregulated in PD mouse and cell models. LINC00943 (or KPNA4) overexpression or miR-142-5p inhibition abated the neuro-protective role of berberine in PD cell model. Moreover, miR-142-5p was a target of LINC00943, and KPNA4 could specially bind to miR-142-5p. Additionally, berberine inhibited NF-kB pathway by regulating LINC00943/miR-142-5p/KPNA4 axis. Berberine protected SK-N-SH cell from MPP(+)-induced neuronal damage via regulating LINC00943/miR-142-5p/KPNA4/NF-kB pathway, highlighting novel evidence for the neuro-protective role of berberine in PD.		Neurochem Res. 2021 Aug 24. doi: 10.1007/s11064-021-03431-w.
5128	LncRNA	NEAT1	miR-9-5p	SLC26A2	Human Airway Smooth Muscle Cell	Asthma	Homo sapiens (human)	ELISA;RIP assay;Western blot;	34427073	Role of NEAT1/MiR-9-5p/SLC26A2 Pathway on Human Airway Smooth Muscle Cell.	PURPOSE: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. MATERIALS AND METHODS: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with platelet-derived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. RESULTS: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. CONCLUSION: These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.		Yonsei Med J. 2021 Sep;62(9):858-867. doi: 10.3349/ymj.2021.62.9.858.
5129	LncRNA	LINC01503	miR-766-5p	PD-L1	Ovarian Carcinoma Cells	Ovarian Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34425872	GATA1-induced upregulation of LINC01503 promotes carboplatin resistance in ovarian carcinoma by upregulating PD-L1 via sponging miR-766-5p.	BACKGROUND: Ovarian Carcinoma (OCa) is a high-mortality malignancy derived from female reproductive system. Increasing evidence has identified long non-coding RNAs (lncRNAs) as important regulators in OCa chemoresistance. In this study, we intended to explore the role of LINC01503 in OCa resistance to carboplatin (CBP). METHODS: Gene expression was measured by reverse transcription-quantitative PCR (RT-qPCR) in OCa cells. Western blot was adopted to detect protein levels of GATA1, PD-L1, E-cadherin, N-cadherin, Vimentin, Bcl-2, Bax, cleaved caspase-3. To assess the effects of LINC01503 on the resistance of OCa cells to CBP, Cell Counting Kit-8 (CCK-8), colony formation, Transwell, and flow cytometry experiments were performed to evaluate half-maximal inhibitory concentration (IC(50)), cell viability, migrative and invasive ability, as well as cell apoptosis. Dual-luciferase reporter assay was employed to assess the associations between the genes. RESULTS: LINC01503 was upregulated in CBP-resistant OCa cells. LINC01503 knockdown reduced CBP resistance in OCa cells. Besides, GATA-binding protein 1 (GATA1) activated LINC01503 transcription in CBP-resistant OCa cells. MiR-766-5p was lowly expressed in CBP-resistant cells and confirmed as a target for LINC01503. In addition, miR-766-5p overexpression increased CBP sensitivity in OCa cells. PD-L1 was verified as the target of miR-766-5p. Besides, LINC01503 upregulated PD-L1 level by regulating miR-766-5p. Furthermore, rescue experiments showed that PD-L1 overexpression abrogated the inhibited impacts of blocking LINC01503 on CBP resistance in OCa cells. CONCLUSION: GATA1-induced LINC01503 expedited CBP resistance in OCa cells via the miR-766-5p/PD-L1 axis, providing a new target for improving the efficacy of OCa chemotherapy.		J Ovarian Res. 2021 Aug 23;14(1):108. doi: 10.1186/s13048-021-00856-3.
5130	LncRNA	Zeb1	miR-1258-x	FZD4	Caco-2 Cells	Damaging The Function Of The Intestinal Barrier	Homo sapiens (human)	qRT-PCR 	34425540	Whole transcriptome-based ceRNA network analysis revealed ochratoxin A-induced compromised intestinal tight junction proteins through WNT/Ca(2+) signaling pathway.	Ochratoxin A (OTA) is a widespread environmental pollutant that is a threat to humans and livestock and remains a global concern to public health. It has negative effects on both humans and animals that are in a continuously exposed environment. The compromised intestinal barrier caused by OTA has aroused widespread concern. This study aimed to investigate the mechanism of OTA-induced tight junction (TJ) protein damage and the relevant components of the intestinal barrier through in vivo whole transcriptome analysis combined with in vitro functional verification. Bioinformatics analysis in OTA-treated Balb/c mice demonstrated that regulated TJ protein related mRNAs were perturbed, and activated the WNT/Ca(2+) signaling pathway possibly regulated by key lncRNAs and miRNAs. Competing endogenous RNA (ceRNA) network analysis revealed that lncRNA Zeb1 regulated FZD4 binding with WNT5a to release Ca(2+) by targeting miR-1258-x and reduced the expression of TJ proteins, thus damaging the function of the intestinal barrier. An in vitro experiment with Caco-2 cells verified that an increase in Ca(2+) level was involved in OTA-induced decreases in the expression of TJ proteins. Taken together, these results will help to identify targets in the intestinal barrier that are compromised by OTA, and will provide the basis for preventing the associated hazard and risk.		Ecotoxicol Environ Saf. 2021 Aug 20;224:112637. doi: 10.1016/j.ecoenv.2021.112637.
5131	LncRNA	Zeb1	miR-1258-x	WNT5a	Caco-2 Cells	Damaging The Function Of The Intestinal Barrier	Homo sapiens (human)	qRT-PCR 	34425540	Whole transcriptome-based ceRNA network analysis revealed ochratoxin A-induced compromised intestinal tight junction proteins through WNT/Ca(2+) signaling pathway.	Ochratoxin A (OTA) is a widespread environmental pollutant that is a threat to humans and livestock and remains a global concern to public health. It has negative effects on both humans and animals that are in a continuously exposed environment. The compromised intestinal barrier caused by OTA has aroused widespread concern. This study aimed to investigate the mechanism of OTA-induced tight junction (TJ) protein damage and the relevant components of the intestinal barrier through in vivo whole transcriptome analysis combined with in vitro functional verification. Bioinformatics analysis in OTA-treated Balb/c mice demonstrated that regulated TJ protein related mRNAs were perturbed, and activated the WNT/Ca(2+) signaling pathway possibly regulated by key lncRNAs and miRNAs. Competing endogenous RNA (ceRNA) network analysis revealed that lncRNA Zeb1 regulated FZD4 binding with WNT5a to release Ca(2+) by targeting miR-1258-x and reduced the expression of TJ proteins, thus damaging the function of the intestinal barrier. An in vitro experiment with Caco-2 cells verified that an increase in Ca(2+) level was involved in OTA-induced decreases in the expression of TJ proteins. Taken together, these results will help to identify targets in the intestinal barrier that are compromised by OTA, and will provide the basis for preventing the associated hazard and risk.		Ecotoxicol Environ Saf. 2021 Aug 20;224:112637. doi: 10.1016/j.ecoenv.2021.112637.
5132	LncRNA	FOXD3-AS	microRNA-363	TFF1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	luciferase assay;	34424807	Long non-coding RNA FOXD3 antisense RNA 1 augments anti-estrogen resistance in breast cancer cells through the microRNA-363/ trefoil factor 1/ phosphatidylinositol 3-kinase/protein kinase B axis.	Long non-coding RNA (lncRNA) FOXD3 antisense RNA 1 (FOXD3-AS1) has been reported to participate in multiple processes that contribute toward the development of cancer. The present study aimed to explore the effect of lncRNA FOXD3-AS1 on anti-estrogen resistance in breast cancer (BC) cells. FOXD3-AS1 was found to be highly expressed in BC cell lines. Moreover, FOXD3-AS1 was highly expressed in estrogen receptor-negative (ER(-)) cells compared to the ER-positive (ER(+)) cells. FOXD3-AS1 overexpression in T47D and MCF-7 (ER(+)) cells enhanced the resistance of cells to tamoxifen (TMX), whereas FOX3-AS1 downregulation reduced the TMX resistance in MDA-MB-231 (ER(-)) cells. Similar results were reproduced in vivo that FOXD3-AS1 inhibition reduced the growth of xenograft tumors formed by MDA-MB-231 cells following TMX treatment whereas FOXD3-AS1 overexpression in T47D cells facilitated tumor growth. The bioinformatic analysis and luciferase assays indicated that FOXD3-AS1 sponged microRNA-363 (miR-363) to restore expression of trefoil factor 1 (TFF1) mRNA. Overexpression of miR-363 reduced T47D cell proliferation induced by FOXD3-AS1, whereas overexpression of TFF1 restored growth of MDA-MB-231 cells reduced after FOXD3-AS1 silencing. The phosphorylation of phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) was increased by FOXD3-AS1 but attenuated by miR-363. Inhibition of PI3K/Akt blocked the role of FOXD3-AS1 and reduced the TMX resistance in T47D and MCF-7 cells. Taken together, the present study suggested that FOXD3-AS1 sponges miR-363 to upregulate TFF1 expression, leading to PI3K/Akt signaling activation and anti-estrogen resistance in BC cells.		Bioengineered. 2021 Dec;12(1):5266-5278. doi: 10.1080/21655979.2021.1962694.
5133	LncRNA	LINC00261	miR-620	PTEN	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	34424120	Apatinib inhibits cell proliferation and migration of osteosarcoma via activating LINC00261/miR-620/PTEN axis.	Apatinib has been recently identified as a potential treatment option for osteosarcoma (OS). Nonetheless, the molecular mechanism of Apatinib in regulating OS progression remains unclear. To explore the downstream molecules that mediated the tumor-suppressive effect of Apatinib on OS. Expression levels of genes were detected by RT-qPCR and western blot assays. Functional assays including Transwell assay were applied to detect the proliferation, apoptosis and migration of OS cells. Molecular interactions were detected by luciferase reporter assay and RIP assay. Apatinib inhibited the proliferation and migration of OS cells. LINC00261 was down-regulated in OS cells but then up-regulated after the treatment by Apatinib. Silencing LINC00261 abrogated the suppressive effect of Apatinib on OS cell proliferation and migration. MicroRNA-620 (miR-620) could be sponged by LINC00261. Besides, miR-620 was up-regulated in OS cells and Apatinib treatment reduced miR-620 expression. Furthermore, LINC00261 acted as a competitive endogenous RNA (ceRNA) by sequestering miR-620 to up-regulate the expression of phosphatase and tensin homolog (PTEN). Moreover, Apatinib hindered in vitro cell proliferation and migration as well as the in vivo tumorigenesis of OS through LINC00261/miR-620/PTEN axis. Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.		Cell Cycle. 2021 Aug 23:1-14. doi: 10.1080/15384101.2021.1949132.
5134	LncRNA	LINC00858	miR-134-5p	TRIM44	Ovarian Cancer Cells	Ovarian Cancer	Homo sapiens (human)	MTT assay;qRT-PCR;MTT assay;	34423728	Long noncoding RNA LINC00858 promotes the progression of ovarian cancer via regulating the miR-134-5p/TRIM44 axis.	Recent studies have shown that many long noncoding RNAs (lncRNAs) are abnormally expressed in ovarian cancer and involved in the pathological progress of ovarian cancer. In the present study, we aimed to investigate the role of lncRNA LINC00858 and the potential mechanism in ovarian cancer. The qRT-PCR was used to measure the expression levels of LINC00858 and miR-134-5p in ovarian cancer tissue specimens and cell lines. Loss-of-function assays were performed to investigate the role of LINC00858 in ovarian cancer. MTT assay was carried out to measure cell proliferation. Transwell assays were performed to determine cell migration and invasion. Biological information analysis and luciferase report gene assay were used to verify potential downstream genes of LINC00858. The xenograft mouse model was established to analyze tumor growth in vivo. Our results showed that LINC00858 was highly expressed in human ovarian cancer tissues and cell lines. Knockdown of LINC00858 inhibited cell proliferation, migration and invasion of SKOV3 cells, and suppressed tumor growth in mouse xenograft models. Mechanistic studies revealed that LINC00858 acted as a sponge of miR-134-5p and then regulated TRIM44 expression in SKOV3 cells. Furthermore, rescue experiments illustrated that inhibition of miR-134-5p restored the inhibitory effects of LINC00858 knockdown on cell proliferation, migration and invasion. TRIM44 overexpression could counteract the inhibitory effects of miR-134-5p mimics on ovarian cancer cells. In conclusion, these findings demonstrated that LINC00858 exerted oncogenic role in ovarian cancer, which was mediated by miR-134-5p/TRIM44 axis. Thus, LINC00858 might be a therapeutic target for the treatment of ovarian cancer.		J Recept Signal Transduct Res. 2021 Aug 23:1-8. doi: 10.1080/10799893.2021.1968433.
5135	LncRNA	LINC00858	miR-134-5p	TRIM44	Ovarian Cancer Cells	Ovarian Cancer	Mus musculus (mouse)	MTT assay;qRT-PCR;MTT assay;	34423728	Long noncoding RNA LINC00858 promotes the progression of ovarian cancer via regulating the miR-134-5p/TRIM44 axis.	Recent studies have shown that many long noncoding RNAs (lncRNAs) are abnormally expressed in ovarian cancer and involved in the pathological progress of ovarian cancer. In the present study, we aimed to investigate the role of lncRNA LINC00858 and the potential mechanism in ovarian cancer. The qRT-PCR was used to measure the expression levels of LINC00858 and miR-134-5p in ovarian cancer tissue specimens and cell lines. Loss-of-function assays were performed to investigate the role of LINC00858 in ovarian cancer. MTT assay was carried out to measure cell proliferation. Transwell assays were performed to determine cell migration and invasion. Biological information analysis and luciferase report gene assay were used to verify potential downstream genes of LINC00858. The xenograft mouse model was established to analyze tumor growth in vivo. Our results showed that LINC00858 was highly expressed in human ovarian cancer tissues and cell lines. Knockdown of LINC00858 inhibited cell proliferation, migration and invasion of SKOV3 cells, and suppressed tumor growth in mouse xenograft models. Mechanistic studies revealed that LINC00858 acted as a sponge of miR-134-5p and then regulated TRIM44 expression in SKOV3 cells. Furthermore, rescue experiments illustrated that inhibition of miR-134-5p restored the inhibitory effects of LINC00858 knockdown on cell proliferation, migration and invasion. TRIM44 overexpression could counteract the inhibitory effects of miR-134-5p mimics on ovarian cancer cells. In conclusion, these findings demonstrated that LINC00858 exerted oncogenic role in ovarian cancer, which was mediated by miR-134-5p/TRIM44 axis. Thus, LINC00858 might be a therapeutic target for the treatment of ovarian cancer.		J Recept Signal Transduct Res. 2021 Aug 23:1-8. doi: 10.1080/10799893.2021.1968433.
5136	LncRNA	ZNF667-AS1	miR-523-3p	NA	Synovial Tissues And Fibroblast-Like Synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)  	ELISA;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34423698	LncRNA ZNF667-AS1 alleviates rheumatoid arthritis by sponging miR-523-3p and inactivating the JAK/STAT signalling pathway.	BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune disease, which compromises the synovial membrane resulting in chronic inflammation. Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) are implicated in the pathogenesis of RA. This study investigated the role of lncRNA ZNF667-AS1 in RA progression. METHODS: Synovial tissues and fibroblast-like synoviocytes (FLSs) were obtained from patients with RA. Gene expression was measured using RT-qPCR. Chondrocytes were treated with lipopolysaccharide (LPS) to establish in vitro models of OA. Cell counting kit-8 (CCK-8), western blot, and enzyme-linked immunosorbent assay (ELISA) were used to examine the proliferation and inflammatory cytokine production in chondrocytes. Animal models of OA were established in SD rats. Peripheral blood mononuclear cells (PBMCs) were isolated from the OA rats. Flow cytometry was used to measure the changes of the inflammatory T-helper cell 17 (Th17) cells. The relationship between ZNF667-AS1 and miR-523-3p was verified by luciferase reporter assay. RESULTS: ZNF667-AS1 was downregulated in RA-FLSs and LPS-stimulated chondrocytes. ZNF667-AS1 overexpression significantly promoted cell proliferation and inhibited the production of IL-6, IL-17 and TNF-a in LPS-stimulated chondrocytes. Additionally, ZNF667-AS1 overexpression reduced the generation of CD4 + IL-17+ cells. In mechanism, ZNF667-AS1 acted a sponge for miR-523-3p. MiR-523-3p overexpression reversed the ZNF667-AS1-mediated regulation of cell proliferation and inflammation. Furthermore, miR-523-3p overexpression abolished the inhibitory effects of ZNF667-AS1 on the JAK/STAT signalling activation. CONCLUSION: ZNF667-AS1 exerts protective effects during RA development by sponging miR-523-3p and inactivating the JAK/STAT signalling.		Autoimmunity. 2021 Aug 23:1-9. doi: 10.1080/08916934.2021.1966770.
5137	LncRNA	SNHG16	miR-4500	GALNT1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34423392	Exosome-derived SNHG16 sponging miR-4500 activates HUVEC angiogenesis by targeting GALNT1 via PI3K/Akt/mTOR pathway in hepatocellular carcinoma.	Accumulating evidence suggests cancer-derived exosomes play an important role in promoting angiogenesis. Long noncoding RNA small nucleolar RNA host gene 16 (SNHG16) is known to aggravate hepatocellular carcinoma (HCC) progression. However, the function of exosomal SNHG16 in HCC angiogenesis remains unclear. In this study, the expression of SNHG16 was significantly upregulated in HCC tissues and cell lines. The proliferative, migratory, and angiogenic abilities of HUVECs were enhanced after exposure to exosomes derived from HCC cells by transmitting SNHG16. In addition, SNHG16 was validated to promote the biological function of HUVECs directly. Exosomal SNHG16 increased GALNT1 expression to promote angiogenesis via sponging miR-4500. SNHG16/miR-4500/GALNT1 axis played an important role in exosome-mediated angiogenesis and tumor growth in vitro and vivo. Furthermore, SNHG16 activated PI3K/Akt/mTOR pathway via competing endogenous miR-4500 and GALNT1. Meanwhile, the expression of plasma exosomal SNHG16 upregulated in the plasma of HCC patients. These data elucidated the essential role of exosomal SNHG16 in communication between HCC cells and endothelial cells. Exosomal SNHG16 could be utilized as a therapeutic target for anti-angiogenesis in HCC progression.		J Physiol Biochem. 2021 Aug 23. doi: 10.1007/s13105-021-00833-w.
5138	LncRNA	PANTR1	miR-587	BCL2A1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34423048	lncRNA PANTR1 Upregulates BCL2A1 Expression to Promote Tumorigenesis and Warburg Effect of Hepatocellular Carcinoma through Restraining miR-587.	Hepatocellular carcinoma (HCC) is one of the most common subtypes of malignant liver tumors, characterized by high morbidity and mortality. Due to its poor diagnosis strategy and inefficient clinical intervention, HCC has brought terrible life experiences for patients worldwide. Finding novel curative agents for HCC is urgently needed. In the current study, we hypothesized that lncRNA PANTR1 participates in HCC initiation or progression. Our study found that lncRNA PANTR1 was upregulated in HCC tumor tissues and abundantly expressed in HCC cell lines. PANTR1 knockdown inhibited cell growth and migration, promoted cell apoptosis in vitro, and suppressed tumor cell growth in vivo. Moreover, our results suggest that downregulated PANTR1 inhibited the Warburg effect in HCC cells. Underlying mechanisms of PANTR1 in HCC progression were investigated. PANTR1 acted as a competent sponge for miR-587 and downregulated miR-587 expression in HCC cells. Further, MiR-587 directly targets BCL2A1. lncRNA PANTR1 promotes HCC progression via mediating the miR-587-BCL2A1 axis. Our study identified a novel lncRNA PANTR1/miR-587/BCL2A1 axis in HCC progression. We might provide a new target for HCC basic research and clinical management.		J Immunol Res. 2021 Aug 12;2021:1736819. doi: 10.1155/2021/1736819. eCollection 2021.
5139	LncRNA	TMEM220-AS1	miR-484	MAGI1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;RNA pull-down;	34422806	Long Non-coding RNA TMEM220-AS1 Suppressed Hepatocellular Carcinoma by Regulating the miR-484/MAGI1 Axis as a Competing Endogenous RNA.	Long non-coding RNAs (lncRNAs) have a considerable regulatory influence on multiple biological processes. Nevertheless, the role of TMEM220-AS1 in hepatocellular carcinoma (HCC) remains unclear. We used The Cancer Genome Atlas (TCGA) database to analyze the differentially expressed lncRNAs. qRT-PCR was used to verify the results for a large population. The in vitro effects of TMEM220-AS1 on HCC cells were determined using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and Transwell assays in HCC cells. We used qRT-PCR and western blotting to identify the epithelial-mesenchymal transition (EMT). Moreover, we performed bioinformatics analysis, western blotting, dual luciferase reporter gene assay, RNA pull-down, and RNA binding protein immunoprecipitation (RIP) to investigate the underlying molecular mechanisms of TMEM220-AS1 function. Finally, the function of TMEM220-AS1 was verified in vivo. The results showed that TMEM220-AS1 was expressed at considerably low levels in HCC. It was demonstrated that malignant phenotypes and EMT of HCC cells were promoted by the knock down of TMEM220-AS1 both in vivo and in vitro. TMEM220-AS1, which was detected primarily in the cytoplasm, functioned as an miRNA sponge to bind miR-484 and promote the level of membrane-associated guanylate kinase, WW, and PDZ domain containing 1 (MAGI1), thereby curbing the malignant phenotypes of HCC cells. In conclusion, low levels of TMEM220-AS1 promote proliferation and metastasis through the miR-484/MAGI1 axis in HCC.		Front Cell Dev Biol. 2021 Aug 5;9:681529. doi: 10.3389/fcell.2021.681529. eCollection 2021.
5140	LncRNA	LINC01569	miR-381-3p	RAP2A	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	RT-PCR;	34422671	Long Non-Coding RNA LINC01569 Promotes Proliferation and Metastasis in Colorectal Cancer by miR-381-3p/RAP2A Axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) display regulatory function flexibly in tumor onset and developments. Our study aimed to delve into the roles of lncRNA LINC01569 (LINC01569) in colorectal cancer (CRC) progression to study the potential mechanisms. METHODS: The genetic expression profiles of miR-381-3p and LINC01569 were measured by RT-PCR. The subcellular localization of LINC01569 in CRC cells was identified using subcellular fractionation location. Loss-of-function assays were performed to explore the potential effects of LINC01569 on CRC progression. Dual-luciferase reporter analysis was employed to verify the binding connections among LINC01569, miR-381-3p, and RAP2A. RESULTS: LINC01569 expression was distinctly increased in CRC. Curiously, if LINC01569 is removed, CRC cells will not migrate, proliferate, and invade remarkably. Molecular mechanism exploration uncovered that LINC01569 acted as a ceRNA competing with RAP2A to bind with miR-381-3p. Furthermore, rescue experiments corroborated the fact that miR-381-3p suppression reversed the inhibitory actions of LINC01569 knockdown on the expression of RAP2A and CRC progression. CONCLUSION: Overall, our findings indicate that LINC01569 plays a key role in CRC development by means of aiming at the miR-381-3p/RAP2A axis and can be equivalent to an underlying medicinal target to save CRC patients.		Front Oncol. 2021 Aug 6;11:727698. doi: 10.3389/fonc.2021.727698. eCollection 2021.
5141	LncRNA	MSTRG.29039.1	miR-12119	NA	Multiple Myeloma Cells	Multiple Myeloma	Homo sapiens (human)  	Dual-luciferase reporter assay;Luciferase reporter assay;RNA sequencing;	34422217	lncRNA MSTRG.29039.1 Promotes Proliferation by Sponging hsa-miR-12119 via JAK2/STAT3 Pathway in Multiple Myeloma.	Noncoding RNA (ncRNA) is involved in the occurrence, development, metastasis, and drug resistance of tumors and involves a variety of biological functions. In addition, miRNA can regulate proliferation and migration and even regulate epigenetics to promote the development of multiple myeloma (MM). However, the mechanism of ncRNA involved in MM is still unclear, and there are many unknown ncRNAs to be explored. This research is aimed at discovering the unknown lncRNA in MM through high-throughput sequencing and to study the mechanism and role of competitive endogenous RNA (ceRNA) involved in the pathogenesis of MM for the development of novel molecular markers and potential new targeted drugs. We screened out 262 new lncRNAs with statistical differences by RNA sequencing and selected the lncRNA MSTRG.29039.1 according to the expression and function of lncRNAs and their target genes in MM. We verified that MSTRG.29039.1 and its target gene OSMR were highly expressed in MM. After knockdown of MSTRG.29039.1 in MM cell lines, the expression of OSMR was decreased, and the expression of hsa-miR-12119 was upregulated which can also promote cell apoptosis and inhibit proliferation. Then, we knocked down hsa-miR-12119 and MSTRG.29039.1, we found that apoptosis of MM cells was reduced, and cell proliferation was increased compared with just knocking down hsa-miR-12119. We further verified the direct binding relationship between MSTRG.29039.1 and OSMR by the dual-luciferase reporter assay system. Thus, MSTRG.29039.1 can competitively bind with miRNA to counteract the inhibitory effect of miRNA on OSMR, which regulates cell proliferation and apoptosis through the JAK2/STAT3 pathway. In a conclusion, lncRNA MSTRG.29039.1 could promote proliferation by sponging hsa-miR-12119 via the JAK2/STAT3 pathway in multiple myeloma. This may be a molecular marker and a potential therapeutic target for MM.		Oxid Med Cell Longev. 2021 Aug 11;2021:9969449. doi: 10.1155/2021/9969449. eCollection 2021.
5142	LncRNA	MEG3	miR-182	NA	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	qPCR;	34421993	The Impact of Single Nucleotide Polymorphism in the Long Non-coding MEG3 Gene on MicroRNA-182 and MicroRNA-29 Expression Levels in the Development of Breast Cancer in Egyptian Women.	Early-stage detection of BC is a critical factor for effective treatment of the disease and can increase the survival rate of BC patients. Long non-coding RNAs can act as miRNA decoys by sequestering miRNAs, thus acting as competing endogenous RNAs and leading to re-expression of miRNA target genes. Maternally expressed 3 (MEG3) is LncRNA and it was reported to be tumor suppressor in breast cancer. The study aims to investigate the effect of MEG3 SNP (rs7158663 G/A) and its association with breast cancer risk in the Egyptian population. In addition, demonstrate the consequence of the MEG3 polymorphism on the expression levels of MEG3, miR-182, and miRNA-29. MEG3 rs7158663 G/A was genotyped and serum MEG3, miRNA-182, and miRNA-29 were measured in 180 breast cancer, 120 FA, and 150 controls by the qPCR. Frequencies of MEG3 rs7158663 GA/AA genotype and A allele were significantly higher in BC patients compared to the controls results showed that serum MEG3 levels were significantly lower, according to the presence of the A allele in different study groups while the expression of miR-182 and miRNA 29 were significantly elevated. MEG3, miR-182, and miRNA-29 are key genes involved in the development of BC, are considered as a novel potential non-invasive diagnostic biomarker for BC.		Front Genet. 2021 Aug 4;12:683809. doi: 10.3389/fgene.2021.683809. eCollection 2021.
5143	LncRNA	MEG3	miR-29	NA	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	qPCR;	34421993	The Impact of Single Nucleotide Polymorphism in the Long Non-coding MEG3 Gene on MicroRNA-182 and MicroRNA-29 Expression Levels in the Development of Breast Cancer in Egyptian Women.	Early-stage detection of BC is a critical factor for effective treatment of the disease and can increase the survival rate of BC patients. Long non-coding RNAs can act as miRNA decoys by sequestering miRNAs, thus acting as competing endogenous RNAs and leading to re-expression of miRNA target genes. Maternally expressed 3 (MEG3) is LncRNA and it was reported to be tumor suppressor in breast cancer. The study aims to investigate the effect of MEG3 SNP (rs7158663 G/A) and its association with breast cancer risk in the Egyptian population. In addition, demonstrate the consequence of the MEG3 polymorphism on the expression levels of MEG3, miR-182, and miRNA-29. MEG3 rs7158663 G/A was genotyped and serum MEG3, miRNA-182, and miRNA-29 were measured in 180 breast cancer, 120 FA, and 150 controls by the qPCR. Frequencies of MEG3 rs7158663 GA/AA genotype and A allele were significantly higher in BC patients compared to the controls results showed that serum MEG3 levels were significantly lower, according to the presence of the A allele in different study groups while the expression of miR-182 and miRNA 29 were significantly elevated. MEG3, miR-182, and miRNA-29 are key genes involved in the development of BC, are considered as a novel potential non-invasive diagnostic biomarker for BC.		Front Genet. 2021 Aug 4;12:683809. doi: 10.3389/fgene.2021.683809. eCollection 2021.
5144	LncRNA	RP11-395G23.3	miR-124-3p	ROR1	Anaplastic Thyroid Carcinoma Cells	Anaplastic Thyroid Cancer	Homo sapiens (human)	qRT-PCR;	34421987	Long Non-coding RNA RP11-395G23.3 Acts as a Competing Endogenous RNA of miR-124-3p to Regulate ROR1 in Anaplastic Thyroid Carcinoma.	Anaplastic thyroid carcinoma (ATC) is one of the most aggressive human malignancies with poor prognosis. However, the underlying mechanisms of ATC remain to be elucidated. Recently, increasing studies have focused on competitive endogenous RNA (ceRNA) to discover valuable biomarkers for the diagnosis of ATC. The present study identified 705 differentially expressed mRNAs and 47 differentially expressed lncRNAs. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were also conducted. Additionally, an lncRNA/miRNA/mRNA network was constructed which included 1103 regulatory relations. The upregulation of RP11-395G23.3 in ATC cells was confirmed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). In the loss of function assays, results suggested silencing of RP11-395G23.3 inhibited cell proliferation and induced cell apoptosis. Mechanically, RP11-395G23.3 could increase ROR1 via sponging miR-124-3p as a ceRNA. Moreover, ROR1 expression was decreased with the downregulation of RP11-395G23.3, but was rescued by the co-transfection of the miR-124-3p inhibitor in ATC cells. Our research suggested that the RP11-395G23.3/miR-124-3p/ROR1 axis potentially acted as a potential target for the diagnosis of ATC.		Front Genet. 2021 Aug 5;12:673242. doi: 10.3389/fgene.2021.673242. eCollection 2021.
5145	LncRNA	MALAT1	miR-495-3p	BUB1	Rb And Adjacent Retinal Tissue	Malignant Retinoblastoma	Homo sapiens (human)  	qPCR;	34419445	Weighted genes associated with the progression of retinoblastoma: Evidence from bioinformatic analysis.	Mechanisms underlying the development of malignant retinoblastoma (RB) remain largely unknown. The purpose of this study was to identify weighted genes that are associated with the progression of RB and to assess the usefulness of bioinformatic analysis in RB research. Bioinformatic analysis was performed to construct weighted gene co-expression and protein-protein interaction (PPI) networks and to predict long non-coding RNA (lncRNA)-microRNA (miRNA)-mRNA regulatory networks. RNA extracted from RB and adjacent retinal tissue was used to validate the results obtained from bioinformatic analysis, using a semi-quantitative PCR (qPCR) assay. Twenty-one modules were generated from 5000 most variably expressed genes. Both the light-yellow and red modules were significantly associated with the cellular anaplastic grade of RB. The genes clustered in the light-yellow module included protocadherin beta (PCDHBs) family members. The red module included 5 hub genes involved in cell division. According to the hypothesis that lncRNA may serve as a competing endogenous RNA (ceRNA) for miRNAs and modulates mRNA expression, a network was constructed between lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and cell division-related mRNAs. PCR analysis using 23 tumor tissues and 5 adjacent retinal tissue showed increased expression of PCDHB5 in tumor samples, and supported the predicted upregulation of mitotic checkpoint serine/threonine kinase (BUB1) by MALAT1 via miR-495-3p. Our study highlights the importance of bioinformatic analysis in identifying potential markers and mechanisms associated with the malignant transformation of RB, and provides evidence to suggest that PCDHB5 and the ceRNA regulatory network of MALAT1/miR-495-3p/BUB1 are involved in the progression of RB.		Exp Eye Res. 2021 Aug 19;211:108730. doi: 10.1016/j.exer.2021.108730.
5146	LncRNA	MALAT1	miR-26b	HMGA2	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	34419065	The m6A methyltransferase METTL3 controls epithelial-mesenchymal transition, migration and invasion of breast cancer through the MALAT1/miR-26b/HMGA2 axis.	BACKGROUND: Previous studies have revealed the key functions of N6-methyladenosine (m6A) modification in breast cancer (BC). MALAT1 as a highly m6A modified lncRNA associated with cancer development and metastasis, but the functional relevance of m6A methyltransferase and MALAT1 in BC is still unknown. Here, our study investigated the effects of the novel m6A methyltransferase METTL3 on epithelial-mesenchymal transition (EMT) in BC via the MALAT1/miR-26b/HMGA2 axis. METHODS: Firstly, we collected clinical BC samples and cultured BC cells, and detected mRNA and protein levels in the human samples and human cell lines by RT-qPCR and Western blot, respectively. Then, the binding of MALAT1 and miR-26b and the targeting relationship between miR-26b and HMGA2 were examined by dual-luciferase assay. Moreover, the binding of MALAT1 and miR-26b was tested by RNA pull down and RNA immunoprecipitation (RIP) assays. Methylated-RNA immunoprecipitation (Me-RIP) was used to detect the m6A modification level of MALAT1. The interaction of METTL3 and MALAT1 was detected by photoactivatable ribonucleoside-crosslinking immunoprecipitation (PAR-CLIP). Finally, effects on invasion and migration were detected by Transwell. RESULTS: In BC, the level of miR-26b was consistently low, while the levels of METTL3, MALAT1 and HMGA2 were high. Further experiments showed that METTL3 up-regulated MALAT1 expression by modulating the m6A modification of MALAT1, and that MALAT1 could promote the expression of HMGA2 by sponging miR-26b. In BC cells, we found that silencing METTL3 could inhibit EMT and tumor cell invasion by suppressing MALAT1. Furthermore, MALAT1 mediated miR-26b to target HMGA2 and promote EMT, migration, and invasion. In summary, METTL3 promoted tumorigenesis of BC via the MALAT1/miR-26b/HMGA2 axis. CONCLUSIONS: Silencing METTL3 down-regulate MALAT1 and HMGA2 by sponging miR-26b, and finally inhibit EMT, migration and invasion in BC, providing a theoretical basis for clinical treatment of BC.		Cancer Cell Int. 2021 Aug 21;21(1):441. doi: 10.1186/s12935-021-02113-5.
5147	LncRNA	OIP5-AS1	miR-152-3p	SLC7A5	Endometrial Carcinoma Cells	Endometrial Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Luciferase reporter assay;Rescue assay;	34419049	OIP5-AS1 contributes to the development in endometrial carcinoma cells by targeting miR-152-3p to up-regulate SLC7A5.	BACKGROUND: Endometrial carcinoma (EC) is one common gynecological tumor, threatening physical and psychological health of females. Huge amount of essays indicated that long non-coding RNAs (lncRNAs) were widely reported to serve as a crucial regulator in the biological movements among multiple carcinomas, including EC. METHODS: RT-qPCR was implemented to detect the expression of target genes. Loss/gain-of-function experiments certified the impacts of OIP5-AS1 and miR-152-3p on EC cell progression. RESULTS: Data of this research suggested that powerful expression of OIP5-AS1 was discovered in EC cell lines. Loss/gain-of-function assays inferred that OIP5-AS1 promoted proliferative, migratory and invasive abilities, and Epithelial-Mesenchymal Transition (EMT). In addition, we identified miR-152-3p expression was negatively modulated by OIP5-AS1. OIP5-AS1 accelerated the development of EC cells via downregulating miR-152-3p expression. SLC7A5 was selected out as a downstream target of miR-152-3p. The competing relationship between OIP5-AS1 and SLC7A5 was corroborated by luciferase reporter assay. Eventually, the results of rescue assays indicated that SLC7A5 overexpression could restore the impacts of OIP5-AS1 ablation on the progression of EC cells. CONCLUSION: Our research confirmed that OIP5-AS1 propeled the development of EC cells through targeting miR-152-3p/SLC7A5. OIP5-AS1 could be utilized as a target for EC treatment.		Cancer Cell Int. 2021 Aug 21;21(1):440. doi: 10.1186/s12935-021-02061-0.
5148	LncRNA	FAM66C	miR-23b-3p	KCND2	Intrahepatic Cholangiocarcinoma Cells	Intrahepatic Cholangiocarcinoma	Homo sapiens (human)	Western blot;	34418280	Long noncoding RNA FAM66C promotes tumor progression and glycolysis in intrahepatic cholangiocarcinoma by regulating hsa-miR-23b-3p/KCND2 axis.	Long noncoding RNAs (lncRNAs) are known to be the important regulators in cancer progression. However, the role of lncRNA FAM66C (FAM66C) is yet to be investigated in intrahepatic cholangiocarcinoma (ICC). This study aimed to investigate the effects and related mechanisms of FAM66C in ICC. Human ICC tissues and cell lines were collected. The expression levels of FAM66C, hsa-miR-23b-3p (miR-23b-3p), and KCND2 were detected by qRT-RCR. The transfection experiments were employed to measure the effect of FAM66C on cell viabilities, migration, and invasion in ICC cells by CCK-8, transwell assays. Glycolysis was investigated by glucose consumption, lactate production and ATP levels. The dual-luciferase reporter and RNA pull down assays were conducted as a means of confirming the interactions between FAM66C, miR-23b-3p, and KCND2. Furthermore, the levels of the EMT-associated proteins (KCND2, GLUT1, PKM2, and LDHA) in ICC cells were detected by western blot. FAM66C was increased in ICC tissues and cells, increased cell viability, glycolysis, migration and invasion, and decreased apoptosis were shown in FAM66C overexpressing cells. Mechanistic analyses revealed that FAM66C regulated the downstream target gene KCND2 by sponging miR-23b-3p. FAM66C effect on ICC was further validated in murine xenograft assays. FAM66C knockdown cells gave rise to tumors that were smaller in size, consistent with the role of FAM66C as a promoter of in vivo tumor growth. These data revealed that FAM66C was able to drive ICC tumor progression and glycolytic activity via the miR-23b-3p/KCND2 axis, indicating FAM66C may be a viable target for treating ICC.		Environ Toxicol. 2021 Aug 21. doi: 10.1002/tox.23346.
5149	LncRNA	PVT1	miR-152-3p	E2F3	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	ChIP;FISH;qPCR;RNA pull-down assay;Western blot;FISH;luciferase assay;RNA pull-down;	34418232	lncRNA PVT1 promotes progression of colorectal cancer by sponging miR-152-3p and regulating E2F3/MAPK8 signaling.	The purpose of this study was to investigate the pathogenesis of colorectal cancer (CRC) and the effects of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on CRC progression. Bioinformatics analysis verified PVT1 expression in tumor and normal tissues. qPCR and Western blotting were used to measure mRNA and protein levels, respectively. MTT, transwell, colony formation, and in vivo assays were used to assess the effects of PVT1 on proliferation, migration, and invasion by CRC cells. PVT1 and miR-152-3p were shown to be colocalized in CRC cells using FISH assay. The target genes of miR-152-3p were predicted and verified by bioinformatics analysis, luciferase assay and RNA pull-down assay. ChIP assay revealed that E2F3 binds with the promoter of MAPK8. PVT1 was overexpressed in CRC specimens, and its expression was higher in CRC cells than normal intestinal cells. PVT1 overexpression enhanced the proliferation, migration, and invasion of CRC cells, while PVT1 knockdown inhibited these processes. miR-152-3p was a target of PVT1, and E2F3 was a target of miR-152-3p. Rescue experiments confirmed the interaction between miR-152-3p and PVT1 and between miR-152-3p and E2F3. Luciferase and ChIP assay results confirmed that E2F3 modulates the transcriptional activation of MAPK8. PVT1 activated E2F3 signaling by sponging miR-152-3p. The PVT1/miR-152-3p/E2F3/MAPK8 axis promoted CRC progression.		Cancer Sci. 2021 Aug 21. doi: 10.1111/cas.15113.
5150	LncRNA	PVT1	miR-152-3p	MAPK8	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	ChIP;FISH;qPCR;RNA pull-down assay;Western blot;FISH;luciferase assay;RNA pull-down;	34418232	lncRNA PVT1 promotes progression of colorectal cancer by sponging miR-152-3p and regulating E2F3/MAPK8 signaling.	The purpose of this study was to investigate the pathogenesis of colorectal cancer (CRC) and the effects of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on CRC progression. Bioinformatics analysis verified PVT1 expression in tumor and normal tissues. qPCR and Western blotting were used to measure mRNA and protein levels, respectively. MTT, transwell, colony formation, and in vivo assays were used to assess the effects of PVT1 on proliferation, migration, and invasion by CRC cells. PVT1 and miR-152-3p were shown to be colocalized in CRC cells using FISH assay. The target genes of miR-152-3p were predicted and verified by bioinformatics analysis, luciferase assay and RNA pull-down assay. ChIP assay revealed that E2F3 binds with the promoter of MAPK8. PVT1 was overexpressed in CRC specimens, and its expression was higher in CRC cells than normal intestinal cells. PVT1 overexpression enhanced the proliferation, migration, and invasion of CRC cells, while PVT1 knockdown inhibited these processes. miR-152-3p was a target of PVT1, and E2F3 was a target of miR-152-3p. Rescue experiments confirmed the interaction between miR-152-3p and PVT1 and between miR-152-3p and E2F3. Luciferase and ChIP assay results confirmed that E2F3 modulates the transcriptional activation of MAPK8. PVT1 activated E2F3 signaling by sponging miR-152-3p. The PVT1/miR-152-3p/E2F3/MAPK8 axis promoted CRC progression.		Cancer Sci. 2021 Aug 21. doi: 10.1111/cas.15113.
5151	LncRNA	CCAT1	miR-140-3p	ATG5	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qPCR;luciferase assay;	34417924	LncRNA CCAT1 Upregulates ATG5 to Enhance Autophagy and Promote Gastric Cancer Development by Absorbing miR-140-3p.	BACKGROUND: Long noncoding RNA colon cancer-associated transcript 1 (LncRNA CCAT1) is highly expressed in gastric cancer tissues and plays a role in autophagy. However, the underlying mechanism still needs to be further clarified. OBJECTIVE: To study the role of LncRNA CCAT1 in regulating autophagy of gastric cancer cells, analyze its downstream targets, and elucidate the mechanism. METHODS: qPCR detected the expression of LncRNA CCAT1 in gastric cancer cells. The proliferation, migration, and invasion ability of LncRNA CCAT1 and the expression level of autophagy-related proteins in gastric cancer cells were detected. Bioinformatics method predicted the downstream targets of LncRNA CCAT1, and they were verified by dual-luciferase assay. The relationship between LncRNA CCAT1, miR-140, and ATG5 was verified by co-transfection, and the expression levels of ATG5 and ATG5-ATG12 complex proteins were detected. Finally, the role of LncRNA CCAT1 in vivo was confirmed by gastric cancer transplantation model. RESULTS: LncRNA CCAT1 was highly expressed in gastric cancer cells. LncRNA CCAT1 can promote the proliferation, migration, invasion, and autophagy activity of gastric cancer cells. LncRNA CCAT1 can bind to miR-140-3p and regulate its expression, while miR-140-3p further regulates the expression of ATG5. Overexpression of LncRNA CCAT1 can promote tumor growth in nude mice. After LncRNA CCAT1 silencing, the positive expression rate of ATG5 in nude mice was low. CONCLUSION: LncRNA CCAT1 may inhibit the expression of miR-140-3p by sponge adsorption, thus weakening its inhibitory effect on ATG5. Eventually, gastric cancer cells were more prone to autophagy under the pressure of stress.		Dig Dis Sci. 2021 Aug 21. doi: 10.1007/s10620-021-07187-9.
5152	LncRNA	NEAT1	miR-29-3p	FRS2	Hypertrophic Scar Fibroblasts	Hypertrophic Scar	Homo sapiens (human)	CCK-8 assay;RACE;RNA pull-down assay;Western blot;RNA pull-down;	34414852	Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts.	Long non-coding RNAs (lncRNAs) play crucial roles in human diseases. However, the detailed role of lncRNAs in hypertrophic scar fibroblasts (HSFs) is inadequately understood. This study aimed to investigate the potential role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in hypertrophic scarring. Expression of lncRNAs, miRNAs, and genes were detected by polymerase chain reaction; protein expression was evaluated using western blotting. Cellular function was determined using the CCK-8 assay. The interaction between microRNA (miR)-29-3p and NEAT1 or fibroblast growth factor receptor substrate 2 (FRS2) was verified by luciferase and RNA pull-down assays. The results showed that NEAT1 was overexpressed in the hypertrophic dermis and in HSFs. However, knockdown of NEAT1 suppressed the proliferation and extracellular matrix (ECM) production of HSFs. Moreover, NEAT1 functioned as a competing endogenous RNA to upregulate FRS2 by sponging miR-29-3p. Downregulation of miR-29-3p or overexpression of FRS2 antagonized the effects of NEAT1 knockdown and promoted HSF proliferation and ECM release. In conclusion, NEAT1 knockdown protected against hypertrophic scarring by modulating the miR-29-3p/FRS2 axis, which is a viable target in scar treatment.		Bioengineered. 2021 Dec;12(1):5210-5219. doi: 10.1080/21655979.2021.1959221.
5153	LncRNA	GAS5	miR-31-5p	ARID1A	Ovarian Clear Cell Carcinoma Cells	Ovarian Clear Cell Carcinoma	Homo sapiens (human)  	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34414664	LncRNA GAS5 inhibits the proliferation and invasion of ovarian clear cell carcinoma via the miR-31-5p/ARID1A axis.	To investigate the role of the lncRNA growth arrest special 5 (GAS5) in ovarian clear cell carcinoma (OCCC), we measured the expression of GAS5 and miR-31-5p in OCCC tissue samples and OCCC cell lines using RT-qPCR. MTT and colony formation assays were used to measure cell viability and colony formation ability. Cell invasion was determined by Transwell assays. The binding between GAS5 and miR-31-5p as well as miR-31-5p and ARID1A was determined by dual-luciferase reporter assays. The ARID1A protein levels were detected using western blotting. Kaplan-Meier curves were used for the analysis of the 5-year survival rate of patients with OCCC. GAS5 and ARID1A levels were significantly decreased, while miR-31-5p levels were strongly elevated in the OCCC tissues and cell lines. Patients with lower GAS5/ARID1A levels had shorter overall survival times. Overexpression of GAS5 or inhibition of miR-31-5p suppressed cell viability and invasion of OCCC cells and upregulated the protein levels of ARID1A. Moreover, overexpression of miR-31-5p reversed the effects of overexpression of GAS5. Cotransfection with pcDNA3.1-GAS5 and miR-31-5p inhibitor led to the lowest cell viability and cell invasion rates. A dual-luciferase reporter assay was performed to confirm the target relationship between GAS5 and miR-31-5p, as well as between miR-31-5p and ARID1A. LncRNA GAS5 inhibited cell viability and invasion of OCCC through activation of ARID1A by sponging miR-31-5p.		Kaohsiung J Med Sci. 2021 Aug 19. doi: 10.1002/kjm2.12420.
5154	LncRNA	RHPN1-AS1	miR-6884-5p	TOP2A	Ovarian Cancer Tissues Or Cell Lines	Ovarian Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Flow Cytometry assay;	34414458	RHPN1-AS1 promotes ovarian carcinogenesis by sponging miR-6884-5p thus releasing TOP2A mRNA.	Ovarian cancer, a severe lethal gynecological malignancy, is characterized by both high morbidity and mortality. Long noncoding RNAs (lncRNAs) have recently caused extensive concern due to their regulatory function in various human tumors. There are a mounting number of lncRNAs that are in extreme need of research, serving as biomarkers for diagnosis and therapy for ovarian cancer. In the present study, RT-qPCR was employed to detect how Rhophilin Rho GTPase binding protein 1 antisense RNA1 (RHPN1-AS1), miR-6884-5p and DNA topoisomerase IIa (TOP2A) are expressed in ovarian cancer tissues or cell lines. BrdU, MTT, colony formation and cell adhesion assays, caspase-3 activity, flow cytometry and wound healing assay were employed to assess cell proliferation, viability, colony number, adhesion, apoptosis and migration in ovarian cancer, respectively. RHPN1-AS1 was determined to be enriched in ovarian cancer tissues and cell lines. Silencing of RHPN1-AS1 was reported to increase cell apoptosis and impair cell proliferation, viability, colony number, adhesion and migration in vitro. Furthermore, RHPN1-AS1 was able to sponge miR-6884-5p which directly targets TOP2A in ovarian cancer. Notably, silencing of RHPN1-AS1 functionally reversed the oncogenic effect induced by the miR-6884-5p inhibitor, while the miR-6884-5p inhibitor markedly restored the inhibition of ovarian carcinogenesis modulated by silencing TOP2A in ovarian cancer. RHPN1-AS1 was found to promote ovarian carcinogenesis via sponging miR-6884-5p thus releasing TOP2A, and RHPN1-AS1 may act as a promising biomarker for the prognosis and therapy of ovarian cancer.		Oncol Rep. 2021 Oct;46(4):221. doi: 10.3892/or.2021.8172. Epub 2021 Aug 20.
5155	LncRNA	XIST	miR-219-5p	NA	Spinal Cord Injury Cells	Spinal Cord Injury	Homo sapiens (human)  	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34414282	Long noncoding RNA XIST knockdown relieves the injury of microglia cells after spinal cord injury by sponging miR-219-5p.	Long noncoding RNAs have been demonstrated to play crucial roles in the pathogenesis of spinal cord injury (SCI). In this study, we aimed to explore the roles and underlying mechanisms of lncRNA X-inactive specific transcript (XIST) in SCI progression. SCI mice model was constructed and evaluated by the Basso-Beattie-Bresnahan method. The SCI cell model was constructed by treating BV2 cells with lipopolysaccharide (LPS). The levels of XIST and miR-219-5p were determined by the reverse transcription quantitative polymerase chain reaction. The concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Protein levels were measured via western blot assay. Cell viability and apoptosis were evaluated by cell counting kit-8 assay and flow cytometry analysis, respectively. The relationship between XIST and miR-219-5p was analyzed by online tool starBase, dual-luciferase reporter assay, and RNA immunoprecipitation assay. As a result, the XIST level was enhanced and the miR-219-5p level was declined in the SCI mice model. XIST was also upregulated in LPS-induced BV2 cells. LPS treatment restrained BV2 cell viability and accelerated apoptosis and inflammatory response. XIST knockdown effectively weakened LPS-induced BV2 cell injury. miR-219-5p was identified as a target of XIST. Moreover, inhibition of miR-219-5p restored the impacts of XIST knockdown on cell viability, apoptosis, and inflammation in LPS-treated BV2 cells. In addition, LPS-induced XIST promoted the activation of the nuclear factor-kB (NF-kB) pathway by sponging miR-219-5p. In conclusion, XIST silencing promoted microglial cell viability and repressed apoptosis and inflammation by sponging miR-219-5p, thus promoting the recovery of SCI.		Open Med (Wars). 2021 Aug 3;16(1):1090-1100. doi: 10.1515/med-2021-0292. eCollection 2021.
5156	LncRNA	GAS5	miR-26a-5p	PTEN	Degenerative Nucleus Pulposus Cells	Intervertebral Disc Degeneration	Homo sapiens (human)  	RACE;	34413821	LncRNA GAS5 as miR-26a-5p Sponge Regulates the PTEN/PI3K/Akt Axis and Affects Extracellular Matrix Synthesis in Degenerative Nucleus Pulposus Cells in vitro.	The role of lncRNA growth arrest specific 5 (GAS5) in degenerative nucleus pulposus cell (NPC) apoptosis has been reported, but the mechanism of GAS5 in extracellular matrix (ECM) synthesis in intervertebral disc degeneration (IDD) remains unknown. We aimed to investigate the mechanism of GAS5 in ECM synthesis in degenerative NPCs. GAS5 expression was measured in degenerative NPCs (CP-H170) and normal NPCs (CP-H097). siRNA-mediated GAS5 knockdown was transfected to NPCs to detect cell viability and the expression of ECM-related genes (Collagen II, aggrecan, Collagen I, and MMP-3). Subcellular localization of GAS5 was analyzed. The downstream gene and pathway of GAS5 in degenerative NPCs were explored. As our results indicated, lncRNA GAS5 was upregulated in degenerative NPCs. Silencing GAS5 improved the viability of degenerative NPCs and increased ECM synthesis. GAS5 was mainly located in the cytoplasm of NPCs. LncRNA GAS5 sponged miR-26a-5p to regulate PTEN. Overexpression of miR-26a-5p promoted ECM synthesis in degenerative NPCs. Akt inhibitor LY294002 reversed the promotion of silencing GAS5 on ECM synthesis of degenerative NPCs. In conclusion, lncRNA GAS5 sponged miR-26a-5p to upregulate PTEN and inhibit the PI3K/Akt pathway, thus inhibiting ECM synthesis of degenerative NPCs.		Front Neurol. 2021 Aug 3;12:653341. doi: 10.3389/fneur.2021.653341. eCollection 2021.
5157	LncRNA	TUG1	miR-505-3p	VEGFA	Endothelial Cells	Corneal Neovascularization	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase reporter assay;	34411571	Knockdown of lncRNA TUG1 suppresses corneal angiogenesis through regulating miR-505-3p/VEGFA.	OBJECTIVES: Vascular endothelial growth factor A (VEGFA) is one of the major factors initiating and regulating angiogenesis. LncRNA taurine up-regulated gene 1 (TUG1) has been implicated in the pathological neovascularization. The aim of this study is to explore the function of TUG1 in regulating VEGFA-mediated angiogenesis in endothelial cells. METHODS: A total of 12 corneal neovascularization (CRNV) samples were collected form patient undergoing corneal transplantation at Tongji Hospital, Wuhan, China. qRT-PCR and Western blotting were performed to examine gene expression and protein levels. Human umbilical vein endothelial cells (HUVECs) were used as an in vitro angiogenesis model. CCK-8 proliferation assay was used to determine cell proliferation capacity and wound healing was performed to analyze cell migration ability. Dual luciferase reporter assay was used for functional interaction validation between miR-505-3p and its targets. The in vitro angiogenic potential was evaluated by tube formation assay. RESULTS: TUG1 and VEGFA were upregulated in CRNV tissues and VEGFA-treated HUVECs. TUG1 knockdown inhibited proliferation, migration and tube formation capacity of HUVECs. TUG1 regulated the angiogenesis of HUVECs by modulating VEGFA expression through targeting miR-505-3p. CONCLUSIONS: Our results suggest that lncRNA TUG1 promotes the angiogenesis of HUVECs through modulating miR-505-3p/VEGFA axis.		Microvasc Res. 2021 Aug 16:104233. doi: 10.1016/j.mvr.2021.104233.
5158	LncRNA	CRNDE	miR-543	ATG4B	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34409031	LncRNA CRNDE Promotes ATG4B-Mediated Autophagy and Alleviates the Sensitivity of Sorafenib in Hepatocellular Carcinoma Cells.	Autophagy is closely related to the growth and drug resistance of cancer cells, and autophagy related 4B (ATG4B) performs a crucial role in the process of autophagy. The long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) promotes the progression of hepatocellular carcinoma (HCC), but it is unclear whether the tumor-promoting effect of CRNDE is associated with the regulation of ATG4B and autophagy. Herein, we for the first time demonstrated that CRNDE triggered autophagy via upregulating ATG4B in HCC cells. Mechanistically, CRNDE enhanced the stability of ATG4B mRNA by sequestrating miR-543, leading to the elevation of ATG4B and autophagy in HCC cells. Moreover, sorafenib induced CRNDE and ATG4B as well as autophagy in HCC cells. Knockdown of CRNDE sensitized HCC cells to sorafenib in vitro and in vivo. Collectively, these results reveal that CRNDE drives ATG4B-mediated autophagy, which attenuates the sensitivity of sorafenib in HCC cells, suggesting that the pathway CRNDE/ATG4B/autophagy may be a novel target to develop sensitizing measures of sorafenib in HCC treatment.		Front Cell Dev Biol. 2021 Aug 2;9:687524. doi: 10.3389/fcell.2021.687524. eCollection 2021.
5159	LncRNA	TRG-AS1	miR-224-5p	SMAD4	Lung Cancer Cells	Lung Cancer	Homo sapiens (human)  	CCK-8 assay;RIP assay;RNA pull-down assay;Western blot;luciferase assay;RNA pull-down;	34408438	Long Non-Coding RNA TRG-AS1 Promoted Proliferation and Invasion of Lung Cancer Cells Through the miR-224-5p/SMAD4 Axis.	INTRODUCTION: The aim of this study was to investigate the role and mechanism of long non-coding RNA (lncRNA) TRG-AS1 in mediating the proliferation, invasion and migration of lung cancer cells as well lung tumor growth. METHODS: Firstly, the expression levels of TRG-AS1, miR-224-5p in lung cancer tissues or cells were quantified by quantitative real-time PCR. Western blot analysis was conducted to measure the expression levels of protein SMAD4. CCK-8 assay, wound healing assay and transwell assay were conducted to evaluate cell proliferation, migration and invasion, respectively. The interaction between TRG-AS1 and miR-224-5p was predicted by bioinformatics analysis. Dual-luciferase assay and RNA pull-down assay were performed to further confirm their interaction. In addition, the interaction between miR-224-5p and SMAD4 was detected by RIP assay. RESULTS: The results showed that TRG-AS1 was highly upregulated and miR-224-5p was downregulated in lung cancer. A negative correlation was found between TRG-AS1 and miR-224-5p. Furthermore, upregulation of TRG-AS1 promoted cell proliferation and invasion, while overexpression of miR-224-5p attenuated the effects of TRG-AS1. The downstream protein SMAD4 played an important role. In vivo study showed that knockdown of TRG-AS1 effectively retarded tumor growth. DISCUSSION: Our data suggested that the TRG-AS1/miR-224-5p/SMAD4 axis may be a potential therapeutic target in lung cancer.		Onco Targets Ther. 2021 Aug 10;14:4415-4426. doi: 10.2147/OTT.S297336. eCollection 2021.
5160	LncRNA	CHL1-AS1	miR-610	MDM2	Endometrial Stromal Cells	Endometriosis	Mus musculus (mouse)	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	34408418	Exosomal lncRNA CHL1-AS1 Derived from Peritoneal Macrophages Promotes the Progression of Endometriosis via the miR-610/MDM2 Axis.	BACKGROUND: Exosomes secreted by peritoneal macrophages (pMφ) are deeply involved in the development of endometriosis (EMs). Exosomes can mediate cell-to-cell communication by transferring biological molecules. This study aimed to explore the effect and mechanism of exosomal long non-coding RNA (lncRNA) CHL1-AS1 derived from pMφ on EMs. MATERIALS AND METHODS: Exosomes (exo) from pMφ were isolated, identified, and co-cultured with ectopic endometrial stromal cells (eESCs) to investigate the biological functions of pMφ-exo. qRT-PCR was used to detect the expression of lncRNA CHL1-AS1 in pMφ-exo from EMs and control patients and verify the transportation of lncRNA CHL1-AS1 from pMφ to eESCs. The effects of exosomal lncRNA CHL1-AS1 on eESC proliferation, migration, invasion, and apoptosis were also detected. The relationships among lncRNA CHL1-AS1, miR-610, and MDM2 (mouse double minute 2) were verified by dual-luciferase reporter assay. The in vivo experiments were conducted to verify the effects of exosomal lncRNA on EMs using a xenograft model of EMs. RESULTS: Exosomes from pMφ were successfully isolated. EMs-pMφ-exo promoted eESC proliferation, migration, and invasion and inhibited their apoptosis. lncRNA CHL1-AS1 was upregulated in EMs-pMφ-exo and transported from pMφ to eESCs via exosomes. lncRNA CHL1-AS1 was found to act as a competing endogenous RNA of miR-610 to promote the expression of MDM2. EMs-pMφ-exo shuttled lncRNA CHL1-AS1 to promote eESC proliferation, migration, and invasion and inhibit apoptosis by downregulating miR-610 and upregulating MDM2. Furthermore, exosomal lncRNA CHL1-AS1 promoted EMs lesions growth by increasing MDM2 in vivo. CONCLUSION: The results demonstrate that exosomal lncRNA CHL1-AS1 promotes the proliferation, migration, and invasion of eESCs and inhibits their apoptosis by downregulating miR-610 and upregulating MDM2, which might be a potential therapeutic target for EMs.		Int J Nanomedicine. 2021 Aug 12;16:5451-5464. doi: 10.2147/IJN.S323671. eCollection 2021.
5161	LncRNA	CRNDE	miR-136-5p	MCM5	Acute Myeloid Leukemia Kg-1A Cells	Acute Myeloid Leukemia	Homo sapiens (human)  	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;Rescue assay;	34408205	CRNDE enhances the expression of MCM5 and proliferation in acute myeloid leukemia KG-1a cells by sponging miR-136-5p.	The long-noncoding RNA colorectal neoplasia differentially expressed (CRNDE) gene has been considered to be crucial in tumor malignancy. Although CRNDE is highly expressed in acute myeloid leukemia (AML), its mechanism of action remains unknown. In this study, GEPIA and qRT-PCR were performed to confirm the expression of CRNDE in AML samples and cell lines, respectively. CRNDE shRNA vectors were transfected to explore the biological functions of CRNDE. The cell proliferation was assessed by the CCK8 assay, while apoptosis and cell cycle distribution were measured by flow cytometry and Western blotting. The results showed that CRNDE was overexpressed in both AML samples and cell lines. CRNDE silencing inhibited proliferation and increased apoptotic rate and cell cycle arrest of KG-1a cells. The luciferase reporter assay coupled with RIP assay revealed that CRNDE act as a ceRNA. Rescue assays demonstrated that the effects of CRNDE silencing could be reversed by miR-136-5p inhibitors. In conclusion, our results expound that the CRNDE/miR-136-5p/MCM5 axis modulates cell progression and provide a new regulatory network of CRNDE in KG-1a cells.		Sci Rep. 2021 Aug 18;11(1):16755. doi: 10.1038/s41598-021-96156-3.
5162	LncRNA	CASC9	miR-424-5p	TXNIP	Hk-2 Human Renal Tubular Epithelial Cells	Acute Kidney Injury	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;	34407684	The lncRNA CASC9 alleviates lipopolysaccharide-induced acute kidney injury by regulating the miR-424-5p/TXNIP pathway.	OBJECTIVE: This study aimed to clarify the mechanism by which the long non-coding RNA cancer susceptibility candidate 9 (CASC9) alleviates sepsis-related acute kidney injury (S-AKI). METHODS: A lipopolysaccharide (LPS)-induced AKI model was established to simulate S-AKI. HK-2 human renal tubular epithelial cells were treated with LPS to establish an in vitro model, and mice were intraperitoneally injected with LPS to generate an in vivo model. Subsequently, the mRNA expression of inflammatory and antioxidant factors was validated by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Reactive oxygen species (ROS) production was assessed using an assay kit. Apoptosis was detected by western blotting and fluorescence-activated cell sorting. RESULTS: CASC9 was significantly downregulated in the LPS-induced AKI model. CASC9 attenuated cell inflammation and apoptosis and enhanced the antioxidant capacity of cells. Regarding the mechanism, miR-424-5p was identified as the downstream target of CASC9, and the interaction between CASC9 and miR-424-5p promoted thioredoxin-interacting protein (TXNIP) expression. CONCLUSIONS: CASC9 alleviates LPS-induced AKI in vivo and in vitro, and CASC9 directly targets miR-424-5p and further promotes the expression of TXNIP. We have provided a possible reference strategy for the treatment of S-AKI.		J Int Med Res. 2021 Aug;49(8):3000605211037495. doi: 10.1177/03000605211037495.
5163	LncRNA	PURPL	MiR-338-3p	NA	Ovarian Cancer Tissues	Epithelial Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34405027	Disregulations of PURPL and MiR-338-3p Could Serve As Prognosis Biomarkers for Epithelial Ovarian Cancer.	Objective: The present study aimed to explore the expressions of long noncoding RNA (lncRNA) p53 upregulated regulator of p53 levels (PURPL) in different ovarian tissues, and to evaluate the significance of disregulations of PURPL and microRNA-338-3p (miR-338-3p) in epithelial ovarian cancer (EOC). Methods: The expressions of PURPL in ovarian cancer, the relations between PURPL and the prognosis of ovarian cancer, and the relation between PURPL and miR-338-3p were queried in multiple biomedical databases. Real-time PCR was performed to detect the expressions of PURPL in different ovarian tissues. Logistic regression analysis was used to analyze the risk factors of recurrence and death. Kaplan-Meier analysis was implemented to evaluate the relations between PURPL and miR-338-3p expressions and the survival of ovarian cancer. Results: PURPL could target miR-338-3p, PURPL were upregulated in ovarian cancer tissues, upregulation of PURPL in ovarian cancer was negatively related with the recurrence free survival (RFS) and overall survival (OS), which were indicated by biomedical databases query. Our data showed upregulations of PURPL were noted in ovarian cancer tissues. Higher expressions of PURPL were associated with more advanced FIGO stage and developed lymph node metastasis in epithelial ovarian cancer. Upregulation of PURPL was related with the recurrence (P=0.002, OR=21.482, 95%CI: 3.457~94.251) and death (P=0.004, OR=35.643, 95%CI: 2.453~84.359) of ovarian cancer patient. PURPL expressions were negatively correlated to miR-338-3p expressions in different ovarian tissues (r = -0.968, P<0.0001). Poor RFS (χ(2)=19.410, P=0.0002) and OS (χ(2)=17.600, P=0.0005) were found in patients with high level PURPL and low level miR-338-3p expressions. Conclusions: Upregulation of PURPL and downregulation of miR-338-3p were related with the poor RFS and OS of ovarian cancer, which indicated disregulations of PURPL and miR-338-3p could serve as prognosis biomarkers for epithelial ovarian cancer.		J Cancer. 2021 Jul 25;12(18):5674-5680. doi: 10.7150/jca.61327. eCollection 2021.
5164	LncRNA	NEAT1	miR-101	DNA-PKcs	Pancreatic Ductal Adenocarcinoma Tissues And Cells	Pancreatic Ductal Adenocarcinoma	Homo sapiens (human)	Western blot;luciferase assay;	34405022	NEAT1/miR-101-dependent Up-regulation of DNA-PKcs Enhances Malignant Behaviors of Pancreatic Ductal Adenocarcinoma Cells.	Background: Although we previously revealed that DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is overexpressed in pancreatic ductal adenocarcinoma (PDAC) and important for gemcitabine resistance, the role of DNA-PKcs in the progression and metastasis of PDAC remain unclear. To date, the upstream signaling events stimulating DNA-PKcs overexpression in PDAC are still not well characterized. Methods: Expression of DNA-PKcs was measured by western blot. The levels of miRNA-101 and lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) were detected by real-time PCR. Cell viability was determined by CCK-8. Cell migration and cell invasion were measured by transwell assay. The regulatory relationship between NEAT1 and miR-101 was determined by a luciferase assay. Results: DNA-PKcs expression was significantly elevated in human PDAC tissues and cells. DNA-PKcs overexpression was correlated with TNM stage and lymph node metastasis. Higher expression of DNA-PKcs was closely correlated with patients of worse overall survival (OS). DNA-PKcs knockdown suppresses malignant behaviors of PDAC cells. Further study showed that miRNA-101 level was decreased in PDAC tissues and cells, which could be responsible for DNA-PKcs overexpression and DNA-PKcs mediated oncogenic actions in PDAC cells. Moreover, NEAT1 functions as an oncogene influencing cell proliferation, migration and invasion in part by serving as a competing endogenous RNA (ceRNAs) modulating miR-101 expression, leading to up-regulation of DNA-PKcs. Conclusion: These findings suggest that NEAT1/miR-101-dependent up-regulation of DNA-PKcs promotes the malignant behaviors of PDAC cells. The NEAT1/miR-101/DNA-PKcs axis may serve as a viable prognostic marker and therapeutic target for PDAC.		J Cancer. 2021 Jul 25;12(18):5622-5632. doi: 10.7150/jca.58824. eCollection 2021.
5165	LncRNA	ALOX12-AS1	miR-3171	AGO2	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	microarray;RNA sequencing;	34407056	Long noncoding RNA ALOX12-AS1 inhibits cervical cancer cells proliferation via targeting miR-3171.	Cervical cancer is a common female malignancy worldwide, and the molecular mechanism of cervical tumorigenesis remains poorly understood. A large piece of evidence have demonstrated the important roles of long noncoding RNAs (lncRNAs) in tumorigenesis, cancer progression and drug resistance. In this study, we comprehensively analyzed the lncRNAs expression pattern in cervical cancer using RNA sequencing and microarray data from the cancer genome atlas, gene expression omnibus and Genotype Tissue Expression. Moreover, we assessed the correlation between lncRNA expression levels and cervical cancer patient's survival. We uncovered hundreds of lncRNAs that are upregulated or downregulated in cervical cancer tissues. Among these aberrantly lncRNAs, some are significantly associated with cervical patients' poorer prognosis, such as ALOX12-AS1 and LINC00173. ALOX12-AS1 expression is downregulated in cervical cancer, and over-expression of ALOX12-AS1 could inhibit cervical cancer cells proliferation in vitro. Further, mechanistically investigation revealed that ALOX12-AS1 could interact with AGO2 and sponge miR-3171, thereby antagonizing its' repression of tumor suppressor phosphatase and tensin homolog expression in cervical cancer cell. Taken together, this study provides lncRNA candidates in cervical cancer and highlights the critical role of ALOX12-AS1 in cervical cancer.		Anticancer Drugs. 2021 Aug 16. doi: 10.1097/CAD.0000000000001214.
5166	LncRNA	LINC01224	miR-2467	NA	Non-Small Lung Cancer Tissue	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RIP assay;RNA pull-down assay;Luciferase reporter assay;Rescue assay;RNA pull-down;	34403779	Long non-coding RNA LINC01224 promotes progression and cisplatin resistance in non-small lung cancer by sponging miR-2467.	Copious evidence reveals that long non-coding RNAs (lncRNAs) exert great regulatory functions in various human cancers. LINC01224 is a novel lncRNA, identified as a cancer regulator of HCC. However, the underlying mechanisms and clinical significance of LINC01224 in other types of cancers need further researches to explore. In this study, we aimed to elucidate the biological role of LINC01224 in NSCLC progression. Presently, LINNC01224 expression was elevated and miR-2467 expression was down-regulated in NSCLC, compared with standard control. Then we described the reciprocal correlation between LINC01224 and miR2467. Afterward, the dual-luciferase reporter assay, RIP assay and RNA pull-down assay validated the base-pair interaction between LINC01224 and miR-2467. Moreover, our findings demonstrated that the silence of LINC01224 inhibited cell proliferation and invasion in NSCLC and enhanced cisplatin (CDDP) sensitivity in vitro. Besides, rescue assays verified that miR-2467 inhibitor could reverse the effects on cell biological activities and CDDP resistance caused by knockdown of LINC01224. Finally, in vivo experiments implicated that knockdown of LINC01224 could inhibit NSCLC tumor growth. To sum up, LINC01224 can promote tumor progression and CDDP resistance in NSCLC via sponging miR-2467, suggesting a promising therapeutic target for better diagnosis and prognosis of NSCLC patients.		Pulm Pharmacol Ther. 2021 Aug 14:102070. doi: 10.1016/j.pupt.2021.102070.
5167	LncRNA	FOXD1-AS1	miR-369-3p	FOXD1	Oral Squamous Cell Carcinoma Cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Rescue assay;	34403535	FOXD1-AS1 upregulates FOXD1 to promote oral squamous cell carcinoma progression.	OBJECTIVES: Recently, increasing attention has been concentrated on decrypting the potential of long non-coding RNAs (lncRNAs) in influencing the progression of human tumors, oral squamous cell carcinoma (OSCC) included. The role of a novel lncRNA, forkhead box D1 antisense RNA 1 (FOXD1-AS1), has been discussed in multiple cancers. Nevertheless, its function and relevant mechanism in OSCC have been not probed yet. MATERIALS AND METHODS: FOXD1-AS1 expression was detected via RT-qPCR. Colony formation, EdU, transwell and Western blot analyses tested the functional role of FOXD1-AS1 in OSCC cells. The relationship between RNAs was assessed by a series of mechanical assays. RESULTS: FOXD1-AS1 was expressed at a high level in head and neck squamous cell carcinoma (HNSC). Knockdown of FOXD1-AS1 exerted repressive impacts on OSCC cell proliferation, migration, invasion, and EMT. Moreover, FOXD1-AS1 positively regulated its nearby gene FOXD1 via interacting with miR-369-3p. In addition, adenosine deaminase RNA specific (ADAR), known as a RNA-binding protein (RBP), was capable to bind with FOXD1-AS1 and FOXD1 simultaneously, and could regulate the stability of FOXD1 mRNA. Aside from that, rescue assays delineated that FOXD1-AS1 promoted OSCC progression via upregulating FOXD1. CONCLUSIONS: FOXD1-AS1 elevates FOXD1 expression to promote OSCC malignant phenotypes through miR-369-3p and ADAR.		Oral Dis. 2021 Aug 17. doi: 10.1111/odi.14002.
5168	LncRNA	AC016405.3	miR-22-3p	ERBB3	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	FISH;qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;FISH;luciferase assay;RNA immunoprecipitation;	34403532	AC016405.3 functions as an oncogenic long non-coding RNA by regulating ERBB3 via sponging miR-22-3p in breast cancer.	BACKGROUND: Increasing studies reported that long non-coding RNAs are involved in regulating breast cancer (BRCA) progression. However, the specific roles and mechanisms of lncRNAs in BRCA remain largely unknown. Here, we sought to explore the functions and mechanisms of AC016405.3 in BRCA progression. METHODS: Bioinformatic analysis for AC016405.3, miR-22-3p, and ERBB3 were performed on starBase. The expressions of AC016405.3, miR-22-3p, and ERBB3 were examined by RT-qPCR. The functions of AC016405.3 on the proliferation, migration, and invasion of cells were evaluated by conducting CCK-8, colony formation, wound-healing, and Transwell assays. The subcellular distribution of AC016405.3 in BRCA cells was identified by performing fluorescence in situ hybridization (FISH) and subcellular fractionation techniques. Dual-luciferase assay was applied to validate the interactions of miR-22-3p with AC016405.3 or ERBB3. The interaction between ERBB3 and miR-22-3p was also tested by Anti-Ago2 RNA immunoprecipitation (RIP) assay. RESULTS: The results showed that AC016405.3 is highly expressed in BRCA tissues as well as cells and positively correlated with poor prognosis in BRCA patients. Silencing AC016405.3 obviously repressed the malignant behaviors of BRCA cells. Mechanistically, AC016405.3 functioned as a competing endogenous RNA (ceRNA) for miR-22-3p in the cytoplasm and sponged miR-22-3p to release its suppression of ERBB3. Rescue experiments revealed that the suppression role induced by AC016405.3 depletion on malignant behaviors of BRCA cells could be obviously counter by inhibiting miR-22-3p or overexpressing ERBB3. CONCLUSION: AC016405.3 promotes BRCA progression by the derepression of ERBB3 via sponging miR-22-3p, which may represent a potential target for BRCA treatment.		J Clin Lab Anal. 2021 Aug 17:e23952. doi: 10.1002/jcla.23952.
5169	LncRNA	TUG1	miR-34a-5p	LDHA	Fibroblast-Like Synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)  	MTT assay;qRT-PCR;RACE;RNA pull-down assay;luciferase assay;MTT assay;RNA pull-down;	34403518	Influences of the lncRNA TUG1-miRNA-34a-5p network on fibroblast-like synoviocytes (FLSs) dysfunction in rheumatoid arthritis through targeting the lactate dehydrogenase A (LDHA).	BACKGROUND: Rheumatoid arthritis (RA) is a systemic and chronic inflammatory disease. The cellular glucose metabolism of fibroblast-like synoviocytes (FLSs) of RA has been revealed to be essential to the pathogenesis and development of RA. To date, the precise roles and molecular mechanisms of long noncoding RNA TUG1 in RA have not been elucidated. METHODS: TUG1 and miR-34a-5p were detected by qRT-PCR. Interactions between lncRNA-miRNA and miRNA-mRNA were validated by RNA pull-down assay and luciferase assay. The glucose metabolism was evaluated by glucose uptake and extracellular acidification rate (ECAR). Cell viability was determined by MTT assay and Annexin V assay. RESULTS: TUG1 expression was significantly upregulated in synovial fibroblast-like synoviocytes (FLSs) compared with normal FLSs. Functional assays uncovered that silence of TUG1 suppressed FLSs-RA invasion, migration, glucose metabolism, and increased apoptosis. Bioinformatics analysis indicated that TUG1 interacted with miR-34a-5p. RNA pull-down assay and luciferase assay validated that TUG1 sponged miR-34a-5p in FLSs-RA. Overexpression of miR-34a-5p effectively inhibited glucose metabolism of FLSs-RA. Furthermore, the glucose metabolism of FLSs-RA was significantly elevated compared with normal FLSs. The glucose metabolism enzyme, LDHA, was directly targeted by miR-34a-5p in FLSs. Rescue experiments validated that the miR-34a-5p-inhibited glucose metabolism of FLSs-RA was through targeting LDHA. Finally, we showed restoration of miR-34a-5p in TUG1-overexpressing FLSs-RA successfully overcame the TUG1-promoted glucose metabolism and apoptosis resistance via targeting LDHA. CONCLUSION: The present study uncovered critical roles and molecular mechanisms underlying the TUG1-mediated glucose metabolism and apoptosis of FLSs-RA through modulating the miR-34a-5p-LDHA pathway in fibroblast-like synoviocytes of rheumatoid arthritis.		J Clin Lab Anal. 2021 Aug 17:e23969. doi: 10.1002/jcla.23969.
5170	LncRNA	LINC01123	miR-1277-5p	LF5	Vascular Smooth Muscle Cells	Carotid Atherosclerosis	Homo sapiens (human)  	qRT-PCR;Western blot;	34403009	LINC01123 promotes cell proliferation and migration via regulating miR-1277-5p/KLF5 axis in ox-LDL-induced vascular smooth muscle cells.	The pathophysiological mechanism of carotid atherosclerosis (CAS) involves endothelial cell dysfunction, vascular smooth muscle cells (VSMCs), and macrophage activation, which ultimately leads to fibrosis of the vessel wall. lncRNA works weightily in the formation of CAS, but the function and mechanism of lncRNA LINC01123 in stable plaque formation are still equivocal. We collected blood samples from 35 CAS patients as well as 33 healthy volunteers. VSMCs treated with oxidized low-density lipoprotein (ox-LDL) were utilized as the CAS cell models. We applied qRT-PCR for detecting LINC01123, miR-1277-5p and KLF5 mRNA expression, CCK-8 method and BrdU test for determining cell proliferation, Transwell test for measuring cell migration, as well as Western blot for assaying KLF5 protein expression. Dual-luciferase reporter experiment was adopted for assessing the interaction between LINC01123 and miR-1277-5p, as well as KLF5 and miR-1277-5p. LINC01123 and KLF5 expression were dramatically up-regulated, while miR-1277-5p expression was down-regulated in CAS patients and ox-LDL-induced CAS cell models. Overexpressed LINC01123 notedly promoted VSMCs migration and proliferation. LINC01123 knockdown repressed cell proliferation and migration. Also, LINC01123 targeted miR-1277-5p and down-regulated its expression, while miR-1277-5p could negatively regulate KLF5 expression. LINC01123 is highly expressed in CAS patients, and promotes cell proliferation and migration via regulating miR-1277-5p/KLF5 axis in ox-LDL-induced VSMCs. It might be involved in the fibrous plaque formation.		J Mol Histol. 2021 Aug 17. doi: 10.1007/s10735-021-10010-4.
5171	LncRNA	TUG1	miR-140-3p	ANXA8	Bladder Tumors And Cells	Bladder Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Immunohistochemistry;luciferase assay;RNA immunoprecipitation;RNA pull-down;	34401471	Annexin A8 regulated by lncRNA-TUG1/miR-140-3p axis promotes bladder cancer progression and metastasis.	Bladder cancer is the ninth most diagnosed cancer in the world. This study aims to investigate the role and mechanisms of the taurine-upregulated gene 1 (TUG1)/miR-140-3p/annexin A8 (ANXA8) axis in bladder cancer. Western blotting and qRT-PCR determined the expression levels of ANXA8, miR-140-3p, TUG1, and epithelial-mesenchymal transition (EMT) markers. RNA immunoprecipitation (RIP), luciferase assay, and RNA pull-down assay validated the association among ANXA8, miR-140-3p, and TUG1. The biological functions were determined by colony formation, Annexin V-fluorescein isothiocyanate (FITC)/propidium (PI) staining, and transwell assays. Xenograft tumorigenesis detected tumor growth and metastasis in vivo. Pathological analysis was examined by hematoxylin and eosin (H&E) and immunohistochemistry (IHC) analyses. ANXA8 was elevated in bladder tumors and cells. Knockdown of ANXA8 suppressed cell growth, migration, invasion, and EMT in UMUC-3 and T24 cells. ANXA8 was determined as a miR-140-3p target gene. Overexpression of miR-140-3p suppressed cell proliferation, migration, invasion, and EMT via targeting ANXA8. TUG1 promoted ANXA8 expression via sponging miR-140-3p. Silencing of miR-140-3p or ANXA8 overexpression abrogated the tumor-suppressive effects of TUG1 silencing on bladder cancer cell growth and metastasis. The TUG1/miR-140-3p/ANXA8 axis was also implicated in tumor growth and lung metastasis in vivo. TUG1 promotes bladder cancer progression and metastasis through activating ANXA8 by sponging miR-140-3p, which sheds light on the mechanisms of bladder cancer pathogenesis.		Mol Ther Oncolytics. 2021 Apr 20;22:36-51. doi: 10.1016/j.omto.2021.04.008. eCollection 2021 Sep 24.
5172	LncRNA	DLEU2	miR-181c-5p	NCAPG	Vascular Endothelial Cells	Hyperoxemia 	Homo sapiens (human)  	qRT-PCR 	34400675	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk.	Oxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O(2) supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capillaries are often the first to be damaged by hyperoxia, causing many serious consequences. Nevertheless, the molecular mechanism by which hyperoxia injures pulmonary capillary endothelial cells (LMECs) has not been fully elucidated. Therefore, we systematically investigated these issues using next-generation sequencing and functional research techniques by focusing on non-coding RNAs. Our results showed that hyperoxia significantly induced apoptosis and profoundly affected the transcriptome profiles of LMECs. Hyperoxia significantly up-regulated miR-181c-5p expression, while down-regulated the expressions of NCAPG and lncRNA-DLEU2 in LMECs. Moreover, LncRNA-DLEU2 could bind complementarily to miR-181c-5p and acted as a miRNA sponge to block the inhibitory effect of miR-181c-5p on its target gene NCAPG. The down-regulation of lncRNA-DLEU2 induced by hyperoxia abrogated its inhibition of miR-181c-5p function, which together with the hyperoxia-induced upregulation of miR-181c-5p, all these significantly decreased the expression of NCAPG, resulting in apoptosis of LMECs. Our results demonstrated a ceRNA network consisting of lncRNA-DLEU2, miR-181c-5p and NCAPG, which played an important role in hyperoxia-induced apoptosis of vascular endothelial injury. Our findings will contribute to the full understanding of the harmful effects of hyperoxia and to find ways for effectively mitigating its deleterious effects.		Sci Rep. 2021 Aug 16;11(1):16582. doi: 10.1038/s41598-021-95712-1.
5173	LncRNA	LINC00882	miR-3619-5p	CTNNB1	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Rescue assay;	34399990	LINC00882 plays a tumor-promoter role in colorectal cancer by targeting miR-3619-5p to up-regulate CTNNB1.	BACKGROUND: Colorectal cancer (CRC) is a common malignant tumor in gastrointestinal tract around the world. Emerging evidence has confirmed that long non-coding RNAs (lncRNAs) are closely connected to cell progression in cancers, including CRC. METHODS: RT-qPCR assays were applied to detect the expression of LINC00882, miR-3619-5p and CTNNB1. Western blot assays were performed to measure the protein level of E-cadherin, N-cadherin and CTNNB1. Transwell assay was conducted to test the cell migration. Immunofluorescence (IF) assay was performed to measure the connected protein of EMT process. RESULTS: LINC00882 was highly expressed in CRC tissues and cell lines. Knockdown of LINC00882 hindered the process of CRC. Studies on gain-of-function and loss-of-function further testified that knockdown of LINC00882 or up-regulation of miR-3619-5p hindered cell migration and EMT process in CRC cells. Moreover, rescue assay proved that the inhibition of migration ability and EMT process resulted from LINC00882 silencing could be rescued when miR-3619-5p inhibitor or pcDNA3.1/CTNNB1 was transfected into CRC cells. CONCLUSION: Our data suggested that LINC00882 promoted the progression of CRC as a ceRNA to regulate CTNNB1 via sponging miR-3619-5p. This finding would supply a novel insight for CRC therapy.		Arch Med Res. 2021 Aug 13:S0188-4409(21)00123-5. doi: 10.1016/j.arcmed.2021.06.001.
5174	LncRNA	FBXL19-AS1	miR-193a-5p.	OL1A1	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	RT-PCR;Western blot;	34399848	LncRNA FBXL19-AS1 promotes proliferation and metastasis of cervical cancer through upregulating COL1A1 as a sponge of miR-193a-5p.	BACKGROUND: Cervical cancer (CC) is one of the most common and malignant tumors in women. In this study, we aim to explore the role and mechanism of F-box and leucine rich repeat protein 19 antisense RNA 1 (FBXL19-AS1), a novel long-chain non coding RNA (lncRNA) with marked roles in a variety of tumors, in regulating the proliferation and metastasis of CC. METHODS: The expression of FBXL19-AS1, miR-193a-5p and COL1A1 were detected by RT-PCR and western blot. Gain- and loss-of functional assays of FBXL19-AS1 and miR-193a-5p were performed in CC cell lines in vitro or in vivo. The proliferation, migration, invasion, apoptosis and epithelial-mesenchymal transition (EMT) of CC cells were determined. RESULTS: FBXL19-AS1 and COL1A1 were significantly up-regulated in CC tissues, while miR-193a-5p was significantly down-regulated. Overexpression of FBXL19-AS1 significantly promoted the proliferation, migration, invasion, EMT and growth of CC cells and inhibited apoptosis, while knockdown of FBXL19-AS1 had the opposite effects. On the other hand, miR-193a-5p inhibited the proliferation and metastasis of CC cells. Mechanistically, FBXL19-AS1 functioned as a competitive endogenous RNA (ceRNA) and inhibited the expression of miR-193a-5p, which targeted at the 3'-UTR site of COL1A1 and negatively regulated COL1A1 expression. CONCLUSIONS: FBXL19-AS1 promotes the proliferation and metastasis of CC cells by sponging miR-193a-5p and up-regulating COL1A1.		J Biol Res (Thessalon). 2021 Aug 16;28(1):20. doi: 10.1186/s40709-021-00151-8.
5175	LncRNA	MEG3	miR-543	IDO1	Non-Small Cell Lung Carcinoma Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RIP assay;	34399782	Effects of LncRNA MEG3 on immunity and autophagy of non-small cell lung carcinoma through IDO signaling pathway.	BACKGROUND: The study was done to investigate the effect of LncRNA MEG3 on the immunity and autophagy of non-small cell lung carcinoma through the IDO signaling pathway. METHODS: A total of 78 cases of early NSCLC patients (research group; RG) and 69 cases of health controls (control group; CG) during the same time were included. The contents of LncRNA MEG3 and miR-543 in peripheral blood and tissues and their diagnostic values for NSCLC were detected. The relationship between LncRNA MEG3 and miR-543 and their posttreatment contents and influence on the prognosis of NSCLC patients were tested. The expression of LncRNA MEG3, miR-543, and IDO (IDO1, IDO2, and TDO proteins) in the lung tissue of rats and the immune function in the CG and the RG were detected. The effects of LncRNA MEG3 and miR-543 on the biological behavior of NSCLC cells were determined. The role of LncRNA MEG3, miR-543, and IDO in NSCLC was verified. RESULTS: LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05). LncRNA MEG3 had a negative correlation with miR-543 (P < 0.05) and influenced the prognosis of NSCLC patients (P < 0.05). LncRNA MEG3 in the lung tissue of rats using IDO inhibitor was elevated compared with that of lung carcinoma model rats (P < 0.05). The level of miR-543 was declined compared with that of lung carcinoma model rats (P < 0.05). The levels of IDO1, IDO2, and TDO proteins were evidently declined compared with those of lung carcinoma model rats (P < 0.05). Compared with lung carcinoma model rats, CD3(+), CD4(+), and CD4(+)/CD8(+) of IDO inhibitor rats were elevated, while CD8(+) was declined (P < 0.05). Cell proliferation and invasion ability and IDO1, IDO2, TDO, Beclin-1, and LC3-II proteins were declined in the sh-LncRNA MEG3 group (P < 0.05), while those in the mimics-miR-543 group were evidently elevated (P < 0.05). However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05). CONCLUSION: MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.		World J Surg Oncol. 2021 Aug 16;19(1):244. doi: 10.1186/s12957-021-02346-8.
5176	LncRNA	MEG3	miR-543	IDO2	Non-Small Cell Lung Carcinoma Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RIP assay;	34399782	Effects of LncRNA MEG3 on immunity and autophagy of non-small cell lung carcinoma through IDO signaling pathway.	BACKGROUND: The study was done to investigate the effect of LncRNA MEG3 on the immunity and autophagy of non-small cell lung carcinoma through the IDO signaling pathway. METHODS: A total of 78 cases of early NSCLC patients (research group; RG) and 69 cases of health controls (control group; CG) during the same time were included. The contents of LncRNA MEG3 and miR-543 in peripheral blood and tissues and their diagnostic values for NSCLC were detected. The relationship between LncRNA MEG3 and miR-543 and their posttreatment contents and influence on the prognosis of NSCLC patients were tested. The expression of LncRNA MEG3, miR-543, and IDO (IDO1, IDO2, and TDO proteins) in the lung tissue of rats and the immune function in the CG and the RG were detected. The effects of LncRNA MEG3 and miR-543 on the biological behavior of NSCLC cells were determined. The role of LncRNA MEG3, miR-543, and IDO in NSCLC was verified. RESULTS: LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05). LncRNA MEG3 had a negative correlation with miR-543 (P < 0.05) and influenced the prognosis of NSCLC patients (P < 0.05). LncRNA MEG3 in the lung tissue of rats using IDO inhibitor was elevated compared with that of lung carcinoma model rats (P < 0.05). The level of miR-543 was declined compared with that of lung carcinoma model rats (P < 0.05). The levels of IDO1, IDO2, and TDO proteins were evidently declined compared with those of lung carcinoma model rats (P < 0.05). Compared with lung carcinoma model rats, CD3(+), CD4(+), and CD4(+)/CD8(+) of IDO inhibitor rats were elevated, while CD8(+) was declined (P < 0.05). Cell proliferation and invasion ability and IDO1, IDO2, TDO, Beclin-1, and LC3-II proteins were declined in the sh-LncRNA MEG3 group (P < 0.05), while those in the mimics-miR-543 group were evidently elevated (P < 0.05). However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05). CONCLUSION: MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.		World J Surg Oncol. 2021 Aug 16;19(1):244. doi: 10.1186/s12957-021-02346-8.
5177	LncRNA	MEG3	miR-543	TDO	Non-Small Cell Lung Carcinoma Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RIP assay;	34399782	Effects of LncRNA MEG3 on immunity and autophagy of non-small cell lung carcinoma through IDO signaling pathway.	BACKGROUND: The study was done to investigate the effect of LncRNA MEG3 on the immunity and autophagy of non-small cell lung carcinoma through the IDO signaling pathway. METHODS: A total of 78 cases of early NSCLC patients (research group; RG) and 69 cases of health controls (control group; CG) during the same time were included. The contents of LncRNA MEG3 and miR-543 in peripheral blood and tissues and their diagnostic values for NSCLC were detected. The relationship between LncRNA MEG3 and miR-543 and their posttreatment contents and influence on the prognosis of NSCLC patients were tested. The expression of LncRNA MEG3, miR-543, and IDO (IDO1, IDO2, and TDO proteins) in the lung tissue of rats and the immune function in the CG and the RG were detected. The effects of LncRNA MEG3 and miR-543 on the biological behavior of NSCLC cells were determined. The role of LncRNA MEG3, miR-543, and IDO in NSCLC was verified. RESULTS: LncRNA MEG3 was low in peripheral blood and tissues, while miR-543 was high (P < 0.05); both had good diagnostic values for NSCLC (P < 0.05). LncRNA MEG3 had a negative correlation with miR-543 (P < 0.05) and influenced the prognosis of NSCLC patients (P < 0.05). LncRNA MEG3 in the lung tissue of rats using IDO inhibitor was elevated compared with that of lung carcinoma model rats (P < 0.05). The level of miR-543 was declined compared with that of lung carcinoma model rats (P < 0.05). The levels of IDO1, IDO2, and TDO proteins were evidently declined compared with those of lung carcinoma model rats (P < 0.05). Compared with lung carcinoma model rats, CD3(+), CD4(+), and CD4(+)/CD8(+) of IDO inhibitor rats were elevated, while CD8(+) was declined (P < 0.05). Cell proliferation and invasion ability and IDO1, IDO2, TDO, Beclin-1, and LC3-II proteins were declined in the sh-LncRNA MEG3 group (P < 0.05), while those in the mimics-miR-543 group were evidently elevated (P < 0.05). However, the double luciferase activity detection and RIP experiment confirmed that there was targeted regulation among them (P < 0.05). CONCLUSION: MEG3 has low expression in NSCLC and affects the immunity and autophagy of NSCLC cells via regulating the miR-543/IDO signaling pathway, which is effective for the treatment of NSCLC.		World J Surg Oncol. 2021 Aug 16;19(1):244. doi: 10.1186/s12957-021-02346-8.
5178	LncRNA	MALAT1	miR-155-5p	ETS1	Periodontal Ligament Stem Cells	Periodontitis	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	34399118	MALAT1 regulates osteogenic differentiation of human periodontal ligament stem cells through mediating miR-155-5p/ETS1 axis.	BACKGROUND: Osteogenic differentiation of human periodontal ligament stem cells is essential to periodontal regeneration treatment for periodontitis. This study investigated the mechanism of lncRNAs-related osteogenic differentiation. METHODS: Human periodontal ligament stem cells were extracted from human periodontal ligament and identified via flow cytometry. After being induced into osteogenic differentiation for three weeks using osteoblast inducing conditional media, human periodontal ligament stem cells were transfected with siRNA-MALAT1, or miR-155-5p inhibitor. Human periodontal ligament stem cells osteogenesis was observed by alkaline phosphatase staining, followed by alizarin red staining for evaluating mineralized nodes formation. Runt-related gene 2, collagen-1 and osteocalcin expressions were assessed by western blot and qRT-PCR. RESULTS: MALAT1 expression was assumed a negative correlation with miR-155-5p expression which was dropping over time in differentiating human periodontal ligament stem cells. MALAT1 could bind with miR-155-5p, and E26 transformation specific-1 (ETS1) was the targeted gene of miR-155-5p. Silenced MALAT1 suppressed ALP activity and mineralized nodes formation and inhibited the expressions of runt-related gene 2, collagen-1 and osteocalcin in differentiating human periodontal ligament stem cells, while miR-155-5p inhibitor reversed the effect of si-MALAT1 on differentiation of human periodontal ligament stem cells. CONCLUSION: MALAT1 modulated differentiation of human periodontal ligament stem cells via regulating miR-155-5p.		Tissue Cell. 2021 Aug 5;73:101619. doi: 10.1016/j.tice.2021.101619.
5179	LncRNA	NEAT1	miR-30a	COX-2	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;FISH;qPCR;RT-qPCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	34396632	Long noncoding RNA NEAT1 promotes tumorigenesis in H. pylori gastric cancer by sponging miR-30a to regulate COX-2/BCL9 pathway.	BACKGROUND: Helicobacter pylori (H. pylori) is a carcinogenic factor for gastric cancer. Our previous study demonstrated that H. pylori decreased the expression of micro-RNA (miRNA)-30a to promote the tumorigenesis of gastric cancer. However, the upstream regulatory molecules of miR-30a are not well elucidated. In this study, we found the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) may sponge miR-30a to regulate COX-2/BCL9 pathway. METHODS: The expression of NEAT1 was detected in gastric cancer tissues and tumor-adjacent tissues by fluorescence in situ hybridization (FISH) analysis and RT-qPCR. LncRNA-miRNA interaction networks were constructed using the RNAhybrid and starBase v.2.0. and then validated using a dual-luciferase reporter assay. The effects of NEAT1 dysregulation on the proliferative, migratory, and invasive abilities of H. pylori filtrate-infected gastric cancer cells were observed by cell counting kit-8 (CCK-8), colony formation, wound healing test, and transwell assays. Western blot and RT-qPCR were performed to detect protein and RNA expression. Immunohistochemistry (IHC) was carried out to analyze the localization and expression of COX-2 and BCL9. RESULTS: FISH and RT-qPCR demonstrated that the expression of NEAT1 was up-regulated in gastric cancer tissues, especially in H. pylori-infected gastric cancer tissues, and the expression of NEAT1 was negatively correlated with miR-30a (miR-30a-3p and miR-30a-5p). The upregulation of NEAT1 enhanced proliferation, migration, and invasion of H. pylori filtrate-infected gastric cancer cells, while the downregulation of NEAT1 decreased these abilities, and miR-30a could reverse the effect of NEAT1 on these abilities. The dual-luciferase reporter assay identified that NEAT1 directly targeted miR-30a (miR-30a-3p and miR-30a-5p). Because miR-30a (miR-30a-3p and miR-30a-5p) negatively regulates the expression of downstream COX-2 and BCL9, NEAT1 was identified to upregulate indirectly the expression of COX-2 and BCL9. IHC showed that the expression of COX-2 and BCL9 was increased in H. pylori gastric cancer tissues. CONCLUSION: The study demonstrated that lncRNA NEAT1 may act as a promoter of tumorigenesis in H. pylori gastric cancer, by sponging miR-30a (miR-30a-3p and miR-30a-5p) to regulate the COX-2/BCL9 pathway.		Helicobacter. 2021 Aug 16:e12847. doi: 10.1111/hel.12847.
5180	LncRNA	NEAT1	miR-30a	BCL9	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;FISH;qPCR;RT-qPCR;Western blot;FISH;Immunohistochemistry;Luciferase reporter assay;	34396632	Long noncoding RNA NEAT1 promotes tumorigenesis in H. pylori gastric cancer by sponging miR-30a to regulate COX-2/BCL9 pathway.	BACKGROUND: Helicobacter pylori (H. pylori) is a carcinogenic factor for gastric cancer. Our previous study demonstrated that H. pylori decreased the expression of micro-RNA (miRNA)-30a to promote the tumorigenesis of gastric cancer. However, the upstream regulatory molecules of miR-30a are not well elucidated. In this study, we found the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) may sponge miR-30a to regulate COX-2/BCL9 pathway. METHODS: The expression of NEAT1 was detected in gastric cancer tissues and tumor-adjacent tissues by fluorescence in situ hybridization (FISH) analysis and RT-qPCR. LncRNA-miRNA interaction networks were constructed using the RNAhybrid and starBase v.2.0. and then validated using a dual-luciferase reporter assay. The effects of NEAT1 dysregulation on the proliferative, migratory, and invasive abilities of H. pylori filtrate-infected gastric cancer cells were observed by cell counting kit-8 (CCK-8), colony formation, wound healing test, and transwell assays. Western blot and RT-qPCR were performed to detect protein and RNA expression. Immunohistochemistry (IHC) was carried out to analyze the localization and expression of COX-2 and BCL9. RESULTS: FISH and RT-qPCR demonstrated that the expression of NEAT1 was up-regulated in gastric cancer tissues, especially in H. pylori-infected gastric cancer tissues, and the expression of NEAT1 was negatively correlated with miR-30a (miR-30a-3p and miR-30a-5p). The upregulation of NEAT1 enhanced proliferation, migration, and invasion of H. pylori filtrate-infected gastric cancer cells, while the downregulation of NEAT1 decreased these abilities, and miR-30a could reverse the effect of NEAT1 on these abilities. The dual-luciferase reporter assay identified that NEAT1 directly targeted miR-30a (miR-30a-3p and miR-30a-5p). Because miR-30a (miR-30a-3p and miR-30a-5p) negatively regulates the expression of downstream COX-2 and BCL9, NEAT1 was identified to upregulate indirectly the expression of COX-2 and BCL9. IHC showed that the expression of COX-2 and BCL9 was increased in H. pylori gastric cancer tissues. CONCLUSION: The study demonstrated that lncRNA NEAT1 may act as a promoter of tumorigenesis in H. pylori gastric cancer, by sponging miR-30a (miR-30a-3p and miR-30a-5p) to regulate the COX-2/BCL9 pathway.		Helicobacter. 2021 Aug 16:e12847. doi: 10.1111/hel.12847.
5181	LncRNA	GAS5	miR-10a-3p	VEGFA	The Serum Samples Of Patients With Osteoporosis	Osteoporosis	Homo sapiens (human)  	Dual-luciferase reporter assay;ELISA;Western blot;Luciferase reporter assay;	34396445	lncRNA GAS5 regulates angiogenesis by targeting miR-10a-3p/VEGFA in osteoporosis.	Osteoporosis is a severe bone disease commonly occurring in older males and postmenopausal females. Previous studies have shown that long non-coding (lnc)RNA growth arrest-specific 5 (GAS5) serves an important role in osteoporosis. However, its role is unclear and requires further exploration. The relative expression levels of GAS5 and miR-10a-3p in the serum samples of patients with osteoporosis, as well as the relative expression levels of GAS5, microRNA (miR)-10a-3p and vascular endothelial growth factor A (VEGFA) mRNA in osteoblasts, were detected by reverse transcription-quantitative PCR. ELISA and western blotting were used to detect the expression levels of VEGFA. A Matrigel angiogenesis test was used to assess the effects on angiogenesis. RNA binding interactions between GAS5/miR-10a-3p and miR-10a-3p/VEGFA were evaluated using dual-luciferase reporter assays. Furthermore, the effects of the GAS5/miR-10a-3p/VEGFA axis were investigated via ELISA, western blotting and Matrigel angiogenesis. GAS5 was significantly downregulated and miR-10a-3p was upregulated in patients with osteoporosis. Overexpression of GAS5 promoted angiogenesis. GAS5 acted as a sponge of miR-10a-3p; VEGFA was a target gene of miR-10a-3p. GAS5 induced angiogenesis by inhibiting miR-10a-3p and enhancing VEGFA expression. These results indicated that GAS5 overexpression increased angiogenesis by inhibiting miR-10a-3p, promoting the expression of VEGFA. The present study revealed a novel mechanism and provided novel targets for the clinical treatment of osteoporosis.		Mol Med Rep. 2021 Oct;24(4):711. doi: 10.3892/mmr.2021.12350. Epub 2021 Aug 13.
5182	LncRNA	FoxD2-AS1	miR-4306	NA	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;Western blot;Cell cycle assay;Luciferase reporter assay;	34396433	miR-4306 inhibits the malignant behaviors of colorectal cancer by regulating lncRNA FoxD2-AS1.	MicroRNA (miR)-4306 and FoxD2-adjacent opposite strand RNA 1 (FOXD2-AS1) are cancer-related genes involved in tumor progression. However, the potential functional roles of miR-4306 and FoxD2-AS1 in colorectal cancer (CRC) development remain unknown. The present study aimed to investigate the biological functions and the molecular mechanisms of miR-4306 and FoxD2-AS1 in CRC. Reverse transcription-quantitative PCR analysis was performed to determine the expression levels of FoxD2-AS1 and miR-4306 in CRC tissues and cell lines. Functional experiments, including Cell Counting Kit-8, colony formation, cell cycle assays and western blotting, were conducted to examine the effects of FoxD2-AS1 and miR-4306 on the malignant behaviors of CRC cells. In addition, the relationship between FoxD2-AS1 and miR-4306 was assessed using a dual-luciferase reporter assay and Pearson's correlation analysis. Compared with normal samples and cells, FoxD2-AS1 expression was increased and miR-4306 expression was decreased in CRC tissues and cells. Functional experiments demonstrated that silencing FoxD2-AS1 inhibited proliferation and induced cell arrest at G(0)/G(1) phase in CRC cells, while the overexpression of FoxD2-AS1 showed opposite results. Ki-67 and proliferating cell nuclear antigen expression levels were decreased after transfection with small interfering RNA FoxD2-AS1, but were increased after transfection with FoxD2-AS1 overexpression plasmid. Furthermore, investigations into the underling mechanism revealed that FoxD2-AS1 functioned as a molecular sponge of miR-4306. The inhibitory effects of FoxD2-AS1 silencing on CRC progression were reversed by miR-4306 knockdown. Collectively, the present study demonstrated that FoxD2-AS1 functioned as an oncogene in CRC progression, and that miR-4306 could inhibit the malignant behaviors of CRC by regulating FoxD2-AS1. Thus, the current study provided a promising therapeutic target for CRC treatment.		Mol Med Rep. 2021 Oct;24(4):723. doi: 10.3892/mmr.2021.12362. Epub 2021 Aug 13.
5183	LncRNA	ADAMTS9-AS1	miR-150	AS2	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qRT-PCR 	34395250	Bioinformatics Analysis and Functional Verification of ADAMTS9-AS1/AS2 in Lung Adenocarcinoma.	Long non-coding RNAs (lncRNAs), as competitive endogenous RNAs (ceRNAs), play a critical role in biological processes of cancer. However, the roles of specific lncRNAs in ceRNA network of lung adenocarcinoma (LUAD) remains largely unclear. Herein, we identified the roles of lncRNA ADAMTS9-AS1/AS2 (ADAMTS-AS1/AS2) in lung adenocarcinoma by bioinformatics analyses and functional verification. First, differentially expressed genes ADAMTS9-AS1, ADAMTS9-AS2 and ADAMTS9 were screened out from GSE130779. Then the expression correlation of these three genes was analyzed. The results showed that ADAMTS9-AS1, ADAMTS9-AS2 and ADAMTS9 were down-regulated in LUAD, and were positively correlated with each other. After that, miRcode was used to find miR-150 which binds to ADAMTS9-AS1/ADAMTS9-AS2/ADAMTS9. Next, co-expression analysis and functional enrichment analyses were performed to further analyze differentially expressed genes. The results showed that the differentially expressed genes were mainly enriched in Beta3 integrin cell surface interactions and epithelial-to-mesenchymal transition. Finally, the cell functions of ADAMTS9-AS1 and ADAMTS9-AS2 in A549 and NCI-H1299 cell lines were verified. In vitro cell studies confirmed that ADAMTS9-AS1 and ADAMTS9-AS2 play an inhibitory role in LUAD cells.		Front Oncol. 2021 Jul 29;11:681777. doi: 10.3389/fonc.2021.681777. eCollection 2021.
5184	LncRNA	NEAT1	miR-124	c-Myc	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34395239	A Novel Mechanism of the c-Myc/NEAT1 Axis Mediating Colorectal Cancer Cell Response to Photodynamic Therapy Treatment.	Photodynamic therapy (PDT) is considered a potential treatment regimen for colorectal cancer cases (CRC). p53 signaling and the miR-124/iASPP axis play an essential role in the PDT resistance of CRC cells. PDT treatment downregulated NEAT1 expression in p53(wt) HCT116 and RKO cells. In these two cell lines, NEAT1 silencing enhanced the suppressive effects of PDT on cell viability and apoptosis. Within the subcutaneously implanted tumor model, NEAT1 silencing enhanced PDT-induced suppression on tumor growth. Regarding p53-deleted HCT116 cells, PDT only moderately affected cell proliferation but induced downregulation of NEAT1. NEAT1 directly targeted miR-124, acting as a ceRNA, competing with iASPP for miR-124 binding, and counteracting miR-124-mediated repression on iASPP under PDT treatment. NEAT1 silencing was enhanced, whereas miR-124 inhibition attenuated PDT effects on CRC cells; miR-124 inhibition significantly reversed the roles of NEAT1 silencing in PDT-treated CRC cells. miR-124 negatively correlated with NEAT1 and iASPP, respectively, whereas NEAT1 and iASPP positively correlated with each other. PDT downregulated c-Myc in CRC cells, and c-Myc activated the transcription of NEAT1 through the targeting of its promoter region. Within p53(mut) SW480 cells, PDT failed to alter cell viability and apoptosis but still downregulated c-Myc, NEAT1, and iASPP and upregulated miR-124. In p53 mutant high-abundant CRC tissues, c-Myc and NEAT1 were up-regulated, and miR-124 was downregulated. In c-Myc high-abundant CRC tissues, NEAT1 and iASPP were up-regulated, and miR-124 was downregulated. The critical role of the c-Myc/NEAT1 axis in mediating CRC response to PDT treatment via the miR-124/iASPP/p53 feedback loop was conclusively demonstrated.		Front Oncol. 2021 Jul 28;11:652831. doi: 10.3389/fonc.2021.652831. eCollection 2021.
5185	LncRNA	SOX2-OT	miR-30d-5p	PDK1	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	34394184	LncRNA SOX2-OT/miR-30d-5p/PDK1 Regulates PD-L1 Checkpoint Through the mTOR Signaling Pathway to Promote Non-small Cell Lung Cancer Progression and Immune Escape.	Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Currently, treatment methods generally cause poor prognosis. Therefore, in order to seek new treatment options, we explored the internal mechanism of NSCLC. Firstly, the SOX2-OT/miR-30d-5p/PDK1 axis regulated by lncRNA SOX2-OT was predicted by bioinformatics methods, and the expression of SOX2-OT, miR-30d-5p, and PDK1 mRNA in cells were detected by qRT-PCR while PDK1 protein expression was detected by western blot. The results expressed that in NSCLC, SOX2-OT, and PDK1 were notably overexpressed while miR-30d-5p was markedly under-expressed. The interaction between them was verified by dual-luciferase reporter and RNA binding protein immunoprecipitation assays. Subsequently, through CCK8, scratch healing, cell invasion and flow cytometry assays, we revealed that inhibiting the expression of SOX2-OT could inhibit the proliferation, migration and invasion of NSCLC cells and promote cell apoptosis; while simultaneous overexpression of PDK1 or inhibition of miR-30d-5p expression could reverse the inhibitory effect of SOX2-OT silence-mediated malignant progression of NSCLC cells. Then, the combined application of overexpressed PDK1 and rapamycin verified that PDK1 could regulate the expression of PD-L1 in NSCLC cells through the mTOR signaling pathway. Co-culture of CD8(+) T cells verified that silencing SOX2-OT could inhibit the apoptosis of CD8(+) T cells through miR-30d-5p/PDK1. Finally, tumor formation assay in animals confirmed that overexpression of SOX2-OT could promote the growth of NSCLC tumor in vivo. In this study, assays in vitro and in vivo were conducted to elucidate the mechanism by which SOX2-OT/miR-30d-5p/PDK1 drives PD-L1 through the mTOR signaling pathway to promote the malignant progression and immune escape of NSCLC.		Front Genet. 2021 Jul 30;12:674856. doi: 10.3389/fgene.2021.674856. eCollection 2021.
5186	LncRNA	MYLK-AS1	miR-217	EZH2	Gbc Cell Lines (Noz, Eh-Gb1, Ocug-1, Gbc-Sd, Sgc-996 And Qbc-939)	Gallbladder Cancer	Homo sapiens (human)	qPCR;Western blot;	34393514	Long Non-Coding RNA Myosin Light Chain Kinase Antisense 1 Plays an Oncogenic Role in Gallbladder Carcinoma by Promoting Chemoresistance and Proliferation.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to play critical roles in human tumours, including gallbladder carcinoma (GBC). However, their biological functions and molecular mechanisms in tumorigenesis and progression remain largely unknown. METHODS: Quantitative polymerase chain reaction (qPCR) was used to verify the expression of lncRNA myosin light chain kinase antisense RNA 1 (MYLK-AS1) in 120 pairs of GBC tissues and paired adjacent non-tumour tissues, as well as in six different GBC cell lines (NOZ, EH-GB1, OCUG-1, GBC-SD, SGC-996 and QBC-939). Cell counting kit 8 was applied to explore cell proliferation and drug sensitivity assays. The target miRNAs (miR) of MYLK-AS1 and downstream target genes were predicted using Starbase 3.0 software and confirmed by double luciferase reporting test. The expression of proteins was assessed using Western blot assay. RESULTS: Here, we demonstrated that MYLK-AS1 was significantly upregulated and correlated with a poor prognosis and poor clinical characteristics in GBC. Furthermore, the forced expression of MYLK-AS1 significantly promoted GBC cell proliferation and resistance to gemcitabine in vitro. Mechanistically, MYLK-AS1 functioned as an efficient miR-217 sponge, thereby releasing the inhibition of enhancer of zeste 2 polycomb repressive complex 2 (EZH2) subunit expression. MYLK-AS1 promoted GBC cell proliferation and resistance to gemcitabine by upregulating EZH2 expression, and EZH2 was confirmed as a direct target of miR-217. DISCUSSION: Our results confirmed that the chemoresistant driver MYLK-AS1 might be a promising candidate as a therapeutic target for the treatment of advanced GBC.		Cancer Manag Res. 2021 Aug 7;13:6219-6230. doi: 10.2147/CMAR.S323759. eCollection 2021.
5187	LncRNA	HOTAIR	miR-148a-3p	KLF6	N2A Cells	Ischemic Stroke	Homo sapiens (human)  	qRT-PCR 	34391823	Silencing lncRNA HOTAIR improves the recovery of neurological function in ischemic stroke via the miR-148a-3p/KLF6 axis.	Ischemic stroke (IS), caused by a permanent or transient local reduction in blood supply to the brain, is one of the most widespread causes of public health problems in modern society. Long non-coding RNA (LncRNA) has been reported to be related to angiogenesis following IS. In this study, we explored the effect and potential molecular mechanism of lncRNA homeobox antisense non-coding RNA (HOTAIR) in IS. Permanent middle cerebral artery occlusion (pMCAO) model and oxygen and glucose deprivation (OGD) model were established. HOTAIR was increased in vivo and in vitro models post-ischemic. HOTAIR knockdown promoted neurological function recovery, manifesting in decreased modified neurological severity score, cerebral infarcted area, apoptosis and inflammation, and improved balance ability, spatial learning and memory ability. Silencing HOTAIR also improved the viability of OGD-induced N2a cells, and attenuated apoptosis and inflammation. HOTAIR can compete with KLF6 to bind to miR-148a-3p. miR-148a-3p knockdown or KLF6 overexpression partially reversed the effect of sh-HOTAIR on OGD-induced N2a cells. HOTAIR suppressed the activation of STAT3 pathway via the miR-148a-3p/KLF6 axis. To summarize, this study demonstrated that lncRNA HOTAIR absorbed miR-148a-3p and up-regulated KLF6 expression through ceRNA mechanism, and inhibited STAT3 pathway, promoted apoptosis and inflammation, and aggravated neurological injury post-IS.		Brain Res Bull. 2021 Aug 12;176:43-53. doi: 10.1016/j.brainresbull.2021.08.003.
5188	LncRNA	XIST	miR-214-3p	Arl2	Mesenchymal Stem Cells	Atrial Fibrillation	Mus musculus (mouse)	ELISA;RACE;RNA immunoprecipitation;Western blot;luciferase assay;RNA immunoprecipitation;	34389797	LncRNA XIST shuttled by adipose tissue-derived mesenchymal stem cell-derived extracellular vesicles suppresses myocardial pyroptosis in atrial fibrillation by disrupting miR-214-3p-mediated Arl2 inhibition.	The mechanisms underlying atrial fibrillation (AF), a type of heart arrhythmia, have not been fully identified. Long noncoding RNAs (lncRNAs) have been implicated in the progression of AF. The current study aimed to ascertain the means by which X-inactive specific transcript (XIST), a lncRNA, contributes to the pathogenesis of AF in an animal model or in atrial myocytes. Extracellular vesicles (EVs) derived from mouse adipose tissue-derived mesenchymal stem cells (AMSCs) were isolated, transfected with XIST, and either injected into AF mouse models or incubated with atrial myocytes. The in vitro and in vivo effects of EV-derived XIST on myocardial pyroptosis were determined by Western blot analysis of pyroptosis-related protein and an ELISA for inflammatory factors. Bioinformatics analysis revealed a relationship between XIST, microRNA (miR)-214-3p, and Arl2, which was subsequently verified by a dual luciferase assay and RNA immunoprecipitation. Functional experiments were performed to elucidate whether changes in miR-214-3p or Arl2 regulated the effect of XIST on myocardial pyroptosis. Overexpressed XIST from AMSC-EVs were found to decrease myocardial pyroptosis while alleviating inflammation, which was demonstrated by reduced expression of nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), cleared-caspase-1/caspase-1 and gasdermin D (GSDMD), as well as the amount of interleukin (IL)-1b and IL-18 in both the cardiomyocytes and AF mouse tissues. Mechanistically, XIST is a competing endogenous RNA (ceRNA) of miR-214-3p, triggering upregulation of its target gene Arl2. Silencing of Arl2 or overexpression miR-214-3p reversed the effects of XIST on inflammation and pyroptosis. Taken together, the key findings of our study suggest that XIST may blunt myocardial pyroptosis by absorbing miR-214-3p to promote Arl2 expression, providing encouraging insight into XIST-based targeted therapy for AF.		Lab Invest. 2021 Aug 13. doi: 10.1038/s41374-021-00635-0.
5189	LncRNA	OGFRP1	miR-4640-5p	eIF5A	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;	34389018	LncRNA OGFRP1 acts as an oncogene in NSCLC via miR-4640-5p/eIF5A axis.	BACKGROUND: Long noncoding RNAs (lncRNAs) OGFRP1 is up-regulated in endometrial cancer and cervical carcinoma, and OGFRP1 suppression inhibits the malignant behavior of cancer cells. Here, we evaluated the expression pattern, biological function and potential mechanism of OGFRP1 in non-small cell lung cancer (NSCLC). METHODS: The expression of target genes in 25 pairs of clinically collected NSCLC and normal lung tissue samples was detected by qRT-PCR or western blot. We screened the siRNA (siOGFRP1) to down-regulate the expression of OGFRP1 in A549 and H1299 cells. The biological function of A549 and H1299 cells were examined by CCK8, wound healing and transwell assays. The molecular mechanism of OGFRP1 was further explored. RESULTS: The expression of OGFRP1 in NSCLC tissues were higher than that in normal lung tissue. siOGFRP1 inhibited the proliferation, migration and invasion of A549 and H1299 cells. In addition, the expression of EMT-related and apoptosis-related proteins was changed by siOGFRP1 transfection. OGFRP1 can directly interact with miR-4640-5p, and siOGFRP1 increased the level of miR-4640-5p. Moreover, miR-4640-5p could directly bind to the 3' UTR region of eIF5A mRNA. eIF5A was highly expressed in NSCLC tissues, and predicted a poor prognosis. In addition, the expression of miR-4640-5p and eIF5A in NSCLC tissues were negatively correlated, while the expression of OGFRP1 and eIF5A were positively correlated. Knockdown of OGFRP1 inhibited the expression of eIF5A, while transfection of miR-4640-5p inhibitor up-regulated the expression of eIF5A. CONCLUSIONS: Taken together, we demonstrated that down-regulation of OGFRP1 inhibited the progression of NSCLC through miR-4640-5p/eIF5A axis.		Cancer Cell Int. 2021 Aug 13;21(1):425. doi: 10.1186/s12935-021-02115-3.
5190	LncRNA	HOXC-AS3	miR-105-5p	SOS1	Cervical Cancer Tissues And Cells	Cervical Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34387789	Long noncoding RNA HOXC-AS3 enhances the progression of cervical cancer via activating ErbB signaling pathway.	Emerging evidence reveals that long noncoding RNAs (lncRNAs) contribute to human tumorigenesis. Nevertheless, the function of HOXC cluster antisense RNA 3 (HOXC-AS3) in human cervical cancer (CC) remains largely unknown. The levels of HOXC-AS3, miR-105-5p and SOS1 in CC tissues and cells were monitored by reverse transcription-polymerase chain reaction (RT-PCR) and western blot (WB). Gain- and loss-of-function experiments were conducted to verify the function of HOXC-AS3 and miR-105-5p in CC cells. Meanwhile, cell proliferation, apoptosis, migration and invasion were examined by the cell counting kit-8 (CCK8) experiment, colony formation assay, flow cytometry and Transwell assay. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to test the regulatory interaction of HOXC-AS3, miR-105-5p and SOS1. In addition, in vivo experiment was performed to certain the role of HOXC-AS3 in tumorigenesis of CC. HOXC-AS3 was overexpressed in CC tissues (vs. adjacent normal tissues) and CC cells. Besides, the higher HOXC-AS3 profile was associated with the poorer clinical prognosis of CC patients. Overexpression of HOXC-AS3 promoted cell growth, migration and invasion, hampered apoptosis, whereas knocking down HOXC-AS3 exhibited the reverse effects. MiR-105-5p was a downstream target of HOXC-AS3, and it mediated the HOXC-AS3-induced oncogenic effects. Mechanistically, the bioinformatic analysis illustrated that SOS1 was targeted by miR-105-5p. Up-regulating SOS1 heightened the growth, migration and invasion of CC cells by enhancing the ErbB signaling pathway, which was reversed by miR-105-5p. Up-regulated HOXC-AS3 aggravates CC by promoting SOS1 expression via targeting miR-105-5p.		J Mol Histol. 2021 Aug 13. doi: 10.1007/s10735-021-10007-z.
5191	LncRNA	GAS5	miR-21	E-cadherin	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34386496	Downregulated lncRNA GAS5 and Upregulated miR-21 Lead to Epithelial-Mesenchymal Transition and Lung Metastasis of Osteosarcomas.	Lung is the primary site of osteosarcoma metastasis, but the underlying genetic or epigenetic factors determining lung metastasis of osteosarcoma are unknown. In this study, we report the status of growth arrest specific 5 (GAS5) in lung metastatic osteosarcomas. GAS5 was generally downregulated in osteosarcoma patients (n = 24) compared to healthy controls (n = 10) and even more so in patients with lung metastatic disease(n = 11) compared to the patients without metastasis (n = 13). We also report a role of miR-21 in GAS5-mediated effects. Downregulation of GAS5 in hFOB 1.19 and U2OS osteosarcoma cells enhanced their migration and invasion, along with an upregulated epithelial-mesenchymal transition (EMT), as evidenced by downregulated E-cadherin and upregulated vimentin, ZEB1, and ZEB2. Downregulation of GAS5 also resulted in a significantly increased expression of miR-21. Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. miR-21 was also found to be elevated in osteosarcoma patients with its levels particularly high in patients with lung metastasis. Our observations reveal a possible role of GAS5 and miR-21 in lung metastasis of osteosarcoma, presenting them as novel targets for therapy.		Front Cell Dev Biol. 2021 Jul 27;9:707693. doi: 10.3389/fcell.2021.707693. eCollection 2021.
5192	LncRNA	GAS5	miR-21	vimentin	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34386496	Downregulated lncRNA GAS5 and Upregulated miR-21 Lead to Epithelial-Mesenchymal Transition and Lung Metastasis of Osteosarcomas.	Lung is the primary site of osteosarcoma metastasis, but the underlying genetic or epigenetic factors determining lung metastasis of osteosarcoma are unknown. In this study, we report the status of growth arrest specific 5 (GAS5) in lung metastatic osteosarcomas. GAS5 was generally downregulated in osteosarcoma patients (n = 24) compared to healthy controls (n = 10) and even more so in patients with lung metastatic disease(n = 11) compared to the patients without metastasis (n = 13). We also report a role of miR-21 in GAS5-mediated effects. Downregulation of GAS5 in hFOB 1.19 and U2OS osteosarcoma cells enhanced their migration and invasion, along with an upregulated epithelial-mesenchymal transition (EMT), as evidenced by downregulated E-cadherin and upregulated vimentin, ZEB1, and ZEB2. Downregulation of GAS5 also resulted in a significantly increased expression of miR-21. Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. miR-21 was also found to be elevated in osteosarcoma patients with its levels particularly high in patients with lung metastasis. Our observations reveal a possible role of GAS5 and miR-21 in lung metastasis of osteosarcoma, presenting them as novel targets for therapy.		Front Cell Dev Biol. 2021 Jul 27;9:707693. doi: 10.3389/fcell.2021.707693. eCollection 2021.
5193	LncRNA	GAS5	miR-21	ZEB1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34386496	Downregulated lncRNA GAS5 and Upregulated miR-21 Lead to Epithelial-Mesenchymal Transition and Lung Metastasis of Osteosarcomas.	Lung is the primary site of osteosarcoma metastasis, but the underlying genetic or epigenetic factors determining lung metastasis of osteosarcoma are unknown. In this study, we report the status of growth arrest specific 5 (GAS5) in lung metastatic osteosarcomas. GAS5 was generally downregulated in osteosarcoma patients (n = 24) compared to healthy controls (n = 10) and even more so in patients with lung metastatic disease(n = 11) compared to the patients without metastasis (n = 13). We also report a role of miR-21 in GAS5-mediated effects. Downregulation of GAS5 in hFOB 1.19 and U2OS osteosarcoma cells enhanced their migration and invasion, along with an upregulated epithelial-mesenchymal transition (EMT), as evidenced by downregulated E-cadherin and upregulated vimentin, ZEB1, and ZEB2. Downregulation of GAS5 also resulted in a significantly increased expression of miR-21. Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. miR-21 was also found to be elevated in osteosarcoma patients with its levels particularly high in patients with lung metastasis. Our observations reveal a possible role of GAS5 and miR-21 in lung metastasis of osteosarcoma, presenting them as novel targets for therapy.		Front Cell Dev Biol. 2021 Jul 27;9:707693. doi: 10.3389/fcell.2021.707693. eCollection 2021.
5194	LncRNA	GAS5	miR-21	ZEB2	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34386496	Downregulated lncRNA GAS5 and Upregulated miR-21 Lead to Epithelial-Mesenchymal Transition and Lung Metastasis of Osteosarcomas.	Lung is the primary site of osteosarcoma metastasis, but the underlying genetic or epigenetic factors determining lung metastasis of osteosarcoma are unknown. In this study, we report the status of growth arrest specific 5 (GAS5) in lung metastatic osteosarcomas. GAS5 was generally downregulated in osteosarcoma patients (n = 24) compared to healthy controls (n = 10) and even more so in patients with lung metastatic disease(n = 11) compared to the patients without metastasis (n = 13). We also report a role of miR-21 in GAS5-mediated effects. Downregulation of GAS5 in hFOB 1.19 and U2OS osteosarcoma cells enhanced their migration and invasion, along with an upregulated epithelial-mesenchymal transition (EMT), as evidenced by downregulated E-cadherin and upregulated vimentin, ZEB1, and ZEB2. Downregulation of GAS5 also resulted in a significantly increased expression of miR-21. Moreover, downregulation of such elevated miR-21 was found to reverse the effects of GAS5 silencing. miR-21 was also found to be elevated in osteosarcoma patients with its levels particularly high in patients with lung metastasis. Our observations reveal a possible role of GAS5 and miR-21 in lung metastasis of osteosarcoma, presenting them as novel targets for therapy.		Front Cell Dev Biol. 2021 Jul 27;9:707693. doi: 10.3389/fcell.2021.707693. eCollection 2021.
5195	LncRNA	GAS5	MiR-665	SDC1	Vascular Smooth Muscle Cell	Cardiovascular Disease	Homo sapiens (human)  	microarray;qRT-PCR;Luciferase reporter assay;	34386495	MiR-665 Regulates Vascular Smooth Muscle Cell Senescence by Interacting With LncRNA GAS5/SDC1.	Background: Vascular aging is considered a special risk factor for cardiovascular diseases, and vascular smooth muscle cells (VSMCs) play a major role in aging-related vascular remodeling and in the pathological process of atherosclerosis. Recent research has reported that long non-coding RNA/microRNA (lncRNA/miRNA) is a critical regulator of cellular senescence. However, the role and mechanism of lncRNA GAS5/miR-665 axis in VSMC senescence remain incompletely understood. Methods: Cellular senescence was evaluated using senescence-associated b-gal activity, the NAD+/NADH ratio, and by immunofluorescence staining of γH2AX immunofluorescence. Differentially expressed miRNAs (DEMs) were identified by miRNA microarray assays and subsequently validated by quantitative real-time PCR (qRT-PCR). A dual luciferase reporter assay was conducted to confirm the binding of lncRNA GAS5 and miR-665 as well as miR-665 and syndecan 1 (SDC1). Serum levels of miR-665, lncRNA GAS5, and SDC1 in 93 subjects were detected by qRT-PCR. The participants were subdivided into control, aging, and early vascular aging (EVA) groups, and their brachial-ankle pulse wave velocity (baPWV) was measured. Results: A total of 20 overlapping DEMs were identified in young and old VSMCs via microarray analysis. MiR-665 showed a significant alteration and, therefore, was selected for further analysis. Upregulation of miR-665 was found in aging VSMCs, and downregulation of miR-665 caused an inhibition of VSMCs senescence. Subsequently, the dual luciferase reporter assay determined the binding site of miR-665 with the 3'-UTR of lncRNA GAS5 and SDC1. Increased expression of lncRNA GAS5 expression inhibited the miR-665 level and VSMC senescence. However, as shown in rescue experiment results, either miR-665 overexpression or SDC1 knockdown significantly reversed the effects of lncRNA GAS5 on VSMC senescence. Finally, compared with that of the control group, miR-665 was highly expressed in serum samples in the aging and EVA groups, especially in the EVA groups. On the contrary, serum levels of lncRNA GAS5 and SDC1 were lower in these two groups. Collectively, in the aging and EVA groups, miR-665 expression was negatively correlated with lncRNA GAS5 and SDC1 expression. Conclusion: miR-665 inhibition functions as a vital modulator of VSMC senescence by negatively regulating SDC1, which is achieved by lncRNA GAS5 that sponges miR-665. Our findings may provide a new treatment strategy for aging-related cardiovascular diseases.		Front Cell Dev Biol. 2021 Jul 27;9:700006. doi: 10.3389/fcell.2021.700006. eCollection 2021.
5196	LncRNA	CCAT2	miR-200b	IGF2BP2	Esophageal Squamous Cell Carcinoma Cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Immunoblotting;Luciferase reporter assay;	34386421	Long Non-Coding RNA CCAT2 Promotes the Development of Esophageal Squamous Cell Carcinoma by Inhibiting miR-200b to Upregulate the IGF2BP2/TK1 Axis.	Long non-coding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). In the current study, we identified CCAT2 as a relevant lncRNA and investigated its role in the progression of ESCC. RT-qPCR was adopted to detect CCAT2 expression in collected clinical samples, ESCC cell lines, and a normal cell line. We tested the correlation between CCAT2 expression and the prognosis of ESCC. RT-qPCR or immunoblotting was adopted to detect the expression of relevant factors in ESCC tissues or cells. Cell proliferation, apoptosis, migration, and invasion were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay, respectively, while subcutaneous tumorigenesis in nude mice was adopted to examine the role of CCAT2 in tumorigenesis of ESCC cells in vivo. Bioinformatics analysis, dual luciferase reporter assay, and RIP were conducted for the target relationship profiling. Me-RIP was adopted to detect m6A modification level of TK1 in ESCC tissues or cells. Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues. CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression. IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification. CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.		Front Oncol. 2021 Jul 27;11:680642. doi: 10.3389/fonc.2021.680642. eCollection 2021.
5197	LncRNA	CCAT2	miR-200b	TK1	Esophageal Squamous Cell Carcinoma Cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;Immunoblotting;Luciferase reporter assay;	34386421	Long Non-Coding RNA CCAT2 Promotes the Development of Esophageal Squamous Cell Carcinoma by Inhibiting miR-200b to Upregulate the IGF2BP2/TK1 Axis.	Long non-coding RNAs (lncRNAs) have been shown to play important roles in human cancers, including esophageal squamous cell carcinoma (ESCC). In the current study, we identified CCAT2 as a relevant lncRNA and investigated its role in the progression of ESCC. RT-qPCR was adopted to detect CCAT2 expression in collected clinical samples, ESCC cell lines, and a normal cell line. We tested the correlation between CCAT2 expression and the prognosis of ESCC. RT-qPCR or immunoblotting was adopted to detect the expression of relevant factors in ESCC tissues or cells. Cell proliferation, apoptosis, migration, and invasion were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay, respectively, while subcutaneous tumorigenesis in nude mice was adopted to examine the role of CCAT2 in tumorigenesis of ESCC cells in vivo. Bioinformatics analysis, dual luciferase reporter assay, and RIP were conducted for the target relationship profiling. Me-RIP was adopted to detect m6A modification level of TK1 in ESCC tissues or cells. Upregulated CCAT2, IGF2BP2, and TK1 expression and inhibited miR-200b expression were observed in ESCC cells and tissues. CCAT2 bound to miR-200b and reduced its expression, leading to upregulated IGF2BP2 expression. IGF2BP2 improved TK1 mRNA stability to enhance its expression by recognizing its m6A modification. CCAT2 promoted the migration and invasion of ESCC cells in vitro, and tumorigenesis in vivo by upregulating TK1 expression, while overexpression of miR-200b reversed these effects of CCAT2. Overall, this study suggests that CCAT2 competitively binds to miR-200b to alleviate its inhibitory effects on IGF2BP2 expression, resulting in elevated TK1 expression, and an ensuing promotion of the development of ESCC.		Front Oncol. 2021 Jul 27;11:680642. doi: 10.3389/fonc.2021.680642. eCollection 2021.
5198	LncRNA	NEAT1	miR-204	SOX4	Arpe19 Cells	Diabetic Retinopathy	Homo sapiens (human)  	qRT-PCR;Western blot;Immunohistochemistry;	34386303	LncRNA NEAT1 regulated diabetic retinal epithelial-mesenchymal transition through regulating miR-204/SOX4 axis.	AIM: Epithelial-mesenchymal transition (EMT) of retinal pigment epithelium (RPE) cells is the key of the development of diabetic retinopathy (DR), and lncRNA NEAT1 could accelerate EMT in diabetic nephropathy. Meanwhile, as a diabetes susceptibility gene, whether sex-determining region Y-related (SRY) high-mobility group box 4 (SOX4) has relationship with lncRNA NEAT1 in DR remains unclear. METHODS: Firstly, NEAT1, SOX4 and miR-204 were evaluated by qRT-PCR (quantitative reverse-transcriptase PCR) under high glucose condition. Then, cell viability, proliferation, migration and invasion were respectively detected by MTT, BrdU staining, wound healing and transwell assay after NEAT1 knockdown or miR-204 overexpression. Also, the EMT-related proteins were examined by western blot and cell immunofluorescence assay. In order to confirm the relationship between miR-204 and NEAT1 or SOX4, dual luciferase reporter gene assay was conducted. At the same time, the protein levels of SOX4 and EMT-related proteins were investigated by immunohistochemistry in vivo. RESULTS: High glucose upregulated NEAT1 and SOX4 and downregulated miR-204 in ARPE19 cells. NEAT1 knockdown or miR-204 overexpression inhibited the proliferation and EMT progression of ARPE19 cells induced by high glucose. NEAT1 was identified as a molecular sponge of miR-204 to increase the level of SOX4. The effect of NEAT1 knockdown on the progression of EMT under high glucose condition in ARPE19 cells could be reversed by miR-204 inhibitor. Also, NEAT1 knockdown inhibited retinal EMT in diabetic mice. CONCLUSION: NEAT1 regulated the development of EMT in DR through miR-204/SOX4 pathway, which could provide reference for clinical prevention and treatment.		PeerJ. 2021 Jul 23;9:e11817. doi: 10.7717/peerj.11817. eCollection 2021.
5199	LncRNA	XLOC_005950	miR-542-3p	NA	Osteosarcoma Mg63 Cells	Osteosarcoma	Homo sapiens (human)  	Dual-luciferase reporter assay;RACE;Flow Cytometry assay;Luciferase reporter assay;	34386091	Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa-miR-542-3p.	Cancer cells use glucose via glycolysis to maintain tumor cell proliferation. However, the effect of long non-coding RNAs (lncRNAs) on glycolysis in osteosarcoma (OS) cells remains unclear. The present study aimed to investigate the involvement of the lncRNA XLOC_005950/hsa-microRNA (miR)-542-3p/phosphofructokinase, muscle (PFKM) axis in the regulation of glucose metabolism, cell proliferation and apoptosis in the progression of OS. lncRNA XLOC_005950, hsa-miR-542-3p and PFKM expression in OS tissues and cells was detected via reverse transcription-quantitative PCR analysis. CRISPR/Cas9 gene editing was used to knockout lncRNA XLOC_005950 expression in MG63 cells. Cell Counting Kit-8 assay, flow cytometry, PFKM activity, and glucose and lactic acid content determination were performed to assess the effects of lncRNA XLOC_005950 knockout and overexpression of hsa-miR-542-3p on the phenotypes of OS cells. The dual-luciferase reporter assay was performed to confirm the targeting associations between lncRNA XLOC_005950, hsa-miR-542-3p and PFKM. The results demonstrated that lncRNA XLOC_005950 expression was upregulated in OS tissues and cells. Functional experiments indicated that lncRNA XLOC_005950 knockout decreased PFKM activity, the intracellular glucose and lactic acid content, and cell proliferation, while increasing apoptosis of OS cells. Furthermore, lncRNA XLOC_005950 knockout upregulated hsa-miR-542-3p expression and downregulated PFKM expression. Overexpression of hsa-miR-542-3p suppressed PFKM expression. Furthermore, lncRNA XLOC_005950, as the molecular sponge of miR-542-3p in OS, modulated the downstream target gene, PFKM. Taken together, the results of the present study suggest that lncRNA XLOC_005950 knockout may inhibit the progression of OS via hsa-miR-542-3p-mediated regulation of PFKM expression.		Oncol Lett. 2021 Sep;22(3):669. doi: 10.3892/ol.2021.12930. Epub 2021 Jul 15.
5200	LncRNA	LINC01272	miR-1303	NA	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Luciferase reporter assay;	34386074	Low LINC01272 predicts poor prognosis of non-small cell lung cancer and its biological function in tumor cells by inhibiting miR-1303.	Non-small cell lung cancer (NSCLC) is a malignant tumor associated with poor prognosis. The clinical value of long non-coding RNAs (lncRNAs) in the pathomechanism of various types of human malignancy has attracted increasing attention. The present study aimed to investigate the expression of LINC01272 in NSCLC and to determine its prognostic value and biological role. Tumor and adjacent non-tumor tissues from 108 patients with NSCLC and NSCLC cell lines were used in this study. The expression levels of LINC01272 and microRNA (miR)-1303 in tissues of patients and NSCLC cell lines were evaluated by reverse transcription quantitative PCR. The relationship between LINC01272 and the overall survival of patients with NSCLC was analyzed by Kaplan-Meier survival curve and log-rank test. Cox regression analysis confirmed the prognostic value of LINC01272 in patients with NSCLC. Cell Counting Kit-8 assay was used to evaluate the proliferation of NSCLC cells. The migration and invasion of NSCLC cells were determined using Transwell assays. The interaction between LINC01272 and miR-1303 in NSCLC was confirmed by dual-luciferase reporter assay. LINC01272 downregulation in NSCLC tissues was associated with worse overall survival in patients based on bioinformatics analysis. Furthermore, LINC01272 expression, which was decreased in NSCLC tumor tissues and NSCLC cells, was considered as an independent prognostic biomarker in NSCLC. In addition, LINC01272 overexpression inhibited NSCLC cell proliferation, migration and invasion. miR-1303 expression, which was increased in tumor tissues, was sponged by LINC01272 and negatively correlated with LINC01272 expression. miR-1303 expression reversed the inhibitory effects of LINC01272 on NSCLC cell function. In summary, the findings from this study suggested that LINC01272 expression, which was decreased in NSCLC tumor tissues and NSCLC cells, may be used as an independent prognostic biomarker for patients with NSCLC and that its overexpression may suppress NSCLC cell proliferation, migration and invasion by inhibiting miR-1303.		Oncol Lett. 2021 Sep;22(3):652. doi: 10.3892/ol.2021.12913. Epub 2021 Jul 9.
5201	LncRNA	OIP5-AS1	miR-30a	VOPP1	Esophageal Cancer Cells	Esophageal Cancer	Homo sapiens (human)	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34386073	Long non-coding RNA OIP5-AS1 promotes the progression of esophageal cancer by regulating miR-30a/VOPP1 expression.	Long non-coding RNAs (lncRNAs) serve an important role in the development of esophageal cancer (EC), which is the eighth most common type of cancer worldwide. lncRNA opa-interacting protein 5 antisense transcript 1 (OIP5-AS1) is associated with human malignancy. However, the biological roles of OIP5-AS1 in the development of EC remain unclear. In the present study, transfection was conducted, and reverse transcription-quantitative PCR and western blot analysis were used for the detection of mRNA and protein expression, respectively. Furthermore, dual-luciferase reporter and RNA immunoprecipitation assays were used to study the interaction between miRNA and lncRNA or genes. The results revealed that OIP5-AS1 expression in EC tissues and cultured EC cells was upregulated, microRNA-30a (miR-30a) expression was downregulated. OIP5-AS1-knockdown suppressed the proliferation, migration and invasion of EC9706 and EC109 cells. miR-30a was confirmed to interact with OIP5-AS1, and miR-30a-mimics transfection ameliorated the effects of OIP5-AS1 in EC cells. Vesicular overexpressed in cancer prosurvival protein 1 (VOPP1) was verified as the direct target of miR-30a. VOPP1 expression was positively correlated with OIP5-AS1 expression in EC cells. Overexpression of VOPP1 ameliorated the negative effects of OIP5-AS1-knockdown on EC9706 and EC109 cells. In conclusion, OIP5-AS1 promoted the proliferation, migration and invasion of EC cells by increasing VOPP1 expression by sponging miR-30a.		Oncol Lett. 2021 Sep;22(3):651. doi: 10.3892/ol.2021.12912. Epub 2021 Jul 9.
5202	LncRNA	lnc-NLC1-C	miR-383	PRDX-3	Glioma Cells	Glioma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	34386062	lnc-NLC1-C inhibits migration, invasion and autophagy of glioma cells by targeting miR-383 and regulating PRDX-3 expression.	Long non-coding RNAs (lncRNAs) serve an important role in tumor progression, and their abnormal expression is associated with tumor development. The lncRNA narcolepsy candidate region 1 gene C (lnc-NLC1-C) is involved in numerous types of cancer, but its biological function in glioma remains unknown. In the present study, lnc-NLC1-C expression was detected using reverse transcription-quantitative (RT-q)PCR in U251, SHG44, U87MG and U118MG glioma cells. U87MG cells were transfected with lnc-NLC1-C overexpression or interference vectors. Cell proliferation was detected using a Cell Counting Kit-8 assay. Cell migration and invasion were examined using a Transwell assay, while apoptosis, cell cycle and reactive oxygen species production were evaluated using flow cytometry, and the expression levels of lnc-NLC1-C, microRNA (miR)-383 and peroxiredoxin 3 (PRDX-3) were measured using western blotting and RT-qPCR. Rescue experiments were performed to verify the function of the lnc-NLC1-C/miR-383/PRDX-3 axis. The highest expression levels of lnc-NLC1-C were identified in U87MG glioma cells. Overexpression of lnc-NLC1-C expression promoted cell proliferation, G(1) phase blocking, migration and invasion, while inhibiting apoptosis and autophagy in U87MG cells. Mechanistically, miR-383 could bind to lnc-NLC1-C to regulate PRDX-3 expression and improve its oncogenic effect. Rescue experiments confirmed that the lnc-NLC1-C/miR-383/PRDX-3 axis was involved in the molecular mechanism of glioma progression. Therefore, lnc-NLC1-C may be a tumor promoter that affects multiple biological functions, such as migration, invasion and autophagy, in glioma cells.		Oncol Lett. 2021 Sep;22(3):640. doi: 10.3892/ol.2021.12901. Epub 2021 Jul 7.
5203	LncRNA	MALAT1	miR-449a	DLL1	Gastric Smooth Muscle Cells	Diabetic Gastroparesis	Homo sapiens (human)	Dual-luciferase reporter assay;RACE;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA sequencing;	34385927	MALAT1: A Pivotal lncRNA in the Phenotypic Switch of Gastric Smooth Muscle Cells via the Targeting of the miR-449a/DLL1 Axis in Diabetic Gastroparesis.	Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus (DM). Our previous study suggested that the expression of the long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is closely related to DGP. However, the role of MALAT1 in DGP pathogenesis remains unclear. Here, we aim to characterize the role of MALAT1 in DGP. First, we analyzed the lncRNA expression profiles through lncRNA sequencing. Next, we detected MALAT1 expression in the stomach tissues of DGP model mice and diabetic patients. Then, we investigated the role and mechanisms of MALAT1 in the proliferation, migration, phenotypic switch, and carbachol-induced intracellular Ca(2+) changes in human gastric smooth muscle cells (HGSMCs) under high glucose (HG) conditions, using short hairpin RNA technology, RNA immunoprecipitation, and dual-luciferase reporter assays. We show that MALAT1 expression was upregulated in the gastric tissues of DGP model mice, the adjacent healthy tissues collected from diabetic gastric cancer patients with DGP symptoms, and in HGSMCs cultured under HG conditions. Functionally, MALAT1 knockdown in vitro impacted the viability, proliferation, migration and promoted the phenotypic switch of HGSMCs under HG conditions. Additionally, we show that MALAT1 sponged miR-449a, regulating Delta-like ligand 1 (DLL1) expression in HGSMCs; any disturbance of the MALAT1/miR-449a/DLL1 pathway affects the proliferation, migration, phenotypic switch, and carbachol-induced Ca(2+) transient signals in HGSMCs under HG conditions. Collectively, our data highlight a novel regulatory signaling pathway, the MALAT1/miR-449a/DLL1 axis, in the context of DGP.		Front Pharmacol. 2021 Jul 27;12:719581. doi: 10.3389/fphar.2021.719581. eCollection 2021.
5204	LncRNA	LOC100505817	miR-20a	WT1	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)	RIP assay;Flow Cytometry assay;	34385891	Tumor Inhibitory Effect of Long Non-coding RNA LOC100505817 on Gastric Cancer.	Gastric cancer (GC) is one of the major malignancies worldwide. Emerging evidence has revealed the potential involvement of long noncoding RNA (lncRNA) in human genetic disorders and cancer, but the role of LOC100505817 remains unknown. Thus, in this study, we isolated tissues from GC patients to characterize the functional importance of LOC100505817 in GC tumorigenesis. We also proposed a hypothesis that the regulation of Wnt/b-catenin pathway by LOC100505817 was regulated by miR-20a-mediated WT1. After the collection of cancer tissues and adjacent tissues were obtained from GC patients, expression of LOC100505817, Wnt/b-catenin pathway- and EMT-related genes was quantified. Ectopic expression and knockdown experiments were applied in order to investigate the protective role of LOC100505817 in the progression of GC. Subsequently, cell viability, flow cytometry for apoptosis and cell cycle were detected via CCK-8, while migration and invasion were determined using scratch test and Transwell assay respectively. Then interactions among LOC100505817, miR-20a and WT1 were explored by dual luciferase reporter gene assay, RNA pull down assay and RNA binding protein immunoprecipitation (RIP) assay. The results found poor expression LOC100505817 was poorly expressed in GC cells and tissues. Overexpressed LOC100505817 resulted in the significant reduction of cell proliferation, migration and invasion as well as the expression of Wnt2b, b-catenin, CyclinD1, N-cadherin, Vimentin and snail, while increased cell apoptosis along with the expression of E-cadherin. Wnt/b-catenin pathway and EMT in GC cells were suppressed by LOC100505817 through miR-20a-inhibted WT1. In summary, our results provided evidence suggesting that LOC100505817 inhibits GC through LOC100505817-mediated inhibition of Wnt/b-catenin pathway, that leads to the overall restraining of GC cell proliferation, migration and invasion through miR-20a-reduced WT1.		Pathol Oncol Res. 2021 May 26;27:581542. doi: 10.3389/pore.2021.581542. eCollection 2021.
5205	LncRNA	CDKN2B-AS1	miR-126-5p	PTPN7	Vascular Smooth Muscle Cells	Coronary Heart Disease	Homo sapiens (human)  	microarray;	34384839	LncRNA CDKN2B-AS1 hinders the proliferation and facilitates apoptosis of ox-LDL-induced vascular smooth muscle cells via the ceRNA network of CDKN2B-AS1/miR-126-5p/PTPN7.	OBJECTIVE: The patterns of lncRNA CDKN2B-AS1 in coronary heart disease (CHD) have been extensively studied. This study investigated the competing endogenous RNA (ceRNA) network of CDKN2B-AS1 in coronary atherosclerosis (CAS). METHODS: Microarray analyses were performed to screen out the CHD-related lncRNAs (CDKN2B-AS1) and the downstream microRNAs (miR-126-5p). The expression of CDKN2B-AS1 in serum of patients with CHD and healthy volunteers was detected. Vascular smooth muscle cells (VSMCs) were treated with oxidized low density lipoprotein (ox-LDL) to establish cell model. Then pcDNA-CDKN2B-AS1 and/or miR-126-5p mimic were transfected into ox-LDL-treated VSMCs to estimate cell proliferation, apoptosis and inflammation. The ceRNA network of CDKN2B-AS1 along with the possible pathway in CHD was testified. RESULTS: CDKN2B-AS1 expression was low in patients with CHD and ox-LDL-treated VSMCs. Upon CDKN2B-AS1 overexpression, TNF-a, NF-kB and IL-1b levels in VSMCs were decreased, the proliferation of VSMCs was inhibited and the apoptosis rate was increased. Overexpression of miR-126-5p could reverse these trends. CDKN2B-AS1 as a ceRNA competitively bound to miR-126-5p to upregulate PTPN7. CDKN2B-AS1 inhibited VSMC proliferation and accelerated apoptosis by inhibiting the PI3K-Akt pathway. CONCLUSION: LncRNA CDKN2B-AS1 upregulates PTPN7 by absorbing miR-126-5p and inhibits the PI3K-Akt pathway, thus hindering the proliferation and accelerating apoptosis of VSMCs induced by ox-LDL, thus being a therapeutic approach for CAS.		Int J Cardiol. 2021 Aug 9:S0167-5273(21)01219-5. doi: 10.1016/j.ijcard.2021.08.009.
5206	LncRNA	LINC00958	miR-4306	SIRT1	Oral Squamous Cell Carcinoma (Oscc) Cells	Oral Squamous Cell Cancer	Homo sapiens (human)  	qPCR;RIP assay;Western blot;Flow Cytometry assay;	34384029	The regulation of long non-coding RNA 00958 (LINC00958) for oral squamous cell carcinoma (OSCC) cells death through absent in melanoma 2 (AIM2) depending on microRNA-4306 and Sirtuin1 (SIRT1) in vitro.	Long non-coding RNAs (lncRNAs) have been proposed as potential targets in OSCC gene therapy. Thus, the study aims to analyze how they exert functions in OSCC. LINC00958, AIM2, Gasdermin D (GSDMD) and tumor protein p53 (TP53) expression levels are analyzed by Quantitative Real-time PCR (qPCR) or Western blotting (WB) in OSCC cells lines. The roles of LINC00958 in cell proliferation, cell death, and GSDMD expression respectively were analyzed by Cell Counting Kit-8 (CCK8) assay, flow cytometry and Immunofluorescence (IF) assay. In addition, expressions of pyroptosis- and autophagy-related proteins are evaluated by WB detection. The targeted binding of LINC00958 and miR-4306 or AIM2 mRNA is predicted by bioinformatics analysis and detected by biodual luciferase system. RIP and qPCR assays analyze whether LINC00958 interacts with SIRT1. We found that LINC00958 showed upregulation in OSCC cells compared to normal oral epithelial cells. LINC00958 silencing significantly suppressed OSCC cell proliferation, induced cell death and reduced autophagy. LINC00958 regulated the levels of miR-4306 which binds to the 3'UTR of AIM2, and interacts with and modulates SIRT1 protein expression. LINC00958 regulated GSDMD and AIM2 levels, as well as p53 and SIRT1 levels. SIRT1 overexpression markedly reversed aforementioned effects of LINC00958. LINC00958 not only downregulated miR-4306 levels to activate the pyroptosis pathway mediated by AIM2 and promoted cancer cell survival but also induced a decrease in SIRT protein expression to further reduce p53 levels.		Bioengineered. 2021 Dec;12(1):5085-5098. doi: 10.1080/21655979.2021.1955561.
5207	LncRNA	lnc-HZ04	miR-hz04	p53	Trophoblast Cells	Miscarriage	Homo sapiens (human)	qRT-PCR 	34383983	Novel lncRNA-HZ04 promotes BPDE-induced human trophoblast cell apoptosis and miscarriage by upregulating IP(3) R(1) /CaMKII/SGCB pathway by competitively binding with miR-hz04.	Normal pregnancy is essential for human reproduction. However, BaP (benzo(a)pyrene) and its metabolite BPDE (benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide) could cause dysfunctions of human trophoblast cells and might further induce miscarriage. Yet, the underlying mechanisms remain largely unknown. Herein, we identified a novel upregulated lnc-HZ04 and a novel downregulated miR-hz04 in villous tissues of unexplained recurrent miscarriage (RM) relative to those in healthy control tissues and also in BPDE-treated human trophoblast cells. Lnc-HZ04 directly and specifically bound with miR-hz04, diminished the reduction effects of miR-hz04 on IP(3) R(1) mRNA expression level and on IP(3) R(1) mRNA stability, and then activated the Ca(2+) -mediated IP(3) R(1) /p-CaMKII/SGCB pathway, which further promoted trophoblast cell apoptosis. The miR-hz04 target site on lnc-HZ04 played crucial roles in these regulations. In normal trophoblast, relatively less lnc-HZ04 and more miR-hz04 suppressed this apoptosis pathway and gave normal pregnancy. After exposure to BPDE or in RM tissues, p53 was upregulated, which might promote p53-mediated lnc-HZ04 transcription. Relatively more lnc-HZ04 and less miR-hz04 activated this apoptosis pathway and might further induce miscarriage. BaP could also induce mice miscarriage by upregulating its corresponding murine apoptosis pathway. Therefore, BPDE-induced apoptosis of human trophoblast cells was associated with the occurrence of miscarriage. This work discovered the regulation roles of lnc-HZ04 and miR-hz04 and provided scientific and clinical understanding of the occurrence of unexplained miscarriage.		FASEB J. 2021 Sep;35(9):e21789. doi: 10.1096/fj.202100376RR.
5208	LncRNA	LOXL1-AS1	miR-590-5p	NA	Endothelial Cells	Atherosclerosis	Homo sapiens (human)	qRT-PCR 	34382896	Inhibition of LOXL1-AS1 alleviates oxidative low-density lipoprotein induced angiogenesis via downregulation of miR-590-5p mediated KLF6/VEGF signaling pathway.	Increasing evidences have confirmed that long non-coding RNA LOXL1-AS1 functions in multiple human diseases. Here, we aim to explore the function and mechanism of LOXL1-AS1 in modulating oxidized low-density lipoprotein (ox-LDL)-induced angiogenesis of endothelial cells (ECs). Presently, we found that LOXL1-AS1 and KLF6 were upregulated in ECs treated by Ox-LDL in a dose- and time-dependent manner while miR-590-5p was downregulated. Overexpression of LOXL1-AS1 aggravated Ox-LDL mediated ECs proliferation and migration, and promoted angiogenesis both in vitro and in vivo. On the contrary, enhancing miR-590-5p or inhibiting LOXL1-AS1 level led to suppressive effects on the proliferation, migration and angiogenesis of ECs. Moreover, LOXL1-AS1 upregulation promoted the expression of vascular endothelial growth factor (VEGF), MMPs (including MMP2, MMP9, and MMP14) and also activated VEGF/VEGFR2/PI3K/Akt/eNOS pathway. Mechanistically, LOXL1-AS1 works as a competitive endogenous RNA (ceRNA) by sponging miR-590-5p, which targeted at the 3'-untranslated region (3'UTR) of KLF6. Additionally, the proliferation, migration, and angiogenesis of ECs were elevated following KLF6 upregulation. By detecting the expression of LOXL1-AS1 and miR-590-5p in the serum of healthy donors and atherosclerosis patients, it was found that LOXL1-AS1 was upregulated in atherosclerosis patients (compared with healthy donors) and had a negative relationship with miR-590-5p. Taken together, LOXL1-AS1 promoted Ox-LDL induced angiogenesis via regulating miR-590-5p-modulated KLF6/VEGF signaling pathway. The LOXL1-AS1-miR-590-5p axis exerts a novel role in the progression of atherosclerosis.		Cell Cycle. 2021 Aug 12:1-18. doi: 10.1080/15384101.2021.1958501.
5209	LncRNA	XIST	miR-19	PTEN	Nucleus Pulposus Cells	Intervertebral Disc Degeneration	Homo sapiens (human)  	qRT-PCR 	34382895	Role of lncRNA XIST/microRNA-19/PTEN network in autophagy of nucleus pulposus cells in intervertebral disc degeneration via the PI3K/Akt signaling pathway.	Intervertebral disc degeneration (IVDD) is a complicated pathological condition accompanying with low back pain. This study was designed to figure out the mechanism of lncRNA XIST in IVDD. Abnormally expressed lncRNAs in IVDD patients were measured. The correlations among XIST, miR-19 and PTEN were identified. Overexpression and silencing of XIST, miR-19 and PTEN were introduced and their roles in NPC autophagy in vitro were detected. The potential signaling pathway involved in these events was identified. Consequently, high expression of XIST was found in IVDD patients. It induced NPC autophagy and reduced NPC viability. XIST could serve as a competing endogenous RNA (ceRNA) for miR-19 and upregulate PTEN expression. The overexpression of XIST reduced miR-19 expression, which was followed by enhanced PTEN expression. Upregulation of miR-19 increased NPC viability and proliferation, while decreased NPC autophagy that regulated by XIST, while overexpressed PTEN reversed the above changes. Moreover, overexpression of XIST inactivated the PI3k/Akt signaling pathway.		Cell Cycle. 2021 Aug 12:1-13. doi: 10.1080/15384101.2021.1924450.
5210	LncRNA	MIR503HG	miR-224-5p	TUSC3	Gastric Cancer Tissues And Cells	Gastric Cancer	Homo sapiens (human)  	MTT assay;qPCR;Western blot;Immunohistochemistry;MTT assay;	34381729	The LncRNA MIR503HG/miR-224-5p/TUSC3 Signaling Cascade Suppresses Gastric Cancer Development via Modulating ATF6 Branch of Unfolded Protein Response.	BACKGROUND: Unfolded protein response (UPR)-mediated tumor-promoting functions have been identified in multiple cancers, and this study focused on investigating the role and molecular mechanisms of UPR in modulating gastric cancer (GC) pathogenesis. METHODS: The bioinformatics analysis was performed to examine the expression status of cancer associated genes in patients with stomach adenocarcinoma (STAD) and predict the targeting sites of miR-224-5p with LncRNA MIR503HG and TUSC3. Genes expressions were quantified by Real-Time qPCR, Western Blot and immunohistochemistry (IHC). Cell proliferation, viability, apoptosis and mobility were evaluated by MTT assay, trypan blue staining assay, flow cytometer and transwell assay, respectively. The binding sites were validated by dual-luciferase reporter gene system assay. RESULTS: LncRNA MIR503HG and TUSC3 were downregulated, but miR-224-5p was upregulated in GC tissues and cells, in contrast with their normal counterparts. Further gain- and loss-of-function experiments validated that the malignant phenotypes in GC cells, including cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and tumorigenesis, were negatively regulated by LncRNA MIR503HG. Mechanistically, LncRNA MIR503HG upregulated TUSC3 in GC cells through sponging miR-224-5p, resulting in the repression of GC progression. Finally, we validated that knock-down of ATF6, but not other two branches of UPR (PERK1 and IRE1), partially rescued cell proliferation and EMT in the GC cells with LncRNA MIR503HG overexpression. CONCLUSIONS: Targeting the LncRNA MIR503HG/miR-224-5p/TUSC3 signaling cascade suppressed ATF6-mediated UPR, resulting in the blockage of GC development.		Front Oncol. 2021 Jul 26;11:708501. doi: 10.3389/fonc.2021.708501. eCollection 2021.
5211	LncRNA	COX10-AS1	miR-641	E2F6	Glioma Cell Lines	Glioma	Homo sapiens (human)  	ChIP;qRT-PCR;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA pull-down;	34381702	The COX10-AS1/miR-641/E2F6 Feedback Loop Is Involved in the Progression of Glioma.	Glioma is the most common primary tumour of the central nervous system and is considered one of the greatest challenges for neurosurgery. Mounting evidence has shown that lncRNAs participate in various biological processes of tumours, including glioma. This study aimed to reveal the role and relevant mechanism of COX10-AS1 in glioma. The expression of COX10-AS1, miR-641 and E2F6 was measured by qRT-PCR and/or western blot. Clone formation assays, EdU assays, Transwell assays and tumour xenograft experiments were performed to evaluate the effects of COX10-AS1, miR-641 and E2F6 on glioma proliferation, migration and invasion. Luciferase reporter assays, RNA pull-down assays and ChIP assays were conducted to analyse the relationship among COX10-AS1, miR-641 and E2F6. We demonstrated that COX10-AS1 was upregulated in glioma tissues and cell lines, which was related to the grade of glioma and patient survival. Next, through functional assays, we found that COX10-AS1 influenced the proliferation, migration and invasion of glioma cell lines. Then, with the help of bioinformatics analysis, we confirmed that COX10-AS1 regulated glioma progress by acting as a sponge of miR-641 to regulate E2F6. Moreover, further study indicated that E2F6 could promote COX10-AS1 expression by binding to its promoter region. Taken together, the data indicated that COX10-AS1 acts as an oncogene in combination with COX10-AS1/miR-641/E2F6 in glioma, which may be beneficial to the diagnosis and treatment of glioma.		Front Oncol. 2021 Jul 26;11:648152. doi: 10.3389/fonc.2021.648152. eCollection 2021.
5212	LncRNA	MIR100HG	miR-146b-5p	CBX6	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR;	34381502	Long Noncoding RNA MIR100HG Knockdown Attenuates Hepatocellular Carcinoma Progression by Regulating MicroRNA-146b-5p/Chromobox 6.	PURPOSE: Hepatocellular carcinoma (HCC) accounts for approximately ninety percent of primary liver cancer. This study attempted to investigate the effects of the long noncoding RNA MIR100HG (MIR100HG) in HCC and the underlying molecular mechanism. MATERIALS AND METHODS: qRT-PCR was implemented to analyze the expression of MIR100HG, microRNA-146b-5p (miR-146b-5p), and Chromobox 6 (CBX6). The correlation between MIR100HG and clinicopathological features of HCC patients was assessed. Additionally, the effects of MIR100HG knockdown on HCC cell viability, migration, and invasion were explored. The interactions among MIR100HG, miR-146b-5p, and CBX6 were confirmed. Furthermore, rescue experiments were conducted to investigate whether MIR100HG knockdown modulates HCC cell behaviors through modulating the miR-146b-5p/CBX6 axis. RESULTS: The expression of MIR100HG and CBX6 was enhanced, while miR-146b-5p was inhibited in HCC cells. High MIR100HG expression was positively associated with the TNM tumor stage and Edmondson-Steiner grading in HCC patients. MIR100HG knockdown considerably reduced the HCC cell viability, migration, and invasion. In addition, MIR100HG directly targeted miR-146b-5p, and miR-146b-5p directly targeted CBX6 in HCC cells. Moreover, miR-146b-5p suppression or CBX6 elevation evidently rescued the suppressed viability, migration, and invasion of HCC cells caused by MIR100HG knockdown. CONCLUSIONS: Knockdown of MIR100HG inhibited the viability, migration, and invasion of HCC cells by targeting the miR-146b-5p/CBX6 axis, offering a potential therapeutic target for HCC therapy.		Gastroenterol Res Pract. 2021 Jul 30;2021:6832518. doi: 10.1155/2021/6832518. eCollection 2021.
5213	LncRNA	HCG18	miR-148b	ETV5	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;	34377255	LncRNA HCG18 promotes cell multiplication and metastasis by miR-148b/ETV5 regulation in osteosarcoma.	OBJECTIVE: To determine the effects of long non-coding RNA (LncRNA) HCG18 on cell multiplication and invasion of osteosarcoma. METHODS: MTT assay and transwell assay were used for cell multiplication and invasion, respectively. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to determine transcriptional and translational expression. Luciferase reporter assay was used to identify the specific target relationships. RESULTS: The expression of LncRNA HCG18 was dramatically increased in osteosarcoma cells compared to the normal tissues. LncRNA-HCG18 accelerated cell multiplication and invasion in vitro, which was achieved by down-regulating the overexpression of miR-148b, and down-regulating ETV5, indicating combination of ETV5 and miR-148b in osteosarcoma. Overexpression of ETV5 could reverse the inhibitory effect of knockout of lncRNA HCG18 on cell multiplication and invasion. CONCLUSION: LncRNA HCG18 acted as a sponge of miR-148b and played an oncogenic role in osteosarcoma, providing therapeutic targets for osteosarcoma.		Am J Transl Res. 2021 Jul 15;13(7):7783-7793. eCollection 2021.
5214	LncRNA	MALAT1	miR-194-5p	DUSP1	Rhabdomyosarcoma (Rd) Cells	Rhabdomyosarcoma	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34377228	Integrative analysis of lncRNA-miRNA-mRNA-associated competing endogenous RNA regulatory network involved in EV71 infection.	The competing endogenous RNA (ceRNA) axis has been shown to play a critical role in the pathogenesis of various viral infections. Generally, the ceRNA network involves long non-coding RNAs (lncRNAs) that act as sponges for miRNA to regulate mRNA expression. However, no information is available regarding the involvement of ceRNA networks in Enterovirus type 71 (EV71) infections. In the present study, data obtained from Gene Expression Omnibus (GEO) database was analyzed using various bioinformatics tools. EV71 infection in rhabdomyosarcoma (RD) cells was associated with differential expression of six lncRNAs, 28 miRNAs, and 349 mRNAs. Gene function enrichment analysis suggested induction of cytoplasmic vesicle process upon EV71 infection. The ceRNA networks were constructed, in which 20 hub genes were predicted by protein-protein interaction. To confirm the MALAT1/miR-194-5p/DUSP1 ceRNA regulatory axis in EV71 infection, real-time quantitative polymerase chain reaction (qRT-PCR) and luciferase reporter assay were performed. The results of the study also revealed the involvement of the MALAT1/miR-194-5p axis in apoptosis induced by EV71 infection, while no association with autophagy was observed. Thus, the present study provided novel insights into the pathogenic mechanism of EV71 infection.		Am J Transl Res. 2021 Jul 15;13(7):7440-7457. eCollection 2021.
5215	LncRNA	CASC21	miR-485-5p	HGH1	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	RT-PCR;Western blot;	34375566	LncRNA CASC21 induces HGH1 to mediate colorectal cancer cell proliferation, migration, EMT and stemness.	Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Long non-coding RNAs (lncRNAs) have been increasingly reported to serve vital parts in malignancies including CRC. Although cancer susceptibility 21 (CASC21) has been uncovered to play a part in CRC, its mechanism still needs further explanation. Thus, our study aimed to further explore the influence and mechanism of CASC21 in CRC progression. Quantitative real-time RT-PCR and western blot were performed to detect gene expression; a series of functional assays were performed to investigate the effect of CASC21 on CRC cells; in vivo tumour growth was evaluated via the nude mice xenograft model. The results revealed that CASC21 facilitated CRC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and stemness. In addition, CASC21 was co-expressed with and bound to transcription factor POU5F1B (POU class 5 homeobox 1B). CASC21 recruited POU5F1B to HGH1 promoter to activate the transcription of HGH1 homolog. Also, CASC21 served as a competitive endogenous RNA (ceRNA) to up-regulate HGH1 via endogenously sponging miR-485-5p. Moreover, HGH1 overexpression counteracted the suppression of CASC21 deficiency on CRC tumour growth. In summary, our study indicated that CASC21 enhanced the expression of HGH1 to promote the malignancy of CRC by recruiting POU5F1B and sponging miR-485-5p, suggesting a key role of CASC21 in CRC progression.		RNA Biol. 2021 Aug 10:1-13. doi: 10.1080/15476286.2021.1950464.
5216	LncRNA	HAGLR	miR-335-3p	WNT2	Tnbc Cells, Bt549 Cells	Triple Negative Breast Cancer	Homo sapiens (human)  	qRT-PCR;luciferase assay;	34375306	LncRNA-HAGLR motivates triple negative breast cancer progression by regulation of WNT2 via sponging miR-335-3p.	BACKGROUND: Triple negative breast cancer (TNBC) is a group of highly heterogeneous mixed breast cancer at the level of gene expression profile. Therefore, it is of great clinical significance to explore the molecular mechanism of TNBC and find a targeted therapeutic approach from the molecular level. METHODS: Long non-coding RNA (lncRNA) HAGLR expression level was measured by and qRT-PCR in TNBC tissues and cell lines. EdU, MTT, wound healing and Transwell assays were performed to explore the role of HAGLR on the malignancy of TNBC cells. Luciferase assay was used to clarify the binding between miR-335-3p with HAGLR and WNT2. The tumor formation experiment in nude mice was used to explore the function of HAGLR in vivo. RESULTS: HAGLR was increased in TNBC tissues and cell lines. Silencing of HAGLR inhibited viability, proliferation, migration, and invasion of BT549 cells. Furthermore, HAGLR acted as a sponge of miR-335-3p and inhibited its expression. And miR-335-3p directly targeted WNT2. Functionally, forced expression of miR-335-3p or knockdown of WNT2 removed the promoted effects of lncRNA HAGLR on TNBC development. In vivo tumorigenesis experiments indicated HAGLR accelerated tumor growth via miR-335-3p/WNT2 axis. CONCLUSION: Our study revealed that HAGLR promoted the growth of TNBC, which was mediated by miR-335-3p/WNT2 axis.		Aging (Albany NY). 2021 Aug 10;13(15):19306-19316. doi: 10.18632/aging.203272. Epub 2021 Aug 10.
5217	LncRNA	NIFK-AS1	miR-637	AKT1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34374933	Upregulation of lncRNA NIFK-AS1 in hepatocellular carcinoma by m(6)A methylation promotes disease progression and sorafenib resistance.	Long non-coding RNAs (LncRNAs) have recently emerged as vital regulators in the development and progression of hepatocellular carcinoma (HCC), providing new opportunities as novel therapeutic targets. Here we identified the lncRNA NIFK-AS1 as being highly expressed in HCC tissues and cells and showed this up-regulation resulted from METTL3-dependent m(6)A methylation. Functionally, knockdown of NIFK-AS1 inhibited the proliferation, colony formation, migration, and invasion of HCC cells. Moreover, these effects were elicited though AKT1 and we uncovered a ceRNA network involving an NIFK-AS1/miR-637/AKT1 axis with downstream effects on HCC progression involving regulation of MMP-7 and MMP-9 expression. From the clinical perspective, we showed that knockdown of NIFK-AS1 sensitized HCC cells to sorafenib through the up-regulation of the drug transporters OATP1B1 and OATP1B3. Clinical investigations showed HCC patients with low NIFK-AS1 expression benefited from sorafenib therapy and this phenomenon was reproduced in patient-derived tumor xenograft models (PDX) comparing HCC with low and high expression of NIFK-AS1. Taken together, these results suggest an essential role for NIFK-AS1 in HCC progression and promote NIFK-AS1 as a new therapeutic target and predictor of sorafenib benefit in HCC patients.		Hum Cell. 2021 Aug 10. doi: 10.1007/s13577-021-00587-z.
5218	LncRNA	LAMTOR5-AS1	miR-let-7b-3p	LAMTOR5	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;	34374893	LAMTOR5 expression level is a biomarker for colorectal cancer and lncRNA LAMTOR5-AS1 predicting miRNA sponging effect.	BACKGROUND: Strong evidence indicated that high expression of HBXIP (also known as LAMTOR5) promotes cancer cells proliferation and helps cancer progression. Long non-coding RNAs (lncRNA) have also a crucial role in developing cancer. In this study, we aimed to determine the expression of LAMTOR5 and its nearby lncRNA, LAMTOR5-AS1 and investigate their potential as a biomarker in colorectal cancer (CRC) patients. METHODS: 75 tissues of colorectal tumors and non-tumor adjacent normal sampled in this study. After RNA procedure then RT-qPCR was applied for expression analysis. Moreover, in silico investigation also enrolled for predicting sponging effect of lncRNA with miRNAs. RESULTS: LAMTOR5 transcription level significantly overexpressed (p value < 0.001) and has shown a diagnostic potential (AUC = 0.8) in CRC. LAMTOR5-AS1 did not indicate any remarkable expression change overall, but showed a significant overexpressed in elderly patients (> 60) with CRC (p value < 0.0097). Moreover, the correlation analysis between LAMTOR5 and LAMTOR5-AS1 revealed a significant association in CRC (p value = 0.0074) which can be partly explained by its predicting act as a mediator with sponging effect on hsa-miR-let-7b-3p and hsa-miR-20a-5p. CONCLUSION: LAMTOR5 gene can be considered as prognostic biomarker for CRC. LAMTOR5-AS5 which is a nearby lncRNA of this gene could play a regulatory impact through its sponging effect on hsa-miR-let-7b-3p and hsa-miR-20a-5p which both have shown a significant impact on overall survival rate in CRC patients in high expression levels.		Mol Biol Rep. 2021 Aug;48(8):6093-6101. doi: 10.1007/s11033-021-06623-3. Epub 2021 Aug 10.
5219	LncRNA	RP11-70C1.3	miR-6736-3p	NRP-1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	microarray;	34374639	Long noncoding RNA RP11-70C1.3 confers chemoresistance of breast cancer cells through miR-6736-3p/NRP-1 axis.	Chemoresistance remains a major obstacle for improving the clinical outcome of patients with breast cancer. Recently, long noncoding RNAs (lncRNAs) have been implicated in breast cancer chemoresistance. However, the function and underlying mechanism are still largely unknown. Using lncRNA microarray, we identified 122 upregulated and 475 downregulated lncRNAs that might be related to the breast cancer chemoresistance. Among them, RP11-70C1.3 was one of the most highly expressed lncRNAs. In breast cancer patients, high RP11-70C1.3 expression predicted poor prognosis. Knockdown of RP11-70C1.3 inhibited the multidrug resistance of breast cancer cells in vitro and in vivo. Further investigations revealed that RP11-70C1.3 functioned as a competing endogenous RNA (ceRNA) for miR-6736-3p to increase NRP-1 expression. Notably, the rescue experiments showed that both miR-6736-3p inhibitor and NRP-1 overexpression could partly reverse the suppressive influence of RP11-70C1.3 knockdown on breast cancer chemoresistance. In conclusion, our study indicated that lncRNA RP11-70C1.3 regulated NRP-1 expression by sponging miR-6736-3p to confer chemoresistance of breast cancer cells. RP11-70C1.3 might be a potential therapeutic target in enhancing the clinical efficacy of chemotherapy in breast cancer.		Bosn J Basic Med Sci. 2021 Jun 29. doi: 10.17305/bjbms.2021.5803.
5220	LncRNA	CDKN2B-AS1	miR-122-5p	STK39	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	qRT-PCR;	34374638	Knockdown of long non-coding RNA CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.	The lncRNAs have been made certain to take part in the development of most cancers in multiple ways. Here, our purpose is to making observation of the biological role and function of lncRNA CDKN2B-AS1 in human breast cancer. Twenty-eight pairs of breast cancer tissue and adjacent normal tissue from breast cancer patients were used to investigate the expression of CDKN2B-AS1 by qRT-PCR. And a lentivirus-shRNA guided CDKN2B-AS1 were to reduce its expression. The function of CDKN2B-AS1 was analyzed using a series of in vitro assays. Meanwhile, the xenograft model was used to further explicate the role of CDKN2B-AS1 in breast cancer. As for the results, there is a relative rich expression of CDKN2B-AS1 in breast cancer tissues compared with the corresponding adjacent normal tissues. Compared with the human breast epithelial cell line, the abundant expression of CDKN2B-AS1 in breast cancer cells were revealed as well. Then, knockdown CDKN2B-AS1 inhibited the malignant biological behaviors of MCF7 and T47D cells. In mechanism, CDKN2B-AS1 sponged the miR-122-5p to regulate STK39 expression. Furthermore, the inhibition effect with sh-CDKN2B-AS1 on breast cancer cells was alleviated by miR-122-5p inhibitor. Last, an in vivo model also confirmed that knockdown CDKN2B-AS1 retarded the growth of breast cancer. Our data concluded that knockdown of CDKN2B-AS1 suppresses the progression of breast cancer by miR-122-5p/STK39 axis.		Bioengineered. 2021 Dec;12(1):5125-5137. doi: 10.1080/21655979.2021.1962685.
5221	LncRNA	MALAT1	miR-124-3p	SphK1	Osteosarcoma Cell Lines And Tissue	Osteosarcoma	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	34373692	Long Noncoding RNA MALAT1 Interacts with miR-124-3p to Modulate Osteosarcoma Progression by Targeting SphK1.	INTRODUCTION: Long noncoding RNAs (lncRNAs) have been implicated in a variety of biological functions, including tumor proliferation, apoptosis, progression, and metastasis. lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in various cancers, as well as osteosarcoma (OS); however, its underlying mechanism in OS is poorly understood. This investigation aims to elucidate the mechanisms of MALAT1 in OS proliferation and migration and to provide theoretical grounding for further targeted therapy in OS. METHODS: In the present study, we applied qRT-PCR to assess the MALAT1 expression in OS tissues and cell lines. The effects of MALAT1 and miR-124-3p on OS cell proliferation and migration were studied by CCK-8 and scratch assays. Cell cycle and apoptosis were tested using a flow cytometer. The competing relationship between MALAT1 and miR-124-3p was confirmed by dual-luciferase reporter assay. RESULTS: MALAT1 was overexpressed in OS cell lines and tissue specimens, and knockdown of MALAT1 significantly inhibited cell proliferation and migration and increased cell apoptosis and the percentage of G0/G1 phase. Furthermore, MALAT1 could directly bind to miR-124-3p and inhibit miR-124-3p expression. Moreover, MALAT1 overexpression significantly relieved the inhibition on OS cell proliferation mediated by miR-124-3p overexpression, which involved the derepression of sphingosine kinase 1 (SphK1). CONCLUSIONS: We propose that lncRNA MALAT1 interacts with miR-124-3p to modulate OS progression by targeting SphK1. Hence, we identified a novel MALAT1/miR-124-3p/SphK1 signaling pathway in the regulation of OS biological behaviors.		J Oncol. 2021 Jul 29;2021:8390165. doi: 10.1155/2021/8390165. eCollection 2021.
5222	LncRNA	ITGB8-AS1	miR-33b-5p	ITGA3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5223	LncRNA	ITGB8-AS1	let-7c-5p	ITGA3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5224	LncRNA	ITGB8-AS1	let-7d-5p	ITGA3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5225	LncRNA	ITGB8-AS1	miR-33b-5p	ITGB3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5226	LncRNA	ITGB8-AS1	let-7c-5p	ITGB3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5227	LncRNA	ITGB8-AS1	let-7d-5p	ITGB3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34371180	LncRNA ITGB8-AS1 functions as a ceRNA to promote colorectal cancer growth and migration through integrin-mediated focal adhesion signaling.	Long non-coding RNAs (lncRNAs) play critical roles in tumorigenesis and progression of colorectal cancer (CRC). However, functions of most lncRNAs in CRC and their molecular mechanisms remain uncharacterized. Here we found that lncRNA ITGB8-AS1 was highly expressed in CRC. Knockdown of ITGB8-AS1 suppressed cell proliferation, colony formation and tumor growth in CRC, suggesting oncogenic roles of ITGB8-AS1. Transcriptomic analysis followed by KEGG analysis revealed that focal adhesion signaling was the most significantly enriched pathway for genes positively-regulated by ITGB8-AS1. Consistently, Knockdown of ITGB8-AS1 attenuated the phosphorylation of SRC, ERK and p38 MAPK. Mechanistically, ITGB8-AS1 could sponge miR-33b-5p and let-7c-5p/let-7d-5p to regulate the expression of integrin family genes ITGA3 and ITGB3, respectively, in the cytosol of cells. Targeting ITGB8-AS1 using antisense oligonucleotide (ASO) remarkedly reduced cell proliferation and tumor growth in CRC, indicating that therapeutic potential of ITGB8-AS1 in CRC. Furthermore, ITGB8-AS1 was easily detected in plasma of CRC patients, which was positively correlated with differentiation and TNM stage, as well as plasma levels of ITGA3 and ITGB3. In conclusion, ITGB8-AS1 functions as a ceRNA to regulate cell proliferation and tumor growth of CRC via regulating focal adhesion signaling. Targeting ITGB8-AS1 is effective in suppressing CRC cell growth and tumor growth. Elevated plasma levels of ITGB8-AS1 were detected in advanced-stage CRC. Thus, ITGB8-AS1 could serve as a potential therapeutic target and circulating biomarker in CRC.		Mol Ther. 2021 Aug 6:S1525-0016(21)00405-6. doi: 10.1016/j.ymthe.2021.08.011.
5228	LncRNA	TMPO-AS1	miR-98-5p	BCAT1	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;	34370878	Long non-coding RNA TMPO-AS1 facilitates the progression of colorectal cancer cells via sponging miR-98-5p to upregulate BCAT1 expression.	BACKGROUND: Colorectal cancer, as a common malignant carcinoma in the gastrointestinal tract, has a high mortality globally. However, the specific molecular mechanisms of long non-coding RNA (lncRNA) thymopoietin antisense transcript 1 (TMPO-AS1) in colorectal cancer were unclear. METHODS: We tested the expression level of TMPO-AS1 via qRT-PCR in colorectal cancer cells while the protein levels of branched chain amino acid transaminase 1 (BCAT1) and the stemness-related proteins were evaluated by Western blot analysis. Colony formation, EdU staining, TUNEL, flow cytometry and sphere formation assays were to assess the biological behaviors of colorectal cancer cells. Then, luciferase reporter, RIP and RNA pull down assay were applied for confirming the combination between microRNA-98-5p (miR-98-5p) and TMPO-AS1/BCAT1. RESULTS: TMPO-AS1 was aberrantly expressed at high levels in colorectal cancer cells. Silenced TMPO-AS1 restrained cell proliferation and stemness and promoted apoptosis oppositely while overexpressing TMPO-AS1 exerted the adverse effects. Furthermore, miR-98-5p was proven to a target of TMPO-AS1 inhibit cell progression in colorectal cancer. Additionally, BCAT1 was proved to enhance cell progression as the target of miR-98-5p, and it offset the effect of silenced TMPO-AS1 on colorectal cancer cells. CONCLUSION: TMPO-AS1 promotes the progression of colorectal cancer cells via sponging miR-98-5p to upregulate BCAT1 expression.		J Gastroenterol Hepatol. 2021 Aug 9. doi: 10.1111/jgh.15657.
5229	LncRNA	SNHG14	miR-30b-5p	Atg5	Mouse Hippocampal Neuron (Ht22 Cells)	Cerebral Ischemia-Reperfusion Injury	Mus musculus (mouse)	qRT-PCR 	34369750	Propofol Protects against Cerebral Ischemia/Reperfusion Injury by Down-Regulating Long Noncoding RNA SNHG14.	Cerebral ischemia-reperfusion (CI/R) injury is a serious central nervous system disease. Propofol (PPF) exerts a neuroprotective effect in CI/R injury; the underlying cause is still unclear. Here, we cultured mouse hippocampal neuron (HT22 cells) in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to mimic CI/R injury in vitro. PPF treatment promoted cell viability and reduced apoptotic cells in the OGD/R-treated HT22 cells, which was effectively abrogated by SNHG14 overexpression. Moreover, we constructed a CI/R injury mouse model on C57BL/6J mice by middle cerebral artery occlusion/reperfusion (MCAO/R), followed by administration of PPF. PPF reduced neuronal damage and loss, enhanced glial cell hyperplasia, and ameliorated cerebral cortex tissue damage and brain infarct in MCAO/R-induced mice. SNHG14 overexpression aggravated MCAO/R-induced CI/R injury in mice. Furthermore, SNHG14 promoted the expression of Atg5 and Beclin 1 via competitively binding miR-30b-5p, which contributed to activate autophagy and apoptosis in HT22 cells. In addition, the levels of p-p38 and p-SP1 were reduced in the OGD/R-treated HT22 cells in the presence of PPF. SP1 interacted with the promoter of SNHG14 and elevated the expression of SNHG14. PPF treatment inhibited the SP1-mediated up-regulation of SNHG14. In conclusion, this work demonstrates that PPF inhibits SNHG14 expression though the p38 MAPK signaling pathway. SNHG14 promotes Atg5 and Beclin 1 expression by sponging miR-30b-5p and thus activates autophagy and aggravates CI/R injury.		ACS Chem Neurosci. 2021 Aug 18;12(16):3002-3014. doi: 10.1021/acschemneuro.1c00059. Epub 2021 Aug 9.
5230	LncRNA	SNHG14	miR-30b-5p	Beclin 1	Mouse Hippocampal Neuron (Ht22 Cells)	Cerebral Ischemia-Reperfusion Injury	Mus musculus (mouse)	qRT-PCR 	34369750	Propofol Protects against Cerebral Ischemia/Reperfusion Injury by Down-Regulating Long Noncoding RNA SNHG14.	Cerebral ischemia-reperfusion (CI/R) injury is a serious central nervous system disease. Propofol (PPF) exerts a neuroprotective effect in CI/R injury; the underlying cause is still unclear. Here, we cultured mouse hippocampal neuron (HT22 cells) in oxygen-glucose deprivation/reoxygenation (OGD/R) conditions to mimic CI/R injury in vitro. PPF treatment promoted cell viability and reduced apoptotic cells in the OGD/R-treated HT22 cells, which was effectively abrogated by SNHG14 overexpression. Moreover, we constructed a CI/R injury mouse model on C57BL/6J mice by middle cerebral artery occlusion/reperfusion (MCAO/R), followed by administration of PPF. PPF reduced neuronal damage and loss, enhanced glial cell hyperplasia, and ameliorated cerebral cortex tissue damage and brain infarct in MCAO/R-induced mice. SNHG14 overexpression aggravated MCAO/R-induced CI/R injury in mice. Furthermore, SNHG14 promoted the expression of Atg5 and Beclin 1 via competitively binding miR-30b-5p, which contributed to activate autophagy and apoptosis in HT22 cells. In addition, the levels of p-p38 and p-SP1 were reduced in the OGD/R-treated HT22 cells in the presence of PPF. SP1 interacted with the promoter of SNHG14 and elevated the expression of SNHG14. PPF treatment inhibited the SP1-mediated up-regulation of SNHG14. In conclusion, this work demonstrates that PPF inhibits SNHG14 expression though the p38 MAPK signaling pathway. SNHG14 promotes Atg5 and Beclin 1 expression by sponging miR-30b-5p and thus activates autophagy and aggravates CI/R injury.		ACS Chem Neurosci. 2021 Aug 18;12(16):3002-3014. doi: 10.1021/acschemneuro.1c00059. Epub 2021 Aug 9.
5231	LncRNA	GLIDR	miR-1270	TCF12	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Flow Cytometry assay;	34369267	Long non-coding RNA GLIDR accelerates the tumorigenesis of lung adenocarcinoma by miR-1270/TCF12 axis.	Lung adenocarcinoma (LUAD) is a deadly cancer with a high incidence worldwide. Long noncoding RNAs (lncRNAs) have been confirmed to have the regulatory effects on the occurrence and development of LUAD. But the specific functions of lncRNA GLIDR in LUAD are still not explicit and need to be investigated. On the basis of the outcomes of RT-qPCR experiments, the relative expression of GLIDR was evidently up-regulated in LUAD cells, while that of miR-1270 was down-regulated. The down-regulation of GLIDR inhibits cell proliferation in accordance with the results of CCK-8, EdU and colony formation assays, and accelerates cell apoptosis according to the results of flow cytometry and JC-1 analyses. Luciferase reporter, RNA pull down and RIP assays indicated that GLIDR could sponge miR-1270 in LUAD. Additionally, TCF12 was proved as the target gene of miR-1270. Furthermore, rescue experiments indicated that overexpression of TCF12 could offset the inhibitory functions of silencing GLIDR on cell behaviors. In brief, this study has demonstrated that GLIDR/miR-1270/TCF12 axis plays the crucial role in LUAD, which offers a new insight into researches on molecular mechanism concerning LUAD and provides with a new perspective for LUAD treatment.		Cell Cycle. 2021 Aug 7:1-10. doi: 10.1080/15384101.2021.1953754.
5232	LncRNA	AK006774	miR-448	bcl-2	Mouse Ischemia/Reperfusion (I/R) Model	Myocardial Infarction	Mus musculus (mouse)	RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	34369259	Long non-coding RNA AK006774 inhibits cardiac ischemia-reperfusion injury via sponging miR-448.	In recent years, the incidence and mortality of myocardial infarction (MI) have been increasing throughout the world, threatening public health. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play critical roles in the progression of MI. The present study aimed to investigate the role of lncRNA AK006774 in the progression of myocardial infarction and find out novel therapeutic or diagnostic target of myocardial infarction. A mouse ischemia/reperfusion (I/R) model and 2,3,5-Triphenyte-trazoliumchloride (TTC) staining were performed to evaluate the effects of AK006774 on I/R injury in vivo. Hypoxia/reoxygenation (H/R) models using primary cardiomyocytes have been established. Flow cytometry and Terminal Deoxynucleotide Transferase dUTP Nick End Labeling (TUNEL) assays were performed to evaluate the effects of AK006774 on cardiomyocyte apoptosis. Luciferase and RNA pull-down assays were performed to verify the interaction between miR-448 and its targets. Western blotting and quantitative PCR were performed to determine protein and gene expression, respectively. We first found that AK006774 overexpression reduced I/R-induced infarct area and cardiomyocyte apoptosis in vivo. Accordingly, AK006774 inhibited apoptosis and oxidative stress in cardiomyocytes subjected to H/R treatment in vitro. Mechanistically, AK006774 modulated the expression of bcl-2 by sponging miR-448. Overexpression of miR-448 antagonized the effects of AK006774 on cardiomyocyte apoptosis. The AK006774/miR-448/bcl-2 signaling axis acts as a key regulator of I/R injury and may be a potential therapeutic or diagnostic target for the treatment of MI.		Bioengineered. 2021 Dec;12(1):4972-4982. doi: 10.1080/21655979.2021.1954135.
5233	LncRNA	DNM3OS	miR-196b-5p	GAPDH	Hd Pc12 Cells	Huntingtons Disease	Rattus (rat)	qRT-PCR 	34369082	DNM3OS regulates GAPDH expression and influences the molecular pathogenesis of Huntington's disease.	Emerging studies have suggested that dysregulated long non-coding RNAs (lncRNAs) are associated with the pathogenesis of neurodegenerative diseases (NDD) including Huntington's disease (HD); however, the pathophysiological mechanism by which lncRNA dysregulation participates in HD remains to be elucidated. Here, we aim to analyse the expression of lncRNA-DNM3OS and identify the possible DNM3OS/miR-196b-5p/GAPDH pathway. PC12 cells induced by rat pheochromocytoma expressing HD gene exon 1 fragment with either 23 or 74 polyglutamine repeats fused to the green fluorescent protein (GFP) were cultured. Our results show that GAPDH and DNM3OS were upregulated in HD PC12 cells, downregulation of which lead to inhibition of aggregate formation accompanied by a decreased apoptosis rate and increased relative ROS levels and cell viability. Moreover, upregulated DNM3OS decreased the expression of miR-196b-5p by sponging, and GAPDH was a direct target of miR-196b-5p, playing an important pathogenic role in the formation of aggregates in the HD cell model. Our study uncovers a novel DNM3OS/miR-196b-5p/GAPDH pathway involved in the molecular pathogenesis of HD, which may offer a potential therapeutic strategy for HD.		J Cell Mol Med. 2021 Aug 8. doi: 10.1111/jcmm.16838.
5234	LncRNA	SNHG7	miR-425-5p	TRAF5	Sprague-Dawley (Sd) Rats And Sh-Sy5Y Cells	Parkinsons Disease	Rattus (rat)	RNA immunoprecipitation;Western blot;Immunohistochemistry;Luciferase activity assay;RNA immunoprecipitation;	34369042	Downregulation of long noncoding RNA SNHG7 protects against inflammation and apoptosis in Parkinson's disease model by targeting the miR-425-5p/TRAF5/NF-kB axis.	Accumulated evidence has manifested that long noncoding RNA (lncRNA) is involved in the progress of Parkinson's disease (PD). SNHG7, a novel lncRNA, has been found to be involved in tumorigenesis. However, SNHG7 expression and its functional effects on PD remain uncharted. Rotenone (Rot) was adopted to construct PD models in Sprague-Dawley (SD) rats and SH-SY5Y cells, respectively. The expression levels of caspase 3, tyrosine hydroxylase (TH), ionized calcium-binding adapter molecule 1 (Iba1) in SD rat striatum were measured via immunohistochemistry and western blot. Additionally, the expressions of inflammatory cytokines (interleukin 1b [IL-1b], IL-6, tumor necrosis factor a) and oxidative stress factors (malondialdehyde, superoxide dismutase, and glutathione peroxidase) in the brain tissues were examined using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Moreover, the protein levels of tumor necrosis factor receptor-associated factor (TRAF5), I-kB, nuclear factor-kB (NF-kB), HO-1, Nrf2 were detected via western blot. Bioinformatics was applied to predict the targeting relationship between SNHG7, miR-425-5p, and TRAF5. Dual-luciferase activity assay and RNA immunoprecipitation assays were conducted to verify their interactions. In comparison to healthy donors, SNHG7 was found upregulated while miR-425-5p expression was downregulated in PD patients. Functional experiments confirmed that SNHG7 downregulation or miR-425-5p overexpression attenuated neuronal apoptosis in the Rot-mediated PD model, TH-positive cell loss, and microglial activation by mitigating inflammation and oxidative stress. Mechanistically, SNHG7 served as a competitive endogenous RNA by sponging miR-425-5p and promoted TRAF5 mediated inflammation and oxidative stress. Inhibition of SNHG7 ameliorated neuronal apoptosis in PD through relieving miR-425-5p/TRAF5/NF-kB signaling pathway modulated inflammation and oxidative stress, and similar results were observed in the Rot-mediated rat model of PD.		J Biochem Mol Toxicol. 2021 Aug 8:e22867. doi: 10.1002/jbt.22867.
5235	LncRNA	SNHG5	miR-181a-5p	TGFBR3	Cartilage Tissues Of Osteoarthritis Patients And C20/A4 Cells	Osteoarthritis	Homo sapiens (human)  	Dual-luciferase reporter assay;qPCR;RACE;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34369033	SNHG5 protects chondrocytes in interleukin-1b-stimulated osteoarthritis via regulating miR-181a-5p/TGFBR3 axis.	Long noncoding RNAs (lncRNAs) have been considered as important modulators in the development of osteoarthritis. The present study investigates whether there is a link between lncRNA small nucleolar RNA host gene 5 (SNHG5) and osteoarthritis pathogenesis, and the underlying molecular mechanism. To establish an in vitro model of osteoarthritis, interleukin 1b (IL-1b) was used to treat chondrocytes (C20/A4 cells) for mimicking the inflammatory condition in osteoarthritis pathogenesis. SNHG5 and miR-181a-5p expression levels were then detected in cartilage tissues of osteoarthritis patients and C20/A4 cells by quantitative polymerase chain reaction (qPCR). Cell counting kit-8 and 5-ethynyl-2'-deoxyuridine assays were applied for detecting the viability of chondrocytes, and the apoptosis of chondrocytes was examined through caspase-3 activity assay and flow cytometry analysis. Western blot and qPCR were employed for determining the expression levels of TGFBR3, ADAMTS5, and MMP-13. The regulatory relationships among SNHG5, miR-181a-5p, and TGFBR3 were verified by RNA immunoprecipitation and dual-luciferase reporter assays. The expression levels of SNHG5 and TGFBR3 were markedly decreased, and miR-181a-5p expression was enhanced in osteoarthritis tissues and chondrocytes treated with IL-1b. SNHG5 knockdown inhibited the viability of chondrocytes, induced apoptosis, and promoted the expression levels of ADAMTS5 and MMP-13. Conversely, SNHG5 overexpression could counteract the effects of IL-1b, increase the viability of chondrocytes and suppress apoptosis. Mechanically, SNHG5 positively regulated TGFBR3 expression via sponging miR-181a-5p. Moreover, miR-181a-5p overexpression and TGFBR3 knockdown counteracted the effects of SNHG5 on chondrocytes. SNHG5 can probably protect chondrocytes from the inflammatory response and reduce the degradation of the extracellular matrix via modulating the miR-181a-5p/TGFBR3 axis.		J Biochem Mol Toxicol. 2021 Aug 8:e22866. doi: 10.1002/jbt.22866.
5236	LncRNA	CDKN2B-AS1	miR-28-5p	URGCP	Colorectal Cancer Tissues	Colorectal Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34368874	LncRNA CDKN2B-AS1 sponges miR-28-5p to regulate proliferation and inhibit apoptosis in colorectal cancer.	Long noncoding RNA (lncRNA) CDKN2B-antisense RNA 1 (AS1) functions as a tumor oncogene in numerous cancers. However, the roles and mechanism of CDKN2B-AS1 in colorectal cancer (CRC) have not been explored. The present study aimed to investigate whether and how CDKN2B-AS1 contributes to CRC progression. The data revealed that CDKN2B-AS1 expression was upregulated in CRC tissues. Loss-of-function assays demonstrated that CDKN2B-AS1 in CRC modulated cell proliferation and apoptosis, which was mediated by cyclin D1, cyclin-dependent kinase (CDK) 4, p-Rb, caspase-9 and caspase-3. Bioinformatics analysis and luciferase reporter assays indicated direct binding of microRNA (miR)-28-5p to CDKN2B-AS1. Moreover, the results herein revealed that the expression of miR-28-5p was negatively correlated with that of CDKN2B-AS1 in CRC tissue. Moreover, CDKN2B-AS1 acted as a miR-28-5p competing endogenous RNA (ceRNA) to target and regulate the expression of URGCP. These findings indicated that CDKN2B-AS1 plays roles in CRC progression, providing a potential therapeutic target or novel diagnostic biomarker for CRC.		Oncol Rep. 2021 Oct;46(4):213. doi: 10.3892/or.2021.8164. Epub 2021 Aug 9.
5237	LncRNA	SNHG22	miR-128-3p	E2F3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34368861	lncRNA SNHG22 sponges miR-128-3p to promote the progression of colorectal cancer by upregulating E2F3.	The long non-coding RNA (lncRNA) small nucleolar RNA host gene 22 (SNHG22) has been reported as a crucial regulator in several types of human cancer. The present study evaluated the function and mechanism of SNHG22 in colorectal cancer (CRC) progression. SNHG22 expression was detected in colorectal adenoma, CRC tumor tissues (TTs) and adjacent non-cancerous tissues (ANTs) using reverse transcription-quantitative PCR (RT-qPCR). The biological behaviors of SNHG22 in CRC cell lines were explored in vitro using Cell Counting Kit-8, flow cytometry, wound scratch assay and Transwell assay, and in vivo using a nude mouse xenograft model. The interaction between SNHG22 and microRNA-128-3p (miR-128-3p), and the target genes of miR-128-3p were explored using online tools, RT-qPCR, western blotting and a dual-luciferase reporter assay. The present study revealed that SNHG22 expression was most highly expressed in TTs followed by adenoma tissues and ANTs. In addition, high SNHG22 expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC. SNHG22 knockdown markedly inhibited CRC cell proliferation, apoptosis resistance, migration and invasion in vitro, and hindered tumor growth in vivo. The mechanistic study revealed that SNHG22 bound to miR-128-3p and attenuated its inhibitory effects on E2F transcription factor 3 (E2F3) expression levels and activity. Rescue experiments demonstrated that inhibiting miR-128-3p or upregulating E2F3 offset the effects of SNHG22 knockdown on CRC cells. The present findings support the existence of an interactive regulatory network involving SNHG22, miR-128-3p and E2F3 in CRC cell lines, indicating that the SNHG22/miR-128-3p/E2F3 axis may be considered a novel diagnostic and therapeutic target in CRC.		Int J Oncol. 2021 Sep;59(3):71. doi: 10.3892/ijo.2021.5251. Epub 2021 Aug 9.
5238	LncRNA	SNHG22	miR-128-3p	E2F3	Colorectal Cancer Cell	Colorectal Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34368861	lncRNA SNHG22 sponges miR-128-3p to promote the progression of colorectal cancer by upregulating E2F3.	The long non-coding RNA (lncRNA) small nucleolar RNA host gene 22 (SNHG22) has been reported as a crucial regulator in several types of human cancer. The present study evaluated the function and mechanism of SNHG22 in colorectal cancer (CRC) progression. SNHG22 expression was detected in colorectal adenoma, CRC tumor tissues (TTs) and adjacent non-cancerous tissues (ANTs) using reverse transcription-quantitative PCR (RT-qPCR). The biological behaviors of SNHG22 in CRC cell lines were explored in vitro using Cell Counting Kit-8, flow cytometry, wound scratch assay and Transwell assay, and in vivo using a nude mouse xenograft model. The interaction between SNHG22 and microRNA-128-3p (miR-128-3p), and the target genes of miR-128-3p were explored using online tools, RT-qPCR, western blotting and a dual-luciferase reporter assay. The present study revealed that SNHG22 expression was most highly expressed in TTs followed by adenoma tissues and ANTs. In addition, high SNHG22 expression levels were significantly associated with advanced clinicopathological factors and worse survival in patients with CRC. SNHG22 knockdown markedly inhibited CRC cell proliferation, apoptosis resistance, migration and invasion in vitro, and hindered tumor growth in vivo. The mechanistic study revealed that SNHG22 bound to miR-128-3p and attenuated its inhibitory effects on E2F transcription factor 3 (E2F3) expression levels and activity. Rescue experiments demonstrated that inhibiting miR-128-3p or upregulating E2F3 offset the effects of SNHG22 knockdown on CRC cells. The present findings support the existence of an interactive regulatory network involving SNHG22, miR-128-3p and E2F3 in CRC cell lines, indicating that the SNHG22/miR-128-3p/E2F3 axis may be considered a novel diagnostic and therapeutic target in CRC.		Int J Oncol. 2021 Sep;59(3):71. doi: 10.3892/ijo.2021.5251. Epub 2021 Aug 9.
5239	LncRNA	OIP5-AS1	miR-200c-3p	PTEN	Endometrial Cancer Cells	Endometrial Cancer	Homo sapiens (human)  	Flow Cytometry assay;	34368370	lncRNA OIP5-AS1 Suppresses Cell Proliferation and Invasion of Endometrial Cancer by Regulating PTEN/AKT via Sponging miR-200c-3p.	BACKGROUND: Endometrial carcinoma (EC) is one of the major gynecologic malignancy cancers affecting females with dismal prognosis and high mortality around the world. Numerous studies have proven that an aberrant level of long noncoding RNAs is present in many endometrial cancer patients, while the underlying molecular mechanism remains unclear. METHOD: The expression levels of lncRNA OIP5-AS1, miR200c-3p, and PTEN were measured by a quantitative real-time polymerase chain reaction in endometrial cancer tissue and endometrial cancer cells. CCK8 assay, wound-healing assay, and cell colony formation were applied to evaluate cell proliferation, cell migration, and cell colony formation ability. Cell cycle and cell apoptosis were detected by flow cytometry. The interactions between OIP5-AS1, miR200c-3p, and PTEN were explored by luciferase activity. RESULTS: In the present study, we demonstrated that long noncoding RNA OIP5-AS1 was significantly reduced in EC tissue compared with normal tissue. The lower expression level of OIP5-AS1 was also confirmed in four kinds of EC cell lines compared with the normal endometrial cell line. Gain- and loss-of-function of experiments indicated that upregulation of OIP5-AS1 could inhibit the proliferation, migration, and invasion of EC cells in vitro. Meanwhile, overexpression of OIP5-AS1 could also suppress the growth of tumor in the xenograft model. Moreover, further study revealed that miR-200c-3p could bind to OIP5-AS1, and the loss function of miR-200c-3p could reverse the elevated OIP5-AS1's inhibitory effect on the progression of EC. Furthermore, we found that downregulation of miR-200c-3p was inversely correlated with PTEN expression in EC cells. Reduced OIP5-AS1 could lead to the accumulation of miR-200c-3p, which could induce the upregulation of PTEN indirectly. CONCLUSION: Our study demonstrated a novel molecular mechanism that lncRNA OIP5-AS1 could modulate the progression of EC by combining competitively with miR-200c-3p to control the PTEN/AKT pathway in EC cells, which might supply important information for developing novel therapeutic strategies for EC patients.		J Immunol Res. 2021 Jul 28;2021:4861749. doi: 10.1155/2021/4861749. eCollection 2021.
5240	LncRNA	OIP5-AS1	miR-200c-3p	AKT	Endometrial Cancer Cells	Endometrial Cancer	Homo sapiens (human)  	Flow Cytometry assay;	34368370	lncRNA OIP5-AS1 Suppresses Cell Proliferation and Invasion of Endometrial Cancer by Regulating PTEN/AKT via Sponging miR-200c-3p.	BACKGROUND: Endometrial carcinoma (EC) is one of the major gynecologic malignancy cancers affecting females with dismal prognosis and high mortality around the world. Numerous studies have proven that an aberrant level of long noncoding RNAs is present in many endometrial cancer patients, while the underlying molecular mechanism remains unclear. METHOD: The expression levels of lncRNA OIP5-AS1, miR200c-3p, and PTEN were measured by a quantitative real-time polymerase chain reaction in endometrial cancer tissue and endometrial cancer cells. CCK8 assay, wound-healing assay, and cell colony formation were applied to evaluate cell proliferation, cell migration, and cell colony formation ability. Cell cycle and cell apoptosis were detected by flow cytometry. The interactions between OIP5-AS1, miR200c-3p, and PTEN were explored by luciferase activity. RESULTS: In the present study, we demonstrated that long noncoding RNA OIP5-AS1 was significantly reduced in EC tissue compared with normal tissue. The lower expression level of OIP5-AS1 was also confirmed in four kinds of EC cell lines compared with the normal endometrial cell line. Gain- and loss-of-function of experiments indicated that upregulation of OIP5-AS1 could inhibit the proliferation, migration, and invasion of EC cells in vitro. Meanwhile, overexpression of OIP5-AS1 could also suppress the growth of tumor in the xenograft model. Moreover, further study revealed that miR-200c-3p could bind to OIP5-AS1, and the loss function of miR-200c-3p could reverse the elevated OIP5-AS1's inhibitory effect on the progression of EC. Furthermore, we found that downregulation of miR-200c-3p was inversely correlated with PTEN expression in EC cells. Reduced OIP5-AS1 could lead to the accumulation of miR-200c-3p, which could induce the upregulation of PTEN indirectly. CONCLUSION: Our study demonstrated a novel molecular mechanism that lncRNA OIP5-AS1 could modulate the progression of EC by combining competitively with miR-200c-3p to control the PTEN/AKT pathway in EC cells, which might supply important information for developing novel therapeutic strategies for EC patients.		J Immunol Res. 2021 Jul 28;2021:4861749. doi: 10.1155/2021/4861749. eCollection 2021.
5241	LncRNA	RUSC1-AS1	miR-101-3p	Notch1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34367901	Long-non-coding RNA RUSC1-AS1 accelerates osteosarcoma development by miR-101-3p-mediated Notch1 signalling pathway.	BACKGROUND: Long non-coding RNA (lncRNA) RUSC1-AS1 has been found to modulate several cancers development. In this study, we explored the role of RUSC1-AS1 on osteosarcoma (OS) progression. METHODS: Quantitative Real-time PCR (qRT-PCR) was conducted to test the relative expression of RUSC1-AS1, Notch1 mRNA and miR-101-3p in OS tissues and adjacent normal tissues. Gain- or loss- of functional assays were carried out to determine the roles of RUSC1-AS1 and miR-101-3p in OS progression both in vitro and in vivo. The expression of E-cadherin, N-cadherin, Vimentin, Snail, Notch1, Ras and ERK was determined by Western blot. Furthermore, the relationships between RUSC1-AS1 and miR-101-3p, Notch1 and miR-101-3p were confirmed through RNA immunoprecipitation (RIP) and dual luciferase reporter gene assay. RESULTS: RUSC1-AS1 and Notch1 were up-regulated in OS cells and tissues. Down-regulating RUSC1-AS1 significantly attenuated the proliferative, epithelial-mesenchymal transition (EMT), growth, lung metastasis, migrative and invasive abilities of MG-63 and Saos-2 cells, and aggravated apoptosis, accompanied with down-regulated Notch1-Ras-ERK1/2 in those cells both in vitro and in vivo, while overexpression of RUSC1-AS1 exerted opposite effects. Overexpressing miR-101-3p in OS cells had similar effects as RUSC1-AS1 inhibition. In addition, RUSC1-AS1 functioned as a competing endogenous RNA (ceRNA) to competitively sponge miR-101-3p, thus upregulating Notch1 expression and mediating the malignant behaviors of OS cells. CONCLUSION: RUSC1-AS1 is a novel oncogenic lncRNA in OS through the miR-101-3p-Notch1-Ras-ERK pathway, which might be a potential therapeutic target for OS.		J Bone Oncol. 2021 Jul 16;30:100382. doi: 10.1016/j.jbo.2021.100382. eCollection 2021 Oct.
5242	LncRNA	KCNMB2-AS1	miR-374a-3p	S100A10	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)  	qRT-PCR 	34367236	KCNMB2-AS1 Promotes Bladder Cancer Progression Through Sponging miR-374a-3p to Upregulate S100A10.	Long non-coding RNAs (lncRNAs) have been reported to play a crucial role in the pathogenesis of numerous cancers. However, the function of lncRNA KCNMB2-AS1 in bladder cancer (BC) remains unclear. In the present study, we aimed to explore the role and underlying mechanisms of KCNMB2-AS1 in bladder cancer progression. We found that lncRNA KCNMB2-AS1 was significantly upregulated both in BC tissues and cell lines, the expression level was highly correlated with pathological TNM stage. Functionally, knockdown of lncRNA KCNMB2-AS1 dramatically inhibited the proliferation, migration, and invasion and of BC cells in vitro, and suppressed tumor growth in vivo. Mechanistically, lncRNA KCNMB2-AS1 could function as a competitive endogenous RNA (ceRNA) through direct sponging miR-374a-3p, which regulated the expression of S100A10. In conclusion, our results demonstrated that lncRNA KCNMB2-AS1 can promote the progression of bladder cancer through regulation of miR-374a-3p/S100A10.		Front Genet. 2021 Jul 22;12:655569. doi: 10.3389/fgene.2021.655569. eCollection 2021.
5243	LncRNA	VCAN-AS1	miR-106a-5p	STAT3	Breast Cancer Tissues And Cells	Breast Cancer	Homo sapiens (human)  	qRT-PCR 	34365889	Long non-coding RNA VCAN-AS1 promotes the malignant behaviors of breast cancer by regulating the miR-106a-5p-mediated STAT3/HIF-1a pathway.	An accumulating number of studies have found that long noncoding RNAs (lncRNAs) participate in breast cancer (BC) development. LncRNA VCAN-AS1, a novel lncRNA, has been confirmed to regulate the progression of gastric cancer, while its role in BC is elusive. Here, our results illustrate that VCAN-AS1 is overexpressed in BC tissues and cells, while miR-106a-5p was downregulated and negatively correlated with VCAN-AS1. In addition, high VCAN-AS1 expression and low miR-106a-5p expression were closely correlated with poor overall survival in BC patients. Functional experiments confirmed that VCAN-AS1 overexpression notably accelerated BC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) and enhanced tumor cell growth while also suppressing cell apoptosis. However, overexpression of miR-106a-5p had the opposite effects. In addition, rescue experiments confirmed that overexpression of VCAN-AS1 inhibited the tumor-suppressive effects mediated by miR-106a-5p. Mechanistically, through bioinformatics analysis, we found that VCAN-AS1 functions as a competitive endogenous RNA (ceRNA) of miR-106a-5p, which targets the 3' untranslated region (UTR) of signal transducer and activator of transcription 3 (STAT3). Further experiments indicated that miR-106a-5p downregulated the STAT3/hypoxia-inducible factor-1alpha (HIF-1a) pathway, while activating the STAT3 pathway reversed miR-106a-5p-mediated antitumor effects. Collectively, our data suggest that VCAN-AS1 is upregulated in breast cancer and promotes its progression by regulating the miR-106a-5p-mediated STAT3/HIF-1a pathway. This study provides a new target for BC therapy.		Bioengineered. 2021 Dec;12(1):5028-5044. doi: 10.1080/21655979.2021.1960774.
5244	LncRNA	CES4	miR-616-5p	DUSP2	Gastric Carcinoma Cells	Gastric Cancer	Homo sapiens (human)  	CCK-8 assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34365722	Apatinib combined with Keytruda treatment induces apoptosis of gastric carcinoma cells through CES4/miR-616-5p/DUSP2 axis.	Gastric carcinoma (GC) is a highly malignant and heterogeneous tumour. Long non-coding RNA CES4 is down-regulated in GC. However, whether CES4 can participate in GC remains unclear, we have carried out research on this topic. GC cells (HGC-27 and MKN-7) were treated with anti-tumour drugs; apatinib combined with Keytruda. Cell viability and apoptosis were detected by CCK-8 assay and flow cytometry. Gene and protein expression were examined by quantitative real-time PCR and western blot. Luciferase reporter assay was performed to verify the relationship among CES4, miR-616-5p and dual-specificity phosphatase-2 (DUSP2). CES4 was highly expressed in the apatinib combined with Keytruda-treated HGC-27 and MKN-7 cells. Apatinib combined with Keytruda treatment repressed cell viability and promoted apoptosis of HGC-27 and MKN-7 cells, which was abrogated by CES4 knockdown. Furthermore, CES4 promoted DUSP2 expression by sponging miR-616-5p in HGC-27 and MKN-7 cells. CES4 knockdown promoted cell viability and inhibited apoptosis of drug-treated HGC-27 and MKN-7 cells by regulating miR-616-5p/DUSP2 axis. In conclusion, these data demonstrate that apatinib combined with Keytruda treatment induces apoptosis of GC cells through CES4/miR-616-5p/DUSP2 axis. Thus, this work provides the experimental basis for the combination of apatinib and Keytruda as a treatment for GC.		Basic Clin Pharmacol Toxicol. 2021 Aug 7. doi: 10.1111/bcpt.13641.
5245	LncRNA	HOTAIR	miR-17-5p	MMP2	The Lungs And A549 Cells	Paraquat (Pq) Poisoning	Homo sapiens (human)  	qRT-PCR 	34364922	Long noncoding RNA HOTAIR functions as ceRNA to regulate MMP2 in paraquat induced lung epithelial-mesenchymal transition.	Paraquat (PQ) poisoning induces epithelial-mesenchymal transition (EMT) in the lungs, resulting in pulmonary fibrosis with a poor prognosis. Although competitive endogenous RNA (ceRNA) networks are known to exert post-transcriptional regulatory effects, the roles of such networks in PQ-induced EMT remain unknown. We explored the potential ceRNA network involved in PQ-induced pulmonary EMT. The male BALB/c mice were injected with 10 mg/kg PQ intraperitoneally and the lungs were harvested at 21(st) day. The A549 cells were treated with 60 μmol/L PQ for 6 days. We determined the expression level of epithelia cadherin (E-cadherin) and a-smooth muscle actin (a-SMA) in the lungs and A549 cells after PQ exposure. We also detected the expression level of the long noncoding RNA (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR), microRNA-17-5p (miR-17-5p), and matrix metalloproteinase 2 (MMP2). We used specific siRNA to determine the influence of HOTAIR on MMP2. We also transfected a mimic or inhibitor of miR-17-5p to explore its role. Moreover, we used the luciferase reporter gene assay to confirm the relationship between miR-17-5p and HOTAIR or MMP2. In this study, we found that MMP2 and HOTAIR were upregulated and miR-17-5p was downregulated in PQ-induced EMT. The knockdown of HOTAIR decreased the expression of MMP2, and the upregulation of miR-17-5p suppressed HOTAIR and MMP2. Apparently, the downregulation of miR-17-5p increased the expression of HOTAIR and MMP2. The expression of a-SMA was negatively regulated by miR-17-5p after PQ exposure. In addition, the luciferase reporter gene assay confirmed that HOTAIR and MMP2 had direct binding sites with miR-17-5p. In conclusion, this study showed that the HOTAIR could act as a ceRNA for miR-17-5p to regulate MMP2 expression in PQ-induced pulmonary EMT.		Toxicology. 2021 Aug 5:152891. doi: 10.1016/j.tox.2021.152891.
5246	LncRNA	LINC01783	miR-199b-5p	NA	Tongue Squamous Cell Carcinoma Cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)  	qPCR;RT-qPCR;	34363308	LINC01783 accelerated tongue squamous cell carcinoma progression via inhibiting miR-199b-5p.	Growing studies illustrated that lncRNAs exert critical roles in development and occurrence of tumours including TSCC. In this research, we indicated that LINC01783 was up-regulated in TSCC cells (SCC1, Cal27, UM1 and SCC4) when compared to NHOK cell. RT-qPCR analysis indicated that LINC01783 was overexpressed in 22 TSCC cases (73.3%, 22/30) compared with no-tumour specimens. LINC01783 level was up-regulated in TSCC specimens when compared to no-tumour specimens. Ectopic expression of LINC01783 promoted TSCC cell cycle and growth and EMT progression in both TSCC cell SCC1 and Cal27. Overexpression of LINC01783 sponged miR-199b-5p in TSCC cell and elevated expression of LINC01783 inhibited miR-199b-5p expression. Moreover, we illustrated that miR-199b-5p was down-regulated in TSCC cells and specimen and LINC01783 level was up-regulated in TSCC specimens when compared to no-tumour specimens. Elevated expression of LINC01783 promoted TSCC cell growth, cycle and EMT progression by sponging miR-199b-5p. These data suggested that LINC01783 functioned as one oncogene and might be one treatment target for TSCC.		J Cell Mol Med. 2021 Aug 7. doi: 10.1111/jcmm.16352.
5247	LncRNA	FEZF1-AS1	MiR-367-3p	SLC12A5	Cervical Carcinoma Cells	Cervical Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Rescue assay;	34362591	Up-Regulated LncRNA FEZF1-AS1 Promotes the Progression of Cervical Carcinoma Cells via MiR-367-3p/SLC12A5 Signal Axis.	BACKGROUND: Cervical cancer (CC) is a common female malignant tumor. With the trend of younger onset, people pay more and more attention to it. Numberless evidence has been indicated that long non-coding RNAs (lncRNAs) can take part in progression of cancers and can exert the regulatory roles in assorted cancers. Nevertheless, the roles of FEZ family zinc finger 1-antisense RNA 1 (FEZF1-AS1) in CC cells are still undiscovered. AIM OF THE STUDY: Thus, the central purpose of our research was to reveal the specific functions and molecular mechanisms of FEZF1-AS1 in CC cells. METHODS: RT-qPCR was utilized to test FEZF1-AS1 expression in CC cells. In addition, functional assays were conducted to evaluate cell proliferation, apoptosis, and migration as well as invasion. In addition, mechanism experiments verified relationship among FEZF1-AS1, miR-367-3p and solute carrier family 12 member 5 (SLC12A5). RESULTS: FEZF1-AS1 was highly expressed in CC cells. Moreover, FEZF1-AS1 depletion suppressed proliferation, migration, invasion, and induced cell apoptosis. Importantly, mechanism experiments confirmed that miR-367-3p could bissnd to FEZF1-AS1 and SLC12A5. The rescue assays determined that FEZF1-AS1 could up-regulate SLC12A5 through binding to miR-367-3p. CONCLUSIONS: The up-regulated FEZF1-AS1 could accelerate the malignant behaviors of CC cells by miR-367-3p/SLC12A5 signal axis.		Arch Med Res. 2021 Aug 3:S0188-4409(21)00119-3. doi: 10.1016/j.arcmed.2021.05.004.
5248	LncRNA	TUG1	miR-137	IGFBP5	Infantile Hemangioma Tissues	Infantile Hemangioma	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34362467	LncRNA-TUG1 promotes the progression of infantile hemangioma by regulating miR-137/IGFBP5 axis.	BACKGROUND: Previous studies indicated that lncRNA taurine upregulated gene 1 (TUG1) played essential roles in human cancers. This study aimed to investigate its function in infantile hemangioma (IH). METHODS: A total of 30 pairs of clinical infantile specimens were used in this study. The expression of TUG1 in IH tissues was assessed by quantitative reverse transcriptase PCR (qRT-PCR). Two short hairpin RNA targeting TUG1 (sh-TUG1-1 and sh-TUG1-2) were transfected into hemangioma-derived endothelial cells, HemECs, to block its expression. The effects of TUG1 on HemECs were evaluated by Cell Counting Kit-8 (CCK-8), colony formation assay, wound healing assay, and Transwell assay. The underlying molecular mechanism of TUG1 was investigated by Starbase prediction and luciferase reporter assay and further determined by loss- and gain-of-function approaches. In addition, the role of TUG1 on tumorigenesis of HemECs was confirmed in an in vivo mouse model. RESULTS: TUG1 was significantly upregulated in infant hemangioma tissues compared with normal adjacent subcutaneous tissues. The loss- and gain-of-function approaches indicated that TUG1 overexpression promoted proliferation, migration, and invasion of HemECs in vitro, and TUG1 knockdown inhibited the tumorigenesis of HemECs in vivo. Specifically, TUG1 could compete with IGFBP5 for miR137 binding. Rescue experiments further confirmed the role of the TUG1/miR137/IGFBP5 axis in HemECs. CONCLUSION: TUG1 was closely associated with the progression of IH by regulating the miR-137/IGFBP5 axis, which might be a potential target for IH treatment.		Hum Genomics. 2021 Aug 6;15(1):50. doi: 10.1186/s40246-021-00349-w.
5249	LncRNA	TUG1	miR-137	IGFBP5	Infantile Hemangioma Tissues	Infantile Hemangioma	Mus musculus (mouse)	qRT-PCR;Luciferase reporter assay;	34362467	LncRNA-TUG1 promotes the progression of infantile hemangioma by regulating miR-137/IGFBP5 axis.	BACKGROUND: Previous studies indicated that lncRNA taurine upregulated gene 1 (TUG1) played essential roles in human cancers. This study aimed to investigate its function in infantile hemangioma (IH). METHODS: A total of 30 pairs of clinical infantile specimens were used in this study. The expression of TUG1 in IH tissues was assessed by quantitative reverse transcriptase PCR (qRT-PCR). Two short hairpin RNA targeting TUG1 (sh-TUG1-1 and sh-TUG1-2) were transfected into hemangioma-derived endothelial cells, HemECs, to block its expression. The effects of TUG1 on HemECs were evaluated by Cell Counting Kit-8 (CCK-8), colony formation assay, wound healing assay, and Transwell assay. The underlying molecular mechanism of TUG1 was investigated by Starbase prediction and luciferase reporter assay and further determined by loss- and gain-of-function approaches. In addition, the role of TUG1 on tumorigenesis of HemECs was confirmed in an in vivo mouse model. RESULTS: TUG1 was significantly upregulated in infant hemangioma tissues compared with normal adjacent subcutaneous tissues. The loss- and gain-of-function approaches indicated that TUG1 overexpression promoted proliferation, migration, and invasion of HemECs in vitro, and TUG1 knockdown inhibited the tumorigenesis of HemECs in vivo. Specifically, TUG1 could compete with IGFBP5 for miR137 binding. Rescue experiments further confirmed the role of the TUG1/miR137/IGFBP5 axis in HemECs. CONCLUSION: TUG1 was closely associated with the progression of IH by regulating the miR-137/IGFBP5 axis, which might be a potential target for IH treatment.		Hum Genomics. 2021 Aug 6;15(1):50. doi: 10.1186/s40246-021-00349-w.
5250	LncRNA	SNHG8	miR-335-5p	PYGO2	Triple-Negative Breast Cancer Cell	Triple Negative Breast Cancerr	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	34362407	Long non-coding RNA SNHG8 enhances triple-negative breast cancer cell proliferation and migration by regulating the miR-335-5p/PYGO2 axis.	BACKGROUND: Growing evidence has demonstrated that long non-coding RNAs (lncRNAs) can function as modulators in the development of triple-negative breast cancer (TNBC). However, the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in TNBC remains unclear. Therefore, our study aimed at investigating the role of SNHG8 in the proliferation and migration of TNBC cells. METHODS: SNHG8 expression was evaluated using RT-qPCR assay. Cell proliferation and migration were assessed by EdU, colony formation and Transwell assays. The levels of proteins related to EMT process were examined by western blot assay. The interaction among SNHG8, miR-335-5p and pygopus family PHD finger 2 (PYGO2) was detected by RIP assay, RNA pull down assay and luciferase reporter assay. RESULTS: SNHG8 expression was significantly up-regulated in TNBC cells. SNHG8 silencing obviously inhibited TNBC cell proliferation, migration and EMT process. Moreover, SNHG8 acted as a sponge to sequester miR-335-5p in TNBC cells. Besides, PYGO2 was proven as a target gene of miR-335-5p, and SNHG8 promoted TNBC cell proliferation, migration and EMT process through regulating miR-335-5p and PYGO2. CONCLUSIONS: Totally, our study indicated that SNHG8 promoted TNBC cell proliferation and migration by regulating the miR-335-5p/PYGO2 axis.		Biol Direct. 2021 Aug 6;16(1):13. doi: 10.1186/s13062-021-00295-6.
5251	LncRNA	CASC18	miR-20a-3p	TGFB2	Tongue Squamous Cell Carcinoma Cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)  	ELISA;qRT-PCR;Western blot;Luciferase reporter assay;	34362313	Association of CASC18/miR-20a-3p/TGFB2 ceRNA axis with occult lymph node metastasis in tongue squamous cell carcinoma.	BACKGROUND: Tongue squamous cell carcinoma (TSCC) ranks as the most prevalent malignancy in the oral cavity. TSCC patients with occult lymph node metastasis (OLNM) are thought to be at risk of worse outcome. However, regulatory mechanisms underlying OLNM remain less investigated. METHODS: In the present study, CASC18/miR-20a-3p/TGFB2 axis was identified and evaluated by bioinformatic and qRT-PCR analyses. Effects of CASC18 knockdown on cell migration and invasion were determined by wound healing and transwell assays. Western blot, ELISA, RNA pulldown and luciferase reporter assays were performed for mechanism verification. RESULTS: CASC18 was identified up-regulating in TSCC tumours, and especially in those from patients with OLNM. Importantly, we found higher CASC18 expression was positively correlated with the presence of OLNM and worse outcome of TSCC patients. Furthermore, we demonstrated that CASC18 knockdown repressed cell migration and invasion through inhibiting epithelial-mesenchymal transition, which could be partly rescued by miR-20a-3p inhibitor. Regarding the molecular mechanism, we further confirmed that CASC18 functioned as a ceRNA to sponge miR-20a-3p to enhanceTGFB2 expression and secretion. CONCLUSION: In conclusion, we have reported a novel CASC18/miR-20a-3p/TGFB2 ceRNA axis in OLNM of TSCC. Our findings will contribute to a deeper understanding of the molecular mechanism of OLNM in TSCC, and facilitate the development of diagnostic methods for assisting treatment decision-making.		Mol Med. 2021 Aug 6;27(1):85. doi: 10.1186/s10020-021-00345-9.
5252	LncRNA	FOXC2-AS1	miR-6868-5p	E2F3	Tongue Squamous Cell Carcinoma Tissues And Cells	Tongue Squamous Cell Carcinoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;	34358374	H3K27ac-induced FOXC2-AS1 accelerates tongue squamous cell carcinoma by upregulating E2F3.	BACKGROUND: The important roles of lncRNAs have been reported in cancers, including tongue squamous cell carcinoma (TSCC). Here, we investigated the functional role and molecular mechanisms of lncRNA FOXC2-AS1 in TSCC. METHODS: The expression level of FOXC2-AS1 in TSCC was determined by RT-qPCR. Its biological role was evaluated through colony formation assay, flow cytometry, wound healing, transwell, and Western blot analyses. The interactions among gene were tested by mechanistic investigations. RESULTS: FOXC2-AS1 expression was high in TSCC tissues and cells. Functional assays in vitro showed that silencing FOXC2-AS1 restrained cell proliferation, cell cycle, migration, invasion, and EMT. In the mechanism, it was verified that H3K27 acetylation (H3K27ac) triggered an increase in FOXC2-AS1 expression. Furthermore, FOXC2-AS1 was identified as a cytoplasmic lncRNA and served as a ceRNA to upregulate E2F3 expression via sponging miR-6868-5p. CONCLUSION: H3K27ac-induced FOXC2-AS1 exhibits carcinogenic property in TSCC by the miR-6868-5p/E2F3 axis.		J Oral Pathol Med. 2021 Aug 6. doi: 10.1111/jop.13232.
5253	LncRNA	NEAT1	miR-766-5p	CDKN1A	Chronic Myelocytic Leukemia Cells	Chronic Myelocytic Leukemia	Homo sapiens (human)  	Flow cytometry assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34354942	m(6)A Modification of lncRNA NEAT1 Regulates Chronic Myelocytic Leukemia Progression via miR-766-5p/CDKN1A Axis.	BACKGROUND: Chronic myeloid leukemia (CML) is an acquired hematopoietic stem malignant disease originating from the myeloid system. Long non-coding RNAs (lncRNAs) have been widely explored in cancer tumorigenesis. However, their roles in CML remain largely unclear. METHODS: The peripheral blood mononuclear cells (PBMCs) and CML cell lines (K562, KCL22, MEG01, BV173) were collected for in vitro research. Real-time quantitative polymerase chain reaction was used to determine the mRNA expression levels. Cell viability and apoptosis were analyzed by cell counting kit 8 and flow cytometry assays. The targeting relationships were predicted using Starbase and TargetScan and ulteriorly verified by RNA pull-down and luciferase reporter assays. Western blotting assay was performed to assess the protein expressions. N6-methyladenosine (m6A) modification sites were predicted by SRAMP and confirmed by Methylated RNA immunoprecipitation (MeRIP) assay. RESULTS: LncRNA nuclear-enriched abundant transcript 1 (NEAT1) expression levels were decreased in the CML cell lines and PBMCs of CML patients. Moreover, METTL3-mediated m6A modification induced the aberrant expression of NEAT1 in CML. Overexpression of NEAT1 inhibited cell viability and promoted the apoptosis of CML cells. Additionally, miR-766-5p was upregulated in CML PBMCs and abrogated the effects of NEAT1 on cell viability and apoptosis of the CML cells. Further, CDKN1A was proved to be the target gene of miR-766-5p and was downregulated in the CML PBMCs. Knockdown of CDKN1A reversed the effects of NEAT1. CONCLUSION: The current research elucidates a novel METTL3/NEAT1/miR-766-5p/CDKN1A axis which plays a critical role in the progression of CML.		Front Oncol. 2021 Jul 20;11:679634. doi: 10.3389/fonc.2021.679634. eCollection 2021.
5254	LncRNA	PITPNA-AS1	miR-520d-5p	SIK2	Triple-Negative Breast Cancer Tissues And Cells	Triple Negative Breast Cancerr	Homo sapiens (human)  	ChIP;qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;Rescue assay;	34353336	MYBL2-induced PITPNA-AS1 upregulates SIK2 to exert oncogenic function in triple-negative breast cancer through miR-520d-5p and DDX54.	BACKGROUND: In recent years, long non-coding RNAs (lncRNAs) have attracted much attention because of its regulatory role in occurrence and progression of tumors, including triple-negative breast cancer (TNBC). LncRNA PITPNA antisense RNA 1 (PITPNA-AS1) has been explored in some cancers, whereas its function and molecular mechanism in TNBC remain unclear. METHODS: PITPNA-AS1 expression in TNBC tissues and cells was determined by RT-qPCR. TNBC cell viability, proliferation, migration, invasion were assessed with CCK-8, colony formation, wound healing, transwell assays. Cell apoptosis was evaluated by flow cytometry. Expression of EMT-related markers was detected by western blot analyses. The molecular mechanism of PITPNA-AS1 was explored by RNA pull down, luciferase reporter, RIP and ChIP assays. RESULTS: PITPNA-AS1 showed high expression levels in TNBC tissues and cells. PITPNA-AS1 knockdown suppressed TNBC cell viability, proliferation, migration, invasion in vitro and inhibited xenograft tumor growth in mice. Mechanistically, PITPNA-AS1 upregulated SIK2 expression by sponging miR-520d-5p and recruiting DDX54 protein. Results of rescue assays suggested that the inhibitive effects of silenced PITPNA-AS1 on TNBC cellular processes were partially rescued by overexpressing SIK2 or combination of miR-520d-5p inhibition and DDX54 overexpression. More importantly, we found that the upregulation of PITPNA-AS1 in TNBC cells was attributed to transcription factor MYBL2. CONCLUSION: PITPNA-AS1 activated by MYBL2 plays an oncogenic role in TNBC through upregulating SIK2.		J Transl Med. 2021 Aug 5;19(1):333. doi: 10.1186/s12967-021-02956-6.
5255	LncRNA	AC092127.1	miR-451a	AEBP2	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34352938	AC092127.1-miR-451a-AE binding protein 2 Signaling Facilitates Malignant Properties of Breast Cancer.	PURPOSE: The purpose of the current study was to explore the functions and potential mechanism of miR-451a in breast cancer (BC). METHODS: Quantitative reverse transcription real-time polymerase chain reaction was used to analyze the expression of miR-451a in human normal mammary cells (MCF-10A) and BC cells. Colony formation assay, terminal-deoxynucleoitidyl transferase mediated nick end labeling assay and transwell assays were conducted to validate the effect of miR-451a on proliferation, apoptosis, migration and invasion of BC cells, respectively. RNA pull-down, RNA immunoprecipitation and luciferase reporter assays were applied to investigate the upstream and downstream mechanisms of miR-451a in BC cells. RESULTS: MiR-451a was expressed at a low level in BC cells. Overexpression of miR-451a repressed BC cells proliferation, migration and invasion. Moreover, long non-coding RNA AC092127.1 acted as a sponge of miR-451a to enhance the expression level of AE binding protein 2 (AEBP2) that was demonstrated to be the target gene of miR-451a in BC cells. Finally, rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion. CONCLUSION: In a word, AC092127.1/miR-451a/AEBP2 axis contributes to BC cell growth, migration and invasion. Our results may help to find novel potential targets for BC treatment.		J Breast Cancer. 2021 Aug 4:e37. doi: 10.4048/jbc.2021.24.e37.
5256	LncRNA	XIST	miR-101-3p	NA	Lung Cancer Cells	Lung Cancer	Homo sapiens (human)  	MTT assay;qRT-PCR;RACE;Western blot;luciferase assay;MTT assay;	34352791	LncRNA XIST Contributes to Cisplatin Resistance of Lung Cancer Cells by Promoting Cellular Glycolysis through Sponging miR-101-3p.	BACKGROUND: Non-small-cell lung carcinoma is one of the most frequently diagnosed cancers. Cisplatin (CDDP) is a currently applied standard anticancer agent for advanced lung cancers. Although effectively clinical response was achieved initially, a large fraction of lung cancer patients developed cisplatin resistance. Therefore, understanding the molecular mechanisms of chemoresistance is crucial for anti-lung cancer therapy. Long non-coding RNA (lncRNA)-X-inactive-specific transcript (XIST) has been reported to be positively associated with multiple cancers. Currently, the precise role and mechanism of XIST in cisplatin resistance of lung cancer have not been elucidated. METHODS: The expression levels of miR-101-3p and lncRNA XIST were detected by qRT-PCR. Cisplatin-resistant lung cancer cell line was established by selecting the survival cells under gradually increased cisplatin treatments. The cell proliferation was detected by MTT assay, and the cellular glucose metabolism rate was evaluated by Seahorse metabolic flux analysis and glucose uptake and lactate product assays. Glycolysis-related protein expression levels were detected by Western blot. Dual luciferase reporter was constructed to determine the lncRNA-miRNA interaction. RESULTS: Here, we report XIST is significantly upregulated in lung cancer tissues compared with normal lung tissues. In addition, cisplatin-resistant lung cancer cells displayed remarkably elevated XIST expression. We demonstrated that miR-101-3p functioned as a tumor suppressor in lung cancer and sensitized lung cancer cells to cisplatin. Bioinformatics analysis predicted miR-101-3p could be a potential target of XIST through direct binding with it as a competing endogenous RNA, which was further validated from lung tumor tissues and cell lines by luciferase assay. Intriguingly, XIST significantly promoted cellular glycolysis rate of lung cancer cells. The extracellular acidification rate, glucose uptake, and lactate product were elevated by XIST overexpression. On the contrary, miR-101-3p effectively suppressed glycolysis rate. Finally, we demonstrated silencing XIST significantly recovered miR-101-3p expression and downregulated expression of glycolysis key enzymes, a phenotype could be further overridden by miR-101-3p inhibition. CONCLUSIONS: This study reveals a new molecular mechanism for the lncRNA-XIST-promoted cisplatin resistance via sponging miR-101-3p, leading to de-repression of cellular glycolysis. Moreover, these findings warrant further in vivo investigations to study XIST as a potential target to overcome cisplatin resistance.		Pharmacology. 2021 Aug 5:1-11. doi: 10.1159/000512621.
5257	LncRNA	TUG1	miR-29a-3p	VEGFA	Human Umbilical Vein Endothelial Cells	Preeclampsia	Homo sapiens (human)	ELISA;qRT-PCR;Western blot;	34352236	Long noncoding TUG1 promotes angiogenesis of HUVECs in PE via regulating the miR-29a-3p/VEGFA and Ang2/Tie2 pathways.	BACKGROUND: Preeclampsia (PE) is a pregnancy-specific disease that is associated with oxidative stress-induced endothelial dysfunction. Long noncoding RNAs (lncRNAs) are related to PE progression. The purpose is to study whether lncRNA taurine-upregulated gene 1 (TUG1) takes part in endothelial dysfunction in PE. METHODS: The placenta tissues were collected from PE patients and normal subjects. Human umbilical vein endothelial cells (HUVECs) were suffered from hypoxia-reoxygenation (H/R). TUG1, miR-29a-3p and vascular endothelial growth factor A (VEGFA) were detected via qRT-PCR. soluble fms-related tyrosine kinase-1 (sFLT1) and soluble endoglin (sENG) levels were detected by ELISA. Cell proliferation, migration, invasion and angiogenesis were examined via MTT, wound healing analysis, transwell and tube formation analysis. The proteins in VEGFA and angiopoietin 2 (Ang2)/tyrosine kinase with immunoglobulin-like and EGF-like domains 2 (Tie2) signaling were measured by western blot. The binding relationship was analyzed via Starbase, Jefferson and dual-luciferase reporter analysis. RESULTS: TUG1 and VEGFA levels were downregulated, and levels of miR-29a-3p, sFLT1 and sENG were increased in PE patients. TUG1 abundance was reduced in H/R-stimulated HUVECs, and TUG1 overexpression increased proliferation, migration, invasion and angiogenesis, and activated the VEGFA and Ang2/Tie2 signaling in H/R-stimulated HUVECs. TUG1 sponged miR-29a-3p, and miR-29a-3p overexpression reversed the function of TUG1 on H/R-induced HUVECs dysfunction. MiR-29a-3p knockdown attenuated H/R-induced inhibition of proliferation, migration, invasion, angiogenesis and activation of the VEGFA and Ang2/Tie2 signaling in HUVECs. VEGFA and Ang2 were targeted by miR-29a-3p, and VEGFA or Ang2 silence weakened the role of miR-29a-3p knockdown in H/R-caused HUVECs dysfunction. CONCLUSION: TUG1 facilitates proliferation, migration, invasion and angiogenesis in H/R-stimulated HUVECs via activating the VEGFA and Ang2/Tie2 signaling by regulating miR-29a-3p.		Microvasc Res. 2021 Aug 2:104231. doi: 10.1016/j.mvr.2021.104231.
5258	LncRNA	SNHG5	miR-299	BACH1	Breast Cancer Cell	Breast Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34351577	LncRNA SNHG5 promotes the glycolysis and proliferation of breast cancer cell through regulating BACH1 via targeting miR-299.	BACKGROUND: Breast cancer (BC) is one of the most common malignant tumors in women. Accumulating studies have been reported that long non-coding RNA (lncRNA) SNHG5 is highly expressed in BC. However, the specific molecular mechanism of SNHG5 in BC is unclear. METHODS: Gene and protein expressions in BC cell were detected by qRT-PCR and western blotting. The proliferation and cell cycle were measured using colony formation assay and flow cytometry analysis, separately. The glucose consumption and lactate production were determined by using the glucose assay kit and lactate assay kit. A dual-luciferase reporter assay was performed to measure the interaction between miR-299 and SNHG5 or BACH1. RESULTS: SNHG5 and BACH1 expressions were increased in BC cell while miR-299 level was decreased. SNHG5 increased BACH1 expression by directly targeting miR-299. SNHG5 silencing or miR-299 overexpression suppressed the proliferation of BC cell, arrested the cell cycle in the G1 cell phase, and decreased the glucose consumption and lactate production of BC cell. However, inhibition of miR-299 or overexpression of BACH1 could reverse the inhibitory effects of sh-SNHG5 on cell proliferation and glycolysis in BC. CONCLUSION: SNHG5 promoted the BC cell growth and glycolysis through up-regulating BACH1 expression via targeting miR-299. These findings may improve the diagnostic and therapeutic approaches to BC.		Breast Cancer. 2021 Aug 5. doi: 10.1007/s12282-021-01281-6.
5259	LncRNA	TUG1	miR-34a	FGFR1	Mc3T3-E1 Cells	Osteoporosis	Homo sapiens (human)  	Luciferase reporter assay;	34350720	Fluid shear stress regulates osteoblast proliferation and apoptosis via the lncRNA TUG1/miR-34a/FGFR1 axis.	LncRNAs and microRNAs play critical roles in osteoblast differentiation and bone formation. However, their exact roles in osteoblasts under fluid shear stress (FSS) and the possible mechanisms remain unclear. The aim of this study was to explore whether and how miR-34a regulates osteoblast proliferation and apoptosis under FSS. In this study, FSS down-regulated miR-34a levels of MC3T3-E1 cells. MiR-34a up-regulation attenuated FSS-induced promotion of proliferation and suppression of apoptosis. Luciferase reporter assay revealed that miR-34a directly targeted FGFR1. Moreover, miR-34a regulated osteoblast proliferation and apoptosis via FGFR1. Further, we validated that lncRNA TUG1 acted as a competing endogenous RNA (ceRNA) to interact with miR-34a and up-regulate FGFR1 protein expression. Furthermore, lncRNA TUG1 could promote proliferation and inhibit apoptosis. Taken together, our study revealed the key role of the lncRNA TUG1/miR-34a/FGFR1 axis in FSS-regulated osteoblast proliferation and apoptosis and may provide potential therapeutic targets for osteoporosis.		J Cell Mol Med. 2021 Aug 5. doi: 10.1111/jcmm.16829.
5260	LncRNA	SPINT1-AS1	miR-214	DNM3OS	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR 	34350182	SPINT1-AS1 Drives Cervical Cancer Progression via Repressing miR-214 Biogenesis.	Accumulating evidences have revealed the dysregulated expressions and critical roles of non-coding RNAs in various malignancies, including cervical cancer. Nevertheless, our knowledge about the vast majority of non-coding RNAs is still lacking. Here we identified long non-coding RNA (lncRNA) SPINT1-AS1 as a novel cervical cancer-associated lncRNA. SPINT1-AS1 was increased in cervical cancer and correlated with advanced stage and poor prognosis. SPINT1-AS1 was a direct downstream target of miR-214, a well-known tumor suppressive microRNA (miRNA) in cervical cancer. Intriguingly, SPINT1-AS1 was also found to repress miR-214 biogenesis via binding DNM3OS, the primary transcript of miR-214. The interaction between SPINT1-AS1 and DNM3OS repressed the binding of DROSHA and DGCR8 to DNM3OS, blocked DNM3OS cleavage, and therefore repressed mature miR-214 biogenesis. The expression of SPINT1-AS1 was significantly negatively correlated with miR-214 in cervical cancer tissues, supporting the reciprocal repression between SPINT1-AS1 and miR-214 in vivo. Through downregulating mature miR-214 level, SPINT1-AS1 upregulated the expression of b-catenin, a target of miR-214. Thus, SPINT1-AS1 further activated Wnt/b-catenin signaling in cervical cancer. Functionally, SPINT1-AS1 drove cervical cancer cellular proliferation, migration, and invasion in vitro, and also tumorigenesis in vivo. Deletion of the region mediating the interaction between SPINT1-AS1 and DNM3OS, overexpression of miR-214, and inhibition of Wnt/b-catenin signaling all reversed the roles of SPINT1-AS1 in cervical cancer. Collectively, these findings identified SPINT1-AS1 as a novel cervical cancer-associated oncogenic lncRNA which represses miR-214 biogenesis and activates Wnt/b-catenin signaling, highlighting its potential as prognostic biomarker and therapeutic target for cervical cancer.		Front Cell Dev Biol. 2021 Jul 19;9:691140. doi: 10.3389/fcell.2021.691140. eCollection 2021.
5261	LncRNA	KCNQ1OT1	MiR-30a-5p	USP22	Colorectal Cancer Tissues And Tumor Cell-Derived Exosomes	Colorectal Cancer	Homo sapiens (human)  	microarray;qPCR;RT-qPCR;RIP assay;	34350172	LncRNA KCNQ1OT1 Secreted by Tumor Cell-Derived Exosomes Mediates Immune Escape in Colorectal Cancer by Regulating PD-L1 Ubiquitination via MiR-30a-5p/USP22.	Background: This study tried to explore the mechanism of long non-coding RNA (lncRNA) KCNQ1OT1 in tumor immune escape. Methods: Gene Expression Omnibus (GEO) and microarray analysis were used to screen the differentially expressed lncRNA and microRNA (miRNA) in normal tissues and tumor tissues. Quantitative reverse transcription PCR (RT-qPCR) was used to quantify KCNQ1OT1, miR-30a-5p, ubiquitin-specific peptidase 22 (USP22), and programmed death-ligand 1 (PD-L1). The interactive relationship between KCNQ1OT1 and miR-30a-5p was verified using dual-luciferase reporter gene assay and ribonucleoprotein immunoprecipitation (RIP) assay. Cell Counting Kit (CCK)-8, clone formation, wound healing, and apoptosis are used to detect the occurrence of tumor cells after different treatments. Protein half-life and ubiquitination detection are used to study the influence of USP22 on PD-L1 ubiquitination. BALB/c mice and BALB/c nude mice are used to detect the effects of different treatments on tumor growth and immune escape in vivo. Results: The expression of lncRNA KCNQ1OT1 in tumor tissues and tumor cell-derived exosomes was significantly increased. The tumor-promoting effect of lncRNA KCNQ1OT1 was through the autocrine effect of tumor cell-derived exosomes, which mediates the miR-30a-5p/USP22 pathway to regulate the ubiquitination of PD-L1 and inhibits CD8+ T-cell response, thereby promoting colorectal cancer development. Conclusion: Tumor cell-derived exosomes' KCNQ1OT1 could regulate PD-L1 ubiquitination through miR-30a-5p/USP22 to promote colorectal cancer immune escape.		Front Cell Dev Biol. 2021 Jul 19;9:653808. doi: 10.3389/fcell.2021.653808. eCollection 2021.
5262	LncRNA	PCDHB17P	miR-145-3p	MELK	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)	qRT-PCR 	34350110	PCDHB17P/miR-145-3p/MELK/NF-kB Feedback Loop Promotes Metastasis and Angiogenesis of Breast Cancer.	Breast cancer is one of the most common life-threatening cancers, mainly because of its aggressiveness and metastasis. Accumulating evidence indicates that long non-coding RNAs (lncRNAs) participate in the development and progression of breast cancer. Nevertheless, the function and expression level of lncRNAs in breast cancer are still not fully understood. Here, we demonstrated that lncRNA PCDHB17P was up-expressed in human breast cancer tissues and cell lines. Knockdown of PCDHB17P remarkably suppressed migration and invasion, as well as tube formation ability of breast cancer cells. MiR-145-3p was significantly decreased in breast cancer samples, which was negatively correlated to the expression of PCDHB17P. In addition, we identified that MELK was a direct target gene of miR-145-3p, which was higher expressed in breast cancer tissues than that in adjacent normal tissues. Mechanistic investigation indicated that PCDHB17P acted as a cancer-promoting competing endogenous RNA (ceRNA) by binding miR-145-3p and upregulating MELK. Interestingly, MELK could in turn increase the promoter activity and expression of PCDHB17P via NF-kB, thus forming a positive feedback loop that drives the metastasis and angiogenesis of breast cancer. Overall, the results demonstrated that the constitutive activation of PCDHB17P/miR-145-3p/MELK/NF-kB feedback loop promotes the metastasis and angiogenesis of breast cancer, suggesting that this lncRNA might be a promising prognostic biomarker and therapeutic target for breast cancer.		Front Oncol. 2021 Jul 19;11:660307. doi: 10.3389/fonc.2021.660307. eCollection 2021.
5263	LncRNA	ZFAS1	miR-186-5p	MCL1	Ischemic Stroke Cell Model	Ischemic Stroke	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34349350	Long non-coding RNA ZFAS1 exerts a protective role to alleviate oxygen and glucose deprivation-mediated injury in ischemic stroke cell model through targeting miR-186-5p/MCL1 axis.	In recent years, accumulating articles have revealed that long non-coding RNAs (lncRNAs) play crucial roles in ischemic stroke (IS). A previous study found that lncRNA zinc finger antisense 1 (ZFAS1) was down-regulated in IS patients compared with healthy controls. However, the precise function of ZFAS1 in IS and its associated mechanism remain unclear. Cell viability was assessed by cell counting kit-8 (CCK8) assay. Cell apoptosis was analyzed by flow cytometry. Western blot assay and quantitative real-time polymerase chain reaction (qRT-PCR) were conducted to measure protein and RNA expression. The interaction between microRNA-186-5p (miR-186-5p) and ZFAS1 or MCL1 apoptosis regulator, BCL2 family member (MCL1) was confirmed by dual-luciferase reporter assay, RNA-pull down assay and RNA immunoprecipitation (RIP) assay. IS cell model was established through exposing N2a cells to oxygen and glucose deprivation (OGD). OGD exposure restrained the viability and induced the apoptosis of N2a cells. OGD exposure down-regulated the expression of ZFAS1 and up-regulated the level of miR-186-5p in a time-dependent manner. ZFAS1 overexpression alleviated OGD-mediated injury in IS cell model. MiR-186-5p was identified as a direct target of ZFAS1, and OGD-induced injury in IS cell model was attenuated by the silence of miR-186-5p. MiR-186-5p interacted with the 3' untranslated region (3'UTR) of MCL1 messenger RNA (mRNA). ZFAS1 positively regulated MCL1 mRNA expression by sequestering miR-186-5p in N2a cells. ZFAS1 overexpression-mediated protective effects in IS cell model were partly overturned by the overexpression of miR-186-5p. MCL1 silencing partly counteracted the protective effects mediated by miR-186-5p silencing in IS cell model. In conclusion, ZFAS1 overexpression exerted a protective role in IS cell model to attenuate OGD-induced injury through targeting miR-186-5p/MCL1 axis. ZFAS1/miR-186-5p/MCL1 signaling might be a novel diagnostic marker and promising treatment target for IS patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10616-021-00481-4.		Cytotechnology. 2021 Aug;73(4):605-617. doi: 10.1007/s10616-021-00481-4. Epub 2021 Jun 24.
5264	LncRNA	MCM3AP-AS1	microRNA-195-5p	E2F3	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	34346845	Long non-coding RNA MCM3AP antisense RNA 1 promotes non-small cell lung cancer progression through targeting microRNA-195-5p.	Lung cancer (LC) ranks first among all causes of cancer-related death, with non-small cell lung cancer (NSCLC) taking up 85% of lung cancer cases. Although lncRNA MCM3AP antisense RNA 1 (MCM3AP-AS1) has been reported to be an oncogenic factor in NSCLC, its detailed mechanism in NSCLC is unknown. In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine MCM3AP-AS1, microRNA (miR)-195-5p and E2F transcription factor 3 (E2F3) mRNA expressions in NSCLC tissues and cells. Western blot was utilized to determine the expression levels of E2F3, BCL2-associated X protein (Bax), B-cell lymphoma-2 (Bcl-2), E-cadherin and N-cadherin. CCK-8 and Transwell assays were conducted to examine cell proliferation, migration and invasion, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation experiments were used to determine the regulatory relationships between MCM3AP-AS1 and miR-195-5p, and miR-195-5p and E2F3. We demonstrated that MCM3AP-AS1 was overexpressed in NSCLC tissues and cells, and MCM3AP-AS1 overexpression accelerated the proliferation, migration and invasion of NSCLC cells. In addition, MCM3AP-AS1 overexpression markedly up-modulated Bcl-2 expression and repressed Bax expression; MCM3AP-AS1 overexpression also significantly up-regulated N-cadherin expression and suppressed E-cadherin expression in NSCLC cells. What is more, in NSCLC cells, miR-195-5p was a target of MCM3AP-AS1, and the latter worked as a molecular sponge for miR-195-5p to regulate E2F3 expression. Collectively, MCM3AP-AS1, serving as a competitive endogenous RNA (ceRNA) to regulate miR-195-5p/E2F3 axis, promotes NSCLC progression, which is a promising therapeutic target for NSCLC.		Bioengineered. 2021 Dec;12(1):3525-3538. doi: 10.1080/21655979.2021.1950282.
5265	LncRNA	OIP5-AS1	miR-223	NLRP3	The Serum Of Ali/Ards Patients	Acute Lung Injury	Homo sapiens (human)  	Dual-luciferase reporter assay;ELISA;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	34346534	LncRNA OIP5-AS1 knockdown or miR-223 overexpression can alleviate LPS-induced ALI/ARDS by interfering with miR-223/NLRP3-mediated pyroptosis.	BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening diseases and endothelial barrier injury is an important contributor to the pathogenesis of ALI/ARDS. LncRNA has been proved to participate in the progression of ALI/ARDS. Our study aimed to investigate the function of lncRNA OIP5-AS1 in LPS-induced ALI/ARDS. METHODS: OIP5-AS1 and miR-223 levels were detected by PCR in the serum of ALI/ARDS patients or healthy donors. MTT assay were performed to detect the proliferation of HPMECs. Flow cytometry were performed to detect the apoptosis of HPMECs. The protein levels of NLRP3, ASC, GSDMD-N, caspase-1 were measured by western blot to detect the pyroptosis of HPMECs. IL-1b, IL-6, IL-18 and IL-10 was detected by ELISA to measure the inflammatory response of HPMECs. And production of ROS, SOD and MDA was measured to determine the oxidative stress of HPMECs. Targets of OIP5-AS1 and miR-223 were predicted by StarBase and confirmed by dual-luciferase reporter assay. RESULTS: We found that OIP5-AS1 was upregulated, while miR-223 was downregulated in the serum of ALI/ARDS patients and LPS-treated HPMECs. Functionally, knockdown of OIP5-AS1 induced proliferation and inhibited apoptosis, pyroptosis, inflammatory response and oxidative stress of LPS-treated HPMECs. Interestingly, miR-223 was a target of OIP5-AS1 and miR-223 inhibition abolished the effects of si-OIP5-AS1 on LPS-induced HPMECs. More importantly, miR-223 directly targeted NLRP3, miR-223 overexpression also promoted proliferation and inhibited apoptosis, pyroptosis, inflammatory response and oxidative stress of LPS-treated HPMECs and which was abolished by NLRP3 overexpression. Finally, we found that OIP5-AS1 knockdown and miR-223 overexpression could both alleviate LPS-induced ALI/ARDS in vivo. CONCLUSION: Together, we find that LncRNA OIP5-AS1 aggravates LPS-induced ALI/ARDS via miR-223/NLRP3 axis and provides new targets for ALI/ARDS therapy.		J Gene Med. 2021 Aug 4:e3385. doi: 10.1002/jgm.3385.
5266	LncRNA	OIP5-AS1	miR-223	NLRP3	The Serum Of Ali/Ards Patients	Acute Respiratory Distress Syndrome	Homo sapiens (human)  	Dual-luciferase reporter assay;ELISA;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	34346534	LncRNA OIP5-AS1 knockdown or miR-223 overexpression can alleviate LPS-induced ALI/ARDS by interfering with miR-223/NLRP3-mediated pyroptosis.	BACKGROUND: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening diseases and endothelial barrier injury is an important contributor to the pathogenesis of ALI/ARDS. LncRNA has been proved to participate in the progression of ALI/ARDS. Our study aimed to investigate the function of lncRNA OIP5-AS1 in LPS-induced ALI/ARDS. METHODS: OIP5-AS1 and miR-223 levels were detected by PCR in the serum of ALI/ARDS patients or healthy donors. MTT assay were performed to detect the proliferation of HPMECs. Flow cytometry were performed to detect the apoptosis of HPMECs. The protein levels of NLRP3, ASC, GSDMD-N, caspase-1 were measured by western blot to detect the pyroptosis of HPMECs. IL-1b, IL-6, IL-18 and IL-10 was detected by ELISA to measure the inflammatory response of HPMECs. And production of ROS, SOD and MDA was measured to determine the oxidative stress of HPMECs. Targets of OIP5-AS1 and miR-223 were predicted by StarBase and confirmed by dual-luciferase reporter assay. RESULTS: We found that OIP5-AS1 was upregulated, while miR-223 was downregulated in the serum of ALI/ARDS patients and LPS-treated HPMECs. Functionally, knockdown of OIP5-AS1 induced proliferation and inhibited apoptosis, pyroptosis, inflammatory response and oxidative stress of LPS-treated HPMECs. Interestingly, miR-223 was a target of OIP5-AS1 and miR-223 inhibition abolished the effects of si-OIP5-AS1 on LPS-induced HPMECs. More importantly, miR-223 directly targeted NLRP3, miR-223 overexpression also promoted proliferation and inhibited apoptosis, pyroptosis, inflammatory response and oxidative stress of LPS-treated HPMECs and which was abolished by NLRP3 overexpression. Finally, we found that OIP5-AS1 knockdown and miR-223 overexpression could both alleviate LPS-induced ALI/ARDS in vivo. CONCLUSION: Together, we find that LncRNA OIP5-AS1 aggravates LPS-induced ALI/ARDS via miR-223/NLRP3 axis and provides new targets for ALI/ARDS therapy.		J Gene Med. 2021 Aug 4:e3385. doi: 10.1002/jgm.3385.
5267	LncRNA	LncIMF2	MiR-217	PPARr	Porcine Intramuscular Adipocytes	Adipogenesis	Homo sapiens (human)  	qRT-PCR 	34346296	LncIMF2 promotes adipogenesis in porcine intramuscular preadipocyte through sponging MiR-217.	Intramuscular fat is positively related to meat quality including tenderness, flavor, and juiciness. Long noncoding RNA (LncRNA) plays a vital role in regulating adipogenesis. However, it is largely unknown about lncRNAs associated with porcine intramuscular adipocyte adipogenesis. In the present study, we focus on a novel LncRNA, which is named lncIMF2, associated with adipogenesis by our previous RNA-sequence analysis and bioinformatics analysis. We demonstrated LncIMF2 knockdown inhibited the proliferation of porcine intramuscular adipocytes while expression of cell cycle-related genes was decreased. Besides, we found LncIMF2 knockdown inhibited expression of adipogenic differentiation marker genes including PPARγ (Peroxisome proliferator-activated reporter gamma) and ATGL (Adipose triglyceride lipase). Similarly, overexpression of LncIMF2 promotes proliferation and differentiation of porcine intramuscular preadipocytes. Moreover, we proved that IncIMF2 acts as a molecular sponge for MicroRNA-217 (miR-217), which has been found associated with adipogenesis, thereby affecting the expression of the miR-217 target gene. Collectively, our findings will contribute to a deeper understanding of the role of LncRNA in pig IMF deposition for the improvement of meat quality.		Anim Biotechnol. 2021 Aug 4:1-12. doi: 10.1080/10495398.2021.1956509.
5268	LncRNA	LncIMF2	MiR-217	ATGL	Porcine Intramuscular Adipocytes	Adipogenesis	Homo sapiens (human)  	qRT-PCR 	34346296	LncIMF2 promotes adipogenesis in porcine intramuscular preadipocyte through sponging MiR-217.	Intramuscular fat is positively related to meat quality including tenderness, flavor, and juiciness. Long noncoding RNA (LncRNA) plays a vital role in regulating adipogenesis. However, it is largely unknown about lncRNAs associated with porcine intramuscular adipocyte adipogenesis. In the present study, we focus on a novel LncRNA, which is named lncIMF2, associated with adipogenesis by our previous RNA-sequence analysis and bioinformatics analysis. We demonstrated LncIMF2 knockdown inhibited the proliferation of porcine intramuscular adipocytes while expression of cell cycle-related genes was decreased. Besides, we found LncIMF2 knockdown inhibited expression of adipogenic differentiation marker genes including PPARγ (Peroxisome proliferator-activated reporter gamma) and ATGL (Adipose triglyceride lipase). Similarly, overexpression of LncIMF2 promotes proliferation and differentiation of porcine intramuscular preadipocytes. Moreover, we proved that IncIMF2 acts as a molecular sponge for MicroRNA-217 (miR-217), which has been found associated with adipogenesis, thereby affecting the expression of the miR-217 target gene. Collectively, our findings will contribute to a deeper understanding of the role of LncRNA in pig IMF deposition for the improvement of meat quality.		Anim Biotechnol. 2021 Aug 4:1-12. doi: 10.1080/10495398.2021.1956509.
5269	LncRNA	XIST	miR-132-3p	MAPK14	Inflammatory Cells	Acute Lung Injury	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34346000	LncRNA XIST knockdown alleviates LPS-induced acute lung injury by inactivation of XIST/miR-132-3p/MAPK14 pathway : XIST promotes ALI via miR-132-3p/MAPK14 axis.	Acute lung injury (ALI) is a fatal inflammatory response syndrome. LncRNA XIST (XIST) is a lung cancer-related gene and participates in pneumonia. However, whether XIST participates in lipopolysaccharides (LPS)-induced ALI remains unclear. LPS-induced inflammation model was constructed in vitro, then cell viability, cytokines, cell apoptosis, protein, and mRNA expressions were individually detected by cell counting kit-8, enzyme-linked immunosorbent assay and flow cytometry, Western blot, and qRT-PCR. A dual-luciferase reporter assay confirmed the relationships among XIST, miR-132-3p, and MAPK14. Furthermore, inflammation and conditions after knockdown of XIST were assessed by hematoxylin and eosin staining, lung wet-to-dry weight ratio, PaO(2)/FiO(2) ratio, and malondialdehyde (MDA) contents using LPS-induced in vivo model. Our findings indicated that the LPS challenge decreased cell viability, increased cell apoptosis, and caused secretions of pro-inflammatory cytokines. Noticeably, LPS significantly upregulated XIST, MAPK14, and downregulated miR-132-3p. Mechanistically, XIST acted as a molecular sponge to suppress miR-132-3p, and MAPK14 was identified as a target of miR-132-3p. Functional analyses demonstrated that XIST silencing remarkably increased cell survival and alleviated cell death and lung injury through decreasing TNF-a, IL-1b, IL-6, accumulation of inflammatory cells, alveolar hemorrhage, MDA release, and increased PaO(2)/FiO(2) ratio, as well as upregulating Bcl-2, and downregulating Bax, MAPK14, and p-extracellular signal-regulated kinases ï¿½. In contrast, inhibition of the miR-132-3p antagonized the effects of XIST silencing. In conclusion, inhibition of XIST exhibited a protective role in LPS-induced ALI through modulating the miR-132-3p/MAPK14 axis.		Mol Cell Biochem. 2021 Aug 3:1-13. doi: 10.1007/s11010-021-04234-x.
5270	LncRNA	UCA1	miR-145-5p	SOCS7	Huh7.5 Cells	Hepatitis C Virus (Hcv) Infection	Homo sapiens (human)  	qRT-PCR 	34345210	Long noncoding RNA UCA1 regulates HCV replication and antiviral response via miR-145-5p/SOCS7/IFN pathway.	Hepatitis C virus (HCV) infection involves a variety of viral and host factors, which leads to the dysregulation of number of relevant genes including long noncoding RNAs (LncRNAs). LncRNA urothelial carcinoma-associated 1 (UCA1) has been reported to be upregulated in HCV-infected individuals. In a bid to elucidate on the contribution of UCA1 on HCV replication, we infected Huh7.5 cells with cell culture-derived HCV and found that UCA1 expression was elevated in time- and dose-dependent manners. Functionally, UCA1 knockdown by siRNA upregulated interferon (IFN) responses, thereby increasing the expression of interferon-stimulating genes (ISGs), and subsequently suppressing HCV replication. Bioinformatics analysis and experimental results indicated that, functioning as competitive endogenous RNA, UCA1 could sponge microRNA (miR)-145-5p, which targeted suppressor of cytokine signaling 7 (SOCS7) mRNA and subsequently mediated SOCS7 silencing. Moreover, SOCS7 protein exerted an inhibitory effect on IFN responses, thereby facilitating HCV replication. Taken together, at first, our findings demonstrate that UCA1 can counteract the expression of miR-145-5p, thereby upregulating the level of SOCS7, and in turn leading to the suppression of antiviral response in Huh7.5 cells.		Int J Biol Sci. 2021 Jul 5;17(11):2826-2840. doi: 10.7150/ijbs.59227. eCollection 2021.
5271	LncRNA	TUG1	miR-590	FGF1	Cardiac Fibroblasts	Acute Myocardial Infarction	Homo sapiens (human)  	Western blot;	34341870	TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction.	Cardiac fibrosis is involved in myocardial remodeling following acute myocardial infarction (AMI), which can result in heart failure, arrhythmias and even sudden cardiac death. Investigating the molecular mechanisms of cardiac fibrosis in acute myocardial infarction (AMI) is essential for better understanding this pathology. The current study aims to investigate the effect of TUG1 on cardiac fibrosis after AMI and elucidated the underlying molecular mechanism of AMI. Rats were randomly divided into four groups (sham-operation group, myocardial infarction group (AMI group), si-NC treated group and si-TUG1 treated group). The biological behavior of cardiac fibroblasts treated with TGF-b1after being transfected by si-TUG1 or miR-590 mimic or miR-590 inhibitor or FGF1 mimic or a combination was evaluated using the cell counting kit-8 (CCK8) and Transwell assays. SatarBase v2.0 was used to predict the target microRNAs binding site candidates with TUG1 and FGF1. Western blot and recovery experiments were used to explore the potential mechanism. TUG1 expression was up-regulated and knockdown of TUG1 improved cardiac function in AMI rats. Knockdown of TUG1 suppressed cell viability and migration and improved collagen production of TGF-b1 treated cardiac fibroblasts. SatarBase v2.0 showed TUG1 served as a sponge for miR-590 and FGF1 is a direct target of miR-590. TUG1 expression was increased in AMI tissue and cardiac fibroblasts treated with TGF-b1. TUG1 knockdown suppressed the biological process of cardiac fibroblasts treated with TGF-b1 by sponging miR-590.		Mamm Genome. 2021 Aug 3. doi: 10.1007/s00335-021-09895-z.
5272	LncRNA	SBF2-AS1	miR-361-5p	TGF-b1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Mus musculus (mouse)	Cell migration assay;Western blot;Luciferase reporter assay;	34341185	Downregulation of lncRNA SBF2-AS1 inhibits hepatocellular carcinoma proliferation and migration by regulating the miR-361-5p/TGF-b1 signaling pathway.	SBF2-AS1 is an oncogenic long non-coding RNA (lncRNA). However, its role and mechanism in hepatocellular carcinoma (HCC) is still not completely clear. The HepG2, Hep3B, Bel-7402 and HL-7702 cell lines were used in our experiments. The CCK-8 kit and EdU staining were applied to detect cell viability and multiplication. The wound healing and Boyden chamber cell migration assays were employed to test the migration ability of cells. The levels of TGF-b1 mRNA, lncRNA SBF2-AS1, and miR-361-5p were assessed by real-time PCR. TGF-b1 protein levels were evaluated by western blotting. The direct interaction between miR-361-5p and TGF-b1 was determined by luciferase reporter assays. A xenograft mouse model (XMM) was established to comprehensively study the effect and mechanisms of lncRNA SBF2-AS1. lncRNA SBF2-AS1 concentration in HCC cells exceeded that in a normal hepatocyte cell line. The downregulation of lncRNA SBF2-AS1 upregulated miR-361-5p levels in HCC cells. And, miR-361-5p negatively regulate TGF-b1 expression in HCC cells. The suppression of miR-361-5p attenuated the influence of lncRNA SBF2-AS1 downregulation on the viability, proliferation, and migration capability of HCC cells. Further, the downregulation of lncRNA SBF2-AS1 inhibited neoplasm growth in an XMM of HCC. Simultaneously, miR-361-5p was upregulated and TGF-b1 was downregulated after lncRNA SBF2-AS1 knocked down. In conclusion, downregulation of lncRNA SBF2-AS1 inhibits HCC proliferation and migration through the regulation of the miR-361-5p/TGF-b1 signaling pathway.		Aging (Albany NY). 2021 Aug 2;13(15):19260-19271. doi: 10.18632/aging.203248. Epub 2021 Aug 2.
5273	LncRNA	ZFAS1	miR-34b-5p	SIRT1	H9C2 Cells	Myocardial Injury	Homo sapiens (human)  	ELISA;RT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	34340571	Long non-coding RNA ZFAS1 alleviates sepsis-induced myocardial injury via target miR-34b-5p/SIRT1.	Long non-coding RNA ZFAS1 is down-regulated in sepsis. However, whether ZFAS1 participates in sepsis-induced cardiomyopathy (SIC) remains largely unknown. LPS injection to rats was used to establish an in vivo sepsis model, while LPS stimulation with H9C2 cell was used to mimic an in vitro sepsis-induced myocardial injury model. Western blots and quantitative RT-PCR were performed to evaluate protein and mRNA levels, respectively. ELISA was conducted to determine cytokine levels in supernatant. Flow cytometry was used to test apoptosis. Dual-luciferase assay was performed to validate binding between ZFAS1 and miR-34b-5p, miR-34b-5p and SIRT1. Our data revealed that ZFAS1 and SIRT1 were down-regulated, while miR-34b-5p was up-regulated in LPS-induced H9C2 cells. Inhibition of miR-34b-5p or overexpression of ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells. A mechanism study revealed that ZFAS1 sponged miR-34b-5p and thus elevated expression of SIRT1, which was prohibited by miR-34b-5p. ZFAS1 alleviated inflammatory response and cell apoptosis in LPS-stimulated H9C2 cells via the miR-34b-5p/SIRT1 axis, providing novel potential therapeutic targets for SIC.		Innate Immun. 2021 Aug 2:17534259211034221. doi: 10.1177/17534259211034221.
5274	LncRNA	Gm11974	miR-122-5p	SEMA3A	N2A Cells	Ischaemic Stroke	Mus musculus (mouse)	qRT-PCR;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	34338972	Long non-coding RNA Gm11974 aggravates oxygen-glucose deprivation-induced injury via miR-122-5p/SEMA3A axis in ischaemic stroke.	Long non-coding RNAs (lncRNAs) play important roles in ischaemic stroke. This study aimed to investigate the role and potential mechanism of lncRNA Gm11974 in ischaemic stroke. Mouse neuroblastoma N2a cells were treated with oxygen-glucose deprivation (OGD). The levels of Gm11974, microRNA-122-5p (miR-122-5p) and semaphorin 3A (SEMA3A) were detected by quantitative real-time PCR (qRT-PCR) or western blot. Cell viability and apoptosis were determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, Caspase-3 Assay Kit and flow Cytometry. The levels of oxidative stress indicators were measured by using commercial kits. The relationship between miR-122-5p and Gm11974 or SEMA3A was verified by dual-luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Middle cerebral artery occlusion (MCAO) in mice was used to mimic ischaemic stroke. Gm11974 and SEMA3A were up-regulated, while miR-122-5p was down-regulated in OGD-treated N2a cells and MCAO mice. Down-regulation of Gm11974 ameliorated OGD-mediated N2a cell damage by increasing cell viability and reducing cell apoptosis and oxidative stress. Gm11974 promoted OGD-induced injury in N2a cells via negatively regulating miR-122-5p. Also, miR-122-5p alleviated OGD-resulted N2a cell injury by targeting SEMA3A. Moreover, silencing of Gm11974 decreased infarct volume and neurological score in MCAO mice. Knockdown of Gm11974 attenuated neuronal injury in ischaemic stroke by regulating miR-122-5p/SEMA3A signaling pathway.		Metab Brain Dis. 2021 Aug 2. doi: 10.1007/s11011-021-00792-7.
5275	LncRNA	MIR3142HG	miR-450b-5p	HMGB1	Human Pulmonary Microvascular Endothelial Cells	Acute Lung Injury	Homo sapiens (human)	RNA pull-down assay;Western blot;RNA pull-down;	34338955	MIR3142HG promotes Lps-Induced Acute Lung Injury by regulating miR-450b-5p/HMGB1 axis.	The present study aimed to evaluate the potential roles of MIR3142HG, a novel long non-coding RNA (lncRNA) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was simulated by the treatment of LPS in human pulmonary microvascular endothelial cells (HPMECs). The expression of MIR3142HG, miR-450b-5p and high-mobility group box 1 (HMGB1) was determined by real-time PCR and western blotting. Functional analysis was performed through the assessment of cell viability, apoptosis and the production of proinflammatory cytokines. The interactions among MIR3142HG, miR-450b-5p and HMGB1 were analyzed by bioinformatics methods, dual-luciferase reporter and RNA pull-down assays. Using gain- and loss-of-function approaches, the in vitro functions of MIR3142HG and miR-450b-5p were subsequently assessed. MIR3142HG expression was upregulated, while miR-450b-5p was decreased in LPS-treated HPMECs. MIR3142HG knockdown protected against ALI induced by LPS through alleviating the apoptosis and inflammation of HPMECs. MIR3142HG impaired miR-450b-5p-mediated inhibition of HMGB1. Besides, the effects of MIR3142HG silencing could be alleviated by miR-4262 inhibition or HMGB1 overexpression. MIR3142HG mediated LPS-induced injury of HPMECs by targeting miR-450b-5p/HMGB1, suggesting that MIR3142HG might serve as a therapeutic potential for the treatment of ALI.		Mol Cell Biochem. 2021 Aug 2. doi: 10.1007/s11010-021-04209-y.
5276	LncRNA	CASC2	miR-21	p53	Luad Patients And Luad Cell Lines	Lung Adenocarcinoma	Homo sapiens (human)  	Flow cytometry assay;Western blot;Flow Cytometry assay;	34337857	LncRNA CASC2 inhibits lung adenocarcinoma progression through forming feedback loop with miR-21/p53 axis.	Lung adenocarcinoma (LUAD) is the most common type of lung cancer. Currently, the survival rate of LUAD patients remains low due to heterogeneity and high invasiveness. The long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is reported to be related to LUAD development. Hence, we investigate the roles and regulatory mechanism of CASC2 in LUAD. The expression levels of CASC2, microRNA (miR)-21, and p53 were quantified by quantitative real-time polymerase chain reaction, and the protein levels of Bax, Bcl-2, p53, and p21 were examined using western blotting. A dual-luciferase reporter experiment was conducted to prove the molecular interactions between CASC2 and miR-21 or p53. CCK-8 and flow cytometry assays were conducted to assess cell proliferation and apoptosis, respectively. CASC2 was expressed at a low level in LUAD patients and LUAD cell lines. CASC2 overexpression markedly suppressed cell proliferation and enhanced apoptosis. Mechanistically, CASC2 overexpression dramatically inhibited miR-21 expression and increased p53 expression by directly targeting miR-21. Moreover, rescue experiments suggested that either miR-21 overexpression or p53 silencing obviously weakened the biological effects of CASC2 overexpression. In addition, p53 was proven to be an upstream transcription factor of CASC2 and can activate CASC2 transcription. These results provide evidence that the lncRNA CASC2/miR-21/p53 form a positive feedback loop to mediate cell proliferation and apoptosis in LUAD, which may provide a new insight into the pathological mechanisms of LUAD.		Kaohsiung J Med Sci. 2021 Aug;37(8):675-685. doi: 10.1002/kjm2.12386. Epub 2021 Aug 1.
5277	LncRNA	HOXA11-AS	miR-24-3p	JPT1	Prostate Cancer Tissues And Cells	Prostate Cancer	Homo sapiens (human)  	Flow cytometry assay;MTT assay;Flow Cytometry assay;MTT assay;	34337714	LncRNA HOXA11-AS promotes cell growth by sponging miR-24-3p to regulate JPT1 in prostate cancer.	OBJECTIVE: Long noncoding RNA (lncRNA) was found to play crucial roles in regulating cancer progression. HOXA11 antisense RNA (HOXA11-AS) was reported to serve an oncogenic lncRNA in cancers but its role in prostate cancer (PCa) remains to be explored. MATERIALS AND METHODS: Expression levels of HOXA11-AS in PCa tissues and cells were analyzed with quantitative Real-Time PCR method. MTT assay, colony formation assay, transwell invasion assay, and flow cytometry assay were conducted to explore the biological roles of HOXA11-AS in PCa. Rescue experiments were conducted to investigate mechanisms of HOXA11-AS in regulating PCa progression. RESULTS: We revealed that HOXA11-AS was upregulated in PCa. Silencing of HOXA11-AS significantly inhibited PCa cell proliferation, colony formation, invasion, and promoted apoptosis in vitro. On the contrary, forcing of HOXA11-AS expression caused opposite effects on cancer cell behaviors. Furthermore, we showed that HOXA11-AS1 serves as a competing endogenous RNA (ceRNA) to regulate Jupiter microtubule associated homolog 1 (JPT1) via sponging microRNA-24-3p (miR-24-3p). Functionally, the overexpression of miR-24-3p or knockdown of JPT1 could partially reverse the effects of HOXA11-AS overexpression on PCa cell behaviors. CONCLUSIONS: This newly identified HOXA11-AS/miR-24-3p/JPT1 axis may provide novel angle for the better control of PCa.		Eur Rev Med Pharmacol Sci. 2021 Jul;25(14):4668-4677. doi: 10.26355/eurrev_202107_26377.
5278	LncRNA	ELFN1-AS1	miR-1250	MTA1	Colorectal Cancer Tissues And Cell Lines	Colorectal Cancer	Homo sapiens (human)	Luciferase reporter assay;	34337713	A long non-coding RNA, ELFN1-AS1, sponges miR-1250 to upregulate MTA1 to promote cell proliferation, migration and invasion, and induce apoptosis in colorectal cancer.	OBJECTIVE: Long non-coding RNA (lncRNA), is essential for the development and progression of cancers. LncRNA regulates target gene expression by sponging the corresponding microRNA (miRNA) during tumorigenesis. This work aimed to explore the role of one lncRNA, ELFN1-AS1, in colorectal cancer (CRC) development and elucidate the pertinent signaling pathway. PATIENTS AND METHODS: First, we found that ELFN1-AS1 was highly abundant in the human CRC tissues and cell lines. Silence of ELFN1-AS1 expression reduced cell proliferation, colony formation, migration and invasion, while inducing apoptosis in vitro; moreover, knockdown of ELFN1-AS1 decreased the size and weight of tumor in vivo. RESULTS: Luciferase reporter assay revealed that ELFN1-AS1 interacted with miR-1205 and suppressed its expression. In addition, miR-1205 could bind to the 3' untranslated region (3'-UTR) of Metastasis Associated Protein1 (MTA1) and inhibited ELFN1-AS1 expression. More importantly, overexpression of MTA1 completely rescued the phenotype of ELFN1-AS1 knockdown. CONCLUSIONS: In sum, our study demonstrated that ELFN1-AS1 sponges miR-1205 to upregulate MTA1, which is essential for CRC cell proliferation, migration, and invasion as well as apoptosis induction.		Eur Rev Med Pharmacol Sci. 2021 Jul;25(14):4655-4667. doi: 10.26355/eurrev_202107_26376.
5279	LncRNA	Linc00312	mir-411-3p	NA	Nasopharyngeal Carcinoma Cells	Nasopharyngeal Cancer	Homo sapiens (human)  	Luciferase reporter assay;	34336850	Genetic Polymorphisms of Long Non-coding RNA Linc00312 Are Associated With Susceptibility and Predict Poor Survival of Nasopharyngeal Carcinoma.	BACKGROUND: Linc00312 is dysregulated in nasopharyngeal carcinoma (NPC) and participates in the initiation and progression of NPC. Our previous studies suggested that linc00312 was able to enhance the sensitivity of NPC cells to irradiation and NPC patients with higher expression of linc00312 was associated with better short-term curative effect and overall survival. The single nucleotide polymorphisms (SNPs) of lncRNAs may influence the disease course and outcome by affecting the expression, secondary structure or function of lncRNAs. However, the role of SNPs in linc00312 on the occurrence and survival of NPC remains unknown. METHODS: We recruited 684 NPC patients and 823 healthy controls to evaluate the association between linc00312 SNPs and NPC susceptibility by using multivariate logistic regression analysis. Kaplan-Meier analysis and Cox proportional hazards regression were applied to assess the effect of linc00312 SNPs on the survival of NPC patients. The relative expression of linc00312 in NPC tissues was determined by real-time PCR. The interaction between linc00312 and mir-411-3p was explored by luciferase reporter assay. In silico prediction of the changes on linc00312 folding structure was conducted by RNAfold WebServer. RESULT: We demonstrated that rs12497104 (G > A) GA genotype carriers had a higher risk than others for suffering from NPC (GA vs GG, OR = 1.437, P = 0.003). Besides, patients with rs12497104 AA genotype showed a poorer overall survival in contrast to GG genotype (AA vs GG, HR = 2.117, P = 0.011). In addition, the heterozygous carriers of rs15734 (G > A) and rs164966 (A > G) were correlated with decreased risk of NPC (GA vs GG, OR = 0.778, P = 0.031; GA vs AA, OR = 0.781, P = 0.033, respectively). We found that the three SNPs might influence the expression of linc00312 in a genotype specific feature. The local centroid secondary structure as well as the minimum free energy of linc00312 were changed following the candidate SNPs alterations. Besides, we revealed that the G to A alteration at rs12497104 disrupted the binding between mir-411-3p and linc00312. CONCLUSION: Our results indicated genetic polymorphisms of linc00312 might serve as potential biomarkers for NPC carcinogenesis and prognosis.		Front Cell Dev Biol. 2021 Jul 16;9:698558. doi: 10.3389/fcell.2021.698558. eCollection 2021.
5280	LncRNA	LINC00261	miR-545-3p	MT1M	Escc Tissues, Cell Lines, And Ddp-Resistant Escc Patients	Esophageal Squamous Cancer	Homo sapiens (human)  	qRT-PCR 	34336838	LINC00261 Suppresses Cisplatin Resistance of Esophageal Squamous Cell Carcinoma Through miR-545-3p/MT1M Axis.	To improve the survival rate and cure rate of patients, it is necessary to find a new treatment scheme according to the molecular composition of (ESCC) in esophageal squamous cell carcinoma. Long non-coding RNAs (lncRNAs) regulate the progression of ESCC by various pathophysiological pathways. We explored the possible function of the lncRNA LINC00261 (LINC00261) on cisplatin (DDP) resistance of ESCC and its relative molecular mechanisms. In the study, we found that LINC00261 was downregulated in ESCC tissues, cell lines, and DDP-resistant ESCC patients. Besides, overexpression of LINC00261 not only inhibited cell proliferation, and DDP resistance but also promotes cell apoptosis. Further mechanistic research showed that LINC00261 sponged miR-545-3p which was negatively correlated with the expression of LINC00261. In addition, functional experiments revealed that upregulation of miR-766-5p promoted proliferation and enhanced DDP resistance. Subsequently, MT1M was testified to be the downstream target gene of miR-545-3p. Rescue experiments revealed that overexpression of MT1M largely restores miR-545-3p mimics-mediated function on ESCC progression. Our results demonstrate that the LINC00261 suppressed the DDP resistance of ESCC through miR-545-3p/MT1M axis.		Front Cell Dev Biol. 2021 Jul 15;9:687788. doi: 10.3389/fcell.2021.687788. eCollection 2021.
5281	LncRNA	lnc-TLCD2-1	miR-193a-5p	YY1	Ccl244 Cell Lines And Radiation-Sensitive Hct116 Cell Lines	Colorectal Cancer	Homo sapiens (human)  	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34336703	Regulation of lnc-TLCD2-1 on Radiation Sensitivity of Colorectal Cancer and Comprehensive Analysis of Its Mechanism.	As is well known that colorectal cancer is the third most common cancer in the world, and radiation treatment plays a vital role in colorectal cancer therapy, but radiation resistance is a significant problem in the treatment of colorectal cancer. As an important member of the non-coding RNA family, long non-coding RNAs (lncRNAs) have been found that it plays a role in the occurrence and progression of colorectal cancer in recent years. However, little is known about the effect of lncRNA on colorectal cancer sensitivity to radiotherapy. We found that lnc-TLCD2-1 was significantly differentially expressed in radiation-tolerant CCL244 cell lines and radiation-sensitive HCT116 cell lines, suggesting that lnc-TLCD2-1 may regulate the radiosensitivity of colorectal cancer, and the relevant underlying mechanism was investigated. Cell clone formation assay, flow cytometry, and cell counting kit 8 (CCK8) were used to detect radiation sensitivity, apoptosis, and proliferation of colorectal cancer cells, respectively; Quantitative real-time PCR and western blot were used to detect the expression of genes; the direct interaction between lnc-TLCD2-1 and hsa-miR-193a-5p was verified by dual luciferase reporter assays; GEPIA, Starbase, TIMER and DAVID were used to complete expression of lnc-TLCD2-1, miR-193a-5p,YY1 and NF-kB-P65 in colorectal cancer, correlation, immune cell infiltration, GO and KEGG enrichment analysis. Clinical prognostic analysis data were obtained from GSE17536 dataset. After radiotherapy for HCT116, the expression of lnc-TLCD2-1 was increased, and the expression of hsa-miR-193a-5p was significantly decreased, while that of CCL244 was the opposite, and the change range of lnc-TLCD2-1 was relatively small. HCT116 with overexpression of lnc-TLCD2-1 after radiation treatment, the number of cell colonies significantly increased, and cell apoptosis decreased compared with the negative control group. The cell colonies and apoptosis of CCL244 with disturbed expression of lnc-TLCD2-1 were opposite to those of HCT116. Lnc-TLCD2-1 can regulate the expression of YY1/NF-kB-P65 by targeting miR-193a-5p. Lnc-TLCD2-1 can promote the proliferation of colorectal cancer. High expression of lnc-TLCD2-1 independently predicted a shorter survival. Lnc-TLCD2-1 is associated with radiation resistance and short survival in colorectal cancer patients. In addition, Lnc-TLCD2-1 can promote the proliferation of colorectal cancer. Our study provides a scientific basis for targeting lnc-TLCD2-1 in colorectal cancer radiation resistance interventions and selection of prognostic biomarker.		Front Oncol. 2021 Jul 15;11:714159. doi: 10.3389/fonc.2021.714159. eCollection 2021.
5282	LncRNA	lnc-TLCD2-1	miR-193a-5p	NF-kB-P65	Ccl244 Cell Lines And Radiation-Sensitive Hct116 Cell Lines	Colorectal Cancer	Homo sapiens (human)  	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34336703	Regulation of lnc-TLCD2-1 on Radiation Sensitivity of Colorectal Cancer and Comprehensive Analysis of Its Mechanism.	As is well known that colorectal cancer is the third most common cancer in the world, and radiation treatment plays a vital role in colorectal cancer therapy, but radiation resistance is a significant problem in the treatment of colorectal cancer. As an important member of the non-coding RNA family, long non-coding RNAs (lncRNAs) have been found that it plays a role in the occurrence and progression of colorectal cancer in recent years. However, little is known about the effect of lncRNA on colorectal cancer sensitivity to radiotherapy. We found that lnc-TLCD2-1 was significantly differentially expressed in radiation-tolerant CCL244 cell lines and radiation-sensitive HCT116 cell lines, suggesting that lnc-TLCD2-1 may regulate the radiosensitivity of colorectal cancer, and the relevant underlying mechanism was investigated. Cell clone formation assay, flow cytometry, and cell counting kit 8 (CCK8) were used to detect radiation sensitivity, apoptosis, and proliferation of colorectal cancer cells, respectively; Quantitative real-time PCR and western blot were used to detect the expression of genes; the direct interaction between lnc-TLCD2-1 and hsa-miR-193a-5p was verified by dual luciferase reporter assays; GEPIA, Starbase, TIMER and DAVID were used to complete expression of lnc-TLCD2-1, miR-193a-5p,YY1 and NF-kB-P65 in colorectal cancer, correlation, immune cell infiltration, GO and KEGG enrichment analysis. Clinical prognostic analysis data were obtained from GSE17536 dataset. After radiotherapy for HCT116, the expression of lnc-TLCD2-1 was increased, and the expression of hsa-miR-193a-5p was significantly decreased, while that of CCL244 was the opposite, and the change range of lnc-TLCD2-1 was relatively small. HCT116 with overexpression of lnc-TLCD2-1 after radiation treatment, the number of cell colonies significantly increased, and cell apoptosis decreased compared with the negative control group. The cell colonies and apoptosis of CCL244 with disturbed expression of lnc-TLCD2-1 were opposite to those of HCT116. Lnc-TLCD2-1 can regulate the expression of YY1/NF-kB-P65 by targeting miR-193a-5p. Lnc-TLCD2-1 can promote the proliferation of colorectal cancer. High expression of lnc-TLCD2-1 independently predicted a shorter survival. Lnc-TLCD2-1 is associated with radiation resistance and short survival in colorectal cancer patients. In addition, Lnc-TLCD2-1 can promote the proliferation of colorectal cancer. Our study provides a scientific basis for targeting lnc-TLCD2-1 in colorectal cancer radiation resistance interventions and selection of prognostic biomarker.		Front Oncol. 2021 Jul 15;11:714159. doi: 10.3389/fonc.2021.714159. eCollection 2021.
5283	LncRNA	PVT1	miR-152-3p	VEGFA	Hct116 And Lovo Cell Lines	Colon Cancer	Mus musculus (mouse)	qRT-PCR 	34336125	Exosomal lncRNA PVT1/VEGFA Axis Promotes Colon Cancer Metastasis and Stemness by Downregulation of Tumor Suppressor miR-152-3p.	BACKGROUND: Treating advanced colon cancer remains challenging in clinical settings because of the development of drug resistance and distant metastasis. Mechanisms underlying the metastasis of colon cancer are complex and unclear. METHODS: Computational analysis was performed to determine genes associated with the exosomal long noncoding (lncRNA) plasmacytoma variant translocation 1 (PVT1)/vascular endothelial growth factor A (VEGFA) axis in patients with colon cancer. The biological importance of the exosomal lncRNA PVT1/VEGFA axis was examined in vitro by using HCT116 and LoVo cell lines and in vivo by using a patient-derived xenograft (PDX) mouse model through knockdown (by silencing of PVT1) and overexpression (by adding serum exosomes isolated from patients with distant metastasis (M-exo)). RESULTS: The in silico analysis demonstrated that PVT1 overexpression was associated with poor prognosis and increased expression of metastatic markers such as VEGFA and epidermal growth factor receptor (EGFR). This finding was further validated in a small cohort of patients with colon cancer in whom increased PVT1 expression was correlated with colon cancer incidence, disease recurrence, and distant metastasis. M-exo were enriched with PVT1 and VEGFA, and both migratory and invasive abilities of colon cancer cell lines increased when they were cocultured with M-exo. The metastasis-promoting effect was accompanied by increased expression of Twist1, vimentin, and MMP2. M-exo promoted metastasis in PDX mice. In vitro silencing of PVT1 reduced colon tumorigenic properties including migratory, invasive, colony forming, and tumorsphere generation abilities. Further analysis revealed that PVT1, VEGFA, and EGFR interact with and are regulated by miR-152-3p. Increased miR-152-3p expression reduced tumorigenesis, where increased tumorigenesis was observed when miR-152-3p expression was downregulated. CONCLUSION: Exosomal PVT1 promotes colon cancer metastasis through its association with EGFR and VEGFA expression. miR-152-3p targets both PVT1 and VEGFA, and this regulatory pathway can be explored for drug development and as a prognostic biomarker.		Oxid Med Cell Longev. 2021 Jul 15;2021:9959807. doi: 10.1155/2021/9959807. eCollection 2021.
5284	LncRNA	LINC00909	miR-23b-3p	MRC2	Ovarian Cancer Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34336102	Elevated LINC00909 Promotes Tumor Progression of Ovarian Cancer via Regulating the miR-23b-3p/MRC2 Axis.	Ovarian cancer (OC), the third common gynecologic malignancy, contributes to the most cancer-caused mortality in women. However, 70% of patients with OC are diagnosed at an advanced stage, of which the 5-year survival is less than 30%. Long noncoding RNAs (long ncRNAs or lncRNA), a type of RNA with exceeding 200 nucleotides in length but no protein-coding capability, have been demonstrated to involve the pathogenesis of various cancers and show considerable potential in the diagnosis of OC. In this study, we found that the LINC00909 expression in tumor and serum specimens of OC patients was elevated, determined by real-time quantitative, and droplet digital PCR. In receiver operating characteristic (ROC) analysis, our results revealed that serum LINC00909 distinguished cancers from normal ovarian tissue with 87.8% of sensitivity and 69.6% of specificity (AUC, 81.2%) and distinguished serous ovarian cancer from normal ovarian tissue with 90.0% of sensitivity and 75.9% of specificity (AUC, 84.5%). Furthermore, we observed that the tumor and serum LINC00909 level was positively associated with the International Federation of Gynecology and Obstetrics (FIGO) stage and the Eastern Cooperative Oncology Group (ECOG) score (reflecting patients' performance status). Also, patients with low serum LINC00909 level showed a longer overall (hazard ratio, HR = 1.874, p = 0.0004) and progression-free (HR = 1.656, p = 0.0017) survival. Functional assays indicated that the elevation of LINC00909 expression contributes to cell proliferation, migration, and invasion capability of ovarian cancer cells. Besides, we demonstrated that LINC00909 functions as a competing endogenous RNA (ceRNA) of MRC2 mRNA by sponging miR-23-3p, and thereby promotes epithelial-to-mesenchymal transition (EMT) of ovarian cancer cells. Therefore, we highlight that the LINC00909/miR-23b-3p/MRC2 axis is implicated in the pathogenesis of ovarian cancer, and serum LINC00909 may be a promising biomarker for the diagnosis of OC.		Oxid Med Cell Longev. 2021 Jul 21;2021:5574130. doi: 10.1155/2021/5574130. eCollection 2021.
5285	LncRNA	TSPEAR-AS2	miR-487a-3p	PPM1A	Oral Squamous Cell Carcinoma Cells	Oral Squamous Cell Cancer	Homo sapiens (human)  	RT-PCR;RNA pull-down;	34336002	lncRNA TSPEAR-AS2, a Novel Prognostic Biomarker, Promotes Oral Squamous Cell Carcinoma Progression by Upregulating PPM1A via Sponging miR-487a-3p.	BACKGROUND: Long noncoding RNA (lncRNA) critically impacts the modulation of tumor developments and progressions. Our study is aimed at investigating the expressing patterns, clinical significance, and biological roles of lncRNA TSPEAR-AS2 (TSPEAR-AS2) in oral squamous cell carcinoma (OSCC). Material and Approach. The expressing states achieved by TSPEAR-AS2 were examined in OSCC specimens and cell lines by RT-PCR. The clinical significance of TSPEAR-AS2 was statistically analyzed. OSCC proliferating, invading, and migrating processes were examined with the use of wound healing assays, transwell, colony formation, and cell counting kit-8. Additionally, the downstream molecular mechanism of TSPEAR-AS2 in OSCC was explored. RESULTS: TSPEAR-AS2 was overexpressed in OSCC tumors and cells. High TSPEAR-AS2 was associated with advanced TNM stage. Patients with high TSPEAR-AS2 expression displayed a shorter disease-free survival and total survival of OSCC patients than those with low TSPEAR-AS2 expressing level. It was found that knockdown of TSPEAR-AS2 could inhibit the proliferating, invading, and migrating processes pertaining to OSCC cells. Luciferase reporter tests and RNA pull-down results revealed that TSPEAR-AS2 enhanced the expressions of PPM1A by regulating miR-487a-3p, and TSPEAR-AS2 could be adopted as a miR-487a-3p sponge to inhibit PPM1A expression. CONCLUSION: Our study highlighted the significance of the TSPEAR-AS2/miR-487a-3p/PPM1A axis within OSCC progression and offered a novel biomarker and novel strategies for OSCC treatments.		Dis Markers. 2021 Jul 17;2021:2217663. doi: 10.1155/2021/2217663. eCollection 2021.
5286	LncRNA	H19	miR-106a	Angpt1	Mesenchymal And Endothelial Cells	Osteogenesis And Angiogenesis	Mus musculus (mouse)	RACE;Luciferase reporter assay;	34335960	Exosomal lncRNA-H19 promotes osteogenesis and angiogenesis through mediating Angpt1/Tie2-NO signaling in CBS-heterozygous mice.	Rationale: Emerging evidence indicates that the growth of blood vessels and osteogenesis is tightly coordinated during bone development. However, the molecular regulators of intercellular communication in the bone microenvironment are not well studied. Therefore, we aim to investigate whether BMMSC-Exo promotes osteogenesis and angiogenesis via transporting lnc-H19 in the CBS- heterozygous mouse model. Methods: Using RT2 lncRNA PCR array screening, we identify a bone-specific, long noncoding RNA-H19 (lncRNA-H19/lnc-H19) in exosomes derived from bone marrow mesenchymal stem cells (BMMSC-Exo) during osteogenesis. Using bioinformatics analysis, we further discovered the seed sequence of miR-106a that could bind to lnc-H19. A luciferase reporter assay was performed to demonstrate the direct binding of miR-106a to the target gene angiopoietin 1 (Angpt1). We employed an immunocompromised Nude mouse model, to evaluate the effects of BMMSC-Exo on angiogenesis in vivo. Using a micro-CT scan, we monitored microstructural changes of bone in the experimental mice. Results: BMMSC-Exo possessed exosomal characteristics including exosome size, and typical markers including CD63, CD9, and TSD101. In vitro, BMMSC-Exo significantly promoted endothelial angiogenesis and osteogenesis. Mechanistic studies have shown that exosomal lnc-H19 acts as "sponges" to absorb miR-106 and regulate the expression of angiogenic factor, Angpt1 that activates lnc-H19/Tie2-NO signaling in mesenchymal and endothelial cells. Both of these effects on osteogenesis and angiogenesis are inhibited by antagonizing Tie2 signaling. Treatment of BMMSC-Exo also restored the bone formation and mechanical quality in vivo. Conclusion: These findings provide a novel insight into how the extracellular role of exosomal lnc-H19 affects osteogenesis and angiogenesis through competing endogenous RNA networks.		Theranostics. 2021 Jun 22;11(16):7715-7734. doi: 10.7150/thno.58410. eCollection 2021.
5287	LncRNA	PCAT6	miR-143-3p	PDIA6	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	34335889	Long non-coding RNA PCAT6 regulates bladder cancer progression via the microRNA-143-3p/PDIA6 axis.	Although long non-coding (lnc)RNAs have been reported to be involved in the pathological development of bladder cancer, the functions of lncRNA prostate cancer-associated transcript 6 (PCAT6) and its underlying mechanism of action in bladder cancer remain unknown. The present study aimed to investigate the effect of PCAT6 in bladder cancer progression and explore its potential application as a novel treatment target. The expression of PCAT6 and miR-143-3p in bladder cancer tissues, adjacent normal tissues and cell lines was measured using reverse transcription-quantitative PCR. Fluorescence in situ hybridization assay was used to detect the subcellular localization of PCAT6. MTT, EdU, Transwell and wound healing assays were conducted to assess the biological function of PCAT6 on cell proliferation, migration and invasion. Putative binding sites between miR-143-3p and PCAT6 or PDIA6 were predicted using starBase, Lncbase and TargetScan analyzes. Dual-luciferase reporter assay was also used to confirm the potential binding between PCAT6 and miR-143-3p. RNA immunoprecipitation assay was performed to verify the possible interaction between PCAT6 and miR-143-3p. Western blotting was used to measure the expression of PDIA6. The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control-transfected cells, whilst the miR-143-3p inhibitor partially mitigated this reduction effect. In addition, rescue experiments revealed that the miR-143-3p inhibitors reversed the effects of PCAT6 silencing on the malignant phenotypes of bladder cancer. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR-143-3p/PDIA6 axis. These results may provide a potential therapeutic target for the treatment of bladder cancer.		Exp Ther Med. 2021 Sep;22(3):947. doi: 10.3892/etm.2021.10379. Epub 2021 Jul 1.
5288	LncRNA	NR2F1-As1	miR-493-5p	MAP3K2	Gastric Cancer Tissues And Cells	Gastric Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	34335755	The Effect and Mechanism of lncRNA NR2F1-As1/miR-493-5p/MAP3K2 Axis in the Progression of Gastric Cancer.	BACKGROUND: LncRNA NR2F1-AS1 has been identified as an oncogene in some human tumors, such as breast cancer, nonsmall cell lung cancer, and esophageal squamous cell carcinoma. Nonetheless, whether NR2F1-AS1 is involved in the progression of gastric cancer (GC) remains unknown. METHODS: The expression patterns of NR2F1-AS1, MAP3K2, and miR-493-5p in GC tissues and cells were detected by RT-qPCR. The protein expression of MAP3K2 was assessed by the Western blotting assay. The MTT assay and flow cytometry were performed to measure cell proliferation and cell apoptosis in GC cells. The transwell assay was adopted to assess cell migration in GC cells. The relationship between NR2F1-AS1, MAP3K2, and miR-493-5p was verified by a dual-luciferase reporter assay. RESULTS: The increased NR2F1-AS1 and MAP3K2 expressions were discovered in GC tissues and cells compared with control groups. Knockdown of NR2F1-AS1 and MAP3K2 dramatically suppressed cell proliferation and migration, while it enhanced cell apoptosis in GC cells. In addition, NR2F1-AS1 was found to be a sponge of miR-493-5p, and MAP3K2 was a downstream gene of miR-493-5p. Moreover, the expression of MAP3K2 was notably reduced by miR-493-5p, and NR2F1-AS1 counteracted the inhibition of miR-493-5p. CONCLUSION: Thus, NR2F1-AS1 was verified to regulate GC cell progression by sponging miR-493-5p to upregulate MAP3K2 expression.		J Oncol. 2021 Jul 13;2021:3881932. doi: 10.1155/2021/3881932. eCollection 2021.
5289	LncRNA	TUG1	miR-29c	B7-H3	Macrophages	Asthma	Homo sapiens (human)  	Dual-luciferase reporter assay;Luciferase reporter assay;	34335559	LncRNATUG1 Facilitates Th2 Cell Differentiation by Targeting the miR-29c/B7-H3 Axis on Macrophages.	The role of long non-coding RNAs (lncRNA) in asthma remains unclear. In this study, we examined the role of long non-coding RNA taurine upregulated 1 (lncRNA TUG1) in asthma. We found that lncRNA TUG1 is one of the differentially expressed lncRNAs in the monocytes of asthmatic children and is associated with Th cell differentiation. LncRNA TUG1 and miR-29c are mainly distributed in the cytoplasm of macrophages. Our data suggested that lncRNA TUG1 increased in macrophages stimulated by House Dust Mite in a dose-dependent manner. Using loss- and gain of function strategy, we found that miR-29c might regulate Th2 cell differentiation by directly targeting co-stimulatory molecule B7-H3. Furthermore, down-regulation of lncRNA TUG1 decreased the level of GATA3 in CD4+T cells and was associated with miR-29c/B7-H3 axis. Moreover, the dual-luciferase reporter assay confirmed that lncRNA TUG1 serves as a competing endogenous RNA to sponge miR-29c. According to the rescue experiment, lncRNA TUG1 regulated Th2 cell differentiation via miR-29c. These data suggest that lncRNA TUG1 in macrophages regulates Th2 cell differentiation via miR-29c/B7-H3 axis.		Front Immunol. 2021 Jul 16;12:631450. doi: 10.3389/fimmu.2021.631450. eCollection 2021.
5290	LncRNA	AFAP1-AS1	miR-27b-3p	VEGF-C	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34334630	LncRNA AFAP1-AS1/miR-27b-3p/VEGF-C axis modulates stemness characteristics in cervical cancer cells.	BACKGROUND: Long non-coding RNA (lncRNA) actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1) functions as a competing endogenous RNA to regulate target genes expression by sponging microRNAs (miRs) to play cancer-promoting roles in cancer stem cells. However, the regulatory mechanism of AFAP1-AS1 in cervical cancer (CC) stem cells is unknown. The present study aimed to provide a new therapeutic target for the clinical treatment of CC. METHODS: Hyaluronic acid receptor cluster of differentiation 44 variant exon 6 (CD44v6)(+) CC cells were isolated by flow cytometry (FCM). Small interfering RNAs of AFAP1-AS1 (siAFAP1-AS1) were transfected into the (CD44v6)(+) cells. The levels of AFAP1-AS1 were measured by quantitative real-time PCR (qRT-PCR). Sphere formation assay, cell cycle analysis, and Western blotting were used to detect the effect of siAFAP1-AS1. RNA Pull-down and Luciferase reporter assay were used to verify the relationship between miR-27b-3p and AFAP1-AS1 or vascular endothelial growth factor (VEGF)-C. RESULTS: CD44v6(+) CC cells had remarkable stemness and a high level of AFAP1-AS1. However, AFAP1-AS1 knockdown with siAFAP1-AS1 suppressed the cell cycle transition of G(1)/S phase and inhibited self-renewal of CD44v6(+) CC cells, the levels of the stemness markers octamer-binding transcription factor 4 (OCT4), osteopontin (OPN), and cluster of differentiation 133 (CD133), and the epithelial-mesenchymal transition (EMT)-related proteins Twist1, matrix metalloprotease (MMP)-9, and VEGF-C. In the mechanism study, miR-27b-3p/VEGF-C signaling was demonstrated to be a key downstream of AFAP1-AS1 in the CD44v6(+) CC cells. CONCLUSIONS: LncRNA AFAP1-AS1 knockdown inhibits the CC cell stemness by upregulating miR-27b-3p to suppress VEGF-C.		Chin Med J (Engl). 2021 Jul 29. doi: 10.1097/CM9.0000000000001665.
5291	LncRNA	MHRT	miR-3185	TGF-b1	Cardiac Fibroblasts	Myocardial Infarction	Mus musculus (mouse)	qRT-PCR;RIP assay;RNA pull-down assay;Western blot;luciferase assay;RNA pull-down;	34334583	LncRNA MHRT Promotes Cardiac Fibrosis via miR-3185 Pathway Following Myocardial Infarction.	Long-chain noncoding RNA (lncRNA) is a new class of molecular regulators in heart development and disease. However, the role of specific lncRNA in cardiac fibrosis remains to be fully explored. This study aimed to investigate the role and potential mechanism of lncRNA MHRT in myocardial fibrosis after myocardial infarction (MI).Cardiac fibroblasts (CFs) were isolated from a mouse model of MI. The expression levels of MHRT and miR-3185 in the hearts of MI and CFs mice treated with transforming growth factor beta 1 (TGF-b1) were analyzed by qRT-PCR. The collagen expression was assessed using qRT-PCR and Western blot. Cell proliferation was assessed by performing MTT and EdU assays. The direct interaction between lncRNA and miRNA was analyzed by luciferase assay, RNA-binding protein immunoprecipitation (RIP) assay, and RNA pull-down assay.The expression levels of MHRT were raised in MI and CFs mice treated with TGF-b1. Overexpression of MHRT promoted collagen production and CF proliferation, while silencing of MHRT showed the opposite effect. MiR-3185 was a target gene of MHRT. In addition, overexpression of MHRT reduced the expression levels of miR-3185, and siMHRT reversed the inhibitory effect of TGF-b1 on the expression of miR-3185. Overexpression of miR-3185 inhibited the upregulation of Col I and Col III induced by TGF-b1.MHRT promoted cardiac fibrosis after MI through miR-3185 and increased myocardial collagen deposition and promoted myocardial fibrosis.		Int Heart J. 2021;62(4):891-899. doi: 10.1536/ihj.20-298.
5292	LncRNA	LOXL1-AS1	miR-590-5p	KLF6	Endothelial Cells	Atherosclerosis	Homo sapiens (human)	qRT-PCR 	34334119	Inhibition of LOXL1-AS1 alleviates oxidative low-density lipoprotein induced angiogenesis via downregulation of miR-590-5p mediated KLF6/VEGF signaling pathway.	Increasing evidences have confirmed that long non-coding RNA LOXL1-AS1 functions in multiple human diseases. Here, we aim to explore the function and mechanism of LOXL1-AS1 in modulating oxidized low-density lipoprotein (ox-LDL)-induced angiogenesis of endothelial cells (ECs). Presently, we found that LOXL1-AS1 and KLF6 were upregulated in ECs treated by Ox-LDL in a dose- and time-dependent manner while miR-590-5p was downregulated. Overexpression of LOXL1-AS1 aggravated Ox-LDL mediated ECs proliferation and migration, and promoted angiogenesis both in vitro and in vivo. On the contrary, enhancing miR-590-5p or inhibiting LOXL1-AS1 level led to suppressive effects on the proliferation, migration and angiogenesis of ECs. Moreover, LOXL1-AS1 upregulation promoted the expression of vascular endothelial growth factor (VEGF), MMPs (including MMP2, MMP9 and MMP14) and also activated VEGF/VEGFR2/PI3K/Akt/eNOS pathway. Mechanistically, LOXL1-AS1 works as a competitive endogenous RNA (ceRNA) by sponging miR-590-5p, which targeted at the 3'-untranslated region (3'UTR) of KLF6. Additionally, the proliferation, migration and angiogenesis of ECs were elevated following KLF6 upregulation. By detecting the expression of LOXL1-AS1 and miR-590-5p in the serum of healthy donors and atherosclerosis patients, it was found that LOXL1-AS1 was upregulated in atherosclerosis patients (compared with healthy donors) and had a negative relationship with miR-590-5p. Taken together, LOXL1-AS1 promoted Ox-LDL induced angiogenesis via regulating miR-590-5p-modulated KLF6/VEGF signaling pathway. The LOXL1-AS1-miR-590-5p axis exerts a novel role in the progression of atherosclerosis.		Cell Cycle. 2021 Jul 31:1-18. doi: 10.1080/15384101.2021.1958484.
5293	LncRNA	SNHG5	miR-375	JAK2	Young Adult Mouse Colon (Yamc) Cells	Ulcerative Colitis	Mus musculus (mouse)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34334085	Long non-coding RNA SNHG5 regulates ulcerative colitis via microRNA-375 / Janus kinase-2 axis.	Ulcerative colitis (UC) is an intestinal inflammatory disorder. Long non-coding RNAs (lncRNAs) are collectively involved in UC. This study is designed to explore the roles of lncRNA (small nucleolar RNA host gene 5) SNHG5 in UC. Gene or microRNA (miRNA) expression was detected using RT-qPCR and western blot, respectively. Cellular functions were analyzed by cell counting kit 8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU) assay, flow cytometry, and the terminal deoxyribonucleotidyl transferase (TDT)-mediated dUTP-digoxigenin nick end labeling (TUNEL) assays. Lactate dehydrogenase (LDH) content was determined by a cell cytotoxicity assay. The interactions between miR-375 and SNHG5 or Janus kinase-2 (JAK2) were verified by a luciferase reporter assay. SNHG5 was up-regulated in intestinal mucosa tissues of UC patients as well as tumor necrosis factor alpha-treated (TNF-a-treated) young adult mouse colon (YAMC) cells. Down-regulated SNHG5 promoted cell proliferation and inhibited apoptosis of YAMC cells. miR-375 was verified to be a target of SNHG5 and was suppressed by TNF-a treatment in YAMC cells. Over-expression of miR-375 restored YAMC cellular functions. Additionally, miR-375 targeted JAK2, which was up-regulated by TNF-a treated YAMC cells. Up-regulation of JAK2 induced the dysfunction of YAMC cells. Knockdown of SNHG5 promoted the proliferation and suppressed the apoptosis of YAMC cells via regulating miR-375/JAK2 axis. Therefore, knockdown of SNHG5 may be a promising therapy for UC.		Bioengineered. 2021 Dec;12(1):4150-4158. doi: 10.1080/21655979.2021.1953219.
5294	LncRNA	ANCR	miR-4731-5p	NMT1	Nasopharyngeal Carcinoma (Npc) Cells	Nasopharyngeal Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;Rescue assay;	34333213	Long noncoding RNA ANCR promotes migration, invasion, EMT progress and stemness of nasopharyngeal carcinoma cells via the miR-4731-5p/NMT1 axis.	BACKGROUND: In our previous study, we revealed that Antidifferentiation noncoding RNA (ANCR) promoted proliferation and radiation resistance of nasopharyngeal carcinoma (NPC) cells. However, the molecular mechanism and function of ANCR are not fully studied. The current study aimed to further investigate the role and underlying molecular mechanism of ANCR in NPC. METHODS: RT-qPCR and western blot analyses were used to detect the levels of RNAs and proteins in NPC cells. Wound healing and Transwell assays were used to examine the migration and invasion of NPC cells. The relationship among ANCR, miR-4731-5p and N-myristoyltransferase 1 (NMT1) was investigated by RIP and luciferase reporter assays. The NPC cell stemness was accessed by the sphere formation assay. RESULTS: ANCR was significantly highly expressed in NPC cell lines. Silenced ANCR suppressed cell migration, invasion epithelial-mesenchymal transition (EMT) process and cell stemness in NPC. Furthermore, ANCR sponged miR-4731-5p to upregulate the NMT1 expression. Rescue assays indicated that NMT1 neutralized the antioncogenic effect induced by silenced ANCR on NPC cells. CONCLUSIONS: Long noncoding RNA ANCR suppresses malignant behaviors of nasopharyngeal carcinoma cells by regulating miR-4731-5p/NMT1 axis.		Pathol Res Pract. 2021 Aug;224:153540. doi: 10.1016/j.prp.2021.153540. Epub 2021 Jul 3.
5295	LncRNA	Lnc-STYK1-2	miR-146b-5p	ITGA2	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;RNA sequencing;	34332611	Lnc-STYK1-2 regulates bladder cancer cell proliferation, migration, and invasion by targeting miR-146b-5p expression and AKT/STAT3/NF-kB signaling.	BACKGROUND: Epigenetic modulation by noncoding RNAs substantially contributes to human cancer development, but noncoding RNAs involvement in bladder cancer remains poorly understood. This study investigated the role of long noncoding RNA (lncRNA) lnc-STYK1-2 in tumorigenesis in cancerous bladder cells. METHODS: Differential lncRNA and mRNA profiles were characterized by high-throughput RNA sequencing combined with validation via quantitative PCR. Bladder cancer cell proliferation was assessed through MTS, and bladder cancer cell migration and invasion were assessed through a Transwell system. The in vivo tumorigenesis of bladder cancer cells was evaluated using the cancer cell line-based xenograft model. The dual-luciferase reporter assay verified the association of miR-146b-5p with lnc-STYK1-2 and the target gene. Protein abundances and phosphorylation were detected by Western blotting. RESULTS: Alterations in lncRNA profiles, including decreased lnc-STYK1-2 expression, were detected in bladder cancer tissues compared with adjacent noncancerous tissues. lnc-STYK1-2 silencing effectively promoted proliferation, migration, and invasion in two bladder cancer cell lines, 5637 and T24, and their tumorigenesis in nude mice. lnc-STYK1-2 siRNA promoted miR-146b-5p and reduced ITGA2 expression in bladder cancer cells. Moreover, miR-146b-5p suppressed ITGA2 expression in bladder cancer cells through direct association. Also, lnc-STYK1-2 directly associated with miR-146b-5p. Finally, miR-146b-5p inhibitors abrogated the alterations in bladder cell functions, ITGA2 expression, and phosphorylation of AKT, STAT3, and P65 proteins in 5637 and T24 cells induced by lnc-STYK1-2 silencing. CONCLUSION: lnc-STYK1-2 inhibited bladder cancer cell proliferation, migration, and tumorigenesis by targeting miR-146b-5p to regulate ITGA2 expression and AKT/STAT3/NF-kB signaling.		Cancer Cell Int. 2021 Jul 31;21(1):408. doi: 10.1186/s12935-021-02114-4.
5296	LncRNA	HCP5	miR-128-3p	PLAGL2	Multiple Myeloma Cells	Multiple Myeloma	Homo sapiens (human)	qRT-PCR;RIP assay;RNA pull-down assay;Western blot;RNA pull-down;	34331612	LncRNA HCP5 acts as a miR-128-3p sponge to promote the progression of multiple myeloma through activating Wnt/b-catenin/cyclin D1 signaling via PLAGL2.	BACKGROUND: Although long non-coding RNA (lncRNA) HCP plays essential roles in human cancers, its function and mechanism in multiple myeloma (MM) have not crystallized. METHODS: HCP5 level in MM was assessed through qRT-PCR. A series of functional investigations were conducted to evaluate the influences of HCP5 on proliferation and apoptosis. Bioinformatics analysis and RIP/RNA pull-down assays were carried out to determine the relationships among HCP5, miR-128-3p, and PLAGL2. Relative protein level was determined through Western blot. A xenograft tumor model was applied for validating the roles of HCP5/miR-128-3p/PLAGL2 axis in vivo. RESULTS: HCP5 was significantly increased in MM. HCP5 knockdown effectively thwarted the proliferative rate and cell cycle of MM cell lines and suppressed tumor growth. HCP5 regulated PLAGL2 expression by sponging miR-128-3p. PLAGL2 overexpression effectively rescued cells from influences by sh-HCP5 on cell proliferative and apoptotic rates. Additionally, HCP5 knockdown significantly inhibited Wnt/b-catenin/cyclin D1 signaling, and these effects were eliminated by PLAGL2 overexpression. CONCLUSION: Our study revealed that HCP5/miR-128-3p/PLAGL2 is closely correlated to MM development by modulating Wnt/b-catenin/cyclin D1 signaling. HCP5 promoted cell proliferation and tumor formation of MM cells by activating the Wnt/b-catenin/CCND1 signaling pathway by sponging miR-128-3p to increase PLAGL2 expression.		Cell Biol Toxicol. 2021 Jul 31. doi: 10.1007/s10565-021-09628-7.
5297	LncRNA	TMPO-AS1	miR-335-5p	NA	Granulosa-Like Tumor (Kgn) Cells	Polycystic Ovary Syndrome	Homo sapiens (human)  	qPCR;RT-qPCR;RNA pull-down assay;RNA pull-down;	34330309	LncRNA TMPO-AS1 suppresses the maturation of miR-335-5p to participate in polycystic ovary syndrome.	BACKGROUND: TMPO-AS1 is a recently characterized oncogenic lncRNA in ovarian cancer. Its role in other ovary diseases is unknown. This study explored its role in polycystic ovary syndrome (PCOS). METHODS: Follicular fluid was extracted from both PCOS patients and controls. The levels of TMPO-AS1 and mature and premature miR-335-5p were analyzed by RT-qPCR. The role of TMPO-AS1 in regulating miR-355-5p maturation in granulosa-like tumor (KGN) cells was analyzed by overexpression experiments. The interaction between TMPO-AS1 and premature miR-335-5p was analyzed by RNA pull-down assay. The subcellular location of TMPO-AS1 in KGN cells was analyzed by nuclear fractionation assay. The role of TMPO-AS1 and miR-335-5p in KGN cell proliferation was analyzed by BrdU assay. RESULTS: TMPO-AS1 was increased in PCOS, while mature miR-355-5p was decreased in PCOS. TMPO-AS1 overexpression decreased mature miR-355-5p level but increased premature miR-355-5p. TMPO-AS1 was localized in both nucleus and cytoplasm. TMPO-AS1 directly interacted with premature miR-355-5p in KGN cells. TMPO-AS1 increased KGN cell proliferation while miR-355-5p decreased cell proliferation. The co-transfection assay showed that TMPO-AS1 reduced the suppressive effects of miR-355-5p on cell proliferation. CONCLUSIONS: TMPO-AS1 might suppress miR-335-5p maturation to participate in PCOS.		J Ovarian Res. 2021 Jul 30;14(1):99. doi: 10.1186/s13048-021-00848-3.
5298	LncRNA	GAS5	miR-146a	Smad4	Synovial Fluid	Osteoarthritis	Homo sapiens (human)  	Cell apoptosis assay;Cell transfection;Cell transfection;qPCR;RT-qPCR;	34329870	LncRNA GAS5 upregulates Smad4 to suppress the apoptosis of chondrocytes induced by lipopolysaccharide.	BACKGROUND: Osteoarthritis (OA) is closely correlated with inflammation. It has been reported that lncRNA GAS5 plays an important role in inflammation, indicating the potential involvement of GAS5 in OA. This study was carried out to investigate the function of GAS5 in OA. METHODS: Expression levels of GAS5 in synovial fluid from 45 OA patients and 45 healthy controls were measured by RT-qPCR. Cell transfections were performed to explore the potential interactions among GAS5, miR-146a, and Smad4 in chondrocytes. Lipopolysaccharide (LPS)-induced cell apoptosis after overexpression of GAS5, miR-146a, and Smad4 was analyzed by cell apoptosis assay. RESULTS: GAS5 was downregulated in OA. Moreover, LPS treatment downregulated GAS5 in chondrocytes. Interaction between GAS5 could with miR-146a was predicted by bioinformatics analysis and further confirmed by RNA-RNA pulldown assay. However, overexpression of GAS5 and miR-146a did not affect the expression of each other. GAS5 overexpression increased Smad4 expression in chondrocytes. In contrast, miR-146a overexpression downregulated Smad4 in chondrocytes. Moreover, GAS5 and Smad4 overexpression inhibited LPS- induced chondrocytes apoptosis, while miR-146a overexpression played an opposite role and attenuated the effects of GAS5 and Smad4 overexpression on cell apoptosis. CONCLUSION: GAS5 might sponge miR-146a to upregulate Smad4, thereby suppressing LPS- induced chondrocytes apoptosis.		Arch Gerontol Geriatr. 2021 Jul 23;97:104478. doi: 10.1016/j.archger.2021.104478.
5299	LncRNA	LINC01559	miR-1343-3p	PARP1	Colorectal Cancer Cells And Tissues	Colorectal Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;	34329839	LINC01559 promotes colorectal cancer via sponging miR-1343-3p to modulate PARP1/PTEN/AKT pathway.	BACKGROUND: Colorectal cancer (CRC) is considered as one of the commonest tumors and is the major reason of cancer-related deaths around the world. Plentiful evidences have validated that long non-coding RNAs (lncRNAs) play a significant part in various cancers, including CRC. LINC01559 is implicated in the development of various cancers. However, the detailed function of LINC01559 in CRC has not been illustrated. METHODS: LINC01559 expression was examined via RT-qPCR, and a series of functional experiments were conducted to explore the role of LINC01559 in CRC progression. Mechanism experiments were carried out to examine the underlying mechanism of LINC01559. RESULTS: LINC01559 expression was increased in CRC cells and tissues, and LINC01559 depletion restrained the biological behaviors of CRC cells. Also, LINC01559 sponged miR-1343-3p in CRC, and PARP1 was the target of miR-1343-3p. Besides, miR-1343-3p overexpression or PARP1 down-regulation affected the biological behaviors of CRC cells. In addition, up-regulation of PARP1 or adding SC79 (AKT pathway activator) could remedy the repressive effects of LINC01559 silencing on CRC cell biological behaviors. CONCLUSIONS: LINC01559 promotes CRC through sponging miR-1343-3p to modulate PARP1/PTEN/AKT pathway, which may be conducive to offering a new idea for CRC therapeutic treatment.		Pathol Res Pract. 2021 Aug;224:153521. doi: 10.1016/j.prp.2021.153521. Epub 2021 Jun 8.
5300	LncRNA	LINC00511	miR-126-5p	DVL3	Glioblastoma Cells	Glioblastoma	Homo sapiens (human)  	RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;RNA sequencing;	34328678	LINC00511 facilitates Temozolomide resistance of glioblastoma cells via sponging miR-126-5p and activating Wnt/b-catenin signaling.	Temozolomide (TMZ) is the first-line chemotherapy drug for glioblastoma (GBM) but acquired TMZ resistance is frequently observed. Thus, a TMZ resistant GBM cell line U87-R was established to search for potential long noncoding RNAs (lncRNAs) used in TMZ resistance. In our study, LINC00511 was identified as a TMZ resistance-associated lncRNA in U87-R cells by transcriptome RNA sequencing. The potential functions of LINC00511 were evaluated by quantitative real-time polymerase chain reaction, cell viability assay, colony formation assay, western blot, soft agar assay, flow cytometry, tumor xenograft model, immunofluorescence, sphere formation assay, fluorescent in situ hybridization, luciferase reporter assay, and RNA pull-down assay. We found that LINC00511 was upregulated in U87-R cells and GBM samples, and correlated with poor prognosis of GBM patients. Silencing LINC00511 impaired TMZ tolerance of U87-R cells, while LINC00511 overexpression increased TMZ resistance of sensitive GBM cells. Wnt/b-catenin signaling was activated in U87-R cells, and inhibiting Wnt/b-catenin signaling enhanced TMZ sensitivity. Furthermore, LINC00511 was mainly distributed in the cytoplasm of GBM cells and regulated Wnt/b-catenin activation by acting as a molecular sponge for miR-126-5p. Multiple genes of Wnt/b-catenin signaling such as DVL3, WISP1, and WISP2 were targeted by miR-126-5p. MiR-126-5p restoration impaired TMZ resistance of GBM cells. In conclusion, our results provided a novel insight into acquired TMZ resistance of GBM cells and suggested LINC00511 as a potential biomarker or therapeutic target for GBM patients.		J Biochem Mol Toxicol. 2021 Jul 30:e22848. doi: 10.1002/jbt.22848.
5301	LncRNA	LINC00511	miR-126-5p	WISP1	Glioblastoma Cells	Glioblastoma	Homo sapiens (human)  	RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;RNA sequencing;	34328678	LINC00511 facilitates Temozolomide resistance of glioblastoma cells via sponging miR-126-5p and activating Wnt/b-catenin signaling.	Temozolomide (TMZ) is the first-line chemotherapy drug for glioblastoma (GBM) but acquired TMZ resistance is frequently observed. Thus, a TMZ resistant GBM cell line U87-R was established to search for potential long noncoding RNAs (lncRNAs) used in TMZ resistance. In our study, LINC00511 was identified as a TMZ resistance-associated lncRNA in U87-R cells by transcriptome RNA sequencing. The potential functions of LINC00511 were evaluated by quantitative real-time polymerase chain reaction, cell viability assay, colony formation assay, western blot, soft agar assay, flow cytometry, tumor xenograft model, immunofluorescence, sphere formation assay, fluorescent in situ hybridization, luciferase reporter assay, and RNA pull-down assay. We found that LINC00511 was upregulated in U87-R cells and GBM samples, and correlated with poor prognosis of GBM patients. Silencing LINC00511 impaired TMZ tolerance of U87-R cells, while LINC00511 overexpression increased TMZ resistance of sensitive GBM cells. Wnt/b-catenin signaling was activated in U87-R cells, and inhibiting Wnt/b-catenin signaling enhanced TMZ sensitivity. Furthermore, LINC00511 was mainly distributed in the cytoplasm of GBM cells and regulated Wnt/b-catenin activation by acting as a molecular sponge for miR-126-5p. Multiple genes of Wnt/b-catenin signaling such as DVL3, WISP1, and WISP2 were targeted by miR-126-5p. MiR-126-5p restoration impaired TMZ resistance of GBM cells. In conclusion, our results provided a novel insight into acquired TMZ resistance of GBM cells and suggested LINC00511 as a potential biomarker or therapeutic target for GBM patients.		J Biochem Mol Toxicol. 2021 Jul 30:e22848. doi: 10.1002/jbt.22848.
5302	LncRNA	LINC00511	miR-126-5p	WISP2	Glioblastoma Cells	Glioblastoma	Homo sapiens (human)  	RNA pull-down assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;RNA sequencing;	34328678	LINC00511 facilitates Temozolomide resistance of glioblastoma cells via sponging miR-126-5p and activating Wnt/b-catenin signaling.	Temozolomide (TMZ) is the first-line chemotherapy drug for glioblastoma (GBM) but acquired TMZ resistance is frequently observed. Thus, a TMZ resistant GBM cell line U87-R was established to search for potential long noncoding RNAs (lncRNAs) used in TMZ resistance. In our study, LINC00511 was identified as a TMZ resistance-associated lncRNA in U87-R cells by transcriptome RNA sequencing. The potential functions of LINC00511 were evaluated by quantitative real-time polymerase chain reaction, cell viability assay, colony formation assay, western blot, soft agar assay, flow cytometry, tumor xenograft model, immunofluorescence, sphere formation assay, fluorescent in situ hybridization, luciferase reporter assay, and RNA pull-down assay. We found that LINC00511 was upregulated in U87-R cells and GBM samples, and correlated with poor prognosis of GBM patients. Silencing LINC00511 impaired TMZ tolerance of U87-R cells, while LINC00511 overexpression increased TMZ resistance of sensitive GBM cells. Wnt/b-catenin signaling was activated in U87-R cells, and inhibiting Wnt/b-catenin signaling enhanced TMZ sensitivity. Furthermore, LINC00511 was mainly distributed in the cytoplasm of GBM cells and regulated Wnt/b-catenin activation by acting as a molecular sponge for miR-126-5p. Multiple genes of Wnt/b-catenin signaling such as DVL3, WISP1, and WISP2 were targeted by miR-126-5p. MiR-126-5p restoration impaired TMZ resistance of GBM cells. In conclusion, our results provided a novel insight into acquired TMZ resistance of GBM cells and suggested LINC00511 as a potential biomarker or therapeutic target for GBM patients.		J Biochem Mol Toxicol. 2021 Jul 30:e22848. doi: 10.1002/jbt.22848.
5303	LncRNA	TPRG1-AS1	miR-4691-5p	RBM24	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34328265	TPRG1-AS1 induces RBM24 expression and inhibits liver cancer progression by sponging miR-4691-5p and miR-3659.	BACKGROUND & AIMS: Noncoding RNAs (ncRNAs) play critical roles in hepatocellular carcinoma (HCC) progression. Here, by performing RNA-sequencing (RNA-Seq) profiling, we sought to identify novel ncRNAs that potentially drive the heterogeneous progression of liver cancers. METHODS: RNA-Seq profiles were obtained from 68 HCC specimens and 10 samples of adjacent non-tumour liver tissues. The functional significance of the potential driver ncRNAs was evaluated by cell experiments. RESULTS: TPRG1-AS1 was identified as a potential driver noncoding RNA that promotes heterogeneous liver cancer progression. TPRG1-AS1 induced tumour suppressor RNA-binding motif protein 24 (RBM24), suppressing tumour growth by activating apoptotic tumour cell death. In addition, we report that TPRG1-AS1 acts as a competing endogenous RNA (ceRNA) for RBM24, sponging miR-4691-5p and miR-3659 to interfere with their binding to RBM24. CONCLUSIONS: We suggest that TPRG1-AS1 is a novel ceRNA sponging miR-4691-5p and miR-3659, resulting in RBM24 expression and suppression of liver cancer growth. Our results provide new insights into the functions of ncRNAs in heterogeneous HCC progression.		Liver Int. 2021 Jul 30. doi: 10.1111/liv.15026.
5304	LncRNA	TPRG1-AS1	miR-3659	RBM24	Hepatocellular Carcinoma Tissues	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34328265	TPRG1-AS1 induces RBM24 expression and inhibits liver cancer progression by sponging miR-4691-5p and miR-3659.	BACKGROUND & AIMS: Noncoding RNAs (ncRNAs) play critical roles in hepatocellular carcinoma (HCC) progression. Here, by performing RNA-sequencing (RNA-Seq) profiling, we sought to identify novel ncRNAs that potentially drive the heterogeneous progression of liver cancers. METHODS: RNA-Seq profiles were obtained from 68 HCC specimens and 10 samples of adjacent non-tumour liver tissues. The functional significance of the potential driver ncRNAs was evaluated by cell experiments. RESULTS: TPRG1-AS1 was identified as a potential driver noncoding RNA that promotes heterogeneous liver cancer progression. TPRG1-AS1 induced tumour suppressor RNA-binding motif protein 24 (RBM24), suppressing tumour growth by activating apoptotic tumour cell death. In addition, we report that TPRG1-AS1 acts as a competing endogenous RNA (ceRNA) for RBM24, sponging miR-4691-5p and miR-3659 to interfere with their binding to RBM24. CONCLUSIONS: We suggest that TPRG1-AS1 is a novel ceRNA sponging miR-4691-5p and miR-3659, resulting in RBM24 expression and suppression of liver cancer growth. Our results provide new insights into the functions of ncRNAs in heterogeneous HCC progression.		Liver Int. 2021 Jul 30. doi: 10.1111/liv.15026.
5305	LncRNA	DARS-AS1	miR-194-5p	RBX1	Ovarian Cancer Cells A2780	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34328246	Long noncoding RNA DARS-AS1 regulates TP53 ubiquitination and affects ovarian cancer progression by modulation miR-194-5p/RBX1 axis.	BACKGROUND: Ovarian cancer is a malignant tumor with a poor prognosis, its underlying mechanism is still unclear. OBJECTIVE: In this study, long noncoding RNA DARS-AS1 was studied to identify its function in the development of ovarian cancer. METHODS: Perform functional experiments to detect the effects of DARS-AS1 on the proliferation, apoptosis, and migration of ovarian cancer cells A2780. The luciferase report, immunoprecipitation (IP) experiment, and ubiquitination level determination verify that RBX1 ubiquitination and mediate the degradation of tumor suppressor gene TP53. RESULTS: Knockdown of DARS-AS1 can inhibit cell proliferation, migration, and apoptosis, and the application of miR-194-5p inhibitors can prevent this process. Luciferase and IP experiments showed that DARS-AS1 regulates the expression of RBX1 by binding to miR-194-5p, and RBX1 mediates its degradation through ubiquitination of TP53.		J Biochem Mol Toxicol. 2021 Jul 30:e22865. doi: 10.1002/jbt.22865.
5306	LncRNA	DARS-AS1	miR-194-5p	TP53	Ovarian Cancer Cells A2780	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34328246	Long noncoding RNA DARS-AS1 regulates TP53 ubiquitination and affects ovarian cancer progression by modulation miR-194-5p/RBX1 axis.	BACKGROUND: Ovarian cancer is a malignant tumor with a poor prognosis, its underlying mechanism is still unclear. OBJECTIVE: In this study, long noncoding RNA DARS-AS1 was studied to identify its function in the development of ovarian cancer. METHODS: Perform functional experiments to detect the effects of DARS-AS1 on the proliferation, apoptosis, and migration of ovarian cancer cells A2780. The luciferase report, immunoprecipitation (IP) experiment, and ubiquitination level determination verify that RBX1 ubiquitination and mediate the degradation of tumor suppressor gene TP53. RESULTS: Knockdown of DARS-AS1 can inhibit cell proliferation, migration, and apoptosis, and the application of miR-194-5p inhibitors can prevent this process. Luciferase and IP experiments showed that DARS-AS1 regulates the expression of RBX1 by binding to miR-194-5p, and RBX1 mediates its degradation through ubiquitination of TP53.		J Biochem Mol Toxicol. 2021 Jul 30:e22865. doi: 10.1002/jbt.22865.
5307	LncRNA	SNHG11	miR-184	IGF-1R	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR 	34328198	lncRNA SNHG11 facilitates prostate cancer progression through the upregulation of IGF-1R expression and by sponging miR-184.	Long non-coding RNA (lncRNA) small nucleolar RNA host gene 11 (SNHG11) has been shown to play an important role in the development and progression of numerous types of cancer. However, to the best of our knowledge, the role of SNHG11 in prostate cancer (PCa) development and metastasis remains unclear. Thus, the aim of the present study was to investigate the functional role and molecular mechanisms of SNHG11 in PCa progression. It was revealed that the SNHG11 expression levels were significantly upregulated in PCa tissues, in comparison with those in adjacent normal tissues. Functionally, SNHG11 knockdown significantly suppressed PCa cell proliferation, migration, invasion and metastasis in vitro and in vivo. Furthermore, SNHG11 was found to positively regulate insulin-like growth factor 1 receptor (IGF-1R) expression by sponging microRNA (miRNA/miR)-184 in PCa cells. The results of rescue experiments demonstrated that IGF-1R overexpression reversed the suppressive effects of SNHG11 knockdown on the proliferation, migration and invasion of PCa cells. On the whole, the findings of the present study suggest that SNHG11 expression is upregulated in PCa and that it facilitates PCa progression, at least in part, via the modulation of the miR-184/IGF-1R signaling axis.		Int J Mol Med. 2021 Sep;48(3):182. doi: 10.3892/ijmm.2021.5015. Epub 2021 Jul 30.
5308	LncRNA	H19	miR-29a-3p	LASP1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	Western blot;	34328197	Long non-coding RNA H19 regulates LASP1 expression in osteosarcoma by competitively binding to miR-29a-3p.	A prevalent type of bone tumor, osteosarcoma (OS) is prone to pulmonary metastasis, which results in a high relapse risk and poor prognosis for patients. The progression of OS is significantly associated with the expression of long non-coding (lnc)RNA H19. To the best of our knowledge, however, the exact molecular mechanism of this lncRNA has not been fully investigated. The present study verified the effect of H19 on the proliferation and invasion of osteosarcoma cells via in vivo and in vitro experiments, including Cell Counting Kit-8, western blot, reverse transcription-quantitative PCR, wound healing and Transwell assays. H19 was found to be overexpressed in OS compared with corresponding normal adjacent tissue. In addition, H19 served as a competing endogenous ncRNA targeting microRNA-29a-3p and activating LIM and SH3 domain protein 1 and modulating the OS cell phenotype. The results of the present study may improve understanding of OS pathogenesis.		Oncol Rep. 2021 Sep;46(3):207. doi: 10.3892/or.2021.8158. Epub 2021 Jul 30.
5309	LncRNA	NEAT1	miR-23a-3p	FOXA1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	luciferase assay;	34327529	lncRNA NEAT1 promotes the Taxol resistance of breast cancer via sponging the miR-23a-3p-FOXA1 axis.	Breast cancer is the most prevalent malignancy among women worldwide. Paclitaxel (Taxol) is a widely applied chemotherapeutic agent against breast cancer. Although Taxol therapy has achieved improvements recently, development of chemoresistance of breast cancer patients is a major obstacle, leading to therapeutic failure. Long non-coding RNAs (lncRNAs) play pivotal roles in tumorigenesis and progresses of breast cancer. However, the biological roles and molecular targets of lncRNA NEAT1 in Taxol-resistant breast cancer remain unclear. Here, we report that NEAT1 is significantly upregulated in breast tumors and cell lines. In addition, silencing NEAT1 effectively sensitizes breast cancer cells to Taxol. Bioinformatical analysis and luciferase assay demonstrated that miR-23a-3p could be sponged and downregulated by NEAT1. We demonstrated that miR-23a-3p was downregulated and functioned as a tumor suppressor in breast cancer. Furthermore, in the established Taxol-resistant MDA-MB-231 breast cancer cell line, we detected significantly increased NEAT1 expression and downregulated miR-23a-3p expression. Importantly, FOXA1 was identified and validated as a direct target of miR-23a-3p in breast cancer cells. Rescue experiments demonstrated that the restoration of miR-23a-3p in NEAT1-overexpressing Taxol-resistant breast cancer cells successfully overcame the NEAT1-promoted Taxol resistance. Taken together, our results revealed the clinical roles and molecular mechanisms for the NEAT1-mediated chemoresistance, providing new insights into the development of non-coding RNA-based therapeutic strategies for enhancing the anti-cancer effects of traditional chemotherapeutic drugs.		Acta Biochim Biophys Sin (Shanghai). 2021 Jul 30:gmab098. doi: 10.1093/abbs/gmab098.
5310	LncRNA	RGMB-AS1	microRNA-574	HDAC4	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qRT-PCR 	34326647	Long Noncoding RNA RGMB-AS1 Acts as a microRNA-574 Sponge Thereby Enhancing the Aggressiveness of Gastric Cancer via HDAC4 Upregulation [Retraction].	[This retracts the article DOI: 10.2147/OTT.S234144.].		Onco Targets Ther. 2021 Jul 22;14:4267. doi: 10.2147/OTT.S329199. eCollection 2021.
5311	LncRNA	NEAT1	miR-129-5p	BMP2	Human Renal Interstitial Fibroblasts	Randalls Plaques	Homo sapiens (human)	qRT-PCR 	34325517	NEAT1 functions as a key mediator of BMP2 to promote osteogenic differentiation of renal interstitial fibroblasts.	Aim: To clarify the mechanism of NEAT1, an aberrantly upregulated lncRNA in Randall's plaques (RP) similar to biomineralization, in mediating osteogenic differentiation of human renal interstitial fibroblasts. Materials & methods: A comprehensive strategy of bioinformatic analysis and experimental verification was performed. Results: BMP2 silence abolished the osteogenic differentiation of human renal interstitial fibroblasts promoted by NEAT1. Mechanically, NEAT1 not only induced the nucleolar translocation of EGR1 binding to BMP2 promotor, but also functioned as a sponge of miR-129-5p in the cytoplasm to promote BMP2 expression. Moreover, there was a positive correlation between NEAT1 and BMP2 expression in RP instead of normal renal papilla. Conclusion: NEAT1 acted as a key mediator of BMP2 to promote human renal interstitial fibroblast osteogenic differentiation, through which NEAT1 might be involved in RP formation.		Epigenomics. 2021 Aug;13(15):1171-1186. doi: 10.2217/epi-2021-0212. Epub 2021 Jul 30.
5312	LncRNA	CASC15	miR-7151-5p	WNT7A	Papillary Thyroid Carcinoma Cells	Thyroid Cancer	Homo sapiens (human)	qRT-PCR 	34325316	LncRNA CASC15 promotes the proliferation of papillary thyroid carcinoma cells by regulating the miR-7151-5p/WNT7A axis.	Long noncoding RNAs (lncRNAs) play crucial roles in the regulation of human thyroid cancer (TC), including papillary thyroid carcinoma (PTC); PTC is the most common pathological subtype of TC. To date, the expression, function, and mechanism of the lncRNA CASC15 in PTC remain unclear. The present study results showed that CASC15 was overexpressed in PTC tissues compared with normal tissues and acted as a potent oncogene to promote the proliferation and tumorigenesis of PTC cells both in vitro and in vivo. Mechanistic studies demonstrated that CASC15 could serve as an endogenous miRNA sponge to absorb and downregulate miR-7151-5p, thereby preventing the inhibition of WNT7A during PTC progression. Furthermore, the study demonstrated that CASC15 activated the WNT/b-catenin signaling pathway by upregulating WNT7A in PTC. Taken together, our findings identified CASC15 as a potential diagnostic marker or therapeutic target for PTC progression. DATA AVAILABILITY: Please contact the corresponding author for a data request.		Pathol Res Pract. 2021 Jul 21;225:153561. doi: 10.1016/j.prp.2021.153561.
5313	LncRNA	IL6-AS1	miR-149-5p	IL-6	Airway Inflammation	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)  	qRT-PCR 	34323408	Long noncoding RNA IL6-AS1 is highly expressed in chronic obstructive pulmonary disease and is associated with interleukin 6 by targeting miR-149-5p and early B-cell factor 1.	Chronic obstructive pulmonary disease is a complex condition with multiple etiologies, including inflammation. We identified a novel long noncoding RNA (lncRNA), interleukin 6 antisense RNA 1 (IL6-AS1), which is upregulated in this disease and is associated with airway inflammation. We found that IL6-AS1 promotes the expression of inflammatory factors, especially interleukin (IL) 6. Mechanistically, cytoplasmic IL6-AS1 acts as an endogenous sponge by competitively binding to the microRNA miR-149-5p to stabilize IL-6 mRNA. Nuclear IL6-AS1 promotes IL-6 transcription by recruiting early B-cell factor 1 to the IL-6 promoter, which increases the methylation of the H3K4 histone and acetylation of the H3K27 histone. We propose a model of lncRNA expression in both the nucleus and cytoplasm that exerts similar effects through differing mechanisms, and IL6-AS1 probably increases inflammation via multiple pathways.		Clin Transl Med. 2021 Jul;11(7):e479. doi: 10.1002/ctm2.479.
5314	LncRNA	PTAR	miR-101	NA	Cervical Cancer Tissues And Cells	Cervical Cancer	Homo sapiens (human)  	CCK-8 assay;Dual-luciferase reporter assay;Flow Cytometry assay;Luciferase reporter assay;	34323178	Long non-coding RNA PTAR inhibits apoptosis but promotes proliferation, invasion and migration of cervical cancer cells by binding miR-101.	In this study, the expression of PTAR in cervical cancer tissues and cells was quantified by real-time PCR. Then, the roles of PTAR in HeLa cell proliferation and cell cycle were analyzed by a CCK-8 assay and flow cytometry, respectively.The effects of PTAR on cell migration and invasion were checked by Transwell and wound healing assays.The effect of PTAR on HeLa cell apoptosis was analyzed using annexin V/FITC staining. Finally, the interaction between PTAR and miR-101 in uterine cancer was verified through a dual-luciferase reporter assay and correlation analysis. The results showed that PTAR expression was aberrantly ascended in cervical cancer tissues and cell lines (Caski, SW756, SiHa, C33A and HeLa cells). Overexpressed PTAR could promote cell proliferation, migration and invasion in HeLa cells, which were suppressed by PTAR knockdown. Moreover, cell cycle progression stalled at the G1-G0 phase could be released with PTAR overexpression. The transfection of a PTAR vector inhibited apoptosis, while si-PTAR transfection increased apoptosis. Furthermore, PTAR could act as an endogenous sponge by directly binding to miR-101 and downregulating miR-101 expression. In conclusion, lncRNAPTAR plays a vital role and may be an effective target for the diagnosis and therapy of cervical cancer.		Bioengineered. 2021 Dec;12(1):4536-4545. doi: 10.1080/21655979.2021.1946634.
5315	LncRNA	COX10-AS1	miR-142-5p	PAICS	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34323174	Regulating COX10-AS1 / miR-142-5p / PAICS axis inhibits the proliferation of non-small cell lung cancer.	Non-small cell lung cancer (NSCLC) is one of the main causes of death in the world. To improve the diagnostic level and find new biological targets，GSE datasets were selected from GEO databaseto analyze the differential expression genes and construct ceRNA network. Cell apoptosis detection showed that both the early and late apoptosis rates were increased after inhibition of COX10-AS1. Glycolysis cell-based assay also found that the content of L-lactate decreased significantly after using miR-142-5p mimics but increased after using si-COX10-AS1. Dual-luciferase reporter analysis showed that the luciferase activity of PAICS-WT reporter vector was inhibited by miR-142-5p mimics, but there was no significant change in PAICS-MUT reporter vector after transfection of miR-142-5p mimics. And overexpression of miR-142-5p reduced the level of PAICS, but inhibition of miR-142-5p expression increased the expression of PAICS. After using COX10-AS1, the expression of PAICS inhibited by miR-142-5p was restored. Through bioinformatics analysis, we constructed the COX10-AS1/miR-142-5p/PAICS axis, which is a ceRNA regulatory network. We confirmed that COX10-AS1 down-expression can restore the inhibitory effect of miR-142-5p on PAICS, promote the apoptosis of NSCLC cells, and inhibit the proliferation of NSCLC cells. This process may be mediated by the activation of glycolysis pathway. The glycolysis-related gene PAICS may be a new and significant target for the regulation of the development of NSCLC.		Bioengineered. 2021 Dec;12(1):4643-4653. doi: 10.1080/21655979.2021.1957072.
5316	LncRNA	HOTTIP	miR-205	ZEB2	Ovarian Cancer Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34322490	HOTTIP-miR-205-ZEB2 Axis Confers Cisplatin Resistance to Ovarian Cancer Cells.	Ovarian cancer is a deadly gynecological malignancy with resistance to cisplatin a major clinical problem. We evaluated a role of long non-coding (lnc) RNA HOTTIP (HOXA transcript at the distal tip) in the cisplatin resistance of ovarian cancer cells, using paired cisplatin sensitive and resistant A2780 cells along with the SK-OV-3 cells. HOTTIP was significantly elevated in cisplatin resistant cells and its silencing reversed the cisplatin resistance of resistant cells. HOTTIP was found to sponge miR-205 and therefore HOTTIP silenced cells had higher levels of miR-205. Downregulation of miR-205 could attenuate HOTTIP-silencing effects whereas miR-205 upregulation in resistant cells was found to re-sensitize cells to cisplatin. HOTTIP silencing also led to reduced NF-kB activation, clonogenic potential and the reduced expression of stem cell markers SOX2, OCT4, and NANOG, an effect that could be attenuated by miR-205. Finally, ZEB2 was identified as the gene target of miR-205, thus completing the elucidation of HOTTIP-miR-205-ZEB2 as the novel axis which is functionally involved in the determination of cisplatin resistance in ovarian cancer cells.		Front Cell Dev Biol. 2021 Jul 12;9:707424. doi: 10.3389/fcell.2021.707424. eCollection 2021.
5317	LncRNA	DGCR5	miR-211-5p	Snail	Ccrcc Tissues	Clear Cell Renal Cancer	Homo sapiens (human)  	qRT-PCR 	34322486	LncRNA DGCR5 Isoform-1 Silencing Suppresses the Malignant Phenotype of Clear Cell Renal Cell Carcinoma via miR-211-5p/Snail Signal Axis.	Long non-coding RNAs (lncRNAs) play important roles during the initiation and progression of cancer. We identified DiGeorge Syndrome Critical Region Gene 5 (DGCR5) as a clear cell renal cell carcinoma (ccRCC) cancer- and lineage-specific lncRNA. Agarose gel electrophoresis analysis and sanger sequencing verified two main isoforms of DGCR5 in ccRCC patient tissues and cell lines. Quantitative polymerase chain reaction further demonstrated that the expression level of DGCR5 major isoform (isoform-1) was higher in ccRCC tissues than that in papillary/chromophobe RCC and other multiple solid malignant tumors. We investigate the biological functions of DGCR5 isoform-1 in ccRCC and show that DGCR5 isoform-1 exerts a tumor-promoting effect in ccRCC. DGCR5 isoform-1 is localized in cytoplasm and shares the same binding sequence to the tumor-suppressive miR-211-5p with the epithelial-to-mesenchymal transition key component SNAI. Furthermore, cellular and molecular experiments demonstrate that DGCR5 isoform-1 could sequester miR-211-5p, leading to the elevation of Snail protein and downregulation of its downstream targets and further promoting ccRCC cell proliferation and migration. Thus, our study indicates that DGCR5 isoform-1 could contribute to ccRCC progression by sponging miR-211-5p through regulating the expression of Snail protein and could serve as a reliable diagnostic biomarker in ccRCC.		Front Cell Dev Biol. 2021 Jul 12;9:700029. doi: 10.3389/fcell.2021.700029. eCollection 2021.
5318	LncRNA	SOX2-OT	miR-143-3p	MSI2	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Mus musculus (mouse)	RNA pull-down assay;luciferase assay;RNA pull-down;	34322386	Downregulation of SOX2-OT Prevents Hepatocellular Carcinoma Progression Through miR-143-3p/MSI2.	OBJECTIVE: LncRNA SOX2-OT is involved in a variety of cancers. This study explored the effect of lncRNA SOX2-OT on hepatocellular carcinoma (HCC) cells. METHODS: SOX2-OT expressions were detected in HCC tissues and normal tissues, normal cells, and HCC cells. The relationship between SOX2-OT and prognosis was analyzed by TCGA. After SOX2-OT expression was inhibited using siRNA, HCC cell malignant behaviors were evaluated. The subcellular localization of SOX2-OT in HCC cells was predicted and analyzed. The binding relationships among SOX2-OT, miR-143-3p, and MSI2 were analyzed by bioinformatics website, dual-luciferase assay, and RNA pull-down assay. The effect of miR-143-3p and MSI2 on the regulation of SOX2-OT on biological behaviors of HCC cells was confirmed by functional rescue experiments. The effect of SOX2-OT on the tumorigenicity of HCC was evaluated by subcutaneous tumorigenesis in nude mice. RESULTS: SOX2-OT was highly expressed in HCC cells and tissues. The prognosis was poor in HCC patients with high SOX2-OT expression. Downregulating SOX2-OT inhibited HCC cell malignant behaviors. SOX2-OT bound to miR-143-3p to promote MSI2 expression. Downregulating miR-143-3p or upregulating MSI2 averted the role of si-SOX2-OT in HCC cells. Nude mouse subcutaneous tumorigenesis showed that SOX2-OT downregulation decreased the tumorigenicity of HCC, and affected the levels of miR-143-3p and MSI2 mRNA in tumor tissues. CONCLUSION: SOX2-OT inhibited the targeted inhibition of miR-143-3p on MSI2 through competitively binding to miR-143-3p, thus promoting MSI2 expression and proliferation, invasion, and migration of HCC cells.		Front Oncol. 2021 Jul 12;11:685912. doi: 10.3389/fonc.2021.685912. eCollection 2021.
5319	LncRNA	IGF2-AS	miR-195	CREB1	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34321174	IGF2-AS knockdown inhibits glycolysis and accelerates apoptosis of gastric cancer cells through targeting miR-195/CREB1 axis.	Dysregulation of long non-coding RNA (lncRNA) insulin growth factor 2 antisense (IGF2-AS) is being found to have relevance to tumorigenesis, including gastric cancer (GC). The purpose of this study was to further explore the detailed role and molecular mechanism of IGF2-AS in GC progression. The expression levels of IGF2-AS, miR-195 and cAMP responsive element binding protein 1 (CREB1) mRNA were assessed by qRT-PCR. Glucose consumption and lactate production were determined using a corresponding Commercial Assay Kit. Hexokinase 2 (HK2) and CREB1 protein levels were detected using western blot. Cell apoptosis was determined by flow cytometry. The targeted interaction between miR-195 and IGF2-AS or CREB1 was validated using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Our data revealed that IGF2-AS was upregulated in GC tissues and predicted poor prognosis. IGF2-AS knockdown hampered glycolysis and accelerated apoptosis of GC cells. Moreover, IGF2-AS acted as a sponge of miR-195 and CREB1 was a direct target of miR-195. MiR-195 mediated the regulatory effect of IGF2-AS knockdown on GC cell glycolysis and apoptosis. MiR-195 exerted its regulatory effect on GC cell glycolysis and apoptosis by CREB1. Furthermore, IGF2-AS regulated CREB1 expression via sponging miR-195. In conclusion, our study suggested that IGF2-AS knockdown suppressed glycolysis and facilitated apoptosis in GC cells at least partly through sponging miR-195 and modulating CREB1 expression, highlighting a novel therapeutic strategy for GC treatment.		Biomed Pharmacother. 2020 Oct;130:110600. doi: 10.1016/j.biopha.2020.110600. Epub 2020 Aug 24.
5320	LncRNA	GNAS-AS1	miR-490-3p	NA	Os Cell Lines	Osteosarcoma	Homo sapiens (human)  	qRT-PCR;	34321018	Biomarker potential of lncRNA GNAS-AS1 in osteosarcoma prognosis and effect on cellular function.	BACKGROUND: Osteosarcoma (OS) is a type of bone cancer that occurs in children and adolescents at a rate of 5%. The purpose of this study is to explore the lncRNA GNAS-AS1 expression profile, prognosis significance in OS, and biological effect on OS cell function. METHODS: One hundred eight pairs of tissues were collected, and OS cell lines were purchased. lncRNA GNAS-AS1 expression in these tissues and cells were analyzed by qRT-PCR. Clinical data were analyzed using chi-square tests, Kaplan-Meier curves (log-rank test), and Cox regression. CCK-8 and transwell assay were conducted to analyze the effect of lncRNA GNAS-AS1 on cell proliferation, invasion, and migration. The downstream miRNA was presumed. RESULTS: The expression of lncRNA GNAS-AS1 was significantly increased in OS cells and tissues, and related to Enneking staging and distant metastasis. Patients with high lncRNA GNAS-AS1 expression represented shorter overall survival and was an independent prognostic predictor of OS. LncRNA GNAS-AS1 knockdown inhibited cell proliferation, migration, and invasion by regulated miR-490-3p partly at least. CONCLUSIONS: LncRNA GNAS-AS1 can be used as a prognostic indicator and its inhibition suppress the development of OS, suggesting its value as novel therapeutic strategies in OS.		J Orthop Surg Res. 2021 Jul 28;16(1):470. doi: 10.1186/s13018-021-02611-2.
5321	LncRNA	HOTAIR	miR-214-3p	HPV16 E7	Hpv16 Positive Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	qPCR;qRT-PCR;Flow Cytometry assay;luciferase assay;	34320988	LncRNA HOTAIR promotes proliferation and inhibits apoptosis by sponging miR-214-3p in HPV16 positive cervical cancer cells.	BACKGROUND: Cervical cancer (CC) is one of the most common gynaecological malignancies all around the world. The mechanisms of cervical carcinoma formation remain under close scrutiny. The long non-coding RNAs (lncRNA) and microRNAs (miRNAs) play important roles in controlling gene expression and promoting the development and progression of cervical cancer by acting as competitive endogenous RNA (ceRNA). However, the roles of lncRNA associated with ceRNAs in cervical carcinogenesis remains unknown. In this study, the expression of long non-coding RNA HOTAIR was investigated in HPV16 positive cervical cancer cells, the candidate miRNAs and target genes were identified to clarify putative ceRNAs of HOTAIR/miRNA in cervical cancer cells. METHODS: The proliferation ability of cells was measured by CCK8 and EdU incorporation assays and cell apoptosis was analyzed by flow cytometry. The expression of HOTAIR, miR-214-3p, HPV16 E7 mRNA were detected by qRT-PCR. As for searching for the interaction between miR-214-3p and HOTAIR, the binding sites for miR-214-3p on HOTAIR was predicted by starbase v2.0 database, then dual-luciferase assay was used to verify the binding sites. In addition, Gene Ontology (GO) and protein-protein interaction (PPI) network analysis of target genes of miR-214-3p were performed with bioinformatics analysis. The potential signal pathway regulated by HOTAIR/miR-214-3p was predicted by KEGG enrichment analysis and confirmed by qPCR and WB analysis in cervical cancer cells. RESULTS: Our results showed that expression of HOTAIR was up-regulated, while that of miR-214-3p was down-regulated in HPV16-positive cervical cancer cells. The expression status of HPV16 E7 played an important role in regulating expression of HOTAIR or miR-214-3p in cervical cancer cells. HOTAIR knockdown could significantly inhibited cell proliferate ability and promote cellular apoptosis, whereas the inhibition of miR-214-3p expression partially reversed such results. Bioinformatics analysis identified 1451 genes as target genes of miR-214-3p. The Gene ontology (GO) and KEGG Pathway enrichment analysis showed that these target genes were mainly related to regulation of cell communication, protein binding, enzyme binding and transferase activity, and Wnt ligand biogenesis. Pathway enrichment analysis results showed that the predicted target genes were significantly enriched in Wnt/b-catenin signaling pathway. Finally, our results confirmed that miR-214-3p could significantly inhibit b-catenin expression in HPV16 positive cancer cells by qPCR and WB analysis. CONCLUSION: HOTAIR could act as a ceRNA through binding to miR-214-3p, promote cell proliferation and inhibit the apoptosis of HPV16 positive cervical cancer. HOTAIR/miR-214-3p/Wnt/b-catenin signal pathway might played important regulated roles in HPV16 positive cervical cancer. Our results provided new insight into defining novel biomarkers for cervical cancer.		Cancer Cell Int. 2021 Jul 28;21(1):400. doi: 10.1186/s12935-021-02103-7.
5322	LncRNA	LINC00707	miR-338-3p	AHSA1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)	qRT-PCR 	34316513	Silencing of LINC00707 suppresses cell proliferation, migration, and invasion of osteosarcoma cells by modulating miR-338-3p/AHSA1 axis.	Osteosarcoma is the most common type of primary malignant tumor of the bone, with a high metastatic rate and poor prognosis. Therefore, it is important to further elucidate the molecular mechanisms involved in the development of osteosarcoma and explore new molecular therapeutic targets. Long intergenic nonprotein-coding RNA 707 (LINC00707) is an oncogenic gene in several cancers. In this study, we further clarified its role and regulatory mechanism in osteosarcoma. We found that LINC00707 levels are significantly higher in the osteosarcoma cell lines SW 1353, HOS, U-2 OS, MG-63, and Saos-2 compared to those in human fetal osteoblastic cell line hFOB1.19. LINC00707 silencing suppressed cell proliferation, migration, and invasion of MG-63 and Saos-2 cells. Moreover, LINC00707 can act as a competitive endogenous RNA of miR-338-3p, and miR-338-3p inhibitor and AHSA1 overexpression alleviated the effect of LINC00707 silencing. In conclusion, we demonstrated high expression of LINC00707 in osteosarcoma cell lines and that silencing LINC00707 suppresses cell proliferation, migration, and invasion by targeting the miR-338-3p/AHSA1 axis in MG-63 and Saos-2 cells. These findings suggest that LINC00707 may serve as a potential target for osteosarcoma treatment.		Open Life Sci. 2021 Jul 16;16(1):728-736. doi: 10.1515/biol-2021-0070. eCollection 2021.
5323	LncRNA	LINC-PINT	miR-26a-5p	PTEN	Airway Smooth Muscle Cells	Asthma	Rattus (rat)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	34315115	Long noncoding RNA LINC-PINT retards the abnormal growth of airway smooth muscle cells via regulating the microRNA-26a-5p/PTEN axis in asthma.	BACKGROUND: Asthma is a chronic respiratory disease worldwide. This study aimed to explore the functions of the long noncoding RNA LINC-PINT (LINC-PINT) in asthma and to determine its underlying molecular mechanisms. METHODS: Rat asthma model was established with ovalbumin sensitization and challenge. The serum level of IgE, airway hyperresponsiveness (AHR), airway inflammation, and pathological changes of lung were evaluated. Airway smooth muscle cells (ASMCs) were stimulated with platelet-derived growth factor-BB (PDGF-BB) to mimic the asthma-like condition at cellular level. QRT-PCR was performed to detect the expression of LINC-PINT, microRNA-26a-5p (miR-26a-5p), and PTEN. MTT and transwell assays were performed to measure the viability and migration of ASMCs. The protein expression of airway remodelling marker MMP-1 and MMP-9 was measured by western blot. The interactions among LINC-PINT, miR-26a-5p, and PTEN were determined by dual-luciferase reporter assay. RESULTS: The expression of LINC-PINT and PTEN was decreased, while miR-26a-5p expression was increased in PDGF-BB-stimulated ASMCs. In vivo, overexpression of LINC-PINT decreased the serum level of IgE, AHR, airway inflammation, and pathological changes of lung in asthma rat model. In vitro, up-regulation of LINC-PINT decreased the viability, migration, and MMP-1 and MMP-9 protein expression in PDGF-BB-stimulated ASMCs. Dual-luciferase reporter assay determined that LINC-PINT targeted miR-26a-5p, and miR-26a-5p targeted PTEN in ASMCs. Feedback approaches confirmed that miR-26a-5p up-regulation or PTEN down-regulation reversed the suppressive effect of LINC-PINT overexpression on the abnormal growth of ASMCs. CONCLUSIONS: LINC-PINT overexpression retarded the abnormal growth of ASMCs by regulating the miR-26a-5p/PTEN axis, offering a potential therapeutic target for asthma.		Int Immunopharmacol. 2021 Jul 24;99:107997. doi: 10.1016/j.intimp.2021.107997.
5324	LncRNA	LINC00667	miR-200b-3p	SLC2A3	Esophageal Cancer Cells	Esophageal Cancer	Homo sapiens (human)	Flow cytometry assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34313922	LINC00667 Promotes Progression of Esophageal Cancer Cells by Regulating miR-200b-3p/SLC2A3 Axis.	BACKGROUND: Recently, more and more evidence indicated that the long non-coding RNA was strictly related to the occurrence and progression of human cancers, including esophageal cancer (EC). We observed that LINC00667 was increased in EC, but the function of LINC00667 was unclear. Therefore, the function and potential molecular mechanism of LINC00667 in the progression of EC need to be further studied. METHODS: Quantitative real-time PCR was used to investigate the levels of LINC00667, miR-200b-3p, and SLC2A3. The levels of protein involved in cell cycle, cell apoptosis, epithelial-mesenchymal transition, as well as SLC2A3 were quantitatived by western blot. The role of LINC00667 in the proliferative, migratory and invasive capabilities of EC cells were measured by cell counting kit-8 assay, EdU assay, flow cytometry assay, wound healing assay and transwell assay, respectively. Interaction between LINC00667 and miR-200b-3p or miR-200b-3p and SLC2A3 were confirmed using a luciferase reporter assay. RESULTS: In this work, we found that LINC00667 expression was up-regulated in EC cell lines, and LINC00667 knockdown inhibited cell proliferation, migration, and invasion in EC cells. In addition, it showed that LINC00667 functioned as competitive endogenous RNA for miR-200b-3p by the DIANA-LncBase database. Moreover, we used targetscan online software to predict SLC2A3 as a target gene of miR-200b-3p. Subsequently, rescue experiments confirmed that knocking out SLC2A3 could reverse the inhibitory effect of miR-200b-3p on EC cells transfected with sh-LINC00667. CONCLUSION: Herein, we revealed the novel mechanism of LINC00667 on regulating metastasis-related gene by sponge regulatory axis during EC metastasis. Our results demonstrated that LINC00667 plays a critical role in metastatic EC by mediating sponge regulatory axis miR-200b-3p/SLC2A3. To explore function of LINC00667/miR-200b-3p/SLC2A3 axis may provide an informative biomarker of malignancy and a highly selective anti-EC therapeutic target.		Dig Dis Sci. 2021 Jul 27. doi: 10.1007/s10620-021-07145-5.
5325	LncRNA	MALAT1	miR-26a-5p	Smad1	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)	qRT-PCR 	34313719	Long noncoding RNA MALAT1 sponging miR-26a-5p to modulate Smad1 contributes to colorectal cancer progression by regulating autophagy.	Accumulating evidences have suggested that bone morphogenetic protein (BMP) -Smad have a functional role in regulating autophagy in the development of human colorectal cancer (CRC). However, the regulatory mechanisms controlling this process remain unclear. Here, we showed that Smad1, the key effector of BMP2-Smad signaling, induces autophagy by upregulating autophagy-related gene 5 (ATG5) expression, and Smad1 binds to the proximal promoter to induce its expression. Moreover, BMP2 induces autophagy in CRC. Overexpression of Smad1 promotes tumorigenesis and migration of CRC cells, and knockdown of ATG5 is able to rescue the Smad1-induced promotion of CRC proliferation and migration partially. Mechanistically, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) may act as a competing endogenous RNA by binding with miR-26a-5p competitively and thus modulating the de-repression of downstream target Smad1. Furthermore, clinical analysis results show that Smad1 is positively correlated with MALAT1 and negatively correlated with miR-26a-5p in CRC samples. In conclusion, our results demonstrated that Smad1 may serve as an oncogene in CRC through autophagy.		Carcinogenesis. 2021 Jul 27:bgab069. doi: 10.1093/carcin/bgab069.
5326	LncRNA	SNHG12	miR-218-5p	IGF2	Human Umbilical Endothelial Cells	Atherosclerosis	Homo sapiens (human)	ELISA;qPCR;RT-qPCR;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	34313533	LncRNA SNHG12 regulates ox-LDL-induced endothelial cell injury by the miR-218-5p/IGF2 axis in atherosclerosis.	Atherosclerosis (AS) is a cardiovascular disorder accompanied by endothelial dysfunction. Extensive evidence demonstrates the regulatory functions of long noncoding RNAs (lncRNAs) in cardiovascular disease, including AS. Here, the function of lncRNA small nucleolar RNA host gene 12 (SNHG12) in AS progression was investigated. A cell model of AS was established in human umbilical endothelial cells (HUVECs) using oxidative low-density lipoprotein (ox-LDL). CCK-8, flow cytometry, TUNEL, ELISA, and western blotting analyses were performed. Apolipoprotein E-deficient (apoE(-/-)) mice fed a Western diet were used as in vivo models of AS. RT-qPCR determined the levels of SNHG12, microRNA-218-5p (miR-218-5p) and insulin-like growth factor-II (IGF2). The molecular mechanisms were investigated using luciferase reporter and RNA pull-down assays. We found that SNHG12 and IGF2 expression levels were high and miR-218-5p expression levels were low in AS patients and ox-LDL-treated HUVECs. SNHG12 depletion attenuated ox-LDL-induced injury in HUVECs, whereas miR-218-5p suppression partially abated this effect. Moreover, IGF2 overexpression prevented the alleviative role of miR-218-5p in ox-LDL-treated HUVECs. SNHG12 upregulated IGF2 expression by sponging miR-218-5p. More importantly, SNHG12 increased proinflammatory cytokine production and augmented atherosclerotic lesions in vivo. Overall, SNHG12 promotes the development of AS by the miR-218-5p/IGF2 axis.		Cell Cycle. 2021 Jul 27:1-17. doi: 10.1080/15384101.2021.1953755.
5327	LncRNA	H19	miR-541-3p	APN	Bone Marrow Mesenchymal Stem Cells	Osteoporosis	Rattus (rat)	Dual-luciferase reporter assay;ELISA;qRT-PCR;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34311444	The lncRNA H19/miR-541-3p/Wnt/b-catenin axis plays a vital role in melatonin-mediated osteogenic differentiation of bone marrow mesenchymal stem cells.	Implant dentures become the first choice for denture restoration in patients with tooth loss. However, oral implants often fail in osteoporosis (OP) patients. Melatonin (MT) induces osteogenic differentiation of bone mesenchymal stem cells (BMSCs), suggesting its therapeutic potential in OP treatment. Long non-coding RNA H19 induces osteogenic differentiation of BMSCs, while its regulatory mechanism in MT-involved osteogenic and adipogenic differentiation of BMSCs remains elusive. Ovariectomized (OVX) rat was used to construct an OP model, and bone quality was assessed. Meanwhile, the expression of H19, miR-541-3p, MT and adiponectin (APN) was examined by quantitative reverse transcription-PCR (qRT-PCR) or ELISA. The adipogenic and osteogenic differentiation of BMSCs were determined by oil red O staining and alizarin red S staining, respectively. The targeting relationships between H19, miR-541-3p and APN mRNA were predicted by bioinformatics and confirmed by RNA immunoprecipitation and dual-luciferase reporter assay. The results showed that MT, H19 and APN were down-regulated, while miR-541-3p was up-regulated in the OVX rat model. At the cellular level, MT reduced adipogenic differentiation, heightened osteogenic differentiation of BMSCs, and activated Wnt/b-catenin pathway, which were reversed by the MT2 selective inhibitor 4-P-PDOT. Overexpressing H19 facilitated the osteogenic differentiation and inhibited the adipogenic differentiation of BMSCs mediated by MT, while H19 knockdown or overexpressing miR-541-3p had the opposite effect. Moreover, H19 functioned as a competitive endogenous RNA and sponged miR-541-3p, and miR-541-3p targeted APN. Overall, MT modulates the osteogenic and adipogenic differentiation of BMSCs by mediating H19/miR-541-3p/APN axis, providing a new reference for the targeted therapy of OP.		Aging (Albany NY). 2021 Jul 26;13(14):18257-18273. doi: 10.18632/aging.203267. Epub 2021 Jul 26.
5328	LncRNA	OIP5-AS1	miR-144-5p	PKM2	Renal Epithelial Cell	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR 	34311128	LncRNA OIP5-AS1 reduces renal epithelial cell apoptosis in cisplatin-induced AKI by regulating the miR-144-5p/PKM2 axis.	BACKGROUND: The abnormal expression of long non-coding RNA (lncRNA) Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) has been observed in many human cancers and the underlying mechanisms have been well studied. However, the function of OIP5-AS1 in acute kidney injury (AKI) remains unclear. MATERIAL AND METHODS: To explore the role of OIP5-AS1 in the progression of AKI, the cisplatin-induced AKI mouse and cell model were established. To confirm the potential protective effect of OIP5-AS1 during cisplatin-induced AKI, rescue experiments were performed. Targetscan was used to predict the potential targets of miR-144-5p. To further determine whether the effect of miR-144-5p during cisplatin-induced AKI was mediated by PMK2, the recuse experiments using PMK2 overexpressing vector was applied. RESULTS: OIP5-AS1 was significantly downregulated both in cisplatin-induced AKI mice and human renal tubular cell line HK-2 cells. Moreover, overexpression of OIP5-AS1 efficiently promoted cell growth and reduced cisplatin-induced apoptosis of HK-2 cells. Furthermore, OIP5-AS1 was identified as a sponge of miR-144-5p, and upregulation of miR-144-5p could significantly reverse overexpression of OIP5-AS1-induced protective effect on the damage of cisplatin to HK-2 cells. In addition, pyruvate kinase M2 (PKM2) was found to be a direct target of miR-144-5p, and overexpression of PKM2 efficiently reversed the effect of miR-144-5p mimics on the damage in cisplatin-stimulated HK-2 cells. CONCLUSIONS: OIP5-AS1 reduced the apoptosis of cisplatin-stimulated renal epithelial cells by targeting the miR-144-5p/PKM2 axis, which extended the regulatory network of lncRNAs in cisplatin-induced AKI and also provided a novel therapeutic target for AKI treatment.		Biomed J. 2021 Jul 23:S2319-4170(21)00096-2. doi: 10.1016/j.bj.2021.07.005.
5329	LncRNA	OIP5-AS1	miR-144-5p	PKM2	Renal Epithelial Cell	Acute Kidney Injury	Mus musculus (mouse)	qRT-PCR 	34311128	LncRNA OIP5-AS1 reduces renal epithelial cell apoptosis in cisplatin-induced AKI by regulating the miR-144-5p/PKM2 axis.	BACKGROUND: The abnormal expression of long non-coding RNA (lncRNA) Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) has been observed in many human cancers and the underlying mechanisms have been well studied. However, the function of OIP5-AS1 in acute kidney injury (AKI) remains unclear. MATERIAL AND METHODS: To explore the role of OIP5-AS1 in the progression of AKI, the cisplatin-induced AKI mouse and cell model were established. To confirm the potential protective effect of OIP5-AS1 during cisplatin-induced AKI, rescue experiments were performed. Targetscan was used to predict the potential targets of miR-144-5p. To further determine whether the effect of miR-144-5p during cisplatin-induced AKI was mediated by PMK2, the recuse experiments using PMK2 overexpressing vector was applied. RESULTS: OIP5-AS1 was significantly downregulated both in cisplatin-induced AKI mice and human renal tubular cell line HK-2 cells. Moreover, overexpression of OIP5-AS1 efficiently promoted cell growth and reduced cisplatin-induced apoptosis of HK-2 cells. Furthermore, OIP5-AS1 was identified as a sponge of miR-144-5p, and upregulation of miR-144-5p could significantly reverse overexpression of OIP5-AS1-induced protective effect on the damage of cisplatin to HK-2 cells. In addition, pyruvate kinase M2 (PKM2) was found to be a direct target of miR-144-5p, and overexpression of PKM2 efficiently reversed the effect of miR-144-5p mimics on the damage in cisplatin-stimulated HK-2 cells. CONCLUSIONS: OIP5-AS1 reduced the apoptosis of cisplatin-stimulated renal epithelial cells by targeting the miR-144-5p/PKM2 axis, which extended the regulatory network of lncRNAs in cisplatin-induced AKI and also provided a novel therapeutic target for AKI treatment.		Biomed J. 2021 Jul 23:S2319-4170(21)00096-2. doi: 10.1016/j.bj.2021.07.005.
5330	LncRNA	HCP5	miR-497	IGF1	Mesenchymal Stem Cells	Myocardial Ischemia Reperfusion Injury	Rattus (rat)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;MTT assay;	34311013	LncRNA HCP5 in hBMSC-derived exosomes alleviates myocardial ischemia reperfusion injury by sponging miR-497 to activate IGF1/PI3K/AKT pathway.	Ischemia/reperfusion (I/R) injury is an inevitable process during heart transplant and suppressing I/R injury could greatly improve the survival rate of recipients. Mesenchymal stem cells (MSCs) have positive effects on I/R. We aimed to investigate the mechanisms underlying the protective roles of MSCs in I/R. Both cell model and rat model of myocardial I/R were used. MTT assay and flow cytometry were used to measure cell viability and apoptosis, respectively. QRT-PCR and western blotting were employed to measure levels of lncRNA HCP5 (HLA complex P5), miR-497, apoptosis-related proteins, and insulin-like growth factor (IGF1)/PI3K/AKT pathway. Dual luciferase assay was used to validate interactions of HCP5 and miR-497, miR-497 and IGF1. Echocardiography was performed to evaluate cardiac function of rats. Serum levels of CK-MB and LDH were measured. H&E and Masson staining were used to examine morphology of myocardial tissues. hBMSC-derived exosomes (hBMSC-Exos) increased the viability of cardiomyocytes following hypoxia/reperfusion (H/R) and decreased apoptosis. H/R diminished HCP5 expression in cardiomyocytes while hBMSC-Exos recovered the level. Overexpression of HCP5 in hBMSC-Exos further enhanced the protective effects in H/R while HCP5 knockdown suppressed. HCP5 directly bound miR-497 and miR-497 targeted IGF1. miR-497 mimics or si-IGF1 blocked the effects of HCP5 overexpression. Further, hBMSC-Exos alleviated I/R injury in vivo and knockdown of HCP5 in hBMSC-Exos decreased the beneficial effects. AntagomiR-497 blocked the effects of HCP5 knockdown. HCP5 from hBMSC-Exos protects cardiomyocytes against I/R injury via sponging miR-497 to disinhibit IGF1/PI3K/AKT pathway. These results shed light on mechanisms underlying the protective role of hBMSC-Exos in I/R.		Int J Cardiol. 2021 Jul 24:S0167-5273(21)01187-6. doi: 10.1016/j.ijcard.2021.07.042.
5331	LncRNA	H19	miR-194	IGF1R	Hypertrophic Scar Fibroblasts	Hypertrophic Scar	Homo sapiens (human)  	Flow Cytometry assay;luciferase assay;	34310900	Long non-coding RNA H19 acts as a microRNA-194 sponge to inhibit the apoptosis and promote the proliferation of hypertrophic scar fibroblasts.	The effects of long non-coding RNAs (lncRNAs) on the proliferation of hypertrophic scars have been described. However, the underlying mechanisms are not well characterized. The present study aimed to investigate the mechanisms of lncRNA H19 in hypertrophic scars. The effects of the lncRNA H19 on the proliferation and apoptosis of hypertrophic scar fibroblasts (HSFs) were analyzed using 5'-Ethynyl-2'-deoxyuridine staining, flow cytometry, and MTT. The results revealed H19 promoted the proliferation and inhibited the apoptosis in HSF. In addition, the binding associations between H19 and microRNA-194 (miR-194), and miR-194 and insulin-like growth factor-I receptor (IGF1R) were identified using bioinformatics screening and verified using dual-luciferase assays. Furthermore, the effects of the IGF1R knockdown on H19-induced HSF phenotypes and regulation over the p38 MAPK pathway were determined. Mechanistically, miR-194 was identified as the downstream effector of the H19-mediated phenotypes of HSFs through its ability to directly target IGF1R, thus modulating the p38 MAPK signaling pathway. In conclusion, the findings suggested that H19 may inhibit the apoptosis and promote the proliferation of HSFs through the miR-194/IGF1R/p38 MAPK signaling axis, thereby contributing to the progression of hypertrophic scars. These findings may provide novel targets for the treatment of hypertrophic scars.		Can J Physiol Pharmacol. 2021 Jul 26. doi: 10.1139/cjpp-2021-0351.
5332	LncRNA	HNRNPU-AS1	miR-205-5p	AXIN2	Cervical Cancer Patients And Cell Lines	Cervical Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Flow Cytometry assay;luciferase assay;	34309414	HNRNPU-AS1 regulates cell proliferation and apoptosis via miR-205-5p/AXIN2 axis and Wnt/b-catenin signaling pathway in cervical cancer.	Long non-coding RNAs (lncRNAs) have key functions in modulating cervical cancer (CC) genesis and progression. This work focused on exploring lncRNA HNRNPU-AS1's function in CC and the underlying mechanism. HNRNPU-AS1, AXIN2 and miR-205-5p levels in CC cases were measured through RT-qPCR. Relationship between miR-205-5p and AXIN2 or HNRNPU-AS1 was validated through dual-luciferase assay. Cell proliferation was examined by CCK-8, while cell apoptosis by colony formation and flow cytometry analysis. HNRNPU-AS1 expression loss could be observed in CC patients and cell lines, which predicted the dismal prognosis of CC cases. Moreover, it was identified that the miR-205-5p level was up-regulated, which acted as an inhibitory target of HNRNPU-AS1 and AXIN2. HNRNPU-AS1 inhibited cell proliferation and promoted apoptosis. As revealed by Kaplan-Meier curve, CC cases showing low HNRNPU-AS1, high miR-205-5p, and low AXIN2 levels had the poorest prognosis. AXIN2 reversed the CC cell proliferation-promoting, apoptosis-inhibiting and Wnt/b-catenin signaling-activating mediated by miR-205-5p or HNRNPU-AS1 knockout. In conclusion, the overexpression of lncRNA HNRNPU-AS1 suppressed CC progression by inhibiting Wnt/b-catenin pathway through miR-205-5p/AXIN2 axis.		Mol Cell Biol. 2021 Jul 26:MCB0011521. doi: 10.1128/MCB.00115-21.
5333	LncRNA	AGAP2-AS	miR-15/16	NA	Colon Cell Lines	Colorectal Cancer	Homo sapiens (human)  	microarray;	34308771	Long non-coding RNA AGAP2-AS1 is up regulated in colorectal cancer.	Accumulating evidence has indicated that, aberrant lncRNA expression plays essential roles in the colorectal cancer (CRC) tumorigenesis. AGAP2-AS1 is upregulated in some cancers, however, its involvement in the CRC tumorigenesis in the population of North-West of Iran has remained unknown. In this study, we evaluated its deregulation in CRC microarray datasets, colon cell lines, CRC tumor, adenomatous colorectal polyps and their paired normal tissues. The results showed that AGAP2-AS1 is upregulated in CRC and might be considered as a potential biomarker for CRC development. Moreover, our results suggest AGAP2-AS1 promoted CRC progression by sponging the hsa-miR-15/16 family and upregulation of their targets.		Nucleosides Nucleotides Nucleic Acids. 2021;40(8):829-844. doi: 10.1080/15257770.2021.1956530. Epub 2021 Jul 26.
5334	LncRNA	ASNR	miR-519e-5p	FGFR2	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	34307360	Long Non-coding RNA ASNR Targeting miR-519e-5p Promotes Gastric Cancer Development by Regulating FGFR2.	Gastric cancer (GC), as a common gastrointestinal tumor, is an important cause of death from cancer all around the world. Long non-coding RNAs (lncRNAs), a novel class of transcripts, have attracted great attention of researchers. However, the mechanisms of the clinical significance of most lncRNAs in human cancer are mainly undocumented. This research desires to explore the clinical significance, biological function, and mechanism of Lnc_ASNR (apoptosis suppressing-non-coding RNA) in GC. Cell proliferation, cell cycle, cell migration, and invasion abilities were respectively determined by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide (MTT), flow cytometry, wound healing, and Transwell assay (Sigma-Aldrich, St. Louis, MO, United States). The association of Lnc_ASNR, miR-519e-5p, and fibroblast growth factor receptor 2 (FGFR2) was evaluated via luciferase reporter experiments. The tumor xenograft assay was conducted to confirm the results of cell experiments. High expressed Lnc_ASNR was detected in both GC cells and tissues using qRT-PCR. Downregulated Lnc_ASNR could reduce proliferation, migration, and invasion in GC cells, while upregulated Lnc_ASNR could promote the cell proliferation, migration, and invasion. Moreover, the effect of Lnc_ASNR on migration and invasion ability is closely related to epithelial-mesenchymal transition (EMT). The bioinformatics analysis, luciferase assay, and Western blot demonstrated that Lnc_ASNR inhibited miR-519e-5p expression but increased FGFR2 expression. Lnc_ASNR and FGFR2 were both targeted to miR-519e-5p, and they were negatively correlated with the expression of miR-519e-5p. All investigations indicated that Lnc_ASNR functioned as a ceRNA targeting miR-519e-5p and facilitated GC development by regulating the pathway of miR-519e-5p/FGFR2.		Front Cell Dev Biol. 2021 Jul 9;9:679176. doi: 10.3389/fcell.2021.679176. eCollection 2021.
5335	LncRNA	NONHSAT079852.2	miR-10401-3p	HSPA1A	Gbm Tissues	Glioblastoma Multiforme	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34307121	Long Noncoding RNA NONHSAT079852.2 Contributes to GBM Recurrence by Functioning as a ceRNA for has-mir-10401-3p to Facilitate HSPA1A Upregulation.	Glioblastoma multiforme (GBM) is the most common brain malignancy and major cause of high mortality in patients with GBM, and its high recurrence rate is its most prominent feature. However, the pathobiological mechanisms involved in recurrent GBM remain largely unknown. Here, whole-transcriptome sequencing (RNA-sequencing, RNA-Seq) was used in characterizing the expression profile of recurrent GBM, and the aim was to identify crucial biomarkers that contribute to GBM relapse. Differentially expressed RNAs in three recurrent GBM tissues compared with three primary GBM tissues were identified through RNA-Seq. The function and mechanism of a candidate long noncoding RNA (lncRNA) in the progression and recurrence of GBM were elucidated by performing comprehensive bioinformatics analyses, such as functional enrichment analysis, protein-protein interaction prediction, and lncRNA-miRNA-mRNA regulatory network construction, and a series of in vitro assays. As the most significantly upregulated gene identified in recurrent GBM, HSPA1A is mainly related to antigen presentation and the MAPK signaling pathway, as indicated by functional enrichment analysis. HSPA1A was predicted as the target gene of the lncRNA NONHSAT079852.2. qRT-PCR revealed that NONHSAT079852.2 was significantly elevated in recurrent GBM relative to that in primary GBM, and high NONHSAT079852.2 expression was associated with the poor overall survival rates of patients with GBM. The knockdown of NONHSAT079852.2 successfully induced tumor cell apoptosis, inhibited the proliferation, migration, invasion and the expression level of HSPA1A in glioma cells. NONHSAT079852.2 was identified to be a sponge for hsa-miR-10401-3p through luciferase reporter assay. Moreover, HSPA1A was targeted and regulated by hsa-miR-10401-3p. Collectively, the results suggested that NONHSAT079852.2 acts as a sponge of hsa-mir-10401-3p and thereby enhances HSPA1A expression, promotes tumor cell proliferation and invasion, and leads to the progression and recurrence of GBM. This study will provide new insight into the regulatory mechanisms of NONHSAT079852.2-mediated competing endogenous RNA in the pathogenesis of recurrent GBM and evidence of the potential of lncRNAs as diagnostic biomarkers or potential therapeutic targets.		Front Oncol. 2021 Jul 8;11:636632. doi: 10.3389/fonc.2021.636632. eCollection 2021.
5336	LncRNA	LINC00665	miR-708	RAP1B	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34306997	LINC00665 Facilitates the Malignant Processes of Osteosarcoma by Increasing the RAP1B Expression via Sponging miR-708 and miR-142-5p.	Osteosarcoma (OS) is a kind of fatal primary bone tumors in adolescents and young adults. Long noncoding RNAs (lncRNAs) are a group of noncoding RNAs which occupy a part of the latest hot topics. We aimed to investigate the roles of lncRNA LINC00665 in OS in this study. In this study, we found that LINC00665 was highly expressed in OS tissues and cell lines, and its high expression was associated with malignant feature and poor prognosis of OS. In OS cells, LINC00665 could facilitate the proliferation, migration, and invasion to play an oncogenic role. Mechanistically, LINC00665 served as a sponge for miR-708 and miR-142-5p and positively mediated the expression of their target RAP1B. Finally, we confirmed that LINC00665 exercised its biological functions by mediating RAP1B. In conclusion, LINC00665 is overexpressed in OS and facilitates the malignant processes of OS cells by increasing the RAP1B expression via sponging miR-708 and miR-142-5p.		Anal Cell Pathol (Amst). 2021 Jul 7;2021:5525711. doi: 10.1155/2021/5525711. eCollection 2021.
5337	LncRNA	LINC00665	miR-142-5p	RAP1B	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34306997	LINC00665 Facilitates the Malignant Processes of Osteosarcoma by Increasing the RAP1B Expression via Sponging miR-708 and miR-142-5p.	Osteosarcoma (OS) is a kind of fatal primary bone tumors in adolescents and young adults. Long noncoding RNAs (lncRNAs) are a group of noncoding RNAs which occupy a part of the latest hot topics. We aimed to investigate the roles of lncRNA LINC00665 in OS in this study. In this study, we found that LINC00665 was highly expressed in OS tissues and cell lines, and its high expression was associated with malignant feature and poor prognosis of OS. In OS cells, LINC00665 could facilitate the proliferation, migration, and invasion to play an oncogenic role. Mechanistically, LINC00665 served as a sponge for miR-708 and miR-142-5p and positively mediated the expression of their target RAP1B. Finally, we confirmed that LINC00665 exercised its biological functions by mediating RAP1B. In conclusion, LINC00665 is overexpressed in OS and facilitates the malignant processes of OS cells by increasing the RAP1B expression via sponging miR-708 and miR-142-5p.		Anal Cell Pathol (Amst). 2021 Jul 7;2021:5525711. doi: 10.1155/2021/5525711. eCollection 2021.
5338	LncRNA	Linc00467	miR-1285-3p	TFAP2A	Head And Neck Squamous Cell Carcinoma Cells	Head And Neck Squamous  Carcinoma	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	34306364	Linc00467 promotes invasion and inhibits apoptosis of head and neck squamous cell carcinoma by regulating miR-1285-3p/TFAP2A.	OBJECTIVE: To explore the invasion and apoptosis of head and neck squamous cell carcinoma (HNSCC) regulated by Linc00467 through the miR-1285-3p/TFAP2A axis. METHODS: qRT-PCR was used to detect the expressions of Linc00467, miR-1285-3p, and TFAP2A in tissues and cells of HNSCC patients. The targeting relationships between Linc00467 and miR-1285-3p, miR-1285-3p, and TFAP2A were verified by dual-luciferase reporter assay. Transfection and grouping were carried out, after HNSCC cell lines were screened. Transwell assay and flow cytometry were used to test cell invasion and apoptosis, respectively. RESULTS: Compared with normal tissues adjacent to the tumor, the expressions of Linc00467 and TFAP2A increased significantly in cancer tissues, while the expression of miR-1285-3p decreased (all P<0.05). Compared with the si-NC group, the invasion of the si-Linc00467 group decreased and the apoptosis rate increased (both P<0.05). In HNSCC cells, over-expression of Linc00467 promoted increased cell invasion and decreased apoptosis rate, which could be partially rescued by over-expression of miR-1285-3p (all P<0.05). Over-expression of miR-1285-3p caused decreased cell invasion and increased apoptosis rate, which was partially reversed by over-expression of TFAP2A (all P<0.05). CONCLUSION: Linc00467 can be used as ceRNA to adsorb miR-1285-3p to regulate the expression of TFAP2A, promote invasion and inhibit apoptosis of HNSCC cells. Linc00467 inhibitors may become one of the targeted therapeutic drugs for HNSCC.		Am J Transl Res. 2021 Jun 15;13(6):6248-6259. eCollection 2021.
5339	LncRNA	LINC00473	miR-195	NA	Ht29 And Sw480 Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34306345	LncRNA LINC00473 promoted colorectal cancer cell proliferation and invasion by targeting miR-195 expression.	Long noncoding RNAs (lncRNAs) have been shown to play crucial roles in cancer development. However, the role of LINC00473 in colorectal cancer has not been explored. In our study, we showed that LINC00473 expression was upregulated in colorectal cancer samples compared to nontumor samples. The expression of LINC00473 in colorectal cancer tissues from patients with distant metastasis was higher than that from cases without distant metastasis. The higher expression level of LINC00473 was positively correlated with advanced clinical stage. The elevated expression of LINC00473 accelerated colorectal cancer cell proliferation, cell cycle progression and invasion. Moreover, overexpression of LINC00473 induced epithelial to mesenchymal (EMT) progression in HT29 and SW480 cells. Ectopic expression of LINC00473 suppressed miR-195 expression in colorectal cancer cells. miR-195 expression was downregulated in colorectal cancer samples compared with nontumor samples. The expression of miR-195 in colorectal cancer tissues from patients with distant metastasis was lower than that from cases without distant metastasis. The lower expression level of miR-195 was positively correlated with advanced clinical stage. In addition, we showed that the expression of miR-195 was negatively correlated with the LINC00473 expression level in colorectal cancer tissues. LINC00473 accelerated colorectal cancer cell proliferation and cell cycle progression and regulated EMT progression by regulating miR-195 expression. These data suggested that LINC00473 induced cell proliferation, cell cycle progression and EMT progression by acting as a ceRNA for miR-195 in colorectal cancer.		Am J Transl Res. 2021 Jun 15;13(6):6066-6075. eCollection 2021.
5340	LncRNA	RP11-874J12.4	miR-3972	SSR2	Mkn-45 And Ags Cells	Gastric Cancer	Homo sapiens (human)	qRT-PCR 	34306333	RP11-874J12.4, a novel lncRNA, confers chemoresistance in human gastric cancer cells by sponging miR-3972 and upregulating SSR2 expression.	Increasing evidence has revealed the contributions of long noncoding RNAs (lncRNAs) in the modulation of drug resistance in gastric cancer. In the present study, we explored the role of a novel lncRNA, RP11-874J12.4, in regulating chemoresistance in gastric cancer and determined the underlying molecular mechanisms. We observed that compared with normal controls, human gastric cancer tissues and cell lines, including MKN-45 and AGS cells, expressed higher RP11-874J12.4 levels. RP11-874J12.4 knockdown sensitized MKN-45 and AGS cells to docetaxel and cisplatin in terms of cell viability and apoptosis rate. In addition, RP11-874J12.4 was found to be a competing endogenous RNA that sponged microRNA (miR)-3972, which showed significantly reduced expression in human gastric cancer tissues and cell lines. Furthermore, signal sequence receptor subunit 2 (SSR2) was identified as a downstream target of miR-3972, and the miR-3972/SSR2 axis was found to regulate chemoresistance in MKN-45 and AGS cells. SSR2 downregulation further sensitized gastric cancer cells with RP11-874J12.4 knockdown to chemotherapeutic drugs via enhanced apoptosis, which was evidenced by significantly upregulated expressions of cleaved caspase-3, cleaved caspase-9, and Bax and downregulated expression of Bcl-2. Furthermore, RP11-874J12.4 knockdown markedly inhibited the growth of xenograft MKN-45 cells in nude mice, which was associated with an increased expression of miR-3972 and decreased expression of SSR2 in tumors. Therefore, the RP11-874J12.4/miR-3972/SSR2 axis plays important roles in the regulation of chemoresistance in MKN-45 and AGS cells and may serve as a target for the diagnosis and treatment of human gastric cancer.		Am J Transl Res. 2021 Jun 15;13(6):5892-5910. eCollection 2021.
5341	LncRNA	H19	miR-625-5p	APEX1	A549 Cells	Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34306329	Long non-coding RNA H19 and the underlying epigenetic function in response to DNA damage of lung cancer cells.	The purpose of the current study is to clarify the epigenetic function of long non-coding RNA (lncRNA) H19 in lung cancer as well as the relevant regulatory mechanism. We first determined H19 upregulation in A549 cells. DNA damage model was established in A549 cells by exposure to X-ray and then ionizing radiation (IR). The degree of DNA damage in the IR cell model was assessed by Comet assay. Gain- and loss-of-function assays were employed to clarify the roles of H19 and miR-675 in DNA damage of A549 cells. The results demonstrated that H19 knockdown inhibited the response of lung cancer cells to IR-induced DNA damage but promoted the damage repair. H19 could interact with miR-675, whereby aggravating IR-induced DNA damage. Furthermore, p62 was identified to be a downstream gene positively regulated by miR-675 while APEX1 was a target gene negatively regulated by miR-625-5p. Meanwhile, silencing of H19 could inhibit APEX1 expression by upregulating miR-625-5p, thereby accelerating DNA damage repair in A549 cells. In conclusion, H19 could function as a modulator of DNA damage response in lung cancer cells.		Am J Transl Res. 2021 Jun 15;13(6):5835-5850. eCollection 2021.
5342	LncRNA	HOTAIRM1-1	miR-125b	NA	Cartilage Tissue	Osteoarthritis	Homo sapiens (human)	RACE;	34306202	Long non-coding RNA HOTAIRM1-1 silencing in cartilage tissue induces osteoarthritis through microRNA-125b.	Aberrations in long noncoding RNA (lncRNA) expression have been recognized in numerous human diseases. In the present study, the of role the long noncoding RNA HOX antisense intergenic RNA myeloid 1 variant (HOTAIRM1-1) in regulating the pathological progression of osteoarthritis (OA) was investigated. The aberrant expression of HOTAIRM1-1 in OA was demonstrated, but the molecular mechanisms require further analysis. The aim of the present study was to explore the function of miR-125b in modulating chondrocyte viability and apoptosis, and to address the functional association between HOTAIRM1-1 and miR-125b as potential targets. A miR-125b inhibitor was used, which laid the foundation for the following investigation. The study confirmed that HOTAIRM1-1 and miR-125b are inversely expressed in chondrocytes. The expression of HOTAIRM1-1 was downregulated and the expression of miR-125b was upregulated in tissues from patients with OA. HOTAIRM1-1 directly interacted with miR-125b in chondrocytes. HOTAIRM1-1 knockdown was associated with chondrocyte proliferation and extracellular matrix degradation. Furthermore, miR-125b reversed the effect of HOTAIRM1-1 on cell proliferation and apoptosis. In conclusion, the present study indicates that the loss of HOTAIRM1-1 function leads to aberrant increases in the proliferation and apoptosis of chondrocytes. miR-125b may be a potential downstream mechanism that regulates the function of HOTAIRM1-1, and this finding provides a therapeutic strategy for OA.		Exp Ther Med. 2021 Sep;22(3):933. doi: 10.3892/etm.2021.10365. Epub 2021 Jul 1.
5343	LncRNA	XIST	miR-96-5p	TNF-a	Microglial Cells	Cerebral Infarction	Mus musculus (mouse)	qRT-PCR 	34306193	Regulation of the long noncoding RNA XIST on the inflammatory polarization of microglia in cerebral infarction.	Proinflammatory polarization of microglia aggravates brain injury in cerebral infarction. The present study focused on the role of long non-coding (lnc)RNA X-inactive specific transcript (XIST) in the phenotype modulation of microglia. It was revealed that lncRNA XIST was significantly upregulated in both a mouse cerebral infarction model induced by middle cerebral artery occlusion (MCAO) and an activated microglial model induced by oxygen/glucose deprivation (OGD). The overexpression of XIST enhanced the expression and release of pro-inflammatory mediators [such as tumor necrosis factor (TNF)-a, IL-6, and iNOS] in microglia. Culture supernatant from lncRNA XIST-overexpressed microglial cells induced the apoptosis of primary neurons, while TNF-a antibody counteracted this neurotoxic effect. LncRNA XIST served as a sponge for miR-96-5p, counteracting its inhibitory effect on IKKb/NF-kB signaling and TNF-a production. Notably, TNF-a was positively regulated by XIST and in turn enhanced XIST expression in microglia. The lncRNA XIST-TNF-a feedback promoted the proinflammatory polarization of microglia, thereby exacerbating cerebral neuron apoptosis.		Exp Ther Med. 2021 Sep;22(3):924. doi: 10.3892/etm.2021.10356. Epub 2021 Jun 30.
5344	LncRNA	ZFAS1	miR-3926	FSTL1	Fibroblast-Like Synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Luciferase reporter assay;MTT assay;	34306188	ZFAS1 knockdown inhibits fibroblast-like synoviocyte proliferation, migration, invasion and inflammation, and promotes apoptosis via miR-3926/FSTL1 in rheumatoid arthritis.	Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by joint disorders. Long non-coding RNA zinc finger antisense 1 (ZFAS1) is aberrantly expressed in numerous human diseases, including RA. The present study aimed to investigate the functions and underlying mechanisms of ZFAS1 in RA. Reverse transcription-quantitative PCR was performed to determine the expression levels of ZFAS1, microRNA (miR)-3926 and follistatin-like protein 1 (FSTL1). MTT assay, flow cytometric analysis and Transwell assay were performed to examine the proliferation, apoptosis, migration and invasion of fibroblast-like synoviocytes (FLSs), respectively. Western blotting was employed to measure the protein expression levels of cleaved caspase-3, interleukin (IL)-6, IL-1b, tumor necrosis factor-a and FSTL1. Dual-luciferase reporter assay was performed to verify the interaction between miR-3926 and ZFAS1 or FSTL1. The results demonstrated that ZFAS1 and FSTL1 were upregulated, and miR-3926 was downregulated in RA synovial tissues and RA-FLSs. ZFAS1 knockdown suppressed cell proliferation, migration, invasion and inflammatory cytokine production, and induced apoptosis in RA-FLSs. ZFAS1 acted as a sponge for miR-3926, and ZFAS1 overexpression abolished the impact of miR-3926 on the development of RA-FLSs. FSTL1 was a direct target of miR-3926, and the effect of FSTL1 knockdown on the progression of RA-FLSs was rescued by miR-3926 inhibition. Furthermore, ZFAS1 regulated FSTL1 expression levels via sponging miR-3926 in RA-FLSs. In conclusion, ZFAS1 knockdown inhibited RA-FLS proliferation, migration, invasion and inflammatory cytokine production, and induced apoptosis in RA via the miR-3926/FSTL1 axis.		Exp Ther Med. 2021 Sep;22(3):914. doi: 10.3892/etm.2021.10346. Epub 2021 Jun 29.
5345	LncRNA	SNHG20	miR-217	NA	Ovarian Cancer Tissues And Cells	Ovarian Cancer	Homo sapiens (human)  	CCK-8 assay;Dual-luciferase reporter assay;qRT-PCR;RIP assay;Luciferase reporter assay;	34302635	LncRNA SNHG20 promotes cell proliferation and invasion by suppressing miR-217 in ovarian cancer.	BACKGROUND: Ovarian cancer is the most common female gynecological malignancy. SNHG20, as a long non-coding RNA, has been proven to be an important regulator in the occurrence and development of various tumors. However, the potential mechanism of SNHG20 in ovarian cancer is unclear. OBJECTIVE: The present study was aimed to investigate the functions and mechanisms of SNHG20 in ovarian cancer. METHODS: The expression of SNHG20 and miR-217 in ovarian cancer tissues and cell lines was detected by qRT-PCR. CCK-8 assay was used to measure cell proliferation in transfected cells. The transwell assay was used to detect the relative invasion rate of transfected cells. The putative binding sites between SNHG20 and miR-217 were predicted by software LncBase v.2, and the interaction between SNHG20 and miR-217 was confirmed by dual-luciferase reporter assays and RIP assay. The rescue experiments were used to illustrate potential mechanisms. RESULTS: SNHG20 was upregulated in ovarian cancer tissues and cell lines. Overexpression of SNHG20 promoted ovarian cancer cell proliferation and invasion. MiR-217 was downregulated in ovarian cancer tissues and cells, and was negatively regulated by SNHG20. Moreover, miR-217 overexpression inhibited ovarian cancer cell proliferation and invasion. Furthermore, miR-217 mimic reversed the inhibitory effect of SNHG20 overexpression on the biological behavior of ovarian cancer cells. CONCLUSIONS: SNHG20 promoted cell proliferation and invasion by sponging miR-217 in ovarian cancer. These results suggested that SNHG20 and miR-217 might provide new targets for therapeutic application in ovarian cancer.		Genes Genomics. 2021 Sep;43(9):1095-1104. doi: 10.1007/s13258-021-01138-4. Epub 2021 Jul 24.
5346	LncRNA	WFDC21P	miR-4293	DCP2	Lung Carcinoma Tissue And Cells	Lung Carcinoma	Homo sapiens (human)  	qRT-PCR 	34301920	miR-4293 upregulates lncRNA WFDC21P by suppressing mRNA-decapping enzyme 2 to promote lung carcinoma proliferation.	Non-coding RNAs (ncRNAs) involve in diverse biological processes by post-transcriptional regulation of gene expression. Emerging evidence shows that miRNA-4293 plays a significant role in the development of non-small cell lung cancer. However, the oncogenic functions of miR-4293 have not been studied. Our results demonstrated that miR-4293 expression is markedly enhanced in lung carcinoma tissue and cells. Moreover, miR-4293 promotes tumor cell proliferation and metastasis but suppresses apoptosis. Mechanistic investigations identified mRNA-decapping enzyme 2 (DCP2) as a target of miR-4293 and its expression is suppressed by miR-4293. DCP2 can directly or indirectly bind to WFDC21P and downregulates its expression. Consequently, miR-4293 can further promote WFDC21P expression by regulating DCP2. With a positive correlation to miR-4293 expression, WFDC21P also plays an oncogenic role in lung carcinoma. Furthermore, knockdown of WFDC21P results in functional attenuation of miR-4293 on tumor promotion. In vivo xenograft growth is also promoted by both miR-4293 and WFDC21P. Overall, our results establish oncogenic roles for both miR-4293 and WFDC21P and demonstrate that interactions between miRNAs and lncRNAs through DCP2 are important in the regulation of carcinoma pathogenesis. These results provided a valuable theoretical basis for the discovery of lung carcinoma therapeutic targets and diagnostic markers based on miR-4293 and WFDC21P.		Cell Death Dis. 2021 Jul 23;12(8):735. doi: 10.1038/s41419-021-04021-y.
5347	LncRNA	MALAT1	miR-145	SMAD3	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;Luciferase reporter assay;	34295718	Long ncRNA MALAT1 promotes cell proliferation, migration, and invasion in prostate cancer via sponging miR-145.	BACKGROUND: The long non-coding (lncRNA) RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is known to promote tumorigenesis, whereas microRNA-145 (miR-145) plays an antitumor role in several cancers. In this study, we aimed to elucidate the role of MALAT1 and miR-145 in prostate cancer cells and investigate the effect of MALAT1 downregulation on prostate cancer (PCa) cells in vitro in vivo. METHODS: The Cancer Genome Atlas (TCGA) datasets were used to carry out the initial bioinformatics analysis; the findings were then tested in LNCaP and CWR22Rv1 cell lines. Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to evaluate the levels of MALAT1 and miR-145 along with related biomarkers. Furthermore, wound-healing and Transwell assays were performed to test the migratory and invasive abilities of PCa cells. Luciferase reporter assays were used to validate the relationship between MALAT1 and miR-145; their down-stream target genes were also studied. To further substantiate these findings in an animal model, tumor studies including immunofluorescence staining of tissues were carried in nude mice. RESULTS: The expression of MALAT1 was upregulated in both LNCaP cell lines and CWR22Rv1 cell lines (F=2.882, t=13.370, P<0.001; F=2.268, t=15.859, P<0.001). Knockdown of MALAT1 reduced the migratory and invasive capabilities of PCa cells (F=0.017, t=12.212, P<0.001; F=10.723, t=6.016, P=0.002). Using direct binding, MALAT1 suppressed the antitumor function of miR-145, which in turn upregulated transforming growth factor-b1 (TGF-b1)-induced epithelial-mesenchymal transition (EMT) via SMAD3 and TGFBR2 (F=2.097, t=5.389, P=0.006; F=1.306, t=4.155, P=0.014). CONCLUSIONS: We confirmed that MALAT1 acts as a competing endogenous RNA (ceRNA) of miR-145. The MALAT1 based regulation of MiR-145-5p-SMAD3/TGFBR2 interactions could be an intriguing molecular pathway for the progression of PCa.		Transl Androl Urol. 2021 Jun;10(6):2307-2319. doi: 10.21037/tau-20-1526.
5348	LncRNA	MALAT1	miR-145	TGFBR2	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;Luciferase reporter assay;	34295718	Long ncRNA MALAT1 promotes cell proliferation, migration, and invasion in prostate cancer via sponging miR-145.	BACKGROUND: The long non-coding (lncRNA) RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is known to promote tumorigenesis, whereas microRNA-145 (miR-145) plays an antitumor role in several cancers. In this study, we aimed to elucidate the role of MALAT1 and miR-145 in prostate cancer cells and investigate the effect of MALAT1 downregulation on prostate cancer (PCa) cells in vitro in vivo. METHODS: The Cancer Genome Atlas (TCGA) datasets were used to carry out the initial bioinformatics analysis; the findings were then tested in LNCaP and CWR22Rv1 cell lines. Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to evaluate the levels of MALAT1 and miR-145 along with related biomarkers. Furthermore, wound-healing and Transwell assays were performed to test the migratory and invasive abilities of PCa cells. Luciferase reporter assays were used to validate the relationship between MALAT1 and miR-145; their down-stream target genes were also studied. To further substantiate these findings in an animal model, tumor studies including immunofluorescence staining of tissues were carried in nude mice. RESULTS: The expression of MALAT1 was upregulated in both LNCaP cell lines and CWR22Rv1 cell lines (F=2.882, t=13.370, P<0.001; F=2.268, t=15.859, P<0.001). Knockdown of MALAT1 reduced the migratory and invasive capabilities of PCa cells (F=0.017, t=12.212, P<0.001; F=10.723, t=6.016, P=0.002). Using direct binding, MALAT1 suppressed the antitumor function of miR-145, which in turn upregulated transforming growth factor-b1 (TGF-b1)-induced epithelial-mesenchymal transition (EMT) via SMAD3 and TGFBR2 (F=2.097, t=5.389, P=0.006; F=1.306, t=4.155, P=0.014). CONCLUSIONS: We confirmed that MALAT1 acts as a competing endogenous RNA (ceRNA) of miR-145. The MALAT1 based regulation of MiR-145-5p-SMAD3/TGFBR2 interactions could be an intriguing molecular pathway for the progression of PCa.		Transl Androl Urol. 2021 Jun;10(6):2307-2319. doi: 10.21037/tau-20-1526.
5349	LncRNA	XIST	miR-497-5p	FOXO1	Trophoblast Cells	Gestational Diabetes Mellitus	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34295698	LncRNA XIST serves as a diagnostic biomarker in gestational diabetes mellitus and its regulatory effect on trophoblast cell via miR-497-5p/FOXO1 axis.	BACKGROUND: Gestational diabetes mellitus (GDM) is increasingly common in pregnancy. This study's purpose was to identify the expression of XIST and manifest the potential mechanism of XIST in GDM. METHODS: Ninety-three patients with GDM and 93 normal pregnant women were included in this investigation. qRT-PCR was conducted to evaluate the expression of miR-497-5p and XIST and the relationship between XIST and fasting blood glucose (FBG) was explored by Pearson assay. The clinical diagnosis of XIST on GDM patients was validated by the receiver operator characteristic (ROC) curve. Cell counting kit-8 (CCK-8) was applied to elucidate cell viability. Luciferase reporter assay was performed to document the relationship among XIST, miR-497-5p, and FOXO1. RESULTS: The expression of XIST was increased in GDM patients and HTR-8/SVneo cell models caused by high glucose (HG). The expression of XIST was associated with the FBG levels and appeared to be a feasible indicator in discriminating GDM patients. The expression of miR-497-5p was prominently reduced in GDM patients and cell models. Inhibition of XIST might alleviate the adverse function of HG on cell viability via sponging miR-497-5p. FOXO1 was proved to be a downstream target gene of miR-497-5p. CONCLUSIONS: Overexpression of XIST and downregulation of miR-497-5p were indicated in this publication. XIST might serve as a promising diagnostic marker for GDM patients. XIST/miR-497-5p/FOXO1 axis played a critical role in the regulation of trophoblast cells.		Cardiovasc Diagn Ther. 2021 Jun;11(3):716-725. doi: 10.21037/cdt-21-110.
5350	LncRNA	SENCR	miR-1	NA	The Serum	Acute Myocardial Infarction	Homo sapiens (human)  	ELISA;qRT-PCR;Luciferase reporter assay;	34295697	Long non-coding RNA SENCR alleviates hypoxia/reoxygenation-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-1.	BACKGROUND: Myocardial cell apoptosis is one of the main reasons for the occurrence of acute myocardial infarction (AMI). The role of smooth muscle and endothelial cell enriched migration/differentiation-associated lncRNA (SENCR) in the cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury and its potential mechanism were investigated in this study to provide a novel biomarker for the development of AMI. METHODS: The expression levels of SENCR in the serum of AMI patients and non-AMI patients with chest pain (control) were detected by qRT-PCR. The function of SENCR in the cardiomyocyte apoptosis and inflammatory response induced by H/R injury was evaluated by MTT, cell apoptosis, and ELISA assay, respectively. The mechanism underlying the function of SENCR was investigated with the luciferase reporter assay. RESULTS: SENCR was significantly downregulated in AMI compared with the control volunteers, which showed negative correlations with the cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) level of patients. The H/R injury-induced cell apoptosis and inflammatory response in cardiomyocytes, which were attenuated by the overexpression of SENCR. The expression of miR-1 was suppressed by the overexpression of SENCR, while the overexpression of miR-1 could alleviate the cell apoptosis, enhance cell viability, and attenuate inflammatory response in cardiomyocyte. SENCR reversed H/R-induced myocardial cell injury by regulating the expression of miR-1. CONCLUSIONS: SENCR was correlated with the clinicopathological features of patients and was revealed to alleviate the cardiomyocyte apoptosis and inflammatory response induced by H/R injury via sponging miR-1.		Cardiovasc Diagn Ther. 2021 Jun;11(3):707-715. doi: 10.21037/cdt-20-1037.
5351	LncRNA	PSMA3-AS1	miR-411-3p	HOXA10	Glioma Cells	Glioma	Homo sapiens (human)  	qPCR;RT-qPCR;	34294084	Long non-coding RNA PSMA3-AS1 promotes glioma progression through modulating the miR-411-3p/HOXA10 pathway.	BACKGROUND: Glioma is a common type of brain tumor and is classified as low and high grades according to morphology and molecules. Growing evidence has proved that long non-coding RNAs (lncRNAs) play pivotal roles in numerous tumors or diseases including glioma. Proteasome 20S subunit alpha 3 antisense RNA 1 (PSMA3-AS1), as a member of lncRNAs, has been disclosed to play a tumor-promoting role in cancer progression. However, the role of PSMA3-AS1 in glioma remains unknown. Therefore, we concentrated on researching the regulatory mechanism of PSMA3-AS1 in glioma. METHODS: PSMA3-AS1 expression was detected using RT-qPCR. Functional assays were performed to measure the effects of PSMA3-AS1 on glioma progression. After that, ENCORI ( http://starbase.sysu.edu.cn/ ) database was used to predict potential genes that could bind to PSMA3-AS1, and miR-411-3p was chosen for further studies. The interaction among PSMA3-AS1, miR-411-3p and homeobox A10 (HOXA10) were confirmed through mechanism assays. RESULTS: PSMA3-AS1 was verified to be up-regulated in glioma cells and promote glioma progression. Furthermore, PSMA3-AS1 could act as a competitive endogenous RNA (ceRNA) for miR-411-3p to regulate HOXA10 and thus affecting glioma progression. CONCLUSION: PSMA3-AS1 stimulated glioma progression via the miR-411-3p/HOXA10 pathway, which might offer a novel insight for the therapy and treatment of glioma.		BMC Cancer. 2021 Jul 22;21(1):844. doi: 10.1186/s12885-021-08465-5.
5352	LncRNA	OGFRP1	miR-149-5p	IL-6	Prostate Cancer Tissues And Cells	Prostate Cancer	Homo sapiens (human)  	CCK-8 assay;qRT-PCR;Luciferase reporter assay;	34293716	The lncRNA OGFRP1/miR-149-5p/IL-6 axis regulates prostate cancer chemoresistance.	BACKGROUND: The long non-coding RNA (lncRNA) OGFRP1 has been found to promote malignancy in prostate cancer (PC) and other cancer types. How this lncRNA functions in the regulation of PC chemoresistance, however, is poorly defined. METHODS: qRT-PCR was employed to measure OGFRP1, miR-149-5p, and IL-6 expression in PC tissues and cells. IC50 values for paclitaxel and docetaxel in PC cells were assessed via a CCK-8 assay approach. Putative miR-149-5p binding targets were identified and validated through bioinformatics assays and luciferase reporter assays, respectively. The impact of OGFRP1 on PC chemoresistance in vivo was validated using a xenograft model system. RESULTS: Docetaxel-resistant PC (PC/DR) cells and tissues exhibited reduced OGFRP1 expression and increased miR-149-5p expression. Knocking down OGFRP1 augmented the sensitivity of these PC cells to docetaxel and paclitaxel in vitro and in vivo. Mechanistically, OGFRP1 was found to bind and sequester miR-149-5p within PC/DR cells, thereby indirectly regulating IL-6 expression. Consistent with this model, the overexpression of IL-6 reversed the OGFRP1 knockdown-mediated reductions in docetaxel and paclitaxel IC50 values for these PC cells. CONCLUSIONS: OGFRP1 can sequester miR-149-5p, thereby indirectly promoting IL-6 upregulation and thereby promoting chemoresistance in PC cells. This OGFRP1/miR-149-5p/IL-6 axis may thus be a promising target for therapeutic efforts aimed at PC chemosensitization and treatment.		Pathol Res Pract. 2021 Aug;224:153535. doi: 10.1016/j.prp.2021.153535. Epub 2021 Jun 22.
5353	LncRNA	HOTTIP	miR-637	LASP1	Cholangiocarcinoma Patients	Cholangiocarcinoma	Homo sapiens (human)  	qRT-PCR 	34290981	HOTTIP Enhances Gemcitabine and Cisplatin Resistance Through Sponging miR-637 in Cholangiocarcinoma.	Chemo-resistance prominently hampers the effects of systemic chemotherapy to cholangiocarcinoma (CCA). Long non-coding RNAs (lncRNAs) have been shown to have great importance not only in tumorigenesis but also in therapeutic prognosis. The aim of this study is to investigate the role of lncRNA HOTTIP in the chemo-resistance to cisplatin and gemcitabine (CG) in CCA. The upregulated expression of HOTTIP was observed in CCA patients and the upregulation was associated with therapeutic responsiveness and prognosis. HOTTIP silencing powerfully increased the chemotherapy sensitivity through weakening proliferation and colony formation and increasing apoptosis. Subsequently, miR-637 was identified as the functional target of HOTTIP, since mechanically it could be targeted by HOTTIP and functionally its overexpression dismissed the changes by HOTTIP silencing in vitro and in vivo. Moreover, LIM and SH3 domain protein 1 (LASP1) could be targeted and regulated by miR-637. In all, HOTTIP modulates the sensitivity to CG in CCA through the HOTTIP/miR-637/LASP1 regulatory axis, providing a new opportunities for CCA treatment.		Front Oncol. 2021 Jul 5;11:664916. doi: 10.3389/fonc.2021.664916. eCollection 2021.
5354	LncRNA	AFAP1-AS1	miR-195	NA	Triple-Negative Breast Cancer Cells	Triple Negative Breast Cancerr	Homo sapiens (human)	MTT assay;MTT assay;	34289449	Formononetin relieves the facilitating effect of lncRNA AFAP1-AS1-miR-195/miR-545 axis on progression and chemo-resistance of triple-negative breast cancer.	This investigation attempted to discern whether formononetin restrained progression of triple-negative breast cancer (TNBC) by blocking lncRNA AFAP1-AS1-miR-195/miR-545 axis. We prepared TNBC cell lines (i.e. MDA-MB-231 and BT-549) and normal human mammary epithelial cell line (i.e. MCF-10A) in advance, and the TNBC cell lines were, respectively, transfected by pcDNA3.1-lncRNA AFAP1-AS1, si-lncRNA AFAP1-AS1, pcDNA6.2/GW/EmGFP-miR-545 or pcDNA6.2/GW/EmGFP-miR-195. Resistance of TNBC cells in response to 5-Fu, adriamycin, paclitaxel and cisplatin was evaluated through MTT assay, while potentials of TNBC cells in proliferation, migration and invasion were assessed via CCK8 assay and Transwell assay. Consequently, silencing of lncRNA AFAP1-AS1 impaired chemo-resistance, proliferation, migration and invasion of TNBC cells (P<0.05), and over-expression of miR-195 and miR-545, which were sponged and down-regulated by lncRNA AFAP1-AS1 (P<0.05), significantly reversed the promoting effect of pcDNA3.1-lncRNA AFAP1-AS1 on proliferation, migration, invasion and chemo-resistance of TNBC cells (P<0.05). Furthermore, CDK4 and Raf-1, essential biomarkers of TNBC progression, were, respectively, subjected to target and down-regulation of miR-545 and miR-195 (P<0.05), and they were promoted by pcDNA3.1-lncRNA AFAP1-AS1 at protein and mRNA levels (P<0.05). Additionally, formononetin significantly decreased expressions of lncRNA AFAP1-AS1, CDK4 and Raf-1, while raised miR-195 and miR-545 expressions in TNBC cells (P<0.05), and exposure to it dramatically contained malignant behaviors of TNBC cells (P<0.05). In conclusion, formononetin alleviated TNBC malignancy by suppressing lncRNA AFAP1-AS1-miR-195/miR-545 axis, suggesting that molecular targets combined with traditional Chinese medicine could yield significant clinical benefits in TNBC.		Aging (Albany NY). 2021 Jul 21;13(14):18191-18222. doi: 10.18632/aging.203156. Epub 2021 Jul 21.
5355	LncRNA	AFAP1-AS1	miR-545	NA	Triple-Negative Breast Cancer Cells	Triple Negative Breast Cancerr	Homo sapiens (human)	MTT assay;MTT assay;	34289449	Formononetin relieves the facilitating effect of lncRNA AFAP1-AS1-miR-195/miR-545 axis on progression and chemo-resistance of triple-negative breast cancer.	This investigation attempted to discern whether formononetin restrained progression of triple-negative breast cancer (TNBC) by blocking lncRNA AFAP1-AS1-miR-195/miR-545 axis. We prepared TNBC cell lines (i.e. MDA-MB-231 and BT-549) and normal human mammary epithelial cell line (i.e. MCF-10A) in advance, and the TNBC cell lines were, respectively, transfected by pcDNA3.1-lncRNA AFAP1-AS1, si-lncRNA AFAP1-AS1, pcDNA6.2/GW/EmGFP-miR-545 or pcDNA6.2/GW/EmGFP-miR-195. Resistance of TNBC cells in response to 5-Fu, adriamycin, paclitaxel and cisplatin was evaluated through MTT assay, while potentials of TNBC cells in proliferation, migration and invasion were assessed via CCK8 assay and Transwell assay. Consequently, silencing of lncRNA AFAP1-AS1 impaired chemo-resistance, proliferation, migration and invasion of TNBC cells (P<0.05), and over-expression of miR-195 and miR-545, which were sponged and down-regulated by lncRNA AFAP1-AS1 (P<0.05), significantly reversed the promoting effect of pcDNA3.1-lncRNA AFAP1-AS1 on proliferation, migration, invasion and chemo-resistance of TNBC cells (P<0.05). Furthermore, CDK4 and Raf-1, essential biomarkers of TNBC progression, were, respectively, subjected to target and down-regulation of miR-545 and miR-195 (P<0.05), and they were promoted by pcDNA3.1-lncRNA AFAP1-AS1 at protein and mRNA levels (P<0.05). Additionally, formononetin significantly decreased expressions of lncRNA AFAP1-AS1, CDK4 and Raf-1, while raised miR-195 and miR-545 expressions in TNBC cells (P<0.05), and exposure to it dramatically contained malignant behaviors of TNBC cells (P<0.05). In conclusion, formononetin alleviated TNBC malignancy by suppressing lncRNA AFAP1-AS1-miR-195/miR-545 axis, suggesting that molecular targets combined with traditional Chinese medicine could yield significant clinical benefits in TNBC.		Aging (Albany NY). 2021 Jul 21;13(14):18191-18222. doi: 10.18632/aging.203156. Epub 2021 Jul 21.
5356	LncRNA	H19	miR-106b-5p	ACSL4	Brain Microvascular Endothelial Cells	Intracerebral Hemorrhage	Homo sapiens (human)  	qPCR;RT-qPCR;RACE;Western blot;Flow Cytometry assay;RNA pull-down;	34288826	Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis.	Intracerebral hemorrhage (ICH) is one of the most common refractory diseases. Long non-coding RNAs (lncRNAs) play crucial roles in ICH. This study was designed to investigate the role of lncRNA H19 in ICH and the underlying molecular mechanisms involved. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to determine mRNA expression. Cell viability was analyzed using Cell Counting Kit 8 (CCK8). PI staining Flow cytometry and TdT-mediated biotinylated nick end-labeling (TUNEL) assays were performed to determine ferroptosis in brain microvascular endothelial cells (BMVECs). Targeting relationships were predicted using Starbase and TargetScan and verified by RNA pull-down and luciferase reporter gene assays. Western blotting was performed to assess protein expression. LncRNA H19 is highly expressed in ICH model cells. Over-expression of H19 suppressed cell viability and promoted ferroptosis of BMVECs. miR-106b-5p is predicted to be a target of H19. The expression of miR-106b-5p was lower in oxygen and glucose deprivation hemin-treated (OGD/H-treated) cells. Over-expression of miR-106b-5p reversed the effects of H19 on cell viability and ferroptosis in BMVECs. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was verified to be a target gene of miR-106b-5p and was highly expressed in OGD/H-treated cells. Upregulation of ACSL4 inhibited the effects of miR-106b-5p and induced BMVEC dysfunction. In conclusion, lncRNA H19 was overexpressed in ICH. Knockdown of H19 promoted cell proliferation and suppressed BMVECs ferroptosis by regulating the miR-106b-5p/ACSL4 axis. Therefore, H19 knockdown may be a promising therapeutic strategy for ICH.		Bioengineered. 2021 Dec;12(1):4004-4015. doi: 10.1080/21655979.2021.1951070.
5357	LncRNA	PROX1-AS1	miR-211-5p	caspase-9	Placental Trophoblast Cells	Preeclampsia	Homo sapiens (human)  	Flow Cytometry assay;RNA pull-down;	34288800	lncRNA PROX1-AS1 mediates the migration and invasion of placental trophoblast cells via the miR-211-5p/caspase-9 axis.	Preeclampsia (PE) is a potentially fatal pregnancy complication; however, its pathogenesis remains unclear. Long non-coding RNAs (lncRNAs) are associated with occurrence and progression of PE. Therefore, this study aimed to explore the function of the lncRNA prospero homeobox 1-antisense RNA 1 (PROX1-AS1) and elucidate its underlying molecular mechanism of action. We found that the expression levels of PROX1-AS1 were elevated in both the placental tissues and blood samples of the patients with PE. Moreover, the results of the flow cytometry and transwell assay showed that the knockdown of PROX1-AS1 inhibited the apoptosis and promoted the migration and invasion of HTR-8/SVneo cells. We also assessed the interactions between PROX1-AS1, caspase-9, and microRNA (miR)-211-5p via dual-luciferase reporter and RNA pull-down analyses. The data indicated that PROX1-AS1 acted as a sponge for miR-211-5p to regulate the expression of caspase-9. Moreover, the expression of miR-211-5p was reduced in PE and negatively related to PROX1-AS1, while that of caspase-9 was increased in PE and negatively regulated by miR-211-5p. Furthermore, inhibition of miR-211-5p rescued the facilitation of cell apoptosis, migration and invasion induced by the knockdown of PROX1-AS1. We also found that caspase-9 improved the apoptosis rate, and suppressed the cell migration and invasion induced by the overexpression of miR-211-5p. In conclusion, the knockdown of PROX1-AS1 promoted the cell morbidity of the trophoblast cells by modulating the miR-211-5p/caspase-9 axis, which may alleviate the progression of PE. This novel regulatory network may contribute to the pathogenesis and progression of PE.		Bioengineered. 2021 Dec;12(1):4100-4110. doi: 10.1080/21655979.2021.1953213.
5358	LncRNA	LINC01320	miR495-5p	RAB19	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qRT-PCR;RIP assay;Luciferase reporter assay;	34288797	N6-methyladenosine (m6A)-mediated up-regulation of long noncoding RNA LINC01320 promotes the proliferation, migration, and invasion of gastric cancer via miR495-5p/RAB19 axis.	Gastric cancer is one of the most common malignant tumors. Long non-coding RNAs play crucial roles in gastric cancer progression. This study investigated the effect of LINC01320 on malignant behaviors of gastric cancer cells and explored its possible molecular mechanism. LINC01320 expression in gastric cancer tissues and cell lines was measured by qRT-PCR. Cell proliferation, transwell, and cell cloning assays were used to detect the effect of LINC01320 on the proliferation, migration, and invasion abilities, respectively, of gastric cancer cells. Bioinformatics analysis was used to predict the binding of miR-495-5p with LINC01320 and RAB19. A luciferase reporter assay was performed to verify their interactions. Finally, the N(6)-methyladenosine (m6A) modification of LINC01320 by METTL14 was identified through RIP experiments. LINC01320 was highly expressed in gastric cancer tissues and cells. LINC01320 overexpression promoted the proliferation, migration, and invasion of gastric cancer cells, while LINC01320 knockdown exerted the opposite effects. Moreover, miR-495-5p was predicted and demonstrated to target LINC01320 and RAB19. LINC01320 sponged miR-495-5p to regulate the expression of RAB19. Additionally, LINC01320-induced increases in cell viability, migration, and invasion of gastric cancer were alleviated by miR-495-5p and silenced RAB19. Furthermore, epigenetic studies showed that METTL14-mediated m6A modification led to LINC01320 up-regulation. METTL14 regulated the m6A modification of LINC01320. Overexpressed LINC01320 contributed to the aggressive phenotype of gastric cancer cells via regulating the miR-495-5p/RAB19 axis. This finding may provide new potential targets for treating gastric cancer.		Bioengineered. 2021 Dec;12(1):4081-4091. doi: 10.1080/21655979.2021.1953210.
5359	LncRNA	PVT1	miR-148a-3p	AGO1	Ovarian Cancer Cells	Ovarian Cancer	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;Western blot;Immunohistochemistry;	34288373	LncRNA PVT1 promotes the progression of ovarian cancer by activating TGF-b pathway via miR-148a-3p/AGO1 axis.	Ovarian cancer is a lethal gynaecologic malignancy with poor diagnosis and prognosis. The long non-coding RNA plasmacytoma variant translocation1 (PVT1) and argonaute 1 (AGO1) are associated with carcinogenesis and chemoresistance; however, the relationship between PVT1 and AGO1 and the downstream mechanisms in ovarian cancer remains poorly known. PVT1 and AGO1 expression was assessed through RT-qPCR and Western blotting in both human tissues and cell lines. The viability and proliferation of ovarian cancer cells were determined by CCK-8 assay and TUNEL assay in vitro and immunohistochemistry in vivo. Cell invasion and migration were investigated through transwell and wound-healing assays. The roles and mechanisms of AGO1 on cell functions were further probed via gain- and loss-of-function analysis. We reveal that PVT1 expression was significantly increased in ovarian cancer tissues which is associated with advanced FIGO stage, lymph-node metastasis, poor survival rate, and high expression of AGO1. PVT1 or AGO1 knockdown significantly reduced the cell viability and increased the cell apoptosis and inhibited ovarian tumour growth and proliferation. Furthermore, we discovered that PVT1 up-regulated the expression of AGO1 and thus regulated the transforming growth factor-b (TGF-b) pathway to promote ovarian cancer progression through sponging miR-148a-3p. Additionally, the activation of ERK1/2, smad2 and smad4 is observed to be related to the PVT1/miR-148a-3p/AGO1/TGF-b pathway-induced cascades. Taken together, the present study reveals that PVT1/miR-148a/AGO1 axis plays an important role in the progression of ovarian cancer and emphasize the potential as a target of value for ovarian cancer therapy.		J Cell Mol Med. 2021 Jul 21. doi: 10.1111/jcmm.16700.
5360	LncRNA	THAP9-AS1	miR-652-3p	VEGFA	Dental Pulp Stem Cells	Dentin-Pulp Regeneration	Homo sapiens (human)  	Rescue assay;	34288157	The role of long noncoding RNA THAP9-AS1 in the osteogenic differentiation of dental pulp stem cells via the miR-652-3p/VEGFA axis.	Dental pulp stem cells (DPSCs) are multipotent and may play crucial roles in dentin-pulp regeneration. Recent studies have revealed that long noncoding RNAs (lncRNAs) are implicated in the osteogenic differentiation of DPSCs. However, the specific role and potential mechanisms of the lncRNA trihydroxyacetophenone domain containing nine antisense RNA 1 (THAP9-AS1) during osteogenic differentiation of DPSCs remain unknown. In the present study, we determined that THAP9-AS1 expression was upregulated during osteogenic differentiation of DPSCs. Moreover, we investigated the biological functions of THAP9-AS1 during osteogenic differentiation of DPSCs by loss-of-function assays. THAP9-AS1 knockdown inhibited osteogenic differentiation of DPSCs by decreasing alkaline phosphatase activity, alkaline phosphatase-positive cell ratio, mineralizing matrix and mRNA, and protein levels of early osteogenic-markers. We also found that THAP9-AS1 interacted with miR-652-3p, whose downstream gene target is vascular endothelial growth factor A (VEGFA). In addition, rescue assays indicated that VEGFA rescued the effects of THAP9-AS1 knockdown during osteogenic differentiation of DPSCs. In summary, we verified that knockdown of THAP9-AS1 inhibits osteogenic differentiation of DPSCs via the miR-652-3p/VEGFA axis. Our findings may be helpful to extend research on the mechanisms underlying osteogenic differentiation of DPSCs.		Eur J Oral Sci. 2021 Aug;129(4):e12790. doi: 10.1111/eos.12790. Epub 2021 Jul 19.
5361	LncRNA	LINC01551	microRNA-122-5p	ADAM10	Hepatocellular Carcinoma Cell	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34288116	Retraction.	Retraction: "Long noncoding LINC01551 promotes hepatocellular carcinoma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of microRNA-122-5p to regulate ADAM10 expression," by Jun Gao, Xiangbao Yin, Xin Yu, Chao Dai, Fan Zhou, J Cell Biochem. 2019; 16393-16407: The above article, published online on 03 July 2019 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/abs/10.1002/jcb.28549), has been retracted by agreement between the journal's Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found. Thus, the editors consider the conclusions of this article to be invalid.		J Cell Biochem. 2021 Jul 19. doi: 10.1002/jcb.30107.
5362	LncRNA	IFITM4P	miR-24-3p	IFITM1	NA	Antiviral Innate Immunity	Homo sapiens (human)  	qRT-PCR 	34287042	LncRNA IFITM4P regulates host antiviral responses by acting as a ceRNA.	Long noncoding RNAs (lncRNAs) are involved in numerous cellular processes. Increasing evidence suggests that some lncRNAs function in immunity through various complex mechanisms. However, implication of a large fraction of lncRNAs in antiviral innate immunity remains uncharacterized. Here, we identified a lncRNA called lncRNA IFITM4P that was transcribed from interferon induced transmembrane protein 4 pseudogene (IFITM4P), a pseudogene belonging to interferon induced transmembrane protein (IFITM) family. We found that expression of lncRNA IFITM4P was significantly induced by infection with several viruses including influenza A virus (IAV). Importantly, lncRNA IFITM4P acted as a positive regulator of innate antiviral immunity. Ectopic expression of lncRNA IFITM4P significantly suppressed IAV replication in vitro, whereas IFITM4P deficiency promoted the viral production. We further observed that expression of lncRNA IFITM4P was up-regulated by interferon (IFN) signaling during viral infection, and altering the expression of this lncRNA had significant effects on the mRNA levels of several IFITM family members including IFITM1, IFITM2 and IFITM3. Moreover, it was identified that lncRNA IFITM4P was a target of miR-24-3p that represses mRNA of IFITM1, IFITM2 and IFITM3. The experiments demonstrated that lncRNA IFITM4P was able to cross-regulate the expression of IFITM family members as a competing endogenous RNA (ceRNA), leading to increased stability of these IFITM mRNAs. Together, our results reveal that lncRNA IFITM4P, as a ceRNA, is involved in innate immunity against viral infection through the lncRNA IFITM4P-miR-24-3p- IFITM1/2/3 regulatory network. IMPORTANCE LncRNAs play important roles in various biological processes, but their involvement in host antiviral responses remains largely unknown. In this study, we revealed that the pseudogene IFITM4P belonging to IFITM family can transcribe a functional long noncoding RNA termed lncRNA IFITM4P. Importantly, results showed that lncRNA IFITM4P was involved in innate antiviral immunity, which resembles some interferon-stimulated genes (ISGs). Furthermore, lncRNA IFITM4P was identified as a target of miR-24-3p and acts as a ceRNA to inhibit the replication of IAV through regulating the mRNA levels of IFITM1, IFITM2 and IFITM3. These data provide a new insight into the role of a previously uncharacterized lncRNA encoded by a pseudogene in the host antiviral response, and a better understanding of the IFITM antiviral network.		J Virol. 2021 Jul 21:JVI0027721. doi: 10.1128/JVI.00277-21.
5363	LncRNA	IFITM4P	miR-24-3p	IFITM2	NA	Antiviral Innate Immunity	Homo sapiens (human)  	qRT-PCR 	34287042	LncRNA IFITM4P regulates host antiviral responses by acting as a ceRNA.	Long noncoding RNAs (lncRNAs) are involved in numerous cellular processes. Increasing evidence suggests that some lncRNAs function in immunity through various complex mechanisms. However, implication of a large fraction of lncRNAs in antiviral innate immunity remains uncharacterized. Here, we identified a lncRNA called lncRNA IFITM4P that was transcribed from interferon induced transmembrane protein 4 pseudogene (IFITM4P), a pseudogene belonging to interferon induced transmembrane protein (IFITM) family. We found that expression of lncRNA IFITM4P was significantly induced by infection with several viruses including influenza A virus (IAV). Importantly, lncRNA IFITM4P acted as a positive regulator of innate antiviral immunity. Ectopic expression of lncRNA IFITM4P significantly suppressed IAV replication in vitro, whereas IFITM4P deficiency promoted the viral production. We further observed that expression of lncRNA IFITM4P was up-regulated by interferon (IFN) signaling during viral infection, and altering the expression of this lncRNA had significant effects on the mRNA levels of several IFITM family members including IFITM1, IFITM2 and IFITM3. Moreover, it was identified that lncRNA IFITM4P was a target of miR-24-3p that represses mRNA of IFITM1, IFITM2 and IFITM3. The experiments demonstrated that lncRNA IFITM4P was able to cross-regulate the expression of IFITM family members as a competing endogenous RNA (ceRNA), leading to increased stability of these IFITM mRNAs. Together, our results reveal that lncRNA IFITM4P, as a ceRNA, is involved in innate immunity against viral infection through the lncRNA IFITM4P-miR-24-3p- IFITM1/2/3 regulatory network. IMPORTANCE LncRNAs play important roles in various biological processes, but their involvement in host antiviral responses remains largely unknown. In this study, we revealed that the pseudogene IFITM4P belonging to IFITM family can transcribe a functional long noncoding RNA termed lncRNA IFITM4P. Importantly, results showed that lncRNA IFITM4P was involved in innate antiviral immunity, which resembles some interferon-stimulated genes (ISGs). Furthermore, lncRNA IFITM4P was identified as a target of miR-24-3p and acts as a ceRNA to inhibit the replication of IAV through regulating the mRNA levels of IFITM1, IFITM2 and IFITM3. These data provide a new insight into the role of a previously uncharacterized lncRNA encoded by a pseudogene in the host antiviral response, and a better understanding of the IFITM antiviral network.		J Virol. 2021 Jul 21:JVI0027721. doi: 10.1128/JVI.00277-21.
5364	LncRNA	IFITM4P	miR-24-3p	IFITM3	NA	Antiviral Innate Immunity	Homo sapiens (human)  	qRT-PCR 	34287042	LncRNA IFITM4P regulates host antiviral responses by acting as a ceRNA.	Long noncoding RNAs (lncRNAs) are involved in numerous cellular processes. Increasing evidence suggests that some lncRNAs function in immunity through various complex mechanisms. However, implication of a large fraction of lncRNAs in antiviral innate immunity remains uncharacterized. Here, we identified a lncRNA called lncRNA IFITM4P that was transcribed from interferon induced transmembrane protein 4 pseudogene (IFITM4P), a pseudogene belonging to interferon induced transmembrane protein (IFITM) family. We found that expression of lncRNA IFITM4P was significantly induced by infection with several viruses including influenza A virus (IAV). Importantly, lncRNA IFITM4P acted as a positive regulator of innate antiviral immunity. Ectopic expression of lncRNA IFITM4P significantly suppressed IAV replication in vitro, whereas IFITM4P deficiency promoted the viral production. We further observed that expression of lncRNA IFITM4P was up-regulated by interferon (IFN) signaling during viral infection, and altering the expression of this lncRNA had significant effects on the mRNA levels of several IFITM family members including IFITM1, IFITM2 and IFITM3. Moreover, it was identified that lncRNA IFITM4P was a target of miR-24-3p that represses mRNA of IFITM1, IFITM2 and IFITM3. The experiments demonstrated that lncRNA IFITM4P was able to cross-regulate the expression of IFITM family members as a competing endogenous RNA (ceRNA), leading to increased stability of these IFITM mRNAs. Together, our results reveal that lncRNA IFITM4P, as a ceRNA, is involved in innate immunity against viral infection through the lncRNA IFITM4P-miR-24-3p- IFITM1/2/3 regulatory network. IMPORTANCE LncRNAs play important roles in various biological processes, but their involvement in host antiviral responses remains largely unknown. In this study, we revealed that the pseudogene IFITM4P belonging to IFITM family can transcribe a functional long noncoding RNA termed lncRNA IFITM4P. Importantly, results showed that lncRNA IFITM4P was involved in innate antiviral immunity, which resembles some interferon-stimulated genes (ISGs). Furthermore, lncRNA IFITM4P was identified as a target of miR-24-3p and acts as a ceRNA to inhibit the replication of IAV through regulating the mRNA levels of IFITM1, IFITM2 and IFITM3. These data provide a new insight into the role of a previously uncharacterized lncRNA encoded by a pseudogene in the host antiviral response, and a better understanding of the IFITM antiviral network.		J Virol. 2021 Jul 21:JVI0027721. doi: 10.1128/JVI.00277-21.
5365	LncRNA	FEZF1-AS1	miR-363-3p	PRRX1	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	34286520	LncRNA FEZF1-AS1 promotes colorectal cancer progression through regulating the miR-363-3p/PRRX1 pathway.	BACKGROUND: Long non-coding RNAs (lncRNAs) are involved in the development of many cancers, including colorectal cancer (CRC). FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) is a key lncRNA in the regulation of CRC progression, but its potential molecular mechanisms need to be further explored. OBJECTIVES: To investigate the mechanism of lncRNA FEZF1-AS1 in the progression of CRC. MATERIAL AND METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure FEZF1-AS1 and miR-363-3p expression. Cell proliferation, migration and invasion were analyzed using Cell Counting Kit-8 (CCK-8) and transwell assays. Protein expression of epithelial-mesenchymal transformation (EMT)-related markers and paired-related homeobox 1 (PRRX1) were determined using western blot analysis. The interactions among FEZF1-AS1, miR-363-3p and PRRX1 were verified with dual-luciferase reporter assay. A xenograft model was constructed in vivo to confirm the role of FEZF1-AS1 in CRC tumor growth. RESULTS: We demonstrated that FEZF1-AS1 expression was upregulated in CRC, and its silencing reduced CRC cell proliferation, migration, invasion, and EMT. MiR-363-3p could be inhibited by FEZF1-AS1, which inhibitor could reverse the suppressive effect of FEZF1-AS1 silencing on CRC progression. Paired-related homeobox 1 could be targeted by miR-363-3p, and the inhibitory effect of FEZF1-AS1 knockdown on CRC progression could also be eliminated by PRRX1 overexpression. Furthermore, interference of FEZF1-AS1 reduced the tumor growth of CRC in vivo. CONCLUSIONS: Our data demonstrate that FEZF1-AS1 regulated PRRX1 expression to promote CRC progression via inhibition of miR-363-3p.		Adv Clin Exp Med. 2021 Aug;30(8):839-848. doi: 10.17219/acem/135693.
5366	LncRNA	PCGEM1	miR-129-5p	ETV1	Hep3B/Oxa Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR;luciferase assay;	34286514	LncRNA PCGEM1 mediates oxaliplatin resistance in hepatocellular carcinoma via miR-129-5p/ETV1 axis in vitro.	BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most severe malignant cancers that leads to high death rate worldwide. Recent research revealed that long non-coding RNAs (lncRNAs) exert a critical role regarding chemoresistance in numerous cancers, including HCC. OBJECTIVES: Our research aimed to explore the function and molecular mechanism of lncRNA PCGEM1 on oxaliplatin resistance of HCC in vitro. MATERIAL AND METHODS: Expression of the lncRNA PCGEM1, together with miR-129-5p, and the mRNA level of ETV1 and drug resistance-related genes including LRPA, MDR1 and MDR3 were determined using quantitative real-time polymerase chain reaction (qRT-PCR) in an oxaliplatin-resistant HCC cell line (Hep3B/OXA). Cell Counting Kit-8 (CCK-8) was employed to assess the viability and cell survival rate, and transwell assays were performed to measure the number of migrated or invaded cells. In addition, the relation among lncRNA PCGEM1, miR-129-5p and ETV1 were determined using luciferase assay. RESULTS: Our data indicated that PCGEM1 and ETV1 expression were enhanced in Hep3B/OXA cells. Furthermore, knockdown of lncRNA PCGEM1 significantly decreased the migration, invasion and mRNA expressions of LRPA, MDR1 and MDR3, and the cell viability in Hep3B/OXA cells. The starBase online tool and luciferase assays verified that miR-129-5p targeted PCGEM1 and ETV1, signifying that PCGEM1 could enhance ETV1 expression via suppressing miR-129-5p. CONCLUSIONS: Our findings demonstrated that PCGEM1 modulated oxaliplatin resistance by targeting the miR-129-5p/ETV1 pathway in HCC in vitro, suggesting a potential strategy for the treatment of chemoresistant HCC.		Adv Clin Exp Med. 2021 Aug;30(8):831-838. doi: 10.17219/acem/135533.
5367	LncRNA	ANRIL	miR-7	FGF2	Vascular Smooth Muscle Cells	Intracranial Aneurysm	Homo sapiens (human)  	RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	34286462	LncRNA ANRIL Facilitates Vascular Smooth Muscle Cell Proliferation and Suppresses Apoptosis via Modulation of miR-7/FGF2 Pathway in Intracranial Aneurysms.	BACKGROUND: Proliferation and apoptosis of vascular smooth muscle cells (VSMCs) are linked to intracranial aneurysm (IA) formation and progression. Long antisense noncoding RNA in the INK4 locus (ANRIL) has been reported to regulate VSMC functions in several cardiovascular diseases. However, little is known about how ANRIL influences VSMC proliferation and apoptosis during IA pathogenesis. METHODS: The expression level of ANRIL in the plasma and arterial wall tissues of patients with IA was detected by real-time quantitative polymerase chain reaction. The functional role of ANRIL in the regulation of VSMC proliferation and apoptosis and its downstream regulatory mechanism were determined using Cell Counting Kit 8, immunofluorescence, terminal-deoxynucleotidyl transferase-mediated UTP nick end labeling, western blotting, luciferase reporter assay, and RNA immunoprecipitation assay. RESULTS: ANRIL was downregulated in the plasma and arterial wall tissues of patients with IA, when compared with control groups. Overexpression of ANRIL significantly promoted VSMC proliferation and blocked cell apoptosis. Mechanistic studies demonstrated that ANRIL directly bound to microRNA-7 (miR-7) and that overexpression of miR-7 overturned the increased cell proliferation and decreased cell apoptosis, which was induced by ANRIL restoration. Besides, further study showed that ANRIL positively regulated fibroblast growth factor 2 (FGF2) expression via targeting miR-7. CONCLUSIONS: These results suggested that ANRIL affects VSMC proliferation and apoptosis via regulation of the miR-7/FGF2 pathway in IA, which provided a potential novel strategy for the treatment of IA.		Neurocrit Care. 2021 Jul 20. doi: 10.1007/s12028-021-01262-9.
5368	LncRNA	NEAT1	miR-148b-3p	ROCK1	Retinoblastoma Tissues, Cells	Retinoblastoma	Homo sapiens (human)  	qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;	34285579	LncRNA NEAT1 Acts as an miR-148b-3p Sponge to Regulate ROCK1 Inhibition of Retinoblastoma Growth.	BACKGROUND: It is reported that long non-coding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) is involved in the occurrence and development of various cancers. However, the detailed biological function and mechanism of LncRNA NEAT1 in retinoblastoma are still unclear. So we will explore the biological function and possible mechanism of LncRNA NEAT1 in retinoblastoma. MATERIALS AND METHODS: Quantitative real-time PCR (qRT-PCR) was used to detect LncRNA NEAT1 in retinoblastoma tissues and cell lines. Cell counting kit 8, Transwell and flow cytometry were applied to explore cell proliferation, invasion and apoptosis. The target miRNAs (miR) of LncRNA NEAT1 and miR and downstream target genes were predicted using Starbase3.0 software and confirmed by double luciferase reporting test and RNA binding protein immunoprecipitation (RIP). Western Blot was applied to explore ROCK1 in cells, and tumor allogeneic experiment was applied to study the role of LncRNA NEAT1 on tumor growth. RESULTS: It was found that LncRNA NEAT1 was up-regulated in retinoblastoma tissues, cells and serum, and the prognosis of patients with high expression of LNC RNA NEAT 1 was poor. Functional analysis showed that knocking down LncRNA NEAT1 could weaken proliferation and invasion, and accelerate apoptosis. Tumor allogeneic experiment showed that sh-NEAT1 injection can inhibit tumor growth. In addition, LncRNA NEAT1 inhibited proliferation and invasion, and promoted apoptosis through miR-148b-3p/ROCK1 axis. CONCLUSION: LncRNA NEAT1 can mediate miR-148b-3p/ROCK1 axis to weaken the proliferation and invasion of retinoblastoma.		Cancer Manag Res. 2021 Jul 12;13:5587-5597. doi: 10.2147/CMAR.S271326. eCollection 2021.
5369	LncRNA	lnc-MMP2-2	miRNA-1207-5p	EPB41L5	Human Brain Microvascular Endothelial Cells, Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)	RNA immunoprecipitation;RNA pull-down assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34285192	TGF-b1-mediated exosomal lnc-MMP2-2 increases blood-brain barrier permeability via the miRNA-1207-5p/EPB41L5 axis to promote non-small cell lung cancer brain metastasis.	Brain metastases remain a major problem in patients with advanced non-small cell lung cancer (NSCLC). The permeability of the blood-brain barrier (BBB) is highly increased during lung cancer brain metastasis; however, the underlying mechanism remains largely unknown. We previously found that lnc-MMP2-2 is highly enriched in tumor growth factor (TGF)-b1-mediated exosomes and regulates the migration of lung cancer cells. This study aimed to explore the role of exosomal lnc-MMP2-2 in the regulation of BBB and NSCLC brain metastasis. Here, using endothelial monolayers and mouse models, we found that TGF-b1-mediated NSCLC-derived exosomes efficiently destroyed tight junctions and the integrity of these natural barriers. Overexpression of lnc-MMP2-2 in human brain microvascular endothelial cells increased vascular permeability in endothelial monolayers, whereas inhibition of lnc-MMP2-2 alleviated these effects. Furthermore, lnc-MMP2-2 knockdown markedly reduced NSCLC brain metastasis in vivo. Mechanistically, through luciferase reporter assays, RNA pull-down assay, and Ago2 RNA immunoprecipitation assay, we showed that lnc-MMP2-2 served as a microRNA sponge or a competing endogenous RNA for miR-1207-5p and consequently modulated the derepression of EPB41L5. In conclusion, TGF-b1-mediated exosomal lnc-MMP2-2 increases BBB permeability to promote NSCLC brain metastasis. Thus, exosomal lnc-MMP2-2 may be a potential biomarker and therapeutic target against lung cancer brain metastasis.		Cell Death Dis. 2021 Jul 20;12(8):721. doi: 10.1038/s41419-021-04004-z.
5370	LncRNA	lnc-MMP2-2	miRNA-1207-5p	EPB41L5	Human Brain Microvascular Endothelial Cells, Lung Cancer Cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	RNA immunoprecipitation;RNA pull-down assay;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34285192	TGF-b1-mediated exosomal lnc-MMP2-2 increases blood-brain barrier permeability via the miRNA-1207-5p/EPB41L5 axis to promote non-small cell lung cancer brain metastasis.	Brain metastases remain a major problem in patients with advanced non-small cell lung cancer (NSCLC). The permeability of the blood-brain barrier (BBB) is highly increased during lung cancer brain metastasis; however, the underlying mechanism remains largely unknown. We previously found that lnc-MMP2-2 is highly enriched in tumor growth factor (TGF)-b1-mediated exosomes and regulates the migration of lung cancer cells. This study aimed to explore the role of exosomal lnc-MMP2-2 in the regulation of BBB and NSCLC brain metastasis. Here, using endothelial monolayers and mouse models, we found that TGF-b1-mediated NSCLC-derived exosomes efficiently destroyed tight junctions and the integrity of these natural barriers. Overexpression of lnc-MMP2-2 in human brain microvascular endothelial cells increased vascular permeability in endothelial monolayers, whereas inhibition of lnc-MMP2-2 alleviated these effects. Furthermore, lnc-MMP2-2 knockdown markedly reduced NSCLC brain metastasis in vivo. Mechanistically, through luciferase reporter assays, RNA pull-down assay, and Ago2 RNA immunoprecipitation assay, we showed that lnc-MMP2-2 served as a microRNA sponge or a competing endogenous RNA for miR-1207-5p and consequently modulated the derepression of EPB41L5. In conclusion, TGF-b1-mediated exosomal lnc-MMP2-2 increases BBB permeability to promote NSCLC brain metastasis. Thus, exosomal lnc-MMP2-2 may be a potential biomarker and therapeutic target against lung cancer brain metastasis.		Cell Death Dis. 2021 Jul 20;12(8):721. doi: 10.1038/s41419-021-04004-z.
5371	LncRNA	CASC9	miR-576-5p	AKT3	Colorectal Cancer Cell	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34285188	Correction to: Silencing long non-coding RNA CASC9 inhibits colorectal cancer cell proliferation by acting as a competing endogenous RNA of miR-576-5p to regulate AKT3.	unknown		Cell Death Discov. 2021 Jul 20;7(1):185. doi: 10.1038/s41420-021-00564-3.
5372	LncRNA	CALML3-AS1	miR-146a	Smad4	Chondrocytes	Osteoarthritis	Homo sapiens (human)  	Cell apoptosis assay;qPCR;RT-qPCR;Western blot;	34282692	LncRNA CALML3-AS1 regulates chondrocyte apoptosis by acting as a sponge for miR-146a.	Chondrocyte apoptosis contributes to osteoarthritis, while miR-146a is a critical player in chondrocyte apoptosis. Our bioinformatics analysis showed that miR-146a may bind with long non-coding RNA (lncRNA) CALML3 antisense RNA 1 (CALML3-AS1). Our study was therefore carried out to investigate the interactions between lncRNA CALML3-AS1 and miR-146a in osteoarthritis. This study included 66 osteoarthritis patients who were admitted at Shanxi People's Hospital from July 2016 to June 2019. Transfections were performed to analyse gene interactions. RT-qPCR and Western blot were performed to determine the expression levels of gene and protein, respectively. Cell apoptosis of chondrocytes induced by lipopolysaccharide (LPS) was analysed by cell apoptosis assay. We found that CALML3-AS1 was downregulated, while miR-146a was upregulated in osteoarthritis. However, no significant correlation was found between them. In addition, overexpression of CALML3-AS1 or miR-146a did not affect the expression of each other. However, overexpression of CALML3-AS1 resulted in the upregulation of Smad family member 4 (Smad4), a downstream target of miR-146a. We also found that the expression of miR-146a and Smad4 were negatively correlated, while the correlation between CALML3-AS1 and smad4 was not significant. In cell apoptosis assay, overexpression of CALML3-AS1 and Smad4 resulted in decreased proliferation of chondrocytes. MiR-146a played an opposite role and reduced the effects of overexpression of CALML3-AS1 and Smad4. Therefore, CALML3-AS1 may regulate chondrocyte apoptosis by acting as a sponge for miR-146a to upregulate Smad4.		Autoimmunity. 2021 Jul 20:1-7. doi: 10.1080/08916934.2021.1943663.
5373	LncRNA	HOTAIR	miR-20a-5p	WT1	Acute Leukemia Cells	Acute Myeloid Leukemia	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34282279	Curcumin attenuates Adriamycin-resistance of acute myeloid leukemia by inhibiting the lncRNA HOTAIR/miR-20a-5p/WT1 axis.	Acute myeloid leukemia (AML) is a common subtype of leukemia, and a large proportion of patients with AML eventually develop drug resistance. Curcumin exerts cancer suppressive effects and increases sensitivity to chemotherapy in several diseases. This study aimed to investigate the mechanism by which curcumin affects the resistance of AML to Adriamycin by regulating HOX transcript antisense RNA (HOTAIR) expression. Cell viability, colony-formation, flow cytometry, and Transwell assays were used to assess cell proliferation, apoptosis, and migration. A dual-luciferase reporter assay was used to verify the interaction between microRNA (miR)-20a-5p and HOTAIR or Wilms' tumor 1 (WT1). RT-qPCR and Western blotting assays were performed to detect gene and protein expression. The results showed that curcumin suppressed the resistance to Adriamycin, inhibited the expression of HOTAIR and WT1, and promoted the expression of miR-20a-5p in human acute leukemia cells (HL-60) or Adriamycin-resistant HL-60 cells (HL-60/ADR). Furthermore, curcumin suppressed proliferation and promoted apoptosis of HL-60/ADR cells. Overexpression of HOTAIR reversed the regulatory effect of curcumin on apoptosis and migration and restored the effect of curcumin on inducing the expression of cleaved caspase3, Bax, and P27. In addition, HOTAIR upregulated WT1 expression by targeting miR-20a-5p, and inhibition of miR-20a-5p reversed the regulation of Adriamycin resistance by curcumin in AML cells. Finally, curcumin inhibited Adriamycin resistance by suppressing the HOTAIR/miR-20a-5p/WT1 pathway in vivo. In short, curcumin suppressed the proliferation and migration, blocked the cell cycle progression of AML cells, and sensitized AML cells to Adriamycin by regulating the HOTAIR/miR-20a-5p/WT1 axis. These findings suggest a potential role of curcumin and HOTAIR in AML treatment.		Lab Invest. 2021 Jul 19. doi: 10.1038/s41374-021-00640-3.
5374	LncRNA	LINC01089	miR-301b-3p	STARD13	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)	Rescue assay;	34281560	LINC01089 suppresses lung adenocarcinoma cell proliferation and migration via miR-301b-3p/STARD13 axis.	BACKGROUND: Lung adenocarcinoma (LUAD) is one of the most common cancers with high morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) serve as tumor promoters or suppressors in the development of various human malignancies, including LUAD. Although long intergenic non-protein coding RNA 1089 (LINC01089) suppresses the progression of breast cancer, its mechanism in LUAD requires further exploration. Thus, we aimed to investigate the underlying function and mechanism of LINC01089 in LUAD. METHODS: The expression of LINC01089 in LUAD and normal cell lines was detected. Functional assays were applied to measure cell proliferation, apoptosis and migration. Besides, mechanism experiments were employed for assessing the interplay among LINC01089, miR-301b-3p and StAR related lipid transfer domain containing 13 (STARD13). Data achieved in this study was statistically analyzed with Student's t test or one-way analysis of variance. RESULTS: LINC01089 expression was significantly down-regulated in LUAD tissues and cells and its overexpression could reduce cell proliferation and migration. Moreover, LINC01089 could regulate STARD13 expression through competitively binding to miR-301b-3p in LUAD. Additionally, rescue assays uncovered that STARD13 depletion or miR-301b-3p overexpression could countervail the restraining effect of LINC01089 knockdown on the phenotypes of LUAD cells. CONCLUSION: LINC01089 served as a tumor-inhibitor in LUAD by targeting miR-301b-3p/STARD13 axis, providing an innovative insight into LUAD therapies. Trial registration Not applicable.		BMC Pulm Med. 2021 Jul 19;21(1):242. doi: 10.1186/s12890-021-01568-6.
5375	LncRNA	DDX11-AS1	miR-514b-3p	RBX1	Esophageal Carcinoma Cell	Esophageal Cancer	Homo sapiens (human)  	qRT-PCR 	34281459	Long non-coding RNA DDX11-AS1 promotes esophageal carcinoma cell proliferation and migration through regulating the miR-514b-3p/RBX1 axis.	Esophageal carcinoma (ESCA) is one of the most aggressive malignancies with extremely high morbidity and mortality. At present, limited advancement in ESCA treatment has achieved. Therefore, it is urgent to explore the pathogenesis and progression mechanism of ESCA to provide the basis for the formulation of novel therapeutic strategies. Previous studies have found that long non-coding RNA (lncRNA) DDX11-AS1 expression enhances the paclitaxel resistance of ESCA cells. However, the mechanisms underlying the drug resistance conferred by lncRNA DDX11-AS1 in ESCA remains to be elucidated. Our research aims to clarify the role and mechanism of lncRNA DDX11-AS1 in regulating the progression of ESCA. We found that the expression of lncRNA DDX11-AS1 in ESCA tissues and cell lines was significantly upregulated. Subsequently, silencing lncRNA DDX11-AS1 significantly inhibited the proliferation, migration and invasion of ESCA cells, and induced the level of cell apoptosis. In terms of mechanism, our data showed that miR-514b-3p/RING box protein 1 (RBX1) axis played a crucial role in the oncogenic function of lncRNA DDX11-AS1. LncRNA DDX11-AS1 expression impaired the inhibitory function of miR-514b-3p on RBX1 through sponging effect. Taken together, our data support the notion that lncRNA DDX11-AS1 promotes the progression of ESCA through miR-514b-3p/RBX1 axis. Our research uncovers the novel regulatory role of lncRNA DDX11-AS1 in ESCA and lays a theoretical basis for developing novel treatment strategy of ESCA.		Bioengineered. 2021 Dec;12(1):3772-3786. doi: 10.1080/21655979.2021.1940617.
5376	LncRNA	MALAT1	miR-26a/26b	ST8SIA4	Breast Cancer Cell Lines	Breast Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	34278507	lncRNA MALAT1/miR-26a/26b/ST8SIA4 axis mediates cell invasion and migration in breast cancer cell lines.	Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is a long non-coding RNA that is overexpressed in various human cancers, including breast cancer. Evidence has associated the function of the a-2,8-sialyltransferase (ST8SIA) family with breast cancer. The present study aimed to investigate the potential roles of MALAT1 in breast cancer development and progression using analyses of both breast cancer tissues and cell lines. The mRNA levels of MALAT1, microRNA (miR)-26a/26b and ST8SIA4 were detected by reverse transcription-quantitative PCR (RT-qPCR) and the protein level of ST8SIA4 was assessed by western blot analysis. Cell proliferation, invasion and migration were detected by CCK-8, wound healing and Transwell assays, respectively. Interactions between MALAT1 and miR-26a/26b were assessed using fluorescence in situ hybridization, RNA immunoprecipitation and luciferase reporter assays. Herein, different levels of MALAT1 were primarily observed in human breast cancer samples and cells. Upregulated MALAT1 was a crucial predictor of poor breast cancer prognosis. Altered MALAT1 modulated cell progression in breast cancer. Moreover, miR-26a/26b was confirmed as a direct regulator of MALAT1, and ST8SIA4 was predicted as a target of miR-26a/26b. Functional analysis in human breast cancer cell lines demonstrated that MALAT1 modulated breast cancer cell tumorigenicity by acting as a competing endogenous lncRNA (ceRNA) to regulate ST8SIA4 levels by sponging miR-26a/26b. The identification of the MALAT1/miR-26a/26b/ST8SIA4 axis which contributes to breast cancer progression may constitute a potential new therapeutic target.		Oncol Rep. 2021 Aug;46(2):181. doi: 10.3892/or.2021.8132. Epub 2021 Jul 19.
5377	LncRNA	LINC01224	miR-485-5p	AKT3	Ec Cells	Endometrial Cancer	Homo sapiens (human)	Flow cytometry assay;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	34278482	Long non-coding RNA LINC01224 promotes cell proliferation and inhibits apoptosis by regulating AKT3 expression via targeting miR-485-5p in endometrial carcinoma.	Endometrial carcinoma (EC) is the most common cancer in women worldwide, yet little is known about the underlying molecular basis of EC development. LINC01224, a novel long non-coding (lnc)RNA, was recently identified as an oncogene in various types of cancer. However, the function and underlying mechanism of LINC01224 in EC is still unclear. A total of 50 pairs of tumor and adjacent normal tissue from patients with EC, three EC cell lines and one human normal endometrial stromal cell (ESC) line were subjected to reverse transcription-quantitative PCR assay to evaluate the expression levels of LINC01224. Cell Counting Kit-8, colony formation and flow cytometry assays were used to assess cell proliferation and apoptosis. Western blotting was used to measure expression levels of apoptosis- and proliferation-associated proteins and AKT3 protein. A xenograft model of HEC1A cells was established to validate the in vivo function of LINC01224 in EC tumor growth. Starbase 3.0 database prediction and luciferase reporter and RNA pull-down assays were performed to verify the binding sites between LINC01224 and microRNA (miR)-485-5p and miR-485-5p and AKT3. LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. The upregulation of LINC01224 was negatively associated with survival of patients with EC. Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells; LINC01224 directly bound to and downregulated miR-485-5p to elevate the expression levels of AKT3, thereby promoting EC progression. LINC01224 depletion in EC cells hindered tumor growth in a xenograft model. The tumor suppressing effect of LINC01224-knockdown on EC progression was partly rescued by treatment with miR-485-5p inhibitor. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR-485-5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.		Oncol Rep. 2021 Sep;46(3):186. doi: 10.3892/or.2021.8137. Epub 2021 Jul 19.
5378	LncRNA	DANCR	miR-135b-5p	KLF9	Multiple Myeloma Cells	Multiple Myeloma	Homo sapiens (human)  	Dual-luciferase reporter assay;MTT assay;Western blot;Luciferase reporter assay;MTT assay;	34278459	Long non-coding RNA DANCR represses the viability, migration and invasion of multiple myeloma cells by sponging miR-135b-5p to target KLF9.	Multiple myeloma (MM) is a malignancy of plasma cells that leads to marrow failure and bone lesions. Numerous studies have verified the link between long non-coding RNAs (lncRNAs) and MM. The present study aimed to examine the role and underlying mechanism of differentiation antagonizing non-protein coding RNA (DANCR) in MM cells. The relative expression levels of DANCR, microRNA (miR)-135b-5p and Krüppel-like factor 9 (KLF9) were examined using reverse transcription-quantitative PCR. Cell viability was assessed using the MTT assay, while relative cell migration and invasion were evaluated using Transwell assays. Moreover, the dual-luciferase reporter assay was used to examine the interplay between DANCR, miR-135b-5p and KLF9. Western blotting was performed to determine the expression level of KLF9. It was found that lncRNA DANCR and KLF9 were downregulated, while miR-135b-5p was upregulated in the serum of patients with MM and in MM cells compared with the controls. Overexpressing DANCR or knocking down miR-135b-5p reduced the viability of the MM cells, as well as restrained MM cells from migrating and invading. Furthermore, DANCR directly targeted miR-135b-5p and was negatively correlated with miR-135b-5p. It was also found that KLF9 was targeted by miR-135b-5p and was inversely correlated with miR-135b-5p expression. The impact of lncRNA DANCR-mediated suppression on cell viability, invasion and migration was partially abolished by short hairpin RNA KLF9 or miR-135b-5p mimics transfection in MM cells. Thus, it was suggested that lncRNA DANCR repressed the viability, migration and invasion of MM cells by sponging miR-135b-5p to target KLF9.		Mol Med Rep. 2021 Sep;24(3):649. doi: 10.3892/mmr.2021.12288. Epub 2021 Jul 19.
5379	LncRNA	FBXL19-AS1	miR-431	PBOV1	Npc Tissues And Cells	Nasopharyngeal Cancer	Homo sapiens (human)  	qRT-PCR 	34278444	FBXL19-AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR-431 and upregulate PBOV1.	Long non-coding RNAs (lncRNAs) have been shown to function as crucial regulators in the progression of various types of cancer, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the mechanisms underlying the role of the FBXL19-AS1/microRNA (miR)-431/prostate and breast cancer overexpressed 1 (PBOV1) axis in the progression of NPC. The expression levels of FBXL19-AS1, miR-431 and PBOV1 were assessed by reverse transcription-quantitative PCR. The Cell Counting Kit-8 assay was utilized to detect cell viability. Cell migration and invasion were determined using a Transwell assay. The associations between FBXL19-AS1 and miR-431 or miR-431 and PBOV1 were verified via bioinformatics analysis, dual-luciferase and RNA-binding protein immunoprecipitation assays. It was demonstrated that the expression levels of FBXL19-AS1 and PBOV1 were upregulated in NPC tissues and cells, whereas miR-431 expression was downregulated. FBXL19-AS1 directly interacted with miR-431. FBXL19-AS1 silencing inhibited the viability, migration and invasion of C666-1 and SUNE1 cells, whereas these effects could be alleviated by suppressing miR-431. miR-431 could target the 3'-untranslated region of PBOV1. Overexpression of PBOV1 neutralized the miR-431-mediated suppression of NPC progression. Moreover, FBXL19-AS1 could regulate PBOV1 by sponging miR-431 in NPC cells. In conclusion, the lncRNA FBXL19-AS1 accelerated NPC progression via the miR-431/PBOV1 axis, suggesting that it may serve as a potential therapeutic target for patients with NPC.		Mol Med Rep. 2021 Sep;24(3):647. doi: 10.3892/mmr.2021.12286. Epub 2021 Jul 19.
5380	LncRNA	TCONS_00004099	NA	PTPRF	U87 And U251 Cell Lines	Glioma	Homo sapiens (human)	Flow cytometry assay;qPCR;Western blot;Flow Cytometry assay;	34277823	LncRNA TCONS_00004099-derived microRNA regulates oncogenesis through PTPRF in gliomas.	BACKGROUND: Glioblastoma is the most common and aggressive primary tumor in the central nervous system (CNS). Patients with glioblastomas have poor prognosis due to its aggressive clinical behavior and resistance to the chemotherapeutic agent temozolomide (TMZ). Aberrant long non-coding RNAs (lncRNAs) are involved in glioma progression and its regulatory mechanisms. Analysis of sequencing data identified a new lncRNA, named lncRNA TCONS_00004099, which could derive a new microRNA and was highly expressed in glioma. METHODS: To elucidate the role of lncRNA TCONS_00004099 in gliomas, Quantitative Real-time PCR (qPCR) was used to assess the differential expression of lncRNA TCONS_00004099 and its related miRNA in glioma tissues, normal brain tissues, glioma cell lines (U87 and U251 cells), and a normal human embryonic brain cell line (HEB). Cell Counting Kit-8 (CCK8) assays to assess cell proliferation, flow cytometry assays examining apoptosis and the cell cycle, colony formation assays, wound healing assay, transwell assays, and zebrafish xenograft models were performed to further clarify the effects of the lncRNA and the related miRNA. Finally, Western blots were carried out to verify the mechanisms related to PTPRF (Protein Tyrosine Phosphatase Receptor Type F). RESULTS: LncRNA TCONS_00004099 was significantly increased in glioma tissues and glioma cell lines. A novel miRNA (miRNA TCONS_00004099) derived from the lncRNA was identified by qPCR. Knockdown of this lncRNA suppressed cell proliferation, migration, invasion and enhanced TMZ-induced apoptosis in U87 and U251 cell lines in vitro and in vivo. The miRNA mimics or inhibitor of miRNA TCONS_00004099 was used to reverse the effects of knockdown or overexpression of lncRNA TCONS_00004099, respectively. Western Blot analyses verified that PTPRF is one of the downstream targets of lncRNA TCONS_00004099. CONCLUSIONS: These results demonstrated that lncRNA TCONS_00004099 promoted malignant behaviors in gliomas, including proliferation, metastasis, and anti-apoptosis. The effect of lncRNA TCONS_00004099 was mediated through miRNA TCONS_00004099 and its target PTPRF. Thus, the lncRNA TCONS_00004099/miRNA/PTPRF axis may be a potential therapeutic target for gliomas.		Ann Transl Med. 2021 Jun;9(12):1023. doi: 10.21037/atm-21-2442.
5381	LncRNA	TCONS_00004099	NA	PTPRF	U87 And U251 Cell Lines	Glioma	Danio rerio (zebrafish)	Flow cytometry assay;qPCR;Western blot;Flow Cytometry assay;	34277823	LncRNA TCONS_00004099-derived microRNA regulates oncogenesis through PTPRF in gliomas.	BACKGROUND: Glioblastoma is the most common and aggressive primary tumor in the central nervous system (CNS). Patients with glioblastomas have poor prognosis due to its aggressive clinical behavior and resistance to the chemotherapeutic agent temozolomide (TMZ). Aberrant long non-coding RNAs (lncRNAs) are involved in glioma progression and its regulatory mechanisms. Analysis of sequencing data identified a new lncRNA, named lncRNA TCONS_00004099, which could derive a new microRNA and was highly expressed in glioma. METHODS: To elucidate the role of lncRNA TCONS_00004099 in gliomas, Quantitative Real-time PCR (qPCR) was used to assess the differential expression of lncRNA TCONS_00004099 and its related miRNA in glioma tissues, normal brain tissues, glioma cell lines (U87 and U251 cells), and a normal human embryonic brain cell line (HEB). Cell Counting Kit-8 (CCK8) assays to assess cell proliferation, flow cytometry assays examining apoptosis and the cell cycle, colony formation assays, wound healing assay, transwell assays, and zebrafish xenograft models were performed to further clarify the effects of the lncRNA and the related miRNA. Finally, Western blots were carried out to verify the mechanisms related to PTPRF (Protein Tyrosine Phosphatase Receptor Type F). RESULTS: LncRNA TCONS_00004099 was significantly increased in glioma tissues and glioma cell lines. A novel miRNA (miRNA TCONS_00004099) derived from the lncRNA was identified by qPCR. Knockdown of this lncRNA suppressed cell proliferation, migration, invasion and enhanced TMZ-induced apoptosis in U87 and U251 cell lines in vitro and in vivo. The miRNA mimics or inhibitor of miRNA TCONS_00004099 was used to reverse the effects of knockdown or overexpression of lncRNA TCONS_00004099, respectively. Western Blot analyses verified that PTPRF is one of the downstream targets of lncRNA TCONS_00004099. CONCLUSIONS: These results demonstrated that lncRNA TCONS_00004099 promoted malignant behaviors in gliomas, including proliferation, metastasis, and anti-apoptosis. The effect of lncRNA TCONS_00004099 was mediated through miRNA TCONS_00004099 and its target PTPRF. Thus, the lncRNA TCONS_00004099/miRNA/PTPRF axis may be a potential therapeutic target for gliomas.		Ann Transl Med. 2021 Jun;9(12):1023. doi: 10.21037/atm-21-2442.
5382	LncRNA	NEAT1	miR-218-5p	TPD52	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34277808	Tumor protein D52 promotes breast cancer proliferation and migration via the long non-coding RNA NEAT1/microRNA-218-5p axis.	BACKGROUND: Breast cancer is an aggressive disease with high morbidity and mortality rates among women globally. Tumor protein D52 (TPD52) is an oncogene in breast cancer; however, its physiological function remains elusive. This study set out to obtain a deeper understanding of the functions of TPD52 in the pathophysiology of breast cancer by exploring its effects on breast cancer cell proliferation and migration. METHODS: Bioinformatics analysis was performed to predict the bonding of TPD52 and nuclear paraspeckle assembly transcript 1 (NEAT1) with miR-218-5p. The bonding of TPD52 and NEAT1 with miR-218-5p were verified by luciferase reporter assays. The mRNA expression of TPD52, miR-218-5p or NEAT1 were tested by Rt-qPCR and the protein expression of TPD52 was tested by western blot. Colony formation and EdU assays were carried out to evaluate cell proliferation. Wound healing and Transwell assays were used to evaluate migration. RESULTS: In this study, TPD52 was upregulated in breast cancer cells, and silencing of TPD52 repressed the proliferation and migration of breast cancer cells in vitro and in vivo. Further, microRNA (miR)-218-5p reduced the expression level of TPD52, while overexpression of TPD52 attenuated the effects of miR-218-5p mimics on breast cancer cell proliferation and migration. Also, NEAT1 acted as a competitive endogenous sponge of miR-218-5p to downregulate free miR-218-5p levels. It was further observed that TPD52 overexpression recovered the inhibition of breast cancer cell growth and migration caused by NEAT1 downregulation. These results confirmed the functions of NEAT1 in breast cancer and supported the mechanism of the NEAT1/miR-218-5p/TPD52 axis. CONCLUSIONS: Our findings highlight the important role of the NEAT1/miR-218-5p/TPD52 axis in breast cancer cell proliferation and migration. This axis may be a potential therapeutic target for breast cancer.		Ann Transl Med. 2021 Jun;9(12):1008. doi: 10.21037/atm-21-2668.
5383	LncRNA	Vof16	miR-205	Gnb3	Rats	Diabetes Mellitus	Rattus (rat)	microarray;luciferase assay;	34277765	Vof16-miR-205-Gnb3 axis regulates hippocampal neuron functions in cognitively impaired diabetic rats.	BACKGROUND: Diabetes is a chronic metabolic disease and an independent risk factor for cognitive damage. Non-protein coding RNAs, including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), are involved in various pathophysiological conditions. METHODS: In this study, cognitive impairment was induced in diabetics rats by streptozotocin (STZ) injection, and the differential lncRNAs and mRNAs in rat hippocampal tissue between control and STZ-treated groups were analyzed with microarray. RESULTS: In the hippocampus of STZ-treated diabetic rats, lncRNA Vof-16, and Gnb3 mRNA were significantly upregulated and silicon analysis showed that Vof-16 and miR-205 share the same miRNA response element (MRE). In addition, the overexpression of Vof-16 in primary hippocampal neurons inhibited the expression of miR-205, and vice versa. Dual luciferase assay verified the binding between Vof-16 and miR-205, and Vof-16 was seen to promote the proliferation of primary hippocampal neurons via sponging miR-205. Silicon analysis predicted that miR-205 could bind with Gnb3, which was verified with dual luciferase assay, and the overexpression of miR-205 could inhibit the protein level of Gnb3, which could be rescued by co-expression with Vof-16. In conclusion, lncRNA Vof-16 regulated Gnb3 expression by competitively binding to miR-205. CONCLUSIONS: These results provided a novel regulation axis for the pathogenesis of STZ-induced diabetes.		Ann Transl Med. 2021 Jun;9(12):965. doi: 10.21037/atm-21-2016.
5384	LncRNA	LINC00665	miR-195-5p	MYCBP	Lung Adenocarcinoma Samples And Cell Lines	Lung Adenocarcinoma	Homo sapiens (human)  	RNA pull-down assay;Luciferase reporter assay;RNA pull-down;	34277412	The Long Noncoding RNA LINC00665 Facilitates c-Myc Transcriptional Activity via the miR-195-5p MYCBP Axis to Promote Progression of Lung Adenocarcinoma.	Long noncoding RNAs (lncRNAs) have recently received growing substantial attention in cancer research due to their important roles in various cancer types. However, the underlying mechanisms and functions of lncRNAs, especially in lung adenocarcinoma (LUAD), remain elusive. Based on pan-cancer screening analyses, we identified that the noncoding RNA LINC00665 was up-regulated in lung adenocarcinoma, which was subsequently confirmed in clinical samples and cell lines. Higher expression of LINC00665 was positively associated with poor prognosis and advanced T stage. Next, using gain- and loss- of function approaches, we revealed that LINC00665 promotes cell proliferation, cell migration, invasion, and suppresses cell apoptosis in LUAD through in vitro and in vivo experiments. Additionally, our findings showed that LINC00665 was predominately localized in the cytoplasm so as to interact with Ago2 protein, which could function as miRNA sponges. The results of bioinformatics prediction and RNA pull-down assay indicated that LINC00665 directly interacted with miR-195-5p. This was also confirmed by fluorescence colocalization. Furthermore, luciferase reporter assay demonstrated that Myc binding protein (MYCBP, also called AMY-1), which enhanced c-Myc transcriptional activity, was the target gene of LINC00665 dependent on miR-195-5p. Finally, rescue functional assay results uncovered that the oncogenic capability of LINC00665 was dependent on miR-195-5p and c-Myc transcriptional activity. In summary, this work elucidates that LINC00665 accelerates LUAD progression via the miR-195-5p/MYCBP axis by acting as a competing endogenous RNA (ceRNA), suggesting that LINC00665 may represent a potential therapeutic target for clinical intervention of LUAD.		Front Oncol. 2021 Jul 1;11:666551. doi: 10.3389/fonc.2021.666551. eCollection 2021.
5385	LncRNA	PCAT6	miR-326	HNRNPA2B1	Pca Cells	Prostate Cancer	Mus musculus (mouse)	qPCR;RT-PCR;Western blot;	34277403	Enzalutamide-Induced Upregulation of PCAT6 Promotes Prostate Cancer Neuroendocrine Differentiation by Regulating miR-326/HNRNPA2B1 Axis.	Our previous studies have demonstrated that Enzalutamide-induced upregulation of long non-coding RNA p21 (lncRNA-p21) facilitates prostate cancer (PCa) neuroendocrine differentiation (NED). Given the important role of lncRNAs in PCa pathogenesis, and given that lots of lncRNAs are dys-regulated in neuroendocrine PCa (NEPC) patients, we next explored the biological function and underlying mechanism of lncRNA-PCAT6 (PCAT6) in mediating Enzalutamide-induced NED. The level of PCAT6 in Enzalutamide-treated PCa cells and NEPC samples were assessed using quantitative RT-PCR (qPCR). The effect of PCAT6 on PCa cell proliferation, invasion, and NED was evaluated through CCK-8, transwell, qPCR, western blot analysis, Xenograft mouse model, and in vivo lung metastasis model. We found that PCAT6 was highly expressed in NE-like cells (PC3, DU145, and NCI-H660) compared with androgen-sensitive LNCaP cells. PCAT6 was also highly expressed in NEPC tissues. Enzalutamide treatment resulted in a significant increase of PCAT6 level in a dose- and time-dependent fashion. Functionally, PCAT6 overexpression promoted NED of C4-2 cells, as evidenced by an increased expression of NE markers (NSE, ChgA, and SYP), whereas PCAT6 knockdown in NCI-H661 cells repressed NED. Furthermore, PCAT6 overexpression promoted PCa cell proliferation and invasion in vitro and in vivo. Mechanistically, PCAT6 functioned as competing endogenous (ce) RNA via absorbing miR-326, thus resulting in a de-suppression of Hnrnpa2b1 target gene. The current results demonstrate that PCAT6 acted as a tumor activator in PCa progression by sponging miR-326 and increasing Hnrnpa2b1 expression and that the PCAT6/miR-326/Hnrnpa2b1 signaling might be a new therapeutic target for PCa.		Front Oncol. 2021 Jun 30;11:650054. doi: 10.3389/fonc.2021.650054. eCollection 2021.
5386	LncRNA	UBE2CP3	miR-138-5p	ITGA2	Gc Cells	Gastric Cancer	Homo sapiens (human)  	Rescue assay;	34274947	The ELF3-regulated lncRNA UBE2CP3 is over-stabilized by RNA-RNA interactions and drives gastric cancer metastasis via miR-138-5p/ITGA2 axis.	LncRNAs play essential roles in tumorigenesis and tumor progression. Pseudogene UBE2CP3 is an antisense intronic lncRNA. However, the biological function of UBE2CP3 in gastric cancer (GC) remains unknown. In this study, we revealed that lncRNA UBE2CP3 was aberrantly upregulated in multiple independent gastric cancer cohorts, and its overexpression was clinically associated with poor prognosis in GC. UBE2CP3 was mainly located in cytoplasm and promoted migratory and invasive capacities of GC cells in vitro and in vivo. Mechanismly, a novel dysregulated ceRNA network UB2CP3/miR-138-5p/ITGA2 was identified in GC by transcriptome sequencing. Furthermore, rescue assay further confirmed that UBE2CP3 mainly promoted GC progression through miR-138-5p/ITGA2 axis. More importantly, our data proved that UBE2CP3/IGFBP7 could form an RNA duplex, thereby directly interacting with the ILF3 protein. In turn, this RNA-RNA interaction between IGFBP7 mRNA and UBE2CP3 mediated by ILF3 protein plays an essential role in protecting the mRNA stability of UBE2CP3. In addition, transcription factor ELF3 was identified to be a direct repressor of lncRNA UBE2CP3 in GC. Taken together, overexpression of UBE2CP3 promotes tumor progression via cascade amplification of ITGA2 upregulation in GC. Our finding has revealed that the dysregulation of UBE2CP3 is probably due to the downregulation of ELF3 and/or the overexpression of IGFBP7 mRNA in GC. Our findings reveal, for the first time, that UBE2CP3 plays crucial a role in GC progression by modulating miR-138-5p/ITGA2 axis, suggesting that UBE2CP3 may serve as a potential therapeutic target in GC.		Oncogene. 2021 Jul 17. doi: 10.1038/s41388-021-01948-6.
5387	LncRNA	MEG3	miR-493-5P	MIF	Neural Stem Cells	Ischemic Stroke	Homo sapiens (human)  	qRT-PCR;Western blot;	34273844	LncRNA MEG3 inhibits the proliferation of neural stem cells after ischemic stroke via the miR-493-5P/MIF axis.	OBJECTIVE: The proliferation of neural stem cells (NSCs(1)), or lack thereof, can have profound effects on brain tissue remodeling for ischemic stroke (IS(2)). In this study, we aimed to reveal the influence of the lncRNA MEG3/miR-493-5p/MIF axis on NSC proliferation after IS. METHODS: We established an oxygen glucose-deprivation/reoxygenation (OGD/R(3)) in vitro model of IS in NSCs. We evaluated NSC isolation efficiency and proliferation by NESTIN, SOX2, and PCNA immunofluorescence staining. MEG3 and miR-493-5P levels were assessed by quantitative real-time polymerase chain reaction (qRT-PCR(4)). Changes in MIF protein expression levels were analyzed using Western blotting. We then evaluated the role of MEG3 and miR-493-5p by transfection of si-MEG3, a miR-493-5p mimic, or miR-493-5p inhibitor. NSC proliferation was quantified using Cell Counting Kit-8 analysis. RESULTS: NESTIN and SOX2 were co-expressed in endogenous NSCs. Following OGD/R, MEG3 and miR-493-5P were significantly upregulated in NSCs, while MIF levels decreased and proliferation was inhibited. Knockdown of MEG3 inhibited miR-493-5p and rescued expression of MIF and PCNA, restoring cellular proliferation levels. In NSCs transfected with a miR-493-5p mimic or inhibitor, MIF levels were down- or upregulated, respectively. Consistently, transfection of a miR-493-5p mimic reduced NSC proliferation, while transfection with a miR-493-5p inhibitor or si-MEG3 rescued the inhibitory effect of OGD/R on NSC proliferation. After co-transfection of si-MEG3 and a miR-493-5p mimic of OGD/R-induced NSCs, levels of PCNA, an indicator of cellular proliferation, were significantly reduced. Conclusion MEG3 inhibits NSC proliferation of after IS via positive regulation of miR-493-5p and potential subsequent downregulation of MIF.		Biochem Biophys Res Commun. 2021 Sep 3;568:186-192. doi: 10.1016/j.bbrc.2021.06.033. Epub 2021 Jul 15.
5388	LncRNA	THAP9-AS1	miR-335-5p	SGMS2	Ecss Cells	Esophageal Squamous Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;Rescue assay;	34273804	LncRNA THAP9-AS1 accelerates cell growth of esophageal squamous cell carcinoma through sponging miR-335-5p to regulate SGMS2.	Esophageal squamous cell carcinoma (ESCC) is kind of common and aggressive malignant tumors with high incidence and mortality all over the world. Accumulating studies have reported that long non-coding RNAs (lncRNAs) can play a vital regulatory role in human cancers. THAP9 antisense RNA 1 (THAP9-AS1) has been identified as an oncogene in several cancers. But its role in ESCC remains to be studied. In our research, THAP9-AS1 expression in ESCC cell lines was analyzed by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration, invasion and apoptosis as well as EMT process were analyzed by 5-Ethynyl-2'-deoxyuridine ( EdU), Transwell, Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) and western blot experiments. The interplay of THAP9-AS1, miR-335-5p and sphingomyelin synthase 2 (SGMS2) was analyzed by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. We discovered that THAP9-AS1 was highly expressed in ESCC cell lines and that the knockdown of THAP9-AS1 inhibited proliferation, migration, and invasion as well as EMT of ECSS cells but enhanced cell apoptosis. Furthermore, miR-335-5p was proved to be sponged by THAP9-AS1 and its up-regulation could repress ESCC progression. Additionally, SGMS2 was verified to be the target gene of miR-335-5p. In rescue assay, SGMS2 overexpression could offset the suppressive role of THAP9-AS1 depletion on ESCC progression. In short, THAP9-AS1 accelerated cell growth of ESCC through sponging miR-335-5p to regulate SGMS2.		Pathol Res Pract. 2021 Aug;224:153526. doi: 10.1016/j.prp.2021.153526. Epub 2021 Jun 17.
5389	LncRNA	LUCAT1	miR-642a	ROCK1	H9C2 Cells	Sepsis-Induced Cardiac Damage	Homo sapiens (human)  	ELISA;MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	34272987	Knockdown of lncRNA LUCAT1 attenuates sepsis-induced myocardial cell injury by sponging miR-642a.	The heart is one of the most common organs involved in sepsis-induced organ dysfunction and about 50% septic patients complicated with myocardial injury. So far, the molecular mechanisms underlying sepsis-induced cardiac damage remain unclear. In this study we aimed to evaluate the effect of miR-642a on sepsis-induced cardiac injury in vitro and explore the possible lncRNA-microRNA mechanism. We first downloaded GSE101639 to identify differentially expressed genes (DEGs) in sepsis. The expression of miR-642a in LPS-induced H9C2 cells was detected by qRT-PCR. MTT assay, cell migration, flow cytometry analysis, ELISA, qRT-PCR and Western blotting analysis were applied to evaluating the effect of miR-642a mimic on LPS-induced H9C2 cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. The results showed miR-642a expression was decreased in septic patients and LPS-induced H9C2 cells. Besides, MiR-642a mimic promoted cell viability and migration, inhibited cell apoptosis of LPS-induced H9C2 cells. Bioinformatics analysis showed miR-642a directly targets with 3'-UTR of ROCK1. Moreover, LUCAT1 regulated ROCK1 expression act as a competing endogenous RNA (ceRNA) for miR-642a. Our data demonstrated that lncRNA LUCAT1 could function via sponging miR-642a to regulate ROCK1 expression in LPS-induced H9C2 cells. And knockdown of lncRNA LUCAT1 could suppress LPS-induced cardiac injury in vitro.		Mamm Genome. 2021 Jul 17. doi: 10.1007/s00335-021-09890-4.
5390	LncRNA	MIR200CHG	miR-200c/141-3p	NA	Breast Cancer Tissues	Breast Cancer	Homo sapiens (human)  	qRT-PCR 	34272387	Long non-coding RNA MIR200CHG promotes breast cancer proliferation, invasion, and drug resistance by interacting with and stabilizing YB-1.	Long non-coding RNAs (lncRNA) have been identified as key regulators of tumorigenesis and development. We aim to explore the biological functions and molecular mechanisms of lncRNA MIR200CHG in breast cancer. We found that MIR200CHG is highly expressed in breast cancer tissues and is related to the tumor size and histopathological grade. In vitro and in vivo experiments confirmed that MIR200CHG can promote breast cancer proliferation, invasion, and drug resistance. MIR200CHG directly binds to the transcription factor Y-box binding protein-1 (YB-1), and inhibits its ubiquitination and degradation. MIR200CHG regulates YB-1 phosphorylation at serine 102, thereby affecting the expression of genes related to tumor cell proliferation, apoptosis, invasion, and drug resistance. Additionally, MIR200CHG partially affects the expression of miR-200c/141-3p encoded by its intron region. Therefore, MIR200CHG can promote the proliferation, invasion, and drug resistance of breast cancer by interacting with and stabilizing YB-1, and has the potential to become a target for breast cancer treatment.		NPJ Breast Cancer. 2021 Jul 16;7(1):94. doi: 10.1038/s41523-021-00293-x.
5391	LncRNA	Lnc049808	miR-101	FUNDC1	Tnbc Cells	Triple Negative Breast Cancerr	Mus musculus (mouse)	microarray;RIP assay;RNA immunoprecipitation;RNA immunoprecipitation;	34272359	Melatonin inhibits triple-negative breast cancer progression through the Lnc049808-FUNDC1 pathway.	Melatonin has been reported to have tumor-suppressive effects via comprehensive molecular mechanisms, and long non-coding RNAs (lncRNAs) may participate in this process. However, the mechanism by which melatonin affects the function of lncRNAs in triple-negative breast cancer (TNBC), the most aggressive subtype of breast cancer, is still unknown. Therefore, we aimed to investigate the differentially expressed mRNAs and lncRNAs in melatonin-treated TNBC cells and the interaction mechanisms. Microarray analyses were performed to identify differentially expressed mRNAs and lncRNAs in TNBC cell lines after melatonin treatment. To explore the functions and underlying mechanisms of the mRNAs and lncRNAs candidates, a series of in vitro experiments were conducted, including CCK-8, Transwell, colony formation, luciferase reporter gene, and RNA immunoprecipitation (RIP) assays, and mouse xenograft models were established. We found that after melatonin treatment, FUNDC1 and lnc049808 downregulated in TNBC cell lines. Knockdown of FUNDC1 and lnc049808 inhibited TNBC cell proliferation, invasion, and metastasis. Moreover, lnc049808 and FUNDC1 acted as competing endogenous RNAs (ceRNAs) for binding to miR-101. These findings indicated that melatonin inhibited TNBC progression through the lnc049808-FUNDC1 pathway and melatonin could be used as a potential therapeutic agent for TNBC.		Cell Death Dis. 2021 Jul 16;12(8):712. doi: 10.1038/s41419-021-04006-x.
5392	LncRNA	CM3AP-AS1	miR-148a	ROCK1	Sclc Cells	Small Cell Lung Cancer	Homo sapiens (human)  	qPCR;Western blot;luciferase assay;RNA pull-down;	34271873	LncRNA MCM3AP-AS1 sponges miR-148a to enhance cell invasion and migration in small cell lung cancer.	BACKGROUND: MCM3AP-AS1 is a recently characterized lncRNA playing an oncogenic role in several cancers. However, its role in lung cancer remains unknown. Here, we aimed to explore the functions of MCM3AP-AS1 in small cell lung cancer (SCLC) and the possible underlying mechanisms. METHODS: MCM3AP-AS1 and ROCK1 levels in SCLC patients were analyzed by qPCR. RNA pull-down and luciferase assays were performed to analyze the interaction between MCM3AP-AS1 and miR-148a. ROCK1 mRNA and protein levels were detected by qPCR and Western blot, respectively. Cell invasion and migration were analyzed by Transwell assays. RESULTS: MCM3AP-AS1 was upregulated in patients with SCLC, and a high MCM3AP-AS1 level was accompanied by a low survival rate. The binding of MCM3AP-AS1 to miR-148a predicted by bioinformatics analysis was verified by RNA pull-down and luciferase assays. However, MCM3AP-AS1 and miR-148a did not affect each other's expression. ROCK1 was upregulated in SCLC tissues and positively correlated with MCM3AP-AS1. In SCLC cells, MCM3AP-AS1 overexpression increased ROCK1 and promoted cancer cell invasion and migration, while miR-148a overexpression showed the opposite effects and attenuated the effects of MCM3AP-AS1 overexpression on ROCK1 expression and cell behaviors. CONCLUSIONS: MCM3AP-AS1 sponges miR-148a, thereby increasing SCLC cell invasion and migration via upregulating ROCK1 expression.		BMC Cancer. 2021 Jul 16;21(1):820. doi: 10.1186/s12885-021-08365-8.
5393	LncRNA	ZFAS1	miR-138-5p	SESN2	Cardiomyocytes	Sepsis-Induced Myocardial Injury	Homo sapiens (human)  	ELISA;qRT-PCR;RNA pull-down assay;Western blot;RNA pull-down;	34271014	Molecular pathways in sepsis-induced cardiomyocyte pyroptosis: Novel finding on long non-coding RNA ZFAS1/miR-138-5p/SESN2 axis.	OBJECTIVE: ZNFX1 antisense RNA1 (ZFAS1) has been emerged as a tumor oncogene or suppressor. However, understanding the biological role and underlying molecular mechanism of ZFAS1 in sepsis induced myocardial injury (SIMI) requires more evidence. This study was assigned to probe the effect of lncRNA ZFAS1 on sepsis-induced pyroptosis in cardiomyocytes and its underlying mechanism. METHODS: Serums of 22 patients with sepsis-induced myocardial injury (SIMI) and 24 healthy controls were collected to determine the expression levels of ZFAS1 and miR-138-5p. Cardiomyocytes (H9C2) or rats were treated by lipopolysaccharide (LPS) to establish in vivo and in vitro sepsis models. H&E staining was applied to observe myocardial injury of rats. The interactions between ZFAS1 and miR-138-5p as well as miR-138-5p and SESN2 were determined by dual-luciferase reporter gene assay and RNA pull-down assay. TUNEL staining was applied to inspect apoptosis level and CCK-8 to measure cell viability. The mRNA levels of ZFAS1, miR-138-5p and SESN2 were measured by qRT-PCR, while the protein expressions of SESN2 and pyroptosis-related proteins (Caspase-1, ASC and NLRP3) were assessed by Western blotting. Levels of inflammatory factors (TNF-a, IL-1b, IL-6 and IL-18) were evaluated by ELISA. RESULTS: Patients with SIMI had suppressed ZFAS1 and increased miR-138-5p expression when compared with those in healthy controls. LPS treatment in rats triggered myocardial injury accompanied by interstitial edema and moderate inflammatory cell infiltration. Besides, LPS caused elevated cell apoptosis rate and enhanced cell pyroptosis and inflammation in sepsis cell models. However, ZFAS1 overexpression or SESN2 overexpression in LPS induced rats and in H9C2 cells had meliorated myocardial injury and inflammatory response, indicating that ZFAS1 and SESN2 can inhibit sepsis-induced pyroptosis of cardiomyocytes. MiR-138-5p is a target gene of ZFAS1, while miR-138-5p can negatively mediate SESN2. ZFAS1 alleviated sepsis induced cardiomyocyte pyroptosis by exerting competing endogenous RNA (ceRNA) function to indirectly regulate SESN2, which evidenced by loss and gain functions of ZFAS1 and SESN2. CONCLUSION: LncRNA ZFAS1 serves as a ceRNA of miR-138-5p to up-regulate the expression of SESN2, thereby ameliorating sepsis-induced cardiomyocyte pyroptosis.		Immunol Lett. 2021 Jul 13;238:47-56. doi: 10.1016/j.imlet.2021.07.003.
5394	LncRNA	LINC00205	miR-185-5p	NA	Luad Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qRT-PCR 	34270733	LINC00205 Promotes Tumor Malignancy of Lung Adenocarcinoma Through Sponging miR-185-5p.	The emerging role of long noncoding RNAs (lncRNAs) in cancer, especially in lung adenocarcinoma (LUAD), is attracting increasingly more attention as a potential therapeutic target. However, whether lncRNA LINC00205 regulates the malignancy of LUAD has not been characterized. In this study, we discovered that LINC00205 was markedly upregulated in LUAD tissues and cell lines and correlated with poor prognosis of patients with LUAD. Our data showed that LINC00205 promoted the migration and proliferation of LUAD cells in vitro and tumor growth in vivo. Notably, the tumor suppressor miR-185-5p was found to be a direct target of LINC00205. In addition, miR-185-5p diminished the promotion of cell proliferation and migration mediated by LINC00205, whereas miR-185-5p inhibition had the opposite effect. In summary, our results show that LINC00205 contributes to LUAD malignancy by sponging miR-185-5p, which provides new insight into LUAD progression.		Lab Med. 2021 Jul 16:lmab041. doi: 10.1093/labmed/lmab041.
5395	LncRNA	LINC00958	MiR-204-3p	KIF2A	Nsclc Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Luciferase reporter assay;	34269081	Knockdown of LncRNA LINC00958 Inhibits the Proliferation and Migration of NSCLC Cells by MiR-204-3p/KIF2A Axis.	Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Increasing evidence suggests that long non-coding RNAs (lncRNAs) function in the tumorigenesis of NSCLC. LINC00958, a newly identified lncRNA, has been reported to be closely linked to tumorigenesis in several cancers. However, its specific role in NSCLC remains unclear. In this study, we determined the expression of LINC00958 in NSCLC by RT-qPCR analysis and evaluated cell proliferation and migration by CCK-8 and transwell assays, respectively. We established a xenograft tumor model to examine the effect of LINC00958 on tumor growth in vivo. Luciferase reporter assays were performed to determine the interaction between LINC00958 and miR-204-3p and the interaction between miR-204-3p and KIF2A. We found that LINC00958 was up-regulated in NSCLC tissues and cell lines. Down-regulation of LINC00958 inhibited cell proliferation and migration in vitro and suppressed tumor growth in vivo. Besides, miR-204-3p was identified as a target of LINC00958 and miR-204-3p inhibitor could reverse the inhibitory effect of LINC00958 knockdown on proliferation and migration of NSCLC cells. We also validated that KIF2A, a direct target of miR-204-3p, was responsible for the biological role of LINC00958. KIF2A antagonized the effect of miR-204-3p on NSCLC cell proliferation and migration and was regulated by LINC00958/miR-204-3p. Taken together, these data indicate that the LINC00958/miR-204-3p/KIF2A axis is critical for NSCLC progression, which might provide a potential therapeutic target of NSCLC.		Cell Transplant. 2021 Jan-Dec;30:9636897211025500. doi: 10.1177/09636897211025500.
5396	LncRNA	MALAT1	miR-613	bax	Glioma Cell	Glioma	Homo sapiens (human)  	qRT-PCR;RT-PCR;	34268963	LncRNA MALAT1 promotes glioma cell growth through sponge miR-613.	PURPOSE: To explore the effect of LncRNA MALAT1 on the growth of glioma cells and its related mechanism. METHODS: The expression of LncRNA MALAT1 and its target gene miR-613 in glioma cells was detected by RT-PCR, and the proliferation, invasion and apoptosis rates and the expression of related proteins were detected by CCK-8, invasion and apoptosis rate tests. RESULTS: The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. Furthermore, the proliferation and invasion ability of glioma cells were evidently inhibited, the apoptosis rate was evidently enhanced, and the expressions of pro-apoptosis related proteins bax and Cle-Caspase-3 were up-regulated while the expression of anti-apoptosis related protein bcl-2 was down-regulated. CONCLUSION: LncRNA MALAT1 can promote the proliferation and invasion of glioma cells and inhibit the apoptosis of glioma cells by sponging miR-613. LncRNA MALAT1 can be applied as a new potential target for glioma treatment.		J BUON. 2021 May-Jun;26(3):984-991.
5397	LncRNA	MALAT1	miR-613	Cle-Caspase-3	Glioma Cell	Glioma	Homo sapiens (human)  	qRT-PCR;RT-PCR;	34268963	LncRNA MALAT1 promotes glioma cell growth through sponge miR-613.	PURPOSE: To explore the effect of LncRNA MALAT1 on the growth of glioma cells and its related mechanism. METHODS: The expression of LncRNA MALAT1 and its target gene miR-613 in glioma cells was detected by RT-PCR, and the proliferation, invasion and apoptosis rates and the expression of related proteins were detected by CCK-8, invasion and apoptosis rate tests. RESULTS: The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. Furthermore, the proliferation and invasion ability of glioma cells were evidently inhibited, the apoptosis rate was evidently enhanced, and the expressions of pro-apoptosis related proteins bax and Cle-Caspase-3 were up-regulated while the expression of anti-apoptosis related protein bcl-2 was down-regulated. CONCLUSION: LncRNA MALAT1 can promote the proliferation and invasion of glioma cells and inhibit the apoptosis of glioma cells by sponging miR-613. LncRNA MALAT1 can be applied as a new potential target for glioma treatment.		J BUON. 2021 May-Jun;26(3):984-991.
5398	LncRNA	MALAT1	miR-613	bcl-2	Glioma Cell	Glioma	Homo sapiens (human)  	qRT-PCR;RT-PCR;	34268963	LncRNA MALAT1 promotes glioma cell growth through sponge miR-613.	PURPOSE: To explore the effect of LncRNA MALAT1 on the growth of glioma cells and its related mechanism. METHODS: The expression of LncRNA MALAT1 and its target gene miR-613 in glioma cells was detected by RT-PCR, and the proliferation, invasion and apoptosis rates and the expression of related proteins were detected by CCK-8, invasion and apoptosis rate tests. RESULTS: The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. Furthermore, the proliferation and invasion ability of glioma cells were evidently inhibited, the apoptosis rate was evidently enhanced, and the expressions of pro-apoptosis related proteins bax and Cle-Caspase-3 were up-regulated while the expression of anti-apoptosis related protein bcl-2 was down-regulated. CONCLUSION: LncRNA MALAT1 can promote the proliferation and invasion of glioma cells and inhibit the apoptosis of glioma cells by sponging miR-613. LncRNA MALAT1 can be applied as a new potential target for glioma treatment.		J BUON. 2021 May-Jun;26(3):984-991.
5399	LncRNA	LOXL1-AS1	miR-377-3p	NFIB	Liver Cancer Cell	Liver Cancer	Homo sapiens (human)	Western blot;Luciferase reporter assay;Rescue assay;RNA pull-down;	34267816	lncRNA LOXL1-AS1 promotes liver cancer cell proliferation and migration by regulating the miR-377-3p/NFIB axis.	Liver cancer is becoming one of the most lethal malignancies due to its high incidence and mortality. Accumulating studies have indicated that long non-coding RNAs (lncRNAs) are critical regulators of the tumorigenesis and development of various types of cancer, including liver cancer. LncRNA LOXL1-antisense RNA 1 (LOXL1-AS1) has been identified as an oncogene in some types of human cancer; however, its role in liver cancer remains obscure. Reverse transcription-quantitative PCR was used to measure LOXL1-AS1 expression in liver cancer tissues and cells. Western blot, MTT, colony formation, glucose uptake and wound healing assays were used to explore the biological function of LOXL1-AS1 in liver cancer cells. Bioinformatics analysis and RNA pull-down and luciferase reporter assays were used to explore the molecular mechanism of LOXL1-AS1 in liver cancer cells. Statistical analysis was used to compare the experimental results of different groups. In the present study, LOXL1-AS1 expression was significantly upregulated in liver cancer tissues and cells compared with in normal liver tissues and cells, respectively. High LOXL1-AS1 expression was associated with poor clinical outcomes in patients with liver cancer. Furthermore, LOXL1-AS1-knockdown suppressed glucose metabolism, proliferation, migration and epithelial-mesenchymal transition (EMT) of liver cancer cells. Subsequently, LOXL1-AS1 acted as a microRNA (miR)-377-3p sponge, and nuclear factor I B (NFIB) was confirmed as the downstream target of miR-377-3p in liver cancer cells. Additionally, rescue assays suggested that NFIB overexpression countervailed the inhibitory influence of LOXL1-AS1 silencing on liver cancer cellular processes. The present study demonstrated that LOXL1-AS1 promoted glucose metabolism, proliferation, migration and EMT of liver cancer cells by sponging miR-377-3p and modulating NFIB, which may provide a novel insight for the treatment of liver cancer.		Oncol Lett. 2021 Aug;22(2):624. doi: 10.3892/ol.2021.12885. Epub 2021 Jun 29.
5400	LncRNA	ANRIL	miR-181a-5p	ANRIL	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34267814	Effects of lncRNA ANRIL-knockdown on the proliferation, apoptosis and cell cycle of gastric cancer cells.	Gastric cancer is one of the most common types of malignant tumor of the gastrointestinal tract worldwide. Cisplatin (DDP) is a commonly used chemotherapeutic drug in the clinic; however, the resistance of gastric cancer cells to DDP limits its efficacy. In the present study, drug-resistant gastric cancer cell lines were constructed using the stepwise continuous selection method, and the relative expression levels of long non-coding RNA (lncRNA) CDKN2B antisense RNA 1 (ANRIL) and microRNA (miR)-181a-5p were detected using reverse transcription-quantitative PCR. The knockdown of lncRNA ANRIL and miR-181a-5p expression was performed by transfection with shRNA-ANRIL and an miR-181a-5p inhibitor, respectively. Cellular proliferation and sensitivity to DDP were assessed using Cell Counting Kit-8 analysis. Cell apoptosis and cell cycle distribution were assessed using flow cytometry and western blotting. The binding relationships between ANRIL, miR-181a-5p and cyclin G1 (CCNG1) were verified using a dual luciferase reporter assay. The results revealed that the expression levels of miR-181a-5p were downregulated in all drug-resistant cell lines. ANRIL-knockdown inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest; however, following the knockdown of miR-181a-5p, the inhibition of cell cycle arrest was alleviated. Notably, miR-181a-5p, ANRIL and CCNG1 were found to have targeting relationships. In conclusion, the findings of the present study suggested that knocking down the expression of ANRIL inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest. Furthermore, its downstream target, miR-181a-5p, inhibited the proliferation of drug-resistant cells and enhanced their sensitivity to DDP.		Oncol Lett. 2021 Aug;22(2):621. doi: 10.3892/ol.2021.12882. Epub 2021 Jun 28.
5401	LncRNA	ANRIL	miR-181a-5p	CCNG1	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34267814	Effects of lncRNA ANRIL-knockdown on the proliferation, apoptosis and cell cycle of gastric cancer cells.	Gastric cancer is one of the most common types of malignant tumor of the gastrointestinal tract worldwide. Cisplatin (DDP) is a commonly used chemotherapeutic drug in the clinic; however, the resistance of gastric cancer cells to DDP limits its efficacy. In the present study, drug-resistant gastric cancer cell lines were constructed using the stepwise continuous selection method, and the relative expression levels of long non-coding RNA (lncRNA) CDKN2B antisense RNA 1 (ANRIL) and microRNA (miR)-181a-5p were detected using reverse transcription-quantitative PCR. The knockdown of lncRNA ANRIL and miR-181a-5p expression was performed by transfection with shRNA-ANRIL and an miR-181a-5p inhibitor, respectively. Cellular proliferation and sensitivity to DDP were assessed using Cell Counting Kit-8 analysis. Cell apoptosis and cell cycle distribution were assessed using flow cytometry and western blotting. The binding relationships between ANRIL, miR-181a-5p and cyclin G1 (CCNG1) were verified using a dual luciferase reporter assay. The results revealed that the expression levels of miR-181a-5p were downregulated in all drug-resistant cell lines. ANRIL-knockdown inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest; however, following the knockdown of miR-181a-5p, the inhibition of cell cycle arrest was alleviated. Notably, miR-181a-5p, ANRIL and CCNG1 were found to have targeting relationships. In conclusion, the findings of the present study suggested that knocking down the expression of ANRIL inhibited cellular proliferation, and promoted apoptosis and cell cycle arrest. Furthermore, its downstream target, miR-181a-5p, inhibited the proliferation of drug-resistant cells and enhanced their sensitivity to DDP.		Oncol Lett. 2021 Aug;22(2):621. doi: 10.3892/ol.2021.12882. Epub 2021 Jun 28.
5402	LncRNA	HOXA-AS2	miR-567	CDK8	Oscc Cells	Oral Squamous Cell Cancer	Homo sapiens (human)	qRT-PCR;Western blot;Luciferase report assay;	34267554	LncRNA HOXA-AS2 Promotes Tumor Progression by Suppressing miR-567 Expression in Oral Squamous Cell Carcinoma.	INTRODUCTION: Growing evidence suggests that long non-coding RNAs (lncRNAs), such as lncRNA HOXA-AS2, are critical regulators involved in human cancer. However, the biological functions and detailed mechanisms underlying how lncRNA HOXA-AS2 affects oral squamous cell carcinoma (OSCC) remain unexplored. METHODS: The expression of lncRNA HOXA-AS2 and miR-567 was determined in OSCC cell lines and clinical tissues by quantitative real-time PCR (qRT-PCR). Target site prediction and luciferase report assays were used to explore their potential interaction and binding sites between lncRNA HOXA-AS2 and miR-567. Overexpression or silencing expression of lncRNA HOXA-AS2 was performed to confirm that miR-567 was suppressed by lncRNA HOXA-AS2. WST-1 assay, crystal staining assay, and cell cycle analysis were used to assess the cell viability and proliferation ability. The target gene of miR-567 was predicted by Targetscan and validated by luciferase report assay as well as qRT-PCR and Western Blot. Xenograft nude mice model was done to demonstrate that lncRNA HOXA-AS2 promoted cell proliferation via targeting miR-567/CDK8 in vivo. RESULTS: LncRNA HOXA-AS2 was up-regulated in OSCC cells and tissues with the expression of miR-567 decreased. The tissue lncRNA HOXA-AS2 expression was found to positively correlate with the TNM stage and lymph node metastasis of OSCC patients. In terms of the mechanism, we found that lncRNA HOXA-AS2 negatively regulates miR-567 expression via a direct interaction. Functionally, overexpression of lncRNA HOXA-AS2 significantly promoted OSCC cell proliferation, while knockdown of lncRNA HOXA-AS2 significantly inhibited it. We also observed that miR-567 directly targets the 3' UTR of CDK8. Moreover, silencing lncRNA HOXA-AS2 inhibited tumor growth with the expression of miR-567 increased and CDK8 decreased in vivo. CONCLUSION: LncRNA HOXA-AS2 was up-regulated in OSCC, and its up-regulation correlated with poor clinical outcomes. The lncRNA also promoted OSCC cell proliferation by directly binding to miR-567, leading to an increase in CDK8 expression. The potential prognostic value of lncRNA HOXA-AS2 should be explored in future studies.		Cancer Manag Res. 2021 Jul 8;13:5443-5455. doi: 10.2147/CMAR.S305946. eCollection 2021.
5403	LncRNA	MEG3	miR-181b	NA	Brain Tissues	Intracerebral Hemorrhage	Rattus (rat)	Dual-luciferase reporter assay;ELISA;RACE;Flow Cytometry assay;Luciferase reporter assay;	34267173	lncRNA MEG3 Downregulation Relieves Intracerebral Hemorrhage by Inhibiting Oxidative Stress and Inflammation in an miR-181b-Dependent Manner.	BACKGROUND This study was designed to illustrate the effects and latent mechanism of lncRNA maternally expressed gene 3 (MEG3) on intracerebral hemorrhage (ICH)-induced brain injury. MATERIAL AND METHODS An ICH rat model was generated to determine the role of lncRNA MEG3 in ICH. The interaction between lncRNA MEG3 and microRNA (miR)-181b were confirmed by Starbase and dual-luciferase reporter assay. One hour (h) or 3 days after ICH stimulation, rat neurological injury was evaluated by modified Neurological Severity Score (mNSS). Brain water content and cell apoptosis were assessed using brain edema assessment and  flow cytometry (FCM), respectively. Caspase3 activity was also determined. Enzyme-linked immunosorbent assay (ELISA) was applied to evaluate the levels of pro-in flammatory cytokines. Moreover, the representative biomarkers of oxidative stress were evidenced using detection kits. RESULTS The lncRNA MEG3 level in ICH rat brain tissues was higher than that in the sham group. miR-181b was a direct target of lncRNA MEG3 and it was downregulated in brain tissues of ICH rats. Notably, we found that neurobehavioral scores, brain water content, and neuronal apoptosis were decreased and caspase3 activity was reduced in MEG3-shRNA-treated ICH rats, while we observed the opposite result in ICH+MEG3-shRNA+miR-181b inhibitor rats. Further analyses revealed that MEG3-shRNA inhibited inflammatory cytokines release and reduced oxidative stress. All these results were reversed by miR-181b inhibitor. In addition, MEG3-shRNA activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway, which was reversed by miR-181b inhibitor. CONCLUSIONS MEG3-shRNA restrained oxidative stress and inflammation following ICH in an miR-181b-dependent manner.		Med Sci Monit. 2021 Jul 16;27:e929435. doi: 10.12659/MSM.929435.
5404	LncRNA	LINC01116	miR-3612	GDF11	Melanoma Cells	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	34266696	LncRNA LINC01116 facilitates melanoma 1 progression via sequestering miR-3612 and up-regulating GDF11 and SDC3.	BACKGROUND: Melanoma is the deadliest cutaneous malignant tumor with high risks. Though increasing evidence has widely referred to the involvement of long non-coding RNAs (lncRNAs) in the mechanism of tumor development, including melanoma, the functional roles of most lncRNAs in melanoma remain to be explored. In this study, we focus on disclosing the role of long intergenic non-protein coding RNA 1116 (LINC01116) in melanoma. METHODS: Firstly, we detected LINC01116 expression through RT-qPCR. Functional analysis and animal experiments were carried out to assess the role of LINC01116 in vivo and in vitro. Western blot analysis was employed for detection of important markers regarding epithelial mesenchymal transition (EMT). In addition, RNA pulls down, RIP and luciferase reporter assays were performed to probe into the regulatory mechanism of LINC01116. RESULTS: LINC01116 was significantly up regulated in melanoma cells. LINC01116 deficiency abrogated cell proliferation, migration, invasion and EMT in melanoma. Moreover, LINC01116 enhanced growth differentiation factor 11 (GDF11) and syndecan 3 (SDC3) expression through sponging microRNA-3612 (miR-3612). The oncogenic role of the LINC01116/miR-3612/GDF11/SDC3 axis in melanoma was finally demonstrated. CONCLUSION: Conclusively, LINC01116 sequestered miR-3612 and targeted GDF11 and SDC3 to contribute to the progression of melanoma.		Arch Med Res. 2021 Jul 13:S0188-4409(21)00143-0. doi: 10.1016/j.arcmed.2021.06.008.
5405	LncRNA	LINC01116	miR-3612	SDC3	Melanoma Cells	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;	34266696	LncRNA LINC01116 facilitates melanoma 1 progression via sequestering miR-3612 and up-regulating GDF11 and SDC3.	BACKGROUND: Melanoma is the deadliest cutaneous malignant tumor with high risks. Though increasing evidence has widely referred to the involvement of long non-coding RNAs (lncRNAs) in the mechanism of tumor development, including melanoma, the functional roles of most lncRNAs in melanoma remain to be explored. In this study, we focus on disclosing the role of long intergenic non-protein coding RNA 1116 (LINC01116) in melanoma. METHODS: Firstly, we detected LINC01116 expression through RT-qPCR. Functional analysis and animal experiments were carried out to assess the role of LINC01116 in vivo and in vitro. Western blot analysis was employed for detection of important markers regarding epithelial mesenchymal transition (EMT). In addition, RNA pulls down, RIP and luciferase reporter assays were performed to probe into the regulatory mechanism of LINC01116. RESULTS: LINC01116 was significantly up regulated in melanoma cells. LINC01116 deficiency abrogated cell proliferation, migration, invasion and EMT in melanoma. Moreover, LINC01116 enhanced growth differentiation factor 11 (GDF11) and syndecan 3 (SDC3) expression through sponging microRNA-3612 (miR-3612). The oncogenic role of the LINC01116/miR-3612/GDF11/SDC3 axis in melanoma was finally demonstrated. CONCLUSION: Conclusively, LINC01116 sequestered miR-3612 and targeted GDF11 and SDC3 to contribute to the progression of melanoma.		Arch Med Res. 2021 Jul 13:S0188-4409(21)00143-0. doi: 10.1016/j.arcmed.2021.06.008.
5406	LncRNA	NEAT1	miR-381	IGF1	Ovarian Granulosa Cells	Polycystic Ovary Syndrome	Rattus (rat)	qRT-PCR 	34266430	Downregulating lncRNA NEAT1 induces proliferation and represses apoptosis of ovarian granulosa cells in polycystic ovary syndrome via microRNA-381/IGF1 axis.	OBJECTIVE: Researchers have revealed the combined functions of long noncoding RNAs (lncRNAs) and microRNA (miRNAs) in polycystic ovary syndrome (PCOS). This study aimed to understand the role of nuclear-enriched abundant transcript 1 (NEAT1) and miR-381 involving insulin-like growth factor 1 (IGF1) in PCOS. METHODS: PCOS rat model was established by dehydroepiandrosterone induction. NEAT1, miR-381 and IGF1 expression in ovarian granulosa cells of PCOS patients and ovarian tissues of PCOS rats were tested. Bioinformatics website and dual luciferase reporter gene assay were utilized to verify the relationship between NEAT1 and miR-381 and that between miR-381 and IGF1. Levels of sex hormone, pathological changes and ovarian granulosa cell apoptosis in ovarian tissues of PCOS rats were detected. Ovarian granulosa cell proliferation and apoptosis were analyzed in vitro. RESULTS: NEAT1 and IGF1 expression increased while miR-381 expression decreased in the ovarian granulosa cells of patients with PCOS and the ovarian tissues of PCOS rats. In in vivo experiments, interference with NEAT1 improved the levels of sex hormones, alleviated pathological changes and suppressed ovarian granulosa cell apoptosis in the ovarian tissues of PCOS rats. In in vitro cell experiments, interference with NEAT1 suppressed apoptosis and enhanced cell proliferation of ovarian granulosa cells. NEAT1 interference-mediated effect would be reversed by up-regulating miR-381. NEAT1 acted as a ceRNA to adsorb miR-381 to target IGF1. Overexpression of IGF1 reversed the inhibitory effect of miR-381 on ovarian granulosa cell apoptosis. CONCLUSION: Interference with NEAT1 increases miR-381 and reduces IGF1 levels, effectively improving the levels of sex hormones and reducing the pathological damage of ovarian tissue in rats with PCOS.		J Biomed Sci. 2021 Jul 15;28(1):53. doi: 10.1186/s12929-021-00749-z.
5407	LncRNA	CASC2	miR-18a-5p	IGF1	16Hbe Cells	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)  	Flow cytometry assay;qRT-PCR;Flow Cytometry assay;Luciferase reporter assay;	34266334	LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis.	AIMS: Chronic obstructive pulmonary disease (COPD) is a systemic disease. Several long non-coding RNAs (lncRNAs) have been identified to be aberrantly expressed in COPD patients. This study investigated the role of lncRNA cancer susceptibility candidate 2 (CASC2) in COPD, as well as its potential mechanism. METHODS: Fifty smokers with COPD and another 50 smokers without COPD were recruited. Receiver operating characteristic curve was constructed to assess the diagnostic value of CASC2 in COPD patients. 16HBE cells were treated with cigarette smoke extract (CSE) to establish a cell model. qRT-PCR was used for the measurement of mRNA levels. The cell viability and apoptosis were detected by using Cell Counting Kit-8 and flow cytometry assay. Enzyme-linked immunosorbent assay was performed to detect the levels of proinflammatory cytokines. Luciferase reporter assay was performed for the target gene analysis. RESULTS: Serum CASC2 was dramatically decreased in COPD patients compared with smokers without COPD, and was positively associated with FEV1 (forced expiratory volume in one second). Serum CASC2 was overexpressed in severe COPD patients, and had the diagnostic accuracy to distinguish COPD patients from smokers. CASC2 overexpression alleviated CSE-induced apoptosis and inflammation in 16HBE cells. CASC2 functions as a ceRNA of miR-18a-5p. Upregulation of miR-18a-5p reversed the influence of CASC2 on cell apoptosis and inflammation in 16HBE cells. IGF1 was the target gene of miR-18a-5p. CONCLUSION: CASC2 was downregulated in COPD patients and it might be a promising biomarker for the disease diagnosis. Overexpression of CASC2 might inhibit the bronchial epithelial cell apoptosis and inflammation via targeting miR-18a-5p/IGF1 axis.The reviews of this paper are available via the supplemental material section.		Ther Adv Respir Dis. 2021 Jan-Dec;15:17534666211028072. doi: 10.1177/17534666211028072.
5408	LncRNA	CCAT1	miR-218-5p	MTF2	Rb Cells	Retinoblastoma	Homo sapiens (human)  	Western blot;Luciferase reporter assay;	34265414	LncRNA CCAT1 sponges miR-218-5p to promote EMT, cellular migration and invasion of retinoblastoma by targeting MTF2.	Retinoblastoma (RB) is the primary neoplasms of the retina that is most common in pediatrics age. Long non-coding RNAs (lncRNAs) has been noticed for strong relation to the occurrence and progress of retinoblastoma. Previously, we have demonstrated that lncRNA colon cancer-associated transcript 1 (CCAT1) in two RB cell lines SO-RB50 and Y79 was obviously overexpressed, and notably, lncRNA CCAT1 attenuated miR-218-5p expressionand induced proliferation, cell migration and invasion. But, how lncRNA CCAT1 acts in RB development and the potential molecular mechanisms remain to be determined. In this study, the expression levels of lncRNA CCAT1 and miR-218-5p were evaluated in RB tissues by Q-PCR, which established the results in the cell lines. Further, lncRNA CCAT1 was shown to promote epithelial-to-mesenchymal transition (EMT), cellular migration and invasion of RB cells by functional analysis of downregulation and overexpression of lncRNA CCAT1 with specific siRNA and pcDNA transfection. By performing bioinformatics and dual luciferase reporter assay, we verified the direct interaction between lncRNA CCAT1 and miR-218-5p. Besides, bioinformatics analysis indicated that metal regulatory transcription factor 2 (MTF2) might be a potent novel target for miR-218-5p, which was further validated with luciferase reporter assay, Q-PCR and also Western blot analysis. Functional analysis and rescue analysis showed that lncRNA CCAT1 via competitive binding to miR-218-5p to modulate MTF2 expression thus accelerate EMT, cell migration and invasion of RB. In conclusion, here we identified the lncRNA CCAT1/miR-218-5p/MTF2 axis in RB cell lines. Our investigations on the function of lncRNA CCAT1 and the roles of the related molecules hint a novel potential target fo RB therapy.		Cell Signal. 2021 Oct;86:110088. doi: 10.1016/j.cellsig.2021.110088. Epub 2021 Jul 13.
5409	LncRNA	MIAT	miR-874-3p	IL1B	Serum	Ischemic Stroke	Homo sapiens (human)  	qRT-PCR 	34265390	Long non-coding RNA MIAT impairs neurological function in ischemic stroke via up-regulating microRNA-874-3p-targeted IL1B.	OBJECTIVE: Long non-coding RNAs (lncRNAs) have diagnostic and therapeutic values in the setting of ischemic stroke (IS). Here, we evaluated the value of myocardial infarction-associated transcript (MIAT) in IS with the involvement of microRNA (miR)-874-3p/interleukin (IL) 1B. METHODS: MIAT, miR-874-3p and IL1B levels in serum of patients with IS were measured. A middle cerebral artery occlusion (MCAO) model was established in mice. MCAO mice were injected with Agomir of miR-874-3p, shRNA or overexpression vector of MIAT or siRNA of IL1B. Subsequently, behavioral activities and neurological function of mice were assessed. The number of Nissl bodies, brain damage, neuronal apoptosis and inflammatory factors in brain tissues of mice were measured. The targeting relationship between MIAT and miR-874-3p, as well as that between miR-874-3p and IL1B was explored. RESULTS: In patients with IS, MIAT and IL1B were up-regulated and miR-874-3p was down-regulated. MIAT absorbed miR-874-3p while miR-874-3p targeted IL1B. Silencing of MIAT or IL1B, or promotion of miR-874-3p improved behavioral activities and neurological function of mice, reduced the number of Nissl bodies, as well as improved brain damage, neuronal apoptosis and inflammation. Overexpression of miR-874-3p abrogated up-regulated MIAT-mediated influence on MCAO mice. CONCLUSION: Shortly, this study figures out that MIAT impairs neurological function in IS via up-regulating miR-874-3p-targeted IL1B.		Brain Res Bull. 2021 Oct;175:81-89. doi: 10.1016/j.brainresbull.2021.07.005. Epub 2021 Jul 13.
5410	LncRNA	SVIL-AS1	miR-103a	ICE1	Luad Cells	Lung Adenocarcinoma	Homo sapiens (human)  	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	34264003	Identification of a competing endogenous RNA axis "SVIL-AS1/miR-103a/ICE1" associated with chemoresistance in lung adenocarcinoma by comprehensive bioinformatics analysis.	BACKGROUND: Chemotherapy is an important treatment for lung cancer. The molecular mechanism of lung adenocarcinoma (LUAD) chemoresistance is not completely understood. METHODS: Weighted gene co-expression network analysis (WGCNA) was applied to screen the modules related to chemosensitivity using the data of LUAD patients receiving chemotherapy in The Cancer Genome Atlas database. GDCRNATools package was used to establish competing endogenous RNA (ceRNA) network based on the key chemotherapy-related module. Kaplan-Meier and risk models were used to analyze the influence of genes in the ceRNA network on the prognosis of LUAD patients receiving chemotherapy. Cell counting kit-8, reverse transcription-quantitative PCR, and dual-luciferase reporter assay were used to detect the effects of abnormal expression of genes in the ceRNA network on the proliferation and IC50 of cisplatin (DDP)-resistant LUAD cells, and the targeting relationship of genes in the ceRNA network. The signaling pathways and functions of ICE1 in LUAD were analyzed by LinkOmics and CancerSEA databases, and validated by Western blot. RESULTS: Midnightblue module was the only WGCNA module positively correlated with chemosensitivity, in which the function of genes was related to cancer progression. SVIL-AS1/miR-103a/ICE1 was constructed based on midnightblue module. High expression of SVIl-AS1 and ICE1 corresponded to a favorable prognosis. High expression of miR-103a corresponded to a dismal prognosis. SVIl-AS1 was downregulated in DDP-resistant LUAD cells. SVIL-AS1 overexpression retarded the proliferation and DDP resistance of DDP-resistant LUAD cell. miR-103a was sponged by SVIL-AS1 and directly targeted ICE1. miR-103a overexpression and ICE1 knockdown overturned the suppressive effect of SVIL-AS1 overexpression on cell proliferation and DDP resistance. Further bioinformatics analysis and experimental verification showed that SVIL-AS1/miR-103a-3p/ICE1 axis can enhance DNA damage caused by chemotherapeutic agents. CONCLUSIONS: SVIL-AS1 inhibited chemoresistance by acting as a sponge for miR-103a and upregulating ICE1 expression, which may be a potential therapeutic target for chemotherapy in LUAD.		Cancer Med. 2021 Jul 15. doi: 10.1002/cam4.4132.
5411	LncRNA	NEAT1	miR-128-3p	ITGA5	Glioma Specimens And Cells	Glioma	Homo sapiens (human)	CCK-8 assay;RNA immunoprecipitation;RNA pull-down assay;RNA immunoprecipitation;RNA pull-down;	34263426	LncRNA NEAT1 Enhances Glioma Progression via Regulating the miR-128-3p/ITGA5 Axis.	Accumulating evidences indicate that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) promotes the progression of glioma. In this study, we postulated that NEAT1 may act as a miR-128-3p sponge. Relative levels of NEAT1 and miR-128-3p expression in human glioma samples and GBM cells were detected using quantitative real-time PCR. By means of CCK-8 assays, transwell assays, and flow cytometric analysis, the biological functions of miR-128-3p and NEAT1 were investigated in U87MG and U251MG human GBM cell lines with stable miR-128-3p and NEAT1 knockdown or overexpression. The luciferase reports, RNA pull-down assay, and RNA immunoprecipitation assay were conducted to determine the relevance of NEAT1 and miR-128-3p in glioma. As a result, high expression of NEAT1 and lack of miR-128-3p were observed in glioma specimens and cells. By binding to anti-oncogene miR-128-3p in the nucleus, NEAT1 enhanced tumorigenesis and glioma development. Further experiments suggested that ITGA5 expression was increased in glioma tissues and was found to be connected with miR-128-3p. Additionally, NEAT1 facilitated ITGA5 expression via competitively binding to miR-128-3p. For this reason, ITGA5 would not be decomposed by miR-128-3p and could activate FAK signaling pathway, thereby promoting cell growth. Collectively, these results indicated that the NEAT1/miR-128-3p/ITGA5 axis was involved in glioma initiation and progression, and might offer a potential novel strategy for treatment of glioma.		Mol Neurobiol. 2021 Jul 15. doi: 10.1007/s12035-021-02474-y.
5412	LncRNA	TCONS_00023297	miR-608	BMP2	Bone Marrow Mesenchymal Stem Cells	Osteoporosis	Homo sapiens (human)	microarray;RIP assay;	34262909	LncRNA TCONS_00023297 Regulates the Balance of Osteogenic and Adipogenic Differentiation in Bone Marrow Mesenchymal Stem Cells and the Coupling Process of Osteogenesis and Angiogenesis.	Long noncoding RNA (lncRNA) is a noncoding RNA with a length of more than 200 bases. It plays an important role in the occurrence and development of diseases. Research on lncRNAs has received increasing attention. Bone is an important organ of the human body. As the population ages, the incidence of osteoporosis gradually increases. The mechanism of action of lncRNAs in the development of osteoporosis is unclear. The imbalance between osteogenic and adipogenic differentiation in bone marrow mesenchymal stem cells (hBMSCs) and the coupling process of osteogenesis and angiogenesis plays an important role in the development of osteoporosis. Therefore, this study focused on the mechanism by which lncRNAs regulate the osteogenic differentiation of bone marrow mesenchymal stem cells and the mechanism of action of lncRNAs in bone metabolism. The expression of lncRNAs in the osteogenic differentiation of hBMSCs was detected by lncRNA microarray. Real-time quantitative PCR was used to detect the expression changes of lncRNA and osteogenic genes during hBMSC osteogenic and adipogenic differentiation. The ceRNA mechanisms were detected by RIP and luciferase reporter gene assays. The effect of lncRNAs on the osteogenesis-angiogenesis coupling process was detected by Transwell assays. TCONS_00023297 increased expression during osteogenic differentiation; TCONS_00023297 overexpression promoted osteogenic differentiation of hBMSCs; BMP2 regulated TCONS_00023297 expression in a concentration- and time-dependent manner; TCONS_00023297 regulated miR-608 via a ceRNA mechanism; TCONS_00023297 inhibited hBMSC adipogenic differentiation; and TCONS_00023297 promoted VEGF secretion by hBMSCs. TCONS_00023297 regulates osteogenic differentiation, adipogenic differentiation, and osteogenic-angiogenic coupling of hBMSCs via the TCONS_00023297/miR-608/RUNX2/SHH signaling axis.		Front Cell Dev Biol. 2021 Jun 28;9:697858. doi: 10.3389/fcell.2021.697858. eCollection 2021.
5413	LncRNA	SNHG11	miR-34b	LIF	Pancreatic Stellate Cells	Chronic Pancreatitis	Homo sapiens (human)	qRT-PCR;RIP assay;Western blot;	34261825	TGF-b1 induced proliferation, migration, and ECM accumulation through the SNHG11/miR-34b/LIF pathway in human pancreatic stellate cells.	Chronic pancreatitis (CP) is a chronic inflammatory and fibrotic disease of the pancreas, and activated pancreatic stellate cells (PSCs) play a vital role in the progression of pancreatic fibrosis in CP. It has been reported that long non-coding RNA small nucleolar RNA host gene 11 (SNHG11) is highly expressed in chronic pancreatitis (CP) patients. However, the role of SNHG11 in CP progression is unclear. The purport of the study was to survey the role of SNHG11 in CP. We employed transforming growth factor (TGF)-beta1 (TGF-b1) to activate human pancreatic stellate cells (PSCs). Expression of SNHG11 was assessed with qRT-PCR. Loss-of-function experiments were executed to evaluate the effects of SNHG11 on the proliferation and migration of TGF-b1-treated PSCs. Some protein levels were detected by western blotting. The regulatory mechanism of SNHG11 was verified by the dual-luciferase reporter and RIP assays. As a result, SNHG11 was upregulated in plasma of CP patients and TGF-b1-treated PSCs. Also, SNHG11 inhibition reduced TGF-b1-induced proliferation, migration, and ECM accumulation in PSCs. Mechanistically, SNHG11 regulated leukemia inhibitory factor (LIF) expression by sponging miR-34b. Furthermore, miR-34b inhibitor abolished SNHG11 silencing-mediated effects on TGF-b1-treated PSC proliferation, migration, and ECM accumulation. LIF overexpression counteracted the repressive influence of miR-34b mimic on proliferation, migration, and ECM accumulation of TGF-b1-treated PSCs. In conclusion, SNHG11 knockdown reduced TGF-b1-induced PSC proliferation, migration, and ECM accumulation by the miR-34b/LIF axis.		Endocr J. 2021 Jul 15. doi: 10.1507/endocrj.EJ21-0176.
5414	LncRNA	TCONS_00077866	miR-297b-5p	SAA3	Mouse Pancreatic B-Tc6 Cells	Type 2 Diabetes	Mus musculus (mouse)	Luciferase reporter assay;	34261739	Inhibition of lncRNA TCONS_00077866 ameliorates the high stearic acid diet-induced mouse pancreatic b-cell inflammatory response by increasing miR-297b-5p to downregulate SAA3 expression.	Long-term consumption of a high-fat diet increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on b-cells, but the underlying molecular mechanisms of this action have not been fully elucidated. Here, we evaluated the role of lncRNA TCONS_00077866 (lnc866) in SA-induced b-cell inflammation. lnc866 was selected for study because lncRNA high-throughput sequencing analysis demonstrated it to have the largest fold-difference in expression of five lncRNAs that were affected by SA treatment. Knockdown of lnc866 by virus-mediated shRNA expression in mice or by Smart Silencer in mouse pancreatic b-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and b-cell inflammation. According to lncRNA-microRNA (miRNAs)-mRNA co-expression network analysis and luciferase reporter assays, lnc866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3). Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in b-TC6 cells and mouse islets. In conclusion, lnc866 silencing ameliorates SA-induced b-cell inflammation by targeting the miR-297b-5p/SAA3 axis. lnc866 inhibition may represent a new strategy to protect b-cells against the effects of SA during the development of type 2 diabetes.		Diabetes. 2021 Jul 14:db201079. doi: 10.2337/db20-1079.
5415	LncRNA	OIP5-AS1	miR-26a-5p	TLR4	Ali Mice And Lps-Treated Primary Bronchial/Tracheal Epithelial Cells	Acute Lung Injury	Mus musculus (mouse)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34261477	Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis.	BACKGROUND: Acute lung injury (ALI) is a pulmonary disorder that leads to acute respiration failure and thereby results in a high mortality worldwide. Increasing studies have indicated that toll-like receptor 4 (TLR4) is a promoter in ALI, and we aimed to explore the underlying upstream mechanism of TLR4 in ALI. METHODS: We used lipopolysaccharide (LPS) to induce an acute inflammatory response in vitro model and a murine mouse model. A wide range of experiments including reverse transcription quantitative polymerase chain reaction, western blot, enzyme linked immunosorbent assay, flow cytometry, hematoxylin-eosin staining, RNA immunoprecipitation, luciferase activity and caspase-3 activity detection assays were conducted to figure out the expression status, specific role and potential upstream mechanism of TLR4 in ALI. RESULT: TLR4 expression was upregulated in ALI mice and LPS-treated primary bronchial/tracheal epithelial cells. Moreover, miR-26a-5p was confirmed to target TLR4 according to results of luciferase reporter assay. In addition, miR-26a-5p overexpression decreased the contents of proinflammatory factors and inhibited cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI by regulating TLR4. Afterwards, OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was identified to bind with miR-26a-5p. Functionally, OIP5-AS1 upregulation promoted the inflammation and miR-26a-5p overexpression counteracted the influence of OIP5-AS1 upregulation on cell inflammatory response and apoptosis. CONCLUSION: OIP5-AS1 promotes ALI by regulating the miR-26a-5p/TLR4 axis in ALI mice and LPS-treated cells, which indicates a promising insight into diagnostics and therapeutics in ALI.		BMC Pulm Med. 2021 Jul 14;21(1):236. doi: 10.1186/s12890-021-01589-1.
5416	LncRNA	PCGEM1	miR-590-3p	SOX11	Non-Small Cell Lung Cancer Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	RIP assay;Luciferase reporter assay;	34261474	LncRNA PCGEM1 induces proliferation and migration in non-small cell lung cancer cells through modulating the miR-590-3p/SOX11 axis.	BACKGROUND: Non-small cell lung cancer (NSCLC) is one of the most prevalent cancers. As reported, long non-coding RNAs (lncRNAs) induce various biological behaviors in cancers. LncRNA PCGEM1 prostate-specific transcript (PCGEM1) is reported to exert carcinogenic effect on certain cancers. Our research aimed to explore the role of PCGEM1 in NSCLC. METHODS: We enrolled forty NSCLC patients to explore PCGEM1 expression in clinical NSCLC tissues. Colony formation assay, CCK-8, Transwell assay were conducted to reveal cell proliferation, viability, migration and invasion. Luciferase reporter assay, RNA pull down, and RIP assay were performed to investigate the downstream axis of PCGEM1. RESULTS: PCGEM1 was significantly upregulated in NSCLC cells and tissues. Subsequently, in vitro loss-of-function experiments illustrated the carcinogenic role of PCGEM1 in NSCLC through promoting viability, proliferation, migration, and invasion. MiR-590-3p was confirmed to be a downstream gene of PCGEM1. Furthermore, SRY-box transcription factor 11 (SOX11) was verified to be a target of miR-590-3p. Additionally, rescue experiments indicated that miR-590-3p inhibitor or pcDNA3.1/SOX11 rescued the impacts of downregulated PCGEM1 on NSCLC cell proliferation, viability, migration and invasion. CONCLUSIONS: LncRNA PCGEM1 aggravated proliferative and migrative abilities in NSCLC via the miR-590-3p/SOX11 axis.		BMC Pulm Med. 2021 Jul 14;21(1):234. doi: 10.1186/s12890-021-01600-9.
5417	LncRNA	DLEU2	miR-30a-5p	ETS2	Ags And Mkn-45 Cells	Gastric Cancer	Homo sapiens (human)  	Flow cytometry assay;qRT-PCR;RACE;Western blot;Flow Cytometry assay;Immunohistochemistry;	34261460	lncRNA DLEU2 promotes gastric cancer progression through ETS2 via targeting miR-30a-5p.	BACKGROUND: Gastric cancer (GC) remains an important cancer worldwide. Further understanding of the molecular mechanisms of gastric carcinogenesis will enhance the diagnosis and treatment of GC. METHODS: The expression of DLEU2 and ETS2 was analyzed in several GC cell lines using GEPIA online analyze, qRT-PCR and immunohistochemistry. The biological behavior of GC cells was detected by CCK8, clone formation, transwell, wound healing, western blot, and flow cytometry assay. More in-depth mechanisms were studied. RESULTS: DLEU2 was significantly up-regulated in GC tissues and cell lines. The expression of DLEU2 was significantly associated with pathological grading and TNM stage of GC patients. Furthermore, knockdown of DLEU2 inhibited the proliferation, migration, and invasion of AGS and MKN-45 cells, while overexpression of DLEU2 promoted the proliferation, migration, and invasion of HGC-27 cells. MiR-30a-5p could directly bind to the 3' UTR region of ETS2. Moreover, DLEU2 bound to miR-30a-5p through the same binding site, which facilitated the expression of ETS2. Knockdown of DLEU2 reduced the protein level of intracellular ETS2 and inhibited AKT phosphorylation, while overexpression of DLEU2 induced the expression of ETS2 and the phosphorylation of AKT. ETS2 was highly expressed in GC tissues. The expression of ETS2 was significantly associated with age, pathological grading, and TNM stage. ETS2 overexpression promoted cell proliferation and migration of AGS and MKN-45 cells. Furthermore, ETS2 overexpression rescued cell proliferation and migration inhibition induced by DLEU2 down-regulation and miR-30a-5p up-regulation in AGS and MKN-45 cells. CONCLUSIONS: DLEU2 is a potential molecular target for GC treatment.		Cancer Cell Int. 2021 Jul 14;21(1):376. doi: 10.1186/s12935-021-02074-9.
5418	LncRNA	LINC00707	miR-382-5p	VEGFA	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	CCK-8 assay;	34258298	LINC00707 Regulates miR-382-5p/VEGFA Pathway to Enhance Cervical Cancer Progression.	Long noncoding RNAs (LncRNAs) are reported to exhibit crucial roles in cancer progression. LINC00707 is recently indicated to be a significant oncogene in various cancers. Up to now, the mechanism of LINC00707 in cervical cancer is still unclear. In this study, our present work was designed to study the biological effects of LINC00707 in cervical cancer. Firstly, the expression level of LINC00707 in cervical cancer was tested. We observed LINC00707 expression was greatly increased in cervical cancer. Then, we assessed the detailed effect of LINC00707 on the development of cervical cancer using CCK-8 assay, Transwell assays, and tumor xenograft experiments. Gain-of-function and loss-of-function assays revealed the function of LINC00707 in cervical cancer progression. In addition, the action of LINC00707 in cervical cancer cells was studied using bioinformatic tools and luciferase reporter experiment. It was displayed that loss of LINC00707 significantly repressed cell growth of cervical cancer. Meanwhile, restoration of LINC00707 expression obviously induced cervical cancer cell growth. Then, we predicted that LINC00707 could serve as a molecular sponge for miR-382-5p to modulate VEGFA expression in cervical cancer. Subsequently, lack of VEGFA expression reversed the influence of miR-382-5p knockdown on cervical cancer cells. In conclusion, our findings evidenced the significant role of LINC00707-miR-382-5p-VEGFA network in cervical cancer and it can provide an attractive target.		J Immunol Res. 2021 Jun 29;2021:5524632. doi: 10.1155/2021/5524632. eCollection 2021.
5419	LncRNA	TUG1	miR-9a-5p	BCL2L11	Human Pulmonary Microvascular Endothelial Cells	Chronic Obstructive Pulmonary Disease	Homo sapiens (human)	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34257718	lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR-9a-5p/BCL2L11 axis in chronic obstructive pulmonary disease.	The aim of the present study was to investigate the function of long non-coding RNA taurine-upregulated gene 1 (lncRNA TUG1) in chronic obstructive pulmonary disease and further assess the underlying molecular mechanisms. Flow cytometry analysis was performed to detect cell apoptosis of human pulmonary microvascular endothelial cells (HPMECs) treated with 1% cigarette smoke extract (CSE). The activity of caspase-3 was measured using a Caspase-3 Activity assay kit and the protein expression of cleaved caspase-3, caspase-3 and Bcl-2 like 11 (BCL2L11) were measured using western blotting. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure the expression of TUG1 mRNA levels in the treated cells. The association between TUG1, the miR-9a-5p/BCL2L11 axis and with miR-9a-5p were predicted and verified using a dual luciferase reporter assay system. The mRNA expression of miR-9a-5p and BCL2L11, and the transfection efficiency were measured by RT-qPCR. The results showed that CSE induced cell apoptosis and increased lncRNA TUG1 expression in HPMECs. CSE significantly reduced the expression of miR-9a-5p in HPMECs compared with the control group. TUG1-short hairpin RNA relieved cell apoptosis induced by CSE by upregulating miR-9a-5p in HPMECs. The present study predicted and verified that BCL2L11 is a direct target of miR-9a-5p. The mRNA expression of BCL2L11 was increased in HPMECs following CSE treatment compared with the control group. miR-9a-5p mimic and BCL2L11-plasmid markedly increased the expression of miR-9a-5p and BCL2L11, respectively. miR-9a-5p mimic reversed the increase in cell apoptosis induced by CSE by inhibiting BCL2L11 expression in HPMECs. To conclude, the present study demonstrated that lncRNA TUG1 exerted roles in cell apoptosis induced by CSE through modulating the miR-9a-5p/BCL2L11 axis.		Exp Ther Med. 2021 Aug;22(2):906. doi: 10.3892/etm.2021.10338. Epub 2021 Jun 25.
5420	LncRNA	SNHG11	miR-2355-5p	CBX5	Tnbc Cells	Triple Negative Breast Cancerr	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Flow Cytometry assay;	34257707	LncRNA SNHG11 aggravates cell proliferation and migration in triple-negative breast cancer via sponging miR-2355-5p and targeting CBX5.	Triple-negative breast cancer (TNBC) is one of the most common malignances worldwide. Concurrently, the incidence of TNBC has continued to rise in recent years. It is reported that long non-coding RNAs (lncRNAs) are involved in biological processes in numerous cancers including TNBC. Small nucleolar RNA host gene 11 (SNHG11) has already been studied and reported in some cancers. However, the role of SNHG11 in TNBC remains unknown. RT-qPCR was used to measure gene expression in the current study. CCK-8, colony formation, flow cytometry, Transwell and western blotting experiments were also performed to determine the biological function of SNHG11 in TNBC cells. Luciferase reporter and RIP assays were performed to measure relationship between genes. In the present study, the results indicated SNHG11 was highly expressed in TNBC tissues and cell lines. Moreover, SNHG11 aggravated cell proliferation and migration, and whereas it attenuated cell apoptosis in TNBC. Furthermore, SNHG11 sponged microRNA 2355-5p (miR-2355-5p) in TNBC. Silencing SNHG11 increased miR-2355-5p expression. In addition, chromobox 5 (CBX5) was identified to be targeted by miR-2355-5p in TNBC. It was also suggested that CBX5 silencing suppressed cell proliferation and migration. Furthermore, overexpressed CBX5 recovered the inhibitive influence of SNHG11 silencing on proliferative and migrative abilities of TNBC cells. Overall, SNHG11 acted as a tumor promoter in TNBC and regulated TNBC cell growth by modulating the miR-2355-5p/CBX5 axis, which indicated that it may be used as a biomarker for TNBC treatment.		Exp Ther Med. 2021 Aug;22(2):892. doi: 10.3892/etm.2021.10324. Epub 2021 Jun 18.
5421	LncRNA	SNHG3	miR-326	TWIST	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34257656	LncRNA SNHG3 Promotes Gastric Cancer Cells Proliferation, Migration, and Invasion by Targeting miR-326.	The function and possible mechanism of lncRNA Small Nucleolar RNA Host Gene 3 (SNHG3) in GC have not been fully studied. The aim of our study was to investigate the role of SNHG3 in the proliferation, migration, and invasion of GC cell lines. The expressions of SNHG3, miR-326, and TWIST in GC9811-P GC cell lines were detected by RT-qPCR. Western blotting was performed to detect the protein levels of TWIST and EMT-related genes. Luciferase reporter gene analysis and RNA immunoprecipitation (RIP) analysis confirmed the interaction between lncRNA SNHG3, miR-326, and TWIST. CCK-8 and Transwell assays were performed to detect cell proliferation, invasion, and migration abilities. The results showed that lncRNA SNHG3 and TWIST were highly expressed in GC cell lines, while miR-326 was expressed to a low degree. Moreover, lncRNA SNHG3 knockdown or miR-326 overexpression significantly inhibited cell proliferation, migration, and invasion of GC cell lines. In addition, TWIST overexpression can reverse the inhibition of lncRNA SNHG3 knockdown or miR-326 overexpression on cell proliferation, migration, and invasion. In conclusion, lncRNA SNHG3 may promote GC progression through the miR-326/TWIST axis, which may provide a new diagnostic and prognostic biomarker for GC.		J Oncol. 2021 Jun 28;2021:9935410. doi: 10.1155/2021/9935410. eCollection 2021.
5422	LncRNA	MALAT1	miR-491-5p	UBE2C	Lung Carcinoma Cells	Lung Carcinoma	Homo sapiens (human)  	qRT-PCR 	34257576	LncRNA MALAT1 Regulating Lung Carcinoma Progression via the miR-491-5p/UBE2C Axis.	Long noncoding RNAs (lncRNAs) play a critical role in the development of lung carcinoma. The mechanism of MALAT1 in lung carcinoma development is not understood very well. This study aimed to investigate the role of MALAT1 in lung carcinoma progression and the mechanism underlying the role of miR-491-5p in the MALAT1 mediated regulation of UBE2C expression. The results indicated that the expression of MALAT1 was often augmented in lung carcinoma cells. Suppression of MALAT1 blocked the proliferation, invasion and migration ability of cancer cells and inhibited the expression of UBE2C. UBE2C restoration attenuated the MALAT1 knockdown-induced anti-cancer effects. Moreover, UBE2C and MALAT1 were indicated as targets of miR-491-5p and inhibition of miR-491-5p restored the MALAT1 knockdown-induced inhibition of the progression of lung carcinoma. Furthermore, MALAT1 sponged miR-491-5p to upregulate UBE2C expression, causing it to act as a competing endogenous RNA. Collectively, MALAT1 downregulation suppressed lung carcinoma progression by regulating the miR-491-5p/UBE2C axis. These results indicate that MALAT1 could be a molecular target for lung carcinoma treatment and prognosis.		Pathol Oncol Res. 2021 Mar 29;27:610159. doi: 10.3389/pore.2021.610159. eCollection 2021.
5423	LncRNA	LINC00636	miR-450a-2-3p	MAPK1	Cardiac Fibroblasts (Cfs) And Human Umbilical Vein Endothelial Cells	Atrial Fibrillation	Homo sapiens (human)	qPCR;RT-qPCR;	34257520	Exosomes Containing LINC00636 Inhibit MAPK1 through the miR-450a-2-3p Overexpression in Human Pericardial Fluid and Improve Cardiac Fibrosis in Patients with Atrial Fibrillation.	The purpose of this study was to investigate the regulatory mechanism of miR-450a-2-3p in myocardial fibrosis in patients with atrial fibrillation. For this purpose, the expression profile of GSE55296 was extracted from the GEO database, and differentially expressed lncRNAs were identified. Gene ontology analysis of the target genes of mir-450a-2-3p indicated that there was a regulatory relationship between LINC00636 and miR-450a-2-3p. Further, the expression levels of the analyzed RNAs were confirmed by RT-qPCR. TGF-b1-induced cardiac fibroblasts (CFs) and human umbilical vein endothelial cells (HUVECs) were used to establish a myocardial fibrosis model and endothelium-mesenchymal transformation (EMT) model in vivo. We hypothesized that exosomes containing LINC00636 regulate the expression of miR-450a-2-3p. LINC00636 was positively correlated with the expression of miR-450a-2-3p. The overexpression of miR-450a-2-3p suppressed the MAPK1 expression in CFs, thereby inhibiting the expression of a-SMA, COL1, and COL3 and preventing CF proliferation. In HUVECs, the miR-450a-2-3p overexpression upregulated the expression of VE-Cadherin (VE-Cad) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) by inhibiting the mitogen-activated protein kinase 1 (MAPK1) expression, whereas the expression levels of vimentin, COL1, and COL3 decreased. These results indicate that LINC00636, which is present in human pericardial fluid, is an antifibrotic molecule that inhibits MAPK1 through the miR-450a-2-3p overexpression and improves cardiac fibrosis in patients with atrial fibrillation.		Mediators Inflamm. 2021 Jun 28;2021:9960241. doi: 10.1155/2021/9960241. eCollection 2021.
5424	LncRNA	MCM3AP-AS1	miR-126	VEGF	Hec-1 Cells	Endometrioid Carcinoma	Homo sapiens (human)  	Cell transfection;Cell transfection;qPCR;RT-qPCR;	34256796	The MCM3AP-AS1/miR-126/VEGF axis regulates cancer cell invasion and migration in endometrioid carcinoma.	BACKGROUND: Long non-coding RNA (lncRNA) MCM3AP-AS1 plays an oncogenic role in several malignancies, but its role in endometrioid carcinoma (EC) is unclear. This study was carried out to explore the role of MCM3AP-AS1 in EC. METHODS: A total of 60 EC patients were enrolled in this study. Expression levels of MCM3AP Antisense RNA 1 (MCM3AP-AS1), microRNA-126 (miR-126), and vascular endothelial growth factor (VEGF) in tissues and transfetced cells were measured by RT-qPCR. Cell transfections were performed to explore the interaction among MCM3AP-AS1, miR-126 and VEGF. Transwell assays were perfromed to evaluate the invasion and migration abilities of HEC-1 cells after transfection. RESULTS: MCM3AP-AS1 was upregulated in EC and predicted poor survival. MCM3AP-AS1 directly interacted with miR-126. In EC cells, overexpression of MCM3AP-AS1 and miR-126 did not significantly affect the expression of each other. In addition, overexpression of MCM3AP-AS1 increased the expression levels of VEGF, a target of miR-126. Moreover, overexpression of MCM3AP-AS1 and VEGF increased the migration and invasion rates of EC cells, while overexpression of miR-126 suppressed these cell behaviors. Overexpression of MCM3AP-AS1 attenuated the role of miR-126 in cell invasion and migration. CONCLUSIONS: Therefore, MCM3AP-AS1 may serve as a competing endogenous RNA (ceRNA) of miR-126 to upregulate VEGF, thereby regulating cancer cell behaviors in EC.		World J Surg Oncol. 2021 Jul 13;19(1):213. doi: 10.1186/s12957-021-02316-0.
5425	LncRNA	NEAT1	miR-135a	HIF1a	Glioma Cells	Bacterial Meningitis	Mus musculus (mouse)	Dual-luciferase reporter assay;Chromatin immunoprecipitation;Luciferase reporter assay;	34256086	Implication of long non-coding RNA NEAT1 in the pathogenesis of bacterial meningitis-induced blood-brain barrier damage.	PURPOSE: Blood-brain barrier (BBB) damage is closely related to various neurological disorders, including bacterial meningitis (BM). Determining a reliable strategy to prevent BBB damage in the context of infection would be highly desirable. In the present study, we investigated the implications of the long non-coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) in moderating BBB damage. METHODS: In vitro BBB models were developed by co-culturing hCMEC/D3 cells with glioma cells, whereupon the glioma-exposed endothelial cells (GECs) were treated with a series of mimics, inhibitors, overexpression plasmids, and shRNAs for evaluating whether NEAT1, microRNA-135a (miR-135a) and hypoxia-inducible factor 1a (HIF1a) mediated BBB integrity and permeability. Furthermore, the in vivo biological function of NEAT1 was validated in a mouse model of BBB damage. RESULTS: NEAT1 and HIF1a were determined to be up-regulated, while miR-135a was under-expressed in GECs. As demonstrated by chromatin immunoprecipitation and dual-luciferase reporter assays, NEAT1 could bind to miR-135a, and HIF1a was confirmed as a target of miR-135a. Either overexpression of NEAT1 or depletion of miR-135a impaired the integrity and augmented the permeability of BBB. However, HIF1a silencing could reverse the BBB damage induced by NEAT1 overexpression or by inhibition of miR-135a. In vivo experiments substantiated that knockdown of NEAT1 could alleviate BBB damage in living mice. CONCLUSIONS: Hence, NEAT1 knockdown prevents BBB disruption and exerts promise as a potential target for BM treatment.		Microvasc Res. 2021 Jul 10;138:104225. doi: 10.1016/j.mvr.2021.104225.
5426	LncRNA	FAM225B	miR-613	CCND2	Nasopharyngeal Carcinoma Cells	Nasopharyngeal Cancer	Homo sapiens (human)	qRT-PCR 	34255617	Long noncoding RNA FAM225B facilitates proliferation and metastasis of nasopharyngeal carcinoma cells by regulating miR-613/CCND2 axis.	Growing evidence has suggested that abnormally expressed long non-coding RNAs (lncRNAs) play critical regulatory roles in nasopharyngeal carcinoma (NPC) pathogenesis. Family with sequence similarity 225 member B (FAM225B) is a novel lncRNA that has been implicated in several human cancers, yet its role in the context of NPC remains largely unclear. The aim of this study was to determine the expression level of FAM225B and its clinical significance in NPC patients. We observed a remarkable increase of FAM225B in NPC tissues and cell lines compared with controls. Also, highly expressed FAM225B was closely correlated with advanced TNM stage, distant metastasis, and poor overall survival. Interestingly, loss-of-function analysis revealed that FAM225B knockdown significantly inhibited tumor growth in vitro and in vivo, and decreased the migratory and invasive capacity of NPC cells. Mechanically, FAM225B functioned as an endogenous sponge by competing for miR-613 binding to up-regulate CCND2 expression. More importantly, rescue experiments further demonstrated that the suppressive impacts of FAM225B knockdown on cell proliferation, migration and invasion were significantly reversed after CCND2 overexpression. Taken all together, these findings highlight FAM225B as an oncogene that promotes NPC proliferation and metastasis through miR-613/CCND2 axis.		Bosn J Basic Med Sci. 2021 Jun 17. doi: 10.17305/bjbms.2021.5691.
5427	LncRNA	PICSAR	miR-485-5p	NA	Hypertrophic Scar Fibroblasts	Hypertrophic Scar Formation	Homo sapiens (human)  	qPCR;Western blot;	34255190	LncRNA PICSAR binds to miR-485-5p and activates TGF-b1/Smad to promote abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and excessive deposition of extracellular matrix (ECM).	The purpose of this study is to explore whether LncRNA PICSAR binds to miR-485-5p and thereby activates TGF-b1/Smad signaling pathway, influencing the abnormal proliferation of fibroblasts and excessive deposition of ECM in hypertrophic scar formation. PICSAR and miR-485-5p expressions were detected by qPCR. Cell proliferation was examined by CCK-8. Protein expressions were determined by western blot. Immunofluorescence detected the Ki-67 expression. Dual-luciferase followed by immunoprecipitation was performed to verify the interaction between PICSAR and miR-485-5p. Interference with PICSAR inhibited the abnormal proliferation of hypertrophic scar fibroblasts (HSFs) and the excessive deposition of ECM. It was also confirmed in our study that MiR-485-5p is a direct target of PICSAR in HSFs. Additionally, inhibition of miR-485-5p reversed the effect of PICSAR knockdown in HSFs. LncRNA PICSAR binds to miR-485-5p and thereby activates TGF-b1/Smad signaling pathway, promoting the abnormal proliferation of fibroblasts and excessive deposition of ECM in hypertrophic scar formation.		Med Mol Morphol. 2021 Jul 13. doi: 10.1007/s00795-021-00296-4.
5428	LncRNA	AGAP2-AS1	miR-628-5p	FOXP2	Pca Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR 	34255057	AGAP2-AS1/miR-628-5p/FOXP2 feedback loop facilitates the growth of prostate cancer via activating WNT pathway.	Increasing studies have indicated the critical roles of long non-coding RNAs (lncRNAs) in the tumorigenesis of cancers. LncRNA AGAP2 antisense RNA 1 (AGAP2-AS1) can serve as an oncogenic role in some cancers, including prostate cancer (PCa). However, the underling mechanism of such lncRNA in PCa has not been fully studied. Therefore, it's meaningful to investigate the role and underlying mechanism of AGAP2-AS1 in PCa. AGAP2-AS1 was confirmed to be highly expressed in PCa cells. Functionally, AGAP2-AS1 silencing inhibited cell proliferation, migration, invasion and EMT process, and induced apoptosis. According to mechanism assays, AGAP2-AS1 sponged miR-628-5p, which was found to restrain PCa cell growth. Besides, FOXP2 was identified as a target gene of miR-628-5p, and its expression was negatively regulated by miR-628-5p and positively modulated by AGAP2-AS1. Importantly, we found that FOXP2 could function as the upstream gene of AGAP2-AS1. Through rescue experiments, we discovered that FOXP2 up-regulation countered AGAP2-AS1 knockdown-mediated inhibition on PCa cell growth. Finally, it was found that AGAP2-AS1 could activate WNT pathway, and LiCl could reverse the influence of AGAP2-AS1 on PCa biological behaviors. To conclude, AGAP2-AS1/miR-628-5p/FOXP2 feedback loop facilitated PCa cell growth via activating WNT pathway.		Carcinogenesis. 2021 Jul 13:bgab062. doi: 10.1093/carcin/bgab062.
5429	LncRNA	Linc00941	miR-877-3p	PMEPA1	Escc Cells	Esophageal Squamous Cancer	Homo sapiens (human)  	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34254950	Linc00941 regulates esophageal squamous cell carcinoma via functioning as a competing endogenous RNA for miR-877-3p to modulate PMEPA1 expression.	Esophageal squamous cell carcinoma (ESCC) represents one of the most common malignancies and is the fifth leading cause of cancer-related deaths. Long intergenic non-coding RNAs (lincRNAs) have been suggested to be dysregulated in various types of cancers, and a growing number of lincRNAs have been implicated to be functional in the ESCC progression. In this study, we examined the role of linc00941 in the ESCC progression and explored the underlying molecular mechanisms. The bioinformatics analysis identified the up-regulation of linc00941 in the ESCC tissues. Further in vitro studies showed that linc00941 was up-regulated in ESCC cell lines. The loss-of-function studies demonstrated that linc00941 knockdown suppressed ESCC cell proliferation, invasion and migration, and also suppressed the in vivo tumor growth. Furthermore, bioinformatics prediction along with luciferase reporter assay and RNA immunoprecipitation assay implied that linc00941 acted as a competing endogenous RNA for miR-877-3p, and linc00941 regulated ESCC cell progression via at least targeting miR-877-3p. Subsequently, miR-877-3p targeted prostate transmembrane protein, androgen induced 1 (PMEPA1) 3' untranslated region and repressed PMEPA1 expression in ESCC cells; overexpression of PMEPA1 attenuated the inhibitory effects of linc00941 knockdown on the ESCC cell progression. Linc00941 knockdown suppressed epithelial-mesenchymal transition (EMT) via targeting miR-877-3p/PMEPA1 axis in ESCC cells. In conclusion, our results indicated the oncogenic role of linc00941 in ESCC, and knockdown of linc00941 suppressed ESCC cell proliferation, invasion, migration and EMT via interacting with miR-877-3p/PMEPA1 axis.		Aging (Albany NY). 2021 Jul 13;13(13):17830-17846. doi: 10.18632/aging.203286. Epub 2021 Jul 13.
5430	LncRNA	LINC01287	miR-3529-5p	RNASEH2A	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)  	Rescue assay;	34254728	Long noncoding RNA LINC01287 promotes proliferation and inhibits apoptosis of lung adenocarcinoma cells via the miR-3529-5p/RNASEH2A axis under the competitive endogenous RNA pattern.	Lung adenocarcinoma (LUAD) is regarded as the most common type of lung cancer. The molecular targeted therapies for LUAD have being extensively studied. Ribonuclease H2 subunit A (RNASEH2A) is a nucleotide degrading enzyme gene that exerts great influence on cell proliferation, DNA replication and genomic stability. According to bioinformatics analysis, RNASEH2A expression in LUAD tissues is predicted to be upregulated and high expression of RNASEH2A might be related to lower survival rate in LUAD patients. In the present study, we investigated functions of RNASEH2A in LUAD. The mRNA RNASEH2A showed high expression in LUAD cells, and its knockdown inhibited proliferation and induced apoptosis in LUAD cells. RNASEH2A was found to be a target gene of microRNA miR-3529-5p after their expression levels and interaction being examined. Long noncoding RNA LINC01287 upregulated RNASEH2A expression in LUAD cells by combining with miR-3529-5p in a competitive way. Rescue assays revealed that the overexpression of RNASEH2A reversed the suppression of cell proliferation and the promotion of cell apoptosis induced by miR-3529-5p overexpression or LINC01287 knockdown. Finally, forkhead box A1 (FOXA1) interacted with RNASEH2A promoter and LINC01287 promoter to upregulate the expression levels of RNASEH2A and LINC01287 in LUAD cells. Overall, FOXA1-induced LINC01287 serves as a competing endogenous RNA to promote proliferation and inhibit apoptosis of LUAD cells via upregulation of RNASEH2A expression at the posttranscriptional level by competitively combining with miR-3529-5p.		Environ Toxicol. 2021 Jul 13. doi: 10.1002/tox.23325.
5431	LncRNA	XIST	miR-27a-3p	FOXO3	Neuro-2A (N2A) Cells	Cerebral Ischemia-Reperfusion Injury	Mus musculus (mouse)	RNA immunoprecipitation;RNA immunoprecipitation;	34254504	Long non-coding RNA XIST promotes cerebral ischemia/reperfusion injury by modulating miR-27a-3p/FOXO3 signaling.	Cerebral ischemia/reperfusion (I/R) injury leads to neuronal damage, which may cause disability and even mortality. Multiple studies have revealed that long non-coding RNAs (lncRNAs) serve pivotal roles in the pathogenesis of cerebral I/R injury. Therefore, the present study aimed to investigate whether the lncRNA X inactivate-specific transcript (XIST) protects neuronal cells from cerebral I/R injury. In the present study, reverse transcription-quantitative PCR demonstrated that XIST expression was upregulated in the brain tissues of an I/R mouse model and in oxygen and glucose deprivation/reperfusion (OGD/R)-treated Neuro-2a (N2a) cells. Knockdown of XIST alleviated cerebral injury, as well as reduced N2a cell apoptosis and reactive oxygen species (ROS) production. Additionally, luciferase reporter and RNA immunoprecipitation assays identified that XIST could bind with microRNA (miR)-27a-3p. It was found that miR-27a-3p expression was downregulated in the brain tissues of an I/R mouse model and in OGD/R-induced N2a cells. In addition, miR-27a-3p overexpression attenuated I/R-induced cerebral injury, and inhibited the apoptosis and ROS production of N2a cells. miR-27a-3p was found to target FOXO3. Silencing of FOXO3 alleviated cerebral injury, as well as inhibited N2a cell apoptosis and ROS production. Collectively, these findings indicated that XIST aggravated cerebral I/R injury by regulating miR-27a-3p/FOXO3 signaling, which may provide a novel insight into the treatment of cerebral I/R injury.		Mol Med Rep. 2021 Aug;24(2):566. doi: 10.3892/mmr.2021.12205. Epub 2021 Jul 13.
5432	LncRNA	NEAT1_1	miR-221-3p	uPAR	Fibroblast-Like Synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)  	qRT-PCR 	34254354	LncRNA NEAT1_1 suppresses tumor-like biologic behaviors of fibroblast-like synoviocytes by targeting the miR-221-3p/uPAR axis in rheumatoid arthritis.	Fibroblast-like synoviocytes (FLSs) are the predominant effector cells in the pathological progression of rheumatoid arthritis (RA). Therefore, elucidating the underlying molecular mechanism of the biologic behaviors in RA-FLSs will be helpful in developing the potent targets for the treatment of RA. We have previously documented that the tumor-like biologic behaviors of RA-FLSs are exacerbated by urokinase-type plasminogen activator receptor (uPAR), a specifically up-regulated receptor in RA-FLSs. Here, we investigate the further mechanism of uPAR and clarify its function in RA-FLSs. We demonstrate that miR-221-3p positively correlates to uPAR and regulates uPAR level in RA-FLSs. Simultaneously, one long noncoding RNA, nuclear paraspeckle assembly transcript 1_1 (NEAT1_1) is identified, which can predictively target miR-221-3p at three sites, indicating a strong possibility of being a competing endogenous RNA in RA-FLSs. Interestingly, NEAT1_1 and miR-221-3p can colocate in the nucleus and cytoplasm in RA-FLSs. Importantly, NEAT1_1 can act as a rheostat for the miR-221-3p/uPAR axis and the downstream JAK signaling. In line with the biologic function, NEAT1_1 negatively regulates the tumor-like characters, and cytokine secretions of RA-FLSs. Collectively, our data provide new insight into the mechanisms of NEAT1_1 in modulating RA-FLSs tumor-like behaviors. The targeting of NEAT1_1 and miR-221-3p/uPAR axis may have a promising therapeutic role in patients with RA.		J Leukoc Biol. 2021 Jul 12. doi: 10.1002/JLB.3A0121-067RRR.
5433	LncRNA	LINC00942	miR-5006-5p	FZD1	A549 And H1299 Cells	Lung Adenocarcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;MTT assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;MTT assay;	34253104	LINC00942 Promotes Tumor Proliferation and Metastasis in Lung Adenocarcinoma via FZD1 Upregulation.	BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported to play important roles in the progression of human cancers. Herein, bioinformatic analysis identified that LINC00942 was a highly overexpressed lncRNA in lung adenocarcinoma (LUAD). The present study aimed to explore the roles and possible molecular mechanisms of LINC00942 in LUAD. METHODS: First, on the basis of TCGA database, the expression and prognosis of LINC00942 were analyzed in LUAD tissues. Then, si-LINC00942 was transfected into A549 and H1299 cells to knockdown the expression of LINC00942. Cell viability was detected by MTT assay. Flow cytometry was used to analyze cell apoptosis. The expressions of PCNA, Bax, Bcl-2, and wnt/b-catenin pathway proteins were detected by western blotting. Dual-luciferase reporter assay was used to evaluate the regulatory relationship between LINC00942 and miR-5006-5p, or miR-5006-5p and FZD1. RESULTS: We discovered that LINC00942 was up-regulated in LUAD tissues compared with adjacent tissues. Besides, we found the increased LINC00942 expression was associated with poor survival. In addition, silencing of LINC00942 suppressed the proliferation, migration, invasion and facilitated the apoptosis of A549 and H1299 cells. Moreover, silencing of LINC00942 repressed the expression of PCNA, Bcl-2, and enhanced Bax expression in A549 and H1299 cells. Mechanically, LINC00942 exerted its effects via enhancing Wnt signaling. LINC00942 functioned as competing endogenous RNA (ceRNA) by binding to miR-5006-5p, upregulating the expression of FZD1, which was a direct target of miR-5006-5p. CONCLUSION: Our findings indicated that LINC00942/miR-5006-5p/FZD1 axis played important roles in LUAD growth through enhancing Wnt signaling. LINC00942/miR-5006-5p/FZD1 axis might serve as a potential biomarker and therapeutic target for LUAD treatment.		Technol Cancer Res Treat. 2021 Jan-Dec;20:1533033820977526. doi: 10.1177/1533033820977526.
5434	LncRNA	LOC366613	miR-532-5p	PTEN	Pc12 Cell Line	Cerebral Infarction	Mus musculus (mouse)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase activity assay;MTT assay;RNA pull-down;	34251959	Long non-coding RNA LOC366613 alleviates the cerebral ischemic injury via regulating the miR-532-5p/phosphatase and tensin homolog axis.	Cerebral infarction (CI) has become a leading cause of death in China. Long non-coding RNAs (lncRNAs) are intensively involved in the progression of CI. Here, we aimed to investigate the effects of lncRNA LOC366613 (LOC366613) on cerebral I/R injury, as well as its possible mechanism. Transient middle cerebral artery occlusion (MCAO) was used to establish a mouse model of cerebral I/R, and the PC12 cell line was used to establish an in vitro oxygen-glucose deprivation (OGD) injury model. The MTT assay was used to determine cell viability, and qRT-PCR was used to determine RNA levels. Western blotting was conducted to detect protein expression levels. The TUNEL assay and flow cytometry were used to measure cell apoptosis, and 2,3,5-triphenyltetrazolium chloride (TTC) was used to determine cerebral infarct volume. Finally, RNA pull-down and luciferase activity assays were used to examine interactions between miR-532-5p and LOC366613, as well as between miR-532-5p and phosphatase and tensin homolog (PTEN). LOC366613 was overexpressed in patients with cerebral I/R injury. In PC12 cells, knockdown of LOC366613 reduced the apoptosis rate and lactic acid dehydrogenase (LDH) expression, while increasing cell viability. Moreover, miR-532-5p was shown to be a target of LOC366613, as predicted. Downregulation of miR-532-5p reversed the effects of LOC366613 knockdown on PC12 cell apoptosis, LDH release, and cell viability. Finally, PTEN was verified as a target of miR-532-5p. LOC366613 participates in cerebral I/R injury by regulating the miR-532-5p/PTEN axis, potentially providing a new CI treatment target.		Bioengineered. 2021 Dec;12(1):2511-2522. doi: 10.1080/21655979.2021.1930966.
5435	LncRNA	H19	miR-146b-3p	NA	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34251499	LncRNA H19 modulated by miR-146b-3p/miR-1539-mediated allelic regulation in transarterial chemoembolization of hepatocellular carcinoma.	Transarterial chemoembolization (TACE) is an effective treatment for unresectable hepatocellular carcinoma (HCC) patients. Although overall survival (OS) of TACE-treated patients has been evidently prolonged, not all unresectable HCC patients can benefit from TACE. Genome-wide association studies identified multiple HCC susceptibility single nucleotide polymorphisms (SNPs). However, it is still unclear how lncRNAs and their functional SNPs impact therapeutic responses of TACE. In the study, we hypothesized that the functional lncRNA H19 SNP(s) might impact H19 expression and, thus, prognosis of TACE-treated HCC patients. We found that the H19 rs3741219 SNP was significantly associated with OS of HCC patients received TACE. Cox proportional hazards model demonstrated that the rs3741219 CC genotype was associated with longer OS and a 37% decreased death risk compared with the TT carriers after TACE therapy (P = 0.001). Interestingly, the rs3741219 T-to-C change led to allelic down-regulation of lncRNA H19 expression via creating the binding sites of miR-146b-3p and miR-1539. Luciferase reporter gene assays indicated that miR-146b-3p and miR-1539 could markedly silence the rs3741219 C-allelic H19 expression but not lncRNA H19 with the T allele. Consistently, there was significantly reduced expression of lncRNA H19 in HCC and normal tissues of the C allele carriers compared with the H19 levels in patients with the T allele. Knock-down of lncRNA H19 significantly promoted the anti-viability efficiency of oxaliplatin (the main chemotherapy drug used in TACE) to HCC cells. In view of these results, we assume that lncRNA H19 might be a potential therapeutic target for unresectable HCC patients.		Arch Toxicol. 2021 Sep;95(9):3063-3070. doi: 10.1007/s00204-021-03119-8. Epub 2021 Jul 12.
5436	LncRNA	H19	miR-1539	NA	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34251499	LncRNA H19 modulated by miR-146b-3p/miR-1539-mediated allelic regulation in transarterial chemoembolization of hepatocellular carcinoma.	Transarterial chemoembolization (TACE) is an effective treatment for unresectable hepatocellular carcinoma (HCC) patients. Although overall survival (OS) of TACE-treated patients has been evidently prolonged, not all unresectable HCC patients can benefit from TACE. Genome-wide association studies identified multiple HCC susceptibility single nucleotide polymorphisms (SNPs). However, it is still unclear how lncRNAs and their functional SNPs impact therapeutic responses of TACE. In the study, we hypothesized that the functional lncRNA H19 SNP(s) might impact H19 expression and, thus, prognosis of TACE-treated HCC patients. We found that the H19 rs3741219 SNP was significantly associated with OS of HCC patients received TACE. Cox proportional hazards model demonstrated that the rs3741219 CC genotype was associated with longer OS and a 37% decreased death risk compared with the TT carriers after TACE therapy (P = 0.001). Interestingly, the rs3741219 T-to-C change led to allelic down-regulation of lncRNA H19 expression via creating the binding sites of miR-146b-3p and miR-1539. Luciferase reporter gene assays indicated that miR-146b-3p and miR-1539 could markedly silence the rs3741219 C-allelic H19 expression but not lncRNA H19 with the T allele. Consistently, there was significantly reduced expression of lncRNA H19 in HCC and normal tissues of the C allele carriers compared with the H19 levels in patients with the T allele. Knock-down of lncRNA H19 significantly promoted the anti-viability efficiency of oxaliplatin (the main chemotherapy drug used in TACE) to HCC cells. In view of these results, we assume that lncRNA H19 might be a potential therapeutic target for unresectable HCC patients.		Arch Toxicol. 2021 Sep;95(9):3063-3070. doi: 10.1007/s00204-021-03119-8. Epub 2021 Jul 12.
5437	LncRNA	HULC	miR-137	ITGB8	Oc Tissues And Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA pull-down;	34250246	Long noncoding RNA HULC contributes to paclitaxel resistance in ovarian cancer via miR-137/ITGB8 axis.	Long noncoding RNA (lncRNA) highly upregulated in liver cancer (HULC) has been reported to be implicated in chemoresistance. However, the potential mechanism of HULC in paclitaxel (PTX)-resistant ovarian cancer (OC) remains undefined. The expression of RNAs and proteins was measured by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and Western blot assay. The PTX resistance and apoptotic rate were assessed via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry, respectively. Furthermore, the interaction between miR-137 and HULC or integrin beta-8 (ITGB8) was predicted by miRcode and starBase v2.0 and then verified by dual luciferase reporter and RNA pull-down assays. In addition, the xenograft mice model was established to explore the effects of HULC in vivo. HULC was significantly upregulated and miR-137 was downregulated in PTX-resistant OC tissues and cells. Also, the HULC depletion suppressed tumor growth and PTX resistance in PTX-treated mice. miR-137 was verified as a target of HULC and directly targeted ITGB8. And HULC knockdown downregulated ITGB8 expression by targeting miR-137. miR-137 inhibitor or ITGB8 overexpression mitigated the suppressive impacts of HULC knockdown on PTX resistance. Collectively, HULC modulated ITGB8 expression to promote PTX resistance of OC by sponging miR-137.		Open Life Sci. 2021 Jul 1;16(1):667-681. doi: 10.1515/biol-2021-0058. eCollection 2021.
5438	LncRNA	SNHG16	miR-892b	PPAPDC1A	Breast Cancer Cell	Breast Cancer	Homo sapiens (human)  	FISH;qPCR;RT-qPCR;RACE;RIP assay;RNA immunoprecipitation;FISH;RNA immunoprecipitation;	34249903	Extracellular Vesicles Carry lncRNA SNHG16 to Promote Metastasis of Breast Cancer Cells via the miR-892b/PPAPDC1A Axis.	Breast cancer (BC) represents the most commonly diagnosed malignancy among women. Long non-coding RNAs (lncRNAs) can be transferred by extracellular vesicles (EVs) to participate in BC progression. This study demonstrated that SNHG16 expression was significantly increased in BC tissues and cells. Overexpression of SNHG16 promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of BC cells. SNHG16 was carried by EVs. Bioinformatics analysis predicted that SNHG16 regulated PPAPDC1A expression by sponging miR-892b, which was confirmed by RNA-fluorescence in situ hybridization (FISH), RT-qPCR, dual-luciferase gene reporter assay, and RNA immunoprecipitation (RIP). MDA-MB-157 and HS578T cells were transfected with pcDNA3.1-SNHG16, miR-892b-mimic, or si-PPAPDC1A for functional rescue experiments in vitro, and the cells were treated with MDA-MB-231 cell-derived EVs. The results confirmed that enhanced miR-892b expression partially eliminated the increase of migration, invasion, and EMT of BC cells mediated by SNHG16 or EVs. The lung metastasis model in nude mice was established by injecting HS578T cells via tail vein. The results showed that si-SNHG16 reduced the metastatic nodules and decreased the vimentin expression. In conclusion, EVs derived from BC cells transferred SNHG16 via the miR-892b/PPAPDC1A axis, thus promoting EMT, migration, and invasion of BC.		Front Cell Dev Biol. 2021 Jun 25;9:628573. doi: 10.3389/fcell.2021.628573. eCollection 2021.
5439	LncRNA	NRP1	miR-204	DCBLD2	Bc Tissues And Cells	Bladder Cancer	Homo sapiens (human)  	Western blot;	34249735	Role of NRP1 in Bladder Cancer Pathogenesis and Progression.	Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA(®) bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers.		Front Oncol. 2021 Jun 23;11:685980. doi: 10.3389/fonc.2021.685980. eCollection 2021.
5440	LncRNA	NRP1	miR-143	DCBLD2	Bc Tissues And Cells	Bladder Cancer	Homo sapiens (human)  	Western blot;	34249735	Role of NRP1 in Bladder Cancer Pathogenesis and Progression.	Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA(®) bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers.		Front Oncol. 2021 Jun 23;11:685980. doi: 10.3389/fonc.2021.685980. eCollection 2021.
5441	LncRNA	NRP1	miR-145	DCBLD2	Bc Tissues And Cells	Bladder Cancer	Homo sapiens (human)  	Western blot;	34249735	Role of NRP1 in Bladder Cancer Pathogenesis and Progression.	Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA(®) bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers.		Front Oncol. 2021 Jun 23;11:685980. doi: 10.3389/fonc.2021.685980. eCollection 2021.
5442	LncRNA	NRP1	miR-195	DCBLD2	Bc Tissues And Cells	Bladder Cancer	Homo sapiens (human)  	Western blot;	34249735	Role of NRP1 in Bladder Cancer Pathogenesis and Progression.	Bladder urothelial carcinoma (BC) is a fatal invasive malignancy and the most common malignancy of the urinary system. In the current study, we investigated the function and mechanisms of Neuropilin-1 (NRP1), the co-receptor for vascular endothelial growth factor, in BC pathogenesis and progression. The expression of NRP1 was evaluated using data extracted from GEO and HPA databases and examined in BC cell lines. The effect on proliferation, apoptosis, angiogenesis, migration, and invasion of BC cells were validated after NRP1 knockdown. After identifying differentially expressed genes (DEGs) induced by NRP1 silencing, GO/KEGG and IPA(®) bioinformatics analyses were performed and specific predicted pathways and targets were confirmed in vitro. Additionally, the co-expressed genes and ceRNA network were predicted using data downloaded from CCLE and TCGA databases, respectively. High expression of NRP1 was observed in BC tissues and cells. NRP1 knockdown promoted apoptosis and suppressed proliferation, angiogenesis, migration, and invasion of BC cells. Additionally, after NRP1 silencing the activity of MAPK signaling and molecular mechanisms of cancer pathways were predicted by KEGG and IPA pathway analysis and validated using western blot in BC cells. NRP1 knockdown also affected various biological functions, including antiviral response, immune response, cell cycle, proliferation and migration of cells, and neovascularisation. Furthermore, the main upstream molecule of the DEGs induced by NRP1 knockdown may be NUPR1, and NRP1 was also the downstream target of NUPR1 and essential for regulation of FOXP3 expression to activate neovascularisation. DCBLD2 was positively regulated by NRP1, and PPAR signaling was significantly associated with low NRP1 expression. We also found that NRP1 was a predicted target of miR-204, miR-143, miR-145, and miR-195 in BC development. Our data provide evidence for the biological function and molecular aetiology of NRP1 in BC and for the first time demonstrated an association between NRP1 and NUPR1, FOXP3, and DCBLD2. Specifically, downregulation of NRP1 contributes to BC progression, which is associated with activation of MAPK signaling and molecular mechanisms involved in cancer pathways. Therefore, NRP1 may serve as a target for new therapeutic strategies to treat BC and other cancers.		Front Oncol. 2021 Jun 23;11:685980. doi: 10.3389/fonc.2021.685980. eCollection 2021.
5443	LncRNA	SNHG17	miR-361-3p	STC2	Rectal Cancer Tissues And Cells	Rectal Cancer	Homo sapiens (human)  	Flow cytometry assay;RIP assay;RNA immunoprecipitation;Flow Cytometry assay;RNA immunoprecipitation;	34249085	SNHG17 Serves as an Oncogenic lncRNA by Regulating the miR-361-3p/STC2 Axis in Rectal Cancer.	Long noncoding RNA (lncRNA) have been reported to be crucial regulators for carcinogenesis, including rectal cancer. This work aimed to explore the roles and associated mechanisms of small nucleolar RNA host gene 17 (SNHG17) in rectal cancer. A quantitative real-time polymerase chain reaction was performed to measure the expression level of SNHG17 in rectal cancer tissues and cells. Cell counting kit-8 (CCK-8) assay and flow cytometry assay were conducted to measure the biological roles of SNHG17 in rectal cancer. In addition, luciferase activity reporter assay, RNA immunoprecipitation (RIP) assay, and rescue experiments were conducted to explore the mechanisms of SNHG17 in rectal cancer. The upregulation status of SNHG17 was identified in rectal cancer tissues and cells. Functionally, knockdown the expression of SNHG17 inhibits rectal cancer cell proliferation via stimulating cell apoptosis. In vivo assay showed that the knockdown of SNHG17 inhibits tumor growth. Furthermore, we showed that microRNA-361-3p (miR-361-3p) has decreased expression in tumor tissues and cells, and SNHG17 functions as a sponge for miR-361-3p. The upregulation status of stanniocalcin 2 (STC2) was also found in rectal cancer, and the knockdown of STC2 hinders cancer progression. In conclusion, lncRNA SNHG17 functions as an oncogenic lncRNA in rectal cancer by regulating the miR-361-3p/STC2 axis.		Front Genet. 2021 Jun 23;12:654686. doi: 10.3389/fgene.2021.654686. eCollection 2021.
5444	LncRNA	NCK1-AS1	miR-526b-5p	ADAM15	Melanoma Cells	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;	34247598	NCK1-AS1 promotes the progression of melanoma by accelerating cell proliferation and migration via targeting miR-526b-5p/ADAM15 axis.	BACKGROUND: Long non-coding RNAs (lncRNAs) are vital regulators of gene expression and cellular processes in multiple cancers, including melanoma. Nevertheless, the function of lncRNA NCK1-antisense 1 (NCK1-AS1) in melanoma remains unknown. METHODS: RT-qPCR was used to analyze the expression of NCK1-AS1, microRNA-526b-5p (miR-526b-5p) and ADAM metallopeptidase domain 15 (ADAM15). Cell proliferation was determined by CCK-8, colony formation and EdU assays. Cell migration was assessed by transwell migration and wound healing assays. Mechanism experiments including luciferase reporter, RIP and RNA pull down assays were conducted to demonstrate the interactions between RNAs. Xenograft model was established to verify the function of NCK1-AS1 and miR-526b-5p in melanoma in vivo. RESULTS: NCK1-AS1 was overexpressed in melanoma cell lines and NCK1-AS1 knockdown hampers the proliferation and migration of melanoma cells. Besides, miR-526b-5p binds to NCK1-AS1 in melanoma and ADAM15 was validated as its downstream target. Further, the inhibitory effects of NCK1-AS1 knockdown on cell proliferation and migration in melanoma were reversed by the depletion of miR-526b-5p and further counteracted by ADAM15 knockdown. The growth of melanoma tumors was hindered by the down-regulation of NCK1-AS1 or up-regulation of miR-526b-5p. CONCLUSION: NCK1-AS1 facilitates cell proliferation and migration in melanoma via targeting miR-526b-5p/ADAM15 axis.		Cancer Cell Int. 2021 Jul 12;21(1):367. doi: 10.1186/s12935-021-02055-y.
5445	LncRNA	TP53TG1	miR-33b	SHCBP1	Rb Cells	Retinoblastoma	Homo sapiens (human)  	qRT-PCR 	34247545	Long Non-Coding RNA TP53TG1 Upregulates SHCBP1 to Promote Retinoblastoma Progression by Sponging miR-33b.	Long non-coding RNA (lncRNA) TP53 target 1 (TP53TG1) is known to be strongly associated with tumor and cancer progression. However, its expression profile, unique role, and regulatory pathways in retinoblastoma (RB) are not known. Here, we revealed a large expression of TP53TG1 in RB tissues and cell lines. Conversely, we showed marked suppression of cell proliferation, migration, and invasion in TP53TG1 knocked down RB cells. Mechanistically, we established that TP53TG1 directly interacted with microRNA (miR)-33b in RB cells. Furthermore, TP53TG1 transcripts were found to be inversely correlated with miR-33b in RB tissues. We also showed that miR-33b suppression partly reversed the TP53TG1 knockdown mediated effects on tumor biology. Finally, TP53TG1 was shown to modulate the levels of SHC Binding and Spindle Associated 1 (SHCBP1), a direct target of miR-33b in RB cells. Based on the above data, we propose that TP53TG1 regulates RB progression via its modulation of the miR-33b/SHCBP1 pathway.		Cell Transplant. 2021 Jan-Dec;30:9636897211025223. doi: 10.1177/09636897211025223.
5446	LncRNA	HYPAL	miR-431-5p	CDK14	Gc Cells	Gastric Cancer	Homo sapiens (human)  	ChIP;microarray;Chromatin immunoprecipitation;Luciferase reporter assay;	34247316	Hypoxia associated lncRNA HYPAL promotes proliferation of gastric cancer as ceRNA by sponging miR-431-5p to upregulate CDK14.	Gastric cancer (GC) is a common malignant solid tumor that is characterized by high hypoxia. The transcription of genes associated with hypoxia affects tumor occurrence and development. Long non-coding RNAs (lncRNAs) have been reported to play important roles in cancer development. In this study, we screened for differentially expressed ncRNAs (non-coding RNA) and mRNAs between hypoxia-inducible factor-1 (HIF-1a) knockdown GC cells and scrambled GC cells. Microarray data revealed that HIF-1a regulated the expression of LINC01355 (Hypoxia Yield Proliferation Associated LncRNA, HYPAL). HYPAL was found to be significantly upregulated in GC cells and tissues and was correlated with poor GC prognosis. Chromatin immunoprecipitation (ChIP) and luciferase reporter assays revealed that HIF-1a promoted HYPAL expression by binding the promoter region. A regulatory network for the competing endogenous RNA (ceRNA) was constructed using bioinformatics tools. Mechanistic studies revealed that HYPAL acted as a ceRNA of miR-431-5p to regulate CDK14 expression. Carcinogenic effects of HYPAL were evaluated in vitro and in vivo. The HIF-1a/HYPAL/miR-431-5p/CDK14 (Cyclin-dependent kinase 14) axis activated the Wnt/b-catenin signaling pathway and induced GC cell proliferation while inhibiting apoptosis. In conclusion, HYPAL is a potential molecular target for GC therapy.		Gastric Cancer. 2021 Jul 11. doi: 10.1007/s10120-021-01213-5.
5447	LncRNA	LINC00662	miR-340-5p	STAT3	Glioma Tissues And Cell Lines	Glioma	Homo sapiens (human)	ChIP;qPCR;RT-qPCR;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34246852	A positive feedback loop of LINC00662 and STAT3 promotes malignant phenotype of glioma.	BACKGROUND: Long noncoding RNAs (lncRNAs) have been reported to be associated with tumorigenesis and development of glioma. LINC00662 has been involved in the pathogenesis of various human cancers. However, the mechanism underlying which LINC00662 exerts its role in glioma needs further exploration. In addition, regulation mechanism of LINC00662 expression in glioma remains unknown. METHODS AND MATERIALS: RT-qPCR was performed to evaluate the expression levels of LINC00662, miR-340-5p in glioma tissues and cell lines. The effect of LINC00662 and miR-340-5p in cell proliferation and invasion was assessed by Cell Counting Kit-8(CCK-8), clone colony formation and Transwell assay. Luciferase reporter assays and RNA immunoprecipitation assay validated the miR-340-5p-target relationships with LINC00662 or STAT3. CHIP-qPCR and Luciferase reporter assays were used to demonstrate the interaction between STAT3 and the promoter region of LINC00662. A tumor xenografts model was implemented to verify the effect of LINC00662 on glioma development in vivo. RESULTS: We found that LINC00662 was frequently highly expressed and related to the malignant phenotype of glioma. LINC00662 knockdown inhibited the proliferation, invasion and glioma genesis of glioma. LINC00662 acted as a ceRNA sponging miR-340-5p to protect the expression of STAT3. In addition, STAT3 was forced to the promoter region of LINC00662 and promoted its transcription. In vivo experiments demonstrated that targeting LINC00662 may be a potential strategy in glioma therapy. CONCLUSION: There was a positive regulation loop between LINC00662 and STAT3 in glioma. LINC00662 might be an oncogene in glioma. Targeting LINC00662 was a potential strategy in glioma therapy.		Pathol Res Pract. 2021 Aug;224:153539. doi: 10.1016/j.prp.2021.153539. Epub 2021 Jul 5.
5448	LncRNA	Pvt1	miR-196b	OSMR	H9C2 Cells	Cardiac Hypertrophy	Rattus (rat)	qRT-PCR 	34245860	Long non-coding RNA Pvt1 modulates the pathological cardiac hypertrophy via miR-196b-mediated OSMR regulation.	Cardiac hypertrophy is the uppermost risk factor for the development of heart failure, leading to irreversible cardiac structural remodeling and sudden death. As a major mediator of cardiac remodeling, oncostatin M (OSM) and its receptor, OSMR, attract plenty of interest. Recent studies have demonstrated key effects of noncoding RNAs on myocardial remodeling. However, whether noncoding RNAs that regulate the expression of OSMR would regulate the process of remodeling remain unclear. Herein, we observed that long noncoding RNA (lncRNA) Pvt1 expression showed to be significantly elicited by aortic banding (AB) operation in vivo and by angiotensin (Ang II) treatment in vitro. Pvt1 knockdown significantly attenuated the myocardial hypertrophy caused by pressure overload within rats and the cardiac myocyte hypertrophy caused by Ang II in vitro. Moreover, Pvt1 knockdown also decreased cellular myomesin and B-raf, which was involved in OSM function in cardiac remodeling. Based on online tools prediction, miR-196b may simultaneously target Pvt1 and OSMR 3' untranslated region (UTR). In rat H9c2 cells and primary cardiac myocyte, Pvt1 and miR-196b exerted negative regulatory effects on each other and miR-196b negatively regulated OSMR expression. Pvt1 directly targeted miR-196b to relieve miR-196b-induced OSMR suppression via acting as a competing endogenous RNA (ceRNA). Moreover, the effect of miR-196b suppression upon the B-raf was opposite to Pvt1 knockdown, and miR-196b suppression might significantly attenuate the effect of Pvt1 knockdown. In summary, Pvt1/miR-196b axis modulating cardiomyocyte hypertrophy and remodeling via OSMR. Our findings provide a rationale for further studies on the potential therapeutic benefits of Pvt1 function and mechanism in cardiac and cardiomyocyte hypertrophy by a lncRNA-miRNA-mRNA network.		Cell Signal. 2021 Oct;86:110077. doi: 10.1016/j.cellsig.2021.110077. Epub 2021 Jul 8.
5449	LncRNA	SOX2	miR-627-3p	Smad2	Non-Small Cell Lung Cancer Cell Line H1975	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34244990	Exosomal long non-coding RNA SOX2 overlapping transcript enhances the resistance to EGFR-TKIs in non-small cell lung cancer cell line H1975.	Crosstalk between cancer cells and macrophages plays a crucial role in the development of cancer. In this study, our data showed that M1 macrophages attenuate, while M2 macrophages and tumor-associated macrophages enhance the EGFR-TKIs resistance in non-small cell lung cancer (NSCLC) cell line H1975. Next, long non-coding RNA SOX2 overlapping transcript (SOX2-OT) is highly expressed in NSCLC cells-derived exosomes. NSCLC cells-derived exosomes promote macrophages M2 polarization and inhibit M1 polarization through transferring SOX2-OT to macrophages. Subsequently, our results indicated that NSCLC cells-induced M2-polarized macrophages enhance the EGFR-TKIs resistance in H1975 cells. Furthermore, our data revealed that NSCLC cells-derived exosomes inhibit the expression of miR-627-3p, while promote Smads expression in THP-1 cells. SOX2-OT acts as miR-627-3p sponge to facilitate Smad2, Smad3 and Smad4 expression. Finally, our results indicated that NSCLC cells promote macrophages M2 polarization and suppress M1 polarization through targeting miR-627-3p/Smads signaling pathway by transferring exosomes to THP-1 cells. In conclusion, our data revealed that NSCLC cells promote macrophages M2 polarization through transferring exosomal SOX2-OT, thus to enhance its own EGFR-TKIs resistance. Mechanismly, NSCLC cells-derived exosomal SOX2-OT promotes macrophages M2 polarization via promoting Smads by sponging miR-627-3p. Our data provide a novel therapeutic target for EGFR-TKIs resistance in NSCLC.		Hum Cell. 2021 Sep;34(5):1478-1489. doi: 10.1007/s13577-021-00572-6. Epub 2021 Jul 9.
5450	LncRNA	SOX2	miR-627-3p	Smad3	Non-Small Cell Lung Cancer Cell Line H1975	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34244990	Exosomal long non-coding RNA SOX2 overlapping transcript enhances the resistance to EGFR-TKIs in non-small cell lung cancer cell line H1975.	Crosstalk between cancer cells and macrophages plays a crucial role in the development of cancer. In this study, our data showed that M1 macrophages attenuate, while M2 macrophages and tumor-associated macrophages enhance the EGFR-TKIs resistance in non-small cell lung cancer (NSCLC) cell line H1975. Next, long non-coding RNA SOX2 overlapping transcript (SOX2-OT) is highly expressed in NSCLC cells-derived exosomes. NSCLC cells-derived exosomes promote macrophages M2 polarization and inhibit M1 polarization through transferring SOX2-OT to macrophages. Subsequently, our results indicated that NSCLC cells-induced M2-polarized macrophages enhance the EGFR-TKIs resistance in H1975 cells. Furthermore, our data revealed that NSCLC cells-derived exosomes inhibit the expression of miR-627-3p, while promote Smads expression in THP-1 cells. SOX2-OT acts as miR-627-3p sponge to facilitate Smad2, Smad3 and Smad4 expression. Finally, our results indicated that NSCLC cells promote macrophages M2 polarization and suppress M1 polarization through targeting miR-627-3p/Smads signaling pathway by transferring exosomes to THP-1 cells. In conclusion, our data revealed that NSCLC cells promote macrophages M2 polarization through transferring exosomal SOX2-OT, thus to enhance its own EGFR-TKIs resistance. Mechanismly, NSCLC cells-derived exosomal SOX2-OT promotes macrophages M2 polarization via promoting Smads by sponging miR-627-3p. Our data provide a novel therapeutic target for EGFR-TKIs resistance in NSCLC.		Hum Cell. 2021 Sep;34(5):1478-1489. doi: 10.1007/s13577-021-00572-6. Epub 2021 Jul 9.
5451	LncRNA	SOX2	miR-627-3p	Smad4	Non-Small Cell Lung Cancer Cell Line H1975	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34244990	Exosomal long non-coding RNA SOX2 overlapping transcript enhances the resistance to EGFR-TKIs in non-small cell lung cancer cell line H1975.	Crosstalk between cancer cells and macrophages plays a crucial role in the development of cancer. In this study, our data showed that M1 macrophages attenuate, while M2 macrophages and tumor-associated macrophages enhance the EGFR-TKIs resistance in non-small cell lung cancer (NSCLC) cell line H1975. Next, long non-coding RNA SOX2 overlapping transcript (SOX2-OT) is highly expressed in NSCLC cells-derived exosomes. NSCLC cells-derived exosomes promote macrophages M2 polarization and inhibit M1 polarization through transferring SOX2-OT to macrophages. Subsequently, our results indicated that NSCLC cells-induced M2-polarized macrophages enhance the EGFR-TKIs resistance in H1975 cells. Furthermore, our data revealed that NSCLC cells-derived exosomes inhibit the expression of miR-627-3p, while promote Smads expression in THP-1 cells. SOX2-OT acts as miR-627-3p sponge to facilitate Smad2, Smad3 and Smad4 expression. Finally, our results indicated that NSCLC cells promote macrophages M2 polarization and suppress M1 polarization through targeting miR-627-3p/Smads signaling pathway by transferring exosomes to THP-1 cells. In conclusion, our data revealed that NSCLC cells promote macrophages M2 polarization through transferring exosomal SOX2-OT, thus to enhance its own EGFR-TKIs resistance. Mechanismly, NSCLC cells-derived exosomal SOX2-OT promotes macrophages M2 polarization via promoting Smads by sponging miR-627-3p. Our data provide a novel therapeutic target for EGFR-TKIs resistance in NSCLC.		Hum Cell. 2021 Sep;34(5):1478-1489. doi: 10.1007/s13577-021-00572-6. Epub 2021 Jul 9.
5452	LncRNA	RCAT1	miR-214-5p	E2F2	Renal Cell Carcinoma Cells	Renal Cancer	Homo sapiens (human)  	qRT-PCR 	34244473	LncRNA RCAT1 promotes tumor progression and metastasis via miR-214-5p/E2F2 axis in renal cell carcinoma.	Renal cell carcinoma is the second malignant tumors in the urinary system with high mortality and morbidity. Increasing evidence suggests that long non-coding RNAs (lncRNAs) play critical roles in tumor development and progression. In the current study, based on the publicly available data obtained from GEO and TCGA database, we identified five prognosis-related lncRNAs with the ability to predict the prognosis of patients with renal cell carcinoma. Among them, the uncharacterized and upregulated lncRNA RCAT1 (renal cancer-associated transcript 1) was identified as the key lncRNA. Our data further revealed that the expression of lncRNA RCAT1 was significantly upregulated in renal cell carcinoma tissues and cells. Gain-of-function and loss-of-function studies showed that lncRNA RCAT1 promoted cell proliferation, migration, and invasion in vitro and in vivo. Furthermore, we verified that lncRNA RCAT1 could abundantly sponge miR-214-5p, which served as a tumor suppressor in renal cell carcinoma. Significantly, miR-214-5p overexpression could attenuate the promotion of cell proliferation and metastasis induced by lncRNA RCAT1. Moreover, we found that E2F2 was a direct target of miR-214-5p, and lncRNA RCAT1 could protect E2F2 from miR-214-5p-mediated degradation. Taken together, our findings suggested that lncRNA RCAT1 could enhance the malignant phenotype of renal cell carcinoma cells by modulating miR-214-5p/E2F2 axis, and lncRNA RCAT1 might be a novel prognostic biomarker and a potential therapeutic target for renal cell carcinoma.		Cell Death Dis. 2021 Jul 9;12(7):689. doi: 10.1038/s41419-021-03955-7.
5453	LncRNA	ZBED3-AS1	miR-381-3p	ARID4B	Melanoma Cells	Melanoma	Homo sapiens (human)	qRT-PCR 	34241580	STAT3-induced ZBED3-AS1 promotes the malignant phenotypes of melanoma cells by activating PI3K/AKT signaling pathway.	Melanoma is considered as the most frequent primary malignancy occurring in skin. Accumulating studies have suggested that long non-coding RNAs (lncRNAs) play critical parts in multiple cancers. In this study, we explored the molecular mechanism of ZBED3 antisense RNA 1 (ZBED3-AS1) in melanoma. We observed that ZBED3-AS1 expression was remarkably up-regulated in melanoma tissues, and high ZBED3-AS1 level was linked to unsatisfactory survival of melanoma patients. Then, we discovered that ZBED3-AS1 was overexpressed in melanoma cells compared with human epidermal melanocytes. In addition, loss-of-function assays verified that ZBED3-AS1 knockdown restrained cell proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness in melanoma. In addition, signal transducer and activator of transcription 3 (STAT3), which also showed tumour-facilitating functions in melanoma, was confirmed as a transcriptional activator of ZBED3-AS1. Moreover, ZBED3-AS1 enhanced the expression of AT-rich interaction domain 4B (ARID4B) through sequestering miR-381-3p. Importantly, we further confirmed that ZBED3-AS1 promoted the malignant progression of melanoma by regulating miR-381-3p/ARID4B axis to activate the phosphatidylinositol 3-kinase/AKT serine/threonine kinase (PI3K/AKT) signalling pathway. In a word, our research might provide a novel therapeutic target for melanoma.		RNA Biol. 2021 Aug 7:1-14. doi: 10.1080/15476286.2021.1950463.
5454	LncRNA	MALAT1	miR-204	APOL1	Hk-2 Cells	Acute Kidney Injury	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA pull-down;	34240756	Knockdown of lncRNA MALAT1 ameliorates acute kidney injury by mediating the miR-204/APOL1 pathway.	BACKGROUND: Acute kidney injury (AKI) was characterized by loss of renal function, associated with chronic kidney disease, end-stage renal disease, and length of hospital stay. Long non-coding RNAs (lncRNAs) participated in AKI development and progression. Here, we aimed to investigate the roles and mechanisms of lncRNA MALAT1 in AKI. METHODS: AKI serum samples were obtained from 129 AKI patients. ROC analysis was conducted to confirm the diagnostic value of MALAT1 in differentiating AKI from healthy volunteers. After hypoxic treatment on HK-2 cells, the expressions of inflammatory cytokines, MALAT1, miR-204, APOL1, p65, and p-p65, were measured by RT-qPCR and Western blot assays. The targeted relationship between miR-204 and MALAT1 or miR-204 and APOL1 was determined by luciferase reporter assay and RNA pull-down analysis. After transfection, CCK-8, flow cytometry, and TUNEL staining assays were performed to evaluate the effects of MALAT1 and miR-204 on AKI progression. RESULTS: From the results, lncRNA MALAT1 was strongly elevated in serum samples from AKI patients, with the high sensitivity and specificity concerning differentiating AKI patients from healthy controls. In vitro, we established the AKI cell model after hypoxic treatment. After experiencing hypoxia, we found significantly increased MALAT1, IL-1b, IL-6, and TNF-a expressions along with decreased miR-204 level. Moreover, the targeted relationship between MALAT1 and miR-204 was confirmed. Silencing of MALAT1 could reverse hypoxia-triggered promotion of HK-2 cell apoptosis. Meanwhile, the increase of IL-1b, IL-6, and TNF-a after hypoxia treatment could be repressed by MALAT1 knockdown as well. After co-transfection with MALAT1 silencing and miR-204 inhibition, we found that miR-204 could counteract the effects of MALAT1 on HK-2 cell progression and inflammation after under hypoxic conditions. Finally, NF-kB signaling was inactivated while APOL1 expression was increased in HK-2 cells after hypoxia treatment, and lncRNA MALAT1 inhibition reactivated NF-kB signaling while suppressed APOL1 expression by sponging miR-204. CONCLUSIONS: Collectively, these results illustrated that knockdown of lncRNA MALAT1 could ameliorate AKI progression and inflammation by targeting miR-204 through APOL1/NF-kB signaling.		J Clin Lab Anal. 2021 Aug;35(8):e23881. doi: 10.1002/jcla.23881. Epub 2021 Jul 9.
5455	LncRNA	HOXA-AS2	miR-509-3p	BTN3A1	Cervical Cancer Tissues And Cells	Cervical Cancer	Homo sapiens (human)  	FISH;qRT-PCR;FISH;	34240204	Long noncoding RNA HOXA-AS2 accelerates cervical cancer by the miR-509-3p/BTN3A1 axis.	OBJECTIVES: Cervical cancer is an aggressive malignant tumour and causes high mortality in women. LncRNA HOXA-AS2 is a tumour promoter in many cancers. The current work was designed to elucidate the functions of HOXA-AS2 in cervical cancer and the underlying regulatory mechanism. METHODS: qRT-PCR was conducted to reveal RNA levels. A FISH assay was conducted for the identification of the subcellular location of HOXA-AS2. MTT, EdU, Transwell and tube formation were used for detection of cell growth, migration and angiogenesis, respectively. In-vivo studies were conducted to reveal the role of HOXA-AS2 on transplanted tumour growth in mice. KEY FINDINGS: The HOXA-AS2 level was found high in tissues and cells of cervical cancer. Silencing of HOXA-AS2 restrained cell proliferation, migration and invasion. Angiogenesis of HUVECs was restrained after silencing HOXA-AS2. Additionally, HOXA-AS2 upregulated the BTN3A1 by interaction with miR-509-3p. BTN3A1 overexpression rescues the inhibitory effect of silenced HOXA-AS2 on cell phenotypes in cervical cancer. Moreover, xenograft tumour growth in mice was suppressed by HOXA-AS2 depletion and was facilitated by BTN3A1 overexpression. CONCLUSIONS: HOXA-AS2 accelerates cellular progression in cervical cancer by the miR-509-3p/BTN3A1 axis.		J Pharm Pharmacol. 2021 Jul 8:rgab090. doi: 10.1093/jpp/rgab090.
5456	LncRNA	SNHG12	miR-199a-5p	Klotho	Intrahepatic Cholangiocarcinoma Cells	Intrahepatic Cholangiocarcinoma	Homo sapiens (human)  	RT-PCR;RIP assay;RNA pull-down assay;luciferase assay;RNA pull-down;	34239888	Long Non-coding RNA SNHG12, a New Therapeutic Target, Regulates miR-199a-5p/Klotho to Promote the Growth and Metastasis of Intrahepatic Cholangiocarcinoma Cells.	Background: Small nucleolar RNA host gene 12 (SNHG12) is a newly identified long non-coding RNA (lncRNA) whose involvements have been explored in several cancers. Our study aimed to explore the functions of SNHG12 on intrahepatic cholangiocarcinoma (ICC) progression and its interaction with miR-199a-5p and Klotho. Methods: RT-PCR was performed to examine the expressions of SNHG12, miR-199a-5p and Klotho in ICC cells. Cell counting kit-8 (CCK-8), colony formation assays and transwell assays were applied to analyze the proliferation, migration and invasion of ICC cells. Luciferase assays, RIP assays and RNA pull-down assays were carried out to demonstrate the direct binding relationships among SNHG12, miR-199a-5p and Klotho. The xenograft nude models were applied to test the effects of SNHG12 on ICC tumor growth. Results: The expression of SNHG12 and Klotho was distinctly increased in ICC cells, while miR-199a-5p expressions were decreased. Functionally, the silence of SNHG12 inhibited the proliferation and metastasis of ICC cells, while miR-199a-5p overexpression exhibited an opposite result. Mechanistically, Knockdown of SNHG12 significantly suppressed the expressions of miR-199a-5p by sponging it, and then increased Klotho expression. The final in vivo experiments suggested that the silence of SNHG12 distinctly inhibited tumor growth. Conclusion: Our findings indicated that SNHG12 inhibited cell proliferation and metastasis process of ICC cells through modulating the miR-199a-5p/Klotho axis and it is expected to become a potential therapeutic target for ICC.		Front Med (Lausanne). 2021 Jun 22;8:680378. doi: 10.3389/fmed.2021.680378. eCollection 2021.
5457	LncRNA	LINC00261	miR-522-3p	TNRC6A	Myocardial Cells	Myocardial Infarction	Homo sapiens (human)  	qRT-PCR;Western blot;	34239606	Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis.	BACKGROUND: Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. METHODS: qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. RESULTS: LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. CONCLUSIONS: LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.		Cardiovasc Ther. 2021 Jun 18;2021:6628194. doi: 10.1155/2021/6628194. eCollection 2021.
5458	LncRNA	NEAT1	let-7 g-5p	BACH1	Colon Cancer Cells	Colon Cancer	Homo sapiens (human)	qRT-PCR 	34238666	Long non-coding RNA NEAT1 absorbs let-7 g-5p to induce epithelial-mesenchymal transition of colon cancer cells through upregulating BACH1.	OBJECTIVE: Long noncoding RNAs (lncRNAs) are critical regulators in diverse human cancers. However, the role of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in colon cancer remains to be further investigated. We aimed to verify the role of NEAT1/let-7 g-5p/BTB and CNC homology 1 (BACH1) axis in colon cancer development. METHODS: Expression of NEAT1, let-7 g-5p and BACH1 in colon cancer tissues and cells was determined. The interactions between NEAT1 and let-7 g-5p, and between let-7 g-5p and BACH1 were assessed. The colon cancer cell lines were treated with plasmids or oligonucleotides to alter NEAT1, BACH1 and let-7 g-5p expression. Then, viability, migration, invasion, and apoptosis of colon cells were evaluated, and the cell growth in vivo was observed as well. RESULTS: NEAT1 and BACH1 were upregulated while let-7 g-5p was downregulated in colon cancer tissues and cells. NEAT1/BACH1 silencing or let-7 g-5p elevation suppressed colon cancer cell growth in vivo and in vitro. The effects of silenced NEAT1 on colon cancer cells and xenografts were reversed by downregulating let-7 g-5p. Down-regulation of BACH1 reversed the effect of NEAT1 overexpression on colon cancer cells. NEAT1 directly bound to let-7 g-5p and let-7 g-5p targeted BACH1. CONCLUSION: Downregulated NEAT1 elevated let-7 g-5p to suppress EMT of colon cancer cells through inhibiting BACH1. This research may contribute to treatment of colon cancer.		Dig Liver Dis. 2021 Jul 5:S1590-8658(21)00216-4. doi: 10.1016/j.dld.2021.04.031.
5459	LncRNA	TPTEP1	miR-454-3p	DLG5	Hcc Cells	Epatocellular Carcinoma	Mus musculus (mouse)	qRT-PCR 	34238665	Long non-coding RNA TPTEP1 exerts inhibitory effects on hepatocellular carcinoma by impairing microRNA-454-3p-mediated DLG5 downregulation.	BACKGROUND: Hepatocellular carcinoma (HCC) is usually diagnosed at late stages, making it the second cause of malignancy-related death across the world. Long noncoding RNAs (lncRNAs) are of significance to tumorigenesis, highly suggestive of their functional roles as novel biomarkers for cancer therapy. The current study investigated the specific role of lncRNA TPTE pseudogene 1 (TPTEP1) in HCC. METHODS: Expression of lncRNA TPTEP1, microRNA-454-3p (miR-454-3p) and discs large homolog 5 (DLG5) was determined in tissues samples from the recruited patients with HCC. Cell proliferation, migration and invasion assays were performed to determine effects of lncRNA TPTEP1, miR-454-3p and DLG5 on the malignant phenotype of tumor cells. Finally, the mouse HCC model was also established to disclose the tumor suppressor effects of lncRNA TPTEP1 in vivo. RESULTS: LncRNA TPTEP1 was downregulated both in HCC cells and tissues, and played a negative regulatory role in HCC cell proliferation, migration and invasion. Mechanistically, lncRNA TPTEP1 competitively bound to miR-454-3p, thereby upregulating its endogenous target DLG5. Moreover, lncRNA TPTEP1 hindered activation of the protein kinase B signaling pathway, causing inhibited malignant phenotypes of HCC cells. Also, lncRNA TPTEP1 suppressed tumor growth and extrahepatic metastasis (lung) via miR-454-3p/DLG5 axis. CONCLUSION: Taken together, this research revealed a concrete mechanism of lncRNA TPTEP1 in HCC.		Dig Liver Dis. 2021 Jul 5:S1590-8658(21)00199-7. doi: 10.1016/j.dld.2021.04.014.
5460	LncRNA	HAND2-AS1	miR-146	RARB	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)	microarray;Western blot;luciferase assay;	34238300	LncRNA HAND2-AS1 exerts anti-oncogenic effects on bladder cancer via restoration of RARB as a sponge of microRNA-146.	BACKGROUND: Growing evidence has shown that long noncoding RNA: microRNA: mRNA is implicated in tumor initiation, development, and progression. Long noncoding RNA HAND2-AS1 exhibits anti-cancer effects in diverse cancers. However, the knowledge of HAND-AS1 in bladder cancer development remains unknown. METHODS: LncRNA and miRNA microarray was conducted to explore different expressed RNA in primary bladder cancer specimens. RNA-RNA interaction prediction tools miRcode ( http://www.mircode.org/ ), DIANA-lncBase v2 ( https://carolina.imis.athena-innovation.gr/diana_tools/web/index.php?r=lncbasev2%2Findex-experimental ), DIANA-TarBase v.8 ( https://carolina.imis.athena-innovation.gr/diana_tools/web/index.php?r=tarbasev8%2Findex ) and miRDB ( http://www.mirdb.org/ ) were employed to predict the interactions between RNA. Bladder cancer cell lines were used to perform cell proliferation and apoptosis assays. Western blot and quantitative Real-time Polymerase Chain Reaction were used to determine the expression of protein and RNA separately. Dual-luciferase assay was conducted to determine the activity of three prime untranslated region of retinoic acid receptor beta (RARB). Furthermore, 5637 human bladder cancer mouse models were established to investigate the interactions of lncRNA: miRNA: mRNA in vivo. RESULTS: Based on the RT2 lncRNA PCR Arrays analysis, we validated HAND2-AS1 declined in bladder cancer and negatively correlated with the depth of invasion and grades. The overexpression of HAND2-AS1 in human bladder cancer cells 5637 and RT4 hampered cell proliferation by provoking Caspase 3-triggered cell apoptosis. Besides, one of the HAND2-AS1 sponges, miR-146, elevated in bladder cancer and targeted the tumor suppressor, retinoic acid receptor beta (RARB). We further demonstrated that the HAND2-AS1: miR-146: RARB complex promoted Caspase 3-mediated apoptosis by suppressing COX-2 expression. Finally, the results gained in mouse xenografts suggested that HAND2-AS1 diminished miR-146 expression, thereby reversing the suppression of miR-146 on RARB-mediated apoptosis and contributing to bladder cancer regression. CONCLUSION: The present study sheds light on the fact that lncRNA HAND2-AS1 exerted as a tumor suppressor by releasing RARB from miR-146, leading to tumor proliferation and invasion inhibition. The findings expanded HAND2-AS-mediated regulatory networks' knowledge and provided novel insights to improve the RARB-targeted regimens against bladder cancer.		Cancer Cell Int. 2021 Jul 8;21(1):361. doi: 10.1186/s12935-021-02063-y.
5461	LncRNA	HAND2-AS1	miR-146	RARB	Bladder Cancer Cells	Bladder Cancer	Mus musculus (mouse)	microarray;Western blot;luciferase assay;	34238300	LncRNA HAND2-AS1 exerts anti-oncogenic effects on bladder cancer via restoration of RARB as a sponge of microRNA-146.	BACKGROUND: Growing evidence has shown that long noncoding RNA: microRNA: mRNA is implicated in tumor initiation, development, and progression. Long noncoding RNA HAND2-AS1 exhibits anti-cancer effects in diverse cancers. However, the knowledge of HAND-AS1 in bladder cancer development remains unknown. METHODS: LncRNA and miRNA microarray was conducted to explore different expressed RNA in primary bladder cancer specimens. RNA-RNA interaction prediction tools miRcode ( http://www.mircode.org/ ), DIANA-lncBase v2 ( https://carolina.imis.athena-innovation.gr/diana_tools/web/index.php?r=lncbasev2%2Findex-experimental ), DIANA-TarBase v.8 ( https://carolina.imis.athena-innovation.gr/diana_tools/web/index.php?r=tarbasev8%2Findex ) and miRDB ( http://www.mirdb.org/ ) were employed to predict the interactions between RNA. Bladder cancer cell lines were used to perform cell proliferation and apoptosis assays. Western blot and quantitative Real-time Polymerase Chain Reaction were used to determine the expression of protein and RNA separately. Dual-luciferase assay was conducted to determine the activity of three prime untranslated region of retinoic acid receptor beta (RARB). Furthermore, 5637 human bladder cancer mouse models were established to investigate the interactions of lncRNA: miRNA: mRNA in vivo. RESULTS: Based on the RT2 lncRNA PCR Arrays analysis, we validated HAND2-AS1 declined in bladder cancer and negatively correlated with the depth of invasion and grades. The overexpression of HAND2-AS1 in human bladder cancer cells 5637 and RT4 hampered cell proliferation by provoking Caspase 3-triggered cell apoptosis. Besides, one of the HAND2-AS1 sponges, miR-146, elevated in bladder cancer and targeted the tumor suppressor, retinoic acid receptor beta (RARB). We further demonstrated that the HAND2-AS1: miR-146: RARB complex promoted Caspase 3-mediated apoptosis by suppressing COX-2 expression. Finally, the results gained in mouse xenografts suggested that HAND2-AS1 diminished miR-146 expression, thereby reversing the suppression of miR-146 on RARB-mediated apoptosis and contributing to bladder cancer regression. CONCLUSION: The present study sheds light on the fact that lncRNA HAND2-AS1 exerted as a tumor suppressor by releasing RARB from miR-146, leading to tumor proliferation and invasion inhibition. The findings expanded HAND2-AS-mediated regulatory networks' knowledge and provided novel insights to improve the RARB-targeted regimens against bladder cancer.		Cancer Cell Int. 2021 Jul 8;21(1):361. doi: 10.1186/s12935-021-02063-y.
5462	LncRNA	LINC00115	miR-30a	SOX9	Ovarian Cancer Stem Cells	Ovarian Cancer	Homo sapiens (human)	microarray;	34238293	LINC00115 promotes stemness and inhibits apoptosis of ovarian cancer stem cells by upregulating SOX9 and inhibiting the Wnt/b-catenin pathway through competitively binding to microRNA-30a.	OBJECTIVE: Long non-coding RNAs (lncRNAs) and microRNAs (miRs) are differentially expressed in ovarian cancer (OC) cells and influence OC progression. This study intended to explore the underlying roles of LINC00115 and miR-30a in OC. METHODS: Gene Expression Omnibus database was used to find OC microarray datasets and bioinformatics analysis predicted the potential molecular mechanism of OC. OC stem cells (OCSCs) surface marker was isolated from human OC cell line and identified. CD133(+) OCSCs were transfected with LINC00115, miR-30a and SOX9 alone or together to detect sphere-forming ability and apoptosis of OCSCs. Caspase-3 activity and DNA damage in cell supernatant were detected. The levels of CD44, NANOG, POU5F1, LINC00115, CD133, miR-30a and SOX9 were measured. Then sh-LNC00115-treated OCSCs were added with Wnt/b-catenin activator SKL2001 to observe the changes of cell stemness and activity. Finally, animal models were established to evaluate the effect of LINC00115 on OCSC in vivo. RESULTS: LINC00115 and SOX9 were highly expressed in OC, while miR-30a was lowly expressed. After silencing LINC00115 or overexpressing miR-30a, the sphere-forming rate of CD133(+) OCSC and levels of CD133, CD44, NANOG and POU5F1 decreased, while apoptotic rate, Caspase-3 activity and histone-related DNA damage increased. SOX9 reversed these trends. Additionally, LINC00115 could bind to miR-30a and miR-30a could target SOX9. SKL2001 partially reversed cell stemness and activity in sh-LNC00115-treated OCSCs. Finally, silencing LINC00115 could inhibit OCSCs growth in vivo. CONCLUSION: LINC00115 promoted stemness and inhibited apoptosis of OCSCs by upregulating SOX9 and in activating the Wnt/b-catenin pathway through competitively binding to miR-30a.		Cancer Cell Int. 2021 Jul 8;21(1):360. doi: 10.1186/s12935-021-02019-2.
5463	LncRNA	UCA1	miR-145	MYO6	Gastric Cancer Cells	Gastric Cancer	Mus musculus (mouse)	CCK-8 assay;qPCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Immunohistochemistry;Luciferase activity assay;RNA immunoprecipitation;	34238213	LncRNA UCA1 promotes development of gastric cancer via the miR-145/MYO6 axis.	BACKGROUND: Long noncoding RNA (lncRNA), urothelial carcinoma-associated 1 (UCA1) is aberrantly expressed in multiple cancers and has been verified as an oncogene. However, the underlying mechanism of UCA1 in the development of gastric cancer is not fully understood. In the present study, we aimed to identify how UCA1 promotes gastric cancer development. METHODS: The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) data were used to analyze UCA1 and myosin VI (MYO6) expression in gastric cancer. Western blot and quantitative real-time PCR (QPCR) were performed to test the expression level of the UCA1/miR-145/MYO6 axis in gastric cancer cell lines and tissues. The roles of the UCA1/miR-145/MYO6 axis in gastric cancer in vitro and in vivo were investigated by CCK-8 assay, flow cytometry, siRNAs, immunohistochemistry, and a mouse xenograft model. The targeted relationship among UCA1, miR-145, and MYO6 was predicted using LncBase Predicted v.2 and TargetScan online software, and then verified by luciferase activity assay and RNA immunoprecipitation. RESULTS: UCA1 expression was higher but miR-145 expression was lower in gastric cancer cell lines or tissues, compared to the adjacent normal cell line or normal tissues. Function analysis verified that UCA1 promoted cell proliferation and inhibited cell apoptosis in the gastric cancer cells in vitro and in vivo. Mechanistically, UCA1 could bind directly to miR-145, and MYO6 was found to be a downstream target gene of miR-145. miR-145 mimics or MYO6 siRNAs could partly reverse the effect of UCA1 on gastric cancer cells. CONCLUSIONS: UCA1 accelerated cell proliferation and inhibited cell apoptosis through sponging miR-145 to upregulate MYO6 expression in gastric cancer, indicating that the UCA1/miR-145/MYO6 axis may serve as a potential therapeutic target for gastric cancer.		Cell Mol Biol Lett. 2021 Jul 8;26(1):33. doi: 10.1186/s11658-021-00275-8.
5464	LncRNA	GLIDR	miR-4677-3p	MAGI2	Glioma Cells	Glioma	Homo sapiens (human)  	qRT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	34237299	GLIDR promotes the progression of glioma by regulating the miR-4677-3p/MAGI2 axis.	Gliomas are the most common and fatal primary brain tumors. Growing evidence suggests that long non-coding RNAs (lncRNAs) constitute novel and potential therapeutic targets for glioma. However, the biological role of glioblastoma down-regulated RNA (GLIDR) in glioma remains largely elusive. In the current study, we used quantitative real-time polymerase chain reaction (qRT-PCR) to detect GLIDR expression in glioma cells. Cell counting kit 8 (CCK-8) assay, colony formation assay, JC-1 staining, and flow cytometry were used to evaluate the role of GLIDR in proliferation and apoptosis of glioma cells. Western blotting was performed to assess the effect of GLIDR on the level of apoptosis-related proteins. In addition, bioinformatics prediction, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter gene assays were used to study the regulatory mechanisms of GLIDR in glioma. GLIDR was found to be highly expressed in glioma cells and silencing of GLIDR inhibited cell proliferation and promoted apoptosis. Functionally, GLIDR bound to miR-4677-3p that directly targeted membrane-associated guanylate kinase, WW, and PDZ domain-containing protein 2 (MAGI2). Our data showed that GLIDR affects the proliferation and apoptosis of glioma cells by targeting miR-4677-3p to regulate the expression of MAGI2. In conclusion, our study determined the oncogenic role of GLIDR in glioma, which may provide a new perspective for the treatment of glioma.		Exp Cell Res. 2021 Sep 1;406(1):112726. doi: 10.1016/j.yexcr.2021.112726. Epub 2021 Jul 6.
5465	LncRNA	LncRNA-42060	miR-204-5p	SOX4	Canine Mammary Gland Tumor Cells	Breast Cancer	Homo sapiens (human)  	RNA sequencing;	34235197	LncRNA-42060 Regulates Tamoxifen Sensitivity and Tumor Development via Regulating the miR-204-5p/SOX4 Axis in Canine Mammary Gland Tumor Cells.	Tamoxifen is the drug of choice for endocrine therapy of breast cancer. Its clinical use is limited by the development of drug resistance. There is increasing evidence that long non-coding RNAs (lncRNAs) are associated with tumor drug resistance. Therefore, we established two TAM-resistant cell lines, CHMp(TAM) and CHMm(TAM). The different expression levels of lncRNA and miRNA in CHMm(TAM) and CHMm were screened by RNA sequencing, and the lncRNA-miRNA interactions were analyzed. LncRNA ENSCAFG42060 (lnc-42060) was found to be significantly upregulated in drug-resistant cells and tumor tissues. Further functional validation revealed that the knockdown of lnc-42060 inhibited proliferation, migration, clone formation, restoration of TAM sensitivity, and reduction of stem cell formation in drug-resistant cells, whereas overexpression of lnc-4206 showed opposite results. Bioinformatics and dual-luciferase reporter gene assays confirmed that lnc-42060 could act as a sponge for miR-204-5p, further regulating SOX4 expression activity and thus influencing tumor cell progression. In conclusion, we screened lncRNAs and miRNAs associated with TAM resistance in canine mammary gland tumor cells for the first time. lnc-42060 served as a novel marker that may be used as an important biomarker for future diagnosis and treatment.		Front Vet Sci. 2021 Jun 21;8:654694. doi: 10.3389/fvets.2021.654694. eCollection 2021.
5466	LncRNA	SNHG14	miR-519b-3p	DDX5	Crc Tissues And Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	34234865	LncRNA SNHG14 promotes cell proliferation and invasion in colorectal cancer through modulating miR-519b-3p/DDX5 axis.	Numbers of studies suggest that long non-coding RNAs (lncRNAs) exert an important role in cancer progression. It is reported that lncRNA SNHG14 (SNHG14) promotes cell proliferation and invasion in many cancers. However, the underlying molecular mechanism of SNHG14 in colorectal cancer (CRC) remains unclear. In our study, we found that SNHG14 is highly expressed in CRC tissues and cells, especially in SW480 and HT-29 cells. In addition, sh-SNHG14 inhibits cell proliferation, cell migration and invasion, promotes cell apoptosis in CRC cell lines. Furthermore, we found that SNHG14 functions as a sponge for miR-519b-3p, while the DEAD box protein 5 (DDX5) is a downstream target gene of miR-519b-3p, and the functions of miR-519b-3p inhibitors on the CRC progression could be rescued by downregulation of DDX5. Our findings suggest that SNHG14 promotes the CRC progression by miR-519b-3p/DDX5 axis, implying the promising therapeutic target of SNHG4 for CRC patients.		J Cancer. 2021 Jun 11;12(16):4958-4970. doi: 10.7150/jca.55495. eCollection 2021.
5467	LncRNA	AFAP1-AS1	miR-205-5p	AFAP1	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	microarray;qPCR;	34234560	LncRNA AFAP1-AS1 Modulates the Proliferation and Invasion of Gastric Cancer Cells by Regulating AFAP1 via miR-205-5p.	PURPOSE: The present study investigated the expression and function of the long noncoding RNA (lncRNA) actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) related to gastric cancer (GC), based on previous results from a microarray analysis. METHODS: Real-time quantitative polymerase chain reaction (qPCR) was used to verify the expression of AFAP1-AS1 in 97 fresh GC tissues and paired non-GC tissues, as well as in six different GC cell lines (BGC-823, SGC-7901, MGC-803, AGS, MKN-45, and MKN-28). The expression levels were subsequently correlated with the clinicopathological features of patients. siRNA against AFAP1-AS1 was transfected into GC cell lines, and cell proliferation, migration, and invasion were detected before and after silencing of AFAP1-AS1 expression. Luciferase reporter gene analysis was used to confirm the target gene of microRNA-205-5p (miR-205-5p) in 293T cells. The potential mechanism was subsequently investigated. RESULTS: qPCR results showed that AFAP1-AS1 was significantly overexpressed in GC tumor tissues and also GC cell lines, comparing to their paired non-GC tissues. Furthermore, statistical analysis revealed that the overexpression of AFAP1-AS1 was significantly correlated with tumor size (p=0.018) and grade of differentiation (p=0.042). Subsequently, artificially decreasing the expression of AFAP1-AS1 with its specific siRNA dramatically inhibited the proliferation, migration and invasion of GC cell lines (SGC-7901 and BGC-823 cells). Mechanical analysis suggested that AFAP1-AS1 is involved in regulation of its maternal gene, AFAP1, at both mRNA level and protein level. Luciferase reporter gene assay indicated that lncRNA AFAP1-AS1, as a ceRNA, is able to sponge miR-205-5p. Moreover, miR-205-5p has been well demonstrated to participate in the regulation of AFAP1 expression and the phenotypes of GC cells, including proliferation, migration and invasion. CONCLUSION: AFAP1-AS1, as a novel biomarker of GC, promotes the proliferation migration and invasion of GC cells and function as ceRNA to target AFAP1 by sponging miR-205-5p.		Cancer Manag Res. 2021 Jun 30;13:5163-5175. doi: 10.2147/CMAR.S307424. eCollection 2021.
5468	LncRNA	AATBC	miR-1245b-5p	CASK	Prostate Cancer Cell	Prostate Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;luciferase assay;Rescue assay;	34234553	Long Noncoding RNA AATBC Promotes the Proliferation and Migration of Prostate Cancer Cell Through miR-1245b-5p/CASK Axis.	INTRODUCTION: Long noncoding RNAs (lncRANs) as suppressive or oncogenic genes have been substantiated in prostate cancer (PCa). In the current study, the role and molecular mechanism of lncRNA AATBC in the progression of PCa was evaluated. METHODS: LncRNA AATBC and miR-1245b-5p expression were evaluated using RT-qPCR. CCK-8, colony-formation, apoptosis and transwell assay were used to analyze the in vitro role. The xenograft model was used to explore the in vivo role. Bioinformatics analysis and a dual luciferase assay, RIP and RNA pull down were used to confirm the interaction between lncRNA AATBC and 1245b-5p, as well as 1245b-5p and CASK. RESULTS: Firstly, we certified that the expression of AATBC was augmented in PCa, and knockdown of AATBC could significantly inhibit the growth of PCa in vitro and in vivo. Mechanistically, our results manifested that AATBC could directly bind to miR-1245b-5p. In addition, miR-1245b-5p played cancer-suppressive role in PCa cells. Moreover, CASK was attested as the target of miR-1245b-5p, and CASK was demonstrated to exert as oncogene in the progression of PCa. Finally, rescue assays illustrated that miR-1245b-5p downregulation or CASK restoration could greatly resist the restrained effects of AATBC knockdown on PCa progression. CONCLUSION: AATBC could accelerate the progression of PCa through regulating miR-1245b-5p/CASK axis, which provided a potential therapeutic target for PCa treatment.		Cancer Manag Res. 2021 Jun 28;13:5091-5100. doi: 10.2147/CMAR.S310529. eCollection 2021.
5469	LncRNA	DANCR	miR-145-3p	ZEB1	Cc Cells	Cervical Cancer	Homo sapiens (human)	Chromatin immunoprecipitation;	34233586	Krüppel-like factor 5-induced overexpression of long non-coding RNA DANCR promotes the progression of cervical cancer via repressing microRNA-145-3p to target ZEB1.	Long non-coding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) participates in the development of diverse cancers. Nevertheless, the impact of DANCR on cervical cancer (CC) remains largely unknown. This study aims to explore the effects of DANCR sponging microRNA-145-3p (miR-145-3p) on CC. Expression of KLF5, DANCR, miR-145-3p, and zinc finger E-box binding homeobox 1 (ZEB1) in CC and adjacent normal tissues was determined. Human CC cell lines were, respectively, treated with silenced DANCR or miR145-3p mimic/inhibitor. Then, the viability, migration, invasion, and apoptosis of CC cells were measured. The cell growth in vivo was observed as well. Chromatin immunoprecipitation assay was performed to analyze the binding of KLF5 and DANCR promoter. Interaction among DANCR, miR-145-3p, and ZEB1 was assessed. KLF5, DANCR, and ZEB1 were upregulated but miR-145-3p was downregulated in CC tissues. KLF5 activated DANCR expression and the high DANCR expression was related to tumor staging, infiltrating muscle depth and lymphatic metastasis of CC patients. Reduced DANCR or elevated miR-145-3p repressed malignant behaviors of CC cells. The tumor diameter and weight were also repressed by DANCR silencing or miR-145-3p elevation. The effect of DANCR knockdown on CC cells could be reversed by miR-145-3p inhibitor. MiR-145-3p was targeted by DANCR and ZEB1 was targeted by miR-145-3p. KLF5-induced overexpression of DANCR promotes CC progression via suppressing miR-145-3p to target ZEB1. This study may provide potential targets for CC treatment.		Cell Cycle. 2021 Jul;20(14):1441-1454. doi: 10.1080/15384101.2021.1941625. Epub 2021 Jul 8.
5470	LncRNA	LIPE-AS1	miR-654-3p	HDGF	Pca Cells	Prostate Cancer	Homo sapiens (human)  	RNA immunoprecipitation;RNA immunoprecipitation;	34233322	Long Noncoding RNA LIPE-AS1 Drives Prostate Cancer Progression by Functioning as a Competing Endogenous RNA for microRNA-654-3p and Thereby Upregulating Hepatoma-Derived Growth Factor.	INTRODUCTION: Information regarding the expression and roles of LIPE antisense RNA 1 (LIPE-AS1) in prostate cancer (PCa) progression is currently limited. We experimentally determined LIPE-AS1 expression in PCa tissues and cell lines. The specific functions of LIPE-AS1 in the oncogenicity of PCa were explored by evaluating a series of cellular functions. Moreover, the molecular mechanisms underlying the oncogenic roles of LIPE-AS1 in PCa were investigated. METHODS: The expression level of LIPE-AS1 was determined via quantitative reverse transcription polymerase chain reaction. Functional experiments, including the Cell Counting Kit-8 assay, Transwell migration and invasion assays, and tumor xenograft experiments, were used to determine the effects of LIPE-AS1 on PCa cells. The putative miRNA-binding LIPE-AS1 was predicted via bioinformatics analysis and further verified using the luciferase reporter and RNA immunoprecipitation assays. RESULTS: LIPE-AS1 was expressed at high levels in PCa cells; this result is consistent with that of The Cancer Genome Atlas database. Patients with PCa manifesting high LIPE-AS1 expression had shorter overall survival than those manifesting low LIPE-AS1 expression. Downregulated LIPE-AS1 inhibited PCa cell proliferation, migration, and invasion in vitro and impaired tumor growth in vivo. With respect to its mechanism, LIPE-AS1 functioned as a competing endogenous RNA for microRNA-654-3p (miR-654-3p) in PCa cells, and hepatoma-derived growth factor (HDGF) was the direct target of miR-654-3p. HDGF was positively regulated by LIPE-AS1 in PCa cells via the absorption of miR-654-3p. Rescue experiments confirmed that miR-654-3p downregulation or HDGF overexpression counteracts the inhibitory effects of LIPE-AS1 depletion on PCa cell proliferation, migration, and invasion. CONCLUSION: LIPE-AS1 promotes PCa malignancy by targeting the miR-654-3p/HDGF axis. Determining the LIPE-AS1/miR-654-3p/HDGF pathway may increase our understanding of PCa pathogenesis and contribute toward a wider applied scope.		Urol Int. 2021 Jul 7:1-16. doi: 10.1159/000516676.
5471	LncRNA	CRNDE	miR-146a-5p	NA	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	Flow Cytometry assay;Luciferase reporter assay;	34232111	Long non-coding RNA CRNDE regulates the growth and migration of prostate cancer cells by targeting microRNA-146a-5p.	The function of lncRNA CRNDE and its role in prostate cancer (PC) remains unclear. The aim of this study was to determine the expression level of lncRNA CRNDE in PC tissues and to elucidate its role in PC. The expression levels of lncRNA CRNDE were measured by quantitative reverse transcription polymerase chain reaction. The role of lncRNA CRNDE in PC cells was studied using loss-of-function assays in vitro. Cell proliferation, migration, invasion, and apoptosis were assessed via Cell Counting Kit-8, colony formation, flow cytometry, wound healing, and transwell chamber assays. A luciferase reporter assay was used to characterize the interaction between lncRNA CRNDE and miR-146a-5p. In PC tissues, the expression level of lncRNA CRNDE was upregulated. Moreover, knockdown of lncRNA CRNDE suppressed PC cell proliferation and migration and induced apoptosis in vitro. miR-146a-5p was verified as a direct target of lncRNA CRNDE. Moreover, the inhibition of miR-146a-5p partially counteracted the effects of lncRNA CRNDE on PC cell proliferation, migration, and invasion. In conclusion, lncRNA CRNDE may serve as a cancer promoter in PC by targeting miR-146a-5p. Therefore, lncRNA CRNDE could be a promising target for the clinical treatment of PC.		Bioengineered. 2021 Dec;12(1):2469-2479. doi: 10.1080/21655979.2021.1935402.
5472	LncRNA	PVT1	miR-365	ELF4	Glioma Tissues And Cells	Glioma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Flow Cytometry assay;luciferase assay;	34230224	Long Noncoding RNA PVT1 Promotes Stemness and Temozolomide Resistance through miR-365/ELF4/SOX2 Axis in Glioma.	Long non-coding RNA (lncRNA) are a class of non-coding RNAs demonstrated to play pivotal roles in regulating tumor progression. Therefore, deciphering the regulatory role of lncRNA in the development of glioma may offer a promising therapeutic target for treatment of glioma. We performed RT-qPCR analysis on the expression of lncRNA plasmacytoma variant translocation 1 (PVT1) and miR-365 in glioma tissues and cell lines. Cell proliferation and viability was assessed with CCK8 assay. Cell migration was assessed by wound healing assay. Transwell assay was used to assess cell invasion capacity. Expression of CD133+ cells was detected by flow cytometry. Western blot assay was used to detection the expression of ELF4 and stemness-related protein SOX2, Oct4 and Nanog. Bioinformatics and dual-luciferase assay were used to predict and validate the interaction between PVT1 and miR-365. Elevated PVT1 expression was observed in glioma tissues and cells. Knockdown of PVT1 and overexpression of miR-365 inhibited proliferation, migration, invasion and promoted stemness and Temozolomide (TMZ) resistance of glioma cells. PVT1 regulated ELF4 expression by competitively binds to miR-365. PVT1 regulated the stemness and sensitivity of TMZ of glioma cells through miR-365/ELF4/ SOX2 axis. This study identified that PVT1 promoted glioma stemness through miR-365/ELF4/SOX2 axis.		Exp Neurobiol. 2021 Jun 30;30(3):244-255. doi: 10.5607/en20060.
5473	LncRNA	HCG11	miR-579-3p	MDM2	Pancreatic Carcinoma Cells	Pancreatic Cancer	Homo sapiens (human)  	qPCR;RACE;Rescue assay;	34230221	LncRNA HCG11/miR-579-3p/MDM2 axis modulates malignant biological properties in pancreatic carcinoma via Notch/Hes1 signaling pathway.	BACKGROUND: Increasing reports have revealed that dysregulated expression of long non-coding RNAs (lncRNAs) is involved in pancreatic carcinoma progression. This study intends to explore the function and molecular mechanism of lncRNA HLA complex group 11 (HCG11) in pancreatic carcinoma. METHODS: The expression profiles of HCG11 in pancreatic carcinoma samples were detected by qPCR. Bioinformatics analysis was applied to detect the associations among HCG11/miR-579-3p/MDM2. The malignant properties of pancreatic carcinoma cells were measured by numerous biological assays. Xenograft model was exploited to detect the effect of HCG11 on tumor growth. RESULTS: A significant increase of HCG11 was occurred in pancreatic carcinoma samples. Knockdown of HCG11 suppressed the progression of pancreatic carcinoma cells. Bioinformatics analysis revealed that HCG11 upregulated MDM2 expression by competitively targeting miR-579-3p. The rescue assays showed that miR-579-3p reversed cell behaviors caused by HCG11, and MDM2 reversed cell properties induced by miR-579-3p. The Notch1 intracellular domain (NICD) and Hes1 protein levels were increased by overexpression of HCG11/MDM2. The tumor growth was suppressed after depletion of HCG11, followed by suppressing Ki67, PCNA and Vimentin expression, increasing TUNEL-positive cells and E-cadherin expression. CONCLUSIONS: Our observations highlighted that HCG11 contributed to the progression of pancreatic carcinoma by promoting growth and aggressiveness, and inhibiting apoptosis via miR-579-3p/MDM2/Notch/Hes1 axis.		Aging (Albany NY). 2021 Jun 21;13(12):16471-16484. doi: 10.18632/aging.203167. Epub 2021 Jun 21.
5474	LncRNA	LINC01287	miR-4500	MAP3K13	Colon Cancer Cells	Colon Cancer	Homo sapiens (human)  	Western blot;Flow Cytometry assay;Luciferase reporter assay;	34229645	LINC01287 facilitates proliferation, migration, invasion and EMT of colon cancer cells via miR-4500/MAP3K13 pathway.	BACKGROUND: Accumulated studies indicate that aberrant expression of long noncoding RNAs (lncRNAs) is associated with tumorigenesis and progression of colon cancer. In the present study, long intergenic non-protein coding RNA 1287 (LINC01287) was identified to up-regulate in colon cancer by transcriptome RNA-sequencing, but the exact function remained unclear. METHODS: Transcriptome RNA-sequencing was conducted to identify dysregulated lncRNAs. Expression of LINC01287 was evaluated by real-time quantitative PCR. The downstream targets of LINC01287 and miR-4500 were verified by luciferase reporter assay, pull down assay and western blot. The potential functions of LINC01287 were evaluated by cell viability assay, colony formation assay, soft agar assay, flow cytometry, transwell migration and invasion assay, and tumor xenograft growth in colon cancer cells. RESULTS: Our results indicated that LINC01287 was up-regulated in colon cancer patients. High LINC01287 expression was associated with advanced TNM stage, lymph node metastasis, distant metastasis and shorter overall survival. Knockdown of LINC01287 inhibited cell growth, colony formation in plates and soft agar, transwell cell migration and invasion, and epithelial-mesenchymal transition (EMT) of colon cancer cells, while LINC01287 overexpression had contrary effects. In addition, LINC01287 mediated MAP3K13 expression by sponging miR-4500, thus promoted NF-kB p65 phosphorylation. Restored MAP3K13 expression or miR-4500 knockdown partially abrogated the effects of silencing LINC01287 in colon cancer cells. CONCLUSION: Our findings demonstrated that the LINC01287/miR-4500/MAP3K13 axis promoted progression of colon cancer. Therefore, LINC01287 might be a potential therapeutic target and prognostic marker for colon cancer patients.		BMC Cancer. 2021 Jul 6;21(1):782. doi: 10.1186/s12885-021-08528-7.
5475	LncRNA	XIST	miR-98	BACH1	Neuronal Cell	Ischemic Stroke	Homo sapiens (human)  	qRT-PCR 	34227845	Long Noncoding RNA X-Inactive Specific Transcript Regulates Neuronal Cell Apoptosis in Ischemic Stroke Through miR-98/BACH1 Axis.	Long noncoding RNA X-inactive specific transcript (XIST) has been identified as a crucial regulator in neurodegenerative disorders. However, the role and mechanism of XIST in ischemic stroke remain elusive. In our study, we found that XIST expression was upregulated in both mice subjected to middle cerebral artery occlusion and oxygen-glucose deprivation (OGD)-treated neurons. Functional assays disclosed that the interference of XIST accelerated viability, and suppressed apoptosis and caspase-3 activity in OGD-treated neurons. Moreover, XIST interacted with miR-98, and miR-98 targeted BTB-to-CNC homology 1 (BACH1). miR-98 silencing or BACH1 overexpression counteracted XIST knockdown-mediated effects on cell viability and apoptosis in OGD-treated neurons. In conclusion, our data demonstrated that XIST facilitated the progression of ischemic stroke through regulating the miR-98/BACH1 axis. These findings might provide a novel therapeutic strategy for ischemic stroke treatment.		DNA Cell Biol. 2021 Jul;40(7):979-987. doi: 10.1089/dna.2020.6354. Epub 2021 Jul 6.
5476	LncRNA	FAM201A	miR-101	Vimentin	Nci-H520Nci-H520 And Sk-Mes-1Sk-Mes-1 Cells	Lung Squamous Carcinoma	Homo sapiens (human)  	qRT-PCR;Western blot;Flow Cytometry assay;	34227092	Long non-coding RNA FAM201A promotes lung squamous cell carcinoma progression through interaction with miR-101.	OBJECTIVE: This study aimed to investigate the mechanism of LncRNA FAM201A mediating lung squamous cell carcinoma progression through interaction with miR-101. PATIENTS AND METHODS: NCI-H520 cells and SK-MES-1 cells were transfected with miRNA-101-mimics and miRNA-101-inhibitor, the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect FAM201A and miR-101 expression. CCK-8, Wound healing assay and transwell assay were utilized to detect the influence of FAM201A on the malignancy of NCI-H520NCI-H520 and SK-MES-1SK-MES-1 cells. Cell apoptosis was determined by flow cytometry. The underlying pathways of FAM201A were measured using Western blot. Xenograft tumor experiments were conducted to detect tumor growth and metastasis in vivo.NCI-H520SK-MES-1 Kaplan-Meier method calculated patient survival. RESULTS: (1) Silencing of FAM201A inhibited the proliferation, migration and invasion of NCI-H520 and SK-MES-1cells and stimulated cell apoptosis significantly. Furthermore, FAM201A elimination hindered tumor growth and metastasis in vivo. (2) Compared with the si-control group, the protein expression of Ki67, Vimentin, Cleaved-caspase-3 and N-cadherin were decreased in the si-FAM201A group. (3) After transfection of miR-101-mimics, the expression level of Vimentin protein was significantly increased, while the expression level of Vimentin protein was significantly decreased after miR-101-inhibitor transfection. (4) MiR-101 mimics could alleviate FAM201A silencing-induced inhibitive effects on cell proliferation, migration, invasion and promotive effects on cell apoptosis. CONCLUSIONS: FAM201A could target miR-101 and upregulate Vimentin to inhibit lung cancer progression. FAM201A was expected to be a potential biomarker and therapeutic target for lung cancer.		Eur Rev Med Pharmacol Sci. 2021 Jun;25(12):4247-4257. doi: 10.26355/eurrev_202106_26130.
5477	LncRNA	KCNQ1OT1	miR-335-5p	NLRP1	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qRT-PCR 	34226539	Identification of the pyroptosis-related prognostic gene signature and the associated regulation axis in lung adenocarcinoma.	Lung adenocarcinoma (LUAD) remains the most common deadly disease and has a poor prognosis. Pyroptosis could regulate tumour cell proliferation, invasion, and metastasis, thereby affecting the prognosis of cancer patients. However, the role of pyroptosis-related genes (PRGs) in LUAD remains unclear. In our study, comprehensive bioinformatics analysis was performed to construct a prognostic gene model and ceRNA network. The correlations between PRGs and tumour-immune infiltration, tumour mutation burden, and microsatellite instability were evaluated using Pearson's correlation analysis. A total of 23 PRGs were upregulated or downregulated in LUAD. The genetic mutation variation landscape of PRG in LUAD was also summarised. Functional enrichment analysis revealed that these 33 PRGs were mainly involved in pyroptosis, the NOD-like receptor signalling pathway, and the Toll-like receptor signalling pathway. Prognosis analysis indicated a poor survival rate in LUAD patients with low expression of NLRP7, NLRP1, NLRP2, and NOD1 and high CASP6 expression. A prognostic PRG model constructed using the above five prognostic genes could predict the overall survival of LUAD patients with medium-to-high accuracy. Significant correlation was observed between prognostic PRGs and immune-cell infiltration, tumour mutation burden, and microsatellite instability. A ceRNA network was constructed to identify a lncRNA KCNQ1OT1/miR-335-5p/NLRP1/NLRP7 regulatory axis in LUAD. In conclusion, we performed a comprehensive bioinformatics analysis and identified a prognostic PRG signature containing five genes (NLRP7, NLRP1, NLRP2, NOD1, and CASP6) for LUAD patients. Our results also identified a lncRNA KCNQ1OT1/miR-335-5p/NLRP1/NLRP7 regulatory axis, which may also play an important role in the progression of LUAD. Further study needs to be conducted to verify this result.		Cell Death Discov. 2021 Jun 25;7(1):161. doi: 10.1038/s41420-021-00557-2.
5478	LncRNA	KCNQ1OT1	miR-335-5p	NLRP7	Lung Adenocarcinoma Cells	Lung Adenocarcinoma	Homo sapiens (human)  	qRT-PCR 	34226539	Identification of the pyroptosis-related prognostic gene signature and the associated regulation axis in lung adenocarcinoma.	Lung adenocarcinoma (LUAD) remains the most common deadly disease and has a poor prognosis. Pyroptosis could regulate tumour cell proliferation, invasion, and metastasis, thereby affecting the prognosis of cancer patients. However, the role of pyroptosis-related genes (PRGs) in LUAD remains unclear. In our study, comprehensive bioinformatics analysis was performed to construct a prognostic gene model and ceRNA network. The correlations between PRGs and tumour-immune infiltration, tumour mutation burden, and microsatellite instability were evaluated using Pearson's correlation analysis. A total of 23 PRGs were upregulated or downregulated in LUAD. The genetic mutation variation landscape of PRG in LUAD was also summarised. Functional enrichment analysis revealed that these 33 PRGs were mainly involved in pyroptosis, the NOD-like receptor signalling pathway, and the Toll-like receptor signalling pathway. Prognosis analysis indicated a poor survival rate in LUAD patients with low expression of NLRP7, NLRP1, NLRP2, and NOD1 and high CASP6 expression. A prognostic PRG model constructed using the above five prognostic genes could predict the overall survival of LUAD patients with medium-to-high accuracy. Significant correlation was observed between prognostic PRGs and immune-cell infiltration, tumour mutation burden, and microsatellite instability. A ceRNA network was constructed to identify a lncRNA KCNQ1OT1/miR-335-5p/NLRP1/NLRP7 regulatory axis in LUAD. In conclusion, we performed a comprehensive bioinformatics analysis and identified a prognostic PRG signature containing five genes (NLRP7, NLRP1, NLRP2, NOD1, and CASP6) for LUAD patients. Our results also identified a lncRNA KCNQ1OT1/miR-335-5p/NLRP1/NLRP7 regulatory axis, which may also play an important role in the progression of LUAD. Further study needs to be conducted to verify this result.		Cell Death Discov. 2021 Jun 25;7(1):161. doi: 10.1038/s41420-021-00557-2.
5479	LncRNA	LINC00284	miR-3127-5p	E2F7	Ptc And Adjacent Non-Tumor Tissues	Papillary Thyroid Cancer	Mus musculus (mouse)	qRT-PCR;	34226533	Long noncoding RNA LINC00284 facilitates cell proliferation in papillary thyroid cancer via impairing miR-3127-5p targeted E2F7 suppression.	Accumulating evidence has suggested that long noncoding RNAs (lncRNAs) exert crucial modulation roles in the biological behaviors of multiple malignancies. Nonetheless, the specific function of lncRNA LINC00284 in papillary thyroid cancer (PTC) remains not fully understood. The objective of this research was to explore the influence of LINC00284 in PTC and elucidate its potential mechanism. The Cancer Genome Atlas (TCGA), gene expression omnibus (GEO) datasets were used to analyze LINC00284 expression differences in thyroid cancer and normal samples, followed by the verification of qRT-PCR in our own PTC and adjacent non-tumor tissues. The impacts of LINC00284 on PTC cell growth were detected in vitro via CCK-8, colony formation, EdU assays, and in vivo via a xenograft tumor model. Bioinformatics analyses and biological experiments were conducted to illuminate the molecular mechanism. We found that LINC00284 expression was remarkably increased in PTC tissues and its overexpression was closely correlated with larger tumor size. In addition, silencing LINC00284 could effectively attenuate PTC cell proliferation, induce apoptosis and G1 arrest in vitro, as well as suppress tumorigenesis in mouse xenografts. Mechanistic investigations showed that LINC00284 acted as a competing endogenous RNA (ceRNA) for miR-3127-5p, thus resulting in the disinhibition of its endogenous target E2F7. In short, our findings indicated that LINC00284-miR-3127-5p-E2F7 axis exerted oncogenic properties in PTC and may offer a new promising target for the diagnosis and therapy of PTC.		Cell Death Discov. 2021 Jun 26;7(1):156. doi: 10.1038/s41420-021-00551-8.
5480	LncRNA	MIR155HG	MiR-485-3p	PSIP1	Elanoma Cell Lines And Tissues	Melanoma	Mus musculus (mouse)	Cell proliferation assay;ChIP;	34225636	The LncRNA MIR155HG is Upregulated by SP1 in Melanoma Cells and Drives Melanoma Progression via Modulating the MiR-485-3p/PSIP1 Axis.	BACKGROUND: MIR155HG is a long non-coding RNA (lncRNA) that has been shown to be dysregulated in a range of tumor types, but the functions of this lncRNA in melanoma remain to be explored. OBJECTIVES: We explored the functions of lncRNA MIR155HG in melanoma progression. METHODS: The expression of miR155HG was analyzed in clinical melanoma. Bioinformatics analysis was performed to assess the potential tumor-related functions of miR155HG. The interaction of miR155HG and SP1 and the inhibition of PSIP1 by miR-485-3p were analyzed by ChIP, luciferase reporter experiments, and biological effects in melanoma were explored by colony formation assays, EdU cell proliferation assays, Transwell analysis and intracranial melanoma mouse model. RESULTS: Herein, we found that MIR155HG was markedly upregulated in melanoma cell lines and tissues. We further determined that the SP1 transcription factor was responsible for driving MIR155HG upregulation in melanoma. Elevated MIR155HG levels were linked to decreased overall survival (OS) in melanoma patients, and we further determined that MIR155HG expression was an independent predictor of melanoma patient prognosis. When MIR155HG was knocked down in melanoma cells, this impaired their proliferative, migratory, and invasive activity. Using predictive bioinformatics analyses, we identified miR-485-3p as a microRNA (miRNA) capable of binding to both MIR155HG and the 3' UTR of PSIP1. CONCLUSION: Together, these results suggest that MIR155HG is capable of promoting melanoma cell proliferation via the miR-485-3p/PSIP1 axis. These novel findings provide new insights into the development of melanoma, potentially highlighting future avenues for therapeutic intervention.		Anticancer Agents Med Chem. 2021 Mar 21. doi: 10.2174/1871520621666210322092906.
5481	LncRNA	SNHG14	miR-181c-5p	BMF	Middle Cerebral Artery Occlusion (Mcao) Model	Ischemic Stroke	Homo sapiens (human)  	ELISA;MTT assay;Western blot;Flow Cytometry assay;MTT assay;	34224818	Downregulation of lncRNA SNHG14 alleviates neurons injury by modulating the miR-181c-5p/BMF axis in ischemic stroke.	PURPOSE: Our study aims to explore the role and mechanism of lncRNA small nucleolar RNA host gene 14 (SNHG14) in brain injury caused by ischemic stroke (IS). METHODS: Middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation (OGD)-induced primary cortical neurons were used to construct in vitro and in vivo models of IS, respectively. Relative SNHG14, miR-181c-5p and Bcl-2-modifying factor (BMF) expression levels were detected by quantitative real-time PCR. MTT assay, EdU staining and flow cytometry were used to measure cell proliferation and apoptosis. The protein levels of apoptosis marker and BMF were determined using western blot analysis. ELISA assay was performed to assess cell inflammatory response and injury. RESULTS: SNHG14 was upregulated and miR-181c-5p was downregulated in MCAO model and OGD-induced primary cortical neurons. Silencing of SNHG14 markedly promoted proliferation, restrained apoptosis and inflammatory response in OGD-induced primary cortical neurons to alleviate neurons injury. In terms of mechanism, miR-181c-5p could be sponged by SNHG14, and its inhibitor reversed the inhibition effect of SNHG14 silencing on OGD-induced neurons injury. Also, BMF was a target of miR-181c-5p, and its overexpression could reverse the suppressive effect of miR-181c-5p on OGD-induced neurons injury. Our data uncovered that BMF expression was positively regulated by SNHG14 and negatively regulated by miR-181c-5p. CONCLUSION: Our results indicated that SNHG14 promoted neurons injury through regulating miR-181c-5p/BMF axis, suggesting that SNHG14 might be a potential target to alleviate IS-induced brain injury.		Brain Res Bull. 2021 Sep;174:379-388. doi: 10.1016/j.brainresbull.2021.06.026. Epub 2021 Jul 2.
5482	LncRNA	MEOX2-AS1	miR-143-3p	VDAC1	Cc Cells	Cervical Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;RT-PCR;Luciferase reporter assay;	34224325	The promotion of cervical cancer progression by signal transducer and activator of transcription 1-induced up-regulation of lncRNA MEOX2-AS1 as a competing endogenous RNA through miR-143-3p/VDAC1 pathway.	Long non-coding RNAs (lncRNAs) are the new regulators and biomarkers for various tumors. However, in cervical cancer (CC), the potential roles of lncRNAs are not well characterized. This research aimed at exploring the roles of MEOX2 antisense RNA 1(MEOX2-AS1) in CC progression and the underlying mechanisms. The examination of MEOX2-AS1 levels in CC specimens and cell lines was conducted by RT-PCR. Loss-of-function experiments were performed for the assays of proliferation, migration, and invasion of CC cells after various treatments. Animal experiments were applied for the determination of the effects of MEOX2-AS1 in vivo. Bioinformatics analysis, together with dual-luciferase reporter assays, was applied to demonstrate the possible relationships among MEOX2-AS1, miR-143-3p and VDAC1. In the paper, we reported that MEOX2-AS1 levels were distinctly upregulated in CC cells and tissues, and higher MEOX2-AS1 expressions indicated a poor clinical outcome. Besides, STAT1 could activate transcriptions of MEOX2-AS1 by binding directly to its promoter region. The silence of MEOX2-AS1 suppressed the metastatic and proliferative ability of CC cells, as revealed by functional assays. Mechanistically, MEOX2-AS1 sponged miR-143-3p to regulate VDAC1 expressions. Furthermore, miR-143-3p inhibitor reversed the anti-proliferation and anti-metastasis effect of MEOX2-AS1 knockdown. Overall, the data indicated that the MEOX2-AS1/miR-143-3p/VDAC1 pathway participated in CC progression, making it a novel therapeutic target for CC cures.		Bioengineered. 2021 Dec;12(1):3322-3335. doi: 10.1080/21655979.2021.1947174.
5483	LncRNA	HULC	miR-383-5p	VAMP2	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34223709	Long noncoding RNA highly upregulated in liver cancer promotes the progression of hepatocellular carcinoma and attenuates the chemosensitivity of oxaliplatin by regulating miR-383-5p/vesicle-associated membrane protein-2 axis.	We aimed to explore the function and underlying mechanism of highly upregulated in liver cancer (HULC; an long noncoding RNAs) in hepatocellular carcinoma (HCC) and chemosensitivity of oxaliplatin (Oxa). The expression of HULC, miR-383-5p, and vesicle-associated membrane protein-2 (VAMP2) was detected by quantitative real-time polymerase chain reaction. Western blot assay was applied for measuring the protein expression of cyclinD1, cleaved-caspase-3, light Chain 3 I/II, p62, and VAMP2. Cell viability and Oxa IC50 value were determined by Cell Counting Kit-8 assay. A colony formation assay was conducted to evaluate colony formation ability. Cell apoptosis was assessed by flow cytometry. The interaction between miR-383-5p and HULC or VAMP2 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. The mice xenograft model was established to investigate the roles of HULC in vivo. HULC and VAMP2 were overexpressed whereas miR-383-5p was lowly expressed in HCC tissues. HULC overexpression promoted the progression of HCC cells and inhibited chemosensitivity of Oxa by increasing cell proliferation and protective autophagy and inhibiting apoptosis, whereas HULC silence presented opposite effects. Moreover, miR-383-5p was a direct target of HULC and miR-383-5p reversed the effects of HULC on the progression of HCC cells and chemosensitivity of Oxa. Besides, HULC acted as a molecular sponge of miR-383-5p to regulate VAMP2 expression. HULC promoted the progression of HCC and inhibited Oxa sensitivity by regulating miR-383-5p/VAMP2 axis, elucidating a novel regulatory mechanism for chemosensitivity of Oxa and providing a potential lncRNA-targeted therapy for HCC.		Pharmacol Res Perspect. 2021 Aug;9(4):e00815. doi: 10.1002/prp2.815.
5484	LncRNA	MALAT1	miR-655-3p	ATAD2	Rb Tissues And Cells	Retinoblastoma	Homo sapiens (human)  	qRT-PCR 	34222668	lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p.	Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB. MALAT1 was upregulated in RB tissues and cells, and it served as a competing endogenous RNA (ceRNA) and inhibited miRNA-655-3p (miR-655-3p) expression, which eventually regulated the expression of miR-655-3p downstream target ATPase Family AAA Domain Containing 2 (ATAD2). The level of ATAD2 significantly increased, while that of miR-655-3p remarkably decreased in RB tissues and cells. MALAT1 depletion inhibited cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT), but promoted apoptosis in vitro and blocked xenograft tumor growth in vivo. MALAT1 exerted its oncogenic functions in RB by regulating miR-655-3p/ATAD2 axis.		Open Med (Wars). 2021 Jun 24;16(1):931-943. doi: 10.1515/med-2021-0290. eCollection 2021.
5485	LncRNA	TUG1	miR-493-3p	NA	Neuro-2A Cells	Cerebral Ischemia-Reperfusion Injury	Homo sapiens (human)  	Flow cytometry assay;Western blot;Flow Cytometry assay;	34222667	Long non-coding RNA TUG1 aggravates cerebral ischemia and reperfusion injury by sponging miR-493-3p/miR-410-3p.	BACKGROUND: Cerebral ischemia and reperfusion injury (CIRI) affects bodily function by causing irreversible damage to brain cells. The diverse pathophysiological course factors hinder the research work to go deeper. Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to be related to CIRI. This study explored the undefined regulatory pathway of TUG1 in CIRI. METHODS: Quantitative real-time polymerase chain reaction was applied to test the expression of TUG1, microRNA (miR)-493-3p and miR-410-3p. The viability and apoptosis of oxygen and glucose deprivation/reoxygen (OGD/R) model cells were evaluated by cell counting kit-8 and flow cytometry assay, respectively. The determination of inflammatory factors of interleukin-6, interleukin-1b and tumor necrosis factor-a was presented by enzyme-linked immunosorbent assay. The oxidative stress was performed by measuring the generation of malondialdehyde, reactive oxygen species and the activity of superoxide dismutase. Cytotoxicity was presented by measuring the generation of lactate dehydrogenase. Western blot assay was devoted to assessing the level of apoptosis-related factors (cleaved-caspase-3 and cleaved-caspase-9) and the protein level of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) pathway-related factors in neuro-2a cells treated by OGD/R. Besides, online database starBase was applied to predict the potential binding sites of TUG1 to miR-493-3p and miR-410-3p, which was further confirmed by the dual-luciferase reporter system. RESULTS: The expression of TUG1 was upregulated, while miR-493-3p or miR-410-3p was downregulated in the serum of CIRI and OGD/R model cells. Meanwhile, knockdown of TUG1 eliminated the suppression in proliferation, the promotion in apoptosis, inflammation and oxidative stress, as well as the cytotoxicity in OGD/R model cells. Interestingly, the inhibition of miR-493-3p or miR-410-3p allayed the above effects. In addition, TUG1 harbored miR-493-3p or miR-410-3p and negatively regulated their expression. Finally, the TUG1 activated JNK and p38 MAPK pathways by sponging miR-493-3p/miR-410-3p. CONCLUSION: TUG1 motivated the development of CIRI by sponging miR-493-3p/miR-410-3p to activate JNK and p38 pathways. The novel role of TUG1 in CIRI may contribute to the advancement of CIRI treatment.		Open Med (Wars). 2021 Jun 24;16(1):919-930. doi: 10.1515/med-2021-0253. eCollection 2021.
5486	LncRNA	TUG1	miR-410-3p	NA	Neuro-2A Cells	Cerebral Ischemia-Reperfusion Injury	Homo sapiens (human)  	Flow cytometry assay;Western blot;Flow Cytometry assay;	34222667	Long non-coding RNA TUG1 aggravates cerebral ischemia and reperfusion injury by sponging miR-493-3p/miR-410-3p.	BACKGROUND: Cerebral ischemia and reperfusion injury (CIRI) affects bodily function by causing irreversible damage to brain cells. The diverse pathophysiological course factors hinder the research work to go deeper. Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to be related to CIRI. This study explored the undefined regulatory pathway of TUG1 in CIRI. METHODS: Quantitative real-time polymerase chain reaction was applied to test the expression of TUG1, microRNA (miR)-493-3p and miR-410-3p. The viability and apoptosis of oxygen and glucose deprivation/reoxygen (OGD/R) model cells were evaluated by cell counting kit-8 and flow cytometry assay, respectively. The determination of inflammatory factors of interleukin-6, interleukin-1b and tumor necrosis factor-a was presented by enzyme-linked immunosorbent assay. The oxidative stress was performed by measuring the generation of malondialdehyde, reactive oxygen species and the activity of superoxide dismutase. Cytotoxicity was presented by measuring the generation of lactate dehydrogenase. Western blot assay was devoted to assessing the level of apoptosis-related factors (cleaved-caspase-3 and cleaved-caspase-9) and the protein level of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) pathway-related factors in neuro-2a cells treated by OGD/R. Besides, online database starBase was applied to predict the potential binding sites of TUG1 to miR-493-3p and miR-410-3p, which was further confirmed by the dual-luciferase reporter system. RESULTS: The expression of TUG1 was upregulated, while miR-493-3p or miR-410-3p was downregulated in the serum of CIRI and OGD/R model cells. Meanwhile, knockdown of TUG1 eliminated the suppression in proliferation, the promotion in apoptosis, inflammation and oxidative stress, as well as the cytotoxicity in OGD/R model cells. Interestingly, the inhibition of miR-493-3p or miR-410-3p allayed the above effects. In addition, TUG1 harbored miR-493-3p or miR-410-3p and negatively regulated their expression. Finally, the TUG1 activated JNK and p38 MAPK pathways by sponging miR-493-3p/miR-410-3p. CONCLUSION: TUG1 motivated the development of CIRI by sponging miR-493-3p/miR-410-3p to activate JNK and p38 pathways. The novel role of TUG1 in CIRI may contribute to the advancement of CIRI treatment.		Open Med (Wars). 2021 Jun 24;16(1):919-930. doi: 10.1515/med-2021-0253. eCollection 2021.
5487	LncRNA	LINC00174	miR-378a-3p	SSH2	Os Cells	Osteosarcoma	Homo sapiens (human)  	RIP assay;Rescue assay;RNA pull-down;	34222341	LINC00174 Facilitates Cell Proliferation, Cell Migration and Tumor Growth of Osteosarcoma via Regulating the TGF-b/SMAD Signaling Pathway and Upregulating SSH2 Expression.	Osteosarcoma (OS), a frequent malignant tumor which mainly occurs in the bone. The roles of long noncoding RNAs (lncRNAs) have been revealed in cancers, including OS. LncRNA long intergenic non-protein coding RNA (LINC00174) has been validated as an oncogene in several cancers. However, the role of LINC00174 in OS has not been explored. In our research, loss-of-function assays were conducted to explore the function of LINC00174 in OS cells. Then, we explored the downstream pathway of LINC00174 in OS cells. Bioinformatics, RNA pull-down and RIP experiments investigated the downstream mechanism of LINC00174 in OS cells. Finally, in vivo assays clarified the effect of LINC00174 on tumorigenesis. We found that LINC00174 was upregulated in OS tissues and cells. LINC00174 knockdown repressed OS cell growth. Mechanistically, LINC00174 knockdown suppressed the TGF-b/SMAD pathway. LINC00174 interacted with miR-378a-3p, and slingshot protein phosphatase 2 (SSH2) 3'UTR was targeted by miR-378a-3p in OS cells. Rescue assays showed that SSH2 upregulation or miR-378a-3p inhibition counteracted the inhibitory effect of LINC00174 depletion in OS cell growth. Additionally, LINC00174 depletion suppressed tumor growth in mice. In conclusion, LINC00174 promotes OS cellular malignancy and tumorigenesis via the miR-378a-3p/SSH2 axis and the TGF-b/SMAD pathway, which might provide a novel insight for OS treatment.		Front Mol Biosci. 2021 Jun 17;8:697773. doi: 10.3389/fmolb.2021.697773. eCollection 2021.
5488	LncRNA	MEG3	MiR-29a	PTEN	Testicular Tissues	Testicular Ischemia-Reperfusion Injury	Homo sapiens (human)  	ELISA;RIP assay;Western blot;Immunohistochemistry;Luciferase reporter assay;	34222244	Long Non-coding RNA MEG3 Promotes Pyroptosis in Testicular Ischemia-Reperfusion Injury by Targeting MiR-29a to Modulate PTEN Expression.	Increasing evidence shows that the abnormal long non-coding RNAs (lncRNAs) expression is closely related to ischemia-reperfusion injury (I/R) progression. Studies have previously described that lncRNA MEG3 regulates pyroptosis in various organs I/R. Nevertheless, the related mechanisms of MEG3 in testicular I/R has not been clarified. The aim of this research is to unravel underlying mechanisms of the regulation of pyroptosis mediated by MEG3 during testicular I/R. We have established a testicular torsion/detorsion (T/D) model and an oxygen-glucose deprivation/reperfusion (OGD/R)-treated spermatogenic cell model. Testicular ischemic injury was assessed by H&E staining. Western blotting, quantitative real-time PCR, MDA, and SOD tests and immunohistochemistry measured the expression of MEG3 and related proteins and the level of ROS production in testicular tissues. Quantitative real-time PCR and western blotting determined the relative expression of MEG3, miR-29a, and relevant proteins in GC-1. Cell viability and cytotoxicity were measured by CCK-8 and LDH assays. Secretion and expression levels of inflammatory proteins were determined by ELISA, immunofluorescence and western blotting. The interaction among MEG3, miR-29a, and PTEN was validated through a dual luciferase reporter assay and Ago2-RIP. In this research, we identified that MEG3 was upregulated in animal specimens and GC-1. In loss of function or gain of function assays, we verified that MEG3 could promote pyroptosis. Furthermore, we found that MEG3 negatively regulated miR-29a expression at the posttranscriptional level and promoted PTEN expression, and further promoted pyroptosis. Therefore, we explored the interaction among MEG3, miR-29a and PTEN and found that MEG3 directly targeted miR-29a, and miR-29a targeted PTEN. Overexpression of miR-29a effectively eliminated the upregulation of PTEN induced by MEG3, indicating that MEG3 regulates PTEN expression by targeting miR-29a. In summary, our research indicates that MEG3 contributes to pyroptosis by regulating miR-29a and PTEN during testicular I/R, indicating that MEG3 may be a potential therapeutic target in testicular torsion.		Front Cell Dev Biol. 2021 Jun 18;9:671613. doi: 10.3389/fcell.2021.671613. eCollection 2021.
5489	LncRNA	FGD5-AS1	miR-497-5p	MACC1	Breast Cancer Cells	Breast Cancer	Homo sapiens (human)  	qPCR;Western blot;	34221989	LncRNA FGD5-AS1 Facilitates the Radioresistance of Breast Cancer Cells by Enhancing MACC1 Expression Through Competitively Sponging miR-497-5p.	BACKGROUND: LncRNA-FGD5-AS1, as an oncogene, participates in the development and progress of various cancers. However, the exact role and the molecular mechanisms by which FGD5-AS1 regulates radiosensitivity in breast cancer (BC) remains largely unknown. METHODS: We used X-Ray weekly-dose-increase method to establish radiation-resistance cell lines. Bioinformatics tools analyze the expression of FGD5-AS1 in breast cancer tissue and evaluated the relationship between FGD5-AS1 and clinic-pathological features. CCK-8 and colony formation were used to analyze cell proliferation. Western blotting and qPCR were applied to detect protein and gene expression, respectively. RNA interference was used to knock down the endogenous gene expression. Luciferase reporter system and immunoprecipitates were applied to verify the target of FGD5-AS1. RESULT: FGD5-AS1 was overexpressed in BC tissues and radiation-resistance cell lines. Higher levels of FGD5-AS1 predicted poorer clinical characteristics and prognosis. Loss-of-function FGD5-AS1 sensitized BC cells to X-ray, meanwhile, the cell gained radiation-resistance when exogenous FGD5-AS1 was expressed. FGD5-AS1 depletion arrested cells at G0/G1 and triggers cell apoptosis. The starBase database (ENCORI), predicted binding site of miR-497-5p in FGD5-AS1 sequence, and luciferase reporter system and immunoprecipitates verified miR-497-5p was the target of FGD5-AS1. Furthermore, MACC1 was predicted and verified as the target of miR-497-5p. Loss-of-function FGD5-AS1 sensitized ionizing radiation was rescued by the up-regulation of MACC1 and the inhibition of miR-497. CONCLUSION: FGD5-AS1 displays an oncogene profile in CRC; patients with high expression of FGD5-AS1 should benefit less from radiotherapy and need a more frequent follow-up. Besides, FGD5-AS1 may be a potential therapeutic target for CRC.		Front Oncol. 2021 Jun 18;11:671853. doi: 10.3389/fonc.2021.671853. eCollection 2021.
5490	LncRNA	MALAT1	miR-124	NA	Cervical Tumor Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR 	34221014	LncRNA MALAT1 Accelerates Cervical Carcinoma Proliferation by Suppressing miR-124 Expression in Cervical Tumor Cells.	Emerging studies have clarified the critical role of LncRNA MALAT1 in various pathological progressions. Here, we identified its positive relationship with cervical carcinoma proliferation. Cervical carcinoma has been considered as one of the most malignant tumors among female. Thus, our study was designed to investigate the underlying mechanism of LncRNA MALAT1 on cervical tumor cell proliferation. We observed that miR-124 was the potential target of LncRNA MALAT1 in cervical tumor cell lines (Hela, C-33A, Caski, and SiHa), the expression level of which is negatively correlated with LncRNA MALAT1 in cervical tumor cells, tissues of cervical patients, and mice. Gain- or loss-of-function analyses in cervical tumor cells have further verified the regulatory role of MALAT1 on miR-124. Additionally, the proliferation of cervical carcinoma was inhibited by miR-124 overexpression, whereas it was blocked by LV-MALAT1 transfection. In vivo assays, overexpression of miR-124, or knockdown of MALAT1 exhibited beneficial effects on tumor weight, size, and volume, together with elevating the survival rate, tightly related with the progression of cervical cancer. In conclusion, LncRNA MALAT1 disabled the effects of miR-124 as an inhibitory sponge, accelerating the progression of cervical carcinoma.		J Oncol. 2021 Jun 15;2021:8836078. doi: 10.1155/2021/8836078. eCollection 2021.
5491	LncRNA	SDCBP2-AS1	miR-100-5p	EPDR1	Oc Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34218800	Long non-coding RNA SDCBP2-AS1 delays the progression of ovarian cancer via microRNA-100-5p-targeted EPDR1.	BACKGROUND: Dysregulation of long non-coding RNAs has been implied to connect with cancer progression. This research was to decipher the mechanism of long non-coding RNA SDCBP2-AS1 in ovarian cancer (OC) through regulation of microRNA (miR)-100-5p and ependymin-related protein 1 (EPDR1). METHODS: LncRNA SDCBP2-AS1 and EPDR1 levels in OC were assessed by Gene Expression Profiling Interactive Analysis. lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 levels in OC tissues and cells were determined. SKOV3 and A2780 cells were transfected with lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1-related plasmids or sequences, and then their functions in cell viability, apoptosis, migration, and invasion were evaluated. The interplay of lncRNA SDCBP2-AS1, miR-100-5p, and EPDR1 was clarified. RESULTS: LncRNA SDCBP2-AS1 and EPDR1 levels were suppressed whilst miR-100-5p level was elevated in OC. After upregulating lncRNA SDCBP2-AS1 or EPDR1, viability, migration, and invasion of OC cells were impaired, and apoptosis rate was increased. Downregulating EPDR1 or upregulating miR-100-5p partially mitigated upregulated lncRNA SDCBP2-AS1-induced impacts on the biological functions of OC cells. LncRNA SDCBP2-AS1 sponged miR-100-5p, and EPDR1 was targeted by miR-100-5p. CONCLUSION: It is illustrated that lncRNA SDCBP2-AS1 regulates EPDR1 by sponge adsorption of miR-100-5p to inhibit the progression of OC.		World J Surg Oncol. 2021 Jul 4;19(1):199. doi: 10.1186/s12957-021-02295-2.
5492	LncRNA	MSC-AS1	miR-302a-3p	IGF2BP2	Melanoma Cell Lines	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	34218464	LncRNA MSC-AS1 motivates the development of melanoma by binding to miR-302a-3p and recruiting IGF2BP2 to elevate LEF1 expression.	Melanoma is considered as the most common malignancy among skin cancers. The roles of many long non-coding RNAs (lncRNAs) have been clearly identified in multiple tumors. Nevertheless, lncRNA MSC antisense RNA 1 (MSC-AS1) has not been deeply investigated melanoma. In the present study, RT-qPCR and western blot analyses were used to measure the expression of RNAs and proteins. Functional and in vivo assays were implemented to detect the function of genes in melanoma. RNA pull-down, RIP and luciferase reporter assays were applied for determining interactions between RNA and protein molecules. It was observed that MSC-AS1 and lymphoid enhancer-binding factor 1 (LEF1) were remarkably up-regulated while microRNA-302a-3p (miR-302a-3p) down-regulated in melanoma cell lines. The silencing of MSC-AS1 hindered cell proliferation, migration and epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo. Furthermore, MSC-AS1 regulated LEF1 expression through sponging miR-302a-3p and recruiting insulin like growth factor 2 mRNA-binding protein 2 (IGF2BP2). Eventually, LEF1 overexpression rescued cell progression impaired by MSC-AS1 knock-down. In summary, our research identified the MSC-AS1/miR-302a-3p/IGF2BP2/LEF1 axis in melanoma development, which indicated that MSC-AS1 is a potential biomarker in the treatment of melanoma.		Exp Dermatol. 2021 Jul 4. doi: 10.1111/exd.14427.
5493	LncRNA	MSC-AS1	miR-302a-3p	LEF1	Melanoma Cell Lines	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RIP assay;Western blot;Luciferase reporter assay;RNA pull-down;	34218464	LncRNA MSC-AS1 motivates the development of melanoma by binding to miR-302a-3p and recruiting IGF2BP2 to elevate LEF1 expression.	Melanoma is considered as the most common malignancy among skin cancers. The roles of many long non-coding RNAs (lncRNAs) have been clearly identified in multiple tumors. Nevertheless, lncRNA MSC antisense RNA 1 (MSC-AS1) has not been deeply investigated melanoma. In the present study, RT-qPCR and western blot analyses were used to measure the expression of RNAs and proteins. Functional and in vivo assays were implemented to detect the function of genes in melanoma. RNA pull-down, RIP and luciferase reporter assays were applied for determining interactions between RNA and protein molecules. It was observed that MSC-AS1 and lymphoid enhancer-binding factor 1 (LEF1) were remarkably up-regulated while microRNA-302a-3p (miR-302a-3p) down-regulated in melanoma cell lines. The silencing of MSC-AS1 hindered cell proliferation, migration and epithelial-mesenchymal transition (EMT) in vitro and tumor growth in vivo. Furthermore, MSC-AS1 regulated LEF1 expression through sponging miR-302a-3p and recruiting insulin like growth factor 2 mRNA-binding protein 2 (IGF2BP2). Eventually, LEF1 overexpression rescued cell progression impaired by MSC-AS1 knock-down. In summary, our research identified the MSC-AS1/miR-302a-3p/IGF2BP2/LEF1 axis in melanoma development, which indicated that MSC-AS1 is a potential biomarker in the treatment of melanoma.		Exp Dermatol. 2021 Jul 4. doi: 10.1111/exd.14427.
5494	LncRNA	ENTPD3-AS1	miR-155	HIF-1a	Rcc Tissues	Renal Cancer	Homo sapiens (human)  	ChIP;CHIP-PCR;Luciferase reporter assay;	34218253	SNP-mediated lncRNA-ENTPD3-AS1 upregulation suppresses renal cell carcinoma via miR-155/HIF-1a signaling.	Over the last decade, more than 10 independent SNPs have been discovered to be associated with the risk of renal cell carcinoma among different populations. However, the biological functions of them remain poorly understood. In this study, we performed eQTL analysis, ChIP-PCR, luciferase reporter assay, and Cox regression analysis to identify the functional role and underlying mechanism of rs67311347 in RCC. The ENCORI database, which contains the lncRNA-miRNA-mRNA interactions, was used to explore the possible target miRNA of ENTPD3-AS1. The results showed that the G > A mutation of rs67311347 created a binding motif of ZNF8 and subsequently upregulated ENTPD3-AS1 expression by acting as an enhancer. The TCGA-KIRC and our cohorts both confirmed the downregulation of ENTPD3-AS1 in RCC tissues and demonstrated that increased ENTPD3-AS1 expression was associated with good OS and PFS. Furthermore, ENTPD3-AS1 interacted with miR-155-5p and activated the expression of HIF-1a, which was an important tumor suppressor gene in the development of RCC. The functional experiments revealed that overexpression of ENTPD3-AS1 inhibited cell proliferation in RCC cell lines and the effect could be rescued by knocking down HIF-1a. Our findings reveal that SNP-mediated lncRNA-ENTPD3-AS1 upregulation suppresses renal cell carcinoma via miR-155/HIF-1a signaling.		Cell Death Dis. 2021 Jul 3;12(7):672. doi: 10.1038/s41419-021-03958-4.
5495	LncRNA	LincRNA-p21	miR-449a	NA	Human Renal Proximal Tubular Epithelial Cells	Acute Kidney Injury	Homo sapiens (human)	qPCR;RT-qPCR;Luciferase activity assay;	34218230	LincRNA-p21 Inhibits Cisplatin-Induced Apoptosis of Human Renal Proximal Tubular Epithelial Cells by Sponging miR-449a.	INTRODUCTION: LincRNA-p21 is predicted to interact with miR-449a, which plays a protective role in cisplatin-induced acute kidney injury (CIA). OBJECTIVE: This study aimed to analyze the involvement of lincRNA-p21 in breast cancer patients with CIA. METHODS: Levels of lincRNA-p21 in plasma from CIA, triple negative breast cancer, and control groups were measured by performing RT-qPCR. The potential interaction between lincRNA-p21 and miR-449a was first predicted by RT-qPCR. The relationship between lincRNA-p21 and miR-449a was analyzed by overexpression experiment. RESULTS: We found that lincRNA-p21 is downregulated in CIA. Dual luciferase activity assay showed that lincRNA-p21 and miR-449a can interact with each other, while overexpression of lincRNA-p21 and miR-449a failed to affect the expression of each other. In human renal proximal tubular epithelial cells (HRPTEpCs), cisplatin led to the upregulated miR-449a but downregulated lincRNA-p21. Interestingly, lincRNA-p21 overexpression led to reduced enhancing effects of miR-449a on the cisplatin-induced apoptosis of HRPTEpCs. CONCLUSION: Therefore, lincRNA-p21 is downregulated in CIA and may sponge miR-449a to inhibit cisplatin-induced apoptosis of HRPTEpCs.		Kidney Blood Press Res. 2021;46(4):495-501. doi: 10.1159/000509229. Epub 2021 Jul 2.
5496	LncRNA	SOX2OT	miRNA-194-5p	RAC1	Nsclc Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	34215717	Tumour-derived exosomal lncRNA-SOX2OT promotes bone metastasis of non-small cell lung cancer by targeting the miRNA-194-5p/RAC1 signalling axis in osteoclasts.	Bone is a frequent metastatic site of non-small cell lung cancer (NSCLC), and bone metastasis (BoM) presents significant challenges for patient survival and quality of life. Osteolytic BoM is characterised by aberrant differentiation and malfunction of osteoclasts through modulation of the TGF-b/pTHrP/RANKL signalling pathway, but its upstream regulatory mechanism is unclear. In this study, we found that lncRNA-SOX2OT was highly accumulated in exosomes derived from the peripheral blood of NSCLC patients with BoM and that patients with higher expression of exosomal lncRNA-SOX2OT had significantly shorter overall survival. Additionally, exosomal lncRNA-SOX2OT derived from NSCLC cells promoted cell invasion and migration in vitro, as well as BoM in vivo. Mechanistically, we discovered that NSCLC cell-derived exosomal lncRNA-SOX2OT modulated osteoclast differentiation and stimulated BoM by targeting the miRNA-194-5p/RAC1 signalling axis and TGF-b/pTHrP/RANKL signalling pathway in osteoclasts. In conclusion, exosomal lncRNA-SOX2OT plays a crucial role in promoting BoM and may serve as a promising prognostic biomarker and treatment target in metastatic NSCLC.		Cell Death Dis. 2021 Jul 2;12(7):662. doi: 10.1038/s41419-021-03928-w.
5497	LncRNA	LINC00654	miR-210-5p	OGFRL1	Chondrocytes	NA	Homo sapiens (human)  	RT-PCR;	34215299	Identification and validation of key long non-coding RNAs in resveratrol protect against IL-1b-treated chondrocytes via integrated bioinformatic analysis.	BACKGROUND: Long non-coding RNAs (lncRNAs) participate in regulation of gene transcription, but little is known about the correlation among resveratrol and lncRNAs. This study aimed to identify and validate the key lncRNAs in resveratrol protect against IL-1b-treated chondrocytes. METHODS: In this experiment, high-throughput sequencing technique was performed to identify the differentially expressed lncRNAs, miRNAs, and mRNAs between IL-1b-treated chondrocytes with or not resveratrol. Moreover, gene ontology and KEGG pathway of the differentially expressed genes were carried out by R software. Then, lncRNA-miRNA-mRNA network was constructed by Cytoscape software. Venn diagram was performed to identify the potentially target miRNAs of LINC00654. Then, real-time polymerase chain reaction (RT-PCR) was performed to validate the most significantly differentially expressed lncRNAs. RESULTS: Totally, 1016 differentially expressed lncRNAs were identified (493 downregulated) between control and resveratrol-treated chondrocytes. Totally, 75 differentially expressed miRNAs were identified (downregulated = 54, upregulated = 21). Totally, 3308 differentially expressed miRNAs were identified (downregulated = 1715, upregulated = 1593). GO (up) were as follows: skin development, response to organophosphorus. GO (down) mainly included visual perception, single fertilization, and sensory perception of smell. KEGG (up) were as follows: TNF signaling pathway and TGF-beta signaling pathway. KEGG (down) were as follows: viral protein interaction with cytokine and cytokine receptor. We identified that LINC00654 and OGFRL1 were upregulated in resveratrol-treated chondrocytes. However, miR-210-5p was downregulated in resveratrol-treated chondrocytes. CONCLUSION: In sum, the present study for the first time detected the differential expressed lncRNAs involved in resveratrol-treated chondrocytes via employing bioinformatic methods.		J Orthop Surg Res. 2021 Jul 2;16(1):421. doi: 10.1186/s13018-021-02574-4.
5498	LncRNA	PVT1	miR-146a	TRAF6	Regulatory T Cells	Transplant Rejection	Homo sapiens (human)  	qRT-PCR;Western blot;	34214903	The lncRNA PVT1 regulates autophagy in regulatory T cells to suppress heart transplant rejection in mice by targeting miR-146a.	Regulatory T cells (Tregs) are indispensable for the maintenance of immune tolerance. The purpose of this study was to investigate the effect of the interaction of the lncRNA PVT1 and miR-146a on Treg autophagy and reveal the mechanism to alleviate transplant rejection. PVT1 and miR-146a expression levels were analyzed by qRT-PCR. Bioinformatic analysis and methylation profiling were used to determine the relationship between PVT1 and miR-146a. Altered autophagic status in Tregs was detected by western blotting. The effect of autophagy on Treg function was assessed in cell coculture in vitro and in animal models. Our results showed that PVT1 expression was reduced in Tregs during rejection and negatively correlated with miR-146a expression. Higher PVT1 expression was associated with higher autophagy in Tregs. Further, highly autophagic Tregs had stronger inhibitory effects on CD4(+) T cells in vitro, prolonged allograft survival and alleviated rejection in vivo. Mechanistic studies showed that overexpression of PVT1 enhanced TNF receptor-associated factor (TRAF) 6 expression by directly targeting miR-146a. MiR-146a overexpression reversed PVT1-induced Treg autophagy and inhibited PVT1-induced TRAF6 expression. The present study shows a novel regulatory pathway of the autophagy program that comprises PVT1, miR-146a, and TRAF6. Our findings may provide potential targets and new therapeutic strategies for transplant rejection.		Cell Immunol. 2021 Sep;367:104400. doi: 10.1016/j.cellimm.2021.104400. Epub 2021 Jun 26.
5499	LncRNA	uc003pxg.1	miR-25-5p	cyclin D1	Human Umbilical Vein Endothelial Cell	Coronary Artery Disease	Homo sapiens (human)	Dual-luciferase reporter assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34212983	Long noncoding RNA uc003pxg.1 regulates endothelial cell proliferation and migration via miR-25-5p in coronary artery disease.	Long noncoding RNAs (lncRNAs) have been reported to be associated with the progression of coronary artery disease (CAD). In our previous study, the levels of lncRNA uc003pxg.1 were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of uc003pxg.1 in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of uc003pxg.1 in CAD. First, uc003pxg.1 expression levels were assessed in peripheral blood mononuclear cells isolated from patients with CAD by reverse transcription-quantitative (RT-q)PCR. The results demonstrated that the levels of uc003pxg.1 were significantly upregulated (~4.6-fold) in samples from 80 patients with CAD compared with those in 80 healthy subjects. Subsequently, the present study demonstrated that small interfering RNA-mediated uc003pxg.1 knockdown inhibited human umbilical vein endothelial cell (HUVEC) proliferation and migration, which was analyzed using the Cell Counting Kit-8, cell cycle, EdU and Transwell assays. Additionally, the results of RT-qPCR and western blot analyses revealed that uc003pxg.1 regulated the mRNA and protein levels of cyclin D1 and cyclin-dependent kinase. Through high-throughput sequencing and dual-luciferase reporter assays, the present study demonstrated that microRNA (miR)-25-5p was a downstream target of uc003pxg.1. Further experiments verified that uc003pxg.1 regulated HUVEC proliferation and migration via miR-25-5p. The results of the present study may enhance the current understanding of the role of lncRNA uc003pxg.1 in CAD.		Int J Mol Med. 2021 Aug;48(2):160. doi: 10.3892/ijmm.2021.4993. Epub 2021 Jul 2.
5500	LncRNA	HOTTIP	miR-744-5p	PTBP1	A549 Cells	Fibrosis Of Lung Tissue	Homo sapiens (human)  	Western blot;Luciferase reporter assay;	34212978	Long non-coding RNA HOTTIP enhances the fibrosis of lung tissues by regulating the miR-744-5p/PTBP1 signaling axis.	Fibrosis of lung tissue can induce the occurrence and development of numerous types of lung disease. The expression levels of the long non-coding RNA (lncRNA) HOXA distal transcript antisense RNA (HOTTIP) have been reported to be upregulated during the development of fibrosis in liver tissues, which subsequently activated hepatic stellate cells. However, whether the lncRNA HOTTIP participates in the occurrence and development of lung fibrosis remains unknown. The present study aimed to investigate the role of lncRNA HOTTIP in lung fibrosis and its potential mechanism. In the present study, A549 cells were stimulated with TGF-b1 to induce lung fibrosis in vitro. A549 was transfected with short hairpin RNA-HOTTP, overexpression-polypyrimidine tract binding protein 1 (PTBP1), microRNA (miR)-744-5p mimic or miR-744-5p to regulate gene expression. Cell proliferation and migration were determined using 5'-ethynl-2'-deoxyuridine and wound healing assays, respectively. The expression levels of a-smooth muscle actin, collagen I, collagen III and fibronectin 1 were analyzed using western blotting. starBase was used to identify molecules that may interact with the lncRNA HOTTIP and dual luciferase reporter assays were used to validate the findings. Moreover, an in vivo lung fibrosis model was established by bleomycin induction in mice. Histological injury was observed using hematoxylin and eosin and masson staining. The results of the present study revealed that the proliferation and migration of A549 cells were both suppressed following the knockdown of HOTTIP. The lncRNA HOTTIP was found to target and downregulate the expression levels of miR-744-5p. The overexpression of miR-744-5p inhibited the proliferation and migration of A549 cells. Furthermore, miR-744-5p targeted and downregulated the expression levels of PTBP1. It was subsequently demonstrated that the overexpression of PTBP1 rescued miR-744-5p-induced suppression of the proliferation and migration of A549 cells. The knockdown of lncRNA HOTTIP expression also relieved the fibrosis of the lung tissues of mice. In conclusion, the results of the present study suggested that the lncRNA HOTTIP may promote the fibrosis of lung tissues by downregulating the expression levels of miR-744-5p and upregulating the expression levels of PTBP1.		Mol Med Rep. 2021 Sep;24(3):619. doi: 10.3892/mmr.2021.12258. Epub 2021 Jul 2.
5501	LncRNA	LncRSPH9-4	miR-17-5p	MMP3	Brain Microvascular Endothelial Cells	Bacterial Meningitis	Homo sapiens (human)  	Western blot;	34198485	LncRSPH9-4 Facilitates Meningitic Escherichia coli-Caused Blood-Brain Barrier Disruption via miR-17-5p/MMP3 Axis.	Brain microvascular endothelial cells (BMECs) constitute the structural and functional basis for the blood-brain barrier (BBB) and play essential roles in bacterial meningitis. Although the BBB integrity regulation has been under extensive investigation, there is little knowledge regarding the roles of long non-coding RNAs (lncRNAs) in this event. The present study aimed to investigate the roles of one potential lncRNA, lncRSPH9-4, in meningitic E. coli infection of BMECs. LncRSPH9-4 was cytoplasm located and significantly up-regulated in meningitic E. coli-infected hBMECs. Electrical cell-substrate impedance sensing (ECIS) measurement and Western blot assay demonstrated lncRSPH9-4 overexpression in hBMECs mediated the BBB integrity disruption. By RNA-sequencing analysis, 639 mRNAs and 299 miRNAs were significantly differentiated in response to lncRSPH9-4 overexpression. We further found lncRSPH9-4 regulated the permeability in hBMECs by competitively sponging miR-17-5p, thereby increasing MMP3 expression, which targeted the intercellular tight junctions. Here we reported the infection-induced lncRSPH9-4 aggravated disruption of the tight junctions in hBMECs, probably through the miR-17-5p/MMP3 axis. This finding provides new insights into the function of lncRNAs in BBB integrity during meningitic E. coli infection and provides the novel nucleic acid targets for future treatment of bacterial meningitis.		Int J Mol Sci. 2021 Jun 14;22(12):6343. doi: 10.3390/ijms22126343.
5502	LncRNA	SNHG16	miR-20a-5p	E2F1	Peripheral Blood Samples	Diabetic Retinopathy	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34197720	Long non-coding RNA SNHG16 regulates E2F1 expression by sponging miR-20a-5p and aggravating proliferative diabetic retinopathy.	Long non-coding RNAs (lncRNAs) were reported that related to microvascular dysfunction in diabetic retinopathy (DR), but the potential mechanism remains unknown. This study was designed to elucidate the effects of lncRNA SNHG16 in proliferative DR progression. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the levels of SNHG16 and miR-20a-5p from peripheral blood samples of different participants. Pearson's correlation analysis on the plasma data was applied to detect correlations between SNHG16 and miR-20a-5p. Finally, the interactions of miR-20a-5p and SNHG16 or E2F1 were assessed by luciferase reporter assays. SNHG16 and E2F1 were increased and miR-20a-5p was decreased in proliferative DR both in vivo and in vitro, when compared with control or non-proliferative DR. E2F1 was identified as the target of miR-20a-5p. MiR-20a-5p interacted with SNHG16 and E2F1, and was controlled by SNHG16. The regulation of SNHG16 on E2F1 was mediated by miR-20a-5p. Cells transfected with SNHG16 OE plasmid markedly increased cell apoptosis and vessel-like formation, whereas the miR-20a-5p mimic partially reversed these effects. Transfection with si-E2F1 plasmid rescued SNHG16 overexpression-aggravated proliferative DR. This study indicated that SNHG16 regulated E2F1 expression by sponging miR-20a-5p and aggravating proliferative DR.		Can J Physiol Pharmacol. 2021 Jul 1. doi: 10.1139/cjpp-2020-0693.
5503	LncRNA	Linc1749808	miR-206	YAP1	Hcc Tissues And Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	microarray;qRT-PCR;luciferase assay;	34196215	Novel long noncoding RNA Linc1749808 promotes hepatocellular carcinoma metastasis by negatively regulating miR-206.	Notably, a growing number of long noncoding RNAs (lncRNAs) have been recognized to play critical roles in hepatocellular carcinoma (HCC) progression. In this study, we identified a new lncRNA, Linc1749808 (ID: XR_001749808.1) based on microarray data from HCC tissues. Linc1749808 levels in 72 HCC tissues and paracancerous samples were detected by qRT-PCR. The interaction between Linc1749808 and microRNA-206 (miR-206) was assessed by bioinformatic analysis and luciferase assays. Linc1749808 depletion assays, Transwell assays, and miR-206-inhibitor rescue experiments were performed to examine the role of the Linc1749808/miR-206 axis in HCC cells. Our results showed that Linc1749808 was highly expressed in both HCC tissues and cell lines. Linc1749808 expression was significantly correlated with microvascular invasion, metastasis, and prognosis. After the knockdown of Linc1749808, the metastatic potential of 97H and HepG2 cells was attenuated in vitro and in vivo, but the proliferative capacity did not significantly change. Furthermore, Linc1749808 was found to act as a sponge of miR-206. Inhibition of miR-206 counteracted the effect of Linc1749808 knockdown in 97H cells by regulating YAP1 and epithelial-mesenchymal transition (EMT). In summary, these findings show that Linc1749808 can exacerbate the metastasis of HCC by sponging miR-206.		Neoplasma. 2021 Jun 29:210310N314. doi: 10.4149/neo_2021_210310N314.
5504	LncRNA	HCP5	miR-138-5p	EZH2	Cscc Cells	Cutaneous Squamous Cell Carcinoma	Homo sapiens (human)	microarray;RNA pull-down;	34195851	lncRNA HCP5 acts as a ceRNA to regulate EZH2 by sponging miR-138-5p in cutaneous squamous cell carcinoma.	Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are essential for the progression of tumors, including cutaneous squamous cell carcinoma (CSCC). The present study aimed to examine the competing endogenous RNA (ceRNA) network in CSCC. Differentially expressed genes in CSCC were analyzed using the GSE66359 microarray data set, and the upstream miRNAs and lncRNAs were predicted using online database analysis (TargetScan 7.1, mirDIP 4.1, miRSearch V3.0, miRDB and RNA22 2.0) and were verified in clinical tissues. RNA pull-down and dual luciferase reporter gene assays were used to verify the targeting relationships among lncRNA human histocompatibility leukocyte antigen complex P5 (HCP5), miR-138-5p and enhancer of zeste homolog 2 (EZH2). Cell lines with a high and low HCP5 expression were screened, and a pcDNA-3.1-HCP5 overexpression vector, small interfering RNA against HCP5, miR-138-5p mimics and miR-138-5p inhibitors were transfected into the CSCC cells. Cell viability, invasion, migration, apoptotic rate and autophagy were evaluated. The effects of HCP5 on autophagy and apoptosis of CSCC cells were verified in vivo using Ki67 and TUNEL staining. EZH2 was demonstrated to be upregulated in CSCC cells. miR-138-5p target sequences were identified in HCP5 and EZH2. HCP5 was revealed to function as a putative ceRNA of miR-138-5p to positively regulate EZH2, and EZH2 was shown to regulate autophagy and apoptosis of CSCC cells through the STAT3/VEGFR2 pathway. HCP5 overexpression decreased miR-138-5p levels, increased EZH2 levels and promoted cell malignant behaviors and autophagy but decreased the apoptosis rate. These trends were opposite when HCP5 was silenced. In conclusion, HCP5 may competitively bind to miR-138-5p to regulate EZH2 in CSCC cells, promoting autophagy and reducing apoptosis through the STAT3/VEGFR2 pathway. This study may provide a new perspective for understanding the molecular mechanism and treatment of CSCC.		Int J Oncol. 2021 Aug;59(2):56. doi: 10.3892/ijo.2021.5236. Epub 2021 Jul 1.
5505	LncRNA	HOTAIR	miR-761	PPME1	Thyroid Cancer Cells	Thyroid Cancer	Homo sapiens (human)  	RT-PCR;Western blot;Luciferase reporter assay;	34195365	Long non-coding RNA HOTAIR/microRNA-761 sponge regulates PPME1 and further influences cell biological functions in thyroid carcinoma.	BACKGROUND: Most well-differentiated thyroid carcinomas display good therapeutic outcomes, but there are still some patients who are not sensitive to the general treatments lose their treatment opportunities. Thus, it is important to understand the molecular mechanisms that cause thyroid carcinoma, so as to find effective diagnostic and therapeutic targets. AIM OF THE STUDY: To explore the role of homeobox transcript antisense RNA (HOTAIR) in thyroid carcinoma through protein phosphatase methylesterase 1 (PPME1) by sponging microRNA 761 (miR-761). METHODS: The regulation network amongst HOTAIR, miR-761 and PPME1 was predicted by online sources. RT-PCR was conducted to evaluate the expression of HOTAIR and miR-761 in tumor tissues. Clinical data was collected and analyzed by Chi-square test. Cell apoptosis and proliferation was evaluated using three types of cancer cells (HTh-7, CAL-62, BCPAP) after treated with si-HOTAIR and miR-761inhibitor. The binding site among HOTAIR, miR-761 and PPME1 was verified by dual luciferase reporter assay. PPME1 expression was measured after HOTAIR and miR-761 were suppressed by western blot. Survival time was measured in nude mice using log-rank test. RESULTS: HOTAIR was expressed to a significantly greater extent than miR-761 in thyroid tumor tissues (P < .001). miR-761 and PPME1 were negatively correlated (coef = -1.91, P < .001). HOTAIR competitively binds to miR-761 and miR-761 directly targets PPME1. HOTAIR was highly correlated with TNM (χ (2) = 5.797, P = .016), tumor size (χ (2) = 7.955, P = .005) and lymphatic metastasis (χ (2) = 6.0, P = .014). HOTAIR promoted cell proliferation and inhibited cell apoptosis, whereas miR-761 did not. HOTAIR elevated and miR-761 suppressed PPME1 expression. HOTAIR expression appears to affect the survival time in vivo. CONCLUSION: HOTAIR regulated thyroid cancer cells by binding to miR-761 through PPME1.		Laryngoscope Investig Otolaryngol. 2021 May 26;6(3):438-445. doi: 10.1002/lio2.593. eCollection 2021 Jun.
5506	LncRNA	RP11-81H3.2	miR-1539	COL2A1	Human Nucleus Pulposus Cells	Intervertebral Disc Degeneration	Homo sapiens (human)  	luciferase assay;	34194562	Long non-coding RNA RP11-81H3.2 suppresses apoptosis by targeting microRNA-1539/COL2A1 in human nucleus pulposus cells.	Intervertebral disk degeneration (IDD) is a severe health problem that results in lower back pain and disability. Previous evidence has indicated that excessive apoptosis of nucleus pulposus (NP) cell is involved in the occurrence and development of IDD. However, the underlying mechanisms regulating NP cell apoptosis are unclear. The present study aimed to investigate the function of a novel long non-coding RNA RP11-81H3.2 in modulating NP cell apoptosis and the potential underlying mechanisms. The results demonstrated that the RP11-81H3.2 expression levels were significantly decreased in NP tissues from patients with IDD compared with those from healthy controls, and that lower expression levels were associated with higher-grade disk degeneration. Functionally, RP11-81H3.2 silencing promoted apoptosis and decreased the viability of NP cells derived from tissue samples of patients with IDD, whereas RP11-81H3.2 overexpression induced opposite effects. Bioinformatics analysis, luciferase assays and reverse transcription-quantitative PCR revealed that microRNA (miR)-1539 was a direct target of RP11-81H3.2. A mechanistic analysis demonstrated that RP11-81H3.2 functioned as an RNA sink to downregulate miR-1539, which led to the upregulation of collagen type 2 a 1 chain (COL2A1), a target of miR-1539. Collectively, the present results suggested that lower RP11-81H3.2 expression levels were associated with higher-grade IDD, and that RP11-81H3.2 inhibited NP cell apoptosis by decreasing the levels of miR-1539 to increase COL2A1 expression levels. The present study identified a beneficial role of RP11-81H3.2 against NP cell apoptosis.		Exp Ther Med. 2021 Aug;22(2):884. doi: 10.3892/etm.2021.10316. Epub 2021 Jun 16.
5507	LncRNA	HAGLROS	miR-26b-5p	NA	Ovarian Cancer Cells	Ovarian Cancer	Homo sapiens (human)  	Western blot;Luciferase reporter assay;Rescue assay;	34194557	Interference of long non-coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR-26b-5p.	Ovarian cancer (OV) is the fifth most common type of cancer affecting women worldwide. Long non-coding RNAs (lncRNAs) serve essential roles in the progression of OV. As such, the present study aimed to investigate the specific role of HAGLR opposite strand lncRNA (HAGLROS) in OV and the underlying mechanism of action through which HAGLROS exerts its effects on OV cells. In the present study, the expression of HAGLROS in several OV cell lines was first detected using reverse transcription-quantitative PCR. HAGLROS was then silenced to evaluate cell viability, proliferation and apoptosis, which were determined using Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Additionally, immunofluorescence staining and western blotting were used to confirm the expression profile of proliferation- and apoptosis-related proteins. Moreover, a dual luciferase reporter assay was used to verify the potential interactions between HAGLROS and microRNA (miR)-26b-5p. Subsequently, rescue assays were performed to investigate the effects of HAGLROS and miR-26b-5p on OV progression. The results indicated that HAGLROS was highly expressed in OV cells. Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. miR-26b-5p inhibitor transfection partially reversed the effects of HAGLROS knockdown on the proliferation and apoptosis of OV cells. In conclusion, the results of the present study suggested that interference of HAGLROS suppressed the proliferation and promoted the apoptosis of OV cells through regulating miR-26b-5p, indicating that HAGLROS may be a promising biomarker in OV diagnosis and treatment.		Exp Ther Med. 2021 Aug;22(2):879. doi: 10.3892/etm.2021.10311. Epub 2021 Jun 15.
5508	LncRNA	NORAD	miR-485	NRF1	Human Mesangial Cells	Diabetic Nephropathy	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;MTT assay;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;MTT assay;	34194552	Knockdown of lncRNA NORAD inhibits the proliferation, inflammation and fibrosis of human mesangial cells under high-glucose conditions by regulating the miR-485/NRF1 axis.	Long non-coding RNAs (lncRNAs) serve major roles in diabetic nephropathy (DN). The present study investigated the regulatory mechanism of lncRNA non-coding RNA activated by DNA damage (NORAD) on DN in vitro. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of lncRNA NORAD, microRNA-485 (miR-485) and nuclear respiratory factor 1 (NRF1) in the tissues of patients with DN and high-glucose (HG)-induced human mesangial cells (HMCs). The viability of HMCs was determined using an MTT assay. The levels of inflammatory [tumour necrosis factor (TNF)-a, interleukin (IL)-1b and IL-6] and fibrotic [type IV collagen (Col. IV), fibronectin (FN) and plasminogen activator inhibitor 1 (PAI-1)] factors in HMCs were measured by ELISA. The interactions between miR-485 and NORAD/NRF1 were predicted using StarBase and miRDB softwares and confirmed by a dual-luciferase reporter assay. Western blot analysis was utilized to measure NRF1 protein levels. lncRNA NORAD was highly expressed in tissues and HG-induced HMCs. NORAD knockdown suppressed cell viability in HG-induced HMCs. The levels of the inflammatory and fibrotic factors in HG-induced HMCs were inhibited by NORAD knockdown. miR-485 was the direct target of NORAD. NORAD reversed the inhibitory effects of miR-485 on HG-induced HMCs. Furthermore, NRF1 was the target gene of miR-485. Downregulation of miR-485 and upregulation of NRF1 reversed the inhibitory effects of NORAD knockdown on HG-induced HMCs. NORAD knockdown inhibited HG-induced HMC proliferation, inflammation and fibrosis by regulating miR-485/NRF1, providing a possible therapeutic strategy for DN.		Exp Ther Med. 2021 Aug;22(2):874. doi: 10.3892/etm.2021.10306. Epub 2021 Jun 14.
5509	LncRNA	WDFY3-AS2	miR-18a	PTEN	Ec Samples And Cells	Esophageal Cancer	Homo sapiens (human)	qPCR;RT-qPCR;RIP assay;	34194502	Long Noncoding RNA WDFY3-AS2 Represses the Progression of Esophageal Cancer through miR-18a/PTEN Axis.	BACKGROUND: Understanding the role of lncRNAs in the development of human malignancies is necessary for the targeted therapy of malignant tumors, including esophageal cancer (EC). Nevertheless, the specific role and regulatory mechanism of lncRNA WDFY3-AS2 in EC are still unclear. Here, we examined the functional role and regulatory mechanism of WDFY3-AS2 in EC. MATERIALS AND METHODS: RT-qPCR assay was applied to measure the expression of WDFY3-AS2 and miR-18a in EC samples and cells. The luciferase reporter and RIP assays were used to check the relationship between WDFY3-AS2, miR-18a, and PTEN. Counting Clock Kit-8 (CCK-8) assay was carried out to detect cell viability, and transwell assays were used for measuring cell migration and invasion. RESULTS: Underexpression of WDFY3-AS2 was found in EC specimens and cells, which predicted a poor prognosis of EC patients. Reexpression of WDFY3-AS2 repressed the progression of EC via inhibiting cell proliferation, migration, and invasion. Additionally, WDFY3-AS2 was negatively correlated with miR-18a and positively with PTEN. Furthermore, we discovered that the expression of PTEN decreased by miR-18a mimic was rescued by WDFY3-AS2 overexpression. CONCLUSIONS: WDFY3-AS2 modulates the expressional level of PTEN as a competitive endogenous RNA via sponging miR-18a in EC, which suggests that the WDFY3-AS2/miR-18a/PTEN pathway might be involved in the progression of EC.		J Oncol. 2021 Jun 5;2021:9951010. doi: 10.1155/2021/9951010. eCollection 2021.
5510	LncRNA	MONC	MiR-636	GLCE	Endometrial Cancer Stem Cells And Endometrial Carcinoma Cells	Endometrial Cancer	Homo sapiens (human)	CCK-8 assay;qRT-PCR;Western blot;Flow Cytometry assay;luciferase assay;	34193130	LncRNA MONC suppresses the malignant phenotype of Endometrial Cancer Stem Cells and Endometrial Carcinoma Cells by regulating the MiR-636/GLCE axis.	BACKGROUND: Emerging evidence shows that abnormal expression of long non-coding RNA is involved in the occurrence and development of various tumors. LncRNA MONC is abnormally expressed in head and neck squamous cell carcinoma, lung cancer, colorectal cancer, and acute megakaryocytic leukemia, but the biological function and potential regulatory mechanism of MONC in endometrial cancer stem cells (ECSCs) and endometrial cancer cells (ECCs) have not been studied. In this study, we aimed to explore the tumor suppressive effect and mechanism of MONC in regulating ECSCs and ECCs. METHODS: We used qRT-PCR to detect the expression of MONC, miR-636 and GLCE in normal human endometrial tissues and endometrial carcinoma (EC) tissues. Luciferase assay was used to verify the binding sites between MONC and miR-636 and between miR-636 and GLCE. Double fluorescence in situ hybridization was used to locate MONC and miR-636 in cells. ECSCs were obtained by flow cytometry sorting assay. Sphere formation assay, CCK-8 assay, transwell invasion assay, cell cycle analysis and apoptosis assay were used to detect the effects of MONC/miR-636/GLCE axis on the malignant biological behavior of ECSCs and ECCs. The effect of MONC on the epithelial-to-mesenchymal transition (EMT) process was detected using western blot. Finally, we conducted in vivo verification through Tumor xenografts in BALB/C nude mice. RESULTS: In this study, we found MONC is low expression in endometrial carcinoma (EC) and patients in the MONC high-expression group had a better prognosis. MONC and miR-636 are relatively co-localized in the cytoplasm. MONC directly inhibits the malignant biological behavior of ECSCs and ECCs by directly inhibiting miR-636. Simultaneously, miR-636 may indirectly reduce the expression of MONC. Down-regulation of miR-636 may promote GLCE expression by targeting the 3'-untranslated region (UTR) of the downstream gene GLCE, thereby inhibiting the progression of ECSCs. MONC combined with miR-636 inhibited tumor epithelial-to-mesenchymal transition (EMT) process. In addition, we verified the tumor suppressive effect of MONC in nude mice, miR-636 can rescue the tumor suppressive effect of overexpressing MONC. CONCLUSIONS: In conclusion, this study showed that MONC inhibits the malignant phenotypes of ECSCs and ECCs by regulating the miR-636/GLCE axis. Thus the MONC/miR-636/GLCE axis may provide novel treatment avenues for human EC.		Cancer Cell Int. 2021 Jun 30;21(1):331. doi: 10.1186/s12935-021-01911-1.
5511	LncRNA	LINC00707	miR-145	CDCA3	Bc Cells	Dder Cancer	Homo sapiens (human)  	RT-PCR;Western blot;Flow Cytometry assay;	34192702	Long Noncoding RNA LINC00707 Accelerates Tumorigenesis and Progression of Bladder Cancer via Targeting miR-145/CDCA3 Regulatory Loop.	INTRODUCTION: Growing studies reveal that long noncoding RNA is involved in oncogenesis and progression. Previous studies have demonstrated that long intergenic noncoding RNA 00707 (LINC00707) stimulated tumor progress in numerous neoplasm types; however, the function of LINC00707 in bladder cancer (BC) was not yet clear. Our researches aimed to determine whether LINC00707 was dysregulated in BC and further study its biological functions. METHODS: LINC00707 levels in BC tissues and cells were measured using reverse transcription-PCR (RT-PCR), and the associations between the levels of LINC00707 and clinicopathological features and the months of survival were also examined. Then, Cell Counting Kit-8 assays, flow cytometry, colony formation assays, and Transwell assays were applied for the assessment of the impact of LINC00707 on the abilities of BC cells. The interaction between LINC00707 and miR-145 or cell division cycle associated 3 was determined by luciferase reporter system and RT-PCR. Protein expressions of Wnt/b-catenin signaling were examined using RT-PCR and Western blot. RESULTS: We found that LINC00707 expressions were notably upregulated in BC samples and cells. Higher expressions of LINC00707 were associated with T stage, grade, and shorter overall survival in BC patients. LINC00707 was also an independent prognostic factor for BC. In vitro assays confirmed that silencing LINC00707 expressions suppressed cell proliferation, colony formation, and metastasis. Mechanistic studies elucidated that LINC00707 was directly targeted to miR-145/CDCA3. Western blot assays revealed that Wnt/b-catenin signaling was inactivated by LINC00707 knockdown. CONCLUSION: Our work offers new insight into the function of LINC00707 in the tumorigenesis of BC.		Urol Int. 2021 Jun 30:1-15. doi: 10.1159/000514388.
5512	LncRNA	HOTAIR	miR-222-3p	ADAM10	Chondrocytes	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;RACE;Western blot;Flow Cytometry assay;Luciferase reporter assay;	34192661	Blocking HOTAIR protects human chondrocytes against IL-1b-induced cell apoptosis, ECM degradation, inflammatory response and oxidative stress via regulating miR-222-3p/ADAM10 axis.	BACKGROUND: Long non-coding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) contributes to cartilage damages including osteoarthritis (OA). While, its role and mechanism in chondrocytes is incompletely clear. METHODS: HOTAIR, microRNA (miR)-222-3p and ADAM metalloproteinase-like domain 10 (ADAM10) expressions were detected by real-time quantitative PCR and western blotting. The interaction between miR-222-3p and HOTAIR or ADAM10 was confirmed by dual-luciferase reporter assay. Cell injury was measured by MTS method, flow cytometry, western blotting, enzyme-linked immunosorbent assay for collagen Type II, type X, sex determining region Y-box 9 (SOX9), matrix metalloproteinase (MMP)-13, interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-a, and special assay kits for malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase (SOD). RESULTS: HOTAIR was highly expressed in human OA cartilages and IL-1b-induced OA model in immortalized chondrocytes (C-28/I2). Under IL-1b stress, blocking HOTAIR was responsible to high mitochondrial activity and low early apoptosis rate, accompanied with increased B cell lymphoma (Bcl)-2 and LC3B-II/I proteins, boosted IL-10 and SOD productions, suppressed cleaved caspase-3 and p62 proteins, and decreased MDA and ROS levels, as well as elevated secretions of Type II collagen, Type X collagen, SOX9, MMP-13, IL-6, and TNF-a. Moreover, miR-222-3p was a target of HOTAIR, and its overexpression and knockdown could suppress and aggravate IL-1b-induced chondrocytes injury. Furthermore, restoring ADAM10, a target gene of miR-222-3p, counteracted the protective role of miR-222-3p upregulation. CONCLUSION: HOTAIR might contribute to IL-1b-induced chondrocytes death, inflammation, extracellular matrix degradation, and oxidative stress in OA via miR-222-3p/ADAM10 axis.		Int Immunopharmacol. 2021 Sep;98:107903. doi: 10.1016/j.intimp.2021.107903. Epub 2021 Jun 27.
5513	LncRNA	NORAD	miR-155-5p	SOCS1	Breast Cancer Cell	Breast Cancer	Homo sapiens (human)  	RNA immunoprecipitation;Western blot;RNA immunoprecipitation;	34190442	Long Non-Coding RNA NORAD Inhibits Breast Cancer Cell Proliferation and Metastasis by Regulating miR-155-5p/SOCS1 Axis.	PURPOSE: Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified. METHODS: Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays. Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p. Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting. RESULTS: NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD. CONCLUSION: NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.		J Breast Cancer. 2021 Jun;24(3):330-343. doi: 10.4048/jbc.2021.24.e32.
5514	LncRNA	HCP5	miR-139-5p	PDE4A	Escc Cells	Esophageal Squamous Cancer	Homo sapiens (human)  	FISH;MTT assay;RIP assay;FISH;Luciferase reporter assay;MTT assay;Rescue assay;	34190001	LncRNA HCP5 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/mTOR signaling.	The role of lncRNA HCP5 in esophageal squamous cell carcinoma (ESCC) remains unknown despite its involvement in different malignancies. MTT assay, EdU assay, TUNEL assay, transwell assay, and sphere formation assay were conducted to reveal ESCC cell viability, proliferation, apoptosis, migration, invasion, and stemness characteristics. FISH and subcellular fraction assays were performed to reveal the subcellular location of HCP5 in ESCC cells. Luciferase reporter assay and RIP assay were conducted to explore the downstream axis of HCP5. Our findings revealed that HCP5 expression was at a higher level in ESCC tissues and cells compared to that in control tissues and cells. Additionally, HCP5 promoted ESCC cellular activities by promoting proliferation, migration, invasion ability and stemness characteristics of ESCC cells as well as suppressing cell apoptosis. Furthermore, we found that HCP5 bound with miR-139-5p to upregulate PDE4A via the competing endogenous RNA network in ESCC cells. Importantly, HCP5 was discovered to stimulate the PI3K/AKT/mTOR signaling by regulating the downstream target genes. Finally, rescue assays indicated that HCP5 promoted ESCC cell growth by activating the PDE4A-medaited PI3K/AKT/mTOR pathway. HCP5 promotes ESCC cellular development by modulating the miR-139-5p/PDE4A pathway and stimulating the PI3K/AKT/mTOR signaling pathway, which may be conducive for the improvement of ESCC treatment.		Cell Cycle. 2021 Jul;20(14):1374-1388. doi: 10.1080/15384101.2021.1944512. Epub 2021 Jun 30.
5515	LncRNA	MT1JP	miR-32	PTEN	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	Cell transfection;Cell transfection;qPCR;RT-qPCR;Western blot;	34188706	lncRNA MT1JP-overexpression abolishes the silencing of PTEN by miR-32 in hepatocellular carcinoma.	Previous studies have shown that long non-coding RNA (lncRNA) MT1JP plays a role as a tumor suppressor in several types of cancer. The present study aimed to explore the role of MT1JP in hepatocellular carcinoma (HCC). Paired HCC and non-tumor tissues from 64 patients with HCC were subjected to RNA isolation and reverse transcription-quantitative PCR (RT-qPCR) to analyze the differential expression of MT1JP, microRNA (miR)-32 and phosphatase and tensin homolog (PTEN) in HCC. Cell transfections, followed by RT-qPCR and western blotting, were carried out to investigate the interactions among MT1JP, miR-32 and PTEN. The role of MT1JP, miR-32 and PTEN in regulating HCC cell proliferation was assessed using a Cell Counting Kit-8 assay. It was found that MT1JP was downregulated in HCC cancer tissues compared with that in non-cancer tissues. Survival analysis showed that patients with low MT1JP expression levels exhibited a significantly higher 5-year overall survival rate compared with patients with high MT1JP levels. The expression of MT1JP in HCC tissues was positively associated with PTEN and negatively associated with miR-32. Overexpression of MT1JP increased the expression levels of PTEN and decreased the expression levels of miR-32. Overexpression of miR-32 did not affect the expression of MT1JP but decreased the expression levels of PTEN and attenuated the effect of overexpression of MT1JP on the expression of PTEN. Overexpression of MT1JP and PTEN decreased the proliferation of HCC cells. Overexpression of miR-32 played an opposite role and attenuated the effects of overexpression of MT1JP. Therefore, MT1JP may upregulate PTEN by downregulating miR-32 to regulate HCC cell proliferation.		Oncol Lett. 2021 Aug;22(2):604. doi: 10.3892/ol.2021.12865. Epub 2021 Jun 15.
5516	LncRNA	SNHG17	miR-375-3p	NA	Cc Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR;Luciferase reporter assay;	34188550	LncRNA SNHG17 Contributes to the Progression of Cervical Cancer by Targeting microRNA-375-3p.	PURPOSE: Cervical cancer is a great threat to women's health all over the world. Non-coding RNAs performed a wide range of functions. This study aimed to clarify the clinical significance and biological function of lncRNA SNHG17 and miRNA-375-3p (miR-375-3p) in cervical cancer (CC). PATIENTS AND METHODS: Blood samples from 124 CC patients and 119 healthy volunteers were collected. The relative expression of SNHG17 and miR-375-3p in CC patient serums and cells was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The receiver operating curve (ROC) was plotted for diagnostic value estimation. The CCK-8 and transwell assay were conducted to explore the function of SNHG17 on CC cells. A luciferase reporter assay was carried out to confirm the interaction of SNHG17 and miR-375-3p. Rescue experiments were performed to verify the interaction. RESULTS: SNHG17 showed an ascending expression while miR-375-3p descended in the serum of CC patients. For SNHG17 and miR-375-3p, respectively, the AUC was 0.863 and 0.869, the sensitivity was 84.7% and 75.8%, and the specificity was 78.2% and 86.6%. Knockdown of SNHG17 inhibited proliferation, migration, and invasion of CC cells. Serum SNHG17 expression was negatively correlated with miR-375-3p expression, and miR-375-3p was the target miRNA of SNHG17. Rescue experiments verified the knockdown of SNHG17 inhibited cell growth through repressing miR-375-3p expression. CONCLUSION: SNHG17 and miR-375-3p have the potential to be diagnostic markers for CC. Overexpression of SNHG17 in CC promoted the progression of CC partly via targeting miR-375-3p, implying a novel therapeutic target for CC emerging.		Cancer Manag Res. 2021 Jun 23;13:4969-4978. doi: 10.2147/CMAR.S312469. eCollection 2021.
5517	LncRNA	MALAT1	miR144	mTOR	Hippocampus Cells	Hg-Induced Neuronal Cell Injury	Homo sapiens (human)  	Western blot;	34188461	MALAT1 Regulated mTOR-Mediated Tau Hyperphosphorylation by Acting as a ceRNA of miR144 in Hippocampus Cells Exposed to High Glucose.	AIM: High glucose (HG)-induced activation of mTOR promotes tau phosphorylation and leads to diabetes-associated dementia. This study aimed to explore the role of metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) in HG-induced neuronal cell injury. METHODS: Hippocampus cells were isolated from C57BL/6J mice. After 6 days of culture, the cells were incubated with 5.5 mM glucose in normal medium or 75 mM glucose for 4 days. Cells were transfected with miR-144 mimic, miR-144 inhibitor, siRNA for MALAT1 or corresponding controls. Gene expression was detected by PCR and Western blot analysis. RESULTS: HG increased the levels of MALAT1 and p-tau in hippocampal cells. Knockdown of MALAT1 partially reversed the effects of HG on mTOR activity and p-tau protein levels. MALAT1 functioned as competing endogenous RNA (ceRNA) for miR-144, and pre-treatment with MALAT1 siRNA decreased mTOR activity and p-tau protein level in HG-treated hippocampal cells, which was significantly attenuated by miR-144 mimics. Moreover, miR-144 negatively regulated the expression of mTOR and knockdown of MALAT1 suppressed mTOR, while overexpression of mTOR abrogated protective effects of MALAT1 knockdown in HG-treated hippocampal cells. CONCLUSION: MALAT1 knockdown prevented HG-induced mTOR activation and inhibited tau phosphorylation. MALAT1 may be a therapy target for diabetes associated dementia.		Clin Interv Aging. 2021 Jun 22;16:1185-1191. doi: 10.2147/CIA.S304827. eCollection 2021.
5518	LncRNA	MIR22HG	miR-9-3p	ADAMTS5	Chondrocytes	Osteoarthritis	Homo sapiens (human)	Dual-luciferase reporter assay;qRT-PCR;RACE;RIP assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	34187303	LncRNA MIR22HG promotes osteoarthritis progression via regulating miR-9-3p/ADAMTS5 pathway.	Dysregulation of long non-coding RNAs (lncRNAs) plays a fundamental role in the development and progression of osteoarthritis (OA), but the potential functions of lncRNAs in OA were not fully clarified. In the present work, we want to clarify the underlying functions and mechanisms of MIR22HG in OA. qRT-PCR was employed to detect the mRNA expression of MIR22HG, miR-9-3p, and ADAMTS5, while the protein expressions were measured using Western blot. The cell proliferation was examined through CCK8, while apoptosis was used in flow cytometry. Luciferase reporter assay and RNA immunoprecipitation (RIP) assays were undertaken to investigate the binding relationship among MIR22HG, ADAMTS5, and miR-9-3p. MIR22HG was significantly overexpressed in OA cartilages, OA chondrocytes and IL-1b-induced chondrocytes. Functionally, MIR22HG knockdown promoted cell proliferation, suppressed apoptosis, and contributed to downregulation of MMP13 and ADAMTS5 and upregulation of COL2A1 and ACAN in IL-1b-stimulated chondrocytes. Mechanistically, bioinformatic analysis indicated that MIR22HG may serve as a sponge for miR-9-3p and ADAMTS5 may be a potential targeted gene for miR-9-3p, which were subsequently verified through a dual-luciferase reporter assay. Moreover, rescue experiments showed that MIR22HG participated in the regulation of chondrocytes proliferation, apoptosis, and degradation of extracellular matrix via miR-9-3p/ADAMTS5 pathway. In conclusion, our findings illuminated that inhibition of MIR22HG ameliorated IL-1b-induced apoptosis and ECM degradation of human chondrocytes through miR-9-3p/ADAMTS5 pathway, which may provide a potentially promising target for OA treatment.		Bioengineered. 2021 Dec;12(1):3148-3158. doi: 10.1080/21655979.2021.1945362.
5519	LncRNA	HOXB-AS3	miR-498-5p	ADAM9	Ec Tissues And Cells	Endometrial Cancer	Homo sapiens (human)  	CCK-8 assay;qPCR;RT-qPCR;RNA pull-down assay;Flow Cytometry assay;RNA pull-down;	34187214	Long non-coding RNA (lncRNA) HOXB-AS3 promotes cell proliferation and inhibits apoptosis by regulating ADAM9 expression through targeting miR-498-5p in endometrial carcinoma.	OBJECTIVE: Long non-coding RNA (lncRNA) expression is closely related to the pathogenesis and progression of various tumors. In this study, we investigated the mechanisms of lncRNA HOXB cluster antisense RNA 3 (HOXB-AS3), miRNA(miR)-498-5p, and disintegrin and metalloproteinase domain-containing protein 9 (ADAM9) in endometrial carcinoma (EC) cells. METHODS: The expression levels of lncRNA HOXB-AS3 in EC tissues and cells were detected using RT-qPCR assays. The effects of HOXB-AS3 knockdown on EC cell proliferation and apoptosis were measured using CCK-8 assays, colony formation assays, and flow cytometry. In addition, putative miR-498-5p binding sites were identified in HOXB-AS3 and ADAM9. The targeted relationships were further verified using dual-luciferase reporter and RNA pull-down assays. RESULTS: HOXB-AS3 expression was upregulated in EC tissues and cells. EC cell proliferation and viability decreased significantly in HOXB-AS3 knockdown groups. A putative miR-498-5p binding site in HOXB-AS3 was verified. Inhibition of miR-498-5p rescued the effects of HOXB-AS3 knockdown on cell proliferation and apoptosis. Finally, ADAM9 was verified as a direct target gene of miR-498-5p. CONCLUSIONS: Our results suggest that lncRNA HOXB-AS3 is highly expressed in EC tissues and cells. Downregulation of HOXB-AS3 inhibits cell proliferation and promotes apoptosis in EC cells. HOXB-AS3 can upregulate ADAM9 expression by sponging miR-498-5p.		J Int Med Res. 2021 Jun;49(6):3000605211013548. doi: 10.1177/03000605211013548.
5520	LncRNA	Xist	miR-590-3p	Tgif2	Osteoclast	Osteoporosis	Mus musculus (mouse)	qRT-PCR 	34187170	LncRNA X inactive-specific transcript promotes osteoclast differentiation through Tgif2 by acting as a ceRNA of miR-590-3p in a murine model.	Aim: This study aims to investigate whether long noncoding RNA (lncRNA)  X-inactive specific transcript (Xist) can regulate osteoclast differentiation in osteoporosis and the mechanism. Materials & methods: The mouse model of osteoporosis was established by ovariectomy surgery. Osteoclast differentiation from RAW264.7 cells was induced in vitro. The relationships between associated genes were assessed. Results: Xist and Tgif2 were upregulated, but miR-590-3p was downregulated in ovariectomy mouse femurs and cell models. Xist knockdown or miR-590-3p overexpression inhibited Tgif2 expression and osteoclast differentiation. Tgif2 and Xist were the targets of miR-590-3p. Increased miR-590-3p expression inhibited Tgif2 level and osteoclast differentiation, while Xist overexpression reversed these effects. Conclusion: Xist serves as a ceRNA of miR-590-3p to promote Tgif2 level; thereby, contributing to osteoclast differentiation.		Regen Med. 2021 Jul;16(7):643-653. doi: 10.2217/rme-2020-0174. Epub 2021 Jun 30.
5521	LncRNA	SNHG5	mir-205-5p	SMAD4	Vascular Smooth Muscle Cells	Abdominal Aortic Aneurysm	Homo sapiens (human)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34185955	Based on bioinformatics analysis lncrna SNHG5 modulates the function of vascular smooth muscle cells through mir-205-5p/SMAD4 in abdominal aortic aneurysm.	OBJECTIVE: The aim of this study was to explore expression profiles of long noncoding RNA (lncRNA)-messenger RNA (mRNA) in abdominal aortic aneurysm (AAA) patients. Further, we explored the mechanisms by which lncRNA SNHG5 modulates the function of vascular smooth muscle cells (VSMC) in AAA. METHODS: Human gene expression profile GSE57691 dataset, was retrieved from Gene Expression Omnibus database. The dataset included gene expression array data of 49 AAA patients and 10 control aortic specimens from organ donors. To explore the main roles of the biological network, differentially expressed lncRNA and mRNAs in the aortic aneurysm (AAA) and normal aortic specimens were determined. Differentially expressed lncRNA and mRNAs were then used to construct a competing endogenous RNA (ceRNA) network using Cytoscape software, and the five key lncRNA were identified. SNHG5 which was significantly downregulated in the AAA was chosen and analysis showed that it regulates mir-205-5p and SMAD4 by binding to mir-205-5p. Double luciferase reporter gene assays, RNA immunoprecipitation, and RNA knockdown studies were used to establish the relationship between SNHG5 and mir-205-5p. Apoptosis rate was determined using flow cytometry, whereas cell proliferation was evaluated using Edu, and 24 well Transwell assay. Western blot analysis was used to determine protein expression levels. RESULTS: The five differentially expressed lncRNAs were significantly correlated with 34 microRNAs and 112 mRNAs. mRNAs in the ceRNA network are implicated in protein binding, signal transduction, DNA and RNA transcription, development, and cell differentiation. SNHG5 was downregulated in the AAA and acts as a molecular sponge for mir-205. Downregulation of SNHG5 induces expression of mir-205-5p. Increased mir-205-5p expression level inhibits SMAD4 production, thus inhibiting proliferation and migration and promotes apoptosis of smooth muscle cells. CONCLUSION: Bioinformatics were used to explore molecular mechanism of AAA progression. The findings of this study show that lncRNA SNHG5 regulates proliferation and apoptosis of VSMC cells through modulation of the mir-205-5p/SMAD4 axis. Therefore, SNHG5 is a potential therapeutic target for AAA disease.		Immun Inflamm Dis. 2021 Jun 29. doi: 10.1002/iid3.478.
5522	LncRNA	HHAS1	miR-204-5p	RUNX2	Bone Marrow-Derived Mesenchymal Stem Cells	Osteogenic Differentiation	Homo sapiens (human)	FISH;microarray;qRT-PCR;RNA immunoprecipitation;Western blot;FISH;Immunohistochemistry;RNA immunoprecipitation;RNA pull-down;	34185419	IRF2-mediated upregulation of lncRNA HHAS1 facilitates the osteogenic differentiation of bone marrow-derived mesenchymal stem cells by acting as a competing endogenous RNA.	BACKGROUND: Mesenchymal stem cells (MSCs) are the major source of osteoblasts. Long noncoding RNAs (lncRNAs) are abundantly expressed RNAs that lack protein-coding potential and play an extensive regulatory role in cellular biological activities. However, the regulatory network of lncRNAs in MSC osteogenesis needs further investigation. METHODS: QRT-PCR, western blot, immunofluorescence, and immunohistochemistry assays were used to determine the levels of relevant genes. The osteogenic differentiation capability was evaluated by using Alizarin Red S (ARS) staining, alkaline phosphatase activity assays, hematoxylin & eosin staining or micro-CT. RNA fluorescence in situ hybridization (FISH) and RNAscope were used to detect HHAS1 expression in cells and bone tissue. A microarray assay was performed to identify differentially expressed microRNAs. RNA immunoprecipitation and RNA pull-down were used to explore the interactions between related proteins and nucleic acids. RESULTS: The level of lncRNA HHAS1 increased during bone marrow-derived MSC (BMSC) osteogenesis and was positively related to the levels of osteogenic genes and ARS intensity. HHAS1 was located in both the cytoplasm and the nucleus and was expressed in human bone tissue. HHAS1 facilitated BMSC osteogenic differentiation by downregulating miR-204-5p expression and enhancing the level of RUNX family transcription factor 2 (RUNX2). In addition, interferon regulatory factor 2 (IRF2) was increased during BMSC osteogenic differentiation and interacted with the promoter of HHAS1, which resulted in the transcriptional activation of HHAS1. Furthermore, IRF2 and HHAS1 helped improve bone defect repair in vivo. CONCLUSIONS: Our study identified a novel lncRNA, HHAS1, that facilitates BMSC osteogenic differentiation and proposed a role for the IRF2/HHAS1/miR-204-5p/RUNX2 axis in BMSC osteogenesis regulation. These findings help elucidate the regulatory network of BMSC osteogenesis and provide potential targets for clinical application.		Clin Transl Med. 2021 Jun;11(6):e429. doi: 10.1002/ctm2.429.
5523	LncRNA	LSINCT5	miR-222	PTEN	Ac16 Cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)  	qRT-PCR;Western blot;Flow Cytometry assay;	34184201	LncRNA LSINCT5/miR-222 regulates myocardial ischemia-reperfusion injury through PI3K/AKT pathway.	Cardiovascular diseases rank the top cause of morbidity and mortality worldwide and are usually associated with blood reperfusion after myocardial ischemia/reperfusion injury (MIRI), which often causes severe pathological damages and cardiomyocyte apoptosis. LSINCT5 expression in the plasma of MI patients (n = 53), healthy controls (n = 42) and hypoxia-reoxygenation (HR)-treated cardiomyocyte AC16 cells was examined using qRT-PCR. The effects of LSINCT5 on cell viability and apoptosis were detected by MTT and flow cytometry, respectively. The expression of apoptosis-related proteins Bcl2, Bax and caspase 3 were tested by Western blot. The interaction between LSINCT5 and miR-222 was predicted by bioinformatic analysis. Moreover, changes in viability and apoptosis of AC16 cells co-transfected with siLSINCT5 and miR-222 inhibitor after HR treatment were examined. At last, the expression of proteins in PI3K/AKT pathway, namely PTEN, PI3K and AKT, was examined to analyze the possible pathway participating in LSINCT5-mediated MI/RI. Our study showed that LSINCT5 expression was upregulated in the plasma of MI patients and HR-treated AC16 cells. LSINCT5 overexpression significantly decreased cell viability and apoptosis. Luciferase reporter gene assay and RNA pulldown assay showed that LSINCT5 was a molecular sponge of miR-222. MiR-222 silencing in AC16 cells simulated the phenotypes of MIRI patients and HR-treated cells, indicating that LSINCT5 functions via miR-222 to regulate proliferation and apoptosis of HR-treated AC16 cells. We also showed that proteins of PI3K/AKT signaling pathway were affected in HR-treated AC16 cells, and LSINTC5 knockdown rescued these effects. LncRNA LSINCT5 was upregulated during MI pathogenesis, and LSINCT5 regulated MIRI possibly via a potential LSINCT5/miR-222 axis and PI3K/AKT signaling pathway. Our findings may provide novel evidence for MIRI prevention.		J Thromb Thrombolysis. 2021 Jun 28. doi: 10.1007/s11239-021-02506-3.
5524	LncRNA	LSINCT5	miR-222	PI3K	Ac16 Cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)  	qRT-PCR;Western blot;Flow Cytometry assay;	34184201	LncRNA LSINCT5/miR-222 regulates myocardial ischemia-reperfusion injury through PI3K/AKT pathway.	Cardiovascular diseases rank the top cause of morbidity and mortality worldwide and are usually associated with blood reperfusion after myocardial ischemia/reperfusion injury (MIRI), which often causes severe pathological damages and cardiomyocyte apoptosis. LSINCT5 expression in the plasma of MI patients (n = 53), healthy controls (n = 42) and hypoxia-reoxygenation (HR)-treated cardiomyocyte AC16 cells was examined using qRT-PCR. The effects of LSINCT5 on cell viability and apoptosis were detected by MTT and flow cytometry, respectively. The expression of apoptosis-related proteins Bcl2, Bax and caspase 3 were tested by Western blot. The interaction between LSINCT5 and miR-222 was predicted by bioinformatic analysis. Moreover, changes in viability and apoptosis of AC16 cells co-transfected with siLSINCT5 and miR-222 inhibitor after HR treatment were examined. At last, the expression of proteins in PI3K/AKT pathway, namely PTEN, PI3K and AKT, was examined to analyze the possible pathway participating in LSINCT5-mediated MI/RI. Our study showed that LSINCT5 expression was upregulated in the plasma of MI patients and HR-treated AC16 cells. LSINCT5 overexpression significantly decreased cell viability and apoptosis. Luciferase reporter gene assay and RNA pulldown assay showed that LSINCT5 was a molecular sponge of miR-222. MiR-222 silencing in AC16 cells simulated the phenotypes of MIRI patients and HR-treated cells, indicating that LSINCT5 functions via miR-222 to regulate proliferation and apoptosis of HR-treated AC16 cells. We also showed that proteins of PI3K/AKT signaling pathway were affected in HR-treated AC16 cells, and LSINTC5 knockdown rescued these effects. LncRNA LSINCT5 was upregulated during MI pathogenesis, and LSINCT5 regulated MIRI possibly via a potential LSINCT5/miR-222 axis and PI3K/AKT signaling pathway. Our findings may provide novel evidence for MIRI prevention.		J Thromb Thrombolysis. 2021 Jun 28. doi: 10.1007/s11239-021-02506-3.
5525	LncRNA	LSINCT5	miR-222	AKT	Ac16 Cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)  	qRT-PCR;Western blot;Flow Cytometry assay;	34184201	LncRNA LSINCT5/miR-222 regulates myocardial ischemia-reperfusion injury through PI3K/AKT pathway.	Cardiovascular diseases rank the top cause of morbidity and mortality worldwide and are usually associated with blood reperfusion after myocardial ischemia/reperfusion injury (MIRI), which often causes severe pathological damages and cardiomyocyte apoptosis. LSINCT5 expression in the plasma of MI patients (n = 53), healthy controls (n = 42) and hypoxia-reoxygenation (HR)-treated cardiomyocyte AC16 cells was examined using qRT-PCR. The effects of LSINCT5 on cell viability and apoptosis were detected by MTT and flow cytometry, respectively. The expression of apoptosis-related proteins Bcl2, Bax and caspase 3 were tested by Western blot. The interaction between LSINCT5 and miR-222 was predicted by bioinformatic analysis. Moreover, changes in viability and apoptosis of AC16 cells co-transfected with siLSINCT5 and miR-222 inhibitor after HR treatment were examined. At last, the expression of proteins in PI3K/AKT pathway, namely PTEN, PI3K and AKT, was examined to analyze the possible pathway participating in LSINCT5-mediated MI/RI. Our study showed that LSINCT5 expression was upregulated in the plasma of MI patients and HR-treated AC16 cells. LSINCT5 overexpression significantly decreased cell viability and apoptosis. Luciferase reporter gene assay and RNA pulldown assay showed that LSINCT5 was a molecular sponge of miR-222. MiR-222 silencing in AC16 cells simulated the phenotypes of MIRI patients and HR-treated cells, indicating that LSINCT5 functions via miR-222 to regulate proliferation and apoptosis of HR-treated AC16 cells. We also showed that proteins of PI3K/AKT signaling pathway were affected in HR-treated AC16 cells, and LSINTC5 knockdown rescued these effects. LncRNA LSINCT5 was upregulated during MI pathogenesis, and LSINCT5 regulated MIRI possibly via a potential LSINCT5/miR-222 axis and PI3K/AKT signaling pathway. Our findings may provide novel evidence for MIRI prevention.		J Thromb Thrombolysis. 2021 Jun 28. doi: 10.1007/s11239-021-02506-3.
5526	LncRNA	MALAT1	miR-125b	HMGA1	Laryngocarcinoma Cells	Laryngocarcinoma	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;	34183954	LncRNA MALAT1 Promote Cell Proliferation and Invasion by Sponging miR-125b to Modulate HMGA1 Expression in Laryngocarcinoma.	BACKGROUND: Laryngocarcinoma is the most frequent head and neck malignant tumor. MALAT1 have a role in promoting cell proliferation and metastasis in several tumors. This research aimed to investigate the great roles of MALAT1in laryngocarcinoma. METHODS: Overall, 54 cases of laryngocarcinoma tissues pathological specimens and paracancerous tissues were collected by surgical resection from the Department of Otolaryngology-Head and Neck Surgery at the Shandong Provincial Hospital affiliated to Shandong University, China from Jan 2012 to Oct 2015. The microRNA and protein levels of genes were evaluated by RT-qPCR and western blot. The proliferative and invasive ability were calculated usingCCK8 and transwell assays. Kaplan-Meier method was used to assess the survival of laryngocarcinoma patients. RESULTS: In laryngocarcinoma tissues and cells, lncRNA MALAT1 expression was significantly increased compared to normal tissues and cells. LncRNA MALAT1 promotes proliferation and migration of laryngocarcinoma cells. LncRNA MALAT1 upregulates HMGA1 expression by acting as a competitive endogenous RNA (ceRNA) for miR-125b. Rescue experiments showed that microRNA-125b inhibitor reversed the change in cell viability and invasion induced by sh-MALAT1. Down regulation of lncRNA MALAT1 inhibits laryngocarcinoma proliferation and invasion by modulating miR-125b/HMGA1. CONCLUSION: LncRNA MALAT1 promotes the development of laryngocarcinoma by regulating the expression level of HMGA1 by acting as a miR-125b ceRNA and may be considered as a new strategy for the development of laryngocarcinoma.		Iran J Public Health. 2021 May;50(5):959-969. doi: 10.18502/ijph.v50i5.6113.
5527	LncRNA	bFaar	miR-138-5p	Ins2	Insulin-Secreting Cells	Obesity	Homo sapiens (human)  	qRT-PCR 	34183666	The long non-coding RNA bFaar regulates islet b-cell function and survival during obesity in mice.	Despite obesity being a predisposing factor for pancreatic b-cell dysfunction and loss, the mechanisms underlying its negative effect on insulin-secreting cells remain poorly understood. In this study, we identify an islet-enriched long non-coding RNA (lncRNA), which we name b-cell function and apoptosis regulator (bFaar). bFaar is dramatically downregulated in the islets of the obese mice, and a low level of bFaar is necessary for the development of obesity-associated b-cell dysfunction and apoptosis. Mechanistically, bFaar promote the synthesis and secretion of insulin by upregulating islet-specific genes Ins2, NeuroD1, and Creb1 through sponging miR-138-5p. In addition, using quantitative mass spectrometry, we identify TRAF3IP2 and SMURF1 as interacting proteins that are specifically associated with bFaar. We demonstrate that SMURF1 ubiquitin ligase activity is essential for TRAF3IP2 ubiquitination and activation of NF-kB-mediate b-cell apoptosis. Our experiments provide direct evidence that dysregulated bFaar contributes to the development of obesity-induced b-cell injury and apoptosis.		Nat Commun. 2021 Jun 28;12(1):3997. doi: 10.1038/s41467-021-24302-6.
5528	LncRNA	bFaar	miR-138-5p	NeuroD1	Insulin-Secreting Cells	Obesity	Homo sapiens (human)  	qRT-PCR 	34183666	The long non-coding RNA bFaar regulates islet b-cell function and survival during obesity in mice.	Despite obesity being a predisposing factor for pancreatic b-cell dysfunction and loss, the mechanisms underlying its negative effect on insulin-secreting cells remain poorly understood. In this study, we identify an islet-enriched long non-coding RNA (lncRNA), which we name b-cell function and apoptosis regulator (bFaar). bFaar is dramatically downregulated in the islets of the obese mice, and a low level of bFaar is necessary for the development of obesity-associated b-cell dysfunction and apoptosis. Mechanistically, bFaar promote the synthesis and secretion of insulin by upregulating islet-specific genes Ins2, NeuroD1, and Creb1 through sponging miR-138-5p. In addition, using quantitative mass spectrometry, we identify TRAF3IP2 and SMURF1 as interacting proteins that are specifically associated with bFaar. We demonstrate that SMURF1 ubiquitin ligase activity is essential for TRAF3IP2 ubiquitination and activation of NF-kB-mediate b-cell apoptosis. Our experiments provide direct evidence that dysregulated bFaar contributes to the development of obesity-induced b-cell injury and apoptosis.		Nat Commun. 2021 Jun 28;12(1):3997. doi: 10.1038/s41467-021-24302-6.
5529	LncRNA	bFaar	miR-138-5p	Creb1	Insulin-Secreting Cells	Obesity	Homo sapiens (human)  	qRT-PCR 	34183666	The long non-coding RNA bFaar regulates islet b-cell function and survival during obesity in mice.	Despite obesity being a predisposing factor for pancreatic b-cell dysfunction and loss, the mechanisms underlying its negative effect on insulin-secreting cells remain poorly understood. In this study, we identify an islet-enriched long non-coding RNA (lncRNA), which we name b-cell function and apoptosis regulator (bFaar). bFaar is dramatically downregulated in the islets of the obese mice, and a low level of bFaar is necessary for the development of obesity-associated b-cell dysfunction and apoptosis. Mechanistically, bFaar promote the synthesis and secretion of insulin by upregulating islet-specific genes Ins2, NeuroD1, and Creb1 through sponging miR-138-5p. In addition, using quantitative mass spectrometry, we identify TRAF3IP2 and SMURF1 as interacting proteins that are specifically associated with bFaar. We demonstrate that SMURF1 ubiquitin ligase activity is essential for TRAF3IP2 ubiquitination and activation of NF-kB-mediate b-cell apoptosis. Our experiments provide direct evidence that dysregulated bFaar contributes to the development of obesity-induced b-cell injury and apoptosis.		Nat Commun. 2021 Jun 28;12(1):3997. doi: 10.1038/s41467-021-24302-6.
5530	LncRNA	HOTAIR	miR-107	CXCL12	Chondrocyte	Osteoarthritis	Homo sapiens (human)  	RACE;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	34183035	Knockdown of long noncoding RNA HOTAIR inhibits osteoarthritis chondrocyte injury by miR-107/CXCL12 axis.	BACKGROUND: Osteoarthritis (OA) is a joint disease characterized via destruction of cartilage. Chondrocyte damage is associated with cartilage destruction during OA. Long noncoding RNAs (lncRNAs) are implicated in the regulation of chondrocyte damage in OA progression. This study aims to investigate the role and underlying mechanism of lncRNA homeobox antisense intergenic RNA (HOTAIR) in OA chondrocyte injury. METHODS: Twenty-three OA patients and healthy controls without OA were recruited. Chondrocytes were isolated from OA cartilage tissues. HOTAIR, microRNA-107 (miR-107) and C-X-C motif chemokine ligand 12 (CXCL12) levels were measured by quantitative real-time polymerase chain reaction and western blot. Cell proliferation, apoptosis and extracellular matrix (ECM) degradation were measured using cell counting kit-8, flow cytometry and western blot. The target interaction was explored by bioinformatics, luciferase reporter and RNA immunoprecipitation assays. RESULTS: HOTAIR expression was enhanced, and miR-107 level was reduced in OA cartilage samples. HOTAIR overexpression inhibited cell proliferation, but induced cell apoptosis and ECM degradation in chondrocytes. HOTAIR knockdown caused an opposite effect. MiR-107 was sponged and inhibited via HOTAIR, and knockdown of miR-107 mitigated the effect of HOTAIR silence on chondrocyte injury. CXCL12 was targeted by miR-107. CXCL12 overexpression attenuated the roles of miR-107 overexpression or HOTAIR knockdown in the proliferation, apoptosis and ECM degradation. CXCL12 expression was decreased by HOTAIR silence, and restored by knockdown of miR-107. CONCLUSION: HOTAIR knockdown promoted chondrocyte proliferation, but inhibited cell apoptosis and ECM degradation in OA chondrocytes by regulating the miR-107/CXCL12 axis.		J Orthop Surg Res. 2021 Jun 28;16(1):410. doi: 10.1186/s13018-021-02547-7.
5531	LncRNA	BRE-AS1	miR-21	PTEN	Tnbc Samples	Triple Negative Breast Cancerr	Homo sapiens (human)	CCK-8 assay;qPCR;RT-qPCR;RNA pull-down assay;RNA pull-down;	34182945	Long non-coding RNA BRE-AS1 inhibits the proliferation, migration, and invasion of cancer cells in triple-negative breast cancer and predicts patients' survival by downregulating miR-21.	BACKGROUND: BRE-AS1 is a recently identified tumor suppressor in non-small cell lung cancer. It role in other human diseases remains elusive. METHODS: Differential expression of BRE-AS1 in with triple-negative breast cancer (TNBC) patients (n = 74, patient group) and healthy volunteers (n = 58, control group) was studied with RT-qPCR. The direct interaction between BRE-AS1 and premature microRNA-21 (miR-21) was assessed by RNA pull-down assay. The interactions among BRE-AS1, miR-21 and PTEN were evaluated by overexpression assays. CCK-8 assay and Transwell assay were used to evaluate cell behaviors. RESULTS: BRE-AS1 was downregulated in TNBC, while miR-21 was highly expressed in TNBC. Low expression levels of lncRNA BRE-AS1 and high expression levels of miR-21 were significantly correlated with unfavorable survival outcomes. BRE-AS1 and miRNA-21 were inversely correlated across TNBC samples, not control samples. BRE-AS1 decreased miR-21 expression and increased PTEN expression while miR-21showed no role in BRE-AS1 expression. RNA pull-down assay illustrated that BRE-AS1 may sponge premature miR-21 to suppress it maturation. Overexpression of BRE-AS1 decreased cell behaviors, while overexpression of miR-21 promoted cell behaviors. MiR-21 suppressed the role of BRE-AS1 in cancer cell behaviors. CONCLUSION: Therefore, BRE-AS1 may inhibit TNBC by downregulating miR-21.		BMC Cancer. 2021 Jun 28;21(1):745. doi: 10.1186/s12885-021-08294-6.
5532	LncRNA	LncRNA-ATB	miR-29b-2-5p	MEKK2	Lung Epithelial Cells	Pulmonary Fibrosis	Homo sapiens (human)  	qRT-PCR 	34180127	LncRNA-ATB regulates epithelial-mesenchymal transition progression in pulmonary fibrosis via sponging miR-29b-2-5p and miR-34c-3p.	Dysregulation of non-coding RNAs (ncRNAs) has been proved to play pivotal roles in epithelial-mesenchymal transition (EMT) and fibrosis. We have previously demonstrated the crucial function of long non-coding RNA (lncRNA) ATB in silica-induced pulmonary fibrosis-related EMT progression. However, the underlying molecular mechanism has not been fully elucidated. Here, we verified miR-29b-2-5p and miR-34c-3p as two vital downstream targets of lncRNA-ATB. As opposed to lncRNA-ATB, a significant reduction of both miR-29b-2-5p and miR-34c-3p was observed in lung epithelial cells treated with TGF-b1 and a murine silicosis model. Overexpression miR-29b-2-5p or miR-34c-3p inhibited EMT process and abrogated the pro-fibrotic effects of lncRNA-ATB in vitro. Further, the ectopic expression of miR-29b-2-5p and miR-34c-3p with chemotherapy attenuated silica-induced pulmonary fibrosis in vivo. Mechanistically, TGF-b1-induced lncRNA-ATB accelerated EMT as a sponge of miR-29b-2-5p and miR-34c-3p and shared miRNA response elements with MEKK2 and NOTCH2, thus relieving these two molecules from miRNA-mediated translational repression. Interestingly, the co-transfection of miR-29b-2-5p and miR-34c-3p showed a synergistic suppression effect on EMT in vitro. Furthermore, the co-expression of these two miRNAs by using adeno-associated virus (AAV) better alleviated silica-induced fibrogenesis than single miRNA. Approaches aiming at lncRNA-ATB and its downstream effectors may represent new effective therapeutic strategies in pulmonary fibrosis.		J Cell Mol Med. 2021 Aug;25(15):7294-7306. doi: 10.1111/jcmm.16758. Epub 2021 Jun 27.
5533	LncRNA	LncRNA-ATB	miR-34c-3p	MEKK2	Lung Epithelial Cells	Pulmonary Fibrosis	Homo sapiens (human)  	qRT-PCR 	34180127	LncRNA-ATB regulates epithelial-mesenchymal transition progression in pulmonary fibrosis via sponging miR-29b-2-5p and miR-34c-3p.	Dysregulation of non-coding RNAs (ncRNAs) has been proved to play pivotal roles in epithelial-mesenchymal transition (EMT) and fibrosis. We have previously demonstrated the crucial function of long non-coding RNA (lncRNA) ATB in silica-induced pulmonary fibrosis-related EMT progression. However, the underlying molecular mechanism has not been fully elucidated. Here, we verified miR-29b-2-5p and miR-34c-3p as two vital downstream targets of lncRNA-ATB. As opposed to lncRNA-ATB, a significant reduction of both miR-29b-2-5p and miR-34c-3p was observed in lung epithelial cells treated with TGF-b1 and a murine silicosis model. Overexpression miR-29b-2-5p or miR-34c-3p inhibited EMT process and abrogated the pro-fibrotic effects of lncRNA-ATB in vitro. Further, the ectopic expression of miR-29b-2-5p and miR-34c-3p with chemotherapy attenuated silica-induced pulmonary fibrosis in vivo. Mechanistically, TGF-b1-induced lncRNA-ATB accelerated EMT as a sponge of miR-29b-2-5p and miR-34c-3p and shared miRNA response elements with MEKK2 and NOTCH2, thus relieving these two molecules from miRNA-mediated translational repression. Interestingly, the co-transfection of miR-29b-2-5p and miR-34c-3p showed a synergistic suppression effect on EMT in vitro. Furthermore, the co-expression of these two miRNAs by using adeno-associated virus (AAV) better alleviated silica-induced fibrogenesis than single miRNA. Approaches aiming at lncRNA-ATB and its downstream effectors may represent new effective therapeutic strategies in pulmonary fibrosis.		J Cell Mol Med. 2021 Aug;25(15):7294-7306. doi: 10.1111/jcmm.16758. Epub 2021 Jun 27.
5534	LncRNA	LncRNA-ATB	miR-29b-2-5p	NOTCH2	Lung Epithelial Cells	Pulmonary Fibrosis	Homo sapiens (human)  	qRT-PCR 	34180127	LncRNA-ATB regulates epithelial-mesenchymal transition progression in pulmonary fibrosis via sponging miR-29b-2-5p and miR-34c-3p.	Dysregulation of non-coding RNAs (ncRNAs) has been proved to play pivotal roles in epithelial-mesenchymal transition (EMT) and fibrosis. We have previously demonstrated the crucial function of long non-coding RNA (lncRNA) ATB in silica-induced pulmonary fibrosis-related EMT progression. However, the underlying molecular mechanism has not been fully elucidated. Here, we verified miR-29b-2-5p and miR-34c-3p as two vital downstream targets of lncRNA-ATB. As opposed to lncRNA-ATB, a significant reduction of both miR-29b-2-5p and miR-34c-3p was observed in lung epithelial cells treated with TGF-b1 and a murine silicosis model. Overexpression miR-29b-2-5p or miR-34c-3p inhibited EMT process and abrogated the pro-fibrotic effects of lncRNA-ATB in vitro. Further, the ectopic expression of miR-29b-2-5p and miR-34c-3p with chemotherapy attenuated silica-induced pulmonary fibrosis in vivo. Mechanistically, TGF-b1-induced lncRNA-ATB accelerated EMT as a sponge of miR-29b-2-5p and miR-34c-3p and shared miRNA response elements with MEKK2 and NOTCH2, thus relieving these two molecules from miRNA-mediated translational repression. Interestingly, the co-transfection of miR-29b-2-5p and miR-34c-3p showed a synergistic suppression effect on EMT in vitro. Furthermore, the co-expression of these two miRNAs by using adeno-associated virus (AAV) better alleviated silica-induced fibrogenesis than single miRNA. Approaches aiming at lncRNA-ATB and its downstream effectors may represent new effective therapeutic strategies in pulmonary fibrosis.		J Cell Mol Med. 2021 Aug;25(15):7294-7306. doi: 10.1111/jcmm.16758. Epub 2021 Jun 27.
5535	LncRNA	LncRNA-ATB	miR-34c-3p	NOTCH2	Lung Epithelial Cells	Pulmonary Fibrosis	Homo sapiens (human)  	qRT-PCR 	34180127	LncRNA-ATB regulates epithelial-mesenchymal transition progression in pulmonary fibrosis via sponging miR-29b-2-5p and miR-34c-3p.	Dysregulation of non-coding RNAs (ncRNAs) has been proved to play pivotal roles in epithelial-mesenchymal transition (EMT) and fibrosis. We have previously demonstrated the crucial function of long non-coding RNA (lncRNA) ATB in silica-induced pulmonary fibrosis-related EMT progression. However, the underlying molecular mechanism has not been fully elucidated. Here, we verified miR-29b-2-5p and miR-34c-3p as two vital downstream targets of lncRNA-ATB. As opposed to lncRNA-ATB, a significant reduction of both miR-29b-2-5p and miR-34c-3p was observed in lung epithelial cells treated with TGF-b1 and a murine silicosis model. Overexpression miR-29b-2-5p or miR-34c-3p inhibited EMT process and abrogated the pro-fibrotic effects of lncRNA-ATB in vitro. Further, the ectopic expression of miR-29b-2-5p and miR-34c-3p with chemotherapy attenuated silica-induced pulmonary fibrosis in vivo. Mechanistically, TGF-b1-induced lncRNA-ATB accelerated EMT as a sponge of miR-29b-2-5p and miR-34c-3p and shared miRNA response elements with MEKK2 and NOTCH2, thus relieving these two molecules from miRNA-mediated translational repression. Interestingly, the co-transfection of miR-29b-2-5p and miR-34c-3p showed a synergistic suppression effect on EMT in vitro. Furthermore, the co-expression of these two miRNAs by using adeno-associated virus (AAV) better alleviated silica-induced fibrogenesis than single miRNA. Approaches aiming at lncRNA-ATB and its downstream effectors may represent new effective therapeutic strategies in pulmonary fibrosis.		J Cell Mol Med. 2021 Aug;25(15):7294-7306. doi: 10.1111/jcmm.16758. Epub 2021 Jun 27.
5536	LncRNA	HOTAIR	miR-17-5p	ATG2	A549 And Beas-2B Cells	Acute Lung Injury	Homo sapiens (human)  	microarray;Luciferase reporter assay;RNA pull-down;	34180119	The lncRNA HOTAIR regulates autophagy and affects Lps-Induced Acute Lung Injury through the miR-17-5p/ATG2/ATG7/ATG16 axis.	Long non-coding ribonucleic acids (lncRNAs) play critical roles in acute lung injury (ALI). We aimed to explore the involvement of lncRNA HOX transcript antisense intergenic ribonucleic acid (HOTAIR) in regulating autophagy in lipopolysaccharide (LPS)-induced ALI. We obtained 1289 differentially expressed lncRNAs or messenger RNAs (mRNAs) via microarray analysis. HOTAIR was significantly upregulated in the LPS stimulation experimental group. HOTAIR knockdown (si-HOTAIR) promoted cell proliferation in LPS-stimulated A549 and BEAS-2B cells, suppressing the protein expression of autophagy marker light chain 3B and Beclin-1. Inhibition of HOTAIR suppressed LPS-induced cell autophagy, apoptosis and arrested cells in the G0/G1 phase prior to S phase entry. Further, si-HOTAIR alleviated LPS-induced lung injury in vivo. We predicted the micro-ribonucleic acid miR-17-5p to target HOTAIR and confirmed this via RNA pull-down and dual luciferase reporter assays. miR-17-5p inhibitor treatment reversed the HOTAIR-mediated effects on autophagy, apoptosis, cell proliferation and cell cycle. Finally, we predicted autophagy-related genes (ATGs) ATG2, ATG7 and ATG16 as targets of miR-17-5p, which reversed their HOTAIR-mediated protein upregulation in LPS-stimulated A549 and BEAS-2B cells. Taken together, our results indicate that HOTAIR regulated apoptosis, the cell cycle, proliferation and autophagy through the miR-17-5p/ATG2/ATG7/ATG16 axis, thus driving LPS-induced ALI.		J Cell Mol Med. 2021 Aug;25(16):8062-8073. doi: 10.1111/jcmm.16737. Epub 2021 Jun 27.
5537	LncRNA	HOTAIR	miR-17-5p	ATG7	A549 And Beas-2B Cells	Acute Lung Injury	Homo sapiens (human)  	microarray;Luciferase reporter assay;RNA pull-down;	34180119	The lncRNA HOTAIR regulates autophagy and affects Lps-Induced Acute Lung Injury through the miR-17-5p/ATG2/ATG7/ATG16 axis.	Long non-coding ribonucleic acids (lncRNAs) play critical roles in acute lung injury (ALI). We aimed to explore the involvement of lncRNA HOX transcript antisense intergenic ribonucleic acid (HOTAIR) in regulating autophagy in lipopolysaccharide (LPS)-induced ALI. We obtained 1289 differentially expressed lncRNAs or messenger RNAs (mRNAs) via microarray analysis. HOTAIR was significantly upregulated in the LPS stimulation experimental group. HOTAIR knockdown (si-HOTAIR) promoted cell proliferation in LPS-stimulated A549 and BEAS-2B cells, suppressing the protein expression of autophagy marker light chain 3B and Beclin-1. Inhibition of HOTAIR suppressed LPS-induced cell autophagy, apoptosis and arrested cells in the G0/G1 phase prior to S phase entry. Further, si-HOTAIR alleviated LPS-induced lung injury in vivo. We predicted the micro-ribonucleic acid miR-17-5p to target HOTAIR and confirmed this via RNA pull-down and dual luciferase reporter assays. miR-17-5p inhibitor treatment reversed the HOTAIR-mediated effects on autophagy, apoptosis, cell proliferation and cell cycle. Finally, we predicted autophagy-related genes (ATGs) ATG2, ATG7 and ATG16 as targets of miR-17-5p, which reversed their HOTAIR-mediated protein upregulation in LPS-stimulated A549 and BEAS-2B cells. Taken together, our results indicate that HOTAIR regulated apoptosis, the cell cycle, proliferation and autophagy through the miR-17-5p/ATG2/ATG7/ATG16 axis, thus driving LPS-induced ALI.		J Cell Mol Med. 2021 Aug;25(16):8062-8073. doi: 10.1111/jcmm.16737. Epub 2021 Jun 27.
5538	LncRNA	HOTAIR	miR-17-5p	ATG16	A549 And Beas-2B Cells	Acute Lung Injury	Homo sapiens (human)  	microarray;Luciferase reporter assay;RNA pull-down;	34180119	The lncRNA HOTAIR regulates autophagy and affects Lps-Induced Acute Lung Injury through the miR-17-5p/ATG2/ATG7/ATG16 axis.	Long non-coding ribonucleic acids (lncRNAs) play critical roles in acute lung injury (ALI). We aimed to explore the involvement of lncRNA HOX transcript antisense intergenic ribonucleic acid (HOTAIR) in regulating autophagy in lipopolysaccharide (LPS)-induced ALI. We obtained 1289 differentially expressed lncRNAs or messenger RNAs (mRNAs) via microarray analysis. HOTAIR was significantly upregulated in the LPS stimulation experimental group. HOTAIR knockdown (si-HOTAIR) promoted cell proliferation in LPS-stimulated A549 and BEAS-2B cells, suppressing the protein expression of autophagy marker light chain 3B and Beclin-1. Inhibition of HOTAIR suppressed LPS-induced cell autophagy, apoptosis and arrested cells in the G0/G1 phase prior to S phase entry. Further, si-HOTAIR alleviated LPS-induced lung injury in vivo. We predicted the micro-ribonucleic acid miR-17-5p to target HOTAIR and confirmed this via RNA pull-down and dual luciferase reporter assays. miR-17-5p inhibitor treatment reversed the HOTAIR-mediated effects on autophagy, apoptosis, cell proliferation and cell cycle. Finally, we predicted autophagy-related genes (ATGs) ATG2, ATG7 and ATG16 as targets of miR-17-5p, which reversed their HOTAIR-mediated protein upregulation in LPS-stimulated A549 and BEAS-2B cells. Taken together, our results indicate that HOTAIR regulated apoptosis, the cell cycle, proliferation and autophagy through the miR-17-5p/ATG2/ATG7/ATG16 axis, thus driving LPS-induced ALI.		J Cell Mol Med. 2021 Aug;25(16):8062-8073. doi: 10.1111/jcmm.16737. Epub 2021 Jun 27.
5539	LncRNA	NEAT1	miR-142-5p	JAG1	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;RNA immunoprecipitation;Western blot;Luciferase reporter assay;RNA immunoprecipitation;	34178135	Long non-coding RNA NEAT1 increases the aggressiveness of gastric cancer by regulating the microRNA-142-5p/JAG1 axis.	Gastric cancer has been indicated to have a high recurrence rate in China. Previous studies have revealed that long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) exerted critical roles in cancers. Therefore, the present study aimed to determine the function of NEAT1 and explore the unknown molecular mechanisms of gastric cancer pathogenesis. Reverse transcription-quantitative PCR assay was used to examine the expression of NEAT1, microRNA (miR)-142-5p and jagged1 (JAG1) in gastric cancer. Cell Counting Kit-8 and Transwell assays were conducted to examine cell proliferation, migration and invasion. The protein expression levels of N-cadherin, Vimentin, E-cadherin and JAG1 were quantified by western blot assay. The associations among NEAT1, miR-142-5p and JAG1 were confirmed by dual-luciferase reporter assay and RNA immunoprecipitation. The effects of NEAT1 silencing on tumor growth were evaluated by tumor xenografts. The results indicated that NEAT1 was highly expressed in tumor tissues and cells compared with that in paracancerous tissues and the normal gastric epithelial cell line GES-1 and significantly associated with poor prognosis in gastric cancer. Functional analyses further demonstrated that NEAT1 knockdown suppressed proliferation, motility and tumor growth in vitro and in vivo. Mechanistically, NEAT1 sponged miR-142-5p to regulate JAG1 expression. In addition, the effects of NEAT1 knockdown on the proliferation, migration and invasion of gastric cancer cells could be rescued by miR-142-5p inhibitor, and JAG1 overexpression reversed the miR-142-5p-mediated effects on gastric cancer cells. These findings demonstrated that long non-coding RNA NEAT1 regulated gastric cancer progression by targeting the miR-142-5p/JAG1 axis.		Exp Ther Med. 2021 Aug;22(2):862. doi: 10.3892/etm.2021.10294. Epub 2021 Jun 10.
5540	LncRNA	lncRNA-MIAT	miR-150-5p	NA	Endometrial Epithelial Cells	Endometrial Fibrosis	Homo sapiens (human)  	qPCR;Western blot;	34178037	ADSC Exosomes Mediate lncRNA-MIAT Alleviation of Endometrial Fibrosis by Regulating miR-150-5p.	BACKGROUND: Secondary infertility remains a major complication of endometrial fibrosis in women. The use of exosomes from adipose-derived mesenchymal stem cells (ADSCs) has shown promising results for the treatment of endometrial fibrosis. However, the mechanisms of action of ADSC-exosome (ADSC-Exo) therapy remain unclear. MATERIALS AND METHODS: An endometrial fibrosis model was established in mice treated with alcohol and endometrial epithelial cells (ESCs) treated with TGF-b1. ADSCs were isolated from Sprague Dawley (SD) rats, and exosomes were isolated from ADSCs using ExoQuick reagent. Exosomes were identified by transmission electron microscopy (TEM), NanoSight, and Western blot analysis. The expression level of lncRNA-MIAT was detected by qPCR analysis. Western blot analysis was carried out to determine the protein levels of fibrosis markers (TGFbR1, a-SMA, and CK19). A dual-luciferase reporter gene assay was used to verify the relationship between target genes. The endometrial tissues of the endometrial fibrosis model were stained with HE and Masson's trichrome. RESULTS: ADSCs and ADSC-Exos were successfully isolated, and the expression level of lncRNA-MIAT was significantly down-regulated in endometrial tissue and the TGF-b1-induced ESC injury model, whereas ADSC-Exos increased the expression of lncRNA-MIAT in the TGF-b1-induced ESC model. Functionally, ADSC-Exo treatment repressed endometrial fibrosis in vivo and in vitro by decreasing the expression of hepatic fibrosis markers (a-SMA and TGFbR1) and increasing the expression of CK19. Moreover, miR-150-5p expression was repressed by lncRNA-MIAT in the TGF-b1-induced ESC injury model. The miR-150-5p mimic promoted TGF-b1-induced ESC fibrosis. CONCLUSION: ADSC-Exos mediate lncRNA-MIAT alleviation of endometrial fibrosis by regulating miR-150-5p, which suggests that lncRNA-MIAT from ADSC-Exos may be a viable treatment for endometrial fibrosis.		Front Genet. 2021 Jun 9;12:679643. doi: 10.3389/fgene.2021.679643. eCollection 2021.
5541	LncRNA	ILF3-AS1	miR-4306	PLAGL2	Ptc Cells	Papillary Thyroid Cancer	Homo sapiens (human)  	ISH;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;	34176471	Long noncoding RNA ILF3-AS1 aggravates papillary thyroid carcinoma progression via regulating the miR-4306/PLAGL2 axis.	BACKGROUND: It have been proven that long non-coding RNAs (lncRNAs) serve as regulators in carcinogenesis. Interleukin enhancer binding factor 3 antisense RNA 1 (ILF3-AS1) has been illuminated as a prognostic factor in some cancers. Nevertheless, its expression pattern and possible functions in papillary thyroid carcinoma (PTC) have not been studied. METHODS: The expression of ILF3-AS1 was measured by RT-qPCR and ISH. Colony formation assay and EdU assay were used to probe cell proliferation. TUNEL assay was used for analysis of cell apoptosis. Immunofluorescence and western blot were conducted to evaluate the expression change of E-cadherin and N-cadherin. The RNA interaction was demonstrated by mechanism experiments, including pull down assay and dual luciferase reporter assay. RESULTS: ILF3-AS1 expression was evidently upregulated in PTC cell lines. ILF3-AS1 knockdown restrained the proliferation, migration and invasion of PTC cells. Mechanical investigation revealed that miR-4306 could interact with ILF3-AS1. PLAGL2 was a downstream target of miR-4306. The effects of ILF3-AS1 knockdown on the cellular processes were abrogated by miR-4306 downregulation or pleiomorphic adenoma gene-like 2 (PLAGL2) overexpression. CONCLUSION: ILF3-AS1 plays tumor-promoting role in PTC via targeting miR-4306/PLAGL2 axis.		Cancer Cell Int. 2021 Jun 27;21(1):322. doi: 10.1186/s12935-021-01950-8.
5542	LncRNA	DLEU2	miR-455	HK2	Ec Cells	Endometrial Cancer	Homo sapiens (human)	qRT-PCR 	34174908	Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway.	BACKGROUND: Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined. METHODS: We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression. RESULTS: HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a. CONCLUSIONS: This study identified DLEU2 as an upstream activator of HK2-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.		J Exp Clin Cancer Res. 2021 Jun 26;40(1):216. doi: 10.1186/s13046-021-02018-1.
5543	LncRNA	LINC01234	miR-525-5p	MEIS2	Tnbc Cells	Triple Negative Breast Cancerr	Mus musculus (mouse)	qPCR;RT-qPCR;Rescue assay;	34173712	LINC01234 aggravates cell growth and migration of triple-negative breast cancer by activating the Wnt pathway.	Triple-negative breast cancer (TNBC) is a common cancer with increasing incidence and mortality in female. Increasing studies have revealed that long noncoding RNAs (lncRNAs) are novel molecules regulating tumors. Long intergenic non-protein coding RNA 1234 (LINC01234) has been demonstrated to function as an oncogene in several tumors. However, the role of LINC01234 in TNBC remains unelucidated. Herein, RT-qPCR showed that LINC01234 expression was upregulated in both TNBC tissues and cell lines. Functionally, knockdown of LINC01234 suppressed proliferation, migration, invasion, epithelial-mesenchymal transition (EMT) process, and promoted apoptosis in TNBC cells. Xenograft mouse models revealed that LINC01234 downregulation inhibited TNBC tumor growth in vivo. Furthermore, LINC01234 was transcriptionally elevated by Sp1 transcription factor (SP1) in TNBC cells. Mechanistically, LINC01234 interacted with miR-525-5p and miR-525-5p targeted MEIS2. Rescue assays manifested that MEIS2 overexpression rescued the cellular processes inhibited by silenced LINC01234. Moreover, we validated that LINC01234 regulated the activation of the Wnt pathway through modulating MEIS2 in TNBC cells. In conclusion, LINC01234 aggravated TNBC cell growth, migration, invasion and EMT by modulating the miR-525-5p/MEIS2 axis and activating the Wnt/b-catenin signaling pathway.		Environ Toxicol. 2021 Jun 26. doi: 10.1002/tox.23318.
5544	LncRNA	THRIL	miR-424	TXNIP	The Myocardial Tissues	Coronary Heart Disease	Mus musculus (mouse)	microarray;qPCR;RT-qPCR;	34171363	Long non-coding RNA THRIL is upregulated in coronary heart disease and binds to microRNA-424 to upregulate TXNIP in mice.	Cardiovascular disease, particularly coronary heart disease (CHD), is one of the diseases with the highest fatality. The close correlation between long non-coding RNAs (lncRNAs) and the occurrence and development of myocardial injury has been highlighted recently. This article mainly focused on the regulation of THRIL on myocardial injury caused by CHD in mice. After establishment of a mouse model with CHD, a lncRNA microarray analysis was performed on mouse myocardial tissues to detect differentially expressed lncRNAs, followed by RT-qPCR validation. CHD was induced in mice by high-fat diet feeding and THRIL was silenced using si-THRIL. The results showed that treating CHD mice with si-THRIL attenuated myocardial damage by restoring LVEF, LVFS, and HDL-C levels, while lowering HMI, LVMI, TC, TG, LDL-C, CK-MB, and cTnI levels. Meanwhile, mechanistical studies using bioinformatics prediction, dual-luciferase and subcellular fractionation assays revealed that THRIL bound to microRNA (miR)-424, inhibited miR-424 interaction with TXNIP and promoted TXNIP expression in the myocardial tissues. The cardioprotective effects of si-THRIL on mice were attenuated when miR-424 was downregulated. Moreover, TXNIP exerted its effects on myocardial injury by mediating the p53 pathway. Taken together, this study demonstrated that THRIL inhibition alleviates myocardial injury in CHD possibly through the miR-424/TXNIP/p53 axis.		Microvasc Res. 2021 Jun 24;138:104215. doi: 10.1016/j.mvr.2021.104215.
5545	LncRNA	ITGB2-AS1	miR-328-5p	HMGA1	Ccrcc Tumor And Cell Lines	Clear Cell Renal Cancer	Homo sapiens (human)  	qRT-PCR 	34170494	LncRNA ITGB2-AS1 promotes the progression of clear cell renal cell carcinoma by modulating miR-328-5p/HMGA1 axis.	Clear cell renal cell carcinoma (ccRCC) is the most common histologic subtype of renal cell carcinoma and long non-coding RNAs (lncRNAs) play important roles in the progression of ccRCC. In this study, we aim to explore the potential function of ITGB2-AS1 in ccRCC progression and its underlying molecular mechanism. We first explored the association between ITGB2-AS1 expression level and ccRCC prognosis. We found that the expression level of ITGB2-AS1 was significantly higher in ccRCC tumor and cell lines, and highly expressed ITGB2-AS1 was also associated with a poorer prognosis. Consistently, silencing ITGB2-AS1 inhibited proliferation, promoted apoptosis in ccRCC cell lines, and curbed the tumorigenesis in the Xenograft model, reduced tumorigenesis in a xenograft tumor growth model. We further identified and confirmed the miRNA miR-328-5p as a target of ITGB2-AS1, and miR-328-5p negatively regulated the expression of HMGA1 protein. The anti-tumor effect of silencing ITGB2-AS1 could be partially rescued by inhibiting miR-328-5p activity or overexpressing HMGA1, indicating that ITGB2-AS1 promotes the survival and progression of ccRCC by modulating miR-328-5p/HMGA1 axis. Collectively, our data demonstrated that ITGB2-AS1 expression level is positively correlated with the survival and tumorigenesis of ccRCC. As a target of ITGB2-AS1, miR-328-5p seems to function as a tumor-suppressor, and the oncogenic effect of ITGB2-AS1 is partially mediated via the miR-328-5p/HMGA1 axis.		Hum Cell. 2021 Sep;34(5):1545-1557. doi: 10.1007/s13577-021-00563-7. Epub 2021 Jun 25.
5546	LncRNA	MEF2C-AS1	miR-592	RSPO1	Cc Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;Luciferase reporter assay;	34169096	A Novel Identified Long Non-coding RNA, lncRNA MEF2C-AS1, Inhibits Cervical Cancer via Regulation of miR-592/RSPO1.	Purpose: Our purpose was to investigate the effect of lncRNA MEF2C antisense RNA 1 (MEF2C-AS1) on cervical cancer and further explore its underlying molecular mechanisms. Methods: The proliferation, migration and invasion of CC cells were determined by counting Kit-8 (CCK-8), colony formation assay, and transwell assays, respectively. qRT-PCR and western blot were conducted to quantitatively detect the expression of lncRNA MEF2C-AS1, miR-592 and R-spondin1 (RSPO1). Kaplan-Meier survival curve from the Cancer Genome Atlas (TCGA) database and the Gene Expression Profiling Interactive Analysis (GEPIA) website was used to describe the overall survival. Bioinformatics analysis was performed to search the downstream target of lncRNA MEF2C-AS1 and miR-592. Luciferase reporter assay was conducted to detect the interaction between lncRNA MEF2C-AS1 and miR-592 or miR-592 and RSPO1. Results: The data from GEPIA website showed that lncRNA MEF2C-AS1 expression was down-regulated in CC tissues and also associated with survival rate of CC patients. Moreover, the results of qRT-PCR also showed lncRNA MEF2C-AS1 was lowly expressed in CC cells. Subsequently, we confirmed that overexpression of lncRNA MEF2C-AS1 inhibited the proliferation, migration and invasion of CC cells. Further research illustrated that lncRNA MEF2C-AS1 was the target of miR-592, and RSPO1 was the downstream target gene of miR-592. Importantly, functional research findings indicated that lncRNA MEF2C-AS1 inhibited CC via suppressing miR-592 by targeting RSPO1. Conclusion: In our study, we demonstrated the functional role of the lncRNA MEF2C-AS1-miR-592-RSPO1 axis in the progression of CC, which provides a latent target for CC treatment.		Front Mol Biosci. 2021 Jun 8;8:687113. doi: 10.3389/fmolb.2021.687113. eCollection 2021.
5547	LncRNA	PRR34-AS1	miR-296-5p	E2F2	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Chromatin immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34168917	lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/b-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12.	Hepatocellular carcinoma (HCC) belongs to the most frequent cancer with a high death rate worldwide. Thousands of long non-coding RNAs (lncRNAs) have been confirmed to influence the development of human cancers, including HCC. Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR) that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in vitro and facilitated tumor growth in vivo. In addition, western blot analysis and TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/b-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/b-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.		Mol Ther Nucleic Acids. 2021 Apr 24;25:37-52. doi: 10.1016/j.omtn.2021.04.016. eCollection 2021 Sep 3.
5548	LncRNA	PRR34-AS1	miR-296-5p	SOX12	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)	ChIP;RT-PCR;RIP assay;RNA immunoprecipitation;Western blot;Chromatin immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34168917	lncRNA PRR34-AS1 promotes HCC development via modulating Wnt/b-catenin pathway by absorbing miR-296-5p and upregulating E2F2 and SOX12.	Hepatocellular carcinoma (HCC) belongs to the most frequent cancer with a high death rate worldwide. Thousands of long non-coding RNAs (lncRNAs) have been confirmed to influence the development of human cancers, including HCC. Nevertheless, the biological role of PRR34 antisense RNA 1 (PRR34-AS1) in HCC remains obscure. Here, we observed via quantitative real-time reverse transcriptase polymerase chain reaction (quantitative real-time RT-PCR) that PRR34-AS1 was highly expressed in HCC cells. Functional assays revealed that PRR34-AS1 promoted HCC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process in vitro and facilitated tumor growth in vivo. In addition, western blot analysis and TOP Flash/FOP Flash reporter assays verified that PRR34-AS1 stimulated Wnt/b-catenin pathway in HCC cells. Furthermore, RNA immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays uncovered that PRR34-AS1 sequestered microRNA-296-5p (miR-296-5p) to positively modulate E2F transcription factor 2 (E2F2) and SRY-box transcription factor 12 (SOX12) in HCC cells. Importantly, chromatin immunoprecipitation (ChIP) and luciferase reporter assays uncovered that E2F2 transcriptionally activated PRR34-AS1 in turn. Further, rescue experiments reflected that PRR34-AS1 affected HCC progression through targeting miR-296-5p/E2F2/SOX12/Wnt/b-catenin axis. Our findings found that PRR34-AS1 elicited oncogenic functions in HCC, which indicated that PRR34-AS1 might be a novel therapeutic target for HCC.		Mol Ther Nucleic Acids. 2021 Apr 24;25:37-52. doi: 10.1016/j.omtn.2021.04.016. eCollection 2021 Sep 3.
5549	LncRNA	FIRRE	miR-520a-3p	YOD1	Gbc Cells	Gallbladder Cancer	Homo sapiens (human)  	RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	34168678	Long Non-coding RNA FIRRE Acts as a miR-520a-3p Sponge to Promote Gallbladder Cancer Progression via Mediating YOD1 Expression.	OBJECTIVES: The role of lncRNAs in gallbladder cancer (GBC) remains poorly understood. In this study, we explored the function of functional intergenic repeating RNA element (FIRRE) in GBC. MATERIALS AND METHODS: Whole transcriptome resequencing was performed in three pairs of GBC tissues and adjacent non-tumor tissues. lncRNA FIRRE expression was verified by real-time PCR. The function of FIRRE in GBC was evaluated by experiments in vitro and in vivo. The mechanism of FIRRE was investigated via fluorescent in situ hybridization, RNA pull-down, dual luciferase reporter assays, and RNA immunoprecipitation. RESULTS: FIRRE level was dramatically increased in GBC tissues compared to that in the adjacent non-tumor tissues. High expression of FIRRE was closely related to clinical stage and poor prognosis in GBC patients. Moreover, FIRRE remarkably enhanced proliferation and migration, and inhibited apoptosis of GBC cells. Mechanistically, FIRRE modulated YOD1 expression by sponging miR-520a-3p, thus contributing to the development of GBC. CONCLUSION: Our data revealed that FIRRE might act as a novel mediator in GBC progression by sponging miR-520a-3p and regulating YOD1. FIRRE might be regarded as a potential diagnostic marker or target for GBC treatment.		Front Genet. 2021 Jun 8;12:674653. doi: 10.3389/fgene.2021.674653. eCollection 2021.
5550	LncRNA	CERS6-AS1	miR-217	YWHAG	Pc Tissues And Cells	Pancreatic Cancer	Homo sapiens (human)  	CCK-8 assay;RIP assay;Western blot;Luciferase report assay;	34168120	LncRNA CERS6-AS1 promotes proliferation and metastasis through the upregulation of YWHAG and activation of ERK signaling in pancreatic cancer.	LncRNAs play essential regulatory roles in pancreatic cancer (PC) tumorigenesis and progression. We aimed to investigate the role of lncRNA CERS6-AS1 in PC. CERS6-AS1 expression was determined in PC tissues and cell lines by PCR analysis. The roles of CERS6-AS1 on proliferation, migration, invasion, and epithelial to mesenchymal transition (EMT) were confirmed via CCK-8 assay, EDU assay, transwell assay, wound healing assay, and western blot assay. Besides, the interaction between CERS6-AS1 and their target genes was verified by luciferase report assays and RIP assays. Animal assays and clinical data analysis were performed to validate the functions in vivo. We found that lncRNA CERS6-AS1 was highly expressed in PC tissues and cells. Additionally, high expression of CERS6-AS1 was obviously associated with poor prognosis. Functional assays demonstrated that CERS6-AS1 downregulation significantly inhibited PC cell growth and migration. Moreover, CERS6-AS1 exerted as a molecular sponge for miR-217-5p (miR-217), and miR-217 was confirmed as a potential target of CERS6-AS1. Subsequently, miR-217 suppressed PC cell proliferation and metastasis by directly targeting YWHAG, which interacted with RAF1 and promoted its phosphorylation, leading to RAF1-mediated ERK signaling activation and translocation of phosphorylated ERK from the cytoplasm to the nucleus. Mechanically, CERS6-AS1 silencing significantly inhibited PC cell proliferation and metastasis via a miR-217/YWHAG/RAF1 signaling axis. CERS6-AS1 exerts as a carcinogen in PC to promote malignant features and behaves as a competitive endogenous RNA for miR-217. We identified CERS6-AS1 as a potential biomarker or therapeutic target to improve PC diagnosis and treatment outcomes.		Cell Death Dis. 2021 Jun 24;12(7):648. doi: 10.1038/s41419-021-03921-3.
5551	LncRNA	XIST	miR-101	EZH2	Gastric Cancer Cells	Gastric Cancer	Homo sapiens (human)  	qRT-PCR 	34167550	Correction to: Long non-coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR-101 to modulate EZH2 expression.	unknown		J Exp Clin Cancer Res. 2021 Jun 24;40(1):208. doi: 10.1186/s13046-021-02002-9.
5552	LncRNA	CASC2	miR-152-3p	PDK4	Sepsis Patients And Lps-Stimulated Hpaepic	Acute Lung Injury	Homo sapiens (human)  	RIP assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Flow Cytometry assay;RNA immunoprecipitation;RNA pull-down;	34165388	LncRNA CASC2 Alleviates Sepsis-induced Acute Lung Injury by Regulating the miR-152-3p/PDK4 Axis.	Background: Acute lung injury (ALI) is an early complication of sepsis and it is also considered as an important cause of high mortality in sepsis patients. This research aimed to explore the potential role and mechanism of long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) in sepsis-induced ALI. Methods: The levels of CASC2, microRNA-152-3p (miR-152-3p) and pyruvate dehydrogenase kinase 4 (PDK4) in sepsis patients and LPS-treated HPAEpiC were detected by quantitative real-time PCR and western blot. Cell viability and apoptosis were assessed by Counting Kit-8 (CCK-8) assay and flow cytometry. The concentrations of inflammatory factors were tested by Enzyme-linked immunosorbent assay. Oxidative stress was evaluated by the levels of reactive oxygen species and superoxide dismutase using corresponding commercial kits. The targeting relationship between miR-152-3p and CASC2 or PDK4 was verified by dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays.Results: CASC2 and PDK4 were down-regulated, while miR-152-3p was up-regulated in sepsis patients and LPS-stimulated HPAEpiC. Overexpression of CASC2 relieved the LPS-resulted cell viability inhibition, apoptosis promotion, inflammatory and oxidative damages in HPAEpiC. In addition, miR-152-3p was a miRNA target of CASC2 and CASC2 alleviated cell injury in LPS-disposed HPAEpiC by sponging miR-152-3p. Moreover, miR-152-3p directly targeted PDK4 and CASC2 increased the PDK4 expression by depending on the sponge effect on miR-152-3p. Meanwhile, inhibition of miR-152-3p attenuated LPS-triggered HPAEpiC injury by upregulating the level of PDK4.Conclusion: These results suggested that CASC2 ameliorated the LPS-induced injury in HPAEpiC via regulating miR-152-3p/PDK4 pathway.		Immunol Invest. 2021 Jun 24:1-15. doi: 10.1080/08820139.2021.1928693.
5553	LncRNA	SNHG8	miR-335	RASA1	H9C2 Cell	Myocardial Injury	Homo sapiens (human)  	ELISA;Western blot;Flow Cytometry assay;	34165173	Inhibition of lncRNA SNHG8 plays a protective role in hypoxia-ischemia-reoxygenation-induced myocardial injury by regulating miR-335 and RASA1 expression.	Long non-coding (lnc)RNAs serve a role in a number of diseases, including different types of cancer and acute myocardial infarction. The aim of the present study was to investigate the protective role of lncRNA small nucleolar RNA host gene 8 (SNHG8) in hypoxia-ischemia-reoxygenation (HI/R)-induced myocardial injury and its potential mechanism of action. Cell viability, proliferation, creatine kinase myocardial band, cell apoptosis and protein expression levels were determined by Cell Counting Kit-8 assay, EdU assay, ELISA, flow cytometry and western blotting, respectively. The association between SNHG8 and microRNA (miR)-335 was confirmed using a dual-luciferase reporter gene assay. The effects of the miR-335 inhibitor transfections had on increasing apoptosis and decreasing H9C2 cell viability were reversed in cells co-transfected with SNHG8 small interfering (si)RNA. Furthermore, it was found that miR-335 could regulate RAS p21 protein activator 1 (RASA1) expression and that transfection with SNHG8 siRNA downregulated RASA1 expression. Silencing of RASA1 protected against HI/R-induced H9C2 cell injury. However, SNHG8 siRNA did not further reduce apoptosis, demonstrating that SNHG8 may act through RASA1, and RASA1 may mediate the protection of SNHG8 siRNA in HI/R myocardial injury. Thus, inhibition of lncRNA SNHG8 alleviated HI/R-induced myocardial damage by regulating miR-335 and RASA1.		Mol Med Rep. 2021 Aug;24(2):597. doi: 10.3892/mmr.2021.12236. Epub 2021 Jun 24.
5554	LncRNA	SLC9A3-AS1	miR-486-5p	E2F6	Npc Cells	Nasopharyngeal Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;	34165171	Long noncoding RNA SLC9A3-AS1 increases E2F6 expression by sponging microRNA-486-5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma.	Long noncoding RNA SLC9A3 antisense RNA 1 (SLC9A3-AS1) plays a central role in lung cancer; yet, its functions in nasopharyngeal carcinoma (NPC) have not been elucidated. The present study revealed the roles of SLC9A3-AS1 in NPC and dissected the mechanisms downstream of SLC9A3-AS1. SLC9A3-AS1 levels in NPC were assessed by applying RT-qPCR. The modulatory role of SLC9A3-AS1 interference on NPC cells was examined using numerous functional experiments. High expression of SLC9A3-AS1 was observed in NPC samples. Patients with NPC with a high level of SLC9A3-AS1 experienced a shorter overall survival than those with a low SLC9A3-AS1 level. Loss of SLC9A3-AS1 reduced NPC cell proliferation, colony formation, migration, and invasion but induced cell apoptosis in vitro. Animal experiments further revealed that the depletion of SLC9A3-AS1 hindered NPC tumour growth in vivo. As a competitive endogenous RNA, SLC9A3-AS1 sponged microRNA-486-5p (miR-486-5p), consequently upregulating E2F transcription factor 6 (E2F6). Finally, the effects of SLC9A3-AS1 silencing on NPC cells were reversed by inhibiting miR-486-5p or overexpressing E2F6. In summary, SLC9A3-AS1 exerted carcinogenic effects on NPC cells by adjusting the miR-486-5p/E2F6 axis. Accordingly, the newly identified SLC9A3-AS1/miR-486-5p/E2F6 pathway may offer attractive therapeutic targets for future development.		Oncol Rep. 2021 Aug;46(2):165. doi: 10.3892/or.2021.8116. Epub 2021 Jun 24.
5555	LncRNA	XIST	miR-126-3p	p-p65	Synovial Tissues And Cells	Rheumatoid Arthritis	Homo sapiens (human)  	MTT assay;qPCR;Western blot;MTT assay;	34165008	LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-kB pathway.	The role and mechanism of lncRNA XIST (XIST) in the development of rheumatoid arthritis (RA) was explored in this study. RT-qPCRs were performed to detect the expression of XIST and miR-126-3p in synovial tissues and cells. Target gene prediction and luciferase gene reporter assay were used to validate downstream target genes of XIST. MTT assay, EdU staining and Annexin V/PI staining were performed to explore the effects of XIST and miR-126-3p on cell proliferation and apoptosis. Western blotting analysis was used to detect the expression of related proteins. We found that the expression levels of XIST in tissues and cells were significantly higher than that in normal tissues and cells. Down-regulation of XIST could inhibit cell proliferation rate and increase apoptosis rate. Luciferase gene reporter assay showed that miR-126-3p was a downstream target gene of XIST. Overexpression of miR-126-3p significantly inhibited RA-FLS cell proliferation and induced RA-FLS cell apoptosis. In addition, down-regulation of XIST could increase the ratio of caspase-3 and Bax/Bcl-2. In addition, overexpression of miR-126-3p could inhibit the NF-kB signalling pathway by reducing the expression levels of p-p65 and p-IkBa in RA-FLS cells. In conclusion, down-regulation of XIST can inhibit the proliferation of synovial fibroblasts by increasing the expression levels of miR-126-3p/NF-kB, thereby inhibiting the occurrence and development of RA.		Autoimmunity. 2021 Jun 24:1-10. doi: 10.1080/08916934.2021.1937608.
5556	LncRNA	XIST	miR-126-3p	p-IkBa	Synovial Tissues And Cells	Rheumatoid Arthritis	Homo sapiens (human)  	MTT assay;qPCR;Western blot;MTT assay;	34165008	LncRNA XIST is involved in rheumatoid arthritis fibroblast-like synoviocytes by sponging miR-126-3p via the NF-kB pathway.	The role and mechanism of lncRNA XIST (XIST) in the development of rheumatoid arthritis (RA) was explored in this study. RT-qPCRs were performed to detect the expression of XIST and miR-126-3p in synovial tissues and cells. Target gene prediction and luciferase gene reporter assay were used to validate downstream target genes of XIST. MTT assay, EdU staining and Annexin V/PI staining were performed to explore the effects of XIST and miR-126-3p on cell proliferation and apoptosis. Western blotting analysis was used to detect the expression of related proteins. We found that the expression levels of XIST in tissues and cells were significantly higher than that in normal tissues and cells. Down-regulation of XIST could inhibit cell proliferation rate and increase apoptosis rate. Luciferase gene reporter assay showed that miR-126-3p was a downstream target gene of XIST. Overexpression of miR-126-3p significantly inhibited RA-FLS cell proliferation and induced RA-FLS cell apoptosis. In addition, down-regulation of XIST could increase the ratio of caspase-3 and Bax/Bcl-2. In addition, overexpression of miR-126-3p could inhibit the NF-kB signalling pathway by reducing the expression levels of p-p65 and p-IkBa in RA-FLS cells. In conclusion, down-regulation of XIST can inhibit the proliferation of synovial fibroblasts by increasing the expression levels of miR-126-3p/NF-kB, thereby inhibiting the occurrence and development of RA.		Autoimmunity. 2021 Jun 24:1-10. doi: 10.1080/08916934.2021.1937608.
5557	LncRNA	SNHG1	miR-216a-3p	BAX	Parkinson'S Disease Model Cells	Parkinsons Disease	Homo sapiens (human)	qRT-PCR 	34164485	Long non-coding RNA SNHG1 mediates neuronal damage in Parkinson's disease model cells by regulating miR-216a-3p/Bcl-2-associated X protein.	BACKGROUND: Parkinson's disease (PD) is a common central nervous system degenerative disease in middle-aged and elderly people. Our study aimed to illuminate the relationship and mechanism of long-chain non-coding RNA SNHG1 and miRNA (miR)-216a-3p in PD. METHODS: Human neuroblastoma cell lines were treated with MPP(+) to construct a PD model. Real-time fluorescent quantitative PCR was used to detect the cellular expression of SNHG1. Neuronal cell activity and apoptosis were compared before and after SNHG1 knock-down, as was neuronal miR-216a-3p expression. Further, a luciferase reporter gene experiment was performed to verify BAX as the target of miR-216a-3p. Anti-miR-216a-3p and BAX were co-transfected into PD model cells, and neuronal cellular activity and apoptosis were observed. Finally, the potential regulatory network of SNHG1/miR-216a-3p/BAX in PD was investigated. RESULTS: The expression of miR-216a-3p was decreased in the PD model cells, and re-expression reversed the high apoptotic rate and cell vitality inhibition in PD model cells. SNHG1 interacted with miR-216a-3p and negatively regulated its upstream molecules, while miR-216a-3p attenuated the effect of SNHG1 knock-down on neurons. The overexpression of BAX in the PD cell model blocked the damage by miR-216a-3p to neurons. At the same time, SNHG1 acted as a coordinator, mediating the regulation of BAX via miR-216a-3p, thereby affecting the activity and apoptotic rate of neurons in the PD model. CONCLUSIONS: SNHG1 interacts with miR-216a-3p to regulate the expression of BAX. This SNHG1/miR-216a-3p/BAX molecular regulatory network is implicated in the pathogenesis of PD.		Ann Transl Med. 2021 May;9(10):851. doi: 10.21037/atm-21-1613.
5558	LncRNA	TUG1	miR-186-5p	XIAP	Serum And Cell	Coronary Microembolization	Rattus (rat)	CCK-8 assay;ELISA;qPCR;RT-qPCR;RIP assay;	34163467	Overexpression of lncRNA TUG1 Alleviates NLRP3 Inflammasome-Mediated Cardiomyocyte Pyroptosis Through Targeting the miR-186-5p/XIAP Axis in Coronary Microembolization-Induced Myocardial Damage.	Coronary microembolization (CME) is a complicated problem that commonly arises in the context of coronary angioplasty. The lncRNA taurine-up regulated gene 1 (TUG1), significantly contributes to cardiovascular diseases; however, its contribution to CME-induced myocardial damage remains elusive. Herein, we establish the rat CME model and investigate the role of TUG1 in CME. The cell viability was evaluated via CCK-8 assay. Serum and cell culture supernatant samples were evaluated via ELISA. The dual luciferase reporter (DLR) assay, RIP, and RNA-pull down were conducted to validate the associations between TUG1 and miR-186-5p as well as miR-186-5p and XIAP. The expression of TUG1, miR-186-5p, and XIAP mRNA were determined by RT-qPCR, and proteins were evaluated via immuneblotting. As a result, TUG1 and XIAP were significantly down-regulated, and the miR-186-5p level was found to be remarkably up-regulated in CME myocardial tissues. Overexpression of TUG1 alleviated CME-induced myocardial injury and pyroptosis, whereas TUG1 knockdown showed the opposite effects. The DLR assay, RIP, and RNA-pull down results reveal that TUG1 directly targets miR-186-5p and miR-186-5p directly targets XIAP. In vitro rescue experiments show that TUG1 overexpression alleviates LPS-caused cardiomyocyte injury and pyroptosis via sponging miR-186-5p and regulating XIAP, and depression of miR-186-5p reduces LPS-induced cardiomyocyte injury and pyroptosis by targeting XIAP. Concludingly, the overexpression of TUG1 alleviates NLRP3 inflammasome-mediated cardiomyocyte pyroptosis through targeting the miR-186-5p/XIAP axis in CME-induced myocardial injury.		Front Immunol. 2021 Jun 7;12:637598. doi: 10.3389/fimmu.2021.637598. eCollection 2021.
5559	LncRNA	MEG3	miR-544b	BTG2	Hcc Tissues And Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR;RIP assay;Luciferase reporter assay;	34163177	m6A-Induced LncRNA MEG3 Suppresses the Proliferation, Migration and Invasion of Hepatocellular Carcinoma Cell Through miR-544b/BTG2 Signaling.	OBJECTIVE: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. Long non-coding RNA plays an important role in the development of HCC. This study analyzed the impact of MEG3 on malignant behavior of HCC and explored its possible molecular mechanism. METHODS: Expression of MEG3 in HCC tissues and cell lines was measured by qRT-PCR. Transfection efficiency of MEG3 was verified by qRT-PCR. Cell proliferation, transwell migration, invasion and cell cloning assays were used to detect the effect of MEG3 on the proliferation, migration and invasion ability of HCC cells. The bioinformatics analysis was applied to predict the binding between miR-544b and MEG3 as well as BTG2. Luciferase reporter assay was performed to verify their interaction. Finally, the m6A modification of MEG3 by METTL3 was identified through RIP experiments. RESULTS: MEG3 was lowly expressed in HCC tissues and cells. Overexpression of MEG3 inhibits the proliferation, migration and invasion of HCC cells. MiR-544b can be sponged by MEG3, and overexpression of miR-544b reverses the anti-cancer effect of MEG3. We further confirmed that BTG2 gene is the target gene of miR-544b. Epigenetic studies have shown that METTL3-mediated N(6)-methyladenosine modification led to MEG3 downregulation. CONCLUSION: In HCC, MEG3 and BTG2 are lowly expressed while miR-544b is highly expressed. MEG3 regulates the expression of BTG2 through miR-544b, thus affecting the malignant behavior of HCC. METTL3 regulates the m6A modification of MEG3 and its expression. This study clarified the role of MEG3/miR-544b/BTG2 axis in HCC and also provided new targets for HCC research.		Onco Targets Ther. 2021 Jun 15;14:3745-3755. doi: 10.2147/OTT.S289198. eCollection 2021.
5560	LncRNA	SPRY4-IT1	NA	TCEB1	Hct 116 Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)	microarray;	34163032	NF-kB-activated SPRY4-IT1 promotes cancer cell metastasis by downregulating TCEB1 mRNA via Staufen1-mediated mRNA decay.	Previous study demonstrated that most long non-coding RNAs (lncRNAs) function as competing endogenous RNAs or molecular sponges to negatively modulate miRNA and regulate tumor development. However, the molecular mechanisms of lncRNAs in cancer are not fully understood. Our study describes the role of the lncRNA SPRY4 intronic transcript 1 (SPRY4-IT1) in cancer metastasis by mechanisms related to Staufen1 (STAU1)-mediated mRNA decay (SMD). Briefly, we found that, high SPRY4-IT1 expression was associated with aggressiveness and poor outcome in human colorectal, breast and ovarian cancer tissues. In addition, functional assays revealed that SPRY4-IT1 significantly promoted colorectal, breast and ovarian cancer metastasis in vitro and in vivo. Mechanistically, microarray analyses identified several differentially-expressed genes upon SPRY4-IT1 overexpression in HCT 116 colorectal cancer cells. Among them, the 3'-UTR of transcription elongation factor B subunit 1 (TCEB1) mRNA can base-pair with the Alu element in the 3'-UTR of SPRY4-IT1. Moreover, SPRY4-IT1 was found to bind STAU1, promote STAU1 recruitment to the 3'-UTR of TCEB1 mRNA, and affect TCEB1 mRNA stability and expression, resulting in hypoxia-inducible factor 1a (HIF-1a) upregulation, and thereby affecting cancer cell metastasis. In addition, STAU1 depletion abrogated TCEB1 SMD and alleviated the pro-metastatic effect of SPRY4-IT1 overexpression. Significantly, we revealed that SPRY4-IT1 is also transactivated by NF-kB/p65, which activates SPRY4-IT1 to inhibit TCEB1 expression, and subsequently upregulate HIF-1a. In conclusion, our results highlight a novel mechanism of cytoplasmic lncRNA SPRY4-IT1 in which SPRY4-IT1 affecting TCEB1 mRNA stability via STAU1-mediated degradation during cancer metastasis.		Oncogene. 2021 Jul;40(30):4919-4929. doi: 10.1038/s41388-021-01900-8. Epub 2021 Jun 23.
5561	LncRNA	UCA1	miR-27a-5p	UBE2N	Oc Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR 	34160887	The lncRNA 'UCA1' modulates the response to chemotherapy of ovarian cancer through direct binding to miR-27a-5p and control of UBE2N levels.	Ovarian cancer (OC) is the leading cause of death in patients with gynecologic cancers. Due to late diagnosis and resistance to chemotherapy, the 5-year survival rate in patients with OC is below 40%. We observed that UCA1, a lncRNA previously reported to play an oncogenic role in several malignancies, is overexpressed in the chemoresistant OC cell line OAW42-R compared to their chemotherapy-sensitive counterpart OAW42. Additionally, UCA1 overexpression was related to poor prognosis in two independent patient cohorts. Currently, the molecular mechanisms through which UCA1 acts in OC are poorly understood. We demonstrated that downregulation of the short isoform of UCA1 sensitized OC cells to cisplatin and that UCA1 acted as competing endogenous RNA to miR-27a-5p. Upon UCA1 downregulation, miR-27a-5p downregulated its direct target UBE2N leading to the upregulation of BIM, a proapoptotic protein of the Bcl2 family. The upregulation of BIM is the event responsible for the sensitization of OC cells to cisplatin. In order to model response to therapy in patients with OC, we used several patient-derived organoid cultures, a model faithfully mimicking patient's response to therapy. Inhibition of UBE2N sensitized patient-derived organoids to platinum salts. In conclusion, response to treatment in patients with OC is regulated by the UCA1/miR-27a-5p/UBE2N axis, where UBE2N inhibition could potentially represent a novel therapeutic strategy to counter chemoresistance in OC.		Mol Oncol. 2021 Jun 23. doi: 10.1002/1878-0261.13045.
5562	LncRNA	PCGEM1	miR-142-5p	RUNX2	Chondrocytes	Osteoarthritis	Homo sapiens (human)  	Flow cytometry assay;qRT-PCR;Western blot;Flow Cytometry assay;	34160339	Fibroblast-like Synoviocytes-derived Exosomal PCGEM1 Accelerates IL-1b-induced Apoptosis and Cartilage Matrix Degradation by miR-142-5p/RUNX2 in Chondrocytes.	Background: Long non-coding RNA (lncRNA) prostate cancer gene expression marker 1 (PCGEM1) has been revealed to participate in the pathogenesis of osteoarthritis (OA). However, the molecular mechanism of PCGEM1 regulating OA progression has not been fully elucidated.Methods: Fibroblast-like synoviocytes (FLSs) were isolated from synovium tissues of OA patients (OA-FLSs) and trauma donors (Normal-FLSs). The size and morphology of the isolated exosomes were analyzed by transmission electron microscopy and nanoparticle tracking analysis. Protein levels were analyzed by western blotting. Expression levels of PCGEM1, microRNA-142-5p (miR-142-5p), runt-related transcription factor 2 (RUNX2) mRNA, and OA related genes were assessed by qRT-PCR. Cell proliferation, viability, and apoptosis were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide or flow cytometry assays. The relationship between miR-142-5p and PCGEM1 or RUNX2 was verified by dual-luciferase reporter and/or RNA pull down assays.Results: PCGEM1 was overexpressed in OA cartilages and exosomes from OA-FLSs. Exosomal PCGEM1 from OA-FLSs facilitated IL-1b-induced apoptosis and cartilage matrix degradation in chondrocytes. MiR-142-5p was downregulated while RUNX2 was upregulated in OA cartilages. Exosomal PCGEM1 from OA-FLSs regulated RUNX2 expression by sponging miR-142-5p in IL-1b-induced chondrocytes. MiR-142-5p inhibitor offset exosomal PCGEM1 knockdown-mediated effects on the apoptosis and cartilage matrix degradation of IL-1b-induced chondrocytes. RUNX2 overexpression counteracted the suppressive effect of miR-142-5p mimic on apoptosis and cartilage matrix degradation of IL-1b-induced chondrocytes.Conclusion: Exosomal PCGEM1 from OA-FLSs facilitated IL-1b-induced apoptosis and cartilage matrix degradation in chondrocytes by sequestering miR-142-5p and upregulating RUNX2, which offered new insights into the pathogenesis of OA.		Immunol Invest. 2021 Jun 23:1-18. doi: 10.1080/08820139.2021.1936010.
5563	LncRNA	CASC19	miR-152-3p	DDX6	Oa Tissues And Cells	Osteoarthritis	Homo sapiens (human)  	Dual-luciferase reporter assay;Flow cytometry assay;qPCR;RT-qPCR;Flow Cytometry assay;Luciferase reporter assay;Rescue assay;	34158095	LncRNA CASC19 accelerates chondrocytes apoptosis and proinflammatory cytokine production to exacerbate osteoarthritis development through regulating the miR-152-3p/DDX6 axis.	BACKGROUND: Osteoarthritis (OA) is one kind of degenerative joint disease that happens in articular cartilage and other joint tissues. Long non-coding RNAs (lncRNAs) have been reported to serve as pivotal regulators in many diseases, including OA. However, the role and relevant regulatory mechanisms of CASC19 in OA remain unknown. METHODS: The expression levels of CASC19, miR-152-3p, and DDX6 were identified by reverse-transcription polymerase chain reaction (RT-qPCR). Cell viability and apoptosis were determined by Cell Counting Kit-8 (CCK-8) and flow cytometry assays, respectively. The relationship between miR-152-3p and CASC19 or DDX6 was predicted by bioinformatics tools and verified by the dual-luciferase reporter assay. RESULTS: CASC19 was verified to exhibit higher expression in OA tissues and cells. Moreover, inhibition of CASC19 weakened proinflammatory cytokine (IL-6, IL-8, and TNF-a) production and cell apoptosis but facilitated cell viability. Experiments of the ceRNA mechanism elucidated that miR-152-3p was a sponge for CASC19, and miR-152-3p targeted DDX6, suggesting that CASC19 sponged miR-152-3p to release DDX6. Finally, results from rescue assays proved that the impacts of CASC19 silencing on chondrocytes apoptosis and proinflammatory cytokine production could be reversed by DDX6 overexpression. CONCLUSIONS: It was concluded that lncRNA CASC19 accelerated chondrocytes apoptosis and proinflammatory cytokine production to exacerbate osteoarthritis development through regulating the miR-152-3p/DDX6 axis. These findings may offer an effective biological target for OA treatment.		J Orthop Surg Res. 2021 Jun 22;16(1):399. doi: 10.1186/s13018-021-02543-x.
5564	LncRNA	BCRT1	miR-1303	FGF7	Osteosarcoma Specimens And Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	34102610	LncRNA BCRT1 facilitates osteosarcoma progression via regulating miR-1303/FGF7 axis.	Growing studies noted that lncRNA was closely related with the initiation and progression of tumors. However, the role of BCRT1 in the progression of osteosarcoma remains unknown. We noted that BCRT1 is significantly upregulated in osteosarcoma specimens and cells. Elevated expression of BCRT1 promotes cell growth and cell cycle in osteosarcoma cell. Moreover, BCRT1 induces EMT and secretion of inflammatory mediators in osteosarcoma cell. We illustrated that elevated expression of BCRT1 decreases miR-1303 expression in MG-63 cell. The expression of miR-1303 is lower in osteosarcoma specimens than in non-tumor specimens. There is an inverse interrelation between miR-1303 levels and BCRT1 levels in osteosarcoma specimens. Furthermore, we identified FGF7 is one direct target gene of miR-1303 in osteosarcoma cell. Ectopic expression of miR-1303 suppresses FGF7 expression and elevated expression of BCRT1 enhanced FGF7 expression in MG-63 cell. Finally, we illustrated that BCRT1 induces osteosarcoma cell cycle and proliferation and promotes EMT progression and inflammatory mediators secretion via modulating FGF7 expression. Our study suggested that BCRT1 acts as one oncogene in osteosarcoma progression.		Aging (Albany NY). 2021 Jun 8;13(11):15501-15510. doi: 10.18632/aging.203106. Epub 2021 Jun 8.
5565	LncRNA	DUXAP9	NA	sox9	Hepatocellular Carcinoma (Hcc) Tissues And Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	34086387	Long non-coding RNA DUXAP9 promotes hepatocellular carcinoma cell stemness via directly interacting with sox9.	Long non-coding RNA (LncRNA) DUXAP9 expression was recently found to be higher in hepatocellular carcinoma (HCC) tissues and cells, and correlated with a shorter overall survival of HCC patients. However, its roles in HCC progression have never been revealed. Here, the roles of DUXAP9 in HCC cell stemness are explored as cancer stem cells (CSCs) contribute to one of the root of cancer progression. We found that DUXAP9 positively regulated HCC cell stemness, as characterized by the change of sphere-formation ability, ALDH activity and stemness marker expression. Further luciferase reporter, mRNA stability and RNA-RNA in vitro interaction assays indicated that DUXAP9 directly bound to the 3' untranslated region (UTR) of sox9, enhanced the mRNA stability of sox9 and thus increased sox9 expression. Notably, the effects induced by DUXAP9 on HCC cell stemness depended on sox9 expression. Therefore, this work identifies a novel DUXAP9/sox9 axis essential for HCC cell stemness.		Environ Toxicol. 2021 Sep;36(9):1793-1801. doi: 10.1002/tox.23300. Epub 2021 Jun 4.
5566	LncRNA	PCA3	MIR-132-3P	SREBP1	Lncap Cells	Prostate Cancer	Homo sapiens (human)  	qRT-PCR 	34052307	LncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.	Antimony is a common environmental contaminant that causes biological toxicity in exposed populations worldwide. Previous studies have revealed that antimony promotes prostate cancer growth by stabilizing the c-Myc protein and mimicking androgen activity. However, the role of lncRNAs in the regulation of antimony-induced carcinogenesis remains unknown, and the precise mechanisms need to be explored. In the present study, we found that chronic exposure to antimony promoted cell growth and lipid metabolic disequilibrium in prostate cancer. Mechanistically, we identified a long noncoding RNA molecule, PCA3, that was substantially upregulated in LNCaP cells in response to long-term antimony exposure. Functional studies indicated that abnormal PCA3 expression modulated antimony-induced proliferation and cellular triglyceride and cholesterol levels. In addition, PCA3 levels were found to be inversely correlated with MIR-132-3 P levels by acting as a decoy for MIR-132-3P. Besides, SREBP1 directly interacted with MIR-132-3 P to increase cell growth and disrupt lipid metabolism by targeting its 3'UTR regions. Taken together, our results revealed that lncRNA PCA3 promotes antimony-induced lipid metabolic disorder in prostate cancer by targeting MIR-132-3 P/SREBP1 signaling.		Toxicol Lett. 2021 Sep 15;348:50-58. doi: 10.1016/j.toxlet.2021.05.006. Epub 2021 May 28.
5567	LncRNA	LINC00997	miR-574-3p	CUL2	Cc Cells	Cervical Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;	34031216	LINC00997/MicroRNA 574-3p/CUL2 Promotes Cervical Cancer Development via Mitogen-Activated Protein Kinase Signaling.	Cervical cancer (CC) is a common gynecological malignancy with high morbidity and mortality. Mounting evidence has highlighted that long noncoding RNAs are essential regulators in cancer development. Long intergenic non-protein-coding RNA 997 (LINC00997) was identified for study due to its high expression in CC tissues. The aim of the study was to investigate the function and mechanism of LINC00997 in CC. Reverse transcription-quantitative PCR (RT-qPCR) revealed that LINC00997 RNA expression was also increased in CC cells and LINC00997 copy number was upregulated in CC tissues. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT), colony formation, and Transwell assays as well as transmission electron microscopy observation exhibited that LINC00997 depletion inhibited CC cell proliferation, migration, invasion, and autophagy. The relationship between LINC00997 and its downstream genes was confirmed by RNA pulldown, luciferase reporter, and RNA-binding protein immunoprecipitation assays. Mechanistically, LINC00997 upregulated the expression of cullin 2 (CUL2) by interacting with microRNA 574-3p (miR-574-3p). Moreover, Western blot analysis was employed to detect the protein levels of mitogen-activated protein kinase (MAPK) pathway-associated factors in CC cells. LINC00997 activated the MAPK signaling by increasing CUL2 expression, thus promoting malignant phenotypes of CC cells. In conclusion, the LINC00997/miR-574-3p/CUL2 axis contributes to CC cell proliferation, migration, invasion, and autophagy via the activation of MAPK signaling.		Mol Cell Biol. 2021 Jul 23;41(8):e0005921. doi: 10.1128/MCB.00059-21. Epub 2021 Jul 23.
5568	LncRNA	TUG1	NA	Runx2	Human Umbilical Vein Endothelial Cells	Atherosclerosis	Homo sapiens (human)	microarray;	33971184	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis.	The role of vascular endothelial cell injury in the course of atherosclerosis (AS) has attracted increasing attention. Long non-coding RNAs (LncRNAs) are demonstrated to be the biomarker for the diagnosis of AS. This study investigated the mechanism of lncRNA taurine upregulated gene 1 (TUG1) in AS. Microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples. TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs). Oxidized low density lipoprotein (ox-LDL)-treated HUVECs were then transfected with sh-TUG1. TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs. TUG1 bound to Runt-related transcription factor 2 (Runx2). Runx2 silencing promoted proliferation and migration of HUVECs. The downstream genes of Runx2 were predicted by hTFtarget database. The binding site of Runx2 and Aminopeptidase N (ANPEP) was determined. Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration. TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration. A mouse model of AS was established. The area of atherosclerotic lesions of mouse aorta was detected, and vascular re-endothelialization was evaluated. TUG1 silencing promoted vascular injury repairing and inhibited AS in vivo. In conclusion, TUG1 silencing enhanced proliferation and migration of ox-LDL-treated HUVECs and promoted vascular injury repairing in vivo via the Runx2/ANPEP axis.		Int J Cardiol. 2021 Sep 1;338:204-214. doi: 10.1016/j.ijcard.2021.05.014. Epub 2021 May 8.
5569	LncRNA	TUG1	NA	ANPEP	Human Umbilical Vein Endothelial Cells	Atherosclerosis	Homo sapiens (human)	microarray;	33971184	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis.	The role of vascular endothelial cell injury in the course of atherosclerosis (AS) has attracted increasing attention. Long non-coding RNAs (LncRNAs) are demonstrated to be the biomarker for the diagnosis of AS. This study investigated the mechanism of lncRNA taurine upregulated gene 1 (TUG1) in AS. Microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples. TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs). Oxidized low density lipoprotein (ox-LDL)-treated HUVECs were then transfected with sh-TUG1. TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs. TUG1 bound to Runt-related transcription factor 2 (Runx2). Runx2 silencing promoted proliferation and migration of HUVECs. The downstream genes of Runx2 were predicted by hTFtarget database. The binding site of Runx2 and Aminopeptidase N (ANPEP) was determined. Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration. TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration. A mouse model of AS was established. The area of atherosclerotic lesions of mouse aorta was detected, and vascular re-endothelialization was evaluated. TUG1 silencing promoted vascular injury repairing and inhibited AS in vivo. In conclusion, TUG1 silencing enhanced proliferation and migration of ox-LDL-treated HUVECs and promoted vascular injury repairing in vivo via the Runx2/ANPEP axis.		Int J Cardiol. 2021 Sep 1;338:204-214. doi: 10.1016/j.ijcard.2021.05.014. Epub 2021 May 8.
5570	LncRNA	TUG1	NA	Runx2	Human Umbilical Vein Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;	33971184	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis.	The role of vascular endothelial cell injury in the course of atherosclerosis (AS) has attracted increasing attention. Long non-coding RNAs (LncRNAs) are demonstrated to be the biomarker for the diagnosis of AS. This study investigated the mechanism of lncRNA taurine upregulated gene 1 (TUG1) in AS. Microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples. TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs). Oxidized low density lipoprotein (ox-LDL)-treated HUVECs were then transfected with sh-TUG1. TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs. TUG1 bound to Runt-related transcription factor 2 (Runx2). Runx2 silencing promoted proliferation and migration of HUVECs. The downstream genes of Runx2 were predicted by hTFtarget database. The binding site of Runx2 and Aminopeptidase N (ANPEP) was determined. Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration. TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration. A mouse model of AS was established. The area of atherosclerotic lesions of mouse aorta was detected, and vascular re-endothelialization was evaluated. TUG1 silencing promoted vascular injury repairing and inhibited AS in vivo. In conclusion, TUG1 silencing enhanced proliferation and migration of ox-LDL-treated HUVECs and promoted vascular injury repairing in vivo via the Runx2/ANPEP axis.		Int J Cardiol. 2021 Sep 1;338:204-214. doi: 10.1016/j.ijcard.2021.05.014. Epub 2021 May 8.
5571	LncRNA	TUG1	NA	ANPEP	Human Umbilical Vein Endothelial Cells	Atherosclerosis	Mus musculus (mouse)	microarray;	33971184	LncRNA TUG1 silencing enhances proliferation and migration of ox-LDL-treated human umbilical vein endothelial cells and promotes atherosclerotic vascular injury repairing via the Runx2/ANPEP axis.	The role of vascular endothelial cell injury in the course of atherosclerosis (AS) has attracted increasing attention. Long non-coding RNAs (LncRNAs) are demonstrated to be the biomarker for the diagnosis of AS. This study investigated the mechanism of lncRNA taurine upregulated gene 1 (TUG1) in AS. Microarray data of AS obtained from GEO database showed that lncRNA TUG1 was differentially expressed in AS samples. TUG1 expression was upregulated in ox-LDL-treated human umbilical vein endothelial cells (HUVECs). Oxidized low density lipoprotein (ox-LDL)-treated HUVECs were then transfected with sh-TUG1. TUG1 silencing promoted proliferation and migration of ox-LDL-treated HUVECs. TUG1 bound to Runt-related transcription factor 2 (Runx2). Runx2 silencing promoted proliferation and migration of HUVECs. The downstream genes of Runx2 were predicted by hTFtarget database. The binding site of Runx2 and Aminopeptidase N (ANPEP) was determined. Runx2 silencing reversed the repression effect of overexpressing ANPEP on cell proliferation and migration. TUG1 silencing inhibited ANPEP expression via Runx2 to promote HUVEC proliferation and migration. A mouse model of AS was established. The area of atherosclerotic lesions of mouse aorta was detected, and vascular re-endothelialization was evaluated. TUG1 silencing promoted vascular injury repairing and inhibited AS in vivo. In conclusion, TUG1 silencing enhanced proliferation and migration of ox-LDL-treated HUVECs and promoted vascular injury repairing in vivo via the Runx2/ANPEP axis.		Int J Cardiol. 2021 Sep 1;338:204-214. doi: 10.1016/j.ijcard.2021.05.014. Epub 2021 May 8.
5572	LncRNA	AFAP1-AS1	miR-424-5p	STAT3	Endometrial Stromal Cells	Endometriosis	Homo sapiens (human)  	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33949053	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-b/Smad signaling via miR-424-5p.	AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-b1 (TGF-b1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-b/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.		J Obstet Gynaecol Res. 2021 Jul;47(7):2394-2405. doi: 10.1111/jog.14801. Epub 2021 May 4.
5573	LncRNA	AFAP1-AS1	miR-424-5p	TGF-b1	Endometrial Stromal Cells	Endometriosis	Homo sapiens (human)  	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33949053	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-b/Smad signaling via miR-424-5p.	AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-b1 (TGF-b1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-b/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.		J Obstet Gynaecol Res. 2021 Jul;47(7):2394-2405. doi: 10.1111/jog.14801. Epub 2021 May 4.
5574	LncRNA	AFAP1-AS1	miR-424-5p	Smad2	Endometrial Stromal Cells	Endometriosis	Homo sapiens (human)  	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase report assay;MTT assay;	33949053	LncRNA AFAP1-AS1 regulates proliferation and apoptosis of endometriosis through activating STAT3/TGF-b/Smad signaling via miR-424-5p.	AIM: Endometriosis is a common gynecological disorder characterized by chronic pelvic pain and infertility, which negatively affects women's health worldwide. AFAP1-AS1 has been implicated in endometriosis lesions recently, but its mechanism of endometriosis progression remains unclear. METHODS: Endometrial stromal cells (ESCs) were used to identify the role of AFAP1-AS1 in endometriosis. The migratory capability was determined by transwell. Gene and protein expressions were identified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell viability and apoptosis were detected by MTT assays and flow cytometry, respectively. Luciferase report assays were used to identify the interaction of AFAP1-AS1, miR-424-5p and signal transducer and activator of transcription 3 (STAT3). RESULTS: AFAP1-AS1 knockdown or miR-424-5p overexpression inhibited proliferation and migration, and promoted apoptosis in ESCs. In addition, knockdown of AFAP1-AS1 repressed the expression of ki-67 and Bcl-2, and promoted the levels of cleaved caspase-3 and Bax. Furthermore, knockdown of AFAP1-AS1 inhibited the conversion of E-cadherin to N-cadherin and the expression of Snail. Moreover, AFAP1-AS1 activated the STAT3/transforming growth factor-b1 (TGF-b1)/Smad2 axis via directly targeting miR-424-5p. The regulatory effect of AFAP1-AS1 silencing in ESC migration, proliferation, and apoptosis was reversed by miR-424-5p inhibition or STAT3 overexpression. CONCLUSIONS: AFAP1-AS1 silencing could inhibit cell proliferation and promote apoptosis by regulating STAT3/TGF-b/Smad signaling pathway via targeting miR-424-5p in ESCs. AFAP1-AS1 may be a potential therapeutic target of controlling the progression of endometriosis.		J Obstet Gynaecol Res. 2021 Jul;47(7):2394-2405. doi: 10.1111/jog.14801. Epub 2021 May 4.
5575	LncRNA	XIST	miR-424-5p	OGT	Liver Cancer Tissues And Cells	Liver Cancer	Mus musculus (mouse)	RIP assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	33909326	The crosstalk network of XIST/miR-424-5p/OGT mediates RAF1 glycosylation and participates in the progression of liver cancer.	BACKGROUND: Liver cancer is a major public health concern, but the mechanistic actions of biomarkers contributing to liver cancer remain to be determined. In this study, we aimed to investigate the regulatory cascade of microRNA-424-5p (miR-424-5p), X-inactive-specific transcript (XIST) and O-GlcNAc transferase (OGT) in liver cancer. METHODS: Differentially expressed miRNAs and target genes related to liver cancer were predicted by bioinformatics analyses, and their expression was determined in liver tissues of patients with liver cancer and liver cancer cells. The RNA immunoprecipitation (RIP), RNA pull-down and dual luciferase reporter assay were used to examine the binding affinity among XIST and miR-424-5p and OGT. Then, gain- and loss-of-function assays were conducted to evaluate the effects of the XIST/miR-424-5p/OGT axis on malignant phenotypes. A nude mouse model of liver cancer was further established for in vivo substantiation. RESULTS: XIST and OGT were up-regulated in liver cancer tissues and cells, responsible for poor prognosis in patients with liver cancer, while miR-424-5p was down-regulated. XIST competitively bound to miR-424-5p to increase OGT expression. XIST silencing inhibited malignant phenotypes of liver cancer cells, while miR-424-5p down-regulation negated its effect. miR-424-5p suppressed RAF1 glycosylation by negatively regulating OGT expression and promoted its ubiquitination/degradation. Furthermore, XIST knockdown inhibited tumour growth and metastasis in nude mice, while ectopic OGT reversed its effect. CONCLUSION: These results reveal a novel mechanism by which the interaction of XIST/miR-424-5p/OGT participates in the malignancy and metastasis of liver cancer.		Liver Int. 2021 Aug;41(8):1933-1944. doi: 10.1111/liv.14904. Epub 2021 May 28.
5576	LncRNA	NEAT1	miR-139	PUMA	Peripheral Blood Mononuclear Cells	Acute Liver Failure	Mus musculus (mouse)	luciferase assay;	33901015	Silencing long noncoding RNA NEAT1 alleviates acute liver failure via the EZH2-mediated microRNA-139/PUMA axis.	This study aimed to investigate the role of long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) in the development of ALF. We collected blood samples from patients with acute liver failure (ALF) and established an ALF mouse model induced by D-galactosamine/Lipopolysaccharide (D-GalN/LPS) for in vivo studies. Peripheral blood mononuclear cells (PMBCs) induced with LPS were isolated for in vitro experiments. Survival tests, histological analysis, and biochemical indicator assays were conducted. Luciferase assay was performed to determine the binding affinity between microRNA-139 (miR-139) and p53-upregulated modulator of apoptosis (PUMA). Expression of lncRNA NEAT1, enhancer of zeste homolog 2 (EZH2), and PUMA was upregulated, while the expression of miR-139 was downregulated in clinical samples and D-GalN/LPS induced ALF mouse model. LncRNA NEAT1 promoted the enrichment of H3K27me3 on the promoter region of miR-139 via EZH2, which led to suppression of miR-139. The inhibition of miR-139 resulted in the upregulation of its downstream target PUMA. The NEAT1/miR-139/PUMA pathway upregulated the production of pro-inflammatory cytokines, tumor necrosis factor alpha, interleukin (IL)-6, and IL-1b, thereby mediating the progression of ALF. In conclusion, silencing lncRNA NEAT1 upregulated the expression of miR-139 through EZH2, leading to the downregulation of PUMA, which alleviated the development of ALF.		Aging (Albany NY). 2021 Apr 26;13(9):12537-12551. doi: 10.18632/aging.202927. Epub 2021 Apr 26.
5577	LncRNA	LINC00665	miR-126-5p	PAK2	Crc Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	33878735	Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p.	Long intergenic noncoding RNAs (lincRNAs) regulate a series of biological processes, and their anomalous expression plays critical roles in the progression of multiple malignancies, including colorectal cancer (CRC). Although many studies have reported the oncogenic function of LINC00665 in multiple cancers, few studies have explored its role in CRC. The aim of this study was to assess the effect of LINC00665 on the malignant behaviors of CRC and explore the underlying regulatory mechanism of LINC00665. LINC00665 was significantly upregulated in CRC. A loss-of-function assay revealed that LINC00665 downregulation inhibited the proliferation and promoted the apoptosis of CRC cells, which was mediated by cyclin D1, CDK4, caspase-9 and caspase-3. Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3. These findings demonstrate that LINC00665 might play an important pro-proliferative and antiapoptotic role in CRC and might be a potential biomarker and a new therapeutic target for CRC.		Aging (Albany NY). 2021 Apr 20;13(10):13571-13584. doi: 10.18632/aging.202874. Epub 2021 Apr 20.
5578	LncRNA	LINC00665	miR-126-5p	FZD3	Crc Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	33878735	Long intergenic noncoding RNA 00665 promotes proliferation and inhibits apoptosis in colorectal cancer by regulating miR-126-5p.	Long intergenic noncoding RNAs (lincRNAs) regulate a series of biological processes, and their anomalous expression plays critical roles in the progression of multiple malignancies, including colorectal cancer (CRC). Although many studies have reported the oncogenic function of LINC00665 in multiple cancers, few studies have explored its role in CRC. The aim of this study was to assess the effect of LINC00665 on the malignant behaviors of CRC and explore the underlying regulatory mechanism of LINC00665. LINC00665 was significantly upregulated in CRC. A loss-of-function assay revealed that LINC00665 downregulation inhibited the proliferation and promoted the apoptosis of CRC cells, which was mediated by cyclin D1, CDK4, caspase-9 and caspase-3. Through mechanistic exploration, we found that miR-126-5p directly bound to LINC00665. Moreover, LINC00665 and miR-126-5p both regulated PAK2 and FZD3 expression. Mechanistically, miR-126-5p was predicted and further verified as a target of both PAK2 and FZD3. These findings demonstrate that LINC00665 might play an important pro-proliferative and antiapoptotic role in CRC and might be a potential biomarker and a new therapeutic target for CRC.		Aging (Albany NY). 2021 Apr 20;13(10):13571-13584. doi: 10.18632/aging.202874. Epub 2021 Apr 20.
5579	LncRNA	lnc-HZ02	miR-hz02	HuR	Bpde-Treated Trophoblast Cells	Miscarriage	Homo sapiens (human)	qRT-PCR 	33851497	Upregulated lnc-HZ02 and miR-hz02 inhibited migration and invasion by downregulating the FAK/SRC/PI3K/AKT pathway in BPDE-treated trophoblast cells.	BPDE (benzo(a)pyren-7,8-dihydrodiol-9,10-epoxide), a metabolite of environmental carcinogenic BaP, weakens the migration and invasion of human villous trophoblast cells and may further induce miscarriage. However, the underlying mechanisms remain largely unknown. In this study, we identified that in trophoblast Swan 71 and HTR-8/SVneo cells, miR-hz02 upregulates the level of lnc-HZ02, which inhibits the expression of an RNA-binding protein HuR. HuR could interact with FAK mRNA and promote its mRNA stability, thus upregulating the FAK level and the FAK/SRC/PI3K/AKT pathway, and finally maintaining the normal migration and invasion of trophoblast cells. If trophoblast cells are exposed to BPDE, both miR-hz02 and lnc-HZ02 are upregulated, which reduce the level of HuR, weaken the interactions of HuR with FAK mRNA, downregulate FAK level and the FAK/SRC/PI3K/AKT pathway, and finally inhibit cell migration and invasion. This study provides a novel scientific understanding of the dysfunctions of human trophoblast cells.		J Biochem Mol Toxicol. 2021 Jun;35(6):1-13. doi: 10.1002/jbt.22757. Epub 2021 Apr 14.
5580	LncRNA	NEAT1	miR-582-5p	HIF-1a	Lung Bronchial Epithelial Cells	Lung Carcinogenesis	Homo sapiens (human)	qRT-PCR 	33829382	LncRNA NEAT1 contributes to the acquisition of a tumor like-phenotype induced by PM 2.5 in lung bronchial epithelial cells via HIF-1a activation.	The hazards of particulate matter (PM2.5) on human respiratory health have been previously reported. However, the molecular mechanisms underlying PM2.5-induced lung carcinogenesis have rarely been studied. In the present study, we explored the effects of PM2.5 on the epithelial-mesenchymal transition (EMT) and acquisition of cancer stem cell (CSC)-like properties in lung bronchial epithelial cells. We found that exposure of PM2.5 enhanced lung bronchial epithelial cell proliferation and EMT. In addition, the expression level of CSC-like biomarkers, CD133 and CD44, was significantly elevated by PM2.5 in vitro. Nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported to participate in lung cancer. Loss of NEAT1 represses the malignant transformation of BEAS-2B and HBE cells induced by PM2.5. NEAT1 interacts with microRNA (miR)-582-5p, and miR-582-5p reverses the pro-tumor effects of NEAT1 overexpression. Hypoxia-inducible factor (HIF)-1a is an important transcription factor in the pathological responses to hypoxia. HIF-1a was a predicted target for miR-582-5p, and a direct correlation between them was identified. Inhibitors of miR-582-5p rescued HIF-1a expression, which was attenuated by a lack of NEAT1. In conclusion, PM2.5 increased NEAT1 expression, which, by binding with miR-582-5p, released HIF-1a and promoted EMT and the acquisition of CSC-like characteristics.		Environ Sci Pollut Res Int. 2021 Aug;28(32):43382-43393. doi: 10.1007/s11356-021-13735-7. Epub 2021 Apr 8.
5581	LncRNA	OGRU	miR-320	USP14	Hg-Stimulated Müller Cells	Diabetic Retinopathy	Homo sapiens (human)  	qRT-PCR 	33762162	Suppressing long noncoding RNA OGRU ameliorates diabetic retinopathy by inhibition of oxidative stress and inflammation via miR-320/USP14 axis.	Long noncoding RNAs (lncRNAs) are important regulators in various diseases including diabetic retinopathy (DR). In this study, DR patients exhibited significantly increased expression of serum LncRNA-OGRU compared with normal individuals. Streptozotocin (STZ)-challenged rats with DR also had higher OGRU expression in retinas than that of the control group, which was confirmed in Müller cells upon high glucose (HG) stimulation. OGRU knockdown remarkably decreased vascular endothelial growth factor (VEGF) and transforming growth factor-b1 (TGF-b1) expression in HG-incubated Müller cells. HG-induced inflammatory response and oxidative stress in vitro were markedly mitigated by OGRU knockdown through restraining IkBɑ/nuclear factor kappa beta (NF-kB) and improving nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways, respectively. Further studies indicated that OGRU suppression greatly restored miR-320 expression, and a negative correlation between them was detected in DR patients. We also found that miR-320 over-expression considerably restrained TGF-b1 signaling, and hindered inflammation and reactive oxygen species (ROS) production in HG-stimulated Müller cells. Additionally, OGRU knockdown or miR-320 over-expression could dramatically down-regulate ubiquitin-specific peptidase 14 (USP14) expression levels in HG-incubated Müller cells, and miR-320 could directly target USP14. Notably, OGRU/miR-320 axis-mediated TGF-b1 signaling, inflammation and ROS were largely dependent on USP14. Intriguingly, our results showed that USP14 directly interacted with transforming growth factor-beta type 1 receptor (TbR1), and impeded TbR1 ubiquitination and degradation. Furthermore, USP14 could also facilitate IkBɑ deubiquitination and degradation, exacerbating IkBɑ phosphorylation and NF-kB activation. Finally, our in vivo studies confirmed that OGRU knockdown considerably ameliorated DR progression in STZ-challenged rats through mediating the mechanisms observed in vitro. Collectively, these findings implicated that LncRNA-OGRU mediated DR progression through competing for miR-320 to regulate USP14 expression, and thus LncRNA-OGRU/miR-320/USP14 axis may be considered as a therapeutic target for DR treatment.		Free Radic Biol Med. 2021 Jun;169:361-381. doi: 10.1016/j.freeradbiomed.2021.03.016. Epub 2021 Mar 21.
5582	LncRNA	MEG8	miR-378d	SOBP	Oc Patients	Ovarian Cancer	Homo sapiens (human)	qRT-PCR 	33742531	Identification of MEG8/miR-378d/SOBP axis as a novel regulatory network and associated with immune infiltrates in ovarian carcinoma by integrated bioinformatics analysis.	BACKGROUND: To investigate the potential molecular mechanism of ovarian cancer (OC) evolution and immunological correlation using the integrated bioinformatics analysis. METHODS: Data from the Gene Expression Omnibus was used to gain differentially expressed genes (DEGs). Gene Ontology and Kyoto Encyclopedia of Gene and Genome pathway analysis were completed by utilizing the Database for Annotation, Visualization, and Integrated Discovery. After multiple validations via The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) projects, the Human Protein Atlas, Kaplan-Meier (KM) plotter, and immune logical relationships of the key gene SOBP were evaluated based on Tumor Immune Estimation Resource, and Gene Set Enrichment Analysis (GSEA) software. Finally, the lncRNAs-miRNAs-mRNAs subnetwork was predicted by starBase, TargetScan, miRBD, and LncBase, individually. Correlation of expression and prognosis for mRNAs, miRNAs, and lncRNAs were confirmed by TCGA, Gene Expression Profiling Interactive Analysis 2 (GEPIA 2), starBase, and KM. RESULTS: A total of 192 shared DEGs were discovered from the four data sets, including 125 upregulated and 67 downregulated genes. Functional enrichment analysis presented that they were mainly enriched in cartilage development, pathway in PI3 K-Akt signaling pathway. Lower expression of SOBP was the independent prognostic factor for inferior prognosis in OC patients. The downregulation of SOBP enhanced the infiltration levels of B cells, CD8+ T cells, Macrophage, Neutrophil, and Dendritic cells. GSEA also disclosed low SOBP showed a significantly associated with the activation of various immune-related pathways. Finally, we first reported that the MEG8/miR-378d/SOBP axis was linked to the development and prognosis of OC through regulating the cytokines pathway. CONCLUSIONS: Our study establishes a novel MEG8/miR-378d/SOBP axis in the development and prognosis of OC, and the triple subnetwork probably affects the progression of the OC by regulating the cytokines pathway.		Cancer Med. 2021 Apr;10(8):2924-2939. doi: 10.1002/cam4.3854. Epub 2021 Mar 19.
5583	LncRNA	RNCR2	miR-495-3p	HK2	Melanoma Tissue Specimens And Cell Lines	Melanoma	Homo sapiens (human)  	CCK-8 assay;qPCR;Western blot;Luciferase reporter assay;	33724862	lncRNA RNCR2 facilitates cell proliferation and epithelial-mesenchymal transition in melanoma through HK2-mediated Warburg effect via targeting miR-495-3p.	Melanoma is a potentially lethal skin cancer with a high death rate. LncRNAs were reported to be implicated in melanoma progression. However, the function and mechanisms of lncRNA RNCR2 in melanoma are little known. In this study, RNCR2, miR-495-3p, and HK2 expression levels were measured in melanoma tissue specimens and cell lines by qPCR. EdU and CCK-8 assays were performed to assess cell proliferation. Enolase activity, ATP level, lactate production, and glucose consumption measurement kits were used to evaluate the glycolysis of tumor cells. Immunofluorescence and western blot were used to detect the expression of epithelial-mesenchymal transition (EMT) and glycolysis-related proteins. Luciferase reporter assay was applied to confirm the target relationships. The role of RNCR2 in tumorigenesis was examined using murine xenograft models. LncRNA RNCR2 was upregulated in melanoma tissues and cell lines. Cell function detection showed that RNCR2 knockdown remarkably inhibited cell proliferation and EMT via glycolysis, as well as reduced the growth of a tumor. Mechanically, RNCR2 was confirmed to bind to miR-495-3p and positively regulated HK2 expression level, and the miR-495-3p level was negatively correlated with RNCR2 or HK2 in melanoma tissues. Further, miR-495-3p downregulation or HK2 upregulation partially reversed RNCR2 knockdown-induced inhibition of melanoma cell growth, EMT, and glycolysis. Collectively, RNCR2 might be an oncogenic lncRNA to promote tumor cell glycolysis and accelerate tumor growth via the miR-495-3p/HK2 axis, providing a promising treatment target for melanoma.		Neoplasma. 2021 Jul;68(4):692-701. doi: 10.4149/neo_2021_201120N1255. Epub 2021 Mar 17.
5584	LncRNA	NKILA	mir-195	NLRX1	Neurons	Traumatic Brain Injury	Homo sapiens (human)	RACE;	33686956	Long noncoding RNA NKILA transferred by astrocyte-derived extracellular vesicles protects against neuronal injury by upregulating NLRX1 through binding to mir-195 in traumatic brain injury.	The study aims to investigate the effects of long noncoding RNA (lncRNA) transmitted nuclear factor-kB interacting lncRNA (NKILA)-containing astrocyte-derived small extracellular vesicles (EVs) on traumatic brain injury (TBI). TBI was modeled in vitro by exposing human neurons to mechanical injury and in vivo by controlled cortical impact in a mouse model. The gain- and loss-function approaches were conducted in injured neurons to explore the role of NKILA, microRNA-195 (miR-195) and nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) in neuronal injury. EVs extracted from NKILA-overexpressing astrocytes were used to treat injured neurons. It was revealed that NKILA was downregulated in injured neurons. Astrocyte co-culture participated in the upregulation of NKILA in injured neurons. Additionally, NKILA could competitively bind to miR-195 that directly targeted NLRX1. Next, the upregulation of NLRX1 or NKILA relived neuronal injury by promoting neuronal proliferation but inhibiting apoptosis. Astrocyte-derived EVs transferred NKILA into neurons, which led to the downregulation of miR-195, upregulation of NLRX1, increased cell proliferation, and decreased cell apoptosis. The in vivo experiments validated that NKILA-containing EVs promoted brain recovery following TBI. Collectively, astrocyte-derived EVs carrying NKILA was found to alleviate neuronal injury in TBI by competitively binding to miR-195 and upregulating NLRX1.		Aging (Albany NY). 2021 Mar 3;13(6):8127-8145. doi: 10.18632/aging.202618. Epub 2021 Mar 3.
5585	LncRNA	NKILA	mir-195	NLRX1	Neurons	Traumatic Brain Injury	Mus musculus (mouse)	RACE;	33686956	Long noncoding RNA NKILA transferred by astrocyte-derived extracellular vesicles protects against neuronal injury by upregulating NLRX1 through binding to mir-195 in traumatic brain injury.	The study aims to investigate the effects of long noncoding RNA (lncRNA) transmitted nuclear factor-kB interacting lncRNA (NKILA)-containing astrocyte-derived small extracellular vesicles (EVs) on traumatic brain injury (TBI). TBI was modeled in vitro by exposing human neurons to mechanical injury and in vivo by controlled cortical impact in a mouse model. The gain- and loss-function approaches were conducted in injured neurons to explore the role of NKILA, microRNA-195 (miR-195) and nucleotide-binding leucine-rich repeat containing family member X1 (NLRX1) in neuronal injury. EVs extracted from NKILA-overexpressing astrocytes were used to treat injured neurons. It was revealed that NKILA was downregulated in injured neurons. Astrocyte co-culture participated in the upregulation of NKILA in injured neurons. Additionally, NKILA could competitively bind to miR-195 that directly targeted NLRX1. Next, the upregulation of NLRX1 or NKILA relived neuronal injury by promoting neuronal proliferation but inhibiting apoptosis. Astrocyte-derived EVs transferred NKILA into neurons, which led to the downregulation of miR-195, upregulation of NLRX1, increased cell proliferation, and decreased cell apoptosis. The in vivo experiments validated that NKILA-containing EVs promoted brain recovery following TBI. Collectively, astrocyte-derived EVs carrying NKILA was found to alleviate neuronal injury in TBI by competitively binding to miR-195 and upregulating NLRX1.		Aging (Albany NY). 2021 Mar 3;13(6):8127-8145. doi: 10.18632/aging.202618. Epub 2021 Mar 3.
5586	LncRNA	ZFAS1	miR-302d-3p	SMAD2	Oa Tissues	Osteoarthritis	Homo sapiens (human)  	qRT-PCR 	33686420	Long noncoding RNA ZFAS1 suppresses chondrocytes apoptosis via miR-302d-3p/SMAD2 in osteoarthritis.	Osteoarthritis (OA) seriously affects people's quality of life due to joint pain, stiffness, disability, and dyskinesia worldwide. Long noncoding RNA zinc finger antisense 1 (ZFAS1) is downregulated and tightly associated with proliferation, migration, apoptosis, and matrix synthesis of chondrocyte in OA. However, the molecular mechanisms of ZFAS1 in OA remain unknown. The expression correlation between ZFAS1, miR-302d-3p, and SMAD2 in OA tissues was analyzed by Pearson correlation analysis. ZFAS1 was a lower expression, and expedited proliferation and repressed apoptosis of chondrocytes. MiR-302d-3p was a direct target of ZFAS1. MiR-302d-3p hindered proliferation and facilitated apoptosis of chondrocytes. MiR-302d-3p partially reversed the effect of ZFAS1 on proliferation and apoptosis of chondrocytes. SMAD2 was positively regulated by the ZFAS1/miR-302d-3p. MiR-302d-3p-mediated proliferation and apoptosis were partly abrogated by targeting SMAD2. ZFAS1 promoted chondrocytes proliferation and repressed apoptosis possibly by regulating miR-302d-3p/SMAD2 axis, providing a potential target for OA treatment.		Biosci Biotechnol Biochem. 2021 Mar 24;85(4):842-850. doi: 10.1093/bbb/zbab008.
5587	LncRNA	SNHG14	miR-152-3p	NA	Dlbcl Cell Lines (Oci-Ly7 And Oci-Ly3) And Specimens	Diffuse Large-B-Cell Lymphoma	Homo sapiens (human)  	qRT-PCR 	33682607	lncRNA SNHG14 promotes oncogenesis and immune evasion in diffuse large-B-cell lymphoma by sequestering miR-152-3p.	This study aimed to explore the role of small nucleolar RNA host gene 14 (SNHG14) in the pathogenesis of diffuse large-B-cell lymphoma (DLBCL). DLBCL cell lines (OCI-Ly7 and OCI-Ly3) and specimens from patients were collected to evaluate the roles of SNHG14 in DLBCL pathogenesis. The results showed that SNHG14 expression increased and miR-152-3p expression decreased in DLBCL tissues and cell lines, indicating a negative correlation between miR-152-3p and SNHG14 expression. Moreover, SNHG14 was found to promote DLBCL growth, migration, and EMT-like processes in vitro, and directly inhibits miR-152-3p gene expression via sequestration of the miR-152-3p transcripts in DLBCL. Additionally, SNHG14/miR-152-3p inhibits apoptosis and promotes cell proliferation on cytotoxic T lymphocytes (CTLs) in DLBCL via the PD-1/PD-L1 checkpoint. Furthermore, both the immune escape and progression of DLBCL are advanced by SNHG14 expression via its interactions with miR-152-3p. Collective, this suggests that SNHG14 is a potential diagnostic, prognostic, and therapeutic target for DLBCL.		Leuk Lymphoma. 2021 Jul;62(7):1574-1584. doi: 10.1080/10428194.2021.1876866. Epub 2021 Mar 8.
5588	LncRNA	LINC01224	MiR-193a-5p	CDK8	Gc Cells	Gastric Cancer	Homo sapiens (human)  	MTT assay;qPCR;RT-qPCR;Western blot;Flow Cytometry assay;luciferase assay;MTT assay;	33655711	LINC01224 accelerates malignant transformation via MiR-193a-5p/CDK8 axis in gastric cancer.	BACKGROUND: Gastric cancer (GC) is a malignant tumor with a significantly high mortality rate, yet, its pathogenesis is not fully understood. Bioinformatics predicted that LINC01224 is highly expressed in stomach adenocarcinoma (STAD), and showed that LINC01224 adsorbed miR-193a-5p to target CDK8. Therefore, this study intended to verify the effect of the LINC01224/miR-193a-5p/CDK8 axis on the biological behavior of gastric cancer. METHODS: Expressions of LINC01224, miR-193a-5p, CDK8, apoptosis-, and EMT-related genes were analyzed using the GEPIA website, RT-qPCR, in situ hybridization, and Western blot as needed. Bioinformatics and dual luciferase assay were used to evaluate the relationship between LINC01224, miR-193a-5p, and CDK8. Functional experiments and rescue experiments (MTT assay, flow cytometry, wound healing assay, and Transwell) were conducted to detect the effects of the above genes on the biological characteristics of GC cells. Tumorigenesis assay was used to verify the results of in vitro experiments. RESULTS: LINC01224 adsorbed miR-193a-5p to target and upregulate CDK8. The expressions of LINC01224 and CDK8 were increased, while the expression of miR-193a-5p was decreased in GC. Overexpressed LINC01224 promoted cell viability, migration and invasion, accelerated tumor formation, attenuated apoptosis, inhibited the expressions of apoptosis-related proteins, and promoted the expressions of EMT-related proteins, whereas silenced LINC01224 led to the opposite effect. MiR-193a-5p inhibitor partially offset the effect of silenced LINC01224; interestingly, siCDK8 significantly reversed the effect of miR-193a-5p inhibitor on GC cells. CONCLUSION: LINC01224 affects the biological behavior of gastric cancer by mediating miR-193a-5p to regulate CDK8.		Cancer Med. 2021 Feb;10(4):1377-1393. doi: 10.1002/cam4.3726.
5589	LncRNA	PVT1	miR-146a	COL2A1	Cartilage Tissue	Osteoarthritis	Mus musculus (mouse)	Western blot;Luciferase reporter assay;	33569722	LncPVT1 promotes cartilage degradation in diabetic OA mice by downregulating miR-146a and activating TGF-b/SMAD4 signaling.	INTRODUCTION: To investigate the role of LncRNA PVT1 (plasmacytoma variant translocation 1) in hyperglycemia-triggered cartilage damage using the diabetic osteoarthritis (OA) mice model. MATERIALS AND METHODS: Streptozotocin (STZ) was used to induce mouse diabetes. Knee OA model was induced through transection of anterior cruciate ligament (ACLT). Severity of arthritis was assessed histologically by Safranin O-Fast Green Staining using Mankin Scores. LncRNA PVT1 and miR-146a were detected by real-time polymerase chain reaction (PCR) in cartilage tissue. Moreover, the interaction among PVT1, miR-146a, and SMAD4 was examined by luciferase reporter assays. Mice were injected intra-articularly with ad-siRNA-PVT1 and ad-siRNA scramble control. Articular concentrations of TNF-a, IL-1, IL-6 and TGF-b1 were determined using enzyme-linked immunosorbent assay. Levels of type II Collagen (COL2A1), TGF-b1, p-SMAD2, SMAD2, p-SMAD3, SMAD3, SMAD4 and nuclear SMAD4 were detected by western blot analysis. RESULTS: PVT1 expression was significantly increased, whereas miR-146a was markedly decreased in diabetic OA mice than in non-diabetic OA and control. Increased PVT1 expression in diabetic OA mice was significantly associated with Mankin score and reduced miR-146a as well as Collagen alpha-1(II) (COL2A1) expressions. In vivo, intra-articular injection of ad-siRNA-PVT1 efficiently increased miR-146a and COL2A1 expressions, alleviated joint inflammation, decreased the expression of pro-inflammatory mediators, and suppressed TGF-b/SMAD4 pathway in diabetic OA mice. CONCLUSIONS: Our results demonstrate LncRNA PVT1 is involved in cartilage degradation in diabetic OA and correlated with disease severity. Efficiency of ad-siRNA-PVT1 in controlling joint inflammation in diabetic OA mice is associated with the suppression of the expression of miR-146a, pro-inflammatory cytokines and activation of TGF-b/SMAD4 pathway.		J Bone Miner Metab. 2021 Jul;39(4):534-546. doi: 10.1007/s00774-020-01199-7. Epub 2021 Feb 10.
5590	LncRNA	CRNDE	miR-335-3p	NA	Os Cells	Osteosarcoma	Homo sapiens (human)  	Luciferase reporter assay;	33522065	Long noncoding RNA CRNDE functions as a diagnostic and prognostic biomarker in osteosarcoma, as well as promotes its progression via inhibition of miR-335-3p.	BACKGROUND: This study was performed to evaluate the diagnostic and prognostic value, as well as the role of long-chain noncoding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) in osteosarcoma (OS). MATERIALS AND METHODS: A quantitative real-time polymerase chain reaction assay was to determine lncRNA CRNDE and microRNA-335-3p (miR-335-3p) expressions. The Kaplan-Meier analysis was to analyze the relationship between lncRNA CRNDE expression and survival in patients with OS. Receiver operating characteristic curves were to evaluate the diagnostic value of lncRNA CRNDE in OS. Bioinformatics analysis and luciferase reporter assays were used to predict and confirm the relationship between lncRNA CRNDE and miR-335-3p. Cell counting Kit-8 and transwell migration assays assessed the role of lncRNA CRNDE and miR-335-3p in OS cells. RESULTS: lncRNA CRNDE expression was upregulated and miR-355-3p expression was downregulated in OS. In patients with OS, low lncRNA CRNDE expression demonstrated higher overall survival, whereas high lncRNA CRNDE expression was an independent poor prognostic factor. Furthermore, increased lncRNA CRNDE expression was associated with distant metastasis and the tumor-node-metastasis stage in patients with OS, which can be considered as an independent diagnostic biomarker in OS. We revealed that miR-335-3p was the target of lncRNA CRNDE. It also demonstrated that knockdown of lncRNA CRNDE inhibited OS cell proliferation, migration, and invasion, and inhibition of miR-355-3p promoted this effect. Finally, miR-335-3p partially mediated the stimulatory effects of lncRNA CRNDE in OS. CONCLUSION: We demonstrated that lncRNA CRNDE is a potential diagnostic and prognostic biomarker for OS, and the lncRNA CRNDE/miR-335-3p axis participates in OS progression.		J Biochem Mol Toxicol. 2021 May;35(5):e22734. doi: 10.1002/jbt.22734. Epub 2021 Feb 1.
5591	LncRNA	MEG3	miR-204	Foxo1	Müller Cells	Diabetes Mellitus	Homo sapiens (human)  	qRT-PCR 	33517190	Melatonin attenuates oxidative stress and inflammation of Müller cells in diabetic retinopathy via activating the Sirt1 pathway.	Oxidative stress and inflammation are important pathogenic factors of diabetic retinopathy (DR). DR remains the most common ocular complication caused by diabetes mellitus (DM) and is the leading cause of visual impairment in working-aged people worldwide. Melatonin has attracted extensive attention due to its potent antioxidant and anti-inflammatory effects. In the present study, melatonin inhibited oxidative stress and inflammation by enhancing the expression and activity of silent information regulator factor 2-related enzyme 1 (Sirt1) both in in vitro and in vivo models of DR, and the Sirt1 inhibitor EX-527 counteracted melatonin-mediated antioxidant and anti-inflammatory effects on Müller cells. Moreover, melatonin enhanced Sirt1 activity through the maternally expressed gene 3 (MEG3)/miR-204 axis, leading to the deacetylation of the Sirt1 target genes forkhead box o1 (Foxo1) and nuclear factor kappa B (NF-kB) subunit p65, eventually contribute to the alleviation of oxidative stress and inflammation. The study revealed that melatonin promotes the Sirt1 pathway, thereby protecting the retina from DM-induced damage.		Biomed Pharmacother. 2021 May;137:111274. doi: 10.1016/j.biopha.2021.111274. Epub 2021 Jan 29.
5592	LncRNA	MEG3	miR-204	NF-kB	Müller Cells	Diabetes Mellitus	Homo sapiens (human)  	qRT-PCR 	33517190	Melatonin attenuates oxidative stress and inflammation of Müller cells in diabetic retinopathy via activating the Sirt1 pathway.	Oxidative stress and inflammation are important pathogenic factors of diabetic retinopathy (DR). DR remains the most common ocular complication caused by diabetes mellitus (DM) and is the leading cause of visual impairment in working-aged people worldwide. Melatonin has attracted extensive attention due to its potent antioxidant and anti-inflammatory effects. In the present study, melatonin inhibited oxidative stress and inflammation by enhancing the expression and activity of silent information regulator factor 2-related enzyme 1 (Sirt1) both in in vitro and in vivo models of DR, and the Sirt1 inhibitor EX-527 counteracted melatonin-mediated antioxidant and anti-inflammatory effects on Müller cells. Moreover, melatonin enhanced Sirt1 activity through the maternally expressed gene 3 (MEG3)/miR-204 axis, leading to the deacetylation of the Sirt1 target genes forkhead box o1 (Foxo1) and nuclear factor kappa B (NF-kB) subunit p65, eventually contribute to the alleviation of oxidative stress and inflammation. The study revealed that melatonin promotes the Sirt1 pathway, thereby protecting the retina from DM-induced damage.		Biomed Pharmacother. 2021 May;137:111274. doi: 10.1016/j.biopha.2021.111274. Epub 2021 Jan 29.
5593	LncRNA	TCL6	miR-155	STAU1	Ccrcc Cell Lines	Clear Cell Renal Cancer	Homo sapiens (human)  	qRT-PCR 	33500248	A lncRNA TCL6-miR-155 Interaction Regulates the Src-Akt-EMT Network to Mediate Kidney Cancer Progression and Metastasis.	Metastasis is the leading cause of mortality from kidney cancer, and understanding the underlying mechanism of this event will provide better strategies for its management. Here we investigated the biological, functional, and clinical significance of lncTCL6 and its interacting miR-155 in clear cell renal cell carcinoma (ccRCC). We employed a comprehensive approach to investigate the lncTCL6-miR-155-Src/Akt-mediated epithelial-to-mesenchymal transition (EMT) pathway as a novel regulatory mechanism in ccRCC progression. Expression analyses revealed that lncTCL6 is downregulated in ccRCC compared with normal tissues. Overexpression of lncTCL6 in ccRCC cell lines impaired their oncogenic functions, such as cell proliferation and migration/invasion, and induced cell-cycle arrest and apoptosis; conversely, depletion of lncTCL6 rescued these phenotypic effects. Furthermore, lncTCL6 directly interacted with miR-155. Unlike lncTCL6, miR-155 was overexpressed in ccRCC. Stable knockdown of miR-155 phenocopied the effects of lncTCL6 overexpression. Conversely, reconstitution of miR-155 and suppression of lncTCL6 in noncancerous renal cell HK2 induced tumorigenic characteristics. Patients with higher expression of lncTCL6 and lower expression of miR-155 had better survival probability. When overexpressed, lncTCL6 recruited STAU1 and mediated decay of Src mRNA, followed by a marked downregulation of an integrated network of Src target genes involved in migration, invasion, and EMT. However, the interaction between miR-155 and lncTCL6 attenuated the regulatory role of lncTCL6 on Src-mediated EMT. In conclusion, this study is the first report documenting the lncTCL6-miR155-Src/Akt/EMT network as a novel regulatory mechanism in aggressive ccRCC and a promising therapeutic target to inhibit renal cancer. SIGNIFICANCE: This study's investigation of noncoding RNA interactions in renal cell carcinoma identify miRNA-155-lncRNA TCL6-mediated regulation of the Src-Akt-EMT network as a novel mechanism of disease progression and metastasis.		Cancer Res. 2021 Mar 15;81(6):1500-1512. doi: 10.1158/0008-5472.CAN-20-0832. Epub 2021 Jan 26.
5594	LncRNA	CHRF	miR-182-5p	ATG7	H9C2 Cells	Myocardial Ischamia Reperfusion Injury	Homo sapiens (human)  	Rescue assay;	33491285	LncRNA CHRF aggravates myocardial ischemia/reperfusion injury by enhancing autophagy via modulation of the miR-182-5p/ATG7 pathway.	Myocardial ischemia/reperfusion (I/R) injury is a very frequent cardiovascular disease and one of the leading causes of death. Abundant evidence has shown that long noncoding RNAs (lncRNAs) are crucial players in myocardial I/R injury. LncRNA cardiac hypertrophy-related factor (CHRF) has been revealed as an important modulator in cardiac disease. However, the function of CHRF in myocardial I/R injury is unclear. In our current work, we found that the expression of CHRF was upregulated in myocardial I/R injury models. Suppression of CHRF relieved myocardial I/R injury in vivo. In addition, in vitro silencing of CHRF enhanced cell viability and attenuated lactate dehydrogenase activity (LDH) as well as apoptosis in H9C2 cells treated with hypoxia/reoxygenation injury. Autophagy has been studied to play an important role in myocardial I/R injury. Thus, experiments related to autophagy were done, and the results showed that CHRF knockdown decreased autophagy. For the exploration of the regulatory mechanism, we found that CHRF sequestered and negatively regulated miR-182-5p to release its inhibition on ATG7. Findings from rescue assays revealed that ATG7 overexpression could suppress the effects of CHRF silence on cell viability, LDH level, apoptosis, and autophagy. To sum up, our results suggested that CHRF exacerbated myocardial I/R injury by enhancing autophagy via modulation of the miR-182-5p/ATG7 pathway. Therefore, this competing endogenous RNA axis may be a potential therapeutic biomarker for myocardial I/R injury.		J Biochem Mol Toxicol. 2021 Apr;35(4):e22709. doi: 10.1002/jbt.22709. Epub 2021 Jan 24.
5595	LncRNA	MAFG-AS1	miR-125b-5p	SphK1	Bladder Cancer Cells	Bladder Cancer	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;Luciferase activity assay;	33400245	LncRNA MAFG-AS1 regulates miR-125b-5p/SphK1 axis to promote the proliferation, migration, and invasion of bladder cancer cells.	MAFG-AS1 is an oncogenic lncRNA in multiple types of cancer. However, its role in bladder cancer (BC) remains unclear. The present study aimed to investigate the function of MAFG-AS1 in BC. BC and paired non-tumor tissues were collected. Two BC cell lines HT01197 and HT-1376 were used. Dual luciferase activity assay, RT-qPCR, western blot, CCK-8, transwell invasion assay, and wound healing assay were performed. We found that MAFG-AS1 was significantly up-regulated in BC tissues and predicted a poor survival rate. MAFG-AS1 interacted with miR-125b-5p. However, the expression levels of MAFG-AS1 and miR-125b-5p were not obviously correlated in BC tissues, and MAFG-AS1 and miR-125b-5p did not regulate the expression of each other. Interestingly, we found that SphK1, a downstream target of miR-125b-5p, was negatively correlated with miR-125b-5p, while it was positively correlated with MAFG-AS1 across BC tissues. In addition, overexpression of MAFG-AS1 upregulated the expression of SphK1 in BC cells, and attenuated the inhibitory effects of miR-125b-5p on the expression of SphK1. Functional assays showed that overexpression of MAFG-AS1 promoted BC cell proliferation, migration, and invasion, while its effects were attenuated by overexpression of miR-125b-5p. Moreover, overexpression of miR-125b-5p inhibited BC cell proliferation, migration, and invasion, while its effects were alleviated by overexpression of SphK1. Taken together, our findings demonstrated that MAFG-AS1 has an oncogenic role in BC by regulating the miR-125b-5p/SphK1 axis. MAFG-AS1 might serve as a good diagnostic marker and a potential therapeutic target of BC.		Hum Cell. 2021 Mar;34(2):588-597. doi: 10.1007/s13577-020-00470-3. Epub 2021 Jan 5.
5596	LncRNA	DRAIC	miR-18a-3p	SET7	Glioma Cells	Glioma	Homo sapiens (human)  	ChIP;qPCR;Luciferase reporter assay;	33336743	SET7/9 promotes H3K4me3 at lncRNA DRAIC promoter to modulate growth and metastasis of glioma.	OBJECTIVE: We aimed at investigating the expression levels of SET7/9 in glioma and the relationship between SET7/9 and LncRNA DRAIC. Further, we explored the relationship between SET7/9 and glioma cell metastasis and mood. PATIENTS AND METHODS: The expression levels of DRAIC and miR-18a-3p in gastric cancer cells were measured by quantitative polymerase chain reaction (qPCR). The binding site of the promoter of DRAIC by H3K4me3 was confirmed by ChIP-Real-time PCR. The direct target of DRAIC and miR-18a-3p in gastric cancer cells was measured by a Luciferase reporter assay. Cell proliferation was detected by Cell counting kit-8 (CCK8), and cell invasion and migration were measured by transwell assays. RESULTS: Compared with adjacent non-cancerous normal tissues, SET7/9 and DRAIC were both downregulated and miR-18a-3p was upregulated in glioma cells. Meanwhile, silencing of SET7/9 enhanced cell proliferation, migration, and invasion in U251 cells. H3K4me3 protein can bind to DRAIC promoter directly. Inhibition of SET7/9 and downregulation of DRAIC in U251 cells reversed the effect of SET7/9 silencing on the growth and metastasis of glioma cells. In U251 cells, SET7/9 and DRAIC overexpression inhibited cell proliferation, migration and invasion. In addition, miR-18a-3p interacts with DRAIC through direct binding. The inhibition of DRAIC promoted the growth and metastasis of U251 cells, while the co-transfection of si- DRAIC and miR-18a-3p further promoted the growth and metastasis of U251 cells. Overexpression of DRAIC inhibited the growth and metastasis of cells, completely reversing the co-transfection of Lnc-DRAIC and miR-18a-3p. CONCLUSIONS: In this research, we discovered that the expression of SET7/9 was low in glioma cells and SET7/9-mediated H3K4me3 enrichment on the DRAIC promoter regulated the growth and metastasis of glioma cells by targeting miR-18a-3p. It potentially provides a new therapeutic marker targeting glioma.		Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12241-12250. doi: 10.26355/eurrev_202012_24016.
5597	LncRNA	DRAIC	miR-18a-3p	SET9	Glioma Cells	Glioma	Homo sapiens (human)  	ChIP;qPCR;Luciferase reporter assay;	33336743	SET7/9 promotes H3K4me3 at lncRNA DRAIC promoter to modulate growth and metastasis of glioma.	OBJECTIVE: We aimed at investigating the expression levels of SET7/9 in glioma and the relationship between SET7/9 and LncRNA DRAIC. Further, we explored the relationship between SET7/9 and glioma cell metastasis and mood. PATIENTS AND METHODS: The expression levels of DRAIC and miR-18a-3p in gastric cancer cells were measured by quantitative polymerase chain reaction (qPCR). The binding site of the promoter of DRAIC by H3K4me3 was confirmed by ChIP-Real-time PCR. The direct target of DRAIC and miR-18a-3p in gastric cancer cells was measured by a Luciferase reporter assay. Cell proliferation was detected by Cell counting kit-8 (CCK8), and cell invasion and migration were measured by transwell assays. RESULTS: Compared with adjacent non-cancerous normal tissues, SET7/9 and DRAIC were both downregulated and miR-18a-3p was upregulated in glioma cells. Meanwhile, silencing of SET7/9 enhanced cell proliferation, migration, and invasion in U251 cells. H3K4me3 protein can bind to DRAIC promoter directly. Inhibition of SET7/9 and downregulation of DRAIC in U251 cells reversed the effect of SET7/9 silencing on the growth and metastasis of glioma cells. In U251 cells, SET7/9 and DRAIC overexpression inhibited cell proliferation, migration and invasion. In addition, miR-18a-3p interacts with DRAIC through direct binding. The inhibition of DRAIC promoted the growth and metastasis of U251 cells, while the co-transfection of si- DRAIC and miR-18a-3p further promoted the growth and metastasis of U251 cells. Overexpression of DRAIC inhibited the growth and metastasis of cells, completely reversing the co-transfection of Lnc-DRAIC and miR-18a-3p. CONCLUSIONS: In this research, we discovered that the expression of SET7/9 was low in glioma cells and SET7/9-mediated H3K4me3 enrichment on the DRAIC promoter regulated the growth and metastasis of glioma cells by targeting miR-18a-3p. It potentially provides a new therapeutic marker targeting glioma.		Eur Rev Med Pharmacol Sci. 2020 Dec;24(23):12241-12250. doi: 10.26355/eurrev_202012_24016.
5598	LncRNA	NRON	miR-23a	NFATc3	Atrial Fibroblasts	Atrial Fibrosis	Mus musculus (mouse)	qRT-PCR 	33246743	LncRNA NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.	BACKGROUND/PURPOSE: miR-23a is a pro-hypertrophic miRNA that inhibits M2 macrophage polarization. A previous study demonstrated that lncRNA NRON alleviated atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes. This study aimed to determine whether NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes. METHODS: Mouse atrial myocytes were transfected with the NRON overexpression vector or empty vector, followed by Ang II treatment. Exosomes were isolated from the treated atrial myocytes and then co-cultured with RAW264.7 macrophages. The culture medium from RAW264.7 macrophages treated as described above was added to mouse atrial fibroblasts for incubation. RESULTS: We found that exosomes derived from Ang II-treated atrial myocytes inhibited M2 macrophage polarization by transferring miR-23a. NFATc3 could directly bind to the miR-23a promoter. Overexpression of NRON inhibited the expression of miR-23a by inhibiting NFATc3 nuclear transport in Ang II-treated atrial myocytes, resulting in a decrease in the level of miR-23a in atrial myocyte-derived exosomes. Meanwhile, exosomes derived from NRON-overexpressing atrial myocytes promoted M2 macrophage polarization and inhibited expression of fibrosis markers in atrial fibroblasts. CONCLUSION: NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.		J Formos Med Assoc. 2021 Jul;120(7):1512-1519. doi: 10.1016/j.jfma.2020.11.004. Epub 2020 Nov 25.
5599	LncRNA	XIST	miR-29a	MYC	Aml Cells	Acute Myeloid Leukemia	Homo sapiens (human)  	microarray;qPCR;RT-qPCR;	33241745	Bioinformatics analysis of long non-coding RNAs involved in nerve regeneration following sciatic nerve injury.	Little is known about the role of epigenetic modification in axon regeneration following peripheral nerve injury. The purpose of the present study was to investigate the role of long non-coding RNAs (lncRNAs) in the regulation of axon regeneration. We used bioinformatics to perform microarray analysis and screened total 476 lncRNAs and 129 microRNAs (miRNAs) of differentially expressed genes after sciatic nerve injury in mice. lncRNA-GM4208 and lncRNA-GM30085 were examined, and the changes in lncRNA expression in the L4-L6 dorsal root ganglia (DRG) following sciatic nerve crush injury were analyzed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression of lncRNAs in the DRG changed, indicating that they might be related to nerve regeneration in the DRG following peripheral nerve injury.		Mol Pain. 2020 Jan-Dec;16:1744806920971918. doi: 10.1177/1744806920971918.
5600	LncRNA	H19	miR-29a-3p	NA	Op Samples	Osteoporosis	Homo sapiens (human)  	qRT-PCR 	33207859	An emerging potential therapeutic target for osteoporosis: LncRNA H19/miR-29a-3p axis.	Osteoporosis (OP) is a complex systemic disease characterized by a loss of bone density, leading to bone fragility and an increase risk of fractures of the hip, spine and wrist. The clinical therapeutic effect is still far from satisfactory. Thus, further studies are urgently needed to explore the pathogenesis of OP. In this study, our aim is to explore the underlying molecular mechanism of lncRNA H19/miR-29a-3p axis for regulating of inflammation, proliferation and apoptosis in OP. The expression of lncRNA H19 was significantly upregulated in OP samples compared with the health control. Subsequently, we found that miR-29a-3p is the target of lncRNA H19 in OP. Furthermore, the knockdown of lncRNA H19 was validated to promote the expression of pro-inflammatory mediators, repress cell proliferation and inhibit cell apoptosis in vitro. Moreover, the modulating effects of lncRNA-H19 on the expressions of pro-inflammatory mediators, cell proliferation and apoptosis in vitro were diminished after co-transfecting with miR-29a-3p inhibitor and siRNA-H19. Thus, we concluded that lncRNA H19/miR-29a-3p axis was involved in the development of OP. This study might provide a better understanding of OP development and a potential therapeutic target for OP intervention.		Eur J Histochem. 2020 Nov 6;64(4):3155. doi: 10.4081/ejh.2020.3155.
5601	LncRNA	MEG3	miR-129-5p	HMGB1	Renal Tubular Epithelial Cells	Acute Kidney Injury	Homo sapiens (human)	qRT-PCR;Western blot;Flow Cytometry assay;	33175458	MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR-129-5p/HMGB1 axis.	The apoptosis of renal tubular epithelial cells (TECs) during ischemia/reperfusion (I/R) facilitates the progression of acute kidney injury (AKI). This study aimed to probe the role of long noncoding RNA maternally expressed 3 (MEG3) in I/R-induced apoptosis of TECs. In this study, with CoCl(2) and hypoxia/reoxygenation treatments, cell models were established to mimic I/R using the human kidney tubular cell line HK-2. In HK-2 cells, expression of MEG3 detected using quantitative real-time polymerase chain reaction (qRT-PCR), was significantly upregulated after CoCl(2) treatment and hypoxia/reoxygenation treatment. The results of cell counting kit-8 assay and flow cytometry suggested that knockdown of MEG3 significantly increased the viability of HK-2 cells but inhibited its apoptosis, while overexpression of MEG3 exerted the reverse effects. Additionally, expression levels of interleukin 6 and tumor necrosis factor-a in the medium were elevated after MEG3 was overexpressed in HK-2 cells. Together with qRT-PCR and Western blot analysis, a dual-luciferase reporter gene assay was used to verify the interactions among MEG3, miR-129-5p, and HMGB1. The results demonstrated that in HK-2 cells, miR-129-5p was a target of MEG3, and HMGB1 served as a target gene of miR-129-5p. Besides this, compared with the control group, the expression levels of MEG3 and HMGB1 in samples derived from AKI patients were remarkably upregulated, and the expression of miR-129-5p was downregulated. Therefore, taken together, we conclude that the overexpression of MEG3 induced by I/R promotes apoptosis of TECs via regulating the miR-129-5p/HMGB1 axis.		J Biochem Mol Toxicol. 2021 Feb;35(2):e22649. doi: 10.1002/jbt.22649. Epub 2020 Nov 11.
5602	LncRNA	DLEU1	miR-133a-3p	SRPK1	Rat Model	Neuropathic Pain	Rattus (rat)	ELISA;qPCR;RT-qPCR;Western blot;Luciferase reporter assay;Rescue assay;	33167866	Downregulation of long noncoding RNA DLEU1 attenuates hypersensitivity in chronic constriction injury-induced neuropathic pain in rats by targeting miR-133a-3p/SRPK1 axis.	BACKGROUND: Neuropathic pain belongs to chronic pain and is caused by the primary dysfunction of the somatosensory nervous system. Long noncoding RNAs (lncRNAs) have been reported to regulate neuronal functions and play significant roles in neuropathic pain. DLEU1 has been indicated to have close relationship with neuropathic pain. Therefore, our study focused on the significant role of DLEU1 in neuropathic pain rat models. METHODS: We first constructed a chronic constrictive injury (CCI) rat model. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were employed to evaluate hypersensitivity in neuropathic pain. RT-qPCR was performed to analyze the expression of target genes. Enzyme-linked immunosorbent assay (ELISA) was conducted to detect the concentrations of interleukin-6 (IL-6), tumor necrosis factor-a (TNF-a) and IL-1b. The underlying mechanisms of DLEU1 were investigated using western blot and luciferase reporter assays. RESULTS: Our findings showed that DLEU1 was upregulated in CCI rats. DLEU1 knockdown reduced the concentrations of IL-6, IL-1b and TNF-a in CCI rats, suggesting that neuroinflammation was inhibited by DLEU1 knockdown. Besides, knockdown of DLEU1 inhibited neuropathic pain behaviors. Moreover, it was confirmed that DLEU1 bound with miR-133a-3p and negatively regulated its expression. SRPK1 was the downstream target of miR-133a-3p. DLEU1 competitively bound with miR-133a-3p to upregulate SRPK1. Finally, rescue assays revealed that SRPK1 overexpression rescued the suppressive effects of silenced DLEU1 on hypersensitivity in neuropathic pain and inflammation of spinal cord in CCI rats. CONCLUSION: DLEU1 regulated inflammation of the spinal cord and mediated hypersensitivity in neuropathic pain in CCI rats by binding with miR-133a-3p to upregulate SRPK1 expression.		Mol Med. 2020 Nov 10;26(1):104. doi: 10.1186/s10020-020-00235-6.
5603	LncRNA	TUG1	miR-29a-3p	NA	Ac16 Cells	Myocardial Ischemia	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33165134	LncRNA TUG1 Contributes to Hypoxia-Induced Myocardial Cell Injury Through Downregulating miR-29a-3p in AC16 Cells.	Myocardial ischemia is a common reason that causes human death globally. Long noncoding RNA taurine upregulated 1 (TUG1) serves as an oncogene in a variety of cancers. In this article, we aimed to investigate the role of TUG1 and its underlying signal pathway in hypoxia-induced myocardial cell injury. Cell viability, apoptosis, and lactate dehydrogenase (LDH) release were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, western blot assay, and LDH cytotoxicity assay. Quantitative real-time polymerase chain reaction was applied to measure the enrichment of TUG1 and miR-29a-3p. MiR-29a-3p was predicted as a target of TUG1 by StarBase bioinformatic software, and the target relationship between TUG1 and miR-29a-3p was verified by dual-luciferase reporter assay. Hypoxia treatment induced the apoptosis and LDH release while inhibited the viability of AC16 cells. TUG1 was markedly upregulated while the level of miR-29a-3p was notably decreased in hypoxia-stimulated AC16 cells. TUG1 contributed to hypoxia-induced AC16 injury. MiR-29a-3p depletion intensified hypoxia-induced AC16 damage. TUG1 negatively regulated the expression of miR-29a-3p through their direct interaction in AC16 cells. TUG1 silencing-mediated influences in hypoxia-induced AC16 cells were partly reversed by the interference of miR-29a-3p. In conclusion, TUG1 accelerated hypoxia-induced AC16 injury through inversely modulating the level of miR-29a-3p. TUG1/miR-29a-3p axis might be an underlying therapeutic target for myocardial ischemia.		J Cardiovasc Pharmacol. 2020 Nov;76(5):533-539. doi: 10.1097/FJC.0000000000000906.
5604	LncRNA	HCP5	miR-27b-3p	MET	Diffuse Large B-Cell Lymphoma Cells	Diffuse Large B-Cell Lymphoma	Homo sapiens (human)	Luciferase reporter assay;	33162801	Geniposide inhibits proliferation and induces apoptosis of diffuse large B-cell lymphoma cells by inactivating the HCP5/miR-27b-3p/MET axis.	Diffuse large B-cell lymphoma (DLBCL) is commonly treated with R-CHOP, but ~30 to 50% of the patients are poorly responsive to this strategy. Geniposide, an extract from the Gardenia jasminoides Ellis, plays antitumor roles in human gastric cancer, hepatocellular carcinoma, and oral squamous carcinoma. However, the effects of geniposide treatment on DLBCL cells, as well as its underlying mechanism, are still unknown. Here, we found that geniposide inhibited the proliferation of OCI-LY7 and OCI-LY3 cells in a dose-dependent manner. Furthermore, geniposide increased the percentage of apoptotic cells and upregulated the levels of cleaved PARP and cleaved caspase-3 in DLBCL cells. Interestingly, geniposide treatment significantly reduced the expression of the long noncoding RNA HLA complex P5 (lncRNA HCP5) in DLBCL cells. HCP5 expression was revealed to be upregulated in DLBCL tissues and cell lines. Moreover, HCP5 knockdown resulted in proliferation inhibition and apoptosis in OCI-LY7 and OCI-LY3 cells. miR-27b-3p was predicted as a potential target of HCP5 using the lnCAR web tool. Both HCP5 silencing and geniposide treatment increased the level of miR-27b-3p in DLBCL cells. Accordingly, a luciferase reporter assay identified miR-27b-3p as a direct target of HCP5. The expression of miR-27b-3p was upregulated and inversely correlated with the HCP5 level in DLBCL tissues. HCP5 knockdown reduced MET protein expression, which was subsequently rescued by miR-27b-3p silencing in DLBCL cells. Importantly, the restoration of MET partially reversed the geniposide-induced proliferation inhibition and apoptosis of DLBCL cells. In conclusion, geniposide inhibits the proliferation and induces the apoptosis of DLBCL cells at least partially by regulating the HCP5/miR-27b-3p/MET axis, indicating a potential strategy for DLBCL treatment.		Int J Med Sci. 2020 Sep 23;17(17):2735-2743. doi: 10.7150/ijms.51329. eCollection 2020.
5605	LncRNA	CASC19	miR-148b	E2F7	Pc Tissues And Cell Lines	Pancreatic Cancer	Homo sapiens (human)	qPCR;RT-qPCR;Luciferase reporter assay;	33155202	LncRNA CASC19 contributed to the progression of pancreatic cancer through modulating miR-148b/E2F7 axis.	OBJECTIVE: Cancer susceptibility 19 (CASC19), a crucial lncRNA associated with multiple cancers, has been reported to play a vital role in the progression of human malignant tumors. However, the underlying mechanism of CASC19 in pancreatic cancer (PC) was still unknown. The purpose of this study was to explore the biological and clinical significance of CASC19 in PC. PATIENTS AND METHODS: RT-qPCR assay was adopted to analyze CASC19 expression in PC tissues and cell lines. Furthermore, the correlation between the CASC19 level and the survival rate of PC patients was assessed by Kaplan-Meier analysis. Bioinformatics analysis and Luciferase reporter assay were utilized to confirm the interaction between miR-148b and CASC19 or E2F7. Cell viability, migration, invasion, and apoptosis were analyzed using MTT, transwell, and TUNEL assays. RESULTS: The results elucidated that CASC19 expression was markedly increased in PC tissues and cell lines. Patients with high expression of CASC19 had a short survival time. Silencing of CASC19 attenuated PC cell proliferation, migration, and invasion. Moreover, we identified that miR-148b was a target of CASC19. CASC19 was negatively correlated with miR-148b and positively correlated with E2F7. The inhibitory effect of CASC19 knockdown on the progression of PC was reversed by the down-regulation of miR-148b or up-regulation of E2F7. CONCLUSIONS: These results demonstrated that CASC19 participated in the development of PC. The CASC19/miR-148b/E2F7 axis might be a new study direction for PC treatment.		Eur Rev Med Pharmacol Sci. 2020 Oct;24(20):10462-10471. doi: 10.26355/eurrev_202010_23399.
5606	LncRNA	MALAT1	miR-211	SIRT1	Epidermis	Vitiligo	Homo sapiens (human)  	RNA sequencing;	33152110	The long noncoding RNA MALAT1 suppresses miR-211 to confer protection from ultraviolet-mediated DNA damage in vitiligo epidermis by upregulating sirtuin 1.	BACKGROUND: The absence of melanocytes poses a challenge for long-term tissue homeostasis in vitiligo. Surprisingly, while individuals with Fitzpatrick phototypes I-II (low melanin content) have a higher incidence of melanoma and nonmelanoma skin cancer, people with vitiligo are at a decreased risk for the same. OBJECTIVES: To understand the molecular mechanisms that protect vitiligo skin from ultraviolet (UV)-induced DNA damage by (i) characterizing differentially expressed microRNAs in lesional vs. nonlesional epidermis and (ii) identifying their upstream regulators and downstream gene targets. METHODS: Genome-wide microRNA profiling of nonlesional and lesional epidermis was performed on five individuals with stable nonsegmental vitiligo using next-generation RNA sequencing. The relevance of the upstream regulator and downstream target gene of the most differentially expressed microRNA was studied. RESULTS: Our study found sirtuin1 (SIRT1), an NAD-dependent deacetylase, to be a direct target of miR-211 - the most significantly downregulated microRNA in lesional epidermis. Inhibition of SIRT1 with EX-527 downregulated keratin 10 and involucrin, suggesting that SIRT1 promotes keratinocyte differentiation. Overexpression of miR-211 mimic led to a significant increase in γ-H2AX positivity and cyclobutane pyrimidine dimer (CPD) formation, hallmarks of UVB-mediated DNA damage. These effects could be ameliorated by the addition of resveratrol, a SIRT1 activator. Furthermore, a long noncoding RNA, MALAT1, was identified as a negative upstream regulator of miR-211. Overexpression of MALAT1 resulted in increased expression of SIRT1 and a concomitant removal of UVB-induced CPDs in primary keratinocytes. CONCLUSIONS: These findings establish a novel MALAT1-miR-211-SIRT1 signalling axis that potentially confers protection to the 'amelanotic' keratinocytes in vitiligo.		Br J Dermatol. 2021 Jun;184(6):1132-1142. doi: 10.1111/bjd.19666. Epub 2020 Dec 30.
5607	LncRNA	MALAT1	miR-185-5p	MDM4	Nsclc Cells	Non-Small Cell Lung Cancer	Mus musculus (mouse)	Dual-luciferase reporter assay;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	33146951	LncRNA MALAT1 accelerates non-small cell lung cancer progression via regulating miR-185-5p/MDM4 axis.	Non-small cell lung cancer (NSCLC) is the commonest malignancy with high death rate around the world. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is greatly overexpressed in multifarious cancers, including NSCLC. However, the precise mechanism of MALAT1 in NSCLC tumorigenesis is blurry. This paper aims to investigate the theory of MALAT1 action in NSCLC progression. The levels of MALAT1, microRNA (miR)-185-5p, and mouse double minute 4 protein (MDM4) were measured by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. Cell proliferation and apoptosis were, respectively, determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and flow cytometry. Cell migratory and invasive abilities were inspected by transwell assay. The binding relationship between miR-185-5p and MALAT1 or MDM4 was confirmed by dual-luciferase reporter assay. The impacts of MALAT1 on tumor growth in vivo were measured by a xenograft experiment. We found MALAT1 and MDM4 were upregulated and MALAT1 positively regulated the MDM4 expression. MALAT1 and MDM4 deletion significantly hindered the proliferation, metastasis, and expedited the apoptosis of NSCLC cells. MDM4 overexpression partly overturned the influence of MALAT1 downregulation on cell development. Moreover, miR-185-5p, as a target of MALAT1, could directly target MDM4, and miR-185-5p upregulation exerted inhibitory effects on NSCLC cells. Besides, knockdown of MALAT1 inhibited tumor growth in vivo through miR-185-5p/MDM4 axis in NSCLC. Collectively, MALAT1 contributed to proliferation, migration, invasion, and impeded apoptosis by regulating the MDM4 expression mediated by miR-185-5p in NSCLC cells.		Cancer Med. 2020 Dec;9(23):9138-9149. doi: 10.1002/cam4.3570. Epub 2020 Nov 4.
5608	LncRNA	SNHG7	miR-15a	NA	Breast Cancer Cells Mcf7 And T47D	Breast Cancer	Homo sapiens (human)  	Cell proliferation assay;Dual-luciferase reporter assay;qRT-PCR;Luciferase reporter assay;	33099915	LncRNA SNHG7 inhibits proliferation and invasion of breast cancer cells by regulating miR-15a expression.	PURPOSE: To explore the inhibition of proliferation and invasion of breast cancer cells by LncRNA SNHG7 via regulating the expression of miR-15a and its mechanism. METHODS: The expression of SNHG7 in breast cancer and adjacent tissues and different breast cancer cells was measured by qRT-PCR and the relationship between SNHG7 and clinicopathological parameters of breast cancer patients was analyzed. The interaction of SNHG7 with miR-15a was explored by dual-luciferase reporter assay. The change in the proliferation of breast cancer cells after silencing SNHG7 was examined by cell proliferation assay. The change in the invasion of breast cancer cells after silencing SNHG7 was examined by Transwell invasion assay. Subcutaneous tumor formation in nude mice was detected to record the tumor size and volume of tumor cells. RESULTS: Compared with adjacent normal tissues, the expression of SNHG7 was significantly increased in breast cancer tissues; the expression of SNHG7 was the highest in breast cancer cells MCF7 and T47D; the expression level of SNHG7 was not notably different among breast cancer patients of different genders and age groups, and the difference was not statistically significant (p>0.05). The expression level of SNHG7 was higher in patients with a higher stage of breast cancer and patients with lymph node metastasis, and the difference was statistically significant. SNHG7 could specifically bind to the 3' UTR of miR-15a. The inhibition of SNHG7 led to constrained proliferation and invasion of breast cancer cells. The tumor volume and weight of the tumor-bearing mice in the si-SNHG7 group were significantly lower than those in the non-specific control (NC) group. CONCLUSION: SNHG7 plays an important role in the development of breast cancer. SNHG7 can affect the proliferation and invasion of breast cancer cells through its targeted regulation of miR-15a activity.		J BUON. 2020 Jul-Aug;25(4):1792-1798.
5609	LncRNA	SNHG10	miR-21	NA	Nsclc Cells	Non-Small Cell Lung Cancer	Homo sapiens (human)  	CCK-8 assay;qPCR;RT-qPCR;	33081752	LncRNA SNHG10 is downregulated in non-small cell lung cancer and predicts poor survival.	BACKGROUND: LncRNA SNHG10 has been reported to be an oncogenic lncRNA in liver cancer. However, its roles in non-small cell lung cancer (NSCLC) remains unknown. METHODS: Tumor and paired non-tumor tissues were harvested from 62 NSCLC patients. RT-qPCR was used to detect the expression of SNHG10 and miR-21 in tissues. Overexpression experiments were used to evaluate the interaction between SNHG10 and miR-21 in NSCLC cells. CCK-8 assay was used to detect the cell proliferation. RESULTS: We observed the expression of SNHG10 was down-regulated in non-small cell lung cancer (NSCLC) compared with that in non-tumor tissues. Moreover, we found that high expression levels of SNHG10 predicted favorable survival of NSCLC patients, and the expression of miR-21 were increased in NSCLC and inversely correlated with SNHG10 expression. In NSCLC cells, overexpression of SNHG10 resulted in increased miR-21 gene methylation and decreased miR-21 expression. Moreover, overexpression of SNHG10 attenuated the enhancing effect of miR-21 overexpression on cell proliferation. CONCLUSIONS: SNHG10 may involve in NSCLC cell proliferation by regulating the miR-21 gene methylation.		BMC Pulm Med. 2020 Oct 20;20(1):273. doi: 10.1186/s12890-020-01281-w.
5610	LncRNA	LINC01094	miR-577	b-catenin	Skov3 And 3Ao Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;	33069244	LINC01094/miR-577 axis regulates the progression of ovarian cancer.	BACKGROUND: Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, b-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. RESULTS: LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of b-catenin, c-Myc and cyclin D1 in OC cells. CONCLUSION: LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.		J Ovarian Res. 2020 Oct 17;13(1):122. doi: 10.1186/s13048-020-00721-9.
5611	LncRNA	LINC01094	miR-577	c-Myc	Skov3 And 3Ao Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;	33069244	LINC01094/miR-577 axis regulates the progression of ovarian cancer.	BACKGROUND: Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, b-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. RESULTS: LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of b-catenin, c-Myc and cyclin D1 in OC cells. CONCLUSION: LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.		J Ovarian Res. 2020 Oct 17;13(1):122. doi: 10.1186/s13048-020-00721-9.
5612	LncRNA	LINC01094	miR-577	cyclin D1	Skov3 And 3Ao Cells	Ovarian Cancer	Homo sapiens (human)  	qRT-PCR;Western blot;	33069244	LINC01094/miR-577 axis regulates the progression of ovarian cancer.	BACKGROUND: Long intergenic non-coding RNA 01094 (LINC01094) is probably a novel regulator in cancer biology. This study aimed to probe into the function and mechanism of LINC01094 in ovarian cancer (OC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was utilized to measure LINC01094 and miR-577 expressions in OC tissues and cell lines. Western blot was used to examine the expressions of epithelial-mesenchymal transition (EMT)-related proteins, b-catenin, c-Myc and cyclin D1. Cell counting kit-8 (CCK-8) and Transwell assays were used to detect the proliferation, migration and invasion of SKOV3 and 3AO cells, respectively. Eventually, dual-luciferase reporter gene assay was employed to detect the regulatory relationship between miR-577 and LINC01094. RESULTS: LINC01094 expression was elevated in OC tissues and cell lines. High LINC01094 expression was associated with higher FIGO stage, lymph node metastasis and the shorter overall survival rate in patients with OC. Meanwhile, LINC01094 knockdown inhibited OC cell proliferation, migration, invasion and EMT. In addition, miR-577 was demonstrated to be a direct downstream target of LINC01094 in OC and inhibition of miR-577 reversed the biological effects of LINC01094 knockdown on OC cells. Additionally, LINC01094 / miR-577 axis regulated the expressions of b-catenin, c-Myc and cyclin D1 in OC cells. CONCLUSION: LINC01094 promotes the proliferation, migration, invasion and EMT of OC cells by adsorbing miR-577.		J Ovarian Res. 2020 Oct 17;13(1):122. doi: 10.1186/s13048-020-00721-9.
5613	LncRNA	LINC01133	miR-30b-5p	Rab3D	Rcc Cell Lines	Renal Cancer	Homo sapiens (human)  	qRT-PCR 	33054325	Long Noncoding RNA LINC01133 Promotes the Malignant Behaviors of Renal Cell Carcinoma by Regulating the miR-30b-5p/Rab3D Axis.	Renal cell carcinoma (RCC) is the most common type of kidney cancer with rising incidence. Long noncoding RNA (lncRNA) LINC01133 is a novel lncRNA that is involved in the development of several types of cancers. However, the role of LINC01133 in RCC has not been reported. Thus, in this study, we investigated the functions of LINC01133 in RCC. The qualitative real-time polymerase chain reaction analysis was performed to examine the levels of LINC01133 in RCC tissues and adjacent tissues, as well as RCC cell lines. The results showed that LINC01133 was highly expressed in RCC tissue specimens and cell lines. Downregulation of LINC01133 significantly inhibited the proliferation, migration, and invasion of RCC cells. Further mechanistic investigations proved that LINC01133 directly interacted with microRNA (miR)-30b-5p and regulated the miR-30b-5p expression in RCC cell lines. Moreover, miR-30b-5p exhibited tumor-suppressive activity in RCC cell lines, which was mediated by targeting Ras-related protein Rab-3D (Rab3D). In vivo study showed that LINC01133 knockdown suppressed tumor growth in the nude mice. Taken together, these findings indicated that LINC01133 might be an oncogene in RCC through regulation of the miR-30b-5p/Rab3D axis. Thus, LINC01133 might serve as a potential therapeutic target for the treatment of RCC.		Cell Transplant. 2020 Jan-Dec;29:963689720964413. doi: 10.1177/0963689720964413.
5614	LncRNA	XIST	Mir-7a-5p	Tfam	Mice Cardiomyocytes (Mcm) Cells	Acute Myocardial Infarction	Homo sapiens (human)  	qRT-PCR;Flow Cytometry assay;siRNA transfection;	33029099	Down-regulation of Xist and Mir-7a-5p improves LPS-induced myocardial injury.	Background: X-inactive specific transcript (Xist) is a lncRNA, which plays a significant role in X-chromosome inactivation, regulates cell proliferation in tumor cells, and inhibits apoptosis in acute myocardial infarction. On the other hand, miR-7a-5p is involved in cardiomyocytes injury in myocardial ischemia/reperfusion. However, their roles in LPS-induced damage remain unclear. Objectives: This study aimed at using siRNA transfection and lentivirus infection to regulate the expression of xist and miR-7a-5p, and to evaluate their effects on LPS-induced myocardial damage. Method: Mice cardiomyocytes (MCM) cells were divided into six groups, namely the control group, the LPS group, the LPS + lncRNA(-) group, the LPS + lncRNA(+) group, the LPS + miRNA(-) group, and the LPS + miRNA(+) group. Quantitative real-time PCR (qRT-PCR) was performed to assay for the RNA expressions of xist, miR-7a-5p, peroxisome proliferator-activated receptor-γ coactivator-1a (PGC-1a), and recombinant mitochondrial transcription factor A (Tfam) in all the groups. The ATP level was determined using the adenosine triphosphate (ATP) assay kit according to the manufacturer's instructions. Flow cytometry was performed to estimate the level of apoptosis and proliferation in cells in each group. Results: The level of xist in the myocardial cells was markedly higher in the LPS group compared with the control group; however, it was reduced in the LPS+ lncRNA(-) group. There was no significant difference in the expression of xist among the LPS+miRNA(-), LPS+miRNA(+), and LPS groups. Moreover, the expression of mir-7a-5p was significantly reduced in myocardial cells in the LPS group, and moderately reduced in the LPS+ miRNA(-) group, but remarkably elevated in the LPS+ miRNA(+) group (P<0.05). The expression of mir-7a-5p was comparably similar in the LPS+ lncRNA(-) group, LPS+ lncRNA(+) group, and LPS groups. Further, the levels of PGC-1a, and Tfam were determined. In the LPS group, the expression of PGC-1a was significantly reduced but elevated in the LPS+lncRNA(-) and LPS+ miRNA(-) groups (P<0.05). There was no significant difference in the level of PGC-1a among the LPS, LPS+ lncRNA(+), and LPS+ miRNA(+) groups. The expression of Tfam was markedly reduced in the LPS group (P < 0.05), but elevated after the suppression of xist and mir-7a-5p. The expression of Tfam was not significantly different among the LPS group, LPS+ lncRNA(+) and LPS+ miRNA(+) groups. Notably, overexpression of mir-7a-5p had a mild effect on the expression of Tfam in the LPS+ miRNA(+) group compared with the control group. Besides, ATP expression in the LPS group was markedly reduced, but elevated after the inhibition of xist and mir-7a-5p. Suppressing the expression of xist or mir-7a-5p resulted in reduced cell apoptosis and increased cell proliferation. Conclusions: In this study, we established that down-regulation of xist and mir-7a-5p reduces apoptosis in response to LPS.		Int J Med Sci. 2020 Sep 16;17(16):2570-2577. doi: 10.7150/ijms.45408. eCollection 2020.
5615	LncRNA	XIST	Mir-7a-5p	ATP	Mice Cardiomyocytes (Mcm) Cells	Acute Myocardial Infarction	Homo sapiens (human)  	qRT-PCR;Flow Cytometry assay;siRNA transfection;	33029099	Down-regulation of Xist and Mir-7a-5p improves LPS-induced myocardial injury.	Background: X-inactive specific transcript (Xist) is a lncRNA, which plays a significant role in X-chromosome inactivation, regulates cell proliferation in tumor cells, and inhibits apoptosis in acute myocardial infarction. On the other hand, miR-7a-5p is involved in cardiomyocytes injury in myocardial ischemia/reperfusion. However, their roles in LPS-induced damage remain unclear. Objectives: This study aimed at using siRNA transfection and lentivirus infection to regulate the expression of xist and miR-7a-5p, and to evaluate their effects on LPS-induced myocardial damage. Method: Mice cardiomyocytes (MCM) cells were divided into six groups, namely the control group, the LPS group, the LPS + lncRNA(-) group, the LPS + lncRNA(+) group, the LPS + miRNA(-) group, and the LPS + miRNA(+) group. Quantitative real-time PCR (qRT-PCR) was performed to assay for the RNA expressions of xist, miR-7a-5p, peroxisome proliferator-activated receptor-γ coactivator-1a (PGC-1a), and recombinant mitochondrial transcription factor A (Tfam) in all the groups. The ATP level was determined using the adenosine triphosphate (ATP) assay kit according to the manufacturer's instructions. Flow cytometry was performed to estimate the level of apoptosis and proliferation in cells in each group. Results: The level of xist in the myocardial cells was markedly higher in the LPS group compared with the control group; however, it was reduced in the LPS+ lncRNA(-) group. There was no significant difference in the expression of xist among the LPS+miRNA(-), LPS+miRNA(+), and LPS groups. Moreover, the expression of mir-7a-5p was significantly reduced in myocardial cells in the LPS group, and moderately reduced in the LPS+ miRNA(-) group, but remarkably elevated in the LPS+ miRNA(+) group (P<0.05). The expression of mir-7a-5p was comparably similar in the LPS+ lncRNA(-) group, LPS+ lncRNA(+) group, and LPS groups. Further, the levels of PGC-1a, and Tfam were determined. In the LPS group, the expression of PGC-1a was significantly reduced but elevated in the LPS+lncRNA(-) and LPS+ miRNA(-) groups (P<0.05). There was no significant difference in the level of PGC-1a among the LPS, LPS+ lncRNA(+), and LPS+ miRNA(+) groups. The expression of Tfam was markedly reduced in the LPS group (P < 0.05), but elevated after the suppression of xist and mir-7a-5p. The expression of Tfam was not significantly different among the LPS group, LPS+ lncRNA(+) and LPS+ miRNA(+) groups. Notably, overexpression of mir-7a-5p had a mild effect on the expression of Tfam in the LPS+ miRNA(+) group compared with the control group. Besides, ATP expression in the LPS group was markedly reduced, but elevated after the inhibition of xist and mir-7a-5p. Suppressing the expression of xist or mir-7a-5p resulted in reduced cell apoptosis and increased cell proliferation. Conclusions: In this study, we established that down-regulation of xist and mir-7a-5p reduces apoptosis in response to LPS.		Int J Med Sci. 2020 Sep 16;17(16):2570-2577. doi: 10.7150/ijms.45408. eCollection 2020.
5616	LncRNA	GAS5	miR-106b	PTEN	Glioma Cells	Glioma	Homo sapiens (human)  	qRT-PCR;Western blot;Luciferase reporter assay;	32991951	LncRNA GAS5 regulates epithelial-mesenchymal transition and viability of glioma cells by targeting microRNA-106b and regulating PTEN expression.	LncRNA growth arrest special 5 (GAS5) and microRNA-106b (miR-106b) have been reported to be involved in the regulation of gliomas. However, their precise mechanisms in regulating the progression and development of gliomas remain unclear. We aimed to investigate the interaction between GAS5 and miR-106b, and their influence on the proliferation, migration, and invasion of gliomas cells. Western blotting and qRT-PCR were applied for measuring expression of protein and mRNA, respectively. The proliferation, migration, and invasion of cells were measured by MTT, wound healing, and transwell assays, respectively. Dual luciferase reporter assay was applied for confirming the binding site between miR-106b and GAS5, miR-106b and PTEN. Significant higher expression of miR-106b, and lower expression of GAS5 and PTEN in the glioma tissues were observed. The binding sites between GAS5 and miR-106b, miR-106b and PTEN were identified. GAS5 could regulate the expression of PTEN through targeting miR-106b, and further influence EMT process, and the proliferation, migration, and invasion of gliomas cells. Meanwhile, PTEN could remarkably inhibited the proliferation, migration and invasion of glioma cells. The influence of PTEN on glioma cells and EMT was similar to GAS5. GAS5 could regulate the EMT process, and the migration of gliomas cells through miR-106b targeting PTEN. Therefore, our findings may provide a new thought for the study of pathogenesis and treatment of glioma.		Neurosci Res. 2021 Sep;170:32-40. doi: 10.1016/j.neures.2020.08.009. Epub 2020 Sep 28.
5617	LncRNA	TCONS_00026334	miR-548n	TP53INP1	Crc Cell Lines	Colorectal Cancer	Homo sapiens (human)  	microarray;	32986920	Long noncoding RNA TCONS_00026334 is involved in suppressing the progression of colorectal cancer by regulating miR-548n/TP53INP1 signaling pathway.	Recently, long noncoding RNAs (lncRNAs) were recognized as significant therapeutic targets in tumors. Our previous microarray analysis showed that lncRNA TCONS_000026334 expression was reduced in metastatic colorectal cancer (CRC) tissues. The objective of this study was to research the biological functions of TCONS_000026334 and the potential mechanism during the development of CRC. TCONS_00026334 transcription levels were detected in CRC tissues from 86 patients and different CRC cell lines. The clinical prognosis factors related to TCONS_00026334 expression were then analyzed. TCONS_000026334 was overexpressed from plasmid pcDNA3.1-TCONS_ 000026334 or knocked down using a small interfering RNA (siRNA). Furthermore, bioinformatics approach and luciferase reporter gene assays were utilized to search for candidate miRNAs of TCONS_00026334 and identify the downstream target genes. The results indicated that TCONS_00026334 expression in 86 CRC tissues was markedly lower than that in non-cancerous tissues. The aberrant expression of TCONS_00026334 correlated negatively with larger tumor size, distant metastasis, serological carcinoembryonic antigen level, and unfavorable survival of patients with CRC. TCONS_00026334 overexpression could inhibit the aggressive phenotypes of CRC in vitro and in vivo. Conversely, TCONS_00026334 silencing accelerated CRC cell proliferation and invasion. We then verified that TCONS_00026334 upregulated the expression level of TP53INP1, a target gene of miR-548n, via direct binding to miR-548n as a competing endogenous RNA. Taken together, our study showed that TCONS_00026334 acts as an anti-tumor and anti-metastatic gene by regulating the miR548n/TP53INP1 axis in the development of CRC.		Cancer Med. 2020 Nov;9(22):8639-8649. doi: 10.1002/cam4.3473. Epub 2020 Sep 28.
5618	LncRNA	ZNF800	NA	PTEN	Vascular Smooth Muscle Cells	Atherosclerosis	Homo sapiens (human)  	qPCR;RT-qPCR;Western blot;	32971395	Long noncoding RNA ZNF800 suppresses proliferation and migration of vascular smooth muscle cells by upregulating PTEN and inhibiting AKT/mTOR/HIF-1a signaling.	BACKGROUND AND AIMS: Long noncoding RNAs (lncRNAs) have recently been implicated in many biological and disease processes, but the exact mechanism of their involvement in atherosclerosis is unclear. The aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) is a major contributor to the development of atherosclerotic lesions. This study aimed to investigate the potential effects of lncRNA ZNF800, a previously uncharacterized lncRNA, on VSMC proliferation and migration. METHODS: The expression of lncRNA ZNF800 in atherosclerotic plaque tissues was detected using reverse transcription-quantitative PCR (RT-qPCR), while the role and mechanism of lncRNA ZNF800 in proliferation and migration of VSMCs were investigated by CCK8 assay, transwell assay, scratch wound assay, RT-qPCR and Western blot. RESULTS: We found that lncRNA ZNF800 was significantly more abundant in atherosclerotic plaque tissues, and substantially suppressed the proliferation and migration of VSMCs. LncRNA ZNF800 had no effect on phosphatase and tensin homolog deleted on chromosome 10 (PTEN) mRNA expression but dramatically increased the levels of PTEN protein. Enhanced lncRNA ZNF800 expression inhibited the activity of the AKT/mTOR/HIF-1a signaling pathway, downregulated the expression of vascular endothelial growth factor a (VEGF-a) and matrix metalloproteinase 1 (MMP1), and suppressed VSMC proliferation and migration. These inhibitory effects of lncRNA ZNF800 were abolished by knockdown of PTEN. The inhibitory effects of lncRNA ZNF800 on cell proliferation and migration and the expression of VEGF-a and MMP1 were exacerbated by HIF-1a knockdown in VSMCs. CONCLUSIONS: These findings demonstrated that lncRNA ZNF800 suppressed VSMC proliferation and migration by interacting with PTEN through a mechanism involving AKT/mTOR/HIF-1a signaling. Therefore, it may play a key atheroprotective role and represent a potential therapeutic target for atherosclerosis-related diseases.		Atherosclerosis. 2020 Nov;312:43-53. doi: 10.1016/j.atherosclerosis.2020.09.007. Epub 2020 Sep 14.
5619	LncRNA	PVT1	miR-181a-5p	TGF-bR1	Hk-2 Cells	Renal Fibrosis	Homo sapiens (human)  	ELISA;qRT-PCR;	32921988	LncRNA PVT1 Suppresses the Progression of Renal Fibrosis via Inactivation of TGF-b Signaling Pathway.	BACKGROUND: Renal fibrosis is a frequent pathway leading to end-stage kidney dysfunction. In addition, renal fibrosis is the ultimate manifestation of chronic kidney diseases (CKD). Long noncoding RNAs (lncRNAs) are known to be involved in occurrence of renal fibrosis, and lncRNA plasmacytoma variant translocation 1 (PVT1) has been reported to act as a key biomarker in renal diseases. However, the role of PVT1 in renal fibrosis remains unclear. MATERIALS AND METHODS: HK-2 cells were treated with TGF-b1 to mimic renal fibrosis in vitro. Gene and protein expressions in HK-2 cells were measured by qRT-PCR and Western-blot, respectively. ELISA was used to test the level of creatinine (CR) and blood urea nitrogen (BUN) in serum of mice. Additionally, unilateral ureteral obstruction (UUO)-induced renal fibrosis mice model was established to investigate the effect of PVT1 on renal fibrosis in vivo. RESULTS: PVT1 was upregulated in TGF-b1-treated HK-2 cells. In addition, TGF-b1-induced upregulation of a-SMA and fibronectin in HK-2 cells was significantly reversed by PVT1 knockdown. Meanwhile, PVT1 bound to miR-181a-5p in HK-2 cells. Moreover, miR-181a-5p directly targeted TGF-bR1. Furthermore, miR-181a-5p antagonist could significantly reverse the anti-fibrotic effect of PVT1 knockdown. Besides, knockdown of PVT1 notably attenuated the symptom of renal fibrosis in vivo. CONCLUSION: Knockdown of PVT1 significantly inhibited the progression of renal fibrosis in vitro and in vivo. Thus, PVT1 may serve as a potential target for the treatment of renal fibrosis.		Drug Des Devel Ther. 2020 Aug 26;14:3547-3557. doi: 10.2147/DDDT.S245244. eCollection 2020.
5620	LncRNA	XIST	miR-200a-3p	NRP1	Y79 Cells	Retinoblastoma	Homo sapiens (human)	qRT-PCR;Flow Cytometry assay;	32904674	Carboplatin Inhibits the Progression of Retinoblastoma Through IncRNA XIST/miR-200a-3p/NRP1 Axis.	OBJECTIVE: This study was set out to explore the expression and related mechanism of XIST and miR-200a-3p in retinoblastoma (Rb). PATIENTS AND METHODS: Fifty-four children with Rb who came to our hospital for surgery from January 2018 to September 2019 were collected. In addition, Rb cells and human retinal epithelial cells were purchased. XIST-siRNA (si-XIST), XIST-shRNA (sh-XIST), empty vector plasmid (siRNA-NC), miR-200a-3p-mimics and miR -200a-3p-inhibition were transfected into Y79 cells. The expression of XIST and miR-200a-3p in the samples were determined by qRT-PCR. b-catenin, cyclin B1, cyclin D1, Bax, Caspase-3, N-cadherin, vimentin, Snail, E-Cadherin and ZO-1 protein levels were measured by WB. MTT, Transwell and flow cytometry were utilized to detect cell proliferation, invasion, and apoptosis, respectively. RESULTS: XIST was highly expressed while miR-200a-3p was lowly expressed in patients' tissues, and the AUC of both was over 0.8. XIST and miR-200a-3p was related to differentiation degree in Rb patients. Y79 cells were selected for transfection. Compared with the siRNA-NC group, XIST was significantly reduced in the siRNA-XIST group, and it was significantly increased in the shRNA-XIST group (P<0.01). The proliferation capacity of siRNA-XIST group was decreased, while that of shRNA-XIST group was up-regulated. The apoptosis rate of siRNA-XIST group was significantly up-regulated, while that of shRNA-XIST group was decreased (P<0.001). The invasive capacity of siRNA-XIST group was decreased, while that of shRNA-XIST group was up-regulated (P<0.001). Silencing XIST and over-expressed miR-200a-3p could inhibit cell epithelial-mesenchymal transition (EMT), proliferation, invasion, and promote apoptosis. WB detection showed that Carboplatin + LncRNA XIST intervention group could more significantly inhibit b-catenin, cyclin B1, cyclin D1, N-cadherin, vimentin, Snail protein, and promote the up-regulation of Bax, Caspase-3, E-Cadherin and ZO-1 expression. CONCLUSION: Inhibition of XIST expression can up-regulate miR-200a-3p-mediated PI3K-Akt/MAPK-ERK signaling pathway and affect cell EMT, proliferation, invasion, and apoptosis, which is expected to be a potential therapeutic target for Rb.		Drug Des Devel Ther. 2020 Aug 21;14:3417-3427. doi: 10.2147/DDDT.S256813. eCollection 2020.
5621	LncRNA	ZFAS1	miR-590-3p	Cdc42	Nsclc Cells	Nonsmall Cell Lung Cancer	Homo sapiens (human)  	Luciferase reporter assay;	32841053	Long Noncoding RNA ZFAS1 Promotes Progression of NSCLC via Regulating of miR-590-3p.	The incidence and mortality rate of nonsmall cell lung cancer (NSCLC) are continuously increasing. Recently, the important roles of long noncoding ribonucleic acid (lncRNA) zinc finger antisense1 (ZFAS1) in the development of many disease have been proved. However, the roles of ZFAS1 in NSCLC are still not completely understood. Thus, this study aimed to explore the potential roles and underlying mechanisms of lncRNA ZFAS1 in the progression of NSCLC. Our results demonstrated that lncRNA ZFAS1 expression was significantly upregulated in NSCLC tissues and cell lines. Loss-of-function experiments revealed that lncRNA ZFAS1 inhibition could remarkably suppress NSCLC cells proliferation in vitro. Bioinformatic analysis and luciferase reporter assay revealed that lncRNA ZFAS1 directly interacted with miR-590-3p. Rescue experiments showed that miR-590-3p inhibitor reversed the cell proliferation function of lncRNA ZFAS1 knockdown in vitro. Furthermore, we confirmed that lncRNA ZFAS1 inhibited cell division cycle 42 (Cdc42) expression by regulating of miR-590-3p in NSCLC cells. Therefore, our study indicates that lncRNA ZFAS1/miR-590-3p axis is involved in NSCLC cell proliferation. It also suggests that lncRNA ZFAS1 is a putative tumor oncogene in NSCLC.		Cell Transplant. 2020 Jan-Dec;29:963689720919435. doi: 10.1177/0963689720919435.
5622	LncRNA	TUG1	miR-532-5p	Sox8	H9C2 Cells	Cardiomyocyte Injury	Rattus (rat)	RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	32833900	Long Noncoding RNA Taurine-Upregulated Gene 1 Knockdown Protects Cardiomyocytes Against Hypoxia/Reoxygenation-induced Injury Through Regulating miR-532-5p/Sox8 Axis.	BACKGROUND: Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to involve in the processing of cardiac ischemia/reperfusion injury after myocardial infarction. Thus, this study further investigates the underlying mechanisms of TUG1 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro. METHODS: Cell viability, apoptosis, and migration and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and transwell assay, respectively. Western blot was used to examine the levels of matrix metallopeptidase 9, matrix metallopeptidase 2, and sex determining region Y-box transcription factor 8 (Sox8) protein. Levels of lactate dehydrogenase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were detected using commercial kits. Levels of TUG1, microRNA-532-5p (miR-532-5p), and Sox8 were detected by quantitative real-time polymerase chain reaction. The interaction between miR-532-5p and Sox8 or TUG1 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assay. RESULTS: H/R induced rat cardiomyocyte H9c2 injury by inhibiting cell viability, migration and invasion, promoting cell apoptosis, and stimulating oxidative stress. H/R-induced H9c2 injury upregulated the level of TUG1, and TUG1 knockdown alleviated H/R-induced cardiomyocyte injury. TUG1 directly bound to miR-532-5p, and miR-532-5p inhibition reversed the action of TUG1 knockdown on H/R-induced cardiomyocyte injury. Sox8 was a target of miR-532-5p, and miR-532-5p blunted H/R-induced cardiomyocyte injury by targeting Sox8. In addition, TUG1 knockdown inhibited H/R-induced Sox8 elevation through miR-532-5p in H9c2 cells. CONCLUSION: TUG1 silence ameliorated H/R-induced cardiomyocytes injury through regulating miR-532-5p/Sox8 axis, suggesting a potential therapeutic target for preventing myocardial ischemia/reperfusion injury.		J Cardiovasc Pharmacol. 2020 Nov;76(5):556-563. doi: 10.1097/FJC.0000000000000895.
5623	LncRNA	OIP5-AS1	miR-26a-5p	NA	Human Umbilical Vein Endothelial Cells	Atherosclerosis	Homo sapiens (human)	Dual-luciferase reporter assay;RNA immunoprecipitation;RNA pull-down assay;Western blot;Luciferase reporter assay;RNA immunoprecipitation;RNA pull-down;	32833899	Long Noncoding RNA OIP5-AS1 Contributes to the Progression of Atherosclerosis by Targeting miR-26a-5p Through the AKT/NF-kB Pathway.	Atherosclerosis (AS) is a cardiovascular disease caused by multiple factors, leading to high mortality and morbidity in aged people. Some long noncoding RNAs have been reported to be associated with AS progression. However, the roles of OIP5-AS1 in AS development are still little known. In this study, the levels of OIP5-AS1 and miR-26a-5p in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs) were determined by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 assay and flow cytometric analysis, respectively. The protein levels of proliferating cell nuclear antigen, B-cell lymphoma-2, cleaved caspase 3, inflammatory cytokines (IL-6 and IL-1b), protein kinase B (AKT), p-AKT, p65, p-p65, IkBa, and p-IkBa were detected by Western blot analysis. The targeting relationship between OIP5-AS1 and miR-26a-5p was verified by dual-luciferase reporter assay, RNA immunoprecipitation assay, and RNA pull-down assay. As a result, the expression of OIP5-AS1 was upregulated and miR-26a-5p was downregulated in ox-LDL-treated HUVECs. MiR-26a-5p was identified as a direct target of OIP5-AS1. OIP5-AS1 knockdown reversed the inhibitory effect on cell proliferation and the promotional effects on apoptosis and inflammation induced by ox-LDL treatment in HUVECs. Interestingly, the effects caused by OIP5-AS1 knockdown were further attenuated by miR-26a-5p inhibition. Furthermore, OIP5-AS1 knockdown blocked the AKT/NF-kB pathway by regulating miR-26a-5p expression. In conclusion, OIP5-AS1 knockdown promoted cell proliferation and suppressed apoptosis and inflammatory response in ox-LDL-treated HUVECs by targeting miR-26a-5p through blocking the AKT/NF-kB pathway, indicating a promising strategy for AS treatment.		J Cardiovasc Pharmacol. 2020 Nov;76(5):635-644. doi: 10.1097/FJC.0000000000000889.
5624	LncRNA	PVT1	miR-149	PAF	Human Small Airway Epithelial Cells	Asthma	Homo sapiens (human)	ELISA;Western blot;	32830409	LncRNA PVT1 exacerbates the inflammation and cell-barrier injury during asthma by regulating miR-149.	BACKGROUND: Asthma is a prevailing respiratory disease among children, characterized by allergic airway inflammation, airway remodeling, and airway hyperresponsiveness. Although it is well-known that long non-coding RNAs (lncRNAs) are linked to a variety of human diseases and well-documented, very few studies explore its role in asthma. In this study, we investigate the effects of lncRNA PVT1 on the promotion of airway inflammation and its associated mechanisms. METHODS AND MATERIALS: Human small airway epithelial cells (HSAECs) with PVT1 overexpressed or knocked down were constructed, and platelet activating factor (PAF) was used to treat HSAECs to mimic the pathological process of asthma in vitro. The expressions of prostaglandin E2 (PGE2), interleukin-1b (IL-1b), IL-6, and tumor necrosis factor-a (TNF-a) were measured by enzyme-linked immunosorbent assay (ELISA). The expressions of PKC, MyD88, and NF-ĸB were measured by Western blot. Monolayer permeability of HSAECs was also compared within different groups. Luciferase reporter gene assay was employed to detect the targeting relationship between PVT1 and miR-149. RESULTS: The knockdown of PVT1 attenuated the levels of inflammatory factors induced by PAF and destruction of cell-barrier function. The overexpression of PVT1 facilitated the pathological development. Additionally, miR-149 was identified as a target microRNA of PVT1, and the overexpression of miR-149 could reverse the effects of PVT1 on PAF-induced HSAECs. CONCLUSION: These findings suggest that PVT1 may represent a novel potential target for treatment of asthma.		J Biochem Mol Toxicol. 2020 Nov;34(11):e22563. doi: 10.1002/jbt.22563. Epub 2020 Aug 24.
5625	LncRNA	lincRNA-COX2	let-7a	STAT3	Pulmonary Arterial Smooth Muscle Cells	Pulmonary Arterial Hypertension	Homo sapiens (human)  	CCK-8 assay;RT-PCR;Western blot;Flow Cytometry assay;	32803651	LincRNA-Cox2 promotes pulmonary arterial hypertension by regulating the let-7a-mediated STAT3 signaling pathway.	It is well supported by the literature that the proliferation and migration of pulmonary arterial smooth muscle cells (PASMCs) are critical for the development of pulmonary arterial hypertension (PAH). Long intergenic noncoding RNA COX2 (lincRNA-COX2) is a regulator of inflammation and might be conducive to the progression of atherosclerosis, while its role in PAH is still unclear. This study was performed to explore the role and mechanism of lincRNA-COX2 in PASMCs proliferation and migration in an anaerobic environment. PASMCs were treated by hypoxia to construct PAH cell models. RT-PCR and western blot were recruited to evaluate the expression levels of lincRNA-COX2, miR-let-7a and STAT3. Their roles in proliferation and cell and migration of PASMCs were determined by the CCK-8 assay, wound-healing assay, and flow cytometry. In peripheral blood samples from PAH patients and hypoxic PASMCs, lincRNA-COX2 expression was enhanced. Silencing lincRNA-COX2 inhibited hypoxia-induced PASMCs proliferation by influencing the G2/M phase of the cell cycle. Meanwhile, lincRNA-COX2 regulated STAT3 through miR-let-7a and its effects on hypoxic PASMCs worked through miR-let-7a/STAT3 axis. To conclude, silencing lincRNA-COX2 attenuated the development of hypoxic PASMCs. LincRNA-COX2/miR-let-7a/STAT3 axis might be considered as a novel target to treat PAH.		Mol Cell Biochem. 2020 Dec;475(1-2):239-247. doi: 10.1007/s11010-020-03877-6. Epub 2020 Aug 14.
5626	LncRNA	LEF1-AS1	miR-10a-5p	MSI1	Hepatocellular Carcinoma Cells	Hepatocellular Carcinoma	Homo sapiens (human)  	microarray;	32786108	Long noncoding RNA LEF1-AS1 acts as a microRNA-10a-5p regulator to enhance MSI1 expression and promote chemoresistance in hepatocellular carcinoma cells through activating AKT signaling pathway.	Long noncoding RNAs (lncRNAs) contribute to the development of hepatocellular carcinoma (HCC), which could regulate various HCC biological characteristics. Here, the study seeks to investigate the role of lncRNA LEF1-AS1 in HCC cell chemoresistance by regulating microRNA (miR)-10a-5p and Musashi1 (MSI1). The microarray-based analysis was employed to identify the HCC-related lncRNA-miRNA-gene regulatory network. Expression patterns of LEF1-AS1, miR-10a-5p, and MSI1 in the HCC cell lines, tissues were accessed by means of reverse transcription-quantitative polymerase chain reaction. Next, the interaction among LEF1-AS1, miR-10a-5p, and MSI1 in HCC was accessed by bioinformatics and dual-luciferase reporter gene assay. Then, the cell line resistant to cisplatin was established, which was then treated with sh/oe-lncRNA LEF1-AS1, miR-10a-5p-mimic, and oe/sh-MSI1 vectors alone or in combination. Afterward, the effect of LEF1-AS1, miR-10a-5p, and MSI1 on HCC cell chemoresistance, proliferation, and apoptosis was assessed. At last, in vivo experiments confirmed the role of MSI1 in tumor growth and chemoresistance in HCC. LEF1-AS1 might potentially affect the growth and chemoresistance of HCC cells by regulating miR-10a-5p and MSI1. LEF1-AS1 and MSI1 expression patterns were elevated, while miR-10a-5p was repressed in HCC tissues and cell lines. LEF1-AS1 combined to miR-10a-5p and regulated MSI1, thereby activating the protein kinase B (AKT) signaling pathway. Knockdown of LEF1-AS1 and MSI1 or elevation of miR-10a-5p compromised the proliferation of Huh7 cell line resistant to DDP and promoted its chemosensitivity and apoptosis. At last, these in vitro findings were also confirmed in vivo. Our results unraveled LEF1-AS1 acts as a miR-10a-5p modulator to promote chemoresistance of HCC cells by stimulating MSI1 and activating the AKT signaling pathway, which might provide a novel therapeutic target for HCC.		J Cell Biochem. 2021 Jan;122(1):86-99. doi: 10.1002/jcb.29833. Epub 2020 Aug 12.
5627	LncRNA	GAS5	miR-92a-3p	E4BP4	Sle Cd4(+) T Cells	Systemic Lupus Erythematous	Homo sapiens (human)  	qRT-PCR 	32781006	LncRNA GAS5 suppresses CD4(+) T cell activation by upregulating E4BP4 via inhibiting miR-92a-3p in systemic lupus erythematosus.	Increasing evidence reveals that long noncoding RNAs (lncRNAs) are associated with autoimmune and inflammatory diseases, such as systemic lupus erythematosus (SLE). In this study, we aimed to explore the role of lncRNA growth arrest specific 5 (GAS5) in the pathogenesis of SLE. We found that lncRNA GAS5 was decreased in CD4(+) T cells and plasma from SLE patients. Overepression of GAS5 inhibited activation of normal CD4(+) T cells and attenuated the self-reactivity of SLE CD4(+) T cells. Additionally, we demonstrated that adenovirus E4 binding protein 4 (E4BP4) was involved in lncRNA GAS5-mediated inhibition of CD4(+) T cell activation. GAS5 could upregulate E4BP4 by inhibiting miR-92a-3p. Taken together, our results indicate that the GAS5/miR-92a-3p/E4BP4 pathway plays an important role in inhibiting CD4(+) T cell activation in SLE, thus providing a potential therapeutic target for SLE treatment.		Immunol Lett. 2020 Nov;227:41-47. doi: 10.1016/j.imlet.2020.08.001. Epub 2020 Aug 8.
5628	LncRNA	DANCR	miR-320a	CTNNB1	Bmscs	Osteoporosis	Homo sapiens (human)  	qRT-PCR;Western blot;luciferase assay;	32778797	LncRNA DANCR and miR-320a suppressed osteogenic differentiation in osteoporosis by directly inhibiting the Wnt/b-catenin signaling pathway.	Our study aimed to determine how lncRNA DANCR, miR-320a, and CTNNB1 interact with each other and regulate osteogenic differentiation in osteoporosis. qRT-PCR and western blotting were performed to determine the expression of DANCR, miR-320a, CTNNB1, and the osteoporosis- or Wnt/b-catenin pathway-related markers T-cell factor 1 (TCF-1), runt-related transcription factor 2 (RUNX2), alkaline phosphatase (ALP), osteocalcin (OCN), and osteopontin (OPN). Interactions between CTNNB1, DANCR, and miR-320a were predicted by bioinformatics approaches and validated using a luciferase assay. Osteoblastic phenotypes were evaluated by ALP staining, ALP activity assay and Alizarin Red staining. The bilateral ovariectomy method was used to establish an in vivo osteoporosis model. Bone morphological changes were examined using hematoxylin and eosin (H&E) and Alcian Blue staining. The expression levels of DANCR and miR-320a in BMSCs derived from osteoporosis patients were upregulated, whereas CTNNB1 expression was downregulated compared with that in healthy controls. Importantly, we demonstrated that miR-320a and DANCR acted independently from each other and both inhibited CTNNB1 expression, whereas the inhibitory effect was additive when miR-320a and DANCR were cooverexpressed. Moreover, we found that DANCR overexpression largely abrogated the effect of the miR-320a inhibitor on CTNNB1 expression and the Wnt/b-catenin signaling pathway in BMSCs during osteogenic differentiation. We further confirmed the results above in BMSCs derived from an osteoporosis animal model. Taken together, our findings revealed that DANCR and miR-320a regulated the Wnt/b-catenin signaling pathway during osteogenic differentiation in osteoporosis through CTNNB1 inhibition. Our results highlight the potential value of DANCR and miR-320a as promising therapeutic targets for osteoporosis treatment.		Exp Mol Med. 2020 Aug;52(8):1310-1325. doi: 10.1038/s12276-020-0475-0. Epub 2020 Aug 11.
5629	LncRNA	SLCO4A1-AS1	miR-4701-5p	NFE2L1	Luad Tissues And Cells	Lung Adenocarcinoma	Homo sapiens (human)	Rescue assay;	32762035	SLCO4A1-AS1 promotes cell growth and induces resistance in lung adenocarcinoma by modulating miR-4701-5p/NFE2L1 axis to activate WNT pathway.	Long noncoding RNAs (lncRNAs) possessed essential functions in the biological behaviors of various human cancers. SLCO4A1 antisense RNA 1 (SLCO4A1-AS1) is a lncRNA that has been reported as a oncogenic regulator in colorectal cancer and bladder cancer. However, whether it exerted functions in the gene expression and cellular processes in lung adenocarcinoma (LUAD) remains still obscure. In the present research, we unveiled the high level of SLCO4A1-AS1 in LUAD tissues and cells. Moreover, functional assays indicated that SLCO4A-AS1 facilitated LUAD cell proliferation, motility, and cisplatin-resistance. Besides, mechanism investigation revealed that miR-4701-5p could interact with SLCO4A1-AS1 and directly target to NFE2L1. The expression correlation between miR-4701-5p and SLCO4A1-AS1 or NFE2L1 was found to be negative. Moreover, NFE2L1 was expressed at a same tendency with SLCO4A1-AS1 in LUAD tissues and cells. In addition, it was confirmed that NFE2L1 was involved in SLCO4A1-AS1-mediated activation of WNT pathway. According to rescue assays, NFE2L1 could involve in SLCO4A1-AS1-mediated LUAD cell growth. Conclusively, our study demonstrated that SLCO4A1-AS1 facilitated cell growth and enhanced the resistance of LUAD cells to chemotherapy via activating WNT pathway through miR-4701-5p/NFE2L1 axis.		Cancer Med. 2020 Oct;9(19):7205-7217. doi: 10.1002/cam4.3270. Epub 2020 Aug 6.
5630	LncRNA	ERICD	miR-664a	E2F1	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	32749762	Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells.	Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD.		Cell Biol Int. 2020 Nov;44(11):2263-2274. doi: 10.1002/cbin.11434. Epub 2020 Aug 10.
5631	LncRNA	ERICD	miR-664a	ARID3A	Osteosarcoma Cells	Osteosarcoma	Homo sapiens (human)  	qRT-PCR 	32749762	Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells.	Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD.		Cell Biol Int. 2020 Nov;44(11):2263-2274. doi: 10.1002/cbin.11434. Epub 2020 Aug 10.
5632	LncRNA	HCG18	miR-141-3p	WIPF1	Gc Cells	Gastric Cancer	Homo sapiens (human)  	RT-PCR;Western blot;Flow Cytometry assay;	32725768	Long noncoding RNA HCG18 up-regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR-141-3p in gastric cancer.	BACKGROUND: Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. METHODS: RT-PCR was used to detect HCG18 and miR-141-3p expression in GC specimen. GC cell lines (AGS and MKN-28) were exploited as cell model. The biological effect of HCG18 on cancer cells was probed by CCK-8, colony formation, flow cytometry, Transwell and wound-healing experiments in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Interaction between HCG18 and miR-141-3p was determined by bioinformatics analysis, RT-PCR, and luciferase reporter experiments. Downstream gene expression of miR-141-3p, including Wiskott-Aldrich syndrome protein interacting protein family member 1 (WIPF1), Yes associated protein 1 (YAP), and tafazzin (TAZ) were detected using Western blot. RESULTS: HCG18 was markedly up-regulated in GC specimens, while miR-141-3p was markedly down-regulated. Down-regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR-141-3p transfection led to opposite effect. HCG18 could down-regulate miR-141-3p through adsorbing it, and a negative association between HCG18 and miR-141-3p was found in GC specimens. HCG18 promoted WIPF1, YAP and TAZ expression, nonetheless, such influence was reversed by co-transfecting with miR-141-3p. CONCLUSION: HCG18 was aberrantly up-regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR-141-3p expression.		Cancer Med. 2020 Sep;9(18):6752-6765. doi: 10.1002/cam4.3288. Epub 2020 Jul 29.
5633	LncRNA	NEAT1	miR-146b	TRAF6	Human Renal Mesangial Cells	Lupus Nephritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32710276	LncRNA NEAT1 accelerates renal mesangial cell injury via modulating the miR-146b/TRAF6/NF-kB axis in lupus nephritis.	Although growing advances have been made in the regulation of lupus nephritis recently, lupus nephritis is still one of the major causes of death in SLE patients and the pathogenesis remains largely unknown. Therefore, exploring the pathological mechanisms is urgently needed for designing and developing novel therapeutic strategies for lupus nephritis. Human renal mesangial cells (HRMCs) were transfected with sh-NEAT1, miR-146b mimic, pcDNA-NEAT1, miR-146b inhibitor, or sh-TRAF6 to modify their expression. Lipopolysaccharide (LPS) was used to induce inflammatory injury. Cell viability was examined with CCK8. Apoptosis was determined by flow cytometry and Hoechst staining. qRT-PCR and western blot were used to analyze gene expression. The secretion of inflammatory cytokines was examined with ELISA. The bindings of NEAT1 with miR-146b and miR-146b with TRAF6 were tested by dual-luciferase reporter assay. NEAT1 was upregulated in LPS-treated HRMCs. Both the knockdown of NEAT1 and TRAF6 suppressed the LPS-induced inflammatory injury in HRMCs. NEAT1 directly targeted miR-146b to control miR-146b-mediated regulation of TRAF6 expression in HRMCs. NEAT1 promoted the expression of TRAF6 via targeting miR-146b to accelerate the LPS-mediated renal mesangial cell injury in HRMCs. Moreover, TRAF6 activated the NF-kB signaling in HRMCs. NEAT1 accelerated renal mesangial cell injury via directly targeting miR-146b, promoting the expression of TRAF6, and activating the NF-kB signaling in lupus nephritis. Our investigation elucidated novel pathological mechanisms and provided potential therapeutic targets for lupus nephritis.		Cell Tissue Res. 2020 Dec;382(3):627-638. doi: 10.1007/s00441-020-03248-z. Epub 2020 Jul 24.
5634	LncRNA	NEAT1	miR-146b	NF-kB	Human Renal Mesangial Cells	Lupus Nephritis	Homo sapiens (human)	Dual-luciferase reporter assay;ELISA;qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;	32710276	LncRNA NEAT1 accelerates renal mesangial cell injury via modulating the miR-146b/TRAF6/NF-kB axis in lupus nephritis.	Although growing advances have been made in the regulation of lupus nephritis recently, lupus nephritis is still one of the major causes of death in SLE patients and the pathogenesis remains largely unknown. Therefore, exploring the pathological mechanisms is urgently needed for designing and developing novel therapeutic strategies for lupus nephritis. Human renal mesangial cells (HRMCs) were transfected with sh-NEAT1, miR-146b mimic, pcDNA-NEAT1, miR-146b inhibitor, or sh-TRAF6 to modify their expression. Lipopolysaccharide (LPS) was used to induce inflammatory injury. Cell viability was examined with CCK8. Apoptosis was determined by flow cytometry and Hoechst staining. qRT-PCR and western blot were used to analyze gene expression. The secretion of inflammatory cytokines was examined with ELISA. The bindings of NEAT1 with miR-146b and miR-146b with TRAF6 were tested by dual-luciferase reporter assay. NEAT1 was upregulated in LPS-treated HRMCs. Both the knockdown of NEAT1 and TRAF6 suppressed the LPS-induced inflammatory injury in HRMCs. NEAT1 directly targeted miR-146b to control miR-146b-mediated regulation of TRAF6 expression in HRMCs. NEAT1 promoted the expression of TRAF6 via targeting miR-146b to accelerate the LPS-mediated renal mesangial cell injury in HRMCs. Moreover, TRAF6 activated the NF-kB signaling in HRMCs. NEAT1 accelerated renal mesangial cell injury via directly targeting miR-146b, promoting the expression of TRAF6, and activating the NF-kB signaling in lupus nephritis. Our investigation elucidated novel pathological mechanisms and provided potential therapeutic targets for lupus nephritis.		Cell Tissue Res. 2020 Dec;382(3):627-638. doi: 10.1007/s00441-020-03248-z. Epub 2020 Jul 24.
5635	LncRNA	CASC2	miR-532-3p	PAPD5	Vascular Smooth Muscle Cells	Atherosclerosis	Homo sapiens (human)  	Cell proliferation assay;Dual-luciferase reporter assay;qRT-PCR;Western blot;Luciferase reporter assay;	32698757	Long noncoding RNA CASC2 inhibits ox-LDL-mediated vascular smooth muscle cells proliferation and migration via the regulation of miR-532-3p/PAPD5.	BACKGROUND: Studies have demonstrated that long noncoding RNAs (lncRNAs) have essential impacts on the development of atherosclerosis (AS). This study aimed to identify the role and functional mechanism of lncRNA CASC2 in the development and migration of vascular smooth muscle cells (VSMCs). METHOD: The serum of 40 pairs of AS patients and healthy volunteers were collected and the expression of CASC2 was evaluated. qRT-PCR and western blotting were carried out to examine the expression levels of at mRNA and protein level, repectively. Cell proliferation assay, colony formation assay, transwell migration assay, dual-luciferase reporter assay, and wound healing assay were conducted to evaluate cell proliferation, colony formation, migration, transcription, targeting, and self-restoration. RESULTS: The expression levels of CASC2 were decreased, while the expression levels of miR-532-3p were elevated in AS patient samples and VSMCs. Overexpression of CASC2 inhibited the proliferation and migration of VSMCs and enhanced cell apoptosis. CASC2 inhibited the expression of miR-532-3p, and inversely upregulated the expression of PAPD5, which was a target of miR-532-3p. In addition, knockdown of miR-532-3p-mimic and PAPD5 could attenuate the impact of overexpression of CASC2 on proliferation, migration, and apoptosis in ox-LDL-VSMCs. CONCLUSION: CASC2 suppressed cell reproduction and promoted cell apoptosis by regulating the miR-532-3p/PAPD5 axis in ox-LDL-mediated VSMCs. This might be important for AS therapeutics.		Mol Med. 2020 Jul 22;26(1):74. doi: 10.1186/s10020-020-00200-3.
5636	LncRNA	NEAT1	miR-183-5p	FOXP1	Neuroblastoma Cells	Neuroblastoma	Homo sapiens (human)	RACE;	32693640	NEAT1 Negatively Regulates Cell Proliferation and Migration of Neuroblastoma Cells by miR-183-5p/FOXP1 Via the ERK/AKT Pathway.	Neuroblastoma, a malignant tumor of the sympathetic nervous system, is an aggressive extracranial tumor in childhood. Long noncoding RNAs (lncRNAs) have been discovered to play a key role in the eukaryotic regulatory gene network and be involved in a wide variety of biological processes. We observed that the expression of lncRNA nuclear-enriched abundant transcript-1 (NEAT1) was significantly decreased in human neuroblastoma tissues and cell lines, compared with the normal. We observed cell proliferation, migration, and invasion with Cell Counting Kit-8 assay, colony formation assay, and Transwell assay to investigate the effects of NEAT1, miR-183-5p, or FOXP1 on neuroblastoma cells. And we also used StarBase and luciferase reporter gene assay to predict and confirm the interaction of NEAT1, miR-183-5p, and FOXP1 in neuroblastoma cells. First, overexpression of NEAT1 suppressed cell proliferation and played a key role in cell migration and invasion. In addition, NEAT1 was demonstrated to directly interact with miR-183-5p and exerted its antioncogenic role in neuroblastoma by negatively regulating miR-183-5p expression. miR-183-5p suppressed the expression of FOXP1 and regulated cell proliferation and migration by directly targeting FOXP1 mRNA 3'-untranslated region. Moreover, FOXP1 antagonized the effect of miR-183-5p on the phosphorylation of extracellular-regulated kinase/protein kinase B (ERK/AKT), while FOXP1 siRNA increased the reduced phosphorylation of ERK/AKT caused by miR-183-5p inhibitor in neuroblastoma cells. Taken together, these data showed that NEAT1 negatively regulated cell proliferation and migration of neuroblastoma by the miR-183-5p/FOXP1 axis via suppression of the ERK/AKT pathway. Our findings may provide a new target for the study of pathogenesis and treatment of neuroblastoma.		Cell Transplant. 2020 Jan-Dec;29:963689720943608. doi: 10.1177/0963689720943608.
5637	LncRNA	PRKCQ-AS1	miR-1287-5p	YBX1	Crc Cell	Colorectal Cancer	Homo sapiens (human)	Rescue assay;	32619070	Long noncoding RNA PRKCQ-AS1 promotes CRC cell proliferation and migration via modulating miR-1287-5p/YBX1 axis.	Colorectal cancer (CRC) brings more than 600 000 deaths every year around the globe, making itself the third most frequently occurred carcinoma. The great progress human achieved in diagnosis and treatment of various cancers has failed to reverse this trend. Fortunately, growing evidence has implied the relationship between lncRNAs and cancer progression. Long noncoding RNA (lncRNA) PRKCQ-AS1 was heightened in CRC cells and tissues and related with dismal prognosis of CRC patients. Knockdown of PRKCQ-AS1 would induce a decrease in proliferative and migrating ability of CRC cells. Also, PRKCQ-AS1 enriched in cytoplasm of CRC cells and negatively regulated miR-1287-5p level. More important, PRKCQ-AS1 could bind to argonaute 2 and function in the RNA-induced silencing complex with miR-1287-5p. Therefore, PRKCQ-AS1 was a competing endogenous RNA for miR-1287-5p. Subsequently, it was validated that miR-1287-5p could suppress the proliferative and migratory functions in CRC. Furthermore, PRKCQ-AS1 could upregulate the mRNA and protein level of YBX1 targeted by miR-1287-5p. And YBX1 expression was elevated in CRC cells and tissues. Rescue assays in vitro and in vivo showed that overexpression of YBX1 could partly offset the effect of CRC progression induced by knocking down PRKCQ-AS1, demonstrating PRKCQ-AS1 mediating CRC progression via miR-1287-5p/YBX1 pathway.		J Cell Biochem. 2020 Oct;121(10):4166-4175. doi: 10.1002/jcb.29712. Epub 2020 Jul 3.
5638	LncRNA	Linc02381	miR-590-5p	MAP2K3	Rheumatoid Arthritis-Fibroblast-Like Synoviocytes	Rheumatoid Arthritis	Homo sapiens (human)  	qRT-PCR 	32608996	Linc02381 Exacerbates Rheumatoid Arthritis Through Adsorbing miR-590-5p and Activating the Mitogen-Activated Protein Kinase Signaling Pathway in Rheumatoid arthritis-fibroblast-like synoviocytes.	Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease. New evidence suggested that linc02381 suppressed colorectal cancer progression by regulating PI3 K signaling pathway, but the role of linc02381 in other diseases, such as RA, remains unclear. This study aimed to reveal the mechanism of linc02381 in RA progression. In vivo and in vitro, we found that linc02381 was upregulated in RA synovial tissues or RA fibroblast-like synoviocytes (RA-FLSs, P < 0.01), which were detected by quantitative real-time polymerase chain reaction. Cell Counting Kit-8, EDU, and Transwell assays revealed that linc02381 overexpression enhanced cell proliferation and invasion, and linc02381 knockdown inhibited cell proliferation and invasion in FLSs. Moreover, the results of bioinformatics analysis, luciferase reporter gene assay, and pull-down assay verified that linc02381 could directly bind with miR-590-5p. MiR-590-5p was downregulated in RA-FLSs, and overexpression of linc02381 suppressed expression of miR-590-5p that post-transcriptionally suppressed the expression of mitogen-activated protein kinase kinase 3 (MAP2K3), and overexpression of miR-590-5p reversed the effect of linc02381 overexpression on MAP2K3 expression. MiR-590-5p inhibitor reversed the inhibition effect of linc02381 knockdown on proliferation and invasion of FLSs, which enhanced expression of MAP2K3, and activation of p38 and AP-1 in the MAPK signaling pathway. In summary, linc02381 was upregulated in RA synovial tissues and RA-FLSs, and it exacerbated RA by adsorbing miR-590-5p to activate the MAPK signaling pathway.		Cell Transplant. 2020 Jan-Dec;29:963689720938023. doi: 10.1177/0963689720938023.
5639	LncRNA	GAS5	miR-21	mTOR	Coronary Artery Disease Patients	Coronary Artery Disease	Homo sapiens (human)  	qRT-PCR 	32557866	Association of genetic variants in lncRNA GAS5/miR-21/mTOR axis with risk and prognosis of coronary artery disease among a Chinese population.	BACKGROUND: Allowing for the significance of single nucleotide polymorphisms (SNPs) in reflecting disease risk, this investigation attempted to uncover whether SNPs situated in lncRNA GAS5/miR-21/mTOR axis were associated with risk and prognosis of coronary heart disease (CHD) among a Chinese Han population. METHODS: Altogether 436 patients with CHD were recruited as cases, and meanwhile, 471 healthy volunteers were included into the control group. Besides, SNPs of GAS5/MIR-21/mTOR axis were genotyped utilizing mass spectrometry. Chi-square test was applied to figure out SNPs that were strongly associated with CHD risk and prognosis, and combined effects of SNPs and environmental parameters on CHD risk were evaluated through multifactor dimensionality reduction (MDR) model. RESULTS: Single nucleotide polymorphisms of GAS5 (ie, rs2067079 and rs6790), MIR-21 (ie, rs1292037), and mTOR (rs2295080, rs2536, and rs1034528) were associated with susceptibility to CHD, and also Gensini score change of patients with CHD (P < .05). MDR results further demonstrated that rs2067079 and rs2536 were strongly interactive in elevating CHD risk (P < .05), while smoking, rs6790 and rs2295080 showed powerful reciprocity in predicting Gensini score change of patients with CHD (P < .05). CONCLUSION: Single nucleotide polymorphisms of lncRNA GAS5/miR-21/mTOR axis might interact with smoking to regulate CHD risk, which was conducive to diagnosis and prognostic anticipation of CHD.		J Clin Lab Anal. 2020 Oct;34(10):e23430. doi: 10.1002/jcla.23430. Epub 2020 Jun 17.
5640	LncRNA	lncRNA- RP11-156p1.3	miRNA-4764-5p	RFTN1	Hepg2 Cell Line	Hepatocellular Carcinoma	Homo sapiens (human)  	qRT-PCR 	32544548	lncRNA- RP11-156p1.3, novel diagnostic and therapeutic targeting via CRISPR/Cas9 editing in hepatocellular carcinoma.	We aim to characterize the expression of RNA panel in HCC. We assessed the expression of HCC-associated mRNA, miRNA and lncRNA network by real time PCR in sera and tissue samples. In a proof-of-principle approach, CRISPR cas9 mediated knock out for lncRNA- RP11-156p1.3 was performed in HEPG2 cell line to validate the role of the chosen RNA in HCC pathogenesis. The differential expression of RFTN1 mRNA, lncRNA- RP11-156p1.3 and miRNA-4764-5p was statistically different among the studied groups. After CRISPR cas9 mediated knockout of lncRNA- RP11-156p1.3 in HEPG2 cells, there was significant decrease in cell count and viability with reversal of the expression of the chosen RNAs. The chosen RNAs play a significant role in HCC pathogenesis and may be potential diagnostic and therapeutic targets.		Genomics. 2020 Sep;112(5):3306-3314. doi: 10.1016/j.ygeno.2020.06.020. Epub 2020 Jun 13.
5641	LncRNA	TSIX	miR-1283	TP53INP2	Sci Patients	Spinal Cord Injury	Homo sapiens (human)  	qRT-PCR 	32535070	Dysregulation in the expression of (lncRNA-TSIX, TP53INP2 mRNA, miRNA-1283) in spinal cord injury.	AIM: The objective of this study is to examine the alterations in the levels of expression of serum lncRNA-TSIX, TP53INP2 mRNA, miRNA-1283 in spinal cord injured (SCI) patients versus healthy control. METHOD: The expression of the selected RNAs in the sera was determined in 23 patients suffering from acute spinal cord injury, 41 individuals with chronic spinal cord injury, and 36 healthy control using real-time reverse-transcription polymerase chain reaction method. RESULTS: The results showed that lncRNA-TSIX and the TP53INP2 mRNA expression levels in SCI patients was overexpressed in comparison to the control group alongside with a significant downregulation of miR-1283. Statistically,there was a highly significant positive correlation between lnc-RNA-TRIX and TP53INP2 mRNA with inverse correlation between miRNA-1283 and lnc-RNA-TRIX based on fold changes. CONCLUSION: Up-regulation of lncRNA-TSIX, TP53INP2 mRNA with downregulation of miRNA-1283 might be closely associated with progression of SCI.		Genomics. 2020 Sep;112(5):3315-3321. doi: 10.1016/j.ygeno.2020.06.018. Epub 2020 Jun 11.
5642	LncRNA	HIX003209	miR-6089	IL-6	Vascular Smooth Muscle Cell	Atherosclerosis	Homo sapiens (human)	qRT-PCR 	32463793	HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089.	Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-a(TNF-a), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-a and IL-1b in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-a, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3'-UTR but not the mut-type 3'-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.		Aging (Albany NY). 2020 May 27;12(10):8913-8922. doi: 10.18632/aging.103079. Epub 2020 May 27.
5643	LncRNA	HIX003209	miR-6089	TNF-a	Vascular Smooth Muscle Cell	Atherosclerosis	Homo sapiens (human)	qRT-PCR 	32463793	HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089.	Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-a(TNF-a), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-a and IL-1b in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-a, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3'-UTR but not the mut-type 3'-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.		Aging (Albany NY). 2020 May 27;12(10):8913-8922. doi: 10.18632/aging.103079. Epub 2020 May 27.
5644	LncRNA	HIX003209	miR-6089	IL-1b	Vascular Smooth Muscle Cell	Atherosclerosis	Homo sapiens (human)	qRT-PCR 	32463793	HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089.	Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-a(TNF-a), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-a and IL-1b in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-a, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3'-UTR but not the mut-type 3'-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.		Aging (Albany NY). 2020 May 27;12(10):8913-8922. doi: 10.18632/aging.103079. Epub 2020 May 27.
5645	LncRNA	SNHG4	miR-138	c-Met	Glioblastoma Cells	Glioblastoma	Homo sapiens (human)  	qRT-PCR 	32427712	LncRNA SNHG4 regulates miR-138/c-Met axis to promote the proliferation of glioblastoma cells.	LncRNA SNHG4 has been reported to be an oncogenic lncRNA in osteosarcoma. Our preliminary analysis of the cancer genome atlas dataset revealed the upregulation of SNHG4 in glioblastoma (GBM). In this study, we confirmed the upregulation of SNHG4 in GBM tissues collected from GBM patients. In addition, lower survival rate of GBM patients was observed in patients with high SNHG4 expression level. SNHG4 can directly interact with miR-138, while SNHG4 expression was no altered after miR-138 overexpression. Interestingly, SNHG4 overexpression led to the upregulation of c-Met, a target of miR-138. Cell counting kit-8 assay showed that miR-138 overexpression resulted in decreased proliferation rate of GBM cells. SNHG4 and c-Met overexpression played opposite roles and reduced the effects of miR-138. Therefore, SNHG4 regulates miR-138/c-Met axis to promote the proliferation of GBM cells.		Neuroreport. 2020 Jun 7;31(9):657-662. doi: 10.1097/WNR.0000000000001469.
5646	LncRNA	MEG3	miR-129-5p	SP-D	Caco2 Cell	Sepsis	Homo sapiens (human)	qRT-PCR 	32410866	MEG3 Alleviated LPS-Induced Intestinal Injury in Sepsis by Modulating miR-129-5p and Surfactant Protein D.	Sepsis and intestinal injury triggered by sepsis are common in intensive care units, which can contribute to a high mortality. lncRNAs can modulate gene expression, and they are closely involved in multiple diseases, including sepsis. In our present study, we investigated the biological function of MEG3 in sepsis, especially during the intestinal injury. Currently, we observed that in LPS-induced sepsis mouse models, the intestinal injury was triggered. Meanwhile, we reported that MEG3 was greatly decreased in vivo, with an increase of miR-129-5p and inhibition of SP-D. Then, MEG3 was overexpressed, and we found that its overexpression repressed the intestinal injury via downregulating miR-129-5p in sepsis mice. Moreover, TNF-a and IL-6 expression was elevated in intestinal tissues compared to the control groups. MEG3 restrained the activation of TNF-a and IL-6, in sepsis models. Subsequently, to induce the inflammatory injury of sepsis, human colorectal Caco2 cells were treated with 10 ng/ml LPS. 10 ng/ml LPS significantly inhibited Caco2 cell proliferation and increased the apoptosis. Additionally, MEG3 was decreased whereas miR-129-5p was obviously increased in Caco2 cells incubated with LPS. Interestingly, we showed that MEG3 repressed cell apoptosis partly and enhanced Caco2 cell proliferation. miR-129-5p overexpression could reverse the effect of MEG3 in vitro. Previously, we proved SP-D was reduced in sepsis and it depressed the intestinal injury in vivo. Finally, the correlation among MEG3, miR-129-5p, and SP-D was predicted and confirmed in our investigation. These findings indicated that MEG3 might be a potential target for intestinal damage caused by sepsis via regulating miR-129-5p and SP-D.		Mediators Inflamm. 2020 Jan 22;2020:8232734. doi: 10.1155/2020/8232734. eCollection 2020.
5647	LncRNA	MEG3	miR-129-5p	SP-D	Caco2 Cell	Sepsis	Mus musculus (mouse)	qRT-PCR 	32410866	MEG3 Alleviated LPS-Induced Intestinal Injury in Sepsis by Modulating miR-129-5p and Surfactant Protein D.	Sepsis and intestinal injury triggered by sepsis are common in intensive care units, which can contribute to a high mortality. lncRNAs can modulate gene expression, and they are closely involved in multiple diseases, including sepsis. In our present study, we investigated the biological function of MEG3 in sepsis, especially during the intestinal injury. Currently, we observed that in LPS-induced sepsis mouse models, the intestinal injury was triggered. Meanwhile, we reported that MEG3 was greatly decreased in vivo, with an increase of miR-129-5p and inhibition of SP-D. Then, MEG3 was overexpressed, and we found that its overexpression repressed the intestinal injury via downregulating miR-129-5p in sepsis mice. Moreover, TNF-a and IL-6 expression was elevated in intestinal tissues compared to the control groups. MEG3 restrained the activation of TNF-a and IL-6, in sepsis models. Subsequently, to induce the inflammatory injury of sepsis, human colorectal Caco2 cells were treated with 10 ng/ml LPS. 10 ng/ml LPS significantly inhibited Caco2 cell proliferation and increased the apoptosis. Additionally, MEG3 was decreased whereas miR-129-5p was obviously increased in Caco2 cells incubated with LPS. Interestingly, we showed that MEG3 repressed cell apoptosis partly and enhanced Caco2 cell proliferation. miR-129-5p overexpression could reverse the effect of MEG3 in vitro. Previously, we proved SP-D was reduced in sepsis and it depressed the intestinal injury in vivo. Finally, the correlation among MEG3, miR-129-5p, and SP-D was predicted and confirmed in our investigation. These findings indicated that MEG3 might be a potential target for intestinal damage caused by sepsis via regulating miR-129-5p and SP-D.		Mediators Inflamm. 2020 Jan 22;2020:8232734. doi: 10.1155/2020/8232734. eCollection 2020.
5648	LncRNA	NR2F1-AS1	miR-371a-3p	TOB1	Colorectal Cancer Cells	Colorectal Cancer	Homo sapiens (human)  	qRT-PCR 	32407174	LncRNA NR2F1-AS1 Regulates miR-371a-3p/TOB1 Axis to Suppress Proliferation of Colorectal Cancer Cells.	A recent study reported the oncogenic function of lncRNA NR2F1-AS1 in liver cancer. Interestingly, by analyzing TCGA data set, downregulation of NR2F1-AS1 in colorectal cancer (CRC) was observed. This observation triggered interest to analyze the functions of NR2F1-AS1 in CRC. It was observed that NR2F1-AS1 was downregulated in CRC and predicted poor survival. NR2F1-AS1 can directly interact with miR-371a-3p but their overexpression failed to affect the expression of each other. However, NR2F1-AS1 overexpression led to the upregulation of TOB1, a target of miR-371a-3p. Cell proliferation analysis revealed reduced proliferation rate of CRC cells after NR2F1-AS1 and TOB1 overexpression. MiR-371a-3p overexpression played an opposite role and reduced the effects of NR2F1-AS1 and TOB1 overexpression. In conclusion, NR2F1-AS1 regulates miR-371a-3p/TOB1 axis to suppress proliferation of CRC cells.	NA	Cancer Biother Radiopharm. 2020 Dec;35(10):760-764. doi: 10.1089/cbr.2019.3237. Epub 2020 May 14.
5649	LncRNA	SOX2-OT	miR-452-5p	HMGB3	Prostate Cancer Cells	Prostate Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;qRT-PCR;RNA immunoprecipitation;Western blot;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;	32407168	Long Noncoding RNA SOX2-OT Knockdown Inhibits Proliferation and Metastasis of Prostate Cancer Cells Through Modulating the miR-452-5p/HMGB3 Axis and Inactivating Wnt/b-Catenin Pathway.	Background: Recent studies have proven that abnormal expression of long noncoding RNAs (lncRNAs) often contributes to growth and invasion of cancer cells. The purpose of this study was to investigate the biological function and regulatory mechanism of lncRNA SOX2 overlapping transcript (SOX2-OT) in prostate cancer (PCa) progression. Materials and Methods: The expression of SOX2-OT, microRNA-452-5p (miR-452-5p), and high mobility group box 3 (HMGB3) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Flow cytometry was performed to determine the cell cycle distribution. Western blot assay was conducted to measure the protein levels of cyclin D1, p21, p27, E-cadherin, vimentin, and N-cadherin. The interaction between miR-452-5p and SOX2-OT or HMGB3 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. The mice xenograft model was established to investigate the role of SOX2-OT in vivo. Results: SOX2-OT and HMGB3 were upregulated, whereas miR-452-5p was downregulated in PCa tissues and cells. Knockdown of SOX2-OT inhibited PCa cell growth and metastasis. MiR-452-5p could directly bind to SOX2-OT and its knockdown reversed the inhibitory effects of SOX2-OT interference on growth and metastasis of PCa cells. HMGB3 was a direct target of miR-452-5p and its knockdown weakened the promotive effects of miR-452-5p silence on growth and metastasis of PCa cells. Moreover, HMGB3 expression was inversely regulated by miR-452-5p and positively modulated by SOX2-OT. Furthermore, SOX2-OT activated the Wnt/b-catenin signaling pathway through increasing HMGB3 expression. Finally, SOX2-OT knockdown hindered tumor growth in vivo by regulating miR-452-5p/HMGB3 axis. Conclusions: SOX2-OT downregulation limited PCa cell growth and metastasis by regulating miR-452-5p/HMGB3 axis and inactivating Wnt/b-catenin signaling pathway, which might offer lncRNA-directed diagnosis and therapy for PCa.	NA	Cancer Biother Radiopharm. 2020 Nov;35(9):682-695. doi: 10.1089/cbr.2019.3479. Epub 2020 May 14.
5650	LncRNA	FOXD3-AS1	miR-127-3p	FJX1	Melanoma Cells	Melanoma	Homo sapiens (human)  	qPCR;RT-qPCR;RNA immunoprecipitation;Western blot;RNA immunoprecipitation;Rescue assay;	32354225	FOXD3-AS1 Contributes to the Progression of Melanoma Via miR-127-3p/FJX1 Axis.	Background: Melanoma, belonging to a kind of skin cancer, takes a big part in cancer-associated deaths globally. Abundant documents have recorded the crucial roles of long noncoding RNA (lncRNA) in the initiation and development of tumors. lncRNA forkhead box D3 antisense RNA 1 (FOXD3-AS1) has been commonly identified as a key regulator in the progression of multiple cancers; however, the way it exerts function remains obscure in melanoma. Materials and Methods: FOXD3-AS1 expression was examined by RT-qPCR. The role of FOXD3-AS1 in melanoma was determined by 5-ethynyl-2'-deoxyuridine (EdU), transwell, and Western blot assays. The combination between microRNA-127-3p and FOXD3-AS1 (or four jointed box 1 [FJX1]) was confirmed by luciferase reporter and RNA immunoprecipitation assays. Results: FOXD3-AS1 was markedly upregulated in melanoma cells. It was validated by loss-of-function assays that cell proliferation and migration were inhibited by FOXD3-AS1 deficiency, while cell apoptosis was facilitated by FOXD3-AS1 knockdown in melanoma. Mechanistic exploration testified that miR-127-3p could bind to FOXD3-AS1 and its expression was negatively modulated by FOXD3-AS1 in melanoma. Besides, overexpression of miR-127-3p repressed melanoma progression. Moreover, miR-127-3p was certified to negatively regulate the expression of the FJX1, and miR-127-3p could combine with FJX1 in melanoma cells. Rescue assays depicted that FJX1 overexpression countervailed FOXD3-AS1 silencing-mediated inhibition on melanoma progression. Conclusions: Overall, FOXD3-AS1 contributes to the progression of melanoma via miR-127-3p/FJX1 axis.	NA	Cancer Biother Radiopharm. 2020 Oct;35(8):596-604. doi: 10.1089/cbr.2019.3093. Epub 2020 Apr 30.
5651	LncRNA	RUSC1-AS1	miR-744	Bcl-2	Cervical Cancer Cells	Cervical Cancer	Homo sapiens (human)  	qRT-PCR 	32264732	Long noncoding RNA RUSC1-AS1 promotes tumorigenesis in cervical cancer by acting as a competing endogenous RNA of microRNA-744 and consequently increasing Bcl-2 expression.	The expression of a long noncoding RNA termed RUSC1-AS1 is dysregulated in breast cancer and laryngeal squamous cell carcinoma, and this dysregulation affects various tumor-associated biological processes. To our knowledge, the expression status and detailed roles of RUSC1-AS1 in cervical cancer as well as its regulatory mechanisms of action remain unknown. Therefore, the objectives of this study were to measure RUSC1-AS1 expression in cervical cancer, investigate the effects of RUSC1-AS1 on cervical cancer cells, and identify the mechanism underlying these effects. Herein, RUSC1-AS1 was found to be highly expressed in cervical cancer tissues and cell lines. High RUSC1-AS1 expression significantly correlated with the International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and shorter overall survival among the patients with cervical cancer. Functional assays revealed that interference with RUSC1-AS1 expression suppressed cervical cancer cell proliferation, migration, and invasion in vitro; induced apoptosis in vitro; and impeded tumor growth in vivo. In addition, RUSC1-AS1 was demonstrated to act as a competing endogenous RNA of microRNA-744 (miR-744) and consequently increase B-cell lymphoma 2 (Bcl-2 or BCL2) expression levels in cervical cancer cells. Furthermore, either inhibition of miR-744 or restoration of Bcl-2 expression neutralized the effects of the RUSC1-AS1 silencing on the malignant characteristics of cervical cancer cells. Thus, RUSC1-AS1 promotes the aggressiveness of cervical cancer in vitro and in vivo by upregulating miR-744-Bcl-2 axis output. The RUSC1-AS1-miR-744-Bcl-2 pathway may be involved in cervical cancer pathogenesis and could serve as a novel target for anticancer therapies.	NA	Cell Cycle. 2020 May;19(10):1222-1235. doi: 10.1080/15384101.2020.1749468. Epub 2020 Apr 8.
5652	LncRNA	HIF1a-AS2	miR-29b-3p	c-FOS	Mouse Muscle And Plasma	Muscle Atrophy	Mus musculus (mouse)	qRT-PCR 	32233025	Muscle atrophy-related myotube-derived exosomal microRNA in neuronal dysfunction: Targeting both coding and long noncoding RNAs.	In mammals, microRNAs can be actively secreted from cells to blood. miR-29b-3p has been shown to play a pivotal role in muscle atrophy, but its role in intercellular communication is largely unknown. Here, we showed that miR-29b-3p was upregulated in normal and premature aging mouse muscle and plasma. miR-29b-3p was also upregulated in the blood of aging individuals, and circulating levels of miR-29b-3p were negatively correlated with relative appendicular skeletal muscle. Consistently, miR-29b-3p was observed in exosomes isolated from long-term differentiated atrophic C2C12 cells. When C2C12-derived miR-29b-3p-containing exosomes were uptaken by neuronal SH-SY5Y cells, increased miR-29b-3p levels in recipient cells were observed. Moreover, miR-29b-3p overexpression led to downregulation of neuronal-related genes and inhibition of neuronal differentiation. Interestingly, we identified HIF1a-AS2 as a novel c-FOS targeting lncRNA that is induced by miR-29b-3p through down-modulation of c-FOS and is required for miR-29b-3p-mediated neuronal differentiation inhibition. Our results suggest that atrophy-associated circulating miR-29b-3p may mediate distal communication between muscle cells and neurons.	NA	Aging Cell. 2020 May;19(5):e13107. doi: 10.1111/acel.13107. Epub 2020 Mar 31.
5653	LncRNA	XIST	miR-889-3p	SIX1	Cc Tissues And Cells	Cervical Cancer	Homo sapiens (human)  	Flow cytometry assay;RNA immunoprecipitation;Western blot;Flow Cytometry assay;RNA immunoprecipitation;	32191528	Long Noncoding RNA XIST Contributes to Cervical Cancer Development Through Targeting miR-889-3p/SIX1 Axis.	Background: Cervical cancer (CC) is one of the most common cancers among women in the world. Long noncoding RNAs and microRNAs were identified as important regulators in many physiological processes. The objective of this study was to illuminate the mechanism of X-inactive-specific transcript (XIST)/miR-889-3p/Sine oculis homeobox 1 (SIX1) axis in CC. Methods: The expression levels of XIST, miR-889-3p, and SIX1 were detected by quantitative real-time polymerase chain reaction. Cell proliferation was assessed by cell counting Kit 8 assay. Cell migration and invasion were evaluated by transwell assay. Cell apoptosis was detected by flow cytometry assay. Murine model was established using transfected Me180 cell. The interaction among XIST, miR-889-3p, and SIX1 was tested by dual-luciferase reporter and RNA immunoprecipitation assays. Protein level of SIX1 was measured by Western blot. Results: XIST was highly expressed in CC tissues and cells. Silenced XIST inhibited proliferation, migration, and invasion and induced apoptosis. Moreover, XIST silencing blocked tumor growth in vivo. XIST directly bound to miR-889-3p, and XIST promoted proliferation, migration, and invasion and hindered apoptosis by suppressing miR-889-3p expression. MiR-889-3p targeted SIX1 and negatively regulated SIX1 expression. Furthermore, miR-889-3p had a low expression and SIX1 had a high expression in CC tissues and cells. XIST knockdown reduced SIX1 level by targeting miR-889-3p. In addition, miR-889-3p inhibition abolished the effects of SIX silencing on proliferation, migration, invasion, and apoptosis. Conclusion: XIST knockdown restrained cell proliferation, migration, and invasion and promoted apoptosis by regulating miR-889-3p/SIX1 axis.	NA	Cancer Biother Radiopharm. 2020 Nov;35(9):640-649. doi: 10.1089/cbr.2019.3318. Epub 2020 Mar 19.
5654	LncRNA	UCA1	miR-873-5p	HIF-1a	Crc Cells	Colorectal Cancer	Homo sapiens (human)  	MTT assay;MTT assay;	32143722	SNP rs12982687 affects binding capacity of lncRNA UCA1 with miR-873-5p: involvement in smoking-triggered colorectal cancer progression.	BACKGROUND: This investigation was arranged to elucidate whether single nucleotide polymorphisms (SNPs) of lncRNA UCA1 was implicated in elevating colorectal cancer (CRC) risk by interacting with environmental exposures. METHODS: LncRNASNP database was firstly adopted to predict SNPs that possibly affected binding of UCA1 with miRNAs and then the interactive effect of SNPs and environmental exposure on CRC risk was evaluated by recurring to type 2 gene-environment interactions (GEI) model. Besides, MTT assay, colony formation assay, transwell assay and wound healing assay were performed to assess the activity of CRC cell lines which carried distinct genotypes of specific SNPs. The impact of nicotine on activity of CRC cells was also appraised. RESULTS: SNP rs12982687 of UCA1 intervened in the binding capacity of UCA1 with several miRNAs, especially miR-873-5p. MiRNAs regulated by UCA1, as predicted by mirPath software, shared genes that were enriched in HIF1 signaling pathway. Moreover, homozygote TT of rs12982687 reduced CRC risk among smokers, and CRC cells that carried rs12982687 (CC) displayed strong migration and invasion. By contrast, miR-873-5p mimic, which reduced UCA1 expression, delayed metastasis of CRC cells (all P < 0.05). Additionally, nicotine not merely elevated UCA1 and HIF-1a expressions in CRC cells, but also facilitated proliferation and metastasis of CRC cells (P < 0.05). CONCLUSIONS: SNP rs12982687 was involved in smoking-triggered CRC progression, given its influence on UCA1's binding with miR-873-5p and HIF-1 signaling.	NA	Cell Commun Signal. 2020 Mar 6;18(1):37. doi: 10.1186/s12964-020-0518-0.
5655	LncRNA	LINC00574	hsa-miR-129-5p	UGT2B15	Heparg Cells	NA	Homo sapiens (human)	qRT-PCR 	32086297	Coordinated Regulation of UGT2B15 Expression by Long Noncoding RNA LINC00574 and hsa-miR-129-5p in HepaRG Cells.	Recent studies have shown that microRNAs and long noncoding RNAs (lncRNAs) regulate the expression of drug metabolizing enzymes (DMEs) in human hepatic cells and that a set of DMEs, including UDP glucuronosyltransferase (UGT) 2B15, is down-regulated dramatically in liver cells by toxic acetaminophen (APAP) concentrations. In this study we analyzed mRNA, microRNA, and lncRNA expression profiles in APAP-treated HepaRG cells to explore noncoding RNA-dependent regulation of DME expression. The expression of UGT2B15 and lncRNA LINC00574 was decreased in APAP-treated HepaRG cells. UGT2B15 levels were diminished by LINC00574 suppression using antisense oligonucleotides or small interfering RNA. Furthermore, we found that hsa-miR-129-5p suppressed LINC00574 and decreased UGT2B15 expression via LINC00574 in HepaRG cells. In conclusion, our results indicate that LINC00574 acts as an important regulator of UGT2B15 expression in human hepatic cells, providing experimental evidence and new clues to understand the role of cross-talk between noncoding RNAs. SIGNIFICANCE STATEMENT: We showed a molecular network that displays the cross-talk and consequences among mRNA, micro RNA, long noncoding RNA, and proteins in acetaminophen (APAP)-treated HepaRG cells. APAP treatment increased the level of hsa-miR-129-5p and decreased that of LINC00574, ultimately decreasing the production of UDP glucuronosyltransferase (UGT) 2B15. The proposed regulatory network suppresses UGT2B15 expression through interaction of hsa-miR-129-5p and LINC00574, which may be achieved potentially by recruiting RNA binding proteins.	NA	Drug Metab Dispos. 2020 Apr;48(4):297-306. doi: 10.1124/dmd.119.090043. Epub 2020 Feb 21.
5656	LncRNA	BDNF-AS	miR-125b-5p	NA	Sh-Sy5Y Cell Model 	Parkinsons Disease	Mus musculus (mouse)	MTT assay;qRT-PCR;Western blot;Flow Cytometry assay;MTT assay;	32057951	LncRNA BDNF-AS promotes autophagy and apoptosis in MPTP-induced Parkinson's disease via ablating microRNA-125b-5p.	BACKGROUNDS: Recently, extensive evidence has indicated that the biological role of long non-coding RNAs (lncRNAs) in neurodegenerative diseases is becoming increasingly evident. The lncRNA brain-derived neurotrophic factor anti-sense (BDNF-AS) has been found to be dysregulated in Huntington's Disease. However, the function of BDNF-AS in Parkinson's disease (PD) remains unknown. The purpose of this present study was to explore the effect of BDNF-AS on PD and its underlying molecular mechanisms. METHODS: The MPTP-induced mouse model of PD and MPP+-induced SH-SY5Y cell model were established. Immunofluorescence was performed to determine the number of TH + positive cells. Mice behavioral changes were detected by pole and rota-rod test. SH-SY5Y cells viability, apoptosis was detected by MTT assay and flow cytometry. The number of autophagosome was measured by transmission electron microscopy. Dopamine content was tested by high performance liquid chromatography. Dual-luciferase reporter gene assay was utilized to verify the correlation between BDNF-AS and miR-125b-5p. qRT-PCR and western blot were used to detect gene expression levels. RESULTS: Our results showed that BDNF-AS was up-regulated in MPTP-induced PD model and dopamine neurons, and MPP + treated SH-SY5Y cells, while miR-125b-5p was down-regulated. The expression of BDNF-AS was positively related with the MPP + concentration. BDNF-AS knockdown could significantly promote cell proliferation, while inhibit apoptosis and autophagy in SH-SY5Y cells treated by MPP + . Silencing BDNF-AS could also increase TH positive neurons and significantly suppress the autophagy of PD mice. Additionally, miR-125b-5p, a putative target gene of BDNF-AS, was involved in the effects of BDNF-AS on SH-SY5Y cell apoptosis and autophagy. CONCLUSIONS: Our study demonstrated that knockdown of BDNF-AS could elevate SH-SY5Y cell viability, inhibit autophagy and apoptosis in MPTP-induced PD models through regulating miR-125b-5p, suggesting that BDNF-AS might act as a potential therapeutic target for PD.	NA	Brain Res Bull. 2020 Apr;157:119-127. doi: 10.1016/j.brainresbull.2020.02.003. Epub 2020 Feb 10.
5657	LncRNA	lncRNA-GS1-358P8.4	has-miR-6715a-3p	KIF2C	Hcc Tissues And Adjacent Nontumor Tissues	Hepatocellular Carcinoma	Homo sapiens (human)  	microarray;luciferase assay;	32056305	Kinesin family member 2C aggravates the progression of hepatocellular carcinoma and interacts with competing endogenous RNA.	Kinesin family member 2C (KIF2C), a substantial mitotic regulator, has been verified to exert a malignant function in several cancers. However, its function in hepatocellular carcinoma (HCC) remains unclear. In this study, the expression profile of KIF2C in HCC was characterized through the dataset from the TCGA and clinical tissue microarrays containing 220 pairs of resected HCC tissues and adjacent nontumor tissues in our hospital. The results indicated that KIF2C was substantially higher expression in tumor tissues than adjacent nontumor tissues. High expression of KIF2C significantly correlated with large tumor (>5.0 cm) (P = .001) and implied a dismal postoperative overall survival (OS) (hazard ratio [HR] = 1.729; P = .002) in our cohort of patients. Gain and loss of function assays displayed that KIF2C promoted HCC cell proliferation, accelerated cell cycle progression, and impeded apoptosis. By bioinformatic tools and mechanistic investigation, we found that KIF2C interacted with various cell-cycle-related proteins and was significantly involved in growth-promoting pathways. KIF2C upregulated PCNA and CDC20 expression. Subsequently, we investigated the regulation of KIF2C by competing endogenous RNA and elucidated that has-miR-6715a-3p was directly bond to the 3'-untranslated region of KIF2C through dual luciferase assays, thereby inhibiting KIF2C expression. Furthermore, the long noncoding RNA GS1-358P8.4 was found to be a candidate of KIF2C for has-miR-6715a-3p binding. HCC patients with high lncRNA-GS1-358P8.4 expression had shorter OS and relapse-free survival compared to those with low expression, which was accordance with the KIF2C. Taken together, KIC2C aggravated HCC progression, it could serve as a prognostic indicator and confer a novel target for clinical treatment.	NA	J Cell Biochem. 2020 Nov;121(11):4419-4430. doi: 10.1002/jcb.29665. Epub 2020 Feb 14.
5658	LncRNA	OIP5-AS1	miR-363-3p	SOX4	Hcc Cells	Hepatocellular Carcinoma	Homo sapiens (human)	RIP assay;RNA pull-down assay;RNA pull-down;	32042127	LncRNA OIP5-AS1 interacts with miR-363-3p to contribute to hepatocellular carcinoma progression through up-regulation of SOX4.	Long noncoding RNA OIP5-AS1 has been observed to be increased in several cancers, however, its role and biological mechanism was poorly understood in HCC. Currently, we found OIP5-AS1 expression was upregulated in HCC cells compared with normal human liver cells. Knockdown of OIP5-AS1 suppressed HCC cell proliferation, induced cells cycle arrest and cells apoptosis. In addition, HCC cell migration and invasion capacity in vitro were also inhibited by OIP5-AS1 inhibition. Bioinformatics analysis revealed OIP5-AS1 could interact with miR-363-3p, thereby repressing HCC development. We also observed miR-363-3p was significantly decreased in HCC cells and overexpression of miR-363-3p repressed HCC progression. The correlation between OIP5-AS1 and miR-363-3p was confirmed by performing RIP assay and RNA pull-down assay. Subsequently, SOX4 was predicted as a target of miR-363-3p and miR-363-3p modulated SOX4 levels negatively in vitro. Apart from these, in vivo experiments established that OIP5-AS1 can suppress HCC development through regulating miR-363-3p and SOX4. Collectively, these demonstrated that OIP5-AS1 was involved in HCC progression via targeting miR-363-3p and SOX4. OIP5-AS1 can act as a novel candidate for HCC diagnosis, prognosis, and therapy.	NA	Gene Ther. 2019 Nov;27(10-11):495-504. doi: 10.1038/s41434-020-0123-2. Epub 2020 Feb 10.
5659	LncRNA	Gas5	miR-320-3p	Tcf3	Cardiomyocyte	Diabetic Cardiomyopathy	Mus musculus (mouse)	RNA pull-down assay;Flow Cytometry assay;Luciferase reporter assay;Rescue assay;RNA pull-down;	32003049	Tcf3-activated lncRNA Gas5 regulates newborn mouse cardiomyocyte apoptosis in diabetic cardiomyopathy.	Diabetic cardiomyopathy can cause cardiac dysfunction and eventually lead to heart failure and sudden death. Long noncoding RNA (lncRNA) Gas5 has been reported to play a function in cardiomyocyte. Here we studied the function of Gas5 on newborn mouse cardiomyocyte (NMC) apoptosis to detect its molecular mechanism. High-glucose treatment was implemented to induce the apoptosis of NMC in this study. And terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, JC-1 assay, and flow cytometry analysis were conducted to know about the apoptosis of NMC when Gas5 and Tcf3 were silenced. Meanwhile, RNA pull-down assay and luciferase reporter assay were conducted to verify the binding of RNAs. Finally, rescue assay was implemented to evaluate the influence on apoptosis situation affected by competing endogenous RNA pathways. Tcf3 was found to bind to the Gas5 promoter to activate the expression of Gas5. Meanwhile, Gas5 and Tcf3 were both found to promote the apoptosis of NMC. Also, mmu-miR-320-3p could bind to Gas5 and Tcf3. Moreover, the Gas5/miR-320-3p/Tcf3 pathway was found to modulate the apoptosis of NMC. In conclusion, Tcf3-activated lncRNA Gas5 regulates NMC apoptosis in diabetic cardiomyopathy.	NA	J Cell Biochem. 2020 Nov;121(11):4337-4346. doi: 10.1002/jcb.29630. Epub 2020 Jan 31.
5660	LncRNA	SNHG16	miR-4500	USP21	Nsclc Cell	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	31956270	The USP21/YY1/SNHG16 axis contributes to tumor proliferation, migration, and invasion of non-small-cell lung cancer.	Deubiquitinases (DUBs) and noncoding RNAs have been the subjects of recent extensive studies regarding their roles in lung cancer, but the mechanisms involved are largely unknown. In our study, we used The Cancer Genome Atlas data set and bioinformatics analyses and identified USP21, a DUB, as a potential contributor to oncogenesis in non-small-cell lung cancer (NSCLC). We further demonstrated that USP21 was highly expressed in NSCLCs. We then conducted a series of in vitro and in vivo assays to explore the effect of USP21 on NSCLC progression and the underlying mechanism involved. USP21 promoted NSCLC cell proliferation, migration, and invasion and in vivo tumor growth by stabilizing a well-known oncogene, Yin Yang-1 (YY1), via mediating its deubiquitination. Furthermore, YY1 transcriptionally regulates the expression of SNHG16. Moreover, StarBase bioinformatics analyses predicted that miR-4500 targets SNHG16 and USP21. A series of in vitro experiments indicated that SNHG16 increased the expression of USP21 through miR-4500. In summary, the USP21/YY1/SNHG16 axis plays a role in promoting the progression of NSCLC. Therefore, the USP21/YY1/SNHG16/miR-4500 axis may be a potential therapeutic target in NSCLC treatment.	NA	Exp Mol Med. 2020 Jan;52(1):41-55. doi: 10.1038/s12276-019-0356-6. Epub 2020 Jan 20.
5661	LncRNA	SNHG16	miR-4500	YY1	Nsclc Cell	Non-Small Cell Lung Cancer	Homo sapiens (human)  	qRT-PCR 	31956270	The USP21/YY1/SNHG16 axis contributes to tumor proliferation, migration, and invasion of non-small-cell lung cancer.	Deubiquitinases (DUBs) and noncoding RNAs have been the subjects of recent extensive studies regarding their roles in lung cancer, but the mechanisms involved are largely unknown. In our study, we used The Cancer Genome Atlas data set and bioinformatics analyses and identified USP21, a DUB, as a potential contributor to oncogenesis in non-small-cell lung cancer (NSCLC). We further demonstrated that USP21 was highly expressed in NSCLCs. We then conducted a series of in vitro and in vivo assays to explore the effect of USP21 on NSCLC progression and the underlying mechanism involved. USP21 promoted NSCLC cell proliferation, migration, and invasion and in vivo tumor growth by stabilizing a well-known oncogene, Yin Yang-1 (YY1), via mediating its deubiquitination. Furthermore, YY1 transcriptionally regulates the expression of SNHG16. Moreover, StarBase bioinformatics analyses predicted that miR-4500 targets SNHG16 and USP21. A series of in vitro experiments indicated that SNHG16 increased the expression of USP21 through miR-4500. In summary, the USP21/YY1/SNHG16 axis plays a role in promoting the progression of NSCLC. Therefore, the USP21/YY1/SNHG16/miR-4500 axis may be a potential therapeutic target in NSCLC treatment.	NA	Exp Mol Med. 2020 Jan;52(1):41-55. doi: 10.1038/s12276-019-0356-6. Epub 2020 Jan 20.
5662	LncRNA	MSC-AS1	miR-3924	WNT5A	Kirc Cells	Kidney Renal Clear Cell Carcinoma	Homo sapiens (human)  	Rescue assay;	31916281	lncRNA MSC-AS1 activates Wnt/b-catenin signaling pathway to modulate cell proliferation and migration in kidney renal clear cell carcinoma via miR-3924/WNT5A.	Kidney renal clear cell carcinoma (KIRC) is the most general subtype of renal cell carcinoma, which composes about 1/20 of adult malignancies. The anomaly of long noncoding RNAs (lncRNAs) expression is proved to mediate cancer progression of various types. The function and mediation mechanism of MSC-AS1 has rarely been detected in KIRC before. This study started with the mediation of MSC-AS1 on cell function. In this study, MSC-AS1 was dramatically upregulated in KIRC and correlated with dismal prognosis of KIRC patients. Knockdown of MSC-AS1 would suppress the proliferative and migratory properties of KIRC cells. MSC-AS1 was found to directly downregulate miR-3924 expression while miR-3924 directly downregulated WNT5A expression. Meanwhile, MSC-AS1 could promote the expression of WNT5A, indicating the existence of MSC-AS1/miR-3924/WNT5A. Further assays indicated that MSC-AS1 could enhance Wnt/b-catenin pathway. By means of rescue assays, the mediation of MSC-AS1/miR-3924/WNT5A/b-catenin axis on KIRC cell proliferation, migration and migration was verified. This study revealed that MSC-AS1 regulates KIRC cell proliferation and migration via miR-3924/WNT5A/b-catenin axis. MSC-AS1 might contribute to new strategies for KIRC treatment.	NA	J Cell Biochem. 2020 Oct;121(10):4085-4093. doi: 10.1002/jcb.29594. Epub 2020 Jan 9.
5663	LncRNA	HOTTIP	miR-124-3p	HMGA2	Otscc Cells	Oral Tongue Squamous Cell Carcinoma	Homo sapiens (human)	Dual-luciferase reporter assay;Western blot;Luciferase reporter assay;	31910357	Downregulation of lncRNA HOTTIP Suppresses the Proliferation, Migration, and Invasion of Oral Tongue Squamous Cell Carcinoma by Regulation of HMGA2-Mediated Wnt/b-Catenin Pathway.	Background: Oral tongue squamous cell carcinoma (OTSCC) is a common type of oral tumor. LncRNAs (long noncoding RNAs) and miRNAs (microRNAs) were identified as regulators in many human cancers. This study aims to explore the molecular basis of HOXA transcript at the distal tip (HOTTIP) in regulating OTSCC progression. Materials and Methods: The expression of HOTTIP, miR-124-3p, and high-mobility group AT-hook 2 (HMGA2) was detected by quantitative real-time polymerase chain reaction. Next, the proliferation was evaluated by 3-(4,5-dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) assay. The migration and invasion were assessed by transwell assay. Furthermore, dual-luciferase reporter assay was performed to confirm the combination between HOTTIP and miR-124-3p, miR-124-3p, and HMGA2. Protein levels of HMGA2, b-catenin, c-Myc, and E-cadherin were examined by Western blot. The nude mice model was employed to test the tumor growth in vivo. Results: HOTTIP was upregulated in OTSCC tissues and cells, and was highly expressed in positive lymph node metastasis and late-stage OTSCC patients. Silencing HOTTIP impeded proliferation, migration, and invasion of OTSCC cells. Moreover, HOTTIP knockdown inhibited proliferation, migration, and invasion of OTSCC cells by targeting miR-124-3p. Besides, miR-124-3p targeted HMGA2 to block proliferation, migration, and invasion. HMGA2 could rescue the inhibitory effects of HOTTIP interference on proliferation, migration, and invasion. In addition, HMGA2 overexpression reversed the downregulation of b-catenin and c-Myc protein levels and upregulation of E-cadherin level affected by HOTTIP silencing. Finally, HOTTIP silencing repressed tumor growth and resulted in a great rise on miR-124-3p and E-cadherin expression and a distinct fall on HMGA2, b-catenin, and c-Myc protein levels. Conclusions: HOTTIP knockdown restrained proliferation, migration, and invasion of OTSCC cells by miR-124-3p/HMGA2 axis through Wnt/b-catenin pathway.	NA	Cancer Biother Radiopharm. 2020 Nov;35(9):720-730. doi: 10.1089/cbr.2019.3017. Epub 2020 Jan 8.
5664	LncRNA	PART1	miR-150-5p	LRG1	Colorectal Cancer Cells	Colorectal Cancer	Mus musculus (mouse)	qRT-PCR 	31898365	LncRNA PART1 facilitates the malignant progression of colorectal cancer via miR-150-5p/LRG1 axis.	Study has shown that long noncoding RNA (lncRNA) prostate androgen-regulated transcript 1 (PART1) was elevated in colorectal cancer tissues and cells, and the proliferation and metastasis of colorectal cancer cells were reduced after its downregulation. The tumor-suppressive role of microRNA-150-5p (miR-150-5p) has been shown in colorectal cancer. In this study, the association between PART1 and miR-150-5p in colorectal cancer was analyzed. Results revealed an increase of PART1, but a decrease of miR-150-5p in 56 colorectal cancer tissues. And there was a strong negative correlation between levels of PART1 and miR-150-5p in these cancer samples. Also, compared with 10 healthy controls, the level of PART1 was increased, whereas miR-150-5p expression was diminished in the serum of 10 colorectal cancer patients. Cell proliferation and migration, along with epithelial-mesenchymal transition, was promoted by PART1 overexpression. However, this lncRNA mitigated apoptosis of colorectal cancer cells. Whereas miR-150-5p mimic abrogated these effects caused by PART1 overexpression. The influences of PART1 knockdown on the above malignant characteristics of colorectal cancer cells were contrary to its overexpression. miR-150-5p inhibitor ablated the effects induced by PART1 knockdown. In xenograft mouse models, silencing of PART1 decreased tumor volume and weight. Our data supported that lncRNA PART1 may regulate leucine-rich a-2-glycoprotein-1 (LRG1) expression through a competing interaction mechanism that hindering miR-150-5p function. In conclusion, PART1 facilitates the malignant progression of colorectal cancer via miR-150-5p/LRG1 pathway. The study further clarified the molecular mechanism of PART1 in colorectal cancer. This study may provide a new approach to diagnose and treat colorectal cancer.	NA	J Cell Biochem. 2020 Oct;121(10):4271-4281. doi: 10.1002/jcb.29635. Epub 2020 Jan 3.
5665	LncRNA	GAS5	miR-21-5p	TLR4	Human Cardiomyocyte-Like Ac16 Cells	Diabetic Cardiomyopathy	Homo sapiens (human)	qRT-PCR 	31865425	Knockdown of long noncoding RNA GAS5 protects human cardiomyocyte-like AC16 cells against high glucose-induced inflammation by inhibiting miR-21-5p-mediated TLR4/NF-kB signaling.	Diabetic cardiomyopathy (DCM) is a common cause of disability and death among diabetic patients. In this study, we aimed to identify the functional role of long noncoding RNA GAS5 in human cardiomyocyte-like AC16 cells under high glucose (HG) condition. The results showed that HG treatment induced damage in AC16 cells by decreasing cell viability and increasing cell apoptosis. We also found that HG increased GAS5 expression in AC16 cells and knockdown of GAS5 protected AC16 cells from HG-induced injury. Furthermore, we confirmed that GAS5 could competitively bind with miR-21-5p and miR-21-5p inhibition alleviated the beneficial effects of GAS5 knockdown against HG stimulation. TLR4 was identified as a target of miR-21-5p in AC16 cells, and GAS5 knockdown alleviated HG-induced inflammation partly by inhibiting miR-21-5p-mediated TLR4/NF-kB signaling. Our results suggested that GAS5/miR-21-5p axis may serve as a candidate therapeutic target for DCM.	NA	Naunyn Schmiedebergs Arch Pharmacol. 2020 Aug;393(8):1541-1547. doi: 10.1007/s00210-019-01795-z. Epub 2019 Dec 21.
5666	LncRNA	KCNQ1OT1	miR-204	EphA7	Imc-3	Maxillary Sinus Squamous Cell Carcinoma	Homo sapiens (human)  	luciferase assay;	31709597	Long noncoding RNA KCNQ1OT1 promotes proliferation, migration, and invasion in maxillary sinus squamous cell carcinoma by regulating miR-204/EphA7 axis.	Long noncoding RNAs have been demonstrated to contribute to the development and progression of various cancers. However, the underlying regulatory mechanisms of KCNQ1OT1 in tumorigenesis of maxillary sinus squamous cell carcinoma (MSSCC) remain unknown. Herein, we found that KCNQ1OT1 expression was markedly upregulated in MSSCC tissues and MSSCC cell line (IMC-3) by using quantitative reverse transcription-polymerase chain reaction. Loss-of-function experiments revealed that the deletion of KCNQ1OT1 inhibited cell proliferation, migration, and invasion. Moreover, we confirmed KCNQ1OT1 could directly interact with miR-204 by bioinformatic prediction and dual luciferase assay, and miR-204 inhibitor markedly reversed MSSCC tumor phenotypes induced by shKCNQ1OT1. Finally, we demonstrated that KCNQ1OT1/miR-204 facilitated MSSCC progression by regulating Eph receptor A7 (EphA7). Taken together, these results revealed a novel regulatory mechanism KCNQ1OT1/miR-204/EphA7 axis, which could provide a new understanding of MSSCC tumorigenesis and develop potential targets for MSSCC therapy.	NA	J Cell Biochem. 2020 Apr;121(4):2962-2969. doi: 10.1002/jcb.29548. Epub 2019 Nov 10.
5667	Pseudogene	HSPB1P1	miR-296-5p	HMGA1	Rcc Cells	Renal Cancer	Homo sapiens (human)  	Dual-luciferase reporter assay;RNA immunoprecipitation;Luciferase reporter assay;RNA immunoprecipitation;	34431162	Pseudogene HSPB1P1 contributes to renal cell carcinoma proliferation and metastasis by targeting miR-296-5p to regulate HMGA1 expression.	With the aid of next-generation sequencing technology, pseudogenes have been widely recognized as functional regulators in the development and progression of certain diseases, especially cancer. Our present study aimed to investigate the functions and molecular mechanisms of HSPB1-Associated Protein 1 Pseudogene 1 (HSPB1P1) in renal cell carcinoma (RCC). HSPB1P1 expression at the mRNA levels was determined by quantitative real-time polymerase chain reaction, and its clinical significance was assessed. Cell viability was detected by cell counting kit-8 assay. Cell migration and invasion were detected by Transwell assays. Location of HSPB1P1 in RCC cells was detected by subcellular distribution analysis. The direct relationship between HSPB1P1 and miR-296-5p/HMGA1 axis was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Our results identify the elevated expression of HSPB1P1 in RCC tissues and cell lines, which predicted advanced progression and poor prognosis in patients with RCC. Knockdown of HSPB1P1 suppressed cell proliferation, migration and invasion and reversed epithelial-mesenchymal transition process in RCC. HSPB1P1 was mostly enriched in the cytoplasm and functioned as a miRNA sponge for miR-296-5p and then regulated high-mobility group A1 expression. In conclusion, our study indicated that HSPB1P1 contributed to RCC progression by targeting miR-296-5p/HMGA1 axis, and should be considered as a promising biomarkers and therapeutic target for clinical applications. This article is protected by copyright. All rights reserved.	NA	Cell Biol Int. 2021 Aug 25. doi: 10.1002/cbin.11694.
